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Are antibiotic-resistant bacteria necessarily less virulent than their original strain?
In the absence of antibiotic treatment, is there a reduction in the average severity of disease caused by resistant strains of pathogenic bacteria compared to wild-type ones?
I would assume that bacteria that have adapted to be able to withstand antibiotics would have to allocate extra resources in order to counter the antibiotics, making them perhaps less growth-efficient than the "original" (non-resistant) strain.

This question is rather vague and unclear, and cannot be succinctly answered in its present state. There are a very large number of pathogenic bacteria (let alone other microbes), a large number of antibiotics, and a multiplicity of routes to antibiotic resistance. Please [edit] your post to focus on a single strain of bacteria and preferentially a single type of antibiotic. From the [help/dont-ask]: Your questions should be reasonably scoped. If you can imagine an entire book that answers your question, you’re asking too much.

I've edited it slightly to narrow the scope; I think it is answerable now (and I'll have a go at answering it if I have time later). It's arguably a duplicate of this, though: http://biology.stackexchange.com/questions/14350/can-antibiotic-resistant-bacteria-compete-with-normal-one-in-an-antibiotic-free?rq=1


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What's the difference between evolution fitness and reproductive success?
What's the difference biological fitness and reproductive success in the biological terminology?

There is the term "evolution" in you title who is not found in the post. But this term is used in an unclear way. did you "evolution, fitness and reproductive success" or do you think that "evolution fitness" is a concept by itself?

The concepts are very similar but there are a few differences.
Firstly, fitness is usually applied to alleles or genotypes, reproductive success to individuals.
Secondly (and partially as a consequence of this), fitness is an average or idealised/expected property across a population; but actual reproductive success per individual is stochastic. Individuals possessing an allele with a relative fitness of "2" will on average have twice as many offpsring as their competitors, all else being equal, but individual reproductive success will vary as a consequence of other factors such as predation, parasitism, starvation etc.
Finally, absolute fitness relates to the proportional representation of a genotype in a population. Reproductive success relates to offspring per individual. For example, in a growing population a genotype could be simultaneously declining in proportion while it is increasing in absolute number, if other genotypes are increasing in number more rapidly.

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How many cells of each cell type are there in C.elegans?
C.elegans is a very well studied organism. Of its approximately 1000 cells in the adult stage, how many of each cell type are there? The only information I could grab from the internet (wormatlas.org) is that there are about 300 neurons. What about the rest of the cells? An answer for other simple animals such as sponges, planaria, jellyfish etc., even in relative proportion of cells, would be accepted.
(I appreciate that this question is somewhat broad and unspecific: eg. are all neurons of the same type? (Yes) Are germ cells included? (No, because they vary) Please ignore such niceties.)
Edit: To clarify, the question asks for a breakdown of the cells along the lines of:
Neurons 300 cells, Epithelium 200 cells, etc., Total 1000 cells

I guess you didn't find this page, then? I'm not a worm biologist, so how did I find such information? I googled list of c elegans cell types. PLEASE do your own research before asking here.

@MattDMo You should make an answer out of the link you post. An answer as simple as There are about n types of cell (see here) would be enough.

The cell map of C.elegans is well known.

Sorry, did I ask "How many cell types are there in C.elegans?" No I did NOT want a list of cell types. PLEASE read the question carefully before answering.

-1 and VTC because this question is unclear (what exact do you define as a "cell type"?) and easily answerable yourself once you have a clear definition.

Thanks to @MattDMo comment...
There are about 17 cell types in hermaphrodites C. elegans (see here). However, it varies very much depending how you count. You might want to have a look at  Sulston and White (1988).

Actually http://www.wormatlas.org/celllistsulston.htm is probably closer to what OP is after, although the whole site is highly relevant.

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How do castes evolve in eusocial species?
I have been reading about eusocial species and have some questions. What is the basis for caste differentiation? Is it entirely genetic? Does the queen have the code for soldiers, workers etc in her own genes, so only a mutation to the queen results in change of the whole colony's castes? As a related question, how do different castes evolve?
It seems to me that if only one individual in a colony is reproducing, the rate of evolution must necessarily be much slower because any genetic change in the queen would affect all castes, which is likely to have some negative effects.

please rephrase: prevent stagnating evolutionary. casts just have a group fitness impact, I don't understand what you mean.

I think this is a great question (and if I have time I'll attempt an answer later) but it had some issues, so I've attempted to rewrite it more clearly. If you feel it no longer reflects what you wanted to ask please revert it; I won't be offended :)

(I'd also suggest adding some more information about the reading you've done so far.)

@arboviral: Thanks for the edit, As far as I understand the edit, it still represents my intend. And what I read so far... well, the linked wiki article.

Does a fertile queen have the code for soldiers/workers in its own genes, so only a mutation to the queen results in change of the whole coloniy's castes?

Yes.

But how that would protect them from just going extinct due to one unfavorable mutation to a queen?

One unfavorable mutation to a queen could make that queen and her lineage "extinct". It wouldn't necessarily have any effect on the rest of the population (i.e. other queens and their lineages).  There's no difference here between eusocial and other species.

that's totally right, although you may add that the queen can be inseminated by many males and the nuptial flights may have individuals of a wide range genetically. a proportion of the new queens may have the defective gene omitted or complemented via egg fertilization.

Ants are eusocial and close relatives of bees and wasps. Ant and bees use Haplodiploidy. it is a sex-determination system in which males develop from unfertilized eggs and are haploid, and females develop from fertilized eggs and are diploid.
Young queen ants leaving the nest can have one or 10 or 20 fathers. The new queens and workers are not necessarilly clones, and defective genes can be omitted in workers and queens.
the queen may be inseminated by more than 15–20 males, it's polygynous, versus mono androus (andros being male in greek).
Some queens can mate with different species of ant and hybridize.
A nuptial flight of 10 queens in the first year and 1000 queens in the 10th year, all those individuals will have different genetics, because they all come from different fertilized eggs. The males are drones and all the same.
It can vary by species of ant, the queens can be all the same: in the ant Cataglyphis cursor, the queens are produced by parthenogenesis but workers arise from fertilized eggs, suggesting that genetic variation is vital for the worker
caste (Pearcy et al. 2004).
Here is an attempt to unify the literature on ant caste development and evolution with a single theoretical framework, drawing on recent advances in evolutionary developmental biology.
They say that ant populations contain a balance little to big ants, a range of sizes, whereby queen like features, ovaries, wings and light receptors between teh eyes called ocelli, appear in steps as the larvae grow. Ants molt and the develop from small workers to large queens progressively.
If you check an soldier ant, she has a large head, it's almost as big as a queen's, although the body stays small. in the next stage of caste size, the body grows into nearly a queen, else with wings too.
If there is a lack of one caste, more of a particular kind are replenished.
To read the paper faster, search for keywords, for example hormones, they say:

Two endocrine hormones, juvenile hormone (JH) and ecdysone, are important regulators of developmental timing in insects. Pupation (and the cessation of larval growth) is triggered by ecdysone, and the action of ecdysone is inhibited by JH (Hiruma and Kaneko, 2013). Thus, treatment of larvae with JH or JH analogs leads to prolonged growth and larger size, as long as necessary nutrition is present. JH removal and/or ecdysone treatment leads to premature pupation and smaller adult size (Hiruma and Kaneko, 2013). This endocrine regulation of insect size has been demonstrated in Coleoptera and Lepidoptera, and is also supported by experiments in ants.

Some of the small ants have the potential to become queens, and when there is lots of food, more of the small ones will grow and make many queens that can fly on a hot day.

In M. rubra, larvae do not have the potential for queen development under normal conditions (Brian, 1979). However, larvae that are forced to diapause just before pupation reorganize their endocrine organs and delay pupation after growth is resumed (Brian, 1979). If sufficient nutrition is available, these totipotent larvae attain a large size and develop into queens

You may laugh by reading the effective genetic ant population mathematics at the end of the first citation. it is completely professor level, with a maths formula, which demonstrates that it's extraordinarily complex and variable effective genetic population distribution and gene expression.
If someone can say more about eusocial gene determination it's quite a difficult topic.

I would be curious why someone downvoted this?!


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Viruses affecting transmission capability of mosquitoes
I've read about bacteria affecting the transmission capability of mosquitoes. For example:

Wolbachia suppresses dengue transmission
When mosquitoes were given antibiotics that decreased their gut microbiota diversity, they became more susceptible to malaria infection

Have there been any studies to show that the presence of certain viruses/viral diversity (rather than bacteria) has an effect on the tranmission of other viruses/pathogens?

There have been some studies looking at this, but not many. One is this study which reported an interaction between Aedes densovirus (AeDNV) and dengue virus (DENV) in Aedes albopictus: mosquitoes already infected with AeDNV were more resistant to infection with DENV, although DENV infection appeared to accelerate the replication of the existing AeDNV infection. A similar interaction was not seen with chikungunya virus (CHIKV).
In addition there are indirect interactions between pathogens of all kinds - viruses such as AeDNV which kill a high proportion of the mosquitoes they infect reduce the average survival and population density of the vector and therefore the ability of the local population to transmit disease (ref).


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Why does my simulation not support the idea that inbreeding is bad?
After reading this post, I wrote some code to simulate inbreeding.

We have a population of $N$ creatures. Each creature has two genes, which come in two forms: recessive (a) and dominant (A). The creatures' initial genomes are random. At each stage, the following happens, in order:

Each creature with the recessive phenotype (aa) dies with probability $p_R$.
Each creature with the dominant phenotype (AA, aA, or Aa) dies with probability $p_D<p_R$.
Each creature then decides to have children with probability $q$. Each creature that decides to have children chooses a mate (see below) and has three children with that mate.

I wrote two different kinds of creature, incest-averse and incest-seking. Each time I ran the simulation, the population consisted of either all incest-averse or all invest-seeking creatures.

An incest-averse creature chooses a mate randomly and uniformly from the set of its non-siblings.
An incest-seeking creature chooses a mate randomly and uniformly from the set of its siblings. If it has no siblings, it just randomly picks anybody.

In practice, since each union produces 3 children, the incest-seeking creatures almost never fail to have siblings after a few generations.
What I found was that whichever type of creature I used, the results were the same: the frequency of the aa genotype plummeted to almost zero. I used the parameters $N=100$, $p_R=0.1$ $p_D=0.05$ $q=0.022$.
Presumably my model is in some way too simple. What am I not taking into account?
Source code

Your question title does not really fit your post. Your simulations do show that inbreeding is bad since the recessive genotype frequency drops to very low non-zero values in your inbreeding scenario, which is expected under high dominance coefficients. What does not fit your expectations is your null model: the outcome of the non-inbreeding scenario. The main problem seems to be that there is no differential fitness effect for recessive genotypes: if all recessive genotypes have such a strong negative fitness effect, you do not have power to separate your two models.

@AlexDeLarge From the reddit post I linked to, my interpretation was that reducing the frequency of aa is what we want (since that phenotype is less fit). In that case, what do we actually expect to happen under non-inbreeding, and why is it a "good" thing?

I notice your simulation doesn't actually compare the spread of phenotypes of "incest-seeking" and "incest-avoiding", you just prescribe one or the other. What your simulation shows is that deleterious phenotypes tend to go extinct, which is what we would expect, incest or no incest (if anything it might happen faster with incest because the deleterious allele is less likely to "hide behind" the non-deleterious one; see: https://en.wikipedia.org/wiki/Genetic_purging). I think the question is, what does "incest is bad" mean to you and how did you expect this simulation to show it?

Given your setting you expect to have low frequency of recessive homozygotes even without inbreeding. But in reality, recessive homozygous genotypes do not need to be deleterious, in fact only a small fraction is. Accordingly, given that recessive deleterious alleles are very rare and most often found in healthy heterozygous carriers, they are rarely combined by chance. The problem with your simulation is that it does not capture that inbreeding, due to excess homozyogotes, strongly increases that probability as you penalise every homozygous recessive genotype.

@RozennKeribin I was trying to understand why inbreeding is considered "bad", genetically. From the reddit post I linked, I thought the idea was that with inbreeding, deleterious alleles go extinct less quickly, although in retrospect that doesn't make much sense. If that's a mistake, then "Why is inbreeding bad?" should be taken to be part of the question.

inbreeding is bad becasue it prevents variety in genotype, the very thing sex evolved to produce. Sex itself is costly and time consuming so doing away with it's benefit but keeping the sex is counterproductive.

With inbreeding, you have a good chance of both parents sharing the same very deleterious mutations, which means their kids are likely to be homozygous for those mutations.  Make your sim have dozens of genes, crank up the penalties for being homozygous, and see what your populations numbers look like in the incestuous group.

I also wonder if your "sibs, then breed randomly" is going to result in a lot of outbreeding once the genetic load of deleterious mutations gets bad, and you get a lot of only children.  If you could change the sim so that singletons try to mate with cousins when there are no sibs, instead of randomly, then you'll have more inbreeding in your inbreeding population.

@Jack M "If that's a mistake, then "Why is inbreeding bad?" should be taken to be part of the question" -> it is a mistake, but given it changes the tenor of your question you might want to edit it taking the new info into account. For why inbreeding is "bad", you might want to try simulations that compare inbreeding vs outbreeding phenotypes (in the long run deleterious alleles go extinct either way, but in the meantime the inbreeders might see less-fit offspring than the outbreeders and be selected against) and asexual vs sexual reproduction (because inbreeding makes sex more like asex)

Try using nonlethal recessive alleles such as those involved in color blindness, then consider the frequency of color blindness on the two groups.

@JeppeNielsen If the alleles have no effect on death rates, then you end up with roughly 25% of each genotype no matter what. This is pretty obvious when you think about it because all four genotypes are entirely equivalent as far as the simulation is concerned.

You do certainly not get 25% of each genotype unless that is your starting frequency. Consider the case were the "a" allele have a frequency of 1% in the general population. Assume that the Hardy-Weinberg principle ( https://en.m.wikipedia.org/wiki/Hardy-Weinberg_principle) is in effect and calculate the equilibrium frequencies. Next consider the situation were inbreeding is occuring, then it should be quite clear that inbreeding increases the frequency of rare recessive allels.


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What effect does taking antibiotics unnecessarily have on future bacterial infections?
I have been told by my biology teacher that you shouldn't take antibiotics unnecessarily because "the body gets used to them" and it reduces the effectiveness of antibiotics against future bacterial infections, which can be dangerous.
I can't understand how the body could "get used to" antibiotics. How does prior use of antibiotics affect their effectiveness against future infections?

Umm, you mean antibiotics, not antibodies.  Eating antibodies won't do anything, for the same reason eating insulin doesn't do anything.

Every time you expose a population of bacteria to an antibiotic, you select for organisms with resistance-granting genes.
Bacteria can pass plasmids full of genes back and forth.  So if you get a nasty E.coli infection, do you really want one of your usual bacteria with a resistance-granting gene sitting right next to it?
Let's say you are so sick you go to the hospital.  Do you think the hospital wants your antibiotic-resistant E-coli around?

As @swbarnes says:

Every time you expose a population of bacteria to an antibiotic, you
  select for organisms with resistance-granting genes.

But you're asking about the situation where you're not 'sick' when you're taking them, and how it affects future infections.
To understand why that's a bad thing, you need to understand a couple more things. Firstly, your body contains a massive number of harmless bacteria. Some of those are the same species as harmful bacteria - for example, your gut contains harmless Escherichia coli, even though some strains are highly pathogenic. Secondly, bacteria exchange genetic information.
When you take antibiotics, the harmless bacteria in your gut are put under enormous selection pressure for resistance. This will increase the frequency of any resistance alleles present in the population. If you then catch food poisoning, the 'bad' E. coli will exchange genetic material with the harmless ones, and some of that may include the genes conferring increased resistance.
So if you take antibiotics for no reason (or give them to animals as a growth promoter, for example) you're putting bacterial populations under selective pressure to develop resistance, which can spread to other strains or even other species, and means more bacteria that are antibiotic resistant.

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Reversal of cross-linking in ChIP-seq
Chromatin immunoprecipitation (ChIP) is a type of immunoprecipitation experimental technique used to investigate the interaction between proteins and DNA in the cell. A summary of the protocol for ChIP is here. Briefly, the steps are:

DNA and associated proteins on chromatin in living cells or tissues are crosslinked;
The DNA-protein complexes are  sheared into ~500 bp DNA fragments by sonication or nuclease digestion;
Cross-linked DNA fragments associated with the protein(s) of interest are selectively immunoprecipitated from the cell debris using an appropriate protein-specific antibody;
The associated DNA fragments are purified and their sequence is determined.

After step 3 (immunoprecipitation of the protein-DNA complex), it is my understanding that the protein–DNA cross-link is reversed and proteins are removed by digestion with proteinase K.
Can anyone tell me if during this step the DNA at site of cross-linking is included in further sequencing step or is washed away with the protein itself?

Welcome to Biology.SE! I've tidied up the question a bit - hope the edits are okay.

So you want to know if in the crosslink reversal step the DNA gets lost?

Yes. More specifically at the point where protein & DNA is attached.

After the crosslink reversal step, you still have some DNA connected to protein fragments.
So at that step, instead of doing a normal DNA purification, we also need to use a phenol-chloroform extraction or special columns to seperate DNA from protein fragments.
Thermofisher usually gives really good explanations too.
Please let me know if I didn't understand the question correctly! :)


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Difference between DNA and Genome
Can we safely use the terms DNA and Genome interchangeably or is there any (even slight) difference between the two?

note that epigenetic aspects are essential to body plan embryo morphology yet are not considered part of the Genome, due in part to current limitations of DNA sequencing

@ScottStensland I learnt the meaning of your comment now after attending Epigenetics course. Thanks Scott!

Oversimplifying:

DNA is a specific form of molecule (desoxyribonucleic acid).
Genome is the information of a specific organism stored on its DNA. (Not just his genes, i.e. the information in the coding parts of his chromosomes, but the whole of it.)

With just a little bit of scientific handwaving, you could conceivably synthesise DNA molecules that are just random sequences of ATCG. It wouldn't be the genome of anything.

I'd add that retroviruses have a genome not encoded by DNA, but RNA; and PCR primers are DNA not encoding a genome.

DNA is any piece of DNA. Genome is a very specific piece (or pieces) of DNA: all of the DNA contained inside one cell, or organelle, or virus particle, from a specific species.
For a species with a single chromosome, like the bacterium, E. coli, then the bacterial genome is equivalent to the cell's chromosome. Same for a virus. For a metazoan, like C. elegans, which has six chromosomes, the nuclear genome is one copy of all the chromosomes and the mitochondrial genome is one copy of the mitochondrial chromosome.
So DNA is a general term, while genome is a specific term that can be used most clearly with a modifier to specify the species you are referring to (e.g., the human genome, or the duckbill platypus genome, etc.).


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Why cold water results in cough
I have a pretty simple question which always kept me intriguing since childhood and I couldn't find its precise answer yet. Why do we cough by cold water. Recently I had flu and found very strange correlation between cold water and coughing. Even seconds after drinking cold[er] water, I started coughing as you all would have experienced as well. So why does it happen?

@rg255 I think the answer below addresses the question and I don't find any reasons why its opinion based if there is a clear linkage with tract called "Respiratory Mucosa". Rest, you better know than me

I am no expert in this but I had asked my doctor the same question the last time I fell sick and I'll try to paraphrase his explanation.
"There is this protective lining on our respiratory tract called "Respiratory Mucosa" that acts as the first line of defense against pathogens. But when you consume cold food and beverages , this membrane gets congested or shrinks such that it exposes the respiratory tract to pathogens . This is more prevalent if your body has an elevated temperature such as after spending a lot time outdoors during summer or after a workout. Cold food as such doesn't make you sick but they make it easier for the pathogens."
A quick Google search turned up this
http://www.thehealthsite.com/diseases-conditions/why-does-drinking-chilled-beverages-cause-sore-throat/#
Your cough could be a symptom of having a sore throat from infection.

any source to add?

Reference added.

Can you add any authoritative reference, like a journal or a well cited expert's blog/website? As for thehealthsite.com it is absolutely uncited and there's no mentioning who the author is.


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If an antiserum was raised in a buffalo by injecting it with monkey red blood cells, what would be the full name for this antiserum?
Im confused, i've attempted this & what i got is buffalo anti-monkey red blood cell antiserum. I'm not sure if this answer is right

its actually Anti-Monkey RBC Buffalo Antiserum as the Ab formed is Anti-monkey RBC Buffalo Ab.

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Can't identify this fish caught off NC coast

It was caught approximately 35 miles off the coast of North Carolina. I've been a charter fisherman for more than 25 years and never seen anything like it. Thanks for your help!

Could you add the size? It's quite difficult to judge from the photo.

i think this is a frogfish. there is multiple types of this fish. i think this is an Ocellated frogfish. frogfishes related to anglerfishes. memorizing animals by classification eventually helps with identification. little google search and using fishbase site about information helps. this sites very helpful about finding fishes.
fisbase frogfishes
frogfish site
this link says it can be found on North Carolina


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What's the rationale behind freezing one's eggs if cells can be cloned?
It seems to me there's a lot of discussions around the topic of somebody freezing her eggs.
What I don't understand though are the following:

Why would you freeze your eggs when you know that the technology for transforming a somatic cell into an egg today exists, or doesn't it see here?
Is it proven that freezing doesn't alter biological activity and hence not diminish the chance of giving birth to a malformed child?

To me it seems way easier and safer (and less expensive) to artificially produce female gametes than freezing them and, 10 years later, unfreeze and hope for them to be still biologically active.

Cloning of humans has yet to be demonstrated. In the reference you provide on artificial gametes notice that all of the sentences use the words "may", and "could". It hasn't actually been done yet, at least not verifiably.

Why Would You Freeze Your Eggs?
For 1, a woman may wish to freeze her eggs if she needs to delay childbirth. This page explores several reasons why, for example, "Women who want or need to delay childbearing in order to pursue educational, career or other personal goals.". Additionally, it explores some basic explanations of the process, if you are interested. If a woman has doubts about her fertility in 10 years time (using your final sentence as an example), such as if she is recently diagnosed with cancer, or needs to finish education but is ready to be committed to having a baby in more than 9 months' time, then she may decide to freeze her eggs for a time when she is more suited to have a baby, using a time when her body is more suited to producing eggs.
Does Freezing Have Adverse Effects?
As for your second question, the same page does mention successfully freezing an embryo for 10 years at -196 degrees Celsius, with no adverse effects on the eventual birth.
Regardless, exploring the risks reveals that the decision on whether the practice is seen as positive or negative is still on the fence - different parties argue for different opinions, as there appears to be no objective truth about proven adverse affects.
The risks described by this clinic are worth considering, albeit minimal compared to a risk of malformed children, however, it is still a popular choice, albeit put forward as 'experimental'. This study (2010, Rudick et al) showed how, in the US, cryopreservation was already being offered in 283 of 442 fertility clinics surveyed. 1/3 of the reasons for the choice was for women with cancer, and the other 2/3 was for women with 'advancing maternal age'.
The ACOG (American College of Obstetricians and Gynecologists), in 2013, stated that they do not endorse freezing of eggs 'for the sole purpose of circumventing reproductive aging in healthy women', however, the ASRM (American Society for Reproductive Medicine) lifted its label as being 'experimental' in 2012. The previously linked article describes a study conducted by the ASRM, which 'reviewed data from four randomized controlled trials and various observational studies that compared fertilization rates, embryo implantation rates and pregnancy rates of fresh eggs versus eggs that were frozen', and 'showed no increase in birth defects, developmental disorders or chromosomal abnormalities when in vitro fertilization cycles were conducted with frozen eggs, leading the society to declare the technique effective and safe'.
Conclusion
Your question is a slightly broad one, and can be answered by the subjective choice of the woman/women involved, however the ASRM still stresses that "we should proceed cautiously in using this as an elective technique", by making a clear line between 'need' and 'want'. However, there is no evidence to show that rates of abnormality are any higher using this method, but considering it is still a fairly new practice that is being marketed as a choice rather than a medical treatment, there is skepticism in the air around whether marketing scientific and medical designs as a mere 'choice' for older women will lead to this technology becoming better or worse.
Additionally, about your comment of it being 'less expensive', this website shows that the average cost of in vitro fertilization in the U.S. is currently about 10,000 - 20,000 USD, whereas the first website I linked (here) estimates the cost at about 10,000 USD to undergo an egg freezing cycle. Although, the prices will change from clinic to clinic. Regardless, the prices are still similar, and the choice lies in the woman choosing to pay and freeze her eggs if, for example, she has recently been diagnosed with cancer, or fears she will not be fertile in 5+ years time.
I hope this answer has been sufficient in answering your questions, and if you have any more questions, feel free to ask me :)
Sources:

http://uscfertility.org/egg-freezing-faqs/
http://www.mayoclinic.org/tests-procedures/egg-
http://www.sciencedirect.com/science/article/pii/S0015028210008009
http://www.ncbi.nlm.nih.gov/pubmed/24463693
http://edition.cnn.com/2012/10/19/health/egg-freezing/
http://www.advancedfertility.com/fertility-treatment-costs.htm


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Does reproduction cause aging ? Is aging just a strategy to increase reproductive success in all organisms?
Background for why I am asking this:
I read a book—modern biological theory and experiments on celibacy— which uses life history theory to imply that reproduction is the reason why organisms grow old. Can this really happen?
The book uses several arguments in support of this argument:

Even if an organism does not age, it would still die from accidents.
Therefore, reproduction becomes a higher priority for the organism than repairing and maintaining its body in order to survive over generations.
Consider two organisms, one that ages and one that does not. Now, if the one that ages can 'tune' its rate of aging so that its life expectancy is more or less the same as that of its non aging peer, it will suffer little loss of lifespan and gain a lot of reproductive success in return, giving it a selective advantage.
The book argues that by aging, organisms reduce the cost of dead bodies. For example, if we don't age, all the people dying would be healthy and robust, implying all the energy gone into maintaining health would be wasted. But if, strategically, we start 'spending' health to gain extra reproductive success, we end up gaining what we would otherwise waste. All the really old people in an aging world like ours become corpses even before dying, implying less loss involved.

So, here is my question:
Is reproduction one of the major causes for ageing? Is ageing a strategy to increase reproductive success, as described in the theory above? Does life history theory imply that a 'well fed' individual will strategically age itself to gain a selective advantage? Is that it? Is that why we age?
Some experiments that favour the above theory:

It has been shown in 'hundreds of dietary restriction experiments' done on animals that a decreased rate of reproduction and of aging go hand in hand.
An increase in the lifespan of eunuchs and castrated animals has been confirmed in many experiments.
It has been observed that if a lactating female lacks calcium, the bones in her body are demineralized to nourish her offspring, implying a higher priority towards the child than her own body, which makes sense because the child would outlive her.
Experiments have confirmed that the cost of ejaculate in male adders and Japanese macaques is non-trivial.

It should be noted that this theory assumes life history theory to be correct, and is therefore supported by all experiments that support life history theory.

After reading disposal soma theory, as suggested by rg255 in the comments, I can see that the theory discussed in this book is disposal soma theory with an extra assertion that the best life strategy of any organism is not to have 0 aging, but to have a species specific rate of aging, in order to reduce waste of resources through dead bodies and increase reproductive success.

Comments are not for extended discussion; this conversation has been moved to chat.

Possible duplicate http://biology.stackexchange.com/questions/17077/why-does-evolution-not-make-our-life-longer


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Which strange fruit is this?
Yesterday, my brother brought a strange fruit resembling Lychee (but much bigger in size). Here is a pic of it:

When cut it, it had smell like banana and fibers were like of the chicken meat, though taste was more or less like banana (sorry have no pic of that).
Can someone kindly help me identify it?

As a complete sidenote, go search for "durian". It is a different kind of tropical fruit that you might not know about and it's fascinating. Especially how the taste/smell of it is commonly described.

The meat-like texture of jackfruit has led some people to use it as a meat substitute for vegetarians/vegans (though of course it's not really comparable in terms of macronutrients.)  See here, for example.

As a sidenote where are you from? This fruit and variants of it is pretty popular in S. Asia.

@J.E I don't think it's a durian according to wikipedia articles.

@AnonymousI yes, you are completely right, but that's why I used words such as "complete sidenote" and "different kind of fruit".

Yep, I've noticed that before I even started the comment but somehow unconsciously I wrote it anyways. My apologies for the mistake.

This appears to be a jackfruit. Jackfruit are a large, tropical fruit, commonly reported as smelling similar to banana.

Oh yeah!! Yes it is what it pretty much looked like from inside. Thanks a lot! I have seen it for the first time in my life.

Jackfruit are famously reported to taste like Wrigley's Juicy Fruit. Both seem to contain a lot of isoamyl acetate, as do bananas. So this all adds up.


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Question about the quantity of orchid species and genera
One flower which I am reminded of is the orchid and conjointly, the Orchidaceae family. I am surprised when discovering there is an abundance of species and genera, hence I would like to know the exact number. Moreover, what is the reason, is this a quality resulting from angiosperms?

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


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Effectiveness of feces as a fertilzer
How effective is feces such as cows, chicken or horses for fertilizing the earth of a garden in order to grow crops.

What crops are we exactly talking about and what feces are we exactly talking about? It mostly depends on those plants' chemical needs and the chemicals in the feces of those animals (and the chemicals present in the soil where that plant is located, and even the current growth stage of the plant).

I am thinking about staple food crops such as carrots, potatoes, cucumbers or yams.

How do you measure effectiveness?  Consider that people have been doing it for probably thousands of years, and still do so today.  Or walk around a cow pasture and notice how the grass grows far more lushly around each cowflop.  Or read throught the 30K or so hits on Google Scholar: https://scholar.google.com/scholar?hl=en&as_sdt=0%2C29&q=effectiveness+of+manure+as+garden+fertilizer&btnG=

It depends largely on the crop there are many papers about it.  You will have an easier time searching for manure instead of feces. https://tropicalsoybean.com/sites/default/files/Comparative%20effectiveness%20of%20cattle%20manure,%20poultry%20manure_Ghosh,%202004.pdf and https://scholar.google.com/scholar?hl=en&as_sdt=0,31&q=effectiveness+of+manure+as+fertilizer

Thank you, I will read into this further.

Horse manure allows the propagation of the plants etc that horses eat as they do not process the seeds.


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How can skeletal muscles in the human body be modeled as levers?
From what I understand, human arms can be thought of as third class levers, so that the distance from your elbow to the place where the muscle attaches is effectively the distance to the fulcrum, so that arms produce proportionally less strength on the end, and proportionally greater distance when lifting a load.  So this is somewhat of an anatomy question (although I suppose if it was to be used for an exoskeleton, it could be robotics) but can leg muscles and the muscles that attach to the ends of arms and legs be roughly modeled in such a way?  What muscles/muscle groups don't classify that way?

Interesting question. I feel like in many cases it would be hard to model the muscles attaching to the hand/foot because of the retinacula in those areas holding them in. I think similar considerations might apply to the muscles moving the fingers/toes. I assume many neck muscles, e.g. sternocleidomastoid might classify in this way, and maybe same for some abdominal muscles.

Well I can imagine the muscle that attaches from your back to your upper arm (pardon me for not using the anatomical name) as having the fulcrum at the attachment point, and maybe the same with the legs.

Your question is not that clear - the title asks how to model muscles as levers, while the body seems to focus more on if they can, and if so which ones can and can't. Going by the title, the question is too broad because you don't specify what sort of modeling you'll be doing. Going by the body, it's also too broad, because there are many different types of muscles with different modes of action and varying degrees of fitting into a "lever" model. Please [edit] your post to focus on a single, clear, answerable question.

AFAIK, you can't model muscles as levers, since they only contract.  The bones are the levers.  In (physical) model terms, you could think of the skeleton as a bunch of sticks bolted together, with ropes tide to the muscle attachment points.  Pull on the rope, and the stick/bone moves.


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What is this compound-leaf tree in Southern India?
I am staying in South India. I didn't find any flowers to this tree; just leaves.
Just seeing the leaf, I am guessing Arabian Jasmine, but my tree doesn't have flowers or seed buds like Arabian Jasmine has.

I added more clarity image, is it ok to ID this plant ?

A clear shot of the whole leaf would be nice. Also a comment about where it's growing and how big it is would be helpful. Thanks.


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To what extent are lifestyle factors taken into account in medical testing?
A glance at any official health bodies advice will show that we are entreated to eat more healthily, take more exercise and reduce stress. Presumably, there is some reasonable evidence that these factors play a relatively significant role in disease formation and response (otherwise, one would presume they would not be within the remit of such organisations).
In what little opportunity I've had to read primary research on medical testing, however (I'm a statistician, not a biologist), I've not come across any attempt at stratification for these factors.
If one is, say, testing the response to a new medicine, presuming these factors will promote recovery in your test subjects, then the apparent efficacy of the medicine might be affected by the distribution of these "lifestyle" factors within your test and control groups.
Similarly, on the other side of the coin, if you are testing the response to a new health threat by epidemiological study, a quoted Odds Ratio of 1.2 might be quite radically different for individuals of different general health, yet (in the studies I've read) there seems to be simply a presumption that the control group and the test group will have a similar spread of lifestyles.
It certainly seems to be a relevant factor in some cases as individuals with a history of smoking are almost always controlled for in such epidemiological studies (especially related to lung conditions), but I have never come across similar treatment of individuals in high stress jobs, eating fewer than 5 fruit and veg per day, taking less than three hours exercise a week etc.
For large effects, these factors would probably be insignificant, but where the effect is small (say a slightly efficacious new treatment, or a low risk environmental contaminant), failure to take account of these factors could theoretically lead to the conclusion that the drug is a slight improvement on what we have, or the threat requires some moderate mitigation, when if fact the drug is virtually ineffective in people who are otherwise unhealthy, or the threat is actually zero to a healthy individual, which would be really important conclusions for public health.
My limited interaction with epidemiological studies was quite a few years ago now, so my question is, have things moved on to start controlling for these factors now we have a better idea of their impact, and more significantly, if they have, have any studies from the past been revised in the light of such controls? Also, does anyone know of any accessible studies on the impact of these factors on epidemiology in general?
To clarify in the light of the close reason. The question is a single one which can be simply answered by anyone involved in epidemiology or researching pathology. Do modern epidemiological studies of disease causal factors control for lifestyle factors, such as diet, obesity, exercise and stress? The answer I'm looking for would come from someone who is either involved in epidemiological research or reads a significant number of epidemiology papers and the would at it's simplest be " Yes, they do" or "No they don't". I'm not sure how much less broad it can get.

I'm voting to close this question as off-topic because it is much better suited for Health.SE.

I don't understand why you think this question would be better suited to Health.SE. That site seems to be primarily about health questions, this question is about pathology and epidemiology research methods. Both tags exist here. If you're suggesting it's off topic simply because it relates to a health issue, then what questions could possibly fall under the epidemiology, health or pathology tags?

While it's true that the majority of questions on that site are personal medical questions, this is the kind of question they would welcome. Tags existed before Health.SE went into public beta.

A well intentioned consideration that another site might like to tackle the question, and voting to close as off-topic are two quite different things.

One of the close reasons is that 'this question is better suited to another SE site.' Not sure of the exact wording, but it is right there. I have nothing against this question; closing it would most likely lead to migration. I simply think there is a better site; both actions ate well-intentioned.

Most studies aren't large or sufficiently powerful enough to consider too many intervening factors. Only the largest trials could even attempt this. Most drug trials are basically as small as they can be, because they are 1) expensive, and 2) you are testing an unknown medication, so you don't want to unnecessarily expose patients to risks that might not yet be understood.

@anongoodnurse The answer to the question here https://biology.meta.stackexchange.com/q/3416/23094 seems to state quite specifically from a diamond mod that "Questions on medical science are on-topic here"

I disagree with the reopen, and the edit does not actually make it more specific. If you really want an answer as simple as that, it isn't really an appropriate question to ask here. The actual answer is obviously it depends: some studies will and some studies won't. Explaining all of the causes and reasons etc to make a solid answer is where it becomes too broad.

@BryanKrause I'm afraid I don't understand your comment at all. You seem to be saying that If I want a short answer the question isn't suitable for this site, but if I want a long answer it isn't suitable either. Also how does "Explaining all of the causes and reasons etc to make a solid answer" make the question too broad. To suggest that the choice to include lifestyle factor stratification in a control group is made considering reasons so vast and complex they couldn't even be summarised in an answer is ludicrous.

I worked (rather tangentially) on statistics for epidemiological studies a few years ago and in that limited experience absolutely none of the studies, no matter what size, stratified their control and test groups for any lifestyle factors, so if it's so "obvious" that some do, simply linking to one of them would have made a simple informative answer. The fact that, instead, everyone just seems to want to dodge the question has served as an answer in itself.

I wouldn't expect subjects to be stratified over lifestyle factors, since the number of groups would get prohibitively large as you add multiple dimensions of factors. However, demographic data is often included and analyzed, the whole fields of population health and epidemiology deal with these factors all the time, just not every factor in every study. Since you are a statistician, I am sure you are aware of the problems with testing too many factors simultaneously. You can design a better powered study if you focus on factors most expected to be of interest.

Testing two factors simultaneously is relatively simple, one only has to use an interactive term on one of the coefficients in a regression analysis, neither is dealing with multiple lifestyle factors complicated where the null hypothesis would be that lifestyle factors did not affect one's risk from the chemical concerned, a compound score for "general healthiness" can be used (and has been in the many studies correlating social status and health). Only if the null hypothesis is rejected would there be any interest in which lifestyle factor had most influence.

Additionally, as I requested in my previous comment, if " the whole fields of population health and epidemiology deal with these factors all the time". I really would be very grateful if you could point me in the direction of one of those many studies, that really was the point of me asking the question. You've twice asserted that at least some studies do take account of lifestyle factors sometimes and yet in my experience I've come across none that do, I'd really like to see an example of how it's done. Some links to the papers that have lead you to this conclusion would be much appreciated.


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How can (or did) Deinococcus radiodurans continue to evolve after developing resistance to mutation?
Deinococcus radiodurans has a remarkable ability to resist damage to its DNA due to radiation, dehydration or (to my knowledge) any other source. It keeps multiple copies of its genome and has a repair mechanism as well.
My question is: how could this thing evolve to be so sophisticated at preventing the processes behind evolution? It seems that a mechanism to prevent errors would also prevent changes, so that as soon as the organism got OK at preventing changes it wouldn't be able to evolve to get better at it. Were genes for these processes borrowed from other extremophiles? Is the assumption that it was in such extreme environments that the damaging influences were keeping up with the repair mechanisms? That's my guess, but I'd love to hear from others with more knowledge of evolutionary processes.

According to the "Functional adaptation" section of this webpage, Deinococcus radiodurans uses repair proteins to stitch up DNA after radiation damage. Meaning, after a burst of radiation, the DNA will be in pieces and the repair proteins put it back together. It seems like this mechanism would not come into play during other forms of DNA mutation that happen during replication, such as point mutations or inversions.

Deinococcus radiodurans did not "develop resistance to mutations".
It is able to repair its chromosome when scatered in pieces by radiations or desiccation, while other bacteria would die in such conditions.
So this is adaptive in extreme environments, such as deserts (where it has evolved) or canned corned beef (where it was discovered).


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Does the false positive covid-19 PCR % referred to by Surkova & Nikolayevskyy in The Lancet mean % of all tests, or % of positive tests?
In False-positive COVID-19 results: hidden problems and costs it is said:

The current rate of operational false-positive swab tests in the UK is
unknown; preliminary estimates show it could be somewhere between 0·8%
and 4·0%

My questions:

Are there any more accurate estimates or research done on the real false positive rate than what Surkova & Nikolayevskyy are referring to?
Is Surkova & Nikolayevskyy referring to a percentage of total tests done, or a percentage of positive tests?

To clarify. Let us, for the sake of example, say that the false positive rate they are talking about is 1%, and one day we test 100.000 people, and that we get 5000 positive results. Will that mean that:
A: 1% of the 100.000 are false positives, therefore there are 1000 false positives?
or that
B: 1% of the 5000 that tested positive are false positives. Therefore, 50 are false positives?

Check the references supplied for those numbers in the article - they explain how the numbers are derived.

I’m voting to close this question because it requires one to read a specific external source to assess and possibly answer. This site is for general problems in biology, not for interpreting particular papers.

Actually, neither A nor B in the example are a correct interpretation of a false positive rate, because there isn't enough information provided to determine a false positive rate. In the terminology of clinical diagnostic testing evaluation, testing outcomes can be classified into one of four fundamental categories: True positive, false positive, true negative, or false negative.
While there are four possible outcomes, any given patient only has two possible test results, positive or negative. And the assessment of that result depends on whether they have the disease or not. So patients with the disease can only have a true positive or a false negative, and patients without the disease can only have a false positive or a true negative.
Since it's not possible for a patient with the disease to have a false positive, we get to ignore them in calculating a false positive rate. So a false positive rate would be the number of false positives out of the total number of possible false positives (or the percentage of patients without the disease who test positive). With an ideal data set in which you knew both the test result and true infection status of each patient, you could calculate it like this:
$$ FPR = \frac {False\ Positives}{False\ Positives + True\ Negatives}$$
The thing is, we don't usually use this in evaluating clinical diagnostics, but rather it's complementary value, which is called "specificity" (for some reason), and is essentially true negative rate.
$$ Specificity = \frac {True\ Negatives}{False\ Positives + True\ Negatives}$$
But note that neither of these values can give you the number of false positives in your example without more information. If you assumed that all 100,000 people tested did not have the disease, then you'd expect 1000 false positives (given your 1% false positive rate). But it gets more complicated when you have a non-zero rate of infection in the tested population. The greater the underlying infection rate, the fewer false positives you expect to see (and vice versa, with a lower infection rate, you expect a greater proportion of positives to be false, which I think is pointed out in the article you linked). Basically, it's really hard to determine something like a false positive rate on the fly and even harder to estimate it's impact in the real word, especially when the test you're trying to evaluate is also the best means you have for determining true infection.
Another consideration is that, for a well designed PCR diagnostic test (most COVID tests are), the majority of false positive results will come from technical errors (i.e. cross contamination, mislabeled specimens, etc.), rather than randomly from the test itself. And the rates of those kinds of errors can vary with the underlying rate of infection, the number of tests being processed by a given lab, the level of training those lab workers have, the number of hours they're putting in (tired people make more mistakes), and probably other factors I'm not considering.


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What species is this large bug? (South India)
I found this bug in South India. What species is it? The tiles in the picture are 5x5 centimeters each. The bug was moving relatively slowly and didn't seem to fear me much.

I tried asking it directly, but it kept claiming to be a feature.

The question has been correclty answered I think but out of curiosity: what do you mean by I tried asking it directly, but it kept claiming to be a feature.?

@Remi.b http://www.urbandictionary.com/define.php?term=It%27s%20not%20a%20bug%2C%20it%27s%20a%20feature

I suppose it's a whip scorpion.

Whip scorpion (order Uropygi, sometimes Thelyphonida), any of approximately 105 species of the arthropod class Arachnida that are similar in appearance to true scorpions except that the larger species have a whiplike telson, or tail, that serves as an organ of touch and has no stinger. The second pair of appendages, the pedipalps, are spiny pincers, and the third pair are long feelers.

It is most common in India and Japan to New Guinea.

In the new picture, why are the mouth-parts different from the specimen in my picture?

Sorry I made a wrong edit. It happened while rolling back an edit made by another member of the community. I've corrected it now,.


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Kegg in Cytoscape: how to get plots with reaction IDs in place of EC numbers using KeggScape?
I found a KeggScape manual page representing Kegg reactions in Reaction ID format, but I couldn't find how to get a Kegg plot with reaction IDs in place of EC numbers. Does anyone know?

Welcome to Biology SE. I think you will need to provide more information if you hope for an answer. I do not use Cytoscape, but believe it is a general networking tool that has nothing intrinsically to do with Kegg. I see there is something called Keggscape. If that is what your question is about, you should edit it to say so, and provide a link to the documentation. Your title doesn't indicate you are talking about Cytoscape so I have edited it for you, putting your old title as a first line. If this is not correct, modify it.


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What is the scientific consensus on whether humans were monogamous during the period of evolutionary adaptedness?
The book The Mating Mind by Geoffrey Miller asserts, as part of its thesis, that humans were not monogamous in the environment of evolutionary adaptedness.
I found the book vivid and persuasive, but I'm interested in what others in the field would say. Is this the scientific consensus among evolutionary psychologists?

"during the period of time wherein evolution shaped our minds" - there was one distinct period?

I'm voting to close this question as off-topic because its non-speculative aspects appear to be answerable by archaeology rather than biology.

@David Any sense of a better site on this network to ask this question?

Not really. There does not appear to be a SE list for archaeology. I just googled for archaeology list and there seem to be a large number, but which would be appropriate I have no idea.

There is no such thing as  "period of time wherein evolution shaped our minds". Our "mind" (whatever you mean by 'mind') is always evolving and has always been. It might not be enough to make your question on-topic but it would be already a good move toward it if you could just specify dates of interest.

I'm referring to the environment of evolutionary adaptedness; do you think this is a useful concept?

It might be worth expanding the question with some background.  For instance, are you asking whether there was a period when humans or pre-humans were "naturally" monogamous, and trying to discover when & how this changed?


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Extraction of arthropod embedded in animal tissue
I'd like to extract an ectoparasite from a biopsy of animal skin for subsequent identification. The mite is small, about 100 um, and embedded in a column of tissue. It's too small to manually excise under magnification. Currently preserved in 70% ethanol.
Ideally I would isolate it by loosening or dissolving the surrounding tissue without destroying its features. I'd like to conduct a visual inspection prior to sequencing for species identification. Specific suggestions and techniques welcome.
See photo:


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The Perplexing Trilobite: What is the Evidence Supporting The Hypothesis That They are Not Crustaceans?
In the field of paleontology, one question that's really bugged me (er, no pun intended) of late is why the subphylum/class Trilobitomorpha/Trilobita is off on its own branch of the Arthropoda phylum, or alternatively should be slotted under the Mandibulata clade.
What is the evidence justifying these hypotheses?
From a layman's perspective it seems compelling both from what is known of the physiology and morphology that it would make more sense to tentatively classify them as a early member of the order Isopoda, a part of the subphylum Crustacea.
Indeed, Alex Chestnut's Master's dissertation, "Using MORPHOMETRICS, Phylogenetic Systematics and Parsimony Analysis to Gain Insight into the Evolutionary Affinities of the Calymenidae Trilobita" states on the history of trilobite studies that Charles Lyttleton, one of the earliest documented discoverers of trilobite species, asserted that trilobites belong not to insects, but to "the crustaceous tribe of animals."
Indeed, if this is the case, morphologically we see that the trilobite shares many features with modern isopods (i.e. "sow bugs", "pill beetles", "roly-polys" etc.).  Look at this newly discovered albino cave isopod, for instance:

And now look at this fossilized Crotalocephalus africanus:

And this Armadillium vulgare (Latreille) pillbug:

And this Crotalocephalus trilobite:

Well, you get the idea.  Trilobites look perhaps look morphologically more like isopods than any other living order (although a certain roach (members of the Laxta genus, i.e. Laxta friedmani) does also look uncannily similar until you get to the legs and wings).
And apparently at one time, they were classed under Crustacea (the subphylum Isopoda is in), hence raising the possibility that Isopoda may be "living fossils" or the modern descendants of trilobites.
However, the Wikipedia entry for trilobites states:

Once soft-part anatomy had been recovered, the trilobites were
  originally allied to the Crustacea; however, this suggestion has since
  fallen out of favour.

While it goes in depth into what is known or believed to be known about trilobite physiology and morphology, it never really explains WHY trilobites are no longer believed to be crustaceans.
It goes on to state, though, that apparently this is being reconsidered... but not in the subphylum Chelicerata (?!) which Isopoda lies under:

A relationship with the Chelicerata, in a clade termed Arachnomorpha
  (Arachnata), was in vogue for some time; a position in the Mandibulata
  (=Myriapoda + Crustacea + Hexapoda) stem-group may be a more
  parsimonious alternative.

Ugh, Myriapoda?  Why?
First, members of Myriapoda generally have simple eye structure, where as members of Crustacea typically have compound eyes.  Trilobites have compound eyes!
Now the other defining characteristic of crustaceans vs. myriapods, from what I've read, is the brain size.  But from what I understand little is known about the trilobite brain.  But I would argue the presence of compound eyes and the believed predatory niche suggests a more complex brain.  So that would make another somewhat hypothetical reason to pick Crustacea over Myriapoda.
I was unable to identify any clear evidence in favor placing trilobites in Myriapoda vs. Crustacea..
Let's look at the overall defining morphological/physiological traits of Crustacea:

Three body regions -- head, thorax, and abdomen (possibly fused).
Exoskeleton is typically hard and molted
Each somite (body segment) can have a pair of appendages which "vary widely"
Abdomen bears pleopods (swimming legs)
Appendages are often biramous.
Open circulatory system Straight digestive track
Brain and kidney structures near the antenna
Eggs hatch as larvae

To my knowledge other than the internal organs (which are not well known) trilobites meet all of these criteria.
And then there's the visual test, as seen above, between living isopods and trilobite fossils.  They look obviously similar.
According to the chapter "The Trilobite Body" in Kaesler, R. L.'s, "Treatise on Invertebrate Paleontology, Part O, Arthropoda 1, Trilobita, revised. Volume 1: Introduction, Order Agnostida, Order Redlichiida", each endopodite (walking leg) had 6 or 7 segments.  This might appear to be a morphological difference between modern isopods, but it is also stated that basically ALL early arthropods (including early Crustacea) are known to have this segmentation.
That brings me to my final point ... whatever scant few traits that do offer some evidence against trilobites being an early member of Isopoda in the Crustacea subphylum appear to be in part, at least, morphological differences that are somewhat ambiguous and may be merely evolutionary artifacts that existed in other Crustacea at the time as well.
So the visual and morphological evidence seems to point strongly to trilobites being isopods.  What compelling evidence exists in favor of putting them under the subphylum Chelicerata?
And why is that evidence viewed as stronger than the aforementioned evidence to put it under the subphylum Crustacea, perhaps as early ancestors of Isopoda.

This question is really long and would benefit greatly from being far more concise

Fair enough @rg255.  I've deleted the first paragraph as it was overly conversational and not overly pertinent.  Do you see anything else that should be removed?  Most of the text appears necessary as I'm outlining the morphological basis for classification, the history, etc. in order to illustrate the evidence to the contrary of the hypothesis I'm asking the justification of.  That allows me to ask the additional later question of why whatever evidence does support the hypothesis is thought to be greater than the aforementioned evidence supporting the Isopoda phylogeny hypothesis.

It is still pretty long and I am personally way too lazy to read it :). Splitting the questions into semantics parts (using section titles) and avoiding redundancy should help. Smaller pictures may make the post less intimidating too.

Trilobites had bodies divided into 3 lobes lengthwise.  Hence the name trilobite = 3-lobed critter.  The head or cephalon of the trilobite is large, nearly as broad as the body and marked by sutures.  These are the easy-to-see differences.  There are several other differences that it would typically take a trained paleontologist to detect, including crystaline calcite lenses in the eyes, a rostral plate, and hypostomal wings.  These are summarized here with nice illustrations: http://www.trilobites.info/triloclass.htm#trilobites.  More details:  http://www.trilobites.us/trilobite-morphology.htm.
The overall similarity between isopods & trilobites may be due to convergent evolution, isopods replaced trilobites in a benthic detritovore niche after the great Permian extinction.  https://en.wikipedia.org/wiki/Permian%E2%80%93Triassic_extinction_event
Claiming that "isopods are trilobites" appears to be the first new argument from the creationists in a century.  https://sciencenotes.wordpress.com/2006/04/29/trilobites-are-not-isopods/
explains and has a prettier isopod picture.


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Does Rüppell's Griffon Vulture Have Greatest Vision Acuity? (Small Carrion Spotted at 10 km+?)
Synopsis:
Some sources seem to imply the Rüppell's (griffon) vulture (Gyps rueppelli) can see objects at a distance in excess of 10 km -- roughly three times the commonly asserted vision distance of an eagle.
What studies have been done on eyes of this species and can any experts comment on the accuracy of this assertion?
Also, do we know whether their eyes perceive a similar color range to that sensed by human photoreceptor cells?

Background
Wikipedia's List of birds by flight heights lists the flight height of Rüppell's (griffon) vulture (Gyps rueppelli) as the highest known bird flight height at 11,300 m (37,000 ft).

The claim appears based on this ornithology journal article [PDF]
 ("Collision between a Vulture and an Aircraft at an Altitude of 37,000 Feet") detailing a collision over Abijan, Ivory Coast.  This is a coastal city...

...so can be estimated to be approximately at see level, inferring this is a height above ground (roughly).
The article adds:

Vultures use their excellent eyesight to scan the landscape below from a relatively static aerial position. Instead of flying over a larger distance, they use elevation to expand their field of vision. If they spot a meal down below, the climb has an immediate payoff.

That piqued my interest, as I came across this while trying to track down what the maximum known distance an animal could see was (per a separate discussion of fantasy vision capabilities).
Human vision is according to quantitative testing limited to "~2.6 km (1.6 miles)" [synopsis], likely varying mildly based on physiologic variability.
A Wikipedia entry on eagles ("Eagle Eye") states (citing a book on eagles as its source):

The eagle eye is among the strongest in the animal kingdom, with an eyesight estimated at 4 to 8 times stronger than that of the average human. An eagle is said to be able to spot a rabbit 3.2 km away.

The statement is a little bit tenuous on the sourcing, but impressive if reasonably accurate.
The note in the list of highest flying birds, though, makes it sound like this high-flying vulture could be able to detect faint objects at a distance of 10+ km!
That in turn suggests this bird to have perhaps the longest range vision acuity of any known species, with a vision range perhaps three times that of an eagle or more.
If so, the record for animal vision would not be "eagle eye", but rather "vulture eye".
Granted, it might also all be bunk; the internet is a very inaccurate place hence why I came here to StackExchange seeking quantitative evidence in support of this claim.

Humans can't see distant objects?  On a clear night with dark skies (all too rare these days) I can make out the Andromeda galaxy, 2.5 million light years away.  If you want something that doesn't produce its own light, Saturn at 1.2 billion km is easily visible.  On Earth, I can see individual trees on mountains 20 km or more away, and on one of those rare clear days, can see Mt Shasta from the summit of Mt Rose (near Reno), about 250 km.  I think what you really need to ask about is angular resolution...

I think the limitations that may have been missed due to my wording is 1) size of the of the object 2) an object that is not a light source.  Your terrestrial examples are impressive and of interest, but deal with objects signficantly larger than those discussed (see MIT candleflame discussion) in this thread and attached links.  Likewise Andromeda to my understanding is a somewhat different example than the one discussed here as it's much larger in relative angular vision than a distant mouse at 1 km+.  Maybe you're right on the angular vision term... is that the proper terminology here?

And how would I quantify how small a range would be implied for this vulture to improve the question?  Feel free to edit my question jamesqf if you feel that putting this in angular terms would improve the clarity!

You might ask whether this vulture has the greatest visual acuity.  The problem is that you don't specify what sort of objects it sees at 10 km.  Large objects, as per my examples, are no problem to see at much greater distances.  A dead (since it's a vulture) critter?  But what sort?  The eagle can spot a rabbit; can the vulture spot a dead rabbit at greater distance?  Then there's the issue of camoflage: I sometimes don't see rabbits until I almost step on them, but can track them at some distance if they're moving.

Thanks, when I get some time I may reword this further per your suggestions in hope of eventually getting an answer.

Tweaked the title @jamesqf ... is that clearer?

I think, but I'm not sure, that one way carrion feeders such as vultures find food over large distances is by observing other vultures closer to the source. Some south American vultures also have a keen sense of smell, and can find carrion on the forest floor.


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Parafilm vs Foil for Retaining Plate Moisture while Allowing Gas Exchange
We often plate Streptomyces aureofaciens and grow them in a 30°C room. A post-doc I work with has always loosely wrapped the agar plates in aluminum foil to retain moisture and prevent cracking of the agar media over extended culturing periods (up to 21 days). Another graduate student is saying that parafilm would be much better as it allows gas exchange. The post-doc agrees that parafilm would retain the moisture, but also believes the parafilm will starve the cells of oxygen over time. The parafilm we use has a reported oxygen permeability of 150 cc/m2/24 hours. I don't really know how much oxygen a plate of streptomyces would consume over a day. Thoughts?

Oxygen consumption depends on the growth rate (and vice-versa). If it takes very long time to culture the organism, then it probably doesn't consume oxygen that fast. Parafilm is a better choice than foils but I am not too sure about its gas permeability. As tweaks, you can use a bigger container for culturing or use a humidified incubator.

This may be a problem that is easier to solve by experiment than anything else. Make a set of cultures with parafilm and compare to a parallel set with foil. If the parafilm cells are fine, everything should be ok. If you get a significant difference in cell number or viability or something, then parafilm might not be ok. As a benefit, parafilm is cheap, so this shouldn't be a difficult experiment.


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Fish and microplastic particles
How does exposure of fish to microplastic particles decrease egg-hatching and give young fish a craving for them?
From Garbage in, garbage out: marine plastic 2016-06-24 | Espresso

There is more than just ocean beautification at stake; many creatures
  ingest plastic, and a recent study showed that exposing fish to
  microplastic particles not only decreases egg-hatching but also gives
  young fish a craving for the stuff.


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Immediate Early Genes during sleep
In Neuroscience 3rd ed by Bear et al. on page 607, immediate early genes are described as related to changing synaptic strength, yet have decreased expression during sleep. The explanation given is that "learning and memory formation are largely absent in [sleep]." But that seems somewhat counterintuitive as LTP occurs during sleep.
What is really going on here?

memory consolidation is highly prominent during sleep. What do you define by memory formation? The gain of new information?

I think it is indeed important to note the difference between consolidation and formation. Serotonin and epinephrin levels (both important for memory formation) are very low during sleep, so the synaptic pathways being modulated by LTP are probably not very active. Just speculating here, but perhaps this is even a mechanism to focus LTP on pathways from events in the near past by minimizing 'present' pathways of the same form.

As @Sleepses suggests, there are theories that memory consolidation involves the pruning of synapses resulting in the lowering of net synaptic "weight" while asleep in order to improve the signal to noise of new memories and to prevent acquisition saturation.


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Neuroscience behind the crash
After experiencing things like stress, intense exercise, or using drugs such as caffeine and amphetamine, subjects often assume a depressive and lethargic state afterwards, known as a "crash." What is the neuroscience behind it? Could it have to do with the depletion of neurotransmitters such as the catecholamines, or a downregulation of certain receptors in response to the overproduction of such neurotransmitters?
(This question is a remix of a previous question I posted, which was not focused enough)

In terms of specifically caffeine, caffeine is an inhibitor of cAMP phosphodiesterase. Your glycogen phosphorylase will be active to a higher level (this also means the glycogen synthase is downregulated!) All the glycogen will clear out of your muscle eventually, and when your caffeine levels fall, all the cellular cAMP will begin to degrade. There's suddenly no glycogen, however, and your muscle cells will pull what they can from the blood to replenish it. Especially combined w/ high sugar intake, the pancreas tends to release too much insulin and clear too much blood sugar.

so if your hypothesis accounts for the main symptoms of the crash (that low blood glucose is at fault), adequate nutrition, for example snacking on carbohydrate heavy foods throughout the day but not having large meals, would eliminate the crash? Or, more directly, a glucose clamp would counter the effect completely?

this study indicates that under a hyperinsulinemic-euglycemic clamp, subjects ingesting caffeine has less glucose disposal than subjects ingesting dextrose.

The "crash" effect is typically perceived as a deterioration in affect. With drugs, this deterioration happens as the drug is cleared from blood circulation, particularly cerebral circulation. With the ingestion of amphetamines, there is a brief reuptake of certain neurotransmitters, particularly dopamine and norepinephrine. Amphetamines also temporarily prevent the 'recycling' of said neurotransmitters, so the reuptake effect can last anywhere from 4 to 24 hours. The brain regulates internal homeostasis of mood based on perceived 'high' and 'low' elevations; thus, after an extended elevation in mood, there must be a 'comedown' period, or a deterioration in affect.
Further essential to this idea of homeostasis are the stress hormones, cortisol and adrenaline. Upon release, these hormones may raise blood sugar levels, blood pressure, and/or heart rate. As heart rate increases, the flow of blood goes to the heart, with less going to the brain. This causes the groggy and tired feeling afterwards that might be associated with a 'crash'. Stress hormones also impact the thyroid (which controls how fast the body uses energy, and controls hormonal sensitivity) as well as the central nervous system.
Exercise also leads to increased heart rate, as well as muscle fatigue. However, exercise itself doesn't typically lead to a depressed, lethargic state, as exercise promotes the release of endorphins (which are known to improve general sense of well-being). However, it is not uncommon for some people to experience "endorphin withdrawal" after suddenly stopping excessive exercise, which could mirror the crash that comes from the 'comedown' after drug use.


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Are memory updates local in mammals?
What I mean is, during long term potentiation (LTP) or long term depression (LTD) for a particular memory, do the strengthening and/or weakening of neuronal connections only occur in a small patch of neurons or regions spread out in the cortex?

LTD and LTP happen at individual synapses (not even whole of neurons). However LTP/LTD at one synapse can affect others in the vicinity.

OK I meant something like when a single episodic memory episode is stored, is the memory stored in diffuse locations or rather localized?

LTP and LTD are processes that operate on single synapses. We don't know how "memories" (there are several types of "memory") are encoded in the human nervous system. As a consequence, we don't yet understand the explicit link between some group of synaptically connected neurons, and a given memory.
So the short answer is "we don't know". Take a look at some of the other questions about memories in human brains: 1, 2


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What does the 4DTv (four-fold synonymous) mean?
I saw this sentence "4DTv is the transversion rate at fourfold synonymous codon positions, and ranged from zero (for recently duplicated paralogs) to ~0.5 (for paralogs derived from an ancient evolutionary past)." at this paper and another paper.
I have searched 4DTv or four-fold synonymous on google, but I did not find the answers showed at the following lines.
And my questions:
(1) Does the value of 4DTv range from 0 to 0.5?
(2) Why 4DTv closed to 0.5 indicate that an ancient evolutionary was happended?

I was about to ask the same question: did you answer yourself? Can you post your answer in that case?

After one month of research, I have some insights about it.
First of all, more than "fourfold-synonymous", the correct research is fourfold degeneracy. The genetic code is degenerate, in the sense that there is usually more than 1 codon encoding a certain amino-acid. The degeneracy usually takes place in the third position of the codon, that can be 2-, 3- or 4-fold degenerate. A 4-fold degenerate site would be the third position of a codon, where regardless of which nucleotide you have, the outcome doesn't change. Example: GGT, GGC, GGA, GGG all code for Glycine. As there are four variants at the third site of the codon, the third site is said to be fourfold-degenerate (4D). As the encoded amino-acid does not change, there is virtually no selective pressure on these variants, therefore they can be used as a "clock" to estimate times, given that you know the mutation rates per position.
Now for your other questions:
Yes, the value ranges from 0 to ~0.5, and this can be explained in a simple way. Transversions (Tv) are considered to be more rare than transitions (Ti). Therefore, if you calculate the ratio of Tv among all the variants, you expect this value to be < 0.5 (i.e. to have less Tv than Ti, otherwise it would be >= 0.5). Now, in order to accumulate Tv at 4D sites you need time to pass, so the more of them you have, the more time has passed, and that's why 4DTv ratios define time.


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Does A/T, G/C pairing exist in haploid?
I'm trying to understanding base pairing. So every linear chromosome is a double stranded double helix. Is this double stranded property the same as saying an organism is diploid? Or do the chromosomes of a haploid eukaryotic organism, like a member of Fungi, each have 2 strands (with the purines always pairing w/ pyrimidines), which would imply that diploids organisms actually have 4 strands?
EDIT: Part of my confusion comes from the fact that in diploid organisms, each parent gives 1 chromosome to the child. If the double stranded property is the same as saying an organism is diploid, does this mean that say if a nucleotide on one chromosome is A, then the nucleotide on the other chromosome in the same loci must be T? Doesn't chromosome mean a paired up strand, not a single strand?

All chromosomes are double-stranded (they wouldn't be stable otherwise). Diploid organisms have two double-strands, for a total of 4 strands. Haploid organisms one have one double-strand, for a total of 2 strands.

Is this double stranded property the same as saying an organism is
  diploid?

No.  You are a diploid organism because you have two copies of every chromosome.*  You got one from your mother, and one from your father.  All your cells are also diploid, except for your gametes, each of which contains only one copy of every chromosome (due to crossing over, each chromosome is partially from your mother, partially from your father).
Bacteria just have one copy of their genome.  They duplicate it prior to cell division, and each resulting cell has one copy of each chromosome.
*Unless your sex chromosomes are XY, or are anuploidic.


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What factors make a sequence evolve non-randomly?
On the wikipedia page about Fay and Wu's H, it talks about a non-randomly evolving sequence may be due to some selection acting or a selective sweep or population expanding/contracting. My questions about these factors that affect non-random sequence evolution are:

Does negative selection differ from a selective sweep because a sweep is a form of positive selection?
After a selective sweep, any rare mutations you see must have come after the selective sweep. Is it because they can't have come during it else they'd 'be diluted' by the positively selected alleles?
Population contraction can create a bottleneck, which makes all individuals come from a common ancestor. But how does population expansion make a sequence evolve non-randomly?

Fay and Wu test is a test that compare expected sequences under a standard coalescent theory model, that is a single panmictic population with non-overlapping generation of constant size $N$ and effective population $Ne=N$, that is the variance in allele frequency at any following generation is $\frac{p(1-p)}{2N}$, where $p$ is the frequency of a given allele. As such Fay and Wu (as well as Tajima's D and other tests) are not only test of selective neutrality but also tests of demographic neutrality as underlined in Nielsen 2001.
It may be hard to make good predictions about the extend and direction at which a given selective or demographic event will affect a given statistic such as Fay and Wu's H. Therefore, in answering the following questions, I am not specific to Fay and Wu's H. Also, answering the questions fully would require making an introduction to coalescent theory which is subject to a whole book rather than a simple post. To fully understand such test, you will need to follow an introduction to coalescent theory. You can have a look at the books recommended in the paragraph General Entry Books to Population Genetics of this answer.

Does negative selection differ from a selective sweep because a sweep is a form of positive selection?

Let's first clarify the terms just in case. Reduction in polymorphism at linked loci due to positive selection is called "selective sweep" while when due to negative selection it is called "background selection".
Generally speaking, selective sweep is much stronger than background selection. Also, selective sweep has a higher impact on Tajima's D, then background selection.
To my knowledge, methods trying to disentangle the two processes of selective sweep and background selection mainly use inter-species comparisons to infer what types of sequences are concerned. If The loss of polymorphism is adjacent to a highly conserved sequences and is found in related species, then it is probably background selection at play. If there is a fixed mutation that isn't found in related species and loss of polymorphism isn't found in these related species, then it is probably selective sweep.

After a selective sweep, any rare mutations you see must have come after the selective sweep. Is it because they can't have come during it else they'd 'be diluted' by the positively selected alleles?

A selective sweep indeed modifies the Site Frequency Spectrum (SFS, distribution of allele frequencies) to create an excess of high frequency variants (or a relative lack of low frequency variants). See wikipedia > Tajima's D

Population contraction can create a bottleneck, which makes all individuals come from a common ancestor. But how does population expansion make a sequence evolve non-randomly?

Population expansion yield to longer coalescent times and therefore lack of rare alleles. See the introduction of Excoffier et al. 2009 for nice explanation and figure.

Thanks! To clarify on the reasoning behind: "If The loss of polymorphism is adjacent to a highly conserved sequences and is found in related species, then it is probably background selection at play. If there is a fixed mutation that isn't found in related species and loss of polymorphism isn't found in these related species, then it is probably selective sweep." Is this because positive selection is an event that may occur in 1 species but not others, while negative selection would occur in all related species?

Yes, I think you got it. Background selection is a thing that is constantly occuring and therefore you would expect to see it in many related species. A selective sweep is a single event that is happen relatively fast in time (esp. in panmictic population) and therefore a loss of polymorphism is necessarily due to a relatively recent sweep and can therefore be witness in only few (if more than just one) related species.

I was thinking about the 3rd question again; my interpretation of population expansion is that longer coalescent times means less new mutations come up that stick around, plus the majority alleles 'dilute out' the rarer ones. Is this the case?

Population growth actually yield to an excess of rare allele (typically an excess of singletons; see Fu and Li test) (Eldon et al. 2015) and beneficial mutations have higher probability of fixation in expanding populations (Otto and Whitlock 1997)

Note understanding the consequences of different selection regime and different demographic events on the site-frequency-spectrum (SFS) is not an easy task. I do not have a perfect intuition either and people are still working out on understanding the impact on the SFS of particular events.


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What is this raptor on a building in California?
So I took this picture of a bird that was sitting just outside my workplace a few weeks ago:

At first I searched the internet for raptors in California and found the Cooper's hawk. It looked so much like this bird so I thought that must be it and left it at that. However I just recently came across this bird and also this recent hawk identification question and they both look very similar to my bird as well. So I realized I don't know what to look for when trying to identify this bird.
Does anyone know what this raptor could be?
If it helps, the specific location was the city of Tustin in Orange County, California (Southern California). It is about 10 miles from the coast.

where in California?

@VanceLAlbaugh Southern California. Near the coast and part of the Greater Los Angeles Area.

It is a Red-shouldered Hawk (Buteo lineatus).

Its breeding range spans eastern North America and along the coast of California and northern to northeastern-central Mexico.

Identifying features:

Presence of dark wings with white spots.
Presence of dark-brownish head, orangish-brown chest.


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Use of Gene Guns
Gene guns (biolistic particle delivery systems) use gold or tungsten atoms coated with plasmid DNA and bombard it on cells. Their use, as far as I understand, is mostly limited to plant cells. From what I found out, this seems to be due to the difficulty of passing vectors through the rigid cell wall that a plant cell has. Is this really the sole reason why gene guns are mostly used for plant hosts? Fungi also possess a chitin cell wall - is the gene gun used for fungi hosts as well?

C elegans respond well. I posted a ? On here few days ago regarding the use of gene guns:  http://biology.stackexchange.com/q/36738/6061 no one cared :-( lol

I think one of the orginal reasons for using biolistic on plant cells was that it seemed to be the only method which proved to be effective.
This is due to some reasons:

A wide range of highly successful methodes for prokaryotic cells (calcium chlorid method, electroporation)
The plant cell has in comparison to animal cells a additional layer (= cell wall) that consists mainly of cellulose chains, which are stabilized by interchain hydrogen bonds to form a crystalline lattice structure (= microfibril), and thus offering the cell high mechanical defense. (book: "Plant Biochemistry", P. 4) This layer mostly needs to be removed before using other methodes than the gene gun, because it can hardly be penetrated. (chemgapedia.de on "Mikroinjektion")
The high inner cell pressure (~3 MPa) of the plant cell, which makes microinjection hard to accomplish: When the cell wall is perforated with a cannula the pressure within the cell drops dramatically resulting in cell death (chemgapedia.de on "Mikroinjektion"). I am not quite sure why the same thing isnt happening when its pierced by the gene "bullet", but I think its because of higher speed and a smaller penetration radius.
Plant cells are big (up to 0,1 mm) and packed up closly and thus an easy target (sparknotes.com on "cell differences")

When it comes to fungi cells, I don't see a reason why they shouldn't be using biolistic on them as well (besides for yeast cells, they might be to small).
The gene gun is the only way to inject even cell organelles, like mitochondria and chloroplasts, into cells. So its already huge area of application will definitly grow in the future. (wikipedia.org on "transfection")

Welcome to Bio and thanks for your answer. If you can include some supporting references I'm happy to upvote.

Can you elaborate a bit on your second point, please? Thank you.


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Myoblasts Formation
Myoblasts arise from mesenchymal stem cells (MSCs), and are precursors to myocytes. In muscles, in the basement membrane, there are also present satellite cells which can divide to generate muscle fibres, to repair injury to muscle. Are satellite cells intermediates in the lineage from MSCs to myocytes?
Is the lineage then MSC > Satellite cells (a committed stem cell or progenitor) > myoblast (precursor) > myocyte?
If not, then what are the progenitors for myocytes, and how do satellite cells fit in this lineage?

Read https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4073943/


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Isolating the gene of interest for protein production
For protein production, the gene of interest is inserted in an expression vector and introduced into a suitable host for expression. But how is the gene of interest for the desired protein isolated from the organism which possesses it?
One way could be to synthetically make the DNA sequence coding for that protein. Another could be to identify the gene of interest from a pre-existing genomic library or cDNA library of that organism. Are they the only methods?
The organism's entire genome could be taken and cleaved with restriction endonucleases, and a Southern blotting technique (i.e. electrophoresis followed by probe hybridisation and autoradiography) could be used to screen the gene of interest from the fragments produced. Of course, for this the gene sequence must be known beforehand, in order to synthesise the probe. Is this method also adopted? It seems inefficient - given that the fragments are assumed to have the intact gene of interest, and the gene should have been sequenced beforehand.

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.

Using existing DNA as in using it from a genomic library or by isolating gene of interest from the organism's genome by the method described in the question?

You could either use a genomic library or you could isolate genomic DNA from the organism. In both cases you wouldn't have to digest it as described in the question, but you could amplify the gene of interest directly from a low amount of DNA (NEB state 10000 copies of DNA are necessary for sufficient amplification in 25-30 cycles).


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Does any specific property decide which DNA strand acts as leading strand template?
Of the two strands of DNA, the one that unwinds in the 3' to 5' direction constitutes the leading strand template, with the other strand of course acting as the lagging strand template. Is there any specific property - such as a specific base pair sequence present on one of the strands - which decides that that strand shall be the leading strand template - whereas the second strand with the complimentary sequence will be the lagging strand template? What decides, in other words, which of the two strands will be unwound in the 3' to 5' direction (effectively rendering it the leading strand template and the second strand the lagging strand template)?

Basically, the orientation of the origin of replication sequence decides that. I'll read up a bit on that and give you a full answer.


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What sequences are between adjacent genes?
The human genome has a lot of non-coding regions, which include regulatory elements, repetitive DNA, and introns. Suppose there are two adjacent genes on a chromosome, and their positions on the chromosome are, say,
For the first gene: 11,785,723 to 11,803,245 bp.
For the second gene: 11,806,096 to 11,806,143 bp. These values include their regulatory elements, promoter and introns as well.
So what sequence is present between bases 11,803,245 and 11,806,096? Are they satellite sequences? Is this non-coding, non-regulatory region 11,803,245 to 11,806,096 bp heterochromatin?

possible duplicate of http://biology.stackexchange.com/q/43120/3340

It is the same question, but with an additional query - are those regions heterochromatin? Are all regions of repititive DNA, like microsatellites, heterochromatin? Or is heterochromatin only the repetitive sequences of telomeres and centomeres?

No. The intergenic regions are not necessarily heterochromatin. Chromatin conformations are usually very long range and are not usually confined to a single gene. The spread of chromatin state can be prevented by insulators/boundary elements, which again are not a part of the transcribed region. The intergenic regions can also harbour distal regulatory elements such as enhancers and silencers; they can have microsatellites, transposons etc too. To know what all are there in a specific region, you can look at the different tracks in the UCSC genome browser.
In short, there can be functional and/or non-functional DNA in-between the transcribed regions.
Repeat regions need not be heterochromatinized and conversely not all heterochromatic regions consist of repeats.

Can it at least be said all repeat sequences are non-functional?

@Charles No you can't really say that. Telomeric repeats are important. So are centromeric repeats. There are non-tandem repeats like LINEs; they have been implicated in somatic heterogeneity in the brain.

Are all non-functional parts of the genome - such as non-functional satellite sequences - heterochromatinized?