DNA is not always negatively supercoiled naturally. It is important to keep in mind that different regions of topologically constrained DNA can have different supercoiling values. For example, the action of unwinding DNA for transcription or replication introduces positive supercoils ahead of the polymerase and negative supercoils behind it.

Additionally, supercoiling is present in DNA normally. Supercoiling is the result of more or less twist in a DNA helix, which is most stable when it has ~10.5 bp/turn (for B-DNA). Supercoiling allows under- or overwound DNA to return to its most stable twist. Negative supercoiling is the result of underwound DNA. Underwound DNA is not thremodynamically favourable and will actually lower the melting point of DNA (the point where strand separation occurs). This can be compensated by introducing supercoils but it is also important for processes such transcription, which require ssDNA. Negative supercoils and ssDNA can be thought of as interchangeable. Negative supercoils are also used to package DNA around histones in eukaryotes and archaea. On the other hand, positive supercoiling is the result of overwound DNA (also not thermodynamically favourable) and will increase the melting point of DNA. Positive supercoiling is often found in thermophiles which live at higher temperatures and need to prevent their DNA from melting excessively. It has also been suggested that positive supercoiling can play a role in regulation of gene expression (by inhibiting promoter melting). Organisms like to keep an approximately constant amount of supercoiling in their DNA for the above reasons; this is called the superhelical density and is characteristic of different classes of organisms.


Can a human cell live indefinetely in a controlled environment?

This question is at least two questions.

Dividing cells

In terms of a dividing human cell line, every time a division occurs the telomeres capping the ends of the chromosomes get a little bit shorter. Once the telomeres get short enough they act as a signal that triggers apoptosis, destroying the cell. There is some human-to-human variation in the initial length of the telomeres, but the impression I've gotten from hanging around cell biologists is that the division limit is somewhere on the order of 10-100.

There are also cells in which the activity of a protein called telomerase is upregulated. Telomerase is a type of polymerase (an enzyme that synthesizes DNA) that acts to add extra length to telomeres. Telomerase+ cells are not affected by the division limit in the normal way. Some examples of telomerase+ cells are stem cells and many kinds of cancer cells.

Stationary cells

In a very real sense, a cell "dies" when it divides. Upon division a cell splits into two daughter cells, but it cannot be said that either daughter cell "is" the original cell. So a more satisfying way to answer to the original question would be to look at how long a single cell can be kept as-is and recognizably alive (i.e. in stationary phase).

If you cheat and freeze the cell at liquid nitrogen temperatures (78 K), then there are plenty of examples of cells surviving for decades, in the sense that a culture can be stored and then thawed, and normal life processes will resume at least some of the time.

Sadly, there may not be a proper answer out there to this version of the question. A quick lit search did not turn up much. It is thought that at least some cells (in particular neurons) last for decades in the human body without dividing, although this is unsurprisingly hard to prove.


What is the distance between the insertion of the distal end of the bicep tendon and the head of the radius?

From {1}:

  Abstract
  PURPOSE:
  There is little information in the literature describing the anatomy of the biceps tendon insertion. The purpose of this study was to map the footprint of the biceps tendon insertion on the bicipital tuberosity and to report on the relevant anatomy to assist surgeons with correct tendon orientation during surgical repair.
  METHODS:
  Fifteen fresh-frozen adult upper extremities were used in this study. The relationships between the long head of the biceps tendon, the short head of the biceps tendon, the muscle bellies, and the distal tendon orientation were examined. The length, width, and area of the biceps tendon insertion were measured.
  RESULTS:
  In all specimens examined, the biceps musculotendinous unit rotated 90 degrees externally from origin to insertion. The long head of the distal tendon was inserted onto the proximal aspect of the bicipital tuberosity, while the short head of the distal tendon was inserted onto the distal aspect of the tuberosity. The lacertus fibrosus, in all specimens, originated from the distal short head of the biceps tendon. On average, the biceps tendon insertion started 23 mm distal to the articular margin of the radial head. The average length of the biceps tendon insertion on the tuberosity was 21 mm, and the average width was 7 mm. The average total area of the biceps tendon insertion (footprint) was 108 mm(2). The average area of the long head of the biceps tendon insertion was 48 mm(2), and the average area of the short head of the biceps tendon insertion was 60 mm(2).
  CONCLUSIONS:
  Landmarks have been identified that will allow anatomic orientation of the distal biceps tendon during operative repair. The distal short head of the biceps tendon has a consistent relationship with the lacertus fibrosus and a distinct insertion on the bicipital tuberosity. The dimensions of the distal biceps tendon footprint have been determined to assist with bone tunnel or suture anchor placement during surgical repair.

(bicipital tuberosity = radial tuberosity)

Some figures from the same study:

FYI:

How correlated are the lengths of tendons in different part of a human body?
How can I measure my tendon length?

References:

{1} Athwal, George S., Scott P. Steinmann, and Damian M. Rispoli. "The distal biceps tendon: footprint and relevant clinical anatomy." The Journal of hand surgery 32, no. 8 (2007): 1225-1229. https://www.ncbi.nlm.nih.gov/pubmed/17923307 ; https://scholar.google.com/scholar?cluster=16116840451671820399&hl=en&as_sdt=0,22 ; http://www.sciencedirect.com/science/article/pii/S0363502307005163 ; http://dx.doi.org/10.1016/j.jhsa.2007.05.027 ; http://sci-hub.cc/10.1016/j.jhsa.2007.05.027


What evolutionary reason is there for hemolytic disease?

Hemolytic disease is not a genetic disease. It is a drawback of how the immune system works. In general, the overall benefits of having the immune system as it is right now are way higher than sporadic disadvantages, like the Hemolytic disease, that is why it is not counter selected. If instead of being a rare condition it would be a common one, then I would expect it to be indeed counter selected.


For allele frequency determination, is it good to take samples from a college/school or a hospital or any other technique?

I suggest this as a starting point.

Basically, if your aim is to determine the population frequency of the alleles, then you should sample from the population.
A possible problem with the university is the age stratification, but also possible different proportion of ethnic groups compared to general population. Also hospital might be biased, because you will have a higher prevalence of people with health issues.
The best thing is to randomly collect samples from the population (but I know it is very hard, especially because you can sample randomly, but the ratio of people willing to give you their blood will be biased!).

One thing that is commonly accepted is to retrieve data from healthy blood donors (which is not unbiased, but is accepted!).
You can give a look at a paper I published a lot of time ago. In that case, the estimation of haplotype frequency was performed on the bone marrow donors registry, and it was considered perfectly fine.

Good luck!


Dimethyltryptamine binding site on Sigma 1 type opioid receptor?

There is no definitive answer to this question since the 3D structure of the receptor has not been determined. In this paper;

  Laurini et al. (2012) Another Brick in the Wall. Validation of the σ1 Receptor 3D Model by Computer-Assisted Design, Synthesis, and Activity of New σ1 Ligands. Molecular Pharmaceutics 9:3107-3126

the authors report the analysis of their molecular model of the receptor. They design 33 new ligands for the putative binding site with binding affinities across five orders of magnitude and then go on to show that the experimentally-determined affinities are in very good agreement with their in silico studies. The paper provides lots of information about the proposed binding site. The paper also describes the use of in silico alanine scanning mutagenesis to assess the relative importance of residues proposed to form the binding site: these are D126,I128,T151,V152,E172,Y173 and L182. Of these D126 and Y173 seem to be critical.

I must stress that this work does not directly investgate the binding of dimethyltryptamine, and the ligands that are used are not based on an indole ring structure. The molecular model used by the authors was first published in an earlier paper.

  Laurini et al. (2011) Homology Model and Docking-Based Virtual Screening for Ligands of the sigma(1) Receptor ACS Medicinal Chemistry Letters 2:834-839

I tried to find out if that paper looks at dimethyltryptamine but unfortunately there seems to be a broken link at the source. Here is the abstract of that paper:

  This study presents for the first time the 3D model of the sigma(1) receptor protein as obtained from homology modeling techniques, shows the applicability of this structure to docking-based virtual screening, defines a computational strategy to optimize the results based on a combination of 3D pharmacophore-based docking and MM/PBSA free energy of binding scoring, and provides evidence that these in silico models and recipes are powerful tools on which virtual screening of new sigma(1) ligands can be based. In particular, the validation of the applicability of docking-based virtual screening to homology models is of utmost importance, since no crystal structure is available to date for the sigma(1) receptor, and this missing information still constitutes a major hurdle for a rational ligand design for this important protein target.


Alleles are variations of a same locus that codes for a protein (gene). These alleles can come in different forms, one of which is SNP. For example, sickle cell anemia arises from an allele of the beta-globin gene which has had a change from A to T.
Meanwhile, for the ABO gene that determines your blood group, the O allele has a missing nucleotide (G) that leads to a frameshift in the gene and a loss of function.
So alleles are caused by SNPs, but can also be due to deletions, additions, insertions and other genetic changes.
Note that SNPs not always lead to new alleles. Sometimes they occur in non-coding areas and nothing happens.

Edit:

SNPs do not need to be gene specific, but this was for simplicty.

@Artem added nicely to the answer, I'm quoting it here:

"Single Nucleotide Polymorphisms (SNPs) are Single Nucleotide Variants (SNVs) at a population allele frequency greater then 1%. Alleles are any variants of the same position of DNA, which includes SNVs, insertion/deletions, or structural variants and at any frequency." - @Artem


Why does oxygen bind to hemoglobin in an specific angle?

summary:
O2 could form a linear complex with the Fe atom, but then it would start to look more like a mineral Fe=O...O bond - a linear bond would be like a transition state to an iron oxide (rust).   An Fe-O-O bent bond preserves more of the electronic character of the O2 molecule and promotes strong but reversible binding to Hemoglobin.

The oxygen molecule forms a partial covalent bond with the iron in the heme (the ringlike molecule in the picture below  ).  The lone pair of electrons of the oxygen atom which forms the bond to the iron has a 120 degree angle with respect to the oxygen molecule itself.  In chemistry we say it is sp2 hybridized.  This implies a slightly greater than 120 degree angle between the Fe-O and the O-O axis would be energetically preferred in oxygen binding.

You can see on the other end of the oxygen, there is a histidine sidechain nitrogen which interacts in a similar way - crooked at a similar angle to the oxygen molecule.

As @MattDMo points out in the comments, it would not be 120 degrees exactly in fact even freshman chemistry molecular orbital theory would say that the double bond would take up more 'space' than the sp2 orbitals, widening out the angle Fe-O=O angle to be greater than 120 degrees.  Then the protein has its own geometry - the histidine and the heme iron are fixed in space and probably have their own location, so this is just an approximate, qualitative bond angle..

The claims of superoxide formation is because the oxygen is diamagnetic the iron and he oxygen, which are both paramagnetic, somehow pair to eliminate their magnetic moment.  The PNAS paper cited here goes in depth on this issue.  The article curiously just says the highly reactive superoxide is kept from being chemically consumed by the hydrophobic pocket around it.

The oxygen almost makes a superoxygen the iron sort of oxidizes but doesn't quite. Its also due to the peroxide like character of the oxygen molecule, partially bonded at both ends.

Still the point is that hemoglobin holds onto the oxygen by making a partial covalent bond.  After all when the O2 unbinds, its just O2 again.  A later study does detect some paramagnetism at low temperatures. In the last word on this that I could find, Pauling does a review and concludes that the electronic state of the heme iron and oxygen complex is a combination of three different electronic states - partly superoxygen, partly oxy-iron and molecular oxygen.

The reference also gives the Fe-O-O angle as 117 degrees.

[Just a note that the reference page I got the picture from refers to rational design of the hemoglobin molecule...in this case they are engineers talking about how they could change the amino acids in the protein to get other properties out of the hemoglobin system - rationally.]


Can frogs see clearly under and above water?

Short answer
Frogs are nearsighted on land and farsighted under water.

Background
Frogs are reported to be nearsighted on land, but farsighted underwater (source: Chegg Study). Nearsightedness (myopia) is a condition in which near objects are perceived clearly, but objects farther away are blurry. Farsightedness (hyperopia) is the reverse. The human counterparts of these conditions are shown in Fig. 1. Humans focus images on the retina by changing the shape of the lens; to focus on near objects, light is more strongly refracted by making the lens more spherical in shape. For far-away objects the lens is flattened such that light is less refracted.

Fig. 1. Near- and farsightedness. source: Hyperphysics

In humans refractive errors are common and can usually be successfully treated with corrective lenses.

The cornea adds substantial refraction to the optical system of the eye, namely about 43 diopters. As a comparison, normal prescription glasses often have only a few diopters worth. In water the refractive index of the cornea is mitigated, as water and the cornea have about the same refractive index (source: lasikmd). Hence vision is blurred for humans under water, because images are focused far behind the retina, resulting in hyperopia.

Frogs have another way of correcting their retinal image. They focus on objects at different distances by using specialized (lentis) muscles to move the lens closer to or farther from the retina (Fig. 2), like the focusing mechanism of a camera (Douglas et al., 1985). However, the lentis muscles can adjust the focus only for approximately 10 diopters worth, with an accompanying shift in lens position of about 150 μm. Hence, because of the huge effect that water has on the corneal refraction (~40 diopters), a frog's lens cannot sufficiently correct the refractive state of the eye to achieve normal vision (emmetropia) both above and below water. Apparently it settled evolutionary spoken somewhere in the middle, namely myopic on land, and hyperopic under water.

Fig. 2. Cichlid eye. Accommodation results from the movement of the lens in the pupillary plane using the lentis muscles; the musculus retractor lentis, and the antagonistic ligamentum suspensorium. source: Vision in cichlids

Reference
- Douglas et al., J Comparative Physiol (1986); 158(1): 33–143


How can evolution make such complicated beings?

If this is a general question about how evolution works then Roland's comment is correct - you should start with one of the excellent resources available online, like http://evolution.berkeley.edu/evolibrary/home.php. However, this specific question sounds more like something we used to call the 'argument from personal incredulity' to me - you're willing to accept that evolution occurs, you're just not sure whether it is sufficient to create something as complex as the organisms you see around you. This is quite a common issue people have with evolution by natural selection, and it's a perfectly reasonable question to ask. Essentially, it originates in the difficulty of appreciating the sheer scale of the processes involved. To paraphrase Douglas Adams, "[life] is big. Really big. You just won't believe how vastly, hugely, mind-bogglingly big it is." But I'll do my best to try to help you understand this a bit better.

The number of single-celled organisms on the ocean floor is estimated at 2.9×10^29 - that's roughly three hundred billion billion billion. The current global human population is about seven billion - that's already effectively impossible to imagine. If every one of those people had seven billion tiny people living on them, and every one of those had seven billion people living on them, that's roughly the number of single-celled organisms on the ocean floor right now. Many of those appeared less than 24 hours ago and will be gone tomorrow. Natural selection is acting on every aspect of every one of those organisms simultaneously and has been doing for roughly 1.5 trillion generations. One-and-a-half thousand, thousand, thousand, thousand, thousand, thousand generations.

Natural selection is also a fantastic mechanism for homing in on solutions to complex problems - so good that we've started using it to solve mathematical and computational optimisation problems.

Essentially, it's one of the best approaches to solving complex problems we have been able to conceive of and it's had an insanely, mind-bogglingly long time to act on a planet-sized test tube. That's how we ended up with so much amazing stuff on our planet.


How long before robin no longer needs the nest on my porch?

According to Cornell's All About Birds website, you will have to wait about a month for the nest to be cleared.

The egg incubation period is 12–14 days.
Following hatching, the nestlings will remain in the nest for another 13 days (i.e., the "nestling period" is 13 days).

However, there are two caveats to this:

A typical robin clutch size (i.e. the # of eggs in the nest at once) is 3-5 eggs. Since you only have two eggs, that could suggest that more eggs are about to be laid very soon, which may extend the nest occupancy another day or so.
Some robins use the nest more than once!

  An American Robin can produce three successful broods in one year.

Here's a visual of what the nestling period (approximately) looks like so that you can track your nest visually :) :

 Source: L. Birnbaum


How is "firing together" detected in Hebbian learning?

The dynamics of Hebbian or associative synaptic plasticity are thought to be governed primarily through the function of the NMDA glutamate receptor. The short answer is that you are basically right on all counts.

Figure of the NMDA receptor present the nervous system.
By Blanca Piedrafita [CC BY-SA 1.0 or CC BY-SA 2.5], via Wikimedia Commons

The NMDA receptor is a non-selective cation ionotropic receptor. The reversal potential of the NMDA receptor is around 0 mV, in contrast to the resting membrane potential of a 'typical' excitatory neuron which is around -70 mV. This means that a pretty strong stimulus is required in order for the NMDA receptor to be activated. Whereas some current can pass through the channel upon binding of its preferred ligands (glutamate or glycine), the pore is normally blocked by a magnesium ion. This mechanism confers some degree of voltage-dependent regulation of ion flow through the channel. When a strong stimulus raises the membrane potential at sufficient levels the magnesium block is lifted, allowing more current to pass through. The slow kinetics of the NMDA receptor allow the temporal integration of incoming signals. This makes the NMDA receptor function as a coincidence detector or AND gate. There are many more known details about the mechanisms involved but the above should suffice to answer your specific question.

Further reading: https://en.wikipedia.org/wiki/NMDA_receptor


Why don't vaccines cause bacterial resistance?

Unfortunately, we do see examples of bacteria and viruses evolving vaccine resistance. For instance, vaccine resistant strains of polio and pertussis have recently been identified.

Yet these seem like the exception rather than the rule. One thing that makes it harder for pathogens to evolve resistance is that vaccines usually generate antibodies to multiple antigens, all of which the pathogen would have to alter.

Another reason vaccines tend not to drive vaccine resistance is that the diseases for which we vaccinate are typically those that are not antigenically variable. (Haemophilus influenza is a notable exception; there we use a conjugate vaccine). This may have something to do with how we view vaccine efficacy. For example, we don't say that the influenza virus evolves vaccine resistance--yet we need a new vaccination each year due to antigenic shift.

If you are interested in learning more, Angela McLean has a nice article looking into this question.


Organism and plants reduce radioactivity?

Your magic search word is 'phyto-remediation'

There a bunch of plants used for this.

None of them remove radioactive material as such.  With the possible exception of deuterium, the chemistry of isotopes aren't distinguishable by biological organisms.

So to remove strontium 90, you need something that picks up strontium.  It will pick up both the radioactive and non-radioactive forms.

In some cases the metal will combine forming compounds.  This may make the radio-isotope inaccessible to a given plant.  If, for example, strontium was in the form of SrO and SrSO4 you might need two different plants, or add a reagent to the soil to convert it to an accessible form.

Once the plant tissue has picked up the radio isotope, the usual process is to drive off the plant tissue by burning or destructive distillation, then processing the material to either make it insoluble for disposal, or convert it for use.  For material with a fairly short half life and low solubility, it may be sufficient just to bury it.


Does avoiding medication that alleviates symptoms shorten the length of a cold?

It is plausible but by no means established that antipyretics (fever suppressors) in particular could increase the duration of infection/symptoms, because fever is part of a functional immune response.

From Graham et al 1990 (a small [n=56] randomized trial of the use of antipyretic pain relievers in volunteers experimentally infected with rhinovirus):

  Use of aspirin and acetaminophen was associated with suppression of serum neutralizing antibody response (P less than .05 vs. placebo) and increased nasal symptoms and signs (P less than .05 vs. placebo) ... There were no significant differences in viral shedding among the four groups, but a trend toward longer duration of virus shedding was observed in the aspirin and acetaminophen groups.

In other words, it looked like the people who took aspirin or acetaminophen had weaker immune responses and more cold symptoms. They might have been infectious for slightly longer, but it's hard to tell (also, duration of infectiousness is not the same as the duration of symptoms ...)

However, a review (Kim et al 2013) concluded that NSAIDs (non-steroidal anti-inflammatory drugs) slightly (but non-significantly) reduced the duration of illness.

  In a pooled analysis, NSAIDs did not significantly reduce the total symptom score (SMD -0.40, 95% CI -1.03 to 0.24, three studies, random-effects model), or duration of colds ([mean difference] -0.23 [days], 95% CI -1.75 to 1.29, two studies, random-effects model) [emphasis added]

Here is the figure from that analysis:

"Common cold" is often considered synonymous with rhinovirus infection, but may also include mild influenza infections. An observational study on influenza A and two other infections (Graham et al 2000) found

  There was a striking correlation between antipyretic therapy and duration of illness in subjects infected with influenza A and S. sonnei, but not R. rickettsii ... Multivariate analysis suggested that antipyretic therapy prolonged illness in subjects infected with influenza A, but its use was the result of prolonged illness in those infected with S. sonnei.

In other words, to the extent that one can really distinguish causality in an observational study, it seemed that taking antipyretics made influenza illness longer, but that causality went in the other direction for S. sonnei (i.e., people took more antipyretics when they were sick for longer).

The usual caveats associated with small studies and researcher degrees of freedom apply when interpreting the results of these studies ...

J Infect Dis. 1990 Dec;162(6):1277-82
Adverse effects of aspirin, acetaminophen, and ibuprofen on immune function, viral shedding, and clinical status in rhinovirus-infected volunteers.
Pharmacotherapy 2000 (20), 1417–1422.
(doi:10.1592/phco.20.19.1417.34865)  Effect of antipyretic
therapy on the duration of illness in experimental
influenza A, Shigella sonnei, and Rickettsia rickettsii
infections.
Cochrane Database Syst Rev. 2013 Jun 4;(6):CD006362. doi: 10.1002/14651858.CD006362.pub3.
Non-steroidal anti-inflammatory drugs for the common cold. Kim SY, Chang YJ, Cho HM, Hwang YW, Moon YS.


What is the standard method for measuring soil and substrate acidity

Soil should first be processed by drying the soil to ensure a standard "dry" sample is analyzed. 55$^o$C in drying ovens for 24 hours works for most non-water-zone soils, but more time at 50 - 55 $^o$C (as long as it's consistent between samples) can be used to dry out wetter samples. One can then put the soil through sieves to remove rocks and other debris (2mm sieve is common).
To actually measure soil pH, one combines 1 part soil with 1 part water and then measure with an electrode (McLean 1982)$^1$.
By always using 1 part soil to 1 part water, you maintain a consistent relative amount of water per sample and therefore can account for different sample sizes.
The final value is reported as pH.
You can find the McLean (1982) resource here for $15 or likely for free from a nearby university library. The paper has been cited over 2800 times.
[1] McLean, E.O. 1982. Soil pH and lime requirement. In A.L. Page et al. (ed.) Methods of soil analysis, part 2. Agronomy Monogr. 9, 2nd ed. ASA and SSSA pp 199–223.
EDIT:
As @Roland pointed out in the comments, other standards do exist.
For example, the International Organization for Standardization (ISO) maintains reports describing  standard protocols for different methods (which therefore are sometimes used):

ISO 10390:2005 specifies an instrumental method for the routine determination of pH using a glass electrode in a 1:5 (volume fraction) suspension of soil in water (pH in H2O), in 1 mol/l potassium chloride solution (pH in KCl) or in 0,01 mol/l calcium chloride solution (pH in CaCl2).
ISO 10390:2005 is applicable to all types of air-dried soil samples, for example pretreated in accordance with ISO 11464.

The USDA describes several standard protocols used by their laboratory at the National Soil Survey Center to measure soil pH (Hydrogen-Ion Activity) in their Soil Survey Laboratory Methods Manual (version 5, 2014). See specifically, pages 265-281 for various soil suspension and soil extract methods.

Note: They cite repeatedly the McLean (1982) paper as a  source for determining pH using an electrode.

They also provide further notes in this technical note.

The EPA (US Environmental Protection Agency) similarly has a protocol that they use. Their electrometric approach using a digital pH meter involves the insertion of a glass electrode into a soil suspension made by mixing the soil 1:1 with a reagent solution (see referenced notes below).

EPA protocol for soil pH (Method 9045D): Revision 4 (2004) available here

References "Chapter One" of technical note SW846 (I link to Update V revision 2, July 2014), which relates back to 2-2 of EPA-600/4-79-019

Again, the overall takeaways are:

Reporting soil acidity as pH is standard
There are multiple standard methods to measure the pH; Just be sure to properly cite your approach!


In general, a read simulator does the following:

Selects regions from a reference sequence with some sort of predefined or user-specified size distribution.
Converts the sequence from those regions into single or paired end reads with quality scores. The quality scores and read lengths are typically user defined.
Introduces errors into the aforementioned sequences, typically with more at the 3' end, which matches what comes from a sequencer.

A simulator may also try to reproduce the uneven coverage that you'd see in real data. In any case, most simulators will place the original coordinates of the simulated reads in the read names so that the quality of the resulting alignments of the reads can be assessed.


Recombination-based vs. Sequence-based genetic mapping

A couple of months ago I listened to a plant physiologist who strongly recommended recombination-based mapping over sequencing based mapping. The main reason he gave was the error-rate of 2nd generation sequencing. The error rate on Illumina platforms are about 1 % if I recall. In a small genome like that of Arabidopsis thaliana (157 Mbp) that accounts for over 1 million sequencing errors. That can of course be reduced having a proper sequencing depth and using the consensus sequence. But it can still cause problems if you're tracking a phenotype caused by an SNV. In plants like A. thaliana where back crossing can be used to create homozygous plants, recombination-based techniques can be particularily effective.

But he was talking from a plant physiologist's view when working with A. thaliana as a model organism. When working with humans which always are heterozygous, can't be back-crossed, don't have a generation time of six weeks and where samples sizes will probably be small I imagine that the situation is different. The classic geneticists' working with human diseases that I have talked have expressed fear that their work will soon be obsolete due to falling sequencing prices and growing sequence data collections.


Have Polyphyodonts ever evolved from Diphyodonts?

Not true polydonty, True polydonty is an animals that grows endless numbers of teeth like reptiles and fish do.  Elephants, kangaroos, and manatees are sometimes called polydont but they are doing something very different, they still only grow a set number of teeth, but instead of growing them in two sets they spread them out growing them a few at a time. the total number of teeth is still the same as other mammals and once that last tooth falls out they can't make anymore. It is worth noting the teeth migrate forward in the jaw as they wear out unlike true polydont in which new teeth grow from below endlessly.In essence they are rationing that limited number of teeth.

True polydonty has never evolved from a non-polydont ancestor.


What is the biding site code recognized by the parts of the spliceosome

Did you try googling "splice site recognition sequences"?

In general, the first two letters of the intron must be GT, the next three are often ARG.

The last three letters of the acceptor site of the intron are virtually always YAG


Mitochondria - are they really separate organisms that once merged into eukaryotic cells?

Yes. But it is incorrect to call mitochondria an organism now.
Most of their genes were lost and are now encoded in the nuclear genome
It gets most of its metabolites
It is not known. See the other post for details.
Why membrane: I guess you know that. Why folded: you guessed right.
Only ovum donates mitochondria and other cytoplasmic factors. Sperm just provides the haploid genome.
No
Most of them are key respiratory enzymes


Does class switching occur both in B cells and Plasma cells?

Short Answer : B-cells class switch to become Plasma cells in the germinal centre of the lymph node.

Long Answer :

There are two important concepts addressed in the question. One is the Immunoglobulin structure - isotype and membrane/soluble type. And the other is the germinal centre B-cell paradigm. Understanding both the concepts are a prerequisite to understand the answer to the issue.

First of all, immunoglobulin synthesized by the lymphocyte can either be membrane bound (known as the B-cell receptor (BCR)) or soluble antibody. After gene rearrangements, the B-cell (still immature) begins to produce membrane bound IgM/IgD. This continues even in the mature B-cell. The membrane bound Ig or mIg has an extra sequence (refer image) on the carboxyl end adding a few hydrophobic amino acid sequences so that it gets anchored well in the hydrophobic part of the membrane. Also at the end is a series of hydrophilic residues involved in downstream cell signalling.

Class switching is process that leads to a change in the isotype of Ig that the cell is producing. Class switching involves excision of DNA which implies that the cell can not revert back to producing the Ig once it used to. The sequence of the gene segments on the heavy chain gene hence becomes important.

When there is a first time exposure to an antigen, the mature B-cells follow a classical paradigm to T-cell dependant antigens, which is shown in this picture below.

Class switching occurs in B cells that are participating in a germinal center reaction, after the naive B-cell has been activated by antigen and a cognate T cell. There also is germinal centre independant class switching that we ignore here.

After a B cell has undergone somatic hypermutation and class switching of its immunoglobulin gene, it may or may not be positively selected to differentiate into a plasmablast. Plasmablasts proliferate rapidly before terminal differentiation to plasma cells, which secrete affinity matured, class-switched antibody. So in other words, class switch recombination is largely restricted to activated, germinal center B cells. These B-cells class switch, as one of many processes to produce soluble antibody producing plasma cells.

Plasma cells and B-cells aren't just one and the same. B-cells undergo a series of processes to form the plasma cells which are also different in morphology.

As already has been mentioned, it should be remembered that class switching involves excision of the intervening DNA between the rearranged VDJ exon and the constant exons being switched to, meaning that they are deleted from the allele. Thus, a B cell that has class switched from IgM to, say, IgG would delete the IgM and IgD heavy chain exons on that allele, and would be restricted to IgG (or IgE and IgA, which lie downstream).

But then, if the B cells bearing IgM had already class switched (to their possible downstream counterparts), how can the primary immune response be IgM dominant? How could IgM antibodies come from class switched plasma cells?

This is because, this whole germinal centre spectacle takes time to happen and in the meanwhile, there are extrafollicular mechanisms of antibody production in place in extrafollicular foci in the spleen or in the medullary cords of lymph nodes. Since antibodies that are develpoed in a germinal centre dependant manner (IgG) are from somatically hypermutated cells, they have more affinity to the antigen than IgM produced by germinal centre independant plasmablasts.

BCR generally has only two types, mIgM and mIgD. If there is a class switch, they turn to soluble antibodies (IgG/IgA/IgD).

Secretory antibody here refers to soluble antibody that is exocytosed from the WBCs, not the IgA that is found in bodily secretions.

Reference, Picture credits :

  Nature reviews immunology, Germinal centres: role in B-cell
  physiology and malignancy
  Kuby Immunology. 6th Edition
  Immonological reviews, Extrafollicular antibody responses


Data on Recombination rate and Gene Positions in Humans

A good baseline for this type of research in human genetics is Standards and guidelines for the interpretation of sequence variants from ACMG. It is a guideline for clinicians, and it gives a good sense of good variants data, bad variants data and setting up confidence level.

Try to consolidate data from:

Population databases

GWAS databases

Exome Aggregation Consortium
1000 Genomes Project (there is data in vcf format which is pretty much what you need)

SNV databases

dbSNP (it is uncurated so you got to be hypercritical)

Disease databases

ClinVar (be aware "12% of interpreted variants have ≥2 submitters in ClinVar , and 21% are interpreted differently")
OMIM
HGMD (it is a gold standard as it is curated, but you could only search for variants but not collect data because you could not download it unless you pay for it)


How can I accurately predict proper transgenic protein function/structure from different species?

By looking at the sequence only?  This is an unsolved problem.

Its not clear to me exactly what you are looking for, but here are some thoughts...

On a relatively narrow question as to whether any gene you plug into a bacterium, yeast, mouse, goat or other transgenic organism - the rna may not translate into protein in detectable levels or at high enough levels to get the desired result.  changing the sequence of the DNA of the gene for better transcription/translation is a common necessary experimental.

On the broader systems biology level, other cofactors, substrates that are necessary for the function of the gene may have to be engineered in the host organism. That is also an open question.

All this is assuming the gene in question codes for an enzyme to make a new or different amount of the metabolic product from the host organism, a commmon synthetic biology target.  If you are adding signaling pathway components, tinkering with a more specific mechanism in the cell, getting the function you desire could be a lot of work.  E.g. if you were inserting a new ribosomal component or a gene related to mitosis, that would be hard to imagine a priori how it would function in the new cell or if it would just kill it.

Also, Olga Troyanskaya at Princeton CS is working on the related problem of finding the function of a gene by looking at its sequence and cross referencing to other known data. Electronic functional inference is difficult, esp when we have no complete gene functional description of any living organism to start with.


What is the formula to calculate $R_0$ (basic reproduction number)?

$$R_0 ∝ \left(\frac{\text{infection}}{\text{contact}}\right) · \left(\frac{\text{contact}}{\text{time}}\right) · \left(\frac{\text{time}}{\text{infection}}\right)$$

  More specifically:

  $$R_0 = τ · \bar{c} · d \quad \quad (1)$$

  where $τ$ is the transmissibility (i.e., probability of infection given contact between a susceptible and infected individual), $\bar{c}$ is the average rate of contact between susceptible and infected individuals, and $d$ is the duration of infectiousness.

Notes On $R_0$ (2007)

Further reading:

https://en.wikipedia.org/wiki/Basic_reproduction_number
Complexity of the Basic Reproduction Number (R0), emerging Infectious Diseases (2019)
Theory versus Data: How to Calculate R0?, PLoS One (2007)
The R0 package: a toolbox to estimate reproduction numbers for epidemic outbreaks, BMC Medical Informatics and Decision Making (2012)


I could only find fairly old literature on the subject, so take this with caution.

Some papers seem to indicate some sort of genetic component to tongue rolling, although the precise molecular basis are not really described (but, again, these are 30-40 years old papers...)

From: Inheritance of ear wax types, ear lobe attachment and tongue rolling ability. - Cruz-Gonzalez and Lisker - Acta Anthropogenet., 1982

  The mode of inheritance of ear wax type, ear lobe attachment and tongue rolling ability were studied in 77 families with a total of 293 children. The results clearly showed that the dry ear wax type and the attached ear lobe type represent the homozygous state for two pairs of autosomal recessive genes. The evidence for the same being true regarding the lack of ability to roll the tongue was less conclusive in our material, but this could be due to difficulties in communication between the examined individuals and the examiners.

Tongue-rolling phenotypes and geographical variation in the United Kingdom

  The distribution of tongue-rolling phenotypes in a sample (n = 477) of undergraduate students of the University College of Swansea (U.K.) was studied. The birthplaces of these students were also recorded. England was divided into six areas, and Wales was left as an area on its own. The data suggest that those students who come from north-east are more non-rollers, which may be due to mixture with Scandinavians.

Left-handedness and tongue-rolling ability.

  948 undergraduates at The Ohio State University were administered the 10-item Edinburgh Handedness Inventory and asked to indicate the extent to which they could turn up the sides of their tongues. Significantly fewer left-handers than right-handers (62.8% and 74.8%, respectively) reported being able to turn up either or both sides. Sex differences in tongue-rolling ability were also noted. Among the 403 men included in the final sample, 77.4% could roll their tongues, whereas only 69.7% of the 491 women could do so.

This paper, however says (luckily Google finds a PDF here... seriously it should be illegal to have papers from the 70s behind paywalls... but I digress):

No evidence for a genetic basis of tongue rolling or hand clasping - Martin, J Hered., 1975

  OCCASIONALLY one still finds in elementary genetics courses and elsewhere, the ability to roll the tongue and the manner of clasping the hands cited as examples of simply inherited human polymorphisms. This is despite extensive evidence to the contrary that has accumulated over several decades. Sturtevant T found that about 65 percent of persons studied were able to tum 1.JP the edges of the tongue and although some people were able to learn the ability, family data indicated that it was inherited as a simple dominant allele. However, Matlock reported 7 out of 33 monozygotic (MZ) twin pairs discordant for the ability, and Sturtevant concluded that there is sufficient nongenetic inftuence to make the character practically useless as a genetic marker. He confessed to being "still embarrassed to see it listed in some current works as an established Mendelian case."

The paper is also cited in the "Myths of Human Genetics" page of the University of Delaware.

So, all in all, it seems that there is evidence against a Mendelian transmission of this character, although these studies are quite old and some further analysis is warranted to exclude non Mendelian (read epigenetic) transmission of tongue rolling.


What happens if nerve impulses go the wrong way?

The propagation of the action potential is MUCH slower than the refractory period. The propagation speed is determined by the cable equation http://www.cnbc.cmu.edu/~bard/passive2/node9.html which is a formalism developed by Hodgkin & Huxley in the 1930s to measure signal transmission through a biological cable (e.g. an axon). The speed of the propagation is measured by a constant. The voltage does decay and thus spread in all directions, but the propagation only matters towards the direction of signal transmission. Ionic action in the soma would destroy the usefulness of transmission not down the axon. With that being said, neurites in arthropod nervous systems for instance http://stg.rutgers.edu/ can receive input and deliver output leading to very complicated patterns of waves inwards and outwards. Despite this, the stomatogastric ganglion can produce very robust and stable rhythmic neural patterns.


They can't see all the birds that are around them as some are hidden behind the others. However, I don't think there is anything so extraordinary; they watch around, have good reflexes and can change direction very abruptly. There is no need for some kind of special sensing abilities to explain bird flocks.

3 simple rules

One can simulate a flock of birds with 3 simples rules:

Adapt your speed on the speed of the other agents

$$\overrightarrow v_{i,1} = \frac{1}{K_L}\sum_j^K\overrightarrow v_j (t) - \overrightarrow v_i(t)$$

, where $K_L$ is the number of birds in the Large area of perception, $\overrightarrow v_j (t)$ is the speed of a given bird in the large area of perception and $\overrightarrow v_i (t)$ is the speed of the focal individual.

Attraction

$$\overrightarrow v_{i,2} = \frac{1}{K_L}\sum_j^K\overrightarrow p_j (t) - \overrightarrow p_i(t)$$

, where $\overrightarrow p_i(t)$ and $\overrightarrow p_j(t)$ are the positions of the focal bird and of a bird present in the large area of perceptio, respectively.

Repulsion

$$\overrightarrow v_{i,3} = -\frac{1}{K_s}\sum_j^K\overrightarrow p_j (t) - \overrightarrow p_i(t)$$

, where $K_s$ is the number of birds present in the Small area of perception.

Then, to update the speed of the birds you just sum up those 3 contributions:

$$\overrightarrow v_i(t+1) =  \overrightarrow v_i(t) + \overrightarrow v_{i,1} + \overrightarrow v_{i,2} + \overrightarrow v_{i,3}$$

see boids for more information.

My point in descrbing this algorithm is that you can get the emergent behaviour of a bird flock out of very simple rules.

Bird Collision

If birds don't often collide each others (what I assume but honestly I don't know much), note that it is estimated that 100 millions birds that die every year after colliding a window (see here). Birds also collide with power lines (ref) and wind turbines (ref).


What is this furry, long-limbed, presumably tree-dwelling creature?

It looks like a taxidermic specimen of a gray slender loris (Loris lydekkerianus), but it does look pale in color. The lack of color distinction in the fur may be because it is a non-living specimen. The links below may be helpful with more detail.

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

https://www.shaldonwildlifetrust.org.uk/page/grey-slender-loris.html

https://www.youtube.com/watch?v=yU3n0BlUP0A


Other than Acetylcarnitine what other orally-bioavailable Acetyl donors exist to assist in the conversion of CoA to acetyl-CoA?

This is only a guess, maybe acetic acid, ie vinegar?

Acids are effectively hydrogen salts, but the acetyl ion might be alkaline like the hydroxyl ion, making acetic acid less acidic than most? As in water, pH neutral, is a combination of hydrogen and hydroxyl, H and OH, ions?


What causes adenosine build up in the brain when awake?

Adenosine causes humans to become sleepy. But how ?

During day time we consume food which is broken down into glucose. This glucose is broken down by "Glycolysis" in cell's cytoplasm during which ATP is produced. This produced ATP is is then used by body as an energy supplier. ATP breaks down into ADP and then AMP with the release of energy which our body consumes for doing work.

(Fig 1- Structure of Adenosine to ATP)

Adenosine is produced continuously and starts to accumulate around and in Adenosine receptors such as A1, A2a, A2b and A3 (as shown in fig below).Adenosine inhibit signal propagation and energy production in at least A1. (Not all the receptors induce sleep when they receive Adenosine.) "A1 receptor" receives adenosine and induces sleep. A1 receptors are implicated in sleep promotion by inhibiting wake-promoting cholinergic neurons in the basal forebrain.

Continuous inhibition of A1 receptor by Adenosine slowly induces sleep by relaxing the brain and muscles but without substantially weakening their abilities!

How is Adenosine metabolized ?

During sleep the accumulated Adenosine is metabolized by Adenosine deaminase enzyme which catalyzes the irreversible deamination of 2'-deoxyadenosine and adenosine to deoxyinosine and inosine. With the reduction in the Adenosine content the body is excited from sleep slowly.

So in short summarize:

  The accumulation of adenosine during waking periods is thus associated
  with the depletion of the ATP reserves stored as glycogen in the
  brain. The increased adenosine levels trigger non-REM sleep, during
  which the brain is less active, thus placing it in a recovery phase
  that is absolutely essential—among other things, to let it rebuild its
  stores of glycogen.

  Because adenosine is continuously metabolized by the enzyme adenosine
  desaminase, the decline in adenosine production during sleep quickly
  causes a general decline in adenosine concentrations in the brain,
  eventually producing conditions more favourable to awakening.

(Refer this page: MOLECULES THAT BUILD UP AND MAKE YOU SLEEP)


Why do I see purple stripes when moving a small source of light (flashlight) quickly in a dark room?

This phenomenon is called afterimage and happens because of adaptations of the photoreceptors in the retina of your eye to the stimulation by light and adaptations by your neurons in the visual processing in your brain.


Role of Fbx15 in ES cells and its use in assaying for iPS cells (Yamanaka paper and others)?

Another paper from Yamanaka's group explains Fbx15.

It says:

  Inactivation of Oct3/4 in ES cells led to rapid extinction of Fbx15 expression.

  Fbx15-null ES cells were normal in morphology, proliferation, and differentiation. These data demonstrate that Fbx15 is a novel target of Oct3/4 but is dispensable for ES cell self-renewal, development, and fertility.

So Fbx15 wont be expressed in Oct4⁻ cells.

I haven't seen any paper describing the function of this gene but in the case of cassette insertions the locus would prove useful in expressing the inserts specifically in Oct3/4⁺ cells


If a person has a specific mutation in a gene, is it more likely he has other mutations in that gene?

A priori, no! Why would it? Do you have any specific hypothesis in mind you would like to discuss?

Below are some expectations from a simple model and possible reasons for why this expectation may break down under more complicated models.

Simple model

Under a simple model (panmictic population and a few other simple assumptions), the number of mutations a given individual has in any sequence considered follows a poisson distribution. Assuming that all mutations occuring have a constance selection coefficient $s$, a constant dominance coefficient $h$ and that the mutation rate for the sequence of interest is $U$, then the number of mutations an individual carry comes from a Poisson distribution with mean $\frac{U}{2hs}$ (Crow 1970).

This model is simple but is probably a pretty good approximation to reality. Below are three assumptions that are not necessarily true and that would yield to a higher variance in the number of mutations (that is a higher probability for an individual that already carry a mutation to get a second mutation).

Population structure

In reality, populations are often not panmictic. As the genetic load depends upon the population size. More specifically, the smaller the population, the higher the genetic load (or the higher the number of mutants alleles present in the population) (Kimura et al. 1963).

Past evolutionary and demographic history

Populations are not stable through time. Some population have recently gone through a bottleneck, others a quickly expanding, some are shrinking, some have recently suffered from a plague, etc... Such processes can all cause populations to differ in the number of mutations they carry and therefore would increase the variance in the distribution of number of mutations individuals carry.

Within a specific short enough sequence, physical linkage associated with specific past evolutionary process will create a relatively long lasting linkage disequilibrium.

Condition-dependent mutation rate

It has been shown in Drosophila melanogaster that individuals with poor genotype tend to have a higher mutation rate causing their lineage to accumulate even more mutations (Sharp and Agrawal 2012).


What is wrong with this analogy: Individuals are to alleles what governments are to individuals

Alleles are passed down (to individuals) and created by individuals (although not fully under their control). But individuals are not passed out or created by the governments (I suppose), although individuals are influenced by the governments and they can influence governments, whereas individuals can not necessarily influence the allele of the gene they already have unless you take epi-genetics into account. Also, the creation of an allele is not entirely influenced by individuals due to independent assortment and chromosomal crossover, but individuals can more or less influence governments.


During interphase, is DNA wrapped around histones?

Yes, DNA is always wrapped around histones.

DNA condensation using histones is not only meant to form the chromatids for mitosis/meiosis, but also one of the factors that control gene expression. Tightly packed heterochromatin is not being expressed, whereas unpacked euchromatin is transcriptionally active. The process of condensation is controlled by enzymes such as histone actelytransferase (HAT) and deacetylase (HDAC) that change the electrostatic properties of the histone proteins. Positively charged lysine in heterochromatin histones allows condensation with negatively charged DNA. By acetylation of these lysines, they become neutral and the heterochromatin turns into euchromatin, which, provided the necessary activators etc., can now be translated. To silence gene expression, the process is reversed.

Gene expression control is very complex and histone acetylation is only one factor out of many. Nonetheless, you see that histones are a crucial part of the chromosomes and are not only formed during mitosis or meiosis.

3.0.jpg

Source: https://en.wikipedia.org/wiki/File:Histone_acetylation_and_deacetylation.jpg


The problem statement says all the proteins have the same molecular weight but does not say how many amino acids they have.  It does say how many cysteine amino acids each has, but not how many other kinds they have.  Cysteine forms disulfide bonds, holding bends in the protein structure.

BiteSizeBio says:

  SDS is a detergent that is present in the SDS-PAGE sample buffer where, along with a bit of boiling, and a reducing agent (normally DTT or B-ME to break down protein-protein disulphide bonds), it disrupts the tertiary structure of proteins. This brings the folded proteins down to linear molecules. SDS also coats the protein with a uniform negative charge, which masks the intrinsic charges on the R-groups.

So the point to SDS-PAGE is to have proteins migrate in the gel according to molecular weight without regard to the natural charges carried by the various component amino acids.  The three proteins should thus migrate at the same rates in SDS-PAGE (not A being slower than B and C, as OP thought).

However, protein C is not treated with β-mercaptoethanol (B-ME) which is an important part of SDS-PAGE, so it retains the disulfide cross-links and thus is not a linear string of amino acids.  Hence C will migrate more slowly than A and B, and the expected result is as stated in choice (c.).


Options:

You can always download the data (as @WYSIWYG has suggested in the comment).
Transfer the data to Galaxy
Convert and export the selection of your choice.

Source: http://modencode.oicr.on.ca/fgb2/gbrowse/fly/


Can anyone identify this spider? (greater Poland region)

That looks like a Funnelweb Weaver (family Agelenidae), specifically Tegenaria atrica,  based on the patterning of the abdomen and thorax.

Female Tegenaria atrica, picture by Jørgen Lissner

Their range includes Poland:

Range: Andorra, Austria, Belgium, Bulgaria, Croatia, Czech Republic, Denmark, Faroe Islands (introduced), Finland, France (Corsica), France (Mainland), Germany, Great Britain (Channel Islands), Great Britain (Mainland), Great Britain (Northern Ireland), Greece (Crete), Greece (Dodecanese Islands), Greece (Mainland), Ireland, Italy (Mainland), Latvia, Liechtenstein, Lithuania, Macedonia, Netherlands, Norway (Mainland), Poland, Portugal (Mainland), Romania, Slovakia, Spain (Mainland), Sweden, Switzerland, Ukraine, Yugoslavia (van Helsdingen 2009.1).

Source: http://www.jorgenlissner.dk/families.aspx


How to add oxygen to indoor air without opening windows?

You should also have in mind that, meanwhile plants produce oxygen through photosynthesis, they also carry out aerobic respiration. In short, this process requires oxygen which is normally not a problem during daytime as photosynthesis covers the oxygen needed. Nonetheless, during nightime, plants remove oxygen from the atmosphere and do not replenish it. This is why nurses normally remove plants from hospital rooms at night. So if you want to put plants in your room, have in mind that is best to take it outside during the night.

Refer to this link for more information: http://www.saps.org.uk/saps-associates/browse-q-and-a/453-do-house-plants-remove-oxygen


Although it is fancy to think of antivenom as a poison for the poison, technically it is a poison only for the poison!

Antivenom is developed in horses (equine) by hyperimmunizing them against the particular venom at a non-lethal dose, followed by collecting the serum. Venoms are complex and have many enzymes and hence are proteins. So, antivenoms are just antibodies against the venom proteins.

Moreover, the antivenoms are classified into monovalent and polyvalent. This signifies whether the sera was prepared by hyperimmunizing the animal with the venom of a single species or many common venomous snake species together.

Usually, a snake bite is an emergency and the victim or the attendants rarely identify the snakes (In our place, patients sometimes to our surprise, even bring the killed snake to the casualty!). Hence, to avoid confusion polyvalent sera are used.

I've written all this just to make an impression that polyvalent sera also carry antibodies against the wrong snake too, but at the end of the day, it's the right antibody that does the job.

As mentioned in the comments, apart from occasional anaphylactic reactions or serum sickness, they are pretty safe (cost/benefit) to use.


Identify this insect with a big "face" pattern on its brown fuzzy wings

I fully admit that I am not an expert on Asian insects but having trawled through various species identification keys and collections I am fairly certain that the insect you observed was:

Deltoplastis commatopa

I lifted the following species description from Wikipedia and I think it matches your description & photo rather well:

  Deltoplastis commatopa is a moth in the family Lecithoceridae. It is
  found in Taiwan and the provinces of Jiangxi, Hunan, Hubei and Sichuan
  in China.

  The wingspan is 16–22 mm. The forewings are light lilac-fuscous with
  blackish-fuscous markings, edged ochreous-whitish. There is a large
  subtriangular antemedian blotch from the dorsum nearly reaching the
  costa, connected with costa by an angulated mark. There is a large
  triangular postmedian blotch, its base posterior, reaching the costa
  and the dorsum, its apex cut off by ochreous-whitish to form a
  tadpole-shaped mark. The terminal area beyond this irrorated
  (speckled) ochreous-whitish, a blackish marginal line round it. The
  hindwings are fuscous, darker posteriorly.

Here is a screenshot of the entry in the Global Biodiversity Information Facility:

You can see from the entry that several occurrences have been reported (with images) by people in Taiwan.

I also found this Taiwanese biodiversity website (in Traditional Chinese) and thought I would include it here (although I have to admit that I am not able to read Traditional Chinese).


Acclimatization increases cold resistance of ants [1]. They have a strong adaptability to different environments [2].

When it comes to the red imported fire ant (Solenopsis invicta) here are some numbers (from [2]):

  When the exposure time was 0.5 h, the survival rate of workers was 15.3% at -14°C. At the exposure time of 1, 2 and 4 h, the entire lethal temperatures for S. invicta were -13°C, -9°C and -9°C, respectively. When the exposure temperature was -10°C, all workers died within 240 min; while at -11°C, it took only 120 min.

References:

Modlmeier AP, Pamminger T, Foitzik S, Scharf I. Cold resistance depends on acclimation and behavioral caste in a temperate ant. Naturwissenschaften. 2012 Oct;99(10):811-9. doi: 10.1007/s00114-012-0963-8. PubMed PMID: 22955370.
Xu YiJuan; Lu YongYue; Huang Jun; Zeng Ling; Liang GuangWen. Cold hardiness of natural populations of the red imported fire ant, Solenopsis invicta Buren (Hymenoptera: Formicidae) in Shenzhen, Guangdong. Acta Entomologica Sinica 2009 Vol. 52 No. 9 pp. 974-983.


In bees that dance in the dark (not all do, some dance in the light) they don't watch the dance, they participate. The follow the dancer using their antenna and sound to keep track of them.

Beehives are often dark, so instead of watching the scout dance, the recruit bees follow the dancer using their antenna and the sounds produced during the dance to determine the directions to the food source.

https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/waggle-dance#:~:text=The%20dance%20conveys%20information%20about,directions%20to%20the%20food%20source.


Is it possible to build a hive for bumblebee or hornet

Yes, it is very common practice and there are many instructions and plans for beehives/nests available online, there are some for wasps


Can Mono-Cell or other organism self-replicate?

The short answer is yes, there are single-celled organisms that can reproduce without another "partner". Probably the most famous example is that of bacteria.

What you're talking about is known as asexual reproduction. In bacteria, the process is known as binary fission, where one bacterium (known as the parent cell) divides into two organisms (known as daughter cells). These two cells will be genetically identical (barring any mutations) to the parent cell, because there has been no combination (for lack of a better term) of DNA, as there is in sexual reproduction.

The process works the same way it does in cells in multicellular organisms, such as humans: DNA "unwinds" (again due to lack of a better term) in the center of the cell, complementary bases are added to each of the now-separate strands (adenine with thymine, guanine with cytosine), the other parts of the cell are duplicated, and, gradually, the bacterium splits in two. The process can be very quick, compared to the nine months humans spend in the womb.

Asexual reproduction is not unique to single-celled organisms, though. While it is prevalent (and easy) in bacteria, some multicellular organisms reproduce asexually. Some plants are capable or this via self-pollination, and there have been some reports (albeit rather dubious) of certain "common" animals reproducing asexually.

There are advantages and disadvantages to asexual reproduction. One advantage is obvious: no mate necessary. As long as an organism has enough energy and nutrients to reproduce, it can. Also, the process is quick, and easy. There are some disadvantages, though. The big one is that there is no recombination from multiple DNA sources - that is, the resulting organism will have exactly (again, barring mutations) the same genes as its parent - for better or for worse. If an asexually-reproducing organism has a defect that still allows it to reproduce, chances are, its offspring will have that defect.

Some sources:

http://plato.acadiau.ca/courses/biol/Microbiology/Replication.htm

http://www.yourarticlelibrary.com/biology/asexual-reproduction-in-animals-characteristics-occurrence-and-types/11727/

http://www.mpipks-dresden.mpg.de/~mbsffe09/talks/Krug.pdf

http://www.britannica.com/EBchecked/topic/498542/reproduction


Can a same gene stretch from one chromosome to another separate chromosome?

Usually not (as described in the other answer, non-contiguous pieces of DNA are not considered as a part of a single gene). However there are some cases of trans-splicing in which the spliceosome can splice together RNAs arising from different genomic locations. But these are rare and do not have a direct effect on distinct phenotypes such as eye colour, to be classified as genes. Not much progress has happened in this aspect of transcriptomics, actually.


Guide to learning about Population biology / ecology / dynamics for a non-Biologist

There are three seminal works that will give you an excellent grounding in the study of dynamical systems in population biology.

The first details the foundations of population genetics:

Crow, James F., and Motoo Kimura. An introduction to population genetics theory. (1970).

The second deals with population ecology:

Maynard-Smith, John. Models in ecology. CUP Archive, 1978.

Finally, the field of evolutionary game theory has recently embraced a dynamical systems approach to studying populations under the guise of a new theoretical framework known simply as evolutionary dynamics:

Nowak, Martin A. Evolutionary dynamics. Harvard University Press, 2006.

I would probably read these in reverse order. The introduction to Maynard Smith's book has a nice discussion about some of the interrelations between population genetics and population ecology. Most of the original work was done by Fisher, but you don't want to read his stuff - it's famously inaccessible.

It is probably worth me telling you that a lot of mathematical biologists don't actually use dynamical systems approaches in their work. Instead, they favour optimisation models. A balanced discussion about the benefits of this approach, and some of the limitations of the dynamical systems approach can be found in these papers:

Smith, J. Maynard. "Optimization theory in evolution." Annual Review of Ecology and Systematics 9 (1978): 31-56.

Parker, Geoffrey A., and J. Maynard Smith. "Optimality theory in evolutionary biology." Nature 348.6296 (1990): 27-33.

As it happens, my soon to be submitted doctoral thesis is on dynamical systems in biology. Hopefully one day I will be able to add my own book to this list :)


How many versions (alleles) of a gene can we carry if every chromosome is in pair?

The phrasing "if every chromosome is in pair" sounds a little bit funny. But it probably mean "or a diploid individual".

If an individual is diploid, then it has two copies of any given locus. If the term is new to you, a locus is a position in the genome (it may correspond to a gene or not). With two copies an individual can carry maximum two different copies, that is two alleles. The answer is two.

  What happens during the gamete formation (meiosis) ? Do the gene pairs stay together?

You nailed it!

  What happens then to the paternal and maternal sets of genes that we inherited ?

This is a slightly vague question IMO but I would suppose the main point that is being expected is a description of segregation and recombination (cross-over). You answer was good but I would suggest.

"The maternally and paternally inherited haplotype will recombine (cross-over) during meiosis so that a gamete resulting from meiosis will contain a single haplotype which is a 'mixture' of the maternally inherited and paternally inherited haplotypes."


Criteria for the numbering of human chromosomes

Why do you think it was "fixed?"  Here's a nice review of the history of human cytogenetics, which included not only the original image from 1956 but points out a report which comments on the standardization of chromosome number.  The autosomes were indeed numbered by length, and the sex chromosomes are traditionally put at the end as they are "numbered" 23 but clearly function quite differently.  Gene content was decades away from being known at the time, and honestly isn't even known now.  It's also just as arbitrary; simple size is easy enough and makes for rather nice pictures.


What is the name of the bird which feeds on penguin blood and meat in Tristan island?

You almost certainly mean the Tristan Thrush, Turdus eremita, which is endemic to Tristan da Cunha. The species is considered to be an opportunistic omnivorous scavenger, but their diet includes the eggs and chicks of many seabird species, as well as the adults of some smaller seabird species.

The Wikipedia page for the species mentions that Tristan Thrush has been recorded drinking penguin blood, citing a BBC documentary which I don't have access to. Five species of penguin have been recorded on Tristan da Cunha, but only the Northern Rockhopper Penguin breeds there (the others are rare visitors to the island). Given the nature of penguin colonies (i.e., densely-packed, and with abundant chicks as well as occasional sick adults), there would be many opportunities for an opportunistic omnivorous scavenger to eat penguin blood, chicks, eggs, or carrion.


Are releasing-hormones and release-inhibiting hormones from the hypothalamus ever present in the blood?

I think your teacher means that these hormones only go from the hypothlamus to the anterior pituitary gland, where they stimulate hormone secretion. Like, for example, of the FSH or LH, who are stimulated by GnRH. GnRH is not present in the systemic sirculation, but it's definately present in the one between the hypothalamus and the APG. FSH and LH are though. I don't remember the name of the small blood-system between the hypothalamus and the APG, but I don't think it's connected to the systemic circulatory system.


What is the difference between a predator and a parasite?

Good question.

There is no fundamental difference between parasites and predators.

Ecological Interaction

In terms of ecological interaction, they are both defined as an interaction where one species benefits and the other suffers from the interaction.

Intuition parasite vs predator

In general predation is viewed as a big individual eating a smaller one while parasitism is when a small individual eats a bigger one. These general intuition however fails to consider a number of cases. Here some cases I can think of

Examples when intuition don't match the above picture

Generally considered as predation but does not fit the above picture-based definition:

social animals attacking in groups preys that are much larger than themselves - non-social animal attacking prey larger than themselves
herbivores browsing on large trees

Generally considered as parasitism but does not fit the above picture-based definition:

indirect effect of habitat modification that would rather be considered as parasitism.
Species that take advantage of parental care of another species by mimicking babies (but being larger)
Individuals of large species stealing the habitat built by a smaller species
Batesian mimicry (see this post; Thank you @WYSIWYG and @NL_Derek for the comments)

Population culture vs science literature

In the popular culture, some people call parasites only endoparasites. This concept is also misleading and not so much in accordance with the general literature in biology.


What features cause mechano sensory adaptation?

At the molecular level this is called receptor desensitization. This is the reason why for example spices (like red hot chili paper) taste more pungent the first time you put them in your mouth and less and less subsequent times (in this case the receptor is called TRPV1).

Mechanosensory perception is mediated, at least in part, by similar transient receptor potential (TRP) channels therefore mechanosensory perception is also subjected to desensitization at the molecular level. In this particular case it is specifically called homologous desensitization.

This is, in my opinion, the primarily reason why a constant stimulus will stop producing action potentials, in essence the receptor will be desensitized and does not provoke a membrane-potential change that mediates the transmission of a neuronal signal.

Footnote

Desensitization in TRP channels happens because those channels open to let $Ca^{2+}$ ions to enter the cell and after prolongated stimulation the intracellular $Ca^{2+}$ concentration will reach the same $Ca^{2+}$ level of the extracellular medium preventing more $Ca^{2+}$ ions to enter the cell.

$Ca^{2+}$ influx into the cell is what provokes a difference in membrane-potential (i.e. the cell is now electrically charged) which mediates a signal that is then transmitted to the neuronal circuitry.


How does lactulose cause the removal of ammonia from the colon?

Excess nitrogen must be excreted by the body and can come from nitrogen in the diet (e.g. amino groups from excess amino acids) or nitrogen-containing compounds produced by bacteria in the gastrointestinal tract (GI tract).
Normally the liver and kidneys are involved in excreting ammonia ($NH_3$) and ammonium ($NH_4^+$) from the body. Ammonia can be toxic in high concentrations, but the body can detoxify it through conversion to other nitrogen-containing substances (i.e. urea) or excrete the ammonia itself.
Ammonia in the blood is freely filtered at the kidney glomerulus and can be "trapped" in the urine flow by accepting a proton to become ammonium (i.e. $H^+ + NH_3 = NH_4^+$) . Because of the positive charge the ammonium ion is unable to passively diffuse back across the tubules into the blood. This is one mechanism that ammonia is excreted. In the liver, the Urea Cycle (see any basic or clinical biochemistry text for more information) is a set of enzymes that converts most of the excess nitrogen in the form of ammonia to urea, which is a non-toxic, water soluble organic compound that can also be excreted in the urine. The body uses these processes to dispose of excess nitrogen from amino acids as well as ammonia that is produced as a by-product of bacterial metabolism in the GI tract.
Some patients with significant liver disease (e.g. cirrhosis from either NAFLD, hepatitis or any other liver-damaging disease) have lost the ability to convert all the excess ammonia to urea. In these patients, an easy way to prevent excessive nitrogen uptake in the gastrointestinal tract is by treating them with lactulose. Lactulose is a carbohydrate that that is not digestible or absorbable by the body, but is osmotically active (pulls water into the intestinal lumen) and acts to speed up intestinal transit. Since lactulose works by speeding up GI transit it makes you stool more frequently (which is why it is very useful for constipation). For liver disease patients, however, the lactulose acidifies (i.e. decreases pH) the lumen of the intestines and ammonia is protonated to form ammonium, which effectively traps it in the intestinal lumen. A lot of the excess ammonium can then pass into the feces and decrease the amount of ammonia that the liver needs to process. This is similar to the mechanism of ammonium in the urine as mentioned above. Additionally, lactulose also decreases the amount of GI bugs that produce ammonia containing compounds as well, which also lessens the amount of ammonia for detoxification by the liver. (Lactulose can also be used for a treatment for small intestinal overgrowth). These GI bacteria metabolize dietary amino acids and other compounds in the gut for energy metabolism, which liberates nitrogen-containing compounds that can be absorbed by the intestines.
Edit: Here is a link for a great reference on NCBI that explains the mechanism of action of lactulose.


What are the disadvantages of forbidding flights to and from the African Ebola region?

I think the disadvantages are mostly economical in that region and so they has nothing to do with epidemiology. Possibly a long term effect can be, that the economy of the region turns from bad to worse, which can affect the healthcare too, but that's just speculation.

The advantages are obvious, ebola is quarantined at some level, so these measures prevent or at least slow down its spread around the world.


**** "What is a genomic imprint? How does genomic imprinting take place?"**

Genomic imprinting is an epigenetic mechanism  of inheritance which allows genes to be expressed differently depending on which parent they come from. This means it is modification of the genome, or changes what the genome produces, without changing the nucleotide (DNA) sequence. The result of imprinting in diploid organisms is that one of the two alleles is silenced.  This page provides a good overview of imprinting.

Two major mechanisms are proposed called DNA methylation and histone modification though others may yet be discovered. DNA methylation silences a gene by adding methyl groups to nucleotides (it modifies the nucleotide but not the sequence) which affects how they are expressed, whilst the exact mechanism is unknown (at least I can't find one on scholar) it does appear to be a key factor in some cancer growths. Genes can also be silenced by histone modification, binding a gene to histones reduces its activity, ie it produces less product.

Genomic imprinting was first described in Mealy Bugs (or at least this is one of the first described) which silence half of their genome in males. Whilst females are fully diploid, the male is also diploid but one half of the genome is silenced, making them effectively haploid. This is done by turning one half of the genome heterochromatic.

  ****"If I say that "this" allele is maternally imprinted does it mean that
  the allele of the gene is passed only by the mother? If a pedigree is
  given, how can we identify whether the trait is paternally imprinted
  or maternally imprinted?"**

Specific control of a gene, rather than entire chromosomes described above, is only known in plants and some mammals. In this case, when a gene is imprinted, the gene is silenced. An example is Igf2 in mice described in the below diagram which is maternal imprinting (ie the mothers allele is silenced). When the mother has a mutant allele and the father a normal allele and normal offspring is produced. When the male passes on the Igf2 mutant the offspring is mutant because the mother's normal copy was imprinted.

  The Igf2 gene can be seen in the above diagram. This is the one of the
  first evidences of genomic imprinting discovered. In the first part of
  the diagram a mutant gene trying to make the mouse offspring dwarf is
  passed from the mother. It can be seen that the mouse is not dwarf
  because the allele for size in this mouse is an imprinted. The
  maternal allele is not expressed, so the dwarf trait is not expressed
  in the offspring, only the normal size trait from the father is. In
  the second part of the diagram the father passes on the mutant gene
  and therefore all the offspring will be dwarf because the size trait
  is completely dependent on the paternal allele, which in this case is
  dwarf. - Creating Variation

The page this diagram and quote comes from also has a good section on genomic imprinting.


does phagocytosis dependent on opsonization?

Well, phagocytosis does not depend on opsonization, but it works better with it because the macrophages can detect the intruders more easily, but the secondary inmune response with IgG depends on the work of the APC cells, so let`s say a bacteria gets in your body for the first time, it can get phagocytated by a macrophage that will after present the parts on his MHC II to start the secondary inmune response.


Features in individuals causing high population variation

I believe there are evidences in both directions in terms of mechanisms to favor variation in a population: outbreeding and crossing within individuals that look alike. There is a fine line between the two. Outbreeding helps in keeping variation and mixing variants that appeared in different parts of the population, but too much outbreeding can generate inviable offspring. Too much inbreeding also reduces viability. Certain plants have features that are selected to favor outbreeding and make inbreeding incompatible by rejecting incompatible ("self") pollen (self-incompatibility mechanisms).


How can the leakage of mitochondrial protons generate heat?

Uncoupling ATP synthesis from the ETC (electron transfer chain; this is where oxidation takes place) by thermogenin or any other method means that the energy used to generate or uphold the proton gradient gets 'lost'.

Since physics teaches us that energy is only transferred and never truly lost, the energy consumed by the ETC must most go somewhere - heat / thermal energy is the easiest and therefore most likely option.

References

Wikipedia article on Uncoupling Proteins
Uncoupling article written in chemical terms
Short general article about brown fat and heat production


How does the brain know where a signal came from? What is the addressing system

The brain knows where a sensory signal came from by what neuron is doing the signalling.  The incoming neuron is dedicated to signals from one source and, since it is not shared by other sources, does not need to have an encoding as to what the source was. When your toe touches something, the sensation causes a pulse which, amazingly, travels along a single nerve cell (neuron) up to the brain stem.  That neuron has its nucleus at a dorsal root ganglion located by the spinal cord, and has a fiber (axon) that extends to the source (toe) and another extending up to the brain stem.  This pathway is called the PCML pathway and the Wikipedia article has some readable details.  This page has a schematic and tabular summary, while this site has a good descriptive overview.

If a robot were built along the same sort of design, to determine what was happening at 1000 places in its body, it would have 1000 wires running to its central computer.  You probably wouldn't choose to use such a design, but then you probably wouldn't be designing a robot that has to build itself from raw materials.


To the best of my knowledge, the only solid organ neoplasm routinely treated by Tx, at the moment, is hepatocellular carcinoma (liver), and even that under very strict conditions. For the rest, transplantation is currently not a standard therapy because of the very real possibility of accelerated growth of micrometastases under severe imunosuppression after the transplant.

And yes... a tumour transplanted into a person would grow, and fast, again because of immunosuppression.

If you're asking this for a practical reason, I'd advise you to talk to the oncologist involved in treatment for a thorough explanation of why this wouldn't work / referral to an applicable study, if there is one.


From wikipedia > tardigrade

[Tardigrades are] considered cosmopolitan and can be located in regions all over the world.
Tardigrades are often found on lichens and mosses. Other environments are dunes, beaches, soil, and marine or freshwater sediments, where they may occur quite frequently (up to 25,000 animals per litre). Tardigrades, in the case of Echiniscoides wyethi,[20] may be found on barnacles.[21] Tardigrades can be often found by soaking a piece of moss in water.

Tardigrades are, in fact, very common. See the simple video how to observe tardigrades. If the people you've met have rarely seen tardigrades, it is probably because they are not looking for them.


Mold is a general name for many species of Fungi, which are heterotroph so they need organic material to feed on. You can see them grow on fiberglass because many organic material can accumulate near or on fiberglass (skin cells, plants root hairs, microbes, oils) and become substrate for the mold.
If you want to grow a specific mold you should first identify it to find the best substrate for that species and not for other. If you simply want mold you can use some kind of starch on the fiberglass and keep it moist (not wet, wetness will give you also oomycetes and bacteria). No need to spray it every 2hrs. You can close the fiberglass with a box, dark box is better (bacteria grow best with light).
You can take (with mask and gloves) some mold and put it on your fiberglass to promote the growing of that mold.
Describing your mold or posting a picture can help to identify. If you see two different colors report both of them and location (center, periphery)


Hundreds of OP's have been made since the 1930's. Phosphoric acid is used in Coca-Cola and organophosphates are esters of H3PO4, you can study ester lipid/aqueous drug chemistry. They have many different targets: http://www.scielo.br/img/revistas/jbchs/v27n5//0103-5053-jbchs-27-05-0809-gf04.jpg

OP's are lipophilic. Lipophilic substances can dissolve into cell walls which are lipid bi-layers, straight into the DNA of cells and also into the nervous system.

They can travel through cellular membrane, alveolar and dermal membranes, through dermal glands, cell walls and from one organ to another. The degree of lipophilicity of drugs cause them to either stay inside the cell membrane or go through. Prozac also being lipophilic. The body is made of a mostly aqueous phase and also a lipid phase.

Many OP's contain Sulphur and they are bioactivated through desulfurative oxidation and turned into the corresponding oxon form by the liver so the organic chemistry inside the body is very complex: dealkylation, dearylation, phosphyrylation, carboxylation, hydrolysis and they are very reactive with metabolic compounds in different phases. They can be combined with absorption facilitators to pass the skin barrier and paired with radicals which are activated by the liver.

A recommended text on the toxicity: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0103-50532016000500809

OP and acetylcholine are both esters.

Here's a good chemistry animation of AChE enzyme inhibitor process: https://youtu.be/fIvF1rhp1nA

And this one, about non-competetive inhibition of AChE:
https://youtu.be/_jfGKbbZStw
general AChE info:
https://www.youtube.com/watch?v=-gIqZ8IxctE

AChE inhibitors that affect lots of organs such as peripheral and central nervous systems, muscles, liver, pancreas, and brain.

They lead to a characteristic toxidrome of hypersecretion, miosis, dyspnea, respiratory insufficiency, convulsions and without an antidote, death.

They can bind to fatty elements inside the body, like the central nervous system. They can exert damage through phosphorous-alkylation of cellular macromolecules (e.g., DNA, proteins) and intense activation of pro-inflammatory pathways.


SYBR green is designed to be much less carcinogenic than ethidium bromide (EtBr).

All these gel dyes work by intercalating themselves into the DNA stack between the bases specifically which has a great potential for causing mutations and messing with the workings of the nucleus.  My remembrance is that the SYBR and GelGreen/Red etc dyes are large and relatively hydrophilic and can't find their way into the nucleus, greatly reducing their toxicity.  They also do not transfer energy to the DNA itself due to their structure and so also cause less DNA damage when being viewed on a transilluminator.


What types of light can't a plant photosynthesize in?

Chlorophyll can use a quite broad range of light for photosynthesis, the only range where it is not working is approximately between 500 and 620nm. See this adsorption spectrum of chlorophyll (from the Wikipedia article on Chlorophyll):

The lack of chlorophyll to absorb light between 500 and 620nm (roughly) results in the green color of leafs, because this light is reflected.
Besides the wavelength also the energy of the light is important, so plants will grow better in sunlight than in the light of your monitor. This link about the maximum effectiveness of photosynthesis is also interesting.


Reference to hypothesis about breast sexual attractiveness?

Eventually, I found it, here it is:

  In considering the human animal, zoologists proposed that the human
  female is the only primate that possesses permanent, full-form breasts
  when not pregnant. Other mammal females develop full breasts only when
  pregnant. The zoologist Desmond Morris proposed that the rounded shape
  of a woman's breasts evolved as frontal, secondary sex characteristic
  that is a sexual-attraction counterpart to the buttocks, and so
  encouraged frontal copulation, the reason being that while other
  primates mate by means of the rear-entry position, the upright,
  bipedal human being was likelier to successfully copulate face to face
  in the missionary position.

https://www.reddit.com/r/askscience/comments/uflgy/why_are_breasts_so_attractive_after_all_theyre/


Approx 1cm, white and brown insect feeding on fruits, what are they?

The picture isn't really focused on the insects. I think those are Crane Flies.  Crane flies have small club like appendages under their wings called halteres,which are used for steering in flight.I dont know the genus or species of these insects. The order is Diptera, the family is Tipulidae. Here are two links.
[https://www.orkincanada.ca/pests/flies/crane-flies/
[https://simple.wikipedia.org/wiki/Crane_fly


Why does the sex of the parent species determines the species of a hybrid offspring

I thought that the only difference between the male and female reproductive cell's DNA code is the X-Y chromosome that determines gender, not differences that can define the species of the offspring. Why does this happen?

Well that is not the only difference, there are certain characters that are only transmitted by one of the parents.

First of all you have to think that the zygote (the cell deriving from the fusion of two gametes) contains the nucleus of the egg and of the sperm but the cytoplasm of the egg only (or at least in great part).
One thing that is present in the cytoplasm are mithocondria, which contain DNA, called mtDNA. mtDNA is therefore transmitted only by the mother (at least, in most species). Therefore a hinny will have donkey mtDNA, while a mule will have horse mtDNA.

Furthermore, cytoplasm contains transcription factors and various proteins that will influence the subsequent development of the zygote into an embryo and, again, these are maternally derived.

Another thing that changes is that there are certain genes on nuclear DNA which are expressed in a single-parent manner. That is, you have 2 copies of these genes, called imprinted genes, one from the mother and one from the father but only one of these copies -that of the mother or of the father, depending on the gene- will be expressed.


It appears to be a California Alligator Lizard - Elgaria multicarinata (subspecies multicarinata), although another photo from the side would be helpful for a positive ID. This species seems to fit the range for the observation as well.

According to CaliforniaHerps.com, there are no associated conservation concerns for this particular species.

Elgaria multicarinata multicarinata conservation status


What is this small black bug found in Turkey?

Looks like a scarab beetle (Coleoptera, Scarabaeidae). Species is difficult to tell without better pictures, but perhaps Scarabaeus typhon?

Edit: OP has IDed in comment as Scarabaeus jalof


The Water hyacinth and its ability to absorb pollutants from the water

Genes don't necessarily work in isolation (most don't). An ability to absorb pollutants would likely be a combination of many genes.

Also, what constitutes a "water pollutant" is very broad - you could be talking about pesticides, heavy metals, fertiliser, organic waste... If water Hyacinth absorbs all of these, it could just be the result of absorbing more water than other plants (with pollutants accumulating in the plants). Who knows - you should state your source of information.

In terms of how to figure out what gene(s) are responsible, you could consider a radioactive tracer to tag the specific compound (or even element) that you consider Hyacinth to absorb better than other plants. This might give you some idea of how it's doing what it's doing. For example, if you think it's absorbing a compound, you can tag that compound with a radioactive tracer, see where it's being accumulated (even it's path), and from there figure out what's happening.

The fastest path to figuring out which gene(s) are responsible from there would be to build up a list of all the genes you think might be involved in this path and create an array of cloned plants with those genes removed. If you remove the correct gene(s) from the equation, the plant will have less or no proclivity for absorbing the type of pollutants in question.


What does differentiation of B-cell mean?

Immature B lymphocytes mature into either plasma cells or memory cells. If a B cell is mature, that means it's already a memory or plasma cell.


Is it possible that there are unknown vitamins?

Yes, it is possible that there is a vitamin or other essential nutrient that has not been identified so far.

Essential nutrient means any substance normally consumed as a constituent of food which is needed for growth and development and/or the maintenance of life and which cannot be synthesized in adequate amounts by the body (fao.org). Essential nutrients include vitamins and some minerals, fatty and amino acids.

Choline: An Essential Nutrient for Public Health (PubMed, 2009):

  Choline was officially recognized as an essential nutrient by the
  Institute of Medicine (IOM) in 1998.

The fact that choline has been recognized an essential nutrient relatively late suggests that there may be other nutrients that are not recognized as essential today but may be in the future, for example:

Aluminum (Biocyclopedia)
Boron (PubMed)
Nickel (WebMD)
Silicon (PubMed)
Vanadium (PubMed)


How do cells know whether they should grow the hyaline cartilage?

Both growth factors and cytokines are involved but the trigger mechanism is unclear [1].

Bones grow in length at the level of epiphyseal plate where chondrocytes produce hyaline cartilage which by addition of calcium and phosphorus ions turns into hard bone [2].

It is believed that the growth process is under the regulation of local mediators like cytokines and growth factors:

  In recent years, a large number of cytokines have been discovered and their molecular structures and biological activities described. A surprisingly large number of cytokines have been shown to affect skeletal tissues, at least experimentally, making this a complex topic, but one which is furthering knowledge of how the cellular events of bone growth may be so precisely regulated [3].

References

Ossification. (2014, July 3). In Wikipedia, The Free Encyclopedia. Retrieved 15:47, September 30, 2014, from http://en.wikipedia.org/w/index.php?title=Ossification&oldid=615387908
http://www.personal.psu.edu/staff/m/b/mbt102/bisci4online/bone/bone5.htm
J.S. Price, B.O. Oyajobi and R.G.G. Russell. The cell biology of bone growth. Available from http://archive.unu.edu/unupress/food2/UID06E/UID06E0U.HTM


The smallest bird in the world is the bee hummingbird.

I think the minimum size is only limited by the size of organs. I mean that certain organs need to have a minimum size to maintain their function in the organism.


The holes are probably caused by one of a family of parasitic sponges.  The holes, as you'd expect, kill the oyster, and the sponge then takes up residence in the shell. A number of species of this family live in the Mediterranean, with Cliona apparently being the most common genus (e.g. Cliona celata and C. viridis).  Images of oyster shells after a Cliona infestation can be seen here and here; these images are more dramatic than the one you found, but show the same general pattern.


What do these novel splicing sites mean?

A splice junction is formed from a pre-mRNA (or primary transcript) whenever an intron is removed, or spliced out.  Two segments of RNA that used to be separated in the pre-mRNA are now ligated to each other, forming a junction of two exons.

RNA-Seq reads that span such a splice junction site would not align very well to the genomic sequence, however if you create a file of all the potential simulated splice junctions there may be some RNA-Seq reads that now align perfectly.

The distinction between what constitutes an intron, and what constitutes an exon is purely empirical.  While it is true that the spliceosomal complex preferentially recognizes and binds to properly juxtaposed splice donor and splice acceptor sites, a variety of different processed, mature, transcripts can result from a single primary transcript.  This differential parsing of the cis-acting sequences at the boundaries of potential introns and exons is called alternative splicing.