A couple reasons come to mind.* The purpose of root hairs is absorbtion. If you consider multiple cells along the length of the hair,  additional cell walls and plasma membranes would somewhat impede the movement of nutrients.

More importantly, the absorbtion is a function of the surface area of the hair. Smaller diameter (one cell thick) hairs provide greater surface area to volume ratio. While it's true that a larger diameter, due to multiple cells, might offer greater overall surface area, it would come at the expense of requiring more volume compared to a greater number of smaller hairs.

For example, suppose you have a certain volume of cutoplasm to spend on making root hairs. For the sake of the example, suppose the hairs are of a fixed length. If you make the hairs half the diameter you will be able to provide twice the overall surface area using the same volume of material.

* By this I mean I don't know the ultimate (evolutionary) reason and I doubt anyone does. This is probabably not an active area of research and you're not likely to find definitive answers with research. So, my answer, if you will, is conjecture.

That said, it is educated conjecture. In 24 years of teaching AP Biology, the relationship of volume versus surface area has arisen multiple times. One of the exercises I gave my students, in preparation for the exam, was to find at least ten examples. Some of the best students found many more.


Biological terminology: "codes for" vs. "codes a"

This is an English usage question more than one of biology.  The verb code has two main meanings(1):

(transitive) to put into the symbols of a code
(intransitive) to be a code symbol

The first, which being transitive takes an object, is used for the act (as by a person) of translating a plain message into a corresponding encoded form. This is not the meaning used in "AAG codes for lysine".

The second form does not take an object.  It is not being done to something, but rather is just a state of being.  This form is almost always followed by a prepositional phrase "for noun", as in "INS codes for insulin".

Hence it is not correct English to say things like "INS codes insulin", as the use of "insulin" as an object implies the first meaning, as if one were saying "INS takes an insulin molecule and puts it into an encoded form" (whatever that would mean).

The reader would likely try to interpret "INS codes insulin" with the intended meaning, but the incorrect usage makes it seem equivalent to something like "INS is a DNA sequence insulin."  Leaving out the preposition for may be shorter, but it gives a bumpier ride.

(1): Merriam-Webster.  For more variants see Wiktionary, esp. encode.


Selection for less efficient egg transfer in Human Botfly life cycle

In multi-host complex life cycles (CLCs), an intermediate host often aids in the dispersal of offspring.

In general terms, an animal, say a botfly, have an ultimate "purpose" or 'goal'  to spread their genetic information as much as possible. This could mean producing a large number of offspring and hoping some survive or it could mean having one offspring, investing a lot of energy and ensuring it does survive. Regardless, spreading genetic information often requires offspring to disperse (or be spread) a great distance, which may allow the individuals' genetic information to dominate an new region.

In the case of botflies, having an intermediate host means the genetic information can be spread a great distance.

If you're looking for a more thorough explanation of complex life cycles, this paper describes it well. There is also this site more specific to the botfly which is not peer reviewed, but well-researched and descriptive.


Why re-label the strand ends in 3' DNA labelling?

There are many ways to label nucleic acids for probes (Summary of Methods).

While there are cases where Klenow fragment-mediated fill-in should sufficiently label both strands of your probe, there are many others where this would not be enough.  Here are two illustrative, although somewhat contrived, examples:

  Example 1: Double digest with 5' and 3' overhangs
  Imagine you did a double digest with BamHI and KpnI to release your probe sequence from the plasmid in which you propagate the sequence.  BamHI will give you a 5' overhang, but KpnI gives a 3' overhang.

Resulting BamHI & KpnI double digest fragment:
  5'-    GATCCNNNNNNNG      - 3'
             |||||||||
  3'-        GNNNNNNNCCATG  - 5'

  Subsequent treatment with the Klenow fragment + $\alpha$P32-dATP + cold dNTPs will both fill-in the 5'-overhang (Klenow's 5'->3' polymerase activity) and remove the 3' overhang (Klenow's 3'->5' exonuclease activity).

Post-Klenow reaction (bold = new bases, * = radio-labeled nucleotide):
  5'-    GATCCNNNNNNNG      - 3'
         |||||||||||||
  3'-    CTAGGNNNNNNNC      - 5'
           *

  At this point only one strand is radio-labeled so the terminal transferase step is needed to add a label to the top strand.

When using $\alpha$P32-dNTPs, you often pick only one base to be radioactive (eg dATP as above).  Sometimes you also just spike the reaction with radioactive dNTP leaving a population of cold dNTPs to be used most of the time.  In either case you now have the chance of not incorporating only non-radioactive bases.

  Example 2: Fill-in reaction that fails to incorporate $\alpha$P32-dATP:

  Imagine a digest with PspI and want to fill-in the 5' overhangs using $\alpha$P32-dATP + cold dNTPs.  PspI recognizes CCWGG sequences where W is either A or T so that some fill-ins will incorporate the $\alpha$P32-dATP, but others will not.

Possible digests and fill-in reactions:
   5'-  CCTGGNNNNNNNNNNCCTGG - 3'
        ||||||||||||||||||||
   3'-  GGACCNNNNNNNNNNGGACC - 5'
                 |
         Digest with PspI
                 |
                 V
   5'-  CCTGGNNNNNNNNNN      - 3'
             ||||||||||
   3'-       NNNNNNNNNNGGACC - 5'
                 |
        Fill-in with Klenow + hot dATP + cold dNTPs
                 |
                 V
   5'-  CCTGGNNNNNNNNNNCCTGG - 3'
        ||||||||||||||||||||
   3'-  GGACCNNNNNNNNNNGGACC - 5'
          *

  Again you are left with only one strand being labeled (or no strand labeling if the sequence was 5'- CCAGGNNNNNCCTGG - 3') and a need for the terminal transferase step.


Would ovoviparous to viviparous mutation have been gradual? How would that work?

I happen to have seen a talk by an anthropologist who was working on this (i can't reference them here i'm sorry to say - forgotten her name).  I can only give an example from their work...

If you look at old world and new world primates, there is a large difference between the gestation time.  If you look at the table in the link, lemurs have half the gestation time that humans and gorillas have.

What I can recall is that the lemurs placenta lacks many of the structures that primates have (see section 5).  The lemur placenta is supposed to be primitive and a lot more like an egg sac which was internalized as opposed to a more articulated womb that primates have.  So her thesis was that eggs would start out being internalized and subsisting only on their own internal structures, still isolated from the mother, then later placental structures would come about that nourish the fetus and enable it to enjoy longer gestation and better development pre-partum.

The stage I'm describing is only the divergence between primitive wombs and 'more advanced' wombs in the sense that they were capable of supporting the fetus for 9 months rather than just 4.  That development happened over about 30 million years.  The divergence of mammals is thought to have happened about 270 million years ago.

So the rough answer would be hundreds of millions of years for the whole shebang, but internalized eggs and live birth would be a relatively smaller amount of time.


How does a cell know what function it has within an organism?

The answer to this question can be split into two parts: cell differentiation from stem cells and simple mitosis. Also, the answer I am providing mainly only applies to species that sexually reproduce.

During the primary stages of growth, immediately following the fertilisation of the female gamete, the zygote begins to divide. Most of these initial cells will not be specialised, they will be stem cells and these have the potential to asymmeterically divide. When they do this, each of the daughter cells will have a specific specialisation path to follow. Which path they will follow, muscular, neural etc. is determined by transcription proteins.

Once the stem cells have produced the correct daughter cells, the general structure of the organism will begin to take form. Once this happens and the cells have followed their development paths until they hit their final specialisation, mitosis takes over. This means that a muscle cell will divide, causing the organism to grow. A muscle cell, will only ever divide into a muscle cell, the same goes for all specialised cells. This is how an organism grows and maintains itself.

However, some stem cells do remain after the organism has matured. For instance, a mature neuron is unable to undergo mitosis, so stem cells are needed to allow for the production of new neurons to replace those that die, to take one example.

You can find out more here.


You are right, this must be a Middle spotted woodpecker Dendrocopos medius. It has clear stripes on its belly, and the black stripe on its cheek does not reach the beak. The beak is also  smaller, but size is always hard to judge.


Making a hole in a tree is okay? Or does it damages the tree?

It can have a negative effect if parasites are able to take advantage of the holes in the tree.The bark is the first line of defense against parasites and making holes without covering them tend to have a negative effect.Furthermore, the bark also protects the plants against adverse weather conditions.


Is apparent competition a suitable term in situations where one species is not negatively affected?

Competition-like interactions where only one species suffers ([0,-]) are usually labelled amensalism, so a suitable term for the situation you describe should be "apparent amensalism". I hadn't actually seen this term in use from before, but a quick Google search reveals that is in fact used. One example is in Jaworski et al. (2015):

  Indirect interactions mediated by shared natural enemies are known as apparent competition, if negative interactions are reciprocal, or apparent amensalism, if one prey suffers from the presence of the other prey (Holt 1977; Holt and Lawton 1994).


Synthesis of Fatty Acids Longer than 16 Carbons

Short Answer: Yes.
Long Answer: See this article:

The diagrams presented show how fatty acids are synthesized in microorganisms and list the enzymes found in Escherichia coli. These reactions are performed by fatty acid synthase II (FASII), which in general contain multiple enzymes that act as one complex. FASII is present in prokaryotes, plants, fungi, and parasites, as well as in mitochondria.
In animals, as well as some fungi such as yeast, these same reactions occur on fatty acid synthase I (FASI), a large dimeric protein that has all of the enzymatic activities required to create a fatty acid. FASI is less efficient than FASII; however, it allows for the formation of more molecules, including "medium-chain" fatty acids via early chain termination.
Once a 16:0 carbon fatty acid has been formed, it can undergo a number of modifications, resulting in desaturation and/or elongation. Elongation, starting with stearate (18:0), is performed mainly in the ER by several membrane-bound enzymes. The enzymatic steps involved in the elongation process are principally the same as those carried out by FAS, but the four principal successive steps of the elongation are performed by individual proteins, which may be physically associated.

Another article from NCBI states:

Primers for several mouse, rat, and human elongases have been reported elsewhere.

...and cites here for this:

Fatty acid elongases and desaturases play an important role in hepatic and whole body lipid composition. We examined the role that key transcription factors played in the control of hepatic elongase and desaturase expression...In conclusion, these studies establish a role for PPARalpha, LXR, SREBP-1, ChREBP, and MLX in the control of hepatic fatty acid elongase and desaturase expression and lipid composition.

Indeed, humans do synthesize stearic acid (C18) in their body; mainly liver and adipose tissue. See this article:

Fatty acid biosynthesis from acetyl-CoA takes place primarily in the liver, adipose tissue, and mammary glands of higher animals. Successive reduction and dehydration reactions yield saturated fatty acids up to a 16-carbon chain length. Stearic acid is synthesized by the condensation of palmitoyl-CoA and acetyl-CoA in the mitochondria, and oleic acid is formed via a mono-oxygenase system in the endoplasmic reticulum.

Now, would it be feasible or not to synthesize unsaturated fatty acids is a matter of debate. Maybe this could be helpful in this matter.


How come all my family have brown eyes and I have blue eyes?

The eye color follow quite well mendelian inheritance rules...
Probably your parents are heterozygote recessive for the blue color, hence the children have 25% of probability of having blue eyes.

Let's say color of the eyes has 2 alleles "BLACK" for the dark eyes and "blue" for the light eyes. Your parents are probably both BLACK-blue, BLACK-blue. They show the dark eyes because that allele is dominant over the blue one.
During recombination all the possible combination can come out:

BLACK x BLACK=25% resulting color=dark
BLACK x blue=25% resulting color=dark
blue x BLACK=25% resulting color=dark
blue x blue=25% resulting color=light

Check out the wiki page about mendelian rules of inheritance if you wanna know more!!
Of course in realty the situation is much more complicated, however you can still approximate the results to mendelian rules...

have fun!!


How is centriole number maintained during meiosis?

When a cell enters the cell cycle and passes through S phase, each centriole is duplicated. A "daughter" centriole grows out of the side of each parent ("mother") centriole. Thus centriole replication — like DNA replication (which is occurring at the same time) — is semiconservative.


Confusion regarding the ventricle system in the brain

I've found the answer. The entire brain and spinal cord is bounded by the arachnoid mater, thus both channels would lead into the subarachnoid space, which also circulates the fluid into the spinal cord region. The CSF exits through the arachnoid granulations, which are like valves, found on the dorsal midline, into the superior sagital sinus, where it returns to the blood stream.


Most often, it seems that Turner syndrome is due to fertilization by a sperm cell lacking a sex chromosome. I wouldn't describe such a cell as "empty": it still has the other 22 chromosomes, but in meiosis the sex chromosomes failed to segregate appropriately.

Monroy et al 2002 note that of 10 people with complete monosomy X, 9 had their single chromosome from the mother.

Monroy, N., López, M., Cervantes, A., García‐Cruz, D., Zafra, G., Canún, S., ... & Kofman‐Alfaro, S. (2002). Microsatellite analysis in Turner syndrome: parental origin of X chromosomes and possible mechanism of formation of abnormal chromosomes. American journal of medical genetics, 107(3), 181-189.


Understanding Genetic Dynamics of Specific Problem

First of all, since two is incorrect, and one is not possible, three is the most probable answer. It is also supported by the format of question that three different types of white purelines are given. Let the genes be A, B, C. Now, there are three possible ways:-

1) Each one has two homozygous dominant genes and one homozygous recessive.

2) Each has one homo dominant and two homo recessive.

3) Any one has all homozygous recessive and the rest two can have any of the above two.

The problem with (2) & (3) is that they do not explain the red F1. Red will require a dominant allele of each gene. But in crosses of (2) or (3), at least one gene will be left out.   For example, AAbbcc x aaBBcc will give all progeny with cc. So none can be red. Same problem with aabbcc x aaBBcc or AABBcc

So lets go with (1). Let

W1 AABBcc

W2 AAbbCC

W3 aaBBCC

W1 x W2. => all AA Bb Cc (Red F1 of cross 1)

F1 x F1 will be like a cross of BbCc with AA in front of all the genotypes. This will give you exactly 9:7 phenotypic ratio as mentioned in question.

Now, lets solve the question.

A) Three genes. So false

B) F1 were homozygous for one gene and heterozygous for other two. So false

C) F1 of cross 1 = AABbCc and W3 aaBBCC
Since it is evident that it is possible to inherit dominant alleles of each gene (eg. AaBbCc or AaBbCC) so red colour can come. So false

D) F1 cross 1 = AABbCc

F1 cross 3 = AaBBCc

It is evident that one segregation of gene alleles of “a” and “b” will have a dominant allele no matter what. So for a white colour, only chances are from cc. So in cross Cc x Cc there is 1/4 probability for cc. So all in all, 1/4 probability for white (since aa and bb genotypes are not possible here).

So D is True.


You can use R-coffee of the T-coffee suite of tools. In general, the *coffee tools are excellent and work very well if you can get over their author's self obsession1. R-coffee can align RNA sequences taking into account structural information:

1 The guy actually adds his name to the output of all his programs! Seriously, he does. Apart from being simply ridiculous, this also affects other programs you might want to pipe your data to. For example, I wanted to pipe t-coffee alignments to an alignment viewer and I had to parse out his effing name in order to be able to do it.


Why are women more susceptible to radiation?

It's actually because of the greater risk "from breast, ovarian, and uterine cancers" (article).  There's a more scientific write-up here, and while I don't have access the abstract implies that a more rigorous update of the exposure criteria upheld sex differences.  From a more terrestrial perspective, The Nuclear Information and Resource Service (nirs.org) has this rather incensed piece on the issue.  They cite a 2006 NAS report which

  finds that harm to women (cancer) is 50% higher than the comparable harm to men from radiation doses that fall within the legal limit to the public over a lifetime.

Basically, it looks like females are more likely to get cancer from radiation, and once they do, those cancers are more likely to cause more harm.  According to the executive summary of NASA's 2014 in-depth report:

  [A] 45-year-old man has a 344-day limit versus a 187-day limit for a 45-year-old woman, due to radiation exposures on the space station that would be typical at the time of solar maximum.

The effect of body size, however, could be the opposite.  Taller women get more cancer, with that study showing a 16% increase in incidence for every 10cm (4in) height increase.  That increase, however, is among certain types, such as melanomas, and not the above-mentioned "breast, ovarian, and uterine cancers."  Males, being taller, could therefore get more cancer overall; it turns out males usually die more from most cancers, just not (obviously) "breast, ovarian, and uterine cancers."


Does caffeine increase the speed at which sperm travels?

The cell response for caffeine, is at the molecular level of RyR (Ryanodine receptor), and the main effect could be a temporal rise in Ca+2 cytosolic concentration, so it can change the electrical behavior for the whole cell, and then affect their mobility. But the main area for RyR research is at spermatogenesis, there are a lot of papers like this one, for that topic


Yes, you can go into shock from bleeding, emotional disturbance, a heart disorder, and/or a blood infection. It causes not enough oxygenated blood to get to important organs in your body and if it isn't treated it's normally fatal.

I would think that enough pain could cause a large emotional disturbance which could result in shock.


The GNOMON and GFF folder contains the files you want, the GNOMON if you check the README relates to the GNOMON gene predictor and the GFF I think links back to the same file. I think the file you want is ref_Stegastes_partitus-1.0.2_scaffolds.gff3.gz which contains the coordinates on the scaffolds.

And as you stated you are on linux, so the best and geeky way to go is awk.

awk '!/#/{if($3=="CDS")print}' ref_Stegastes_partitus-1.0.2_scaffolds.gff3 > SomeFile.gff3

UPDATE

This part is from python. With reference to the previous user's answer if you fetch the GBK file, rna.gbk, this should allow you to fetch CDS using biopython

You should also check out Peter cook's tutorial on handling genbank files in python

from Bio import SeqIO
from __future__ import print_function

Genome = SeqIO.parse("Examples/rna.gbk","genbank")
handle = open("Examples/rna.faa","w")
for genes in Genome:
    i=1
    for Feature in genes.features:
        if Feature.type=="CDS":
            FASTA=Feature.extract(genes.seq)
            print(">"+genes.id+"_CDS_"+str(i),file=handle)
            print(FASTA,file=handle)
            i += 1

I would recommend that you install anaconda, it is a package management software, which when installed installs its own python version and alongside it installs some 400 different packages. Instructions are available on the link. So these packages should come with the link.

After you have installed anaconda, put all that code from up there into a Myfile.py and execute on the command line with python Myfile.py.


Why cannot machines use energy stored in a way similar to biological systems' energy storage?

The activation energy of breaking these covalent bonds is high. Biological systems use phosphorylases to couple ATP to glycogen such that the high energy phosphate bonds then supply some of their energy to break the covalent glycosidic bonds in glycogen

So problem 1, high activation energy.

Secondly, how are you going to store the energy in the machine? Conventional electrochemical cells use something like what was written about membrane potential. Their energy is accessible as it is in a form of an electrical potential. When you expend energy to break storage molecules into glucose, there's not much for you to do on the glucose other than to burn it. Burning it is extremely inefficient and makes up a huge amount of energy loss to wasted heat. The other way would be to oxidize it. You'll need something to accept the electrons (NADH and FADH in biological systems), something to overcome the high activation energy of oxidizing the bonds at every stage (more ATP coupling), something to harness the high-energy electrons from glucose (electron transport chain/chemiosmosis). In all, it is too complicated to be replicated efficiently.

So problem 2, there are many complicated steps involved.

This is why only simpler versions of the above exist. Power to gas shows us the splitting of H2O into H2 and O2. This is akin to only one stage of bond-breakage in respiration, and is simple enough to carry out (through electrolysis). H2O donates and another H2O accepts the electron. Energy is supplied as a electrical potential in the circuit instead of ATP coupling from enzymes.

Last problem is, there really isn't a need to store energy in other forms than an already-existing energy storage molecule. Most of our energy storage is in the form of carbon compounds, and electricity. Carbon compounds are high energy density, and electricity is easy to manipulate. It is perhaps trivial to the world to attempt condensing table sugar (glucose) into starch. It is not efficient enough to be impactful. Biological systems need to do this because storage is on a scale comparable to the cell body, and directly relates to survival. High blood glucose in animals might lead to hyperglycemia, triose phosphate (product of respiration) is used for lipid formation and in turn building of cell membranes, glucose molecules are used as monomers in the production of cellulose, aka cell wall in plants, (a heck ton of other metabolic pathways exist), etc.

This link shows us the different ways of energy storage in our world. We're not limited by biological constraints, so even compressing H2 into a liquid, will be more efficient than interconverting that into other forms of chemical energy, if you're talking about for pure "storage"'s sake.

I highly recommend reading up on photosynthesis, to see how biological systems harness energy from the sun, and store that into covalent bonds between CO2 molecules. More specifically you can look up Krebs Cycle.


Try running software like Censor. If checks in the reference repeat databases and detects microsatellites. So, you can most probably be sure of the microsatellites generated. Moreover, the microsatellites have their information present in the GIRI database. So, you can get more information, if you find the microsatellite in your sequences. Hope this helps.

~Rama.


Can we determine a person's age by dating methods or other means?

No, one can't confirm age by carbon dating. That doesn't mean we can't make a decent guess by other methods.

There is an interesting case of a 33 year old Texas woman who enrolled in 10th grade in Texas. She said she had no transcripts because she had been homeschooled. She looked like a teenager and acted like a one too. She even fooled her new 23 year old boyfriend. So it happens. It also happened in the Little Leagues World Series, if I remember correctly. A twenty-something guy passed himself off as a 14 year old. He was a star (for a while).

In children and adolescents, the combination of a dental exam, dental films and bone X-rays can narrow a one's biological age well. Once the bones are done growing in length, that avenue is closed.

After that, someone might have to provide a tooth. Chemical analysis of tooth dentin, such as aspartic acid racemization, has shown reproducible and fairly precise results.

Global levels of carbon-14 (14C) have been carefully recorded over time. In one 2010 study, forty-four teeth from 41 individuals (one per individual) were analyzed
using aspartic acid racemization analysis of tooth crown dentin or radiocarbon analysis of enamel. Teeth from individuals with dates of birth ranging from 1936 through 1994 (aged 13–70 years) were analyzed, and where the date of birth was known, yielded a 14C-based date of birth estimation accuracy of 1.3 years (S.D. = 0.9 years). In one case, a date of birth was determined to be 1948.4. In another, it was determined to be 1988.

  [T]en of these were split and subjected to both radiocarbon and racemization analysis. Combined analysis showed that the two methods correlated well (R2 = 0.66, p < 0.05). Radiocarbon analysis showed an excellent precision with an overall absolute error of 1.0 ± 0.6 years. Aspartic acid racemization also showed a good precision with an overall absolute error of 5.4 ± 4.2 years. Whereas radiocarbon analysis gives an estimated year of birth, racemization analysis indicates the chronological age of the individual at the time of (tooth extraction).

During the course of aging, l-forms of amino acids are transformed by racemization to the d-forms.

  [T]he extent of racemization of amino acids may be used to estimate the age of various tissues. Of all stable amino acids, aspartic acid has one of the fastest racemization rates and is therefore the amino acid most commonly used for age estimation....[T]eeth are the tissue of choice for age estimation analysis.

Both methods have strengths and limitations.

  The radiocarbon birth dating method can tell the birth date of the person regardless of the time of (extraction). However, the time window for this analysis is limited to subjects born after the early 1940s because the calculations are based on the measurement of bomb pulse-derived 14C.

Clearly this wouldn't be of too much use in people trying to pass themselves off as teens.

Some studies of aspartic acid racemization report accuracies of age ±3 years. The radiocarbon and racemization can further narrow it down.

Why did Charity Johnson pretend to be a teenager for 20 years?
Age Estimation in Forensic Sciences APPLICATION OF COMBINED ASPARTIC ACID RACEMIZATION AND RADIOCARBON ANALYSIS
Strategy for the estimation of chronological age using the aspartic acid racemization method with special reference to coefficient of correlation between D/L ratios and ages


I suspect that you are correct, "subpatellar tendon" is referring to the patellar ligament. Although it is small, in the image below, (3) is the tibial tuberosity and (5) is the patella. (4) which is labeled "subpatellar tendon" is between the two. The only structure between them is the patellar ligament. So, I think this is what it meant (though in 20 years of teaching, I haven't heard that terminology).


Is the knee locking mechanism present in animals?

Yes, the mechanism of patellar locking does occur in quadrupeds too. Although they are 4 limbed, a major portion of the weight is borne by the hind limbs. This is known as the stay apparatus and includes the mechanisms of Patellar locking, reciprocal mechanism and check apparatus.

On the other hand in the forelimb, although there is no locking mechanism as such, there exists a neat difference from the human anatomy. Human forelimbs are majorly adapted for manipulation but for quadrupeds, they are weight bearing. There exists what is called the stay apparatus - which includes the suspensory apparatus and the check apparatus.

For a detailed explanation for the interested reader, heres a helpful link - https://en.wikivet.net/Stay_Apparatus_-_Horse_Anatomy


Isolating the gene of interest for protein production

As you already wrote there are two basic ideas: Synthesis of the desired gene sequence and use of existing DNA.

DNA Synthesis is getting cheaper so it is becoming the method of choice for generating DNA-samples up to about 5000 bp (for example see the IDT-page for commercial gene synthesis). If this is too short for your desired sequence there is the possibility to split the gene to different of those synthetic sequences and to fuse them using Gibson-Cloning (Gibson et al. 2009) - after adjusting the synthetic sequences so that there is an overlapping sequence. Alternatively you could use classical cloning - provided there are suitable cleaving sites in your sequence.

If you don't want to synthesize the DNA and have a template available you could design suitable primers and amplify the gene from the template using PCR and purify it by gel-electrophoresis. Inserting the sequence into a vector then requires that you find suitable cleaving sites within the sequence and the vector.


Salt Bridge for Microbial Fuel Cell: Full or Partly Full?

Main function of the salt bridge is to conduct electrons. It should be in such a way that the agar within the PVC pipe from both end should be in contact with anode and cathode. so I would say keep it completely filled for better conduction.


How does transition of osmoregulation occur in fishes when they migrate from sea to rivers and vice-versa

I found a publication related to the osmoregulation in salmon that might be interesting to you. I'm copying the abstract because it basically answer your question.

  Smoltification, also called parr-smolt transformation, is a complex developmental process that consists of a number of independent, but coordinated changes, in the biochemistry, physiology, morphology and behavior of juvenile salmon in their transition from freshwater to seawater life. A key component of smoltification is represented by the physiological adaptations that enable smolts to thrive in hyperosmotic environments. Instrumental to this process is the ability of smolt gills to gradually become capable of actively secreting salt through specialized cells known as mitochondria-rich (MR) cells, ionocytes or chloride cells. NaCl secretion by teleost gills is therefore accomplished via the secondary active transport of Cl - and the passive transport of Na + . The driving force for active transport is provided by Na + /K + ATPase, which maintains low intracellular Na + and high intracellular K + concentrations. However, this NaCl secretion mechanism needs at least two different ion channels: A CFTR type chloride channel for the passive exit of Cl - and a potassium channel to recycle extracellular K + , which is a thermodynamic prerequisite to work under conditions imposed by high extracellular salinity in seawater. The characteristics of K + channels required for NaCl secretion from MR cells into seawater are still unknown for Salmo salar and only recently have begun to be studied in other teleosts.

You can find the complete paper here.


All flowering plants gives fruits. Why does jasmine flower plant not yield fruits?

Flower gives rise to seeds and fruits which are the ways through them the plant distributes the seeds.

Here, one should differentiate botanic term "fruit" and general common meaning of the word "fruit" which are not the same.

Botanic fruit can be subtle, not fleshy and come as a grain or pods.

Jasmine fruits are black berries.


What is the relation between plasmid concentration and mRNA levels?

The amount of transfected plasmid does not correlate at all with the protein expression level. After transfction, usually each cell is going to get and keep only one copy of the plasmid. Once the plasmid is in the cell, it will be replicated and the cell will contain X copies of it, depending on the plasmid copy number. In general, plasmids with low copy numbers correlate with lower protein expression compared to plasmids with high copy number. But there are also exceptions:

  Expression of genes under control of EF1α promoter appears to correlate with plasmid copy number.  In contrast, expression driven by the more traditional CMV immediate early promoter appears less plasmid copy number dose-responsive (ref).


Number of different clones of B lymphocytes

Alternate spicing of mRNA is a real phenomenon, but it's not the source of immune cell receptor diversity.  The DNA of immune cells is rearranged in a slightly random manner, to make a receptor with a random sequence in the variable portion of the receptor.  As Armatus already said, the process is VDJ recombination.  Here is a link to a textbook on NCBI

https://www.ncbi.nlm.nih.gov/books/NBK27113/


What are important temperature breakpoints for plant distributions?

Can't help with citations.  For temperate climates there are several critical temps that I know of:

First one is 0 or possibly -2.  The freezing point of water.  Most plant cells have enough dissolved material in their sap/protoplasm that there is 1-2 degrees of freezing point reduction.

Next one down seems to be somewhere around -10 C.  There is a big reduction in plant species counts around this temp.

Not sure where the next one is.  Jack Pine can tolerate temps down to -60C  Apparently their protoplasm has enough sugars and alcohols that it becomes a glass -- no expansion.

Climate imposes other limits.

I bought 500 mountain hemlocks one year.  Everything I read said zone 3.  Maybe for the tops.  Where they grow, there is typically several feet of snow in winter.  Roots never got below freezing.
In our region of central Alberta Crimson King Norway maple is hardy -- most of the time.  If it gets cold early, say November, it kills the buds.  It's not just how cold it gets, but when and how fast it gets cold.
Near Edmonton we can grow a variety of birches.  Calgary 300 km south is a growing zone warmer than us, but birches don't do well there.  The chinooks are warm enough that they break bud, then the buds die when it gets cold again.  Other plants avoid this by having a chilling requirement matched to our winters.
Our winters are very long.  Some of the problem isn't cold as much as desiccation.  In some cases a warmer winter will be more fatal -- warmer air can draw off more moisture from buds and twigs.
I think there are temps above freezing that are important:  When trying to grow eggplant, any day that got below +10C seem to make the eggplants sulk and do nothing for about 3 days while they were recovering.
Another critical temp is in the high 80's/low 90's. (Farenheit)  Many plants shut down photosynthesis to conserve water.  Greenhouse operators go to great lengths to keep their houses below 90 F


Is there a Reverse Transcription optimization for long, 9kb, transcripts?

RT-PCR should be able to get you up to ~10kb. If you are finding that it is not working, then you can by long-range RT-PCR kits commercially (look at Stratagene and Qiagen, for example). The Qiagen can handle up to 12.5 kb in a two-step RT-PCR system.


Spider identification assistance Phoenix

That's a nice silhouette of a male Southern House Spider, Kukulcania hibernalis.  That bizarre body, with the gigantic, forward-projecting, 'jackknife' chelicerae is unique and unmistakable.  These are quite harmless spiders.  A link to some useful information is below:
https://bugguide.net/node/view/26400


Why is the opposite of plantar flexion called "dorsiflexion"?

Anatomical terms must be able to fit a wide variety of organisms, from insects to fish, dogs, horses, chimpanzees to humans. That's why the terms are sometimes confusing to people who are thinking only of bipedal humans.

In anatomy, the dorsum is the upper side of animals that typically run fly, swim or crawl in a horizontal position. In vertebrates the dorsum contains the backbone. In such an animal the "ground side" is the ventrum.

Due to varied orientation on quadrupedal mammals (where the term is more appropriately used) the "back"-side of the hand, the "top"-side of the foot and the upper surface of the tongue are referred to by the term dorsum.

Does this picture help? Note the dorsal surfaces of the body, muzzle, feet.

In anatomy, the sole of the foot is called the plantar surface. The top of the foot is called the dorsum of the foot. (Imagine us walking on all fours like apes.) Therefore when you extend your foot, it's called plantar flexion; when you flex your foot upwards towards your head, it's called dorsiflexion.

Similarly, the arteries feeding the bottom of your foot form the plantar arch. Those feeding the top are the dorsal artery (or the dorsalis pedis).

Because anatomy must describe other animals than ourselves with other orientations, it must be consistent. In a quadruped, the dorsum of the tongue and the feet do actually point to it's "back" surface. See the picture below:

Lynxes have big paws, so it's more obvious that the surface facing the backbone is appropriately called the dorsum of the paw/foot. This picture is particularly interesting because it shows three degrees of dorsiflexion and one paw in full plantar flexion.

In humans, the "back" is actually the posterior surface, because we are not primarily in a horizontal orientation. The ventral surface is called "anterior". Thus we speak of the anterior chest wall and the posterior chest wall, not the dorsal and ventral surfaces, although those designations would still be entirely correct.


What is the rationale behind tapering of immunosuppressant dose a while after transplant?

This is a very interesting question. One of the most important considerations in patients on long-term immunosuppression is the risk of complications, whether infections or (more dangerously) cancer development; because of this if we can taper the dose then we would like to. This paper specifically discusses a lot of those risks. You mention prednisolone which is a glucocorticoid, and the side-effects (see also here) of chronic steroids (due to very wide-ranging immunosuppression) are well-known and always borne in mind when they have to be prescribed. The tapering of corticosteroids in long-term immunosuppression is often early to replace them with other drugs (mentioned here). With regards to the other immunosuppressives you mention, I'll mention mycophenolate mofetil and tacrolimus later with regards to how this is feasible biologically; with regards to cyclosporine, this study (admittedly old) has data illustrating the rates of rejection of renal transplants when patients withdrew from or tapered cyclosporine (here for financial reasons, but this drug also has significant adverse effects) and you can see from Figure 1 in the paper that although the patients who withdrew completely had many allograft rejections, those who tapered did not.

I'll start with answering your question about what clinical evidence we have for being able to do this; there have been quite a few studies which might help to throw some light on this. This study specifically considered kidney transplants, testing patients who were on standard immunosuppression for the 2 years after a transplant, and specifically measuring the quantity of CTLs (cytotoxic T-lymphocytes) reactive against donor cells, and they found that these cells were significantly downregulated in most patients 2 years after the transplant (while activity against third-party cells was mostly preserved). Since they found other T-cell responses to be unimpaired, they concluded that there was specific downregulation of the donor-specific cells occurring.

This paper also has some data which you can have a look at. This study specifically looked at moving patients from cyclosporine to azathioprine and mycophenolate mofetil and then tapering those. I've reproduced one of their graphs below which shows the activity of donor-specific CTLs before transplantation (the no dose group), 1 year after (still on high dose immunosuppression) and 2 years after (on low dose immunosuppression). The units are the ratio of activity of donor T-cells to activity against third-party T-blasts from spleen tissue (i.e. a control). Although you can see that some patients have ended up with increased activity after tapering, most patients appear to have low activities similar to (or even lower than) their pre-immunosuppression values, and these would be the patients considered for this tapering. This means that they now respond less vigorously to allograft cells than to control cells, and the ratio has decreased during treatment (presumably the reason why almost all of them have ratios under 1.0 before treatment is that the donor is not a random individual but matched for a lower immunological response):

And for another comparison with the body's response to non-donor substrates, the same study looked at response to tetanus toxoid. As you can see in the graph below, although the high dose caused the response to drop, it appears to have bounced back up again in most following the taper, similarly to the 3rd-party T-cell response but unlike the allograft response (the y-axis is proliferation of patient spleen cells in response to the toxoid divided by control rate):

As to the immunological reasons that we can taper the immunosuppressant dose, this is not particularly clear but there are known processes which might help to elucidate it. This paper (also on kidney transplants) suggests that there is a specific downregulation of the activity of CTLs directed against antigens presented by the direct pathway, and that this could be caused by anergy, deletion or regulation. The authors suggest that the most likely cause is an effect of the chemotherapeutics (here MMF and azathioprine) on the T-reg cells, and they speculate from the tests they did (the Discussion of the paper has the details) that the cessation of suppression of T-regs that occurs during the taper is what is responsible. They also mention a role for IL-2 signalling (necessary for T-reg function, and some immunosuppressants suppress it leading to rebound on tapering) and dendritic cells (whose costimulatory function may be altered by MMF).

As to the precise mechanism, it is not yet particularly clear, but it is thought that in the interaction between a suppressing T-reg cell and a CD4 effector T-cell, the latter actually induces the T-reg cell through as yet unknown mechanisms, so that continued activity of T-cells (e.g. in chronic inflammation or the presence of an allograft) may upregulate T-regs that suppress them. It is known that T-regs are important in downregulating chronic inflammation (presumably this is responsible for the pattern in the first graph I reproduced above where the activity against donor cells seems to drop more than that against control cells, even on high immunosuppression), through mechanisms which have been hypothesized to include CD4 T-cells undergoing receptor-ligand interactions with T-regs and providing signals to them to upregulate their production of IL-35 (which is important in suppressing all types of T-cells). Given that it is known that upregulated suppressive activity of T-regs in chronic inflammation downregulates the immune responses of all non-T-reg cells, it appears that donor-reactive T-helper cells will induce T-regs which will then downregulate donor-reactive CTLs. This paper I mentioned previously postulates that on release of immunosuppression this population of T-regs would bounce back and greatly downregulate the donor-reactive CTLs and T-helper cells.

This paper also mentions the fact that an introduction of tapered mycophenolate mofetil in liver transplant patients promotes immunological tolerance to allogeneic transplants. They mention the effect of this on T-regs as well as other immune cells.

For interest, this paper presents some interesting alternative speculation on the nature of the T-regs involved in organ transplantation tolerance. In certain cases, self-tolerance may develop to 'new' tissues, and the authors postulate that the main T-regs involved in transplantation tolerance are newly formed in response to the prolonged presence of the allograft, rather than predefined. Because of this, the tolerance might develop to some extent regardless of the chemotherapeutic regimen.

Finally with regards to tacrolimus, this study has data on the immune response during weaning off the drug after an intestinal transplant. They found that patients with a low immune response prior to weaning had a better response to the weaning, and that their immune function remained low after weaning. This is a bit different to the MMF situation I mentioned above where immune function in general seems to return and only donor-reactive immunogenicity remains low (this tacrolimus study doesn't specifically mention the effect on infection rates, but their Figure 7 seems to imply that those patients with low immune function (presumably those weaned) had lower intervention rates). Specifically the authors conclude here also that self-downregulation of the immune system (probably by T-regs) is likely to be the cause.

So in summary it is not yet fully elucidated as to why we can do this, but the upregulation of T-regs that downregulate donor-specific effector cells, and (at least for certain chemotherapeutics) the release of T-reg suppression on tapering may be important.


Can a color-deficient person be made to visualize the missing colors?

It is a very interesting question and I did some efforts to investigate the literature on this topic, but yet I don't have a definitive answer for you. But let's start from the beginning.

First of all, the reason for color deficiency can be not only lack (rare) or impairment (more often) of certain types of color-perceiving cells (cones) in retina, but also brain injures: the central color blindness can develop after head trauma or as a result of some neurodegenerative deceases, like Parkinson's decease. In case of brain origin of the color blindness it is usually the complete color blindness (no color is percieved), whereas congenical primary color blindness (receptor-based) is usually just the unability to distinguish one or two colors, whereas the rest can be more or less separated.

I searched Pubmed for the literature on the topic and found a recent PNAS paper about the simulation of primary and secondary visual cortex on humans using intracranial electrodes. As they describe their results (bold font by me):

  When percepts were elicited from late areas, subjects reported that
  they were simple shapes and colors....

But the paper investigated only healthy humans, no color impaired subjects were used for the tests, so cannot conclude from here whether we can elicit the perception of the color the person is incapable to see with the eyes using these stimulations.

I took this paper as the starting point and did some reference research, looking for the paper referenced there and for newer publications referencing this one: PNAS is one of the top journals in this area with very high impact factor and if there were a publication about brain stimulation and color blindness I would have definitely identified it.

During my investigations I came accross a series of interesting articles devoted to "cortical visual neuroprosthesis for the blind" (read this paper<1> from 2005 for review on this topic), but this is the treatment of conventional blindness, not the color blindness. There was no intersection in keywords or titles for color blindness and brain stimulation, both in the referenced articles and in the complete article database.

So, I would suggest that you address some talented experimentalist with your question and maybe one day, who knows, we will read your name under the Nature article dedicated to the novel way to cure color blindness.

<1> -- unfortunately not available publicly for free, I am sorry.


Does food continue to stay sequential once it is inside my body?

In general, food is not kept in any particular sequential order.  The stomach has a lot of smooth muscle which churns the food, very rapidly erasing any "order" to the food.  Beyond that, the stomach digests "the food in the stomach," in parallel.  Whatever is in it, it digests.

Now, in general, food eaten earlier will digest into chyme (the digested slurry which enters the intestines) sooner, but that's a very general pattern and doesn't account for any differences in how long it takes to digest various types of foods.

I don't have any sources to back this next claim up, but I do believe that if you were to chew some steak poorly, and then follow it up by more steak chewed properly, the later steak would actually digest first because it would take less mechanical processing in the stomach to get the digestive enzymes to where they need to be to work.


Can two proteins have equal primary structure but different secondary structure?

By equal I assume you mean identical.

Yes, in fact several known proteins have different folding patterns for the same primary structure as part of their function. but most proteins can take on more than one folding pattern, in fact specialized proteins called chaperones exist to encourage (force) a particular folding pattern in some other proteins, especially ones that are essential or in which the other foldings can be dangerous.

The easy way to understand the difference is the primary structure is the amino acid sequence and the secondary is the first stage in how the protein folds (the other being the tertiary). the primary creates the secondary (and tertiary) but there is usually more than one stable folding.

this video contains a further breakdown of the different levels of structure.


What made this pile of tiny poops at the base of an old oak? Eastern Long Island, NY

UPDATE: I was not paying close enough attention to size. If the feces is as small as the OP mentions in the comment below this post ("20+ of these scat in an acorn"), then this is very unlikely porcupine!! Instead, the size and shape suggests the feces belong to either a rat (perhaps wood rat) or some type of squirrel.

I await an update form the OP with more specifics before diving deeper...

Hollowed-out tree? Pile of pellet-like feces? End of Winter/start of spring?
Almost assuredly these belong to a porcupine.

 Source: user Thomas at http://livingprimitively.com/2012/05/
The North American porcupine (Erethizon dorsatum), which can be found throughout Canada and much of the northern US, is present in New York.

 Source: NH PBS

Animaldiversity.org suggests that porcupines are primarily tree dwellers in the state of NY.

For a suburban example like yours, see here.

Although porcupines do not hibernate, they reduce their range significantly during the winter and will tend to accumulate large piles of scat in and near their winter den (or suite of dens -- source). Although caves are ideal as they keep porcupines warmer, they also will frequently use hollowed-out trees as winter dens.
Since the inner bark of trees is a favorite food of porcupines (source), they will linger quite a bit around their den tree or other nearby trees if available.
Porcupine scat matches what you've found. Scat is oblong, slightly curved, and composed mostly of sawdust (due to their high wood diet) [Source: here]. According to Northwoodguides:

Wood fibers are evident in their scat. Scat may be piles of pellets varying in length from 1/2 to 1 inch long or it may be present in a chainlike pattern connected by wood fibers. Color varies from season to season depending on diet but is usually brown to black.

This site also has some good info, photos, and videos.

It is unlikely your scat belongs to another mammal such as a flying squirrel. Although flying squirrel poop looks similar and is smaller, their feces will not be notable woody as they eat lichens, fungi, berries, leaves, and other non-woody foods. Source. This site suggests that flying squirrel scat can accumulate at the base of a tree, but I have not seen this nor do the other characteristics match your almost textbook example of a porcupine "poop tree."


Wootton (1992) reviewed the anatomy and biomechanics of insect wings. Basically the wing is a lightweight but strong scaffolding of veins, supporting a thin membrane. The veins are composed by a sandwich of cuticle with a potential space in between. The membrane is also a double-layer but without the space.

In the venous space are is circulating hemolymph and often nerves and tracheae. The wikipedia image is pretty good:

The nerves carry sensory information and the tracheae oxygen.The hemolymph is continuous with the body and thus is able to circulate and hydrate the wing (important for maintaining flexibility). As Wootton says:

  desiccation destroys both compliancy and toughness, and a dry cuticle would be mechanically disastrous

So by maintaining a flexible tissue, insects have strong and tough wings that remain light enough.


To answer your last question, I very much doubt it's true in general. It does have unplesant effects in some people though. Form a popsci account

  He [a psychoanalyst] was puzzled about a 24-year-old man whom he viewed as psychiatrically healthy except for intense depression that lasted for several hours after sex. [...] Could it be that some patients have particularly strong rebound activity in the amygdala after orgasm that makes them feel bad?

And this post-coital dysphoria can happen to women too, for which there is some prevalence data:

  Forty‐six percent of respondents reported experiencing PCD symptoms at least once in their lifetime with 5.1% experiencing PCD symptoms a few times within the past 4 weeks.

"No sex before game day" was a tenet in some sports psychology/physiology corners, but more recent research failed to find significant differences of sex acts on mental performance... at least in (healthy) athletes. A 2016 review notes

  Despite the major differences found in the recovery phase, where higher values of HR [heart rate] were found 2 h after sexual intercourse, no significant differences were found in workload achieved and in mental concentration of the athletes.

And, yeah, I know sex doesn't necessarily mean orgasm, but it seems close enough to mention.


How are neurons selective towards specific stimuli?

Sensory receptors and neurons get their selectivity from physical processes and their position in space. For example, photoreceptor cells in the retina respond to light in a specific position in space because the lens and structure of the eye directs light incoming in a particular angle to a specific spot on the retina. Sensory receptors in the skin can sense touch in a particular place because that's where they are located. Hair cells in the cochlea respond to particular frequencies of sound because the membranes in the inner ear vibrate at different frequencies along the length.
For selectivity to lines of a particular orientation, neurons combine receptive fields of retinal cells, like this:

From https://grey.colorado.edu/CompCogNeuro/index.php/CCNBook/Perception
The "LGN" (visual thalamus) cells pictured here have receptive fields that look a lot like the retinal ganglion cells that carry output from the retina. For simplicity, you can think like they are the same. These cells are excited by light in the center (red), and inhibited (indirectly) by their neighbors (blue) (there are also "off-center" cells that respond in the opposite way, preferring dark in the center and light in the surround).
If you add up a bunch in a row, you can make a cell in primary visual cortex (V1, the green cell) that responds to edges. If you summed up the receptive fields of cells in a different orientation you'd get selectivity to a different orientation of lines. The key feature to making selective receptive fields is which cells are connected to which.
These receptive fields are created in development by spontaneous activity in the retina and eventually by actual visual input when the eyes open. The process is pretty complex and occurs in multiple stages, but you can start with a review like this one:
Huberman, A. D., Feller, M. B., & Chapman, B. (2008). Mechanisms underlying development of visual maps and receptive fields. Annu. Rev. Neurosci., 31, 479-509.
Higher in the visual processing hierarchy you will find increasing complexity as receptive fields of different types are combined and recombined.


At what levels of muscle energy intake does catabolism start?

1) Yes, most cells in the body derive energy from oxidative metabolism, unless oxygen is not available for some reason. There are some exceptions, for example red blood cells lack mitochondria and so have no respiration, and various types of rapidly proliferating cells such as activated immune cells have high glycolysis and lactate production (for reasons that are still not well understood).

2) The main fuel of exercising muscle is glycogen, which can account for 60-80% of energy requirements (article). Triacyglycerols (fat) stored in muscle tissue may account for most of the remainder (artice). Normally, muscle protein is not a major energy source during exercise. Some muscle protein breakdown has been observed after 2-3 hours of intense exercise (think marathon runners), when glycogen stores are depleted. See this review article.

If glycogen is not synthesized and stored normally while resting, then muscle may be more likely to catabolize protein during intense exercise. This can happen to some extent in diabetes, see for example this paper. There are also severe genetic disorders that disrupt glycogen synthesis, but those are very rare. I would guess fasting also makes it difficult to replenish muscle glycogen stores (and muscle triglycerides as well), so strenuous exercise combined with fasting might result in muscle protein breakdown, but I don't know of a study on this.


Where is the line between Anaerobic and Aerobic?

Anaerobic respiration is a respiration where the final electron acceptor is different than oxygen. The final acceptor can be a less oxidizing than oxygen, like sulfate (SO42-), nitrate (NO3-), or sulfur (S). For example bacteria that use sulfate are obligate anaerobs.

The Krebs cycle cannot take place in the absence of oxygen, although oxygen is not directly involved in the cycle. The oxygen is required for the electron transport chain, which oxidized NADH and FADH2 back to NAD+ and FAD+, which are involved in the four reduction reactions of the cycle.

Thus, aerobic respiration includes both Krebs cycle and final electron acceptor of oxygen, whereas anaerobic respiration does not.


Why is methylcellulose used in pharmaceuticals?

Methyl cellulose is a dry binder. It is used to make a pill with a small mass of active ingredient and as much binder as required to make the pill a manageable size.

The following properties make methyl cellulose a good dry binder:

inexpensive
non-allergic
vegetarian
soluble in cold water
non-digestable
nontoxic

Most of this information is from the Wikipedia article.


What is the appropriate method to send a strain?

I believe Addgene send strains as bacterial stabs.

This is the protocol from Qiagen.

  E. coli strains can also be stored for up to 1 year as stabs in soft
  agar. Stab cultures are used to transport or send bacterial strains to
  other labs. Prepare stab cultures as follows:

  Prepare and autoclave LB agar (standard LB medium containing 0.7% agar) as described in the last issue of QIAGEN News (1).
  Cool the LB agar to below 50°C (when you can hold it comfortably) and add the appropriate antibiotic(s). While the agar is still liquid,
  add 1 ml agar to a 2-ml screw-cap vial under sterile conditions, then
  leave to solidify.

  Vials of agar can be prepared in batches and stored at room
  temperature until required.

  Using a sterile straight wire, pick a single colony from a freshly streaked plate and stab it deep down into the soft agar several times
  (Figure 1).

  ￼￼￼￼￼￼￼￼￼4. Incubate the vial at 37°C for 8–12 h leaving the cap
  slightly loose.

  Seal the vial tightly and store in the dark, preferably at 4°C.

  When recovering a stored strain, it is advisable to check the
  antibiotic markers by streaking the strain onto a selective plate.

I believe if the shipping is <24hrs you could send a stab in ice.

Hope that helps

Ben


One of the primary reasons to use poly(A) selection is to eliminate the massive amount of ribosomal RNA (rRNA) present in the samples.  The alternative is to use ribosomal RNA depletion kits / techniques to remove as much rRNA as possible before sequencing.  Without rRNA depletion a large proportion (~60-80%) of the reads would map to rRNAs.

poly(A) selection also reduces the amount of pre-mRNA in the samples, which reduces the number of intron aligned reads.


Do trees in a forest generally grow in a lattice formation?

For most trees and plants, distribution is spatially highly variable. Thinking about the lifecycle of plants—their seeds are non-randomly dispersed, the seedlings and saplings grow in different biotic (neighboring trees, distance to herbivores) and abiotic (different soils, shading, etc.) environments, all the plants are at different life/size stages, and that they are highly plastic in their ability to have fluid morphologies in different conditions—it's really difficult to detect a clean lattice pattern with little variance.

Nevertheless, for some species of plants, where the conditions are right (e.g., very limited and highly sought-after resources, species poor areas, synchronicity of generations, strong antagonism), we see some evidence of regular patterns. Ecologists often analyze spatial distributions to see if they are random, clumped, or uniform/regularly distributed (link). We see some distributional uniformity that does resemble lattice-/tiling-like patterns, which you may find in the references from the link above. There is reference to only 1 tree species in that link :/ I can't say that I see ecologists looking for lattices explicitly, but I would be surprised if there isn't a subfield interested in it. HTH.


I'm thinking this is a Quercus imbricaria, which has the nickname of "shingle oak"; they're native to the eastern regions of the United States, which includes your state and county, exhibited immediately below.

Distribution
 Brown = absent; Dark green = present in state/Native; Light green = present in county/Native.
(source)
The leaves
The leaves are mostly linear in shape, with entire margins & a combination of pinnate and dichotomous venation. The overall color, size and sheen also seem to match quite well.

Overall tree
Surprisingly, I had a difficult time finding a decent image that showed a close up of the branching for this tree, so I decided to use an image of a Quercus laurifolia instead, which is of the same genus as the proposed species, and is also found in the eastern [but more southern parts of the] United States.


What the difference between an inverted and everted retina?

Based on your title and description, all that means is that in vertebrates the retina is inverted in a sense that light sensing cells sit at the back of the retina meaning light has to pass through layers of neurons and capillaries before reaching light sensing cells, whereas cephalopod has the photoreceptors at the front side of the retina, with processing neurons and capillaries behind them hence retina is everted i.e. inside out. See this page (http://en.wikipedia.org/wiki/Retina) under "In other animals" section.

Hope this helps!


New work suggests a prominent role for genes in the SRGAP2 family, as explained here. Data suggest a mechanism where incomplete duplication - most likely at SRGAP2C - created a novel gene function some 2–3 mya, which is a time corresponding to the transition from Australopithecus to Homo and the beginning of neocortex expansion. Further, in the mouse neocortex, Srgap2 promotes spine maturation and limits spine density, supporting sustained radial migration and leading to the emergence of human-specific features.


Source for 'EVERY living organism uses ATP as energy carrier', and can we make a synthetic one that doesn't?

Well your request for a source is rather like asking who first reported that 2+2=4. Not quite, but that should give the idea to someone who has not studied biochemistry. I doubt that you will find a source, but the following from Jacques Monod — the Nobel laureate — is worth quoting:

  “Anything found to be true of E. coli must also be true of elephants.”

In fact, this turns out not to be true for anything, but it is true of the role of ATP.

The better question, I think, is not what the source of such a quotation is, but what is the evidence for such an opinion. The evidence that has accumulated over the last 80 years or so is from examining the metabolic pathways present in different organisms, and, more recently, sequencing their genomes to identify the genes for various enzymes. What has been observed is a core of common pathways, involving a core mechanism of energy metabolism involving ATP. This is consistent with the idea that this arose early in evolution and was fixed in the last common ancestor of living things.

If you want a more recent source to the ideas above, I suggest another SE Biology question, Immortal genes common to all organisms, may provide a starting point.


Why can a zygote develop into all different types of cell, whereas a differentiated cell cannot?

Developmental biology is a huge field that we are still working on a lot.

DNA is only half the story.  The other half is gene expression; what subset of the DNA a cell is using at any time.  Your lung cells have the gene for insulin, but in lung cells, that gene is dormant.

The short answer is that in general, a mature cell is using the subset of its DNA that it needs to do its job and can't just change its gene expression to become a different kind of cell.   Cells that do become less like adult cells and less specialized can become cancerous.


Number of spindle fibres during Metaphase?

The number of spindle fibres is actually more than total number of kinetochore pairs. The fibres attached to kinetochores are called K-fibres and the others are called polar fibres. I cant surely say that there is exactly one K-fibre per kinetochore but as per its definition and from the microscopic images you can conclude that there is one per kinetochore.

In a normal mitotic metaphase there are 2n kinetochore pairs, and as you rightly calculated, there will be 96 K-fibres.

In meiosis-I there is a tetrad which has 2 kinetochore pairs but the ones in sister chromatids behave as a single unit. So there would be 23 fibres.

The fusion of kinetochores of sister chromatids is relaxed in meiosis-II and again a separation would require 23 fibres.

Please have a look at this article. Molecular biology of Meiosis nicely explained:
http://www.sciencedirect.com/science/article/pii/S0092867403000837

More about K-fibre formation:

http://link.springer.com/article/10.1007/s00412-005-0028-2/fulltext.html


Did bilateral symmetry evolved just once?

A lack of strong evidence causes the field to be mostly hypothetical. Detailed pre-cambrian fossils are necessary, from the 1bn-600 million years ago, to find a protostome - deuterostome ancestor.

Genetic data is also inconclusive. A search for bilateral common ancestor gives i.e. dev.biologists.org/content/129/13/3021 It's a summary of research, where the accepted view is that there is a common ancestor to all known bilateral organisms.

All the baliteria are classed in the common clade which have a similar cell attributes and physiology, they all have hearts whereas starfish and jellyfish don't, there are various genes that suggest common ancestry. There is currently no evidence of bilateral from parallel evolution, although it's very possible or probable that there were some previously and perhaps even today, i.e. tardigrades don't have hearts, so perhaps some species one day will be found to be convergeant species, although they are thought to be miniaturized lobopodia.

Sea cucumbers and sea anenomes both have a bilateral juvenile stage, so they have perhaps evolved from bilateral ancestors.
researchgate.net/profile/Taha_Soliman4/publication/262415405/…

A new fossil of a bilateral animal has been found from 550mn years ago: phys.org/news/2020-03-ancestor-animals-australian-fossils.html squids are starfish with mollusks on them, there are hybrid symmetries.


Yes, there are some differences between the gametes that a parent produces at different ages!

Mutations in the germline during mitosis

Every time a cell replicates some mutations may occur (even through mitosis). Of course, any mutation that occurs in cells are located in your hand or in your brain, for example, will not be transmitted to the offsprings. Only mutations occurring in the germline (cells in the testis and in the ovaries whose descendent or themselves go through meiosis) are possibly passed to the offsprings. Interestingly, because of the developmental pathways of sperm cells and ovules, sperm cells go through a lot more mitosis than ovules do, resulting in more mutations in the sperms than in the ovules. Therefore, if you look at a mutation in an individual and assuming you know that the mutation occurred during the lifetime of the parents, then you are more likely that the mutation comes from the father than from the mother.

As reviewed by Cochran and Harpending (2013), mothers transmit on average a number x of new mutations to their offspring. This number x is independent of the age of the Mother. Fathers, however, transmit a number of new mutations to their offsprings that is very much dependent on the age of the father for developmental reasons.

Of course, as it has been pointed out there are various environmental factors that may increase or diminish the mutation rate (such as the mutagens (Tobacco, X-ray, ..))

Note on the process of adaptation

It is important to know that a vast majority of mutations are deleterious (impact negatively the reproductive success and survival of the individual carrying it). If we assume that no selection occurs between the cells of the germline, then no adaptation is possible. And in average sperm cells of an old guy should have lower fitness than the sperm cells of the same guy when he was younger. This process is referred to as mutation accumulation (mutation accumulation is not a concept that is specific to somatic lines mutations). However, one may argue the opposite! One might think that the cells that carry the new mutations (the mutation that occurred during the lifetime of the man) may be selected for or counter-selected. In such a case, the few beneficial mutations might be enough to make our cell lineages more fit with age. Whether the fitness of cells increase or decrease through our lifetime is dependent on the effective population size, the mutation rate and distribution of mutational effects. One can calculate the critical parameters yielding to one (mutation accumulation and fitness decrease) or the other (fitness increase through age) thanks to the mutational meltdown literature.

It is important to note however that what increase the fitness of a cell might decrease the fitness of its carrier. Knowing the joint distribution of mutational effect for both the carrier and the cells should allow us to calculate if reproducing late in life allows transmitting better genes than reproducing early in life. Intuitively, I would expect that reproducing early in life would allow a parent to transmit better genes.

Epigenetics

We have to talk about epigenetics also. Epigenetics refers to all the modification that occur "around" or "on" the DNA but which are not the modification of the sequence of nucleotides. It is possible that the transmission of epigenetic modification is dependent on the age of the parents. But I have never heard of any case where this happens.


Some general aspects about miRNA nomenclature in addition to canadianer's answer:

mir refers to the pre-miRNA whereas miR refers to the mature form
mir-x-y mir-x-z for example mir-1-1 and mir-1-2 refer to different precursors that give rise to same mature miRNA (i.e. miR-1). These different precursors can be regulated differently.
The mature miRNA resulting from the 5' arm of the precursor hairpin has a suffix of -5p; similarly the product from the 3' arm has the suffix of -3p. Previously, the lesser expressed/abundant (or unexpressed) of the two products was designated with an asterisk. For e.g. miR-124*. This convention is obsolete now. Any miRNA by default has the -5p/3p suffix. This is useful especially in case of let-7 because there is no uppercase notation to differentiate precursor from the mature miRNA. For example, the mature form is always denoted as hsa-let-7b-5p even though the -3p is never expressed.
A "family" consists of miRNAs with the same seed sequence (usually 2nd-9th residue). Sometimes it can be observed that one of the arms is less conserved than the other between different precursors. For example in the case of let-7 the -3p(s) do not have a conserved seed sequence, however, all -5p(s) have the same seed sequence.

And as mentioned in the other answer, the name let-7 just sticks around because of historical reasons.


Can animals use the nitrogen in chitin to build proteins?

This article suggests a certain amount of chitin digestion is possible.

http://www.bio.unipd.it/agroecology/download/pdf/papers/2009/Chitin-Chitinases-Paoletti-From-Binomium-Chitnchitinase-Recent-Issues-Fp-Version.pdf

I can't quantitatively say how much of any of the myriad potential chitin sources (fungal, crustacean or other arthropods) would be digested within a 'normal' time frame in the human digestive system. That work should probably be undertaken, though.


Why isn't Rh disease present in other mammals?

Rh is just a proteinous(antigenic) factor in red blood cells; not a DISEASE.If it is present in blood you are Rh positive. If not Rh negative.An Rh negative person if exposed to Rh positive blood will form specific antibodies against the Rh antigens. In case of pregnancy, Rh antigens of the foetus do not get exposed to the Rh negative blood of the mother during first pregnancyas the two bloods are well separated by the placenta.

However during the delivery of the first child there is a possibility of the exposure of maternal blood to small amounts of Rh positive blood of the foetus.In such cases the mother starts preparing antibodies against Rh antigens in her blood.

In case of her subsequent pregnancies, the Rh antibodies from the Rh negative mother can leak into the blood of the Rh positive foetus and destroy the foetal RBCs. THis could be fatal to the foetus or could cause severe anaemia and jaundice to the baby.A condition called erythroblastosis foetalis arises.

This condition can be avoided by administering ant- Rh antibodies to the mother immediately after her first delivery.

This is not a disease but is just as a result of antigen- antibody reaction.As far as Rhesus monkeys are concerned, it is an innate factor in them, common to all.It is quite similar to the case of Bacillus thuringiensis in biotechnology. When inserted into plant cells these bacterial phytotoxins cause havoc as an insecticidal agent; whereas they seem to have exactly no effect inside bacteria.You may also consider the case of Penicillium notatum.These organisms are capable of causing harm to other living organisms but are not affected themselves.

Similar is the case with Rhesus monkeys.


Until the late 1980's all enzymes* were believed to be proteins, and were often defined as protein catalysts, often in textbooks which are often not perfect representations of science. At that point every macromolecular biological catalyst known was a protein so they thought all macromolecular catalysts were proteins. But the discovery of ribozymes (RNA strands that act as catalysts) changed that. The discovery that one of the most well known enzymes ribosomes had their functional components made of RNA and not protein also played a factor.

NOW enzymes are generally defined as macromolecular biological catalysts and include ribozymes. But older works or outdated textbooks will still refer to enzymes as only proteins but newer works will not. Don't feel despondent I was taught the same thing initially, and it persisted for a several years in college. Part of this is each successive step in education tends to lag behind and/or get over simplified in scientific knowledge. Textbook manufacturers are not overly concerned with poor phrasing or outdated definitions and are rarely writtten by scientists.

*in its object form, originally and for quite a long time enzyme referred to the process not the agent responsible becasue the agent was unknown.


For sequence data, UPGMA is not really accepted anymore. Maximum parsimony and Neighbour-joining are usually used because they are quite fast and they give you a relatively good idea about the phylogeny.

You should not decide based on which method gives you the highest bootstrap.

For publication, it is recommended to use either Bayesian consensus tree (MrBayes is popular program) or a maximum likelihood tree (RAxML or MEGA are popular for ML). For maximum likelihood bootstrap (BS) is used and the confidence is relatively high if at least reaches 80 (%). For Bayesian, instead of bootstrap Bayesian posterior probability (BPP) is used. For BPP it has to be at least 0.95 to be significant.


How to isolate two plasmids from E. Coli strand?

A retransformation should get you a pure plasmid. Transform the plasmid mix into empty E.coli (don't use too much DNA), plate on Kan / Amp depending on what you need. The probability that one cell took up both plasmids is extremely low, and you could check with colony PCR just to be sure.

Otherwise: ask around, there must be (old) stocks of the single plasmids around, or glycerol stocks of E.coli containing only one of the plasmids.

Third option: take a look at your mutagenesis method. For your needs there might be techniques around that'll work on a mixture of plasmids. If you just need one variant or a single site saturation library you could use Quikchange for example. I don't see a reason why this wouldn't work on a mix of plasmids.


Can Taq polymerase be stored with PCR primers?

Yes, this is perfectly fine. Many companies sell PCR Master Mixes (granted, without primers):

Thermo Fisher
Sigma-Aldrich
BioRad
Promega
Qiagen

If you choose to make your own, make sure it's stored at -20°C, and be sure to aliquot it so it's not going to be subjected to multiple freeze/thaw cycles. Obviously you should mix it well before aliquoting, but even after thawing I would vortex it to make sure all of the components are well-mixed. Make a 2X master mix, and adjust to a final 1X concentration in the PCR tube with your DNA sample and nuclease-free H2O.


Change in conditions of an ecosystem lead to change in organisms

I will try to provide a general answer, starting point and overview to this question, even though it is rather wide ranging and vague.

The biological process

If we start with your description of the process; you are correct that such a dramatic change in the environment as slash-and-burn agriculture will drastically change the living environments on the canopy floor (well, in the entire ecosystem).

To name a few, there will be changes in:

Light conditions, which will alter the competitive balance between plant species, where ones adapted to a closed canopy will disappear.
Moisture
Temperature (maximum, minimum and variance in temperature)
Nutrients The point of slash-and-burn agriculture is to provide a boost of nutrients for farming. However, the boost is short-lived and transient. Afterwards, you are usually left with a very nutrient poor soil, which is common in tropical forests. Tropical forests (where slash-and-burn is often used) are high in biomass, but most if it is bound in the standing biomass. When this is removed by clear-cutting, the natural cycling of nutrients is disrupted, and excess nutrients are leached out of the soil (Ricklefs, 2001).
Loss of host species This will lead to loss of primary consumers (specialists & generalists) feeding on them, and cascading effects into the ecosystem that depends on these.

All these changes and several others will dramatically modify the niche spaces and the competition between species in the forest patch, and most previous species will probably not be able to persist locally. New species will move in to fill the open niches, and over a (long) period of succession a new quasi-stable community will emerge. Due to the extremely high biodiversity in tropical forests it will almost certainly contain fewer species than the original community.

The question of whether the community will eventually return to its previous state (even if that will take an extremely long time), is a relatively open question, and also depends on the conditions at the specific site and if the spatial scale of the disturbance. The biggest issue for conservation biology is that these land-use changes generally happen at a large scale, so fragmentation of species habitats can lead to regional and even global extinction. Since many tropical species have small ranges and are not adapted to fragmented landscapes, many run the risk of going extinct. Therefore, even if the overall appearance of the original forest will return, it will contain a very different set of species. Land-use changes, even in the form of temporary slash-and-burn agriculture, also generally leads to continued/secondary exploitation of the area and seldom to restoration/regrowth (Meffe & Carroll, 1997).

I also want to point out that you are indirectly referring ("...new equilibrium be reached...") to the idea of a Balance of nature in ecosystems, which is largely seen as obsolete and incorrect. However, as shorthand or when referring to a dynamical equilibrium between multiple populations (with ongoing evolutionary change) it can be meaningful.

The philosophical issue

The question of whether an ecosystem change or extinction of species is "...a bad thing" is inherently philosophical and depends on human judgement. The philosophical foundations for conservation biology can be divided into instrumental values and intrinsic/inherent values. Instrumental values can then be subcategorized as services (pollination, water regulation), goods/resources, information (e.g. genetical info to be used in medical research), and esthetic/spiritual values. Intrinsic values refers to a specific value placed on species, ecosystems or evolutionary history due to its uniqueness and it is seen as independent of human needs and wants (although some argue that values independent of humans are impossible). Intrinsic values are also connected to the acknowledgement that organisms have interests and wants themselves (their own 'good'). Different people naturally weight these issues in different ways, and for some the short-term economical gains will weigh heavier. The long-term economic costs are potentially large, but less certain. From a strict biodiversity perspective (i.e. a species counting perspective), the change will certainly be negative, since the change in land-use will decrease diversity and probably lead to more 'trivial' species moving in. From the perspective of the original ecosystem (if it has a say) the change is per definition negative, since it will disappear.

The direct intrumental value of individual species are usually uncertain (irrespectivly of the direct rationales used), so the precautionary principle is often invoked to justify species conservation. Also, numerous examples exist of how aspects of biodiversity are related to human values (some recent examples are Garibaldi et al. 2013 and Gamfeldt et al. 2013), such as production or services, which can also be used to justify both conserving biodiversity or individual species. An example of ecosystem services from tropical environements can be seen in Ricketts (2004). However, sometimes functional diversity is emphasized which focus on preserving functional groups of species instead of 'general' biodiversity (i.e. specific species).


Can the theory of natural selection distinguish between two correlated phenotypic traits?

Are biologists aware of the causation vs correlation problem or are they noobs in statistics?

Evolutionary biologists tend to be pretty good statisticians. For historical consideration, Pearson is the father of the concept of correlation and was a biostatistician and Fisher is (one of) the father of evolutionary genetics and is also a famous statistician (invented the Fisher's exact test, t.test and Anova). Many of the modern developments in modern statistics were brought about by geneticists (incl. developments in HMM, ABC, FDR, etc...).

So, yes we are aware of the causation vs correlation problem.

  In the theory of natural selection, can the two situations be disentangled especially when one is talking about evolutionary accounts that are on the order of hundreds of millions of years[?]

Just like in any other causation vs correlation problem, no it is not easy to disentangle the two. If the specific hypothesis put under testing is subject to experimental manipulation, then yes, it is often feasible to disentangle the two. Otherwise, in a purely observational study, one can logically reason and argue for one rather than another causality relationship but in essence, you cannot know in a purely observational study whether a correlation is representing a direct causation.

The follow-up question might then be

  Is experimental manipulation feasible in evolutionary biology?

The answer is yes. Not for all questions though.

First there are evolution experiments. An evolution experiment is just like what is sounds like. You put a population in a controlled environment and let it evolve. Repeat the process many time to have a decent sample size. There are also many question of interest to evolutionary biology that can be studied through experimental manipulation (and not only observatory studies) that do not require an evolution experiment.

You seem to be particularly interested in the reconstruction of past evolutionary history of a lineage (evolution biology is much more than a 'historic' reconstruction of life on earth), I would like to highlight that in purely observation studies and in experimental studies not involving evolution experiments, there are plenty of methods to reconstruct past events. Consider for example the loss of genetic diversity at linked variants (selective sweep) caused by positive selection. If two traits are correlated through time (which is very hard to figure out in absence of good fossil records) or correlated over several species (consider having a look at phylogenetic contrasts methods and more modern version of inference of selection over phylogenies), then if selection occurred in a single of the two traits, you should expect to see a differential loss of heterozygosity among the genetic markers explaining ariance for one trait and for the other.


Question about the quantity of orchid species and genera

The Plant List records 27,801 accepted species names in 899 genera within Orchidaceae. This estimate probably differs a bit between authorities. For example the Angiosperm Phylogeny website records 26,000 species in around 880 genera. Regardless it is I think the most speciose angiosperm family.

The explosive diversification of orchids, like the diversification of angiosperms, has been a big study point for evolutionary biologists. A lot of explanations center around the wide array of floral morphologies which you can find in the group, as well as (although not independently) the evolution of a whole range of pollination strategies. Other factors include evolving in a tropical environment and the evolution of CAM photosynthesis in the group. You can find more details in, for example Givnish et al. 2015


Prostate, seminal vesicles or testis which one is bigger(by volume and size)?

The average seminal vesicle length was 31±10.3mm and its average volume 7.1±5.2cc. That is verified by another source which states 6-10mm in controls.

The average prostate volume ranges from 20 to 40cc from ages 30  to 80, 3-2-3cm for younger males 5-4-5 for older ones.


What is the family of this insect caught by my Drosera?

This is a Dark-winged fungus gnat (family Sciaridae); the European species of the family are dealt with by Menzel, F.; Mohrig, W., 1999, Revision der paläarktischen Trauermücken (Diptera, Sciaridae) [A Revision of the Palaearctic Black Fungus Gnats (Diptera: Sciaridae)], Studia Dipterologica Supplement, (6):761 pages; copies are sold by Ampyx-Verlag (see http://www.ampyx-verlag.de/lilac_cms/de/4852,,refz,rd,368,2914,12/index.html).  Some species of the family have economic importance, but identification to species usually requires male specimens which must be at least temporarily mounted on microscope slides.


Estimation of species range fragmentation

Very interesting question +1. I don't know the literature on the subject very well but I did not find much by looking for it. I know that a number of methods exist when you have genetic data (STRUCTURE or some of the work of J. Novembre probably).

Here are two possible solutions

Fitting $x$ distributions

You could be fitting 1, 2, 3, ...., n normal (or uniform) distributions to the observed data. Each time, compare their maximum likelihood (for which you might need a MCMC with 2⋅x parameters, where $0≤x≤n$ is the number of distributions you're fitting) and select the "best" model with some information criterion such as AIC or BIC.

The number of fragments is just the $x$ value associated with the lowest AIC.

Logistic regression

Another (faster and simpler) solution would be to fit a logistic regression to your data.

Iteratively fit a logistic regression of degree 1,2,3,...n and then again use some information criteria to select the 'best'.

To find the number of fragments, you can then either use the number of degrees in the model or even better use some threshold on the the probability of getting a zero (which you could compute with the package effects in R).

Notes

It will probably takes you a day or so if you're at ease with these methods and have intro knowledge in programming.

You might want to get opinions from stats.SE as well.


I found the definition here, which is a cool package in R:

  animal - all vertebrate dispersed seeds, without distinction between
  attached(epichorous) and ingested (endochorous) dispersal of seeds


Why do mosquitoes appear to be repelled by magnets?

According to the research cited by the OP (Strickman et al. 2000), mosquitoes alter their behavior in the presence of a magnetic field, and the measured changes in behavior are statistically significant. The authors of the study found that the external surfaces of mosquitoes attract ferromagnetic particles from the air. They speculate that changing their orientation to the earth's magnetic field helps mosquitoes navigate while approaching a potential host.
Reference Cited
Strickman, D., Timberlake, B., Estrada-Franco, J, Weissman, M, Fenimore, PW, and R.J. Novak. 2000. Effects of magnetic fields on mosquitoes. Journal of the American Mosquito Control Association 16(2):131-137.


How to prevent blobs under the microscope?

At least some of the blobs that you have appear to be air. Seating the coverslip carefully will help to prevent air-bubbles from forming under the coverslip. Lay one edge against the fluid and slowly ease it down.

You mention using an oil immersion lens. It is possible that water has come into contact with your lens. Oil finding its way beneath the coverslip could also introduce refractory blobs as well.


Where to download gene list of human genome?

The database you are looking for is ensembl [Yates (2016)].

Go here and chose  Customise your download. There you can select a dataset (e.g. genes and then specify human genes - currently uses build GRCh38; you can also go the same way here to do the same for hg19/GRCh37).

After chosing your dataset, you can click on Attributes to specify what to include in your download (HGNC symbols, IDs, regions, GO terms, and a ton of other stuff), click on Filters to apply filters to your choices (only genes from a chromosome, region, and a ton of other stuff).

Then click Results and download your selection in a format of choice.

(Hint: click Count first and use it as a a sanity check to see if the number of selected genes fits your expectation.)


How much divergence would be needed for classifications as astrobiology?

I think if life was transferred to either body on a probe, it would not count as alien yet because it could not have had time to develop very far on its own, since all probes are recent evolution wise. These would be offshoots from earth life. Truly alien life would most likely use different biochemistry because it originated in a different planet, it would be a totally different tree of life. However, the presence of life on the moon or mars, even if just contaminating earth bacteria, would be incredibly important for astrobiologists, as it would provide direct evidence that life can survive in these harsh environments. Life on the moon would most likely be dormant bacteria, because there is no air or water or food. However, if bacteria could survive prolonged exposure to space and be revived upon entering a suitable environment, that would provide evidence for panspermia. Read this: https://en.wikipedia.org/wiki/Surveyor_3

If panspermia is true, then those aliens might not be that unrelated after all. But until we find one, we can't make any conclusions.


To absorb essential elements, body must get them in form of stable ions.
So for calcium and magnesium, our body absorbs them from the hard water in the same way it obtains from other sources and uses them identically.
For iron, we cannot obtain iron from iron fillings because iron reacts with water and other chemicals in our body which can produce harmful effects.
For further information on absorbtion of calcium from hard water visit http://goaskalice.columbia.edu/answered-questions/calcium-hard-water


How long can a unicellular organism live without nutrition? What happens after that? Does it depend on the domain?

This is very dependent on the organism within each of the groups you mention. While for the most part, archea are the extremophiles and have the ability to withstand many extreme conditions, nutrient limitation survival greatly varies. I think you could easily find organisms in each group that could withstand nutrient limitation well.

A good example would be yeast, which is a single celled organism you may have actually worked with. If you take laboratory yeast, in their diploid state, and starve them, they will undergo meiosis, and in their spore form, live for a very very long time without nutrients, protected by their ascus (which is actual their dead mother cell).

Yeast can also completely desiccate and still live. When you pick up an active yeast packet for baking, those yeast have not only been starved, but have been completely sucked dry of their water. Yet when you add water back, they live (though a great number of them will die).

I think in general, most single celled organisms have a certain tolerance for low nutrient conditions. This does happen to them a lot. All it means is they slow their cell cycle down, stop dividing, and just undergo a caution period. There is all sorts of signaling in the cells that sense the nutrients, and slow growth based on their conditions.


Mathematical model about the relationship between two animal species

The model you present here is a special case of the Lotka-Volterra competition equations, where the two species have the same effect on each other (i.e., symmetric competition). Some things to think about in interpreting this:

each species has a negative effect on the other (i.e., increasing the density of either species lowers the other's population growth rate), hence this is a "negative-negative" interaction; it makes more sense for two species that are competing with each other (for resources, space, enemy-free space, etc ...) than for a predator-prey system such as the shark-whale example you give.
In contrast, in predator-prey (or more broadly "enemy-victim") systems, one species (the predator) benefits from the association - its population growth rate increases when the density of the other species (the prey) increases - and the other species (the prey) suffers (its population growth rate goes down when the predator density increases)
the fact that the competition is symmetric (this happens because you are using the sum of the population, $M+N$, and not using a competitive asymmetry parameter, e.g. $M+\alpha_{MN} N$) means that this would be most suited to modeling the competition between species that were very similar to each other (e.g. the same size, resource-gathering ability, etc.)


In centrioles, what type of fibers connect the triplet microtubules?

Winey M, O'Toole E. 2014. Centriole structure. Phil Trans R Soc B 369:20130457

  Cross-sectional images of centrioles and basal bodies show a linker between the A- and C-tubules in many different organisms... Surprisingly, candidate molecules serving as constituents of these linkers have not yet been identified.

That's as of 2014. I don't have the time right now, but I'll try at some point to find if there are more recent developments.