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What is the difference between taxonomical aids Flora, Manual and Catalogue?
The three type of books mentioned above are taxonomical aids that offer information about species found in an area. However, the exact difference between them is not clear to me. Please explain.

They seem to be non-standard terms. Manual/catalogue can refer to anything.

Flora just tells about the plant species living there but manual tells about all the species living there And catalog is best defined as an array of the species in an understandable manner

A Flora describes plants and where they live. Floras typically include a dichotomous key for identification purposes and often times will include range maps as well. Floras are almost always designed to be simultaneously regionally constrained and regionally exhaustive/complete (i.e., includes all plants that grow in that region or at least all taxonomic divisions of specified taxa). See Example.
A manual applies much more broadly to plants, and typically instructs you on a subject (e.g., identification/differentiation of species).  A manual does not need to be exhaustive and its scope is typically user defined (though often based on the scale/range of it's underlying subject). However, some have used the term manual to be more or less synonymous with Flora or otherwise similar document (e.g., see here).
A catalog is simply a listing of all species organized in some way. These are usually alphabetical (vs. taxonomically organized like a typical Flora). You will also never find a key in a catalog and will often find less phytographic detail.
See Chapter 6 in Describing Species: Practical Taxonomic Procedure for Biologists by Judith Winston for further assistance.


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Clarification about taxon (plural taxa)
If i am right, then any category placed at any rank in the taxonomical hierarchy is a taxon. For example Panthera, Mammalia, Solanaceae etc. But are general group of organism (casual groups which are not biologically defined like Birds, Cats, Fishes) also regarded as taxa? Please clarify.

Definition of taxon (From ICZN glossary):

A taxonomic unit, whether named or not: i.e. a population, or group of
  populations of organisms which are usually inferred to be
  phylogenetically related and which have characters in common which
  differentiate (q.v.) the unit (e.g. a geographic population, a genus,
  a family, an order) from other such units. A taxon encompasses all
  included taxa of lower rank (q.v.) and individual organisms. The Code
  fully regulates the names of taxa only between and including the ranks
  of superfamily and subspecies.

Birds are called Aves and that is a taxon. Cats come under Felidae. If you are asking - "Is a colloquial/vernacular name considered a taxon". Perhaps the group of organisms can be referred to by a colloquial name when they are not given any scientific name but in this case these taxa are well defined by a standard scientific name (according to the nomenclature codes such as ICBN, ICZN, etc).
So "cat" is not a taxon, but cats fall under the taxon called "Felidae".
In some cases certain groups are not even actual clades. A clade is a monophyletic group i.e. all its members have a common ancestor. The group — reptiles, is not a clade.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

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In what way is ADHD genetic?
According to Psychcentral depression, bipolar disorder, ADHD, schizophrenia and autism are traceable to the same inherited genetic variations
According to AsapSCIENCE, depression could be genetic due to a variation in the serotonin transporter gene. Having at least one short seems to give some kind of genetic predisposition to depression.
So what's the analogue of the serotonin transporter gene in ADHD? Is there a dopamine transporter gene?
Double posted on Cognitive Sciences Stackexchange

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4264104/ The diagnosis is observational. One misconception that people have is that a given genotype will, in 100% of cases produce a phenotype. So even if the genetic marker(s) has(have) been identified, it doesn't mean that the expression patterns of a person will be such as to produce the phenotype.  There will be a predisposition, but it is possible that a heterozygote allele could rescue the normal phenotype. It is also possible that even homozygotes will not manifest the phenotype if the deleterious gene is not expressed.

@AMR For a lay person pls? 'There will be a predisposition' --> How? I'm guessing the serotonin transporter gene is what gives a predisposition for depression. What about for ADHD?

I'm voting to close this question as off-topic because it's cross posted and answered on CogSci.SE:http://cogsci.stackexchange.com/questions/12311/what-is-the-underlying-genetic-basis-for-adhd

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Genetics of epilepsy
Is epilepsy genetically inheritable? If yes, is it dominant?

This is going to get closed as a personal medical question as-is, but a simple edit could fix that.  That being said, there is a well-referenced section on Wikipedia: https://en.wikipedia.org/wiki/Epilepsy#Genetics

Sometimes!
The causes of epilepsy are legion.  There's a massive Wikipedia page listing various causes, and, wow, I get tired just reading the table of contents.  None of those are genetic causes, but it should perhaps therefore be not surprising to learn that the genetic causes of epilepsy, although the minority of cases, are also quite varied.  Apparently most of the causative genes involve ion channels (whether voltage- or ligand-gated), but there are a truly large number of genes that can be related to epilepsy.
This 2011 paper has quite a lot of information.  Some facts it presents on the genetics of epilepsy:

Something like 1-2% of all mutations in mice present with epilepsy symptoms.
Concordance is around 50-60% for monozygotic twins, and 15% for dizygotic

The majority of twin concordance is likely from the same (genetic) cause

Monogenic causes (versus complex causes of epilepsy) account for around 1-2% of human cases.

In direct answer to your question, there is this paragraph (emphasis added) explaining the rough breakdwn:

Monogenic inheritance is suggested by the familial aggregation of cases that share a similar phenotype and are distributed in the pedigree according to a Mendelian mode of transmission: autosomal or sex-linked, dominant, or recessive. Autosomal recessive epilepsies are often associated with structural or metabolic abnormalities of the brain and with neurologic comorbidities, so most of them are not in the category of idiopathic epilepsies. Examples of these are pyridoxine-dependent epilepsy (PDE), several progressive myoclonic epilepsies (PMEs), and some malformations of cortical development (MCDs). Most of the monogenic idiopathic epilepsies follow the pattern of autosomal dominant inheritance, implying the presence of multiple cases in successive generations and male-to-male transmission.

In short:

If it's genetic, it's likely to be complicated and controlled by many genes
If it's controlled by one gene, it's likely to be dominant

The paper also presents the following table which may be of interest, listing monogenic causes of epilepsy:

"The causes of epilepsy are legion".. did you mean lesion?

@WYSIWYG Nope.  Adjective form of the word, referencing biblical usage.  Just a fancy way of saying "a lot".


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What is the result of modifying the reagents in the Sanger method?
If one of the dideoxynucleotides is omitted while using the Sanger method how would that affect the chain termination method of DNA sequencing?

Are you talking that you don't put in a whole base (like T) or if you have a deletion?

if by one of the dideoxynucleotides, you mean one of ddatp, or.ddctp, ddgtp, or ddttp was ommited from the process, then the sequencing would only be able to terminate for the other three dideoxynucleotides. And you would not be able to get the full sequence, and only nucleotides of whatever three you had.

@RoSiv if you have an answer then post that as an answer. Comments should be used only to seek clarification or suggest improvements.

@user18817 you would possibly benefit from familiarizing yourself with the BiologySE homework policy: http://biology.stackexchange.com/help/homework

@WYSIWYG         I was not sure if I was right. I am only an undergrad and I dont wanna give out a wrong answer to someone. Sorry.

@RoSiv Then provide a good answer with references. You are right. Just make it a bit elaborate.

If by one of the dideoxynucleotides, you mean one of ddATP, ddCTP, ddGTP, or ddTTP was omitted from the process, then the sequencing would only be able to terminate for the other three dideoxynucleotides. And you would not be able to get the full sequence, and only nucleotides of whatever three you had.
The function of ddNTPs (the dideoxnucleotides) is to stop the elongation of DNA and to subsequently be read by either fluorescence or radioactivity.
Source: https://en.wikipedia.org/wiki/Sanger_sequencing

Note that in Sanger sequencing the ddNTPs are not added together in the same mix. If you omit one ddNTP then you won't be able to sequence that particular base in the DNA. Though you may be able to infer the 4th base from the other three, the confidence of the read would be low.


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Binocular microscope use, diaphragm?
I am try to review my scope work, since my proffesor asked me to calibrate all the scopes for an intro class in biology, and it has been awhile since I used one. I googled "Binocular microscope use" and saw a powerpoint as my first link.
On page 21 it stated:

The diaphragm should be opened just enough to allow the objective lens
  to collect all of the light that comes through the sample. Opening the
  diaphragm too wide, allows some of the light to escape collection by
  the objective lens. Closing the diaphragm too much, causes aberrations
  of the image.

But if the diaphragm controls the amount of light passed through, why is "light escaping" a bad thing? Why cant I keep the light as wide as possible?
As an aside, if anyone has any suggestions for review on binoc. compound microscope use, I would appreciate it.

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


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Do transposons usually jump from one chromosome to another?
If it is usual occurrence, does it mean that my one gene can change its location from one chromosome to another?

Yes of course; they are not like tandem duplications.
However, some transposons have site preferences; for example the Tn7 transposon.

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

An old thread, but I have a similar question: can you (or anyone else) provide an example of a transposon that moves from one chromosome to another chromosome?

Transposons are specialized sequences of DNA that are part of a larger group termed mobile genetic elements. They can move from one position in the genome to another on the same chromosome or another. A specific enzyme called transposase, usually encoded by the transposon itself, acts on specific DNA sequences at each end of the transposon, causing it to insert into a new target DNA site (Alberts et al, 2015). Not only is this a source of genetic variation, genes carried in this way can convey great advantages such as carrying antibiotic resistance in bacterial cells.


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Heterochromatin v Euchromatin. Which is more abundant?
So I was just reading that whether heterochromatin or euchromatin is more abundant in a particular human cell depends on how active that cell is. But considering that most of the 25,000 or so genes in the human genome are transcriptionally inactive in any given cell, how is it possible for cellular activity to affect the chromatin structure to a degree that significantly alters how a nucleus looks on microscopic images? Since, after all, whether the cell is active or not will only affect little of the chromatin.
And since most of the genome is inactive, shouldn't it be in a heterochromatic form, and thus most of the chromatin in any given cell will be heterochromatin?
(I know this is not true, but I was wondering why)

I think whether DNA is in the heterochromatic or euchromatic stage depends on the stages of a cell's life cycle. There is a page on wikipedia with a good comparative image: https://en.wikipedia.org/wiki/Chromatin#/media/File:Chromatin_Structures.png    I think to answer your question though, it varies?

I dont think the forms of chromatin are stages but are rather states that depend on the transcriptional activity of the cell. And yes it does indeed vary but my question was how come such variation affect the overall structural conformation of the chromatin since most of it is inactive anyway.

Percentage of euchromatin varies between cell types and organisms. It has been shown that upto 88% of the human genome is transcribed; a phenomenon called pervasive transcription [1]. Highly specialized cells may have a lower percentage of transcribed regions and in females one entire X-chromosome is silenced (some regions in the silenced-X do show transcriptional activity).
Euchromatic regions not only constitute the geneic regions but also regulatory intergenic regions such as enhancers, locus control regions (LCR), silencers etc. It has been found that ~97% of these elements fall in the DNAse hypersensitve (DHS) region of the chromatin [2].
DNAse hypersensitivity is directly proportional to the chromatin state such that open/accessible regions are more prone to DNAse-I digestion. You may call these regions as euchromatin.
Though the total DHS density is not reported in the paper [2] or supplementary data, the ENCODE project that the paper concerns, will have all the detailed information. You can can find these datasets here, from which you can calculate DHS density distribution for different cell types. However, most of these cells are actually cell lines and not from primary tissues.


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How to remove duplicate results from BLAST?
If I run BLAST using a protein sequence (e.g. human p53), I get many matches to the same protein, presumably from different research projects. As you can see from the screenshot, all are similarly named and close to exact matches. Is there any way I can filter the results to get unique genes only?

imagine, you can. then how do you want to pick those that are "unique"? What makes one accession number better than another for same protein? my point is that those are all a bit different, but all as real as the other

Choose reference protein as a database. Then you can avoid the same sequence from different projects.
http://www.ncbi.nlm.nih.gov/refseq/about/

BLAST against a non-redundant database (for e.g. nr and UniProt). nr contains all non-redundant sequences collected from different primary databases but nonetheless there is some redundancy. You can also specify (or filter out) the species if you are not interested in all species.
Finally, you can also choose the best hit (post-BLAST, using simple scripts).

My point is that those results are already from the nr database, and are nevertheless all the same protein from the same species but with different accession numbers.


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Do all mammals have a Ventricular system?
I am familiar with the human Ventricular system that circulates Cerebrospinal fluid. This is needed among other reasons, to suspend the heavy human brain, and for injury protection. Do all mammals have a need a Ventricular system?
Maybe some did not have as strong of an evolutionary need for cerebrospinal fluid?

Are you asking Do all animals... as in your title or do all mammals... as in your post. Note that after asking do all mammals... in your post you are asking For example don't woodpeckers..., while woodpeckers are obviously not mammals. Note that many animals don't have a circulatory system nor a brain (such as jellyfish for example) and so the answer to the question in the title is no.

Of course not. For the human primates, nearly most of them have the ventrcular system, but for the non-human primates, seldom of them get.

Just mammals then. I forgot about jellyfish. Which are such a great exception to so many attempts at generalizing the kingdom of animals.

A reiteration of the initial question based on the exclusion of jellyfish as invertebrates: How might the evolutionary development of the ventricular system coincide with a functional separation of the central and peripheral nervous systems?

The ventricular system is common to vertebrates. It's also necessary for brain nutrition, assists in preventing under/over perfusion by exerting/releasing pressure, and forms part of the brain's glymphatic clearance pathway.
See also:
Totally Tubular: The Mystery behind Function and Origin of the Brain Ventricular System


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How is sugar in fruit metabolized, or digested and used?
I thought before, in general, when we have sugar in our food, then the sugar goes in our bloodstream, and if there is too much sugar, then insulin is secreted by our pancreas, and the sugar is pushed into our cells for storage, and to lower the blood sugar (and the insulin may over do it, causing our blood sugar to be too low).
But then recently I heard that sugar in fruit goes through a different route: it goes directly to the liver, and not moderated by the pancreas and insulin?  How does it work?

Hello, and welcome to the site! Note that not only don't we do personal health question, but asking what caused somebody's cancer is completely futile, as nobody in the world, not even his doctors, can tell that. Getting cancer is the combination of hundreds of stochastic processes happening in the same time, nobody can say what exactly happened.

Also, I'm flagging your question for migration to Biology, because the metabolic routes of nutrients are quite complicated and not really a matter of medicine practice. They are typically studied by biologists, not medics.

I have to second @rumtscho 's words, that we can't answer the question about someone's cancer and since you called it a side note yourself, the question would be better off if you deleted that last paragraph. As for the metabolism of sugar: the word sugar can refer to a whole class of chemical compounds - there are different sorts of those in fruit and they have different metabolic paths - so if the question is indeed migrated, I would suggest breaking it down to several questions or narrowing it a bit to a particular sugar: i.e. glucose, fructose etc.

@Lucky as far as I'm aware, there are only two monosaccharides a human can digest, glucose and fructose. All other sugars are either broken down to these two, from where the two metabolism paths start (example: sucrose), or are indigestible. But I think the people on Biology will be better informed whether there are indeed only two sugar pathways.

@rumtscho now that I think of it you are right (there are some enzymes for galactose, but that one isn't found in fruit). Depending on the amount of detail this wouldn't be a whole book, but it can definitely be a whole chapter. Still you are right about the second thing as well - if/when the question is migrated, the community at biology SE would have a better way to solve this :-).

This refers to metabolism of fructose. Many fruits contain high amounts of fructose (hence the name :) in addition to glucose. So does ordinary table sugar (sucrose, which contains equal parts glucose and fructose), and most other sweets you can find --- candy, soft drinks and so on.
Dietary fructose is rapidly metabolized, mostly into glucose, glycogen and fat. This happens mostly in the liver, but also in the intestines and kidneys; these are the only tissues known to express the enzymes involved (see the answer given by sunboyharry), as well as the transporter protein that brings fructose into the cells. Neither the transporter nor these enzymes are controlled by insulin, as far as we can tell, they are always active and ready to convert any fructose that comes around. This differs markedly from glucose metabolism, where both the transporter and key metabolic enzymes are activated by insulin. A review article is found here.
This arrangement makes sense given that the "goal" is to rapidly convert fructose to glucose (the "standard" blood sugar in mammals), and into storage forms (glycogen, fat). But since the glucose obtained from fructose is controlled by insulin as usual, in the end the effects of eating glucose or fructose are similar. Also, ingesting fructose does lead to an insulin response, probably because it is converted to glucose. While there is some research that suggests high fructose intake is more dangerous than glucose, particularly for the liver, I'm not sure there is any conclusive evidence or a scientific consensus about this yet.

Do you mean fructolysis?
Here what I found on the textbook  by John L. Tymoczko:
Fructose can take one of two pathways to enter the glycolytic pathway.Much of the ingested fructose is metabolized by the liver, using the fructose 1-phosphate pathway. The first step is the phosphorylation of fructose to fructose-1-phosphate by fructokinase. Fructose-1-phosphate is then split into glyceraldehyde and dihydroxyacetone phosphate, an intermediate in glycolysis. This aldol cleavage is catalyzed by a specific fructose 1-phosphate aldolase. Dihydroxyacetone phosphate continues into stage 2 of glycolysis, whereas glyceraldehyde is then phosphorylated to glyceraldehyde 3-phosphate, a glycolytic intermediate, by triose kinase. In other tissues, fructose can be phosphorylated to the glycolytic intermediate fructose 6-phosphate by hexokinase.

This is my speculation. Converting modified sugars to sugars which are immediately available could take some time. So, blood sugar, which is mainly glucose, might not elevate immediately.
The same reason is suggested when you take starch from plants. Starch does cause less trouble than equivalent amount of glucose.


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How does an increased amplitude affect nerve conduction velocity?
My professor said that increasing the amplitude (the amount of depolarization e.g. depolarizing from -80 mV instead of -50 mV) leads to a greater conduction velocity.

Do you mean that larger-amplitude action potentials have larger speeds? In that case your example is incorrect, as an action potential generated from a resting potential of -80 mV has a larger amplitude than an action potential generated from a resting membrane potential of -50 mV.

@AliceD yes that's what I mean, -80mV has a larger amplitude and will have a greater conduction velocity through the neuron as compared to a 50mV resting potential. Why is this?


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Need clarification on a sentence regarding vesicle-mediated translocation
I've chanced upon a passage that is not entirely clear to me:

In addition to conjugation, transformation and transduction, other less well recognised mechanisms of DNA uptake occur in nature, while other mechanisms of HGT are probably yet to be elucidated, in particular, DNA uptake by eukaryotes:
Vesicle-mediated translocation by a range of gram-negative bacteria such as Neisseria gonorrheae, E. coli and Pseudomonas aeruginosa, which can bud off vesicle structures that contain genetic material (e.g.antibiotic resistance and virulence genes) and then fuse with another bacterium (Dorward et al., 1989; Kadurugamuwa and Beveridge, 1997; Yaron et al., 2000).

(From "Risks from GMOs due to Horizontal Gene Transfer", by Paul Keese)
Is it the bacteria that fuse with another bacterium, or is it the vesicles that fuse another bacterium? I'm not sure.
I thought the vesicles were budded off in the first place so that they could carry gene material to another bacteria.

(asked a parallel question at ELL SE)

If you looked at the PubMed page that you linked to you will see in the right hand column a list of similar articles. The first is a review or HGT from plant to bacteria, so if you read that, you will likely find a better explanation of the process than the article you are referencing.

@AMR - thank you! Got it.


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Catenation and decatenation by DNA Gyrase
Decatenation is done for the replication of DNA and why is Catenation done and is it related to Crossing over

Both DNA Catenation & Decatenation are crucial to the equal distribution of DNA to the daughter cells during the mitotic crossing over. While catenation plays structural role in chromosomal architecture , decatenation facilitates the separation of sister chromatids.

Hi Jank. Can you add some details with some references?


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immune response towards sperm cells
Question 1: Why does the immune system not act on sperm cells as sperm cells are developed after puberty?
Question 2: Does immune response occur when a person's own cells are injected inside their bodies?

Q1: Immune system recognizes gametes as self. Q2: Do you mean filling a syringe with ejaculate and injecting it back into the donor? That would be weird and likely unadvisable, mainly because the proteins, carbohydrates, and lipids found in ejaculate would likely cause an inflammatory response as they are accessing areas, (subcutaneous or intramuscular) that are generally sterile. Also ejaculate can carry bacteria and viruses that could also cause an infection.

@AMR OP is not asking for an advise but presenting a hypothetical situation.

@WYSIWYG Your edit for question two is over specific. Original:  "Question 2: when own cells are injected to same person then strong immune system occurs?" That in no way implies an intravenous injection. That would be an even worse idea as it would likely cause an embolism that would kill you before the immune system had a chance to figure out what was happening.

@WYSIWYG And my comment was not intended for advice. It was to say that it is a bad question to ask. and even if you were looking at it from an actual experimental design perspective, it would be almost impossible to get the permission of an ethics review panel to conduct the experiment. If is also bad in the sense that you could not ascertain what the antigen was even if you did go ahead with the experiment. You would need to isolate individual plasma membrane proteins, lipids and carbohydrates and test each separately to determine what if any antigen was producing an immune response.

@WYSIWYG As there is likely no modern literature published to elucidate question 2, and there would likely not be any ethically acceptable experiments that could determine the outcome. That question should be deleted. Question 1 is simply that the testes are immune privileged parts of the body. While the Wikipedia article speculates that they are immunogenic due to delayed development, the more likely reason is that sperm puts up fewer HLA surface proteins than somatic cells, which would make them a target for NK-cells, as NK's perform quorum sensing to determine whether to kill.

As for immune response elicited in the female http://biology.stackexchange.com/questions/28164/why-white-blood-cells-wbcs-do-not-react-to-foreign-bodies-like-sperm

Body does not act against sperms because the testes are isolated immunologically by the blood testis barrier.
In mumps due to this barrier becoming ineffective due to inflammation, orchiditis (inflammation of testis) may occur and this may render the person infertile in some cases.
Such antigens which are not exposed to body's immune system are called cryptic antigens.
One more example of cryptic antigen is the antigens of the cornea.
For more information see here.
For more you can search for blood testis barrier.
For the second question, immune reaction will occur if the injected cell contains cryptic antigens. If there are no cryptic antigens then there will be no reaction.
For cryptic antigens see here.


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Fastest G protein coupled reactions
As per few references, fastest G protein coupled reaction known is Drosophila melanogaster phototransduction which produces quantum bumps with average latency of 45 ms (and peak response around 200 ms). Another reaction is chemotaxis which is also in that order. I was wondering are there any known examples which are as fast as these responses?
P.S: Many ion channels are GPCR which triggers very fast but most of them takes long time (in order of seconds) to give peak ion concentration
P.S.S: By fastest I mean, minimum time required to give peak response after activation of receptor(s).
Update:
In abstract case, Let's say you got signal from outside at time t = 0. Now this will leads to reaction cascade which will take time 't1'. Assume output of this is opening of channel which will increase concentration of ion X. Now X will reach it's peak concentration at time t = t1 + t2. So I am looking for such reaction cascades with minimum time 't' (t1+t2).

That is not the property of the receptor. There are many other factors that dictate the response time (the time required to achieve steady state).

Yes. I am asking for smallest reaction times which involves GPCRs. And it need not be steady state. Peak time is not steady state.

Even peak time is a function of a lot of different parameters. Btw peak can be observed only in case of certain network architectures. A single reaction doesn't peak; you need a feedback (or some other kinds of motifs). Anyways, what do you exactly mean by reaction time? What is the reaction here. There can be several downstream effects some of which can be early while others are delayed.

Why do you want to know this? A little context might make the question more answerable.

@WYSIWYG , I think you didn't get my question (or I didn't explained properly). Let's say you got signal from outside at time t = 0. Now this will leads to reaction cascade which will take time 't1'. Assume output of this is opening of channel which will increase concentration of ion X. Now X will reach it's peak concentration at time t = t1 + t2. So I am looking for such reaction cascades with minimum time 't' (t1+t2).

@GoodGravy , I just wanted to know smallest time delay between signal and response in GPCR.

@Dexter but there can be several steps in a cascade and some of them might take more time than the others to reach the peak. What I am saying is that the response is not just dependent on the receptor but also on the other molecules interacting with it. Not only that; initial conditions, the magnitude of the signal etc also matter.

@WYSIWYG, exactly. There will be many steps which will ideally create time delay for output of particular signalling cascade. I am looking for such time period. Assuming all other interactions are also involved in setting up this delay, I was curious to know how fast these reactions can be.

So does this question boils down to "What is the shortest GPCR reaction, i.e. with the receptor and effector being separated by a minimum number of steps?"

I wouldn't say minimum number of steps. Time required to execute all these steps should be minimum.

@Dexter I don't really understand what is the purpose of the question. Curiosity or you are looking for parameters for your mathematical model? In any case nobody has checked all the GPCR pathways. The number of downstream steps and also the architecture of the network determine the response time. An example of long term effects of GPCR signalling would be growth, which might take many hours to reach steady state. That would be the maximum limit. Olfactory/visual stimulus should be the fastest because these are quickly converted to electrical signals.

It's my curiosity. I had heated discussion with my friends on same topic. So I wanted to know scientifically what is reality.

Mammalian rod cells, the most numerous photoreceptor cells in the retina, reach a max depolarization after a single photon stimulus at 100-120 ms, implying a time constant (1/k) of about 25 ms (see Chen et al., Nature 404:557).  This is on the same order of speed as the fly eye, maybe a tad faster.  Non-photoreceptor GPCRs are probably slower, but few folks have tried to measure these effects. The m1 muscarinic acetylcholine receptor catalyzes Gq activation with a time constant of about 500 ms (Mukhopadhyay and Ross PNAS 96:9539), but there may be faster ones.

Drosophila photoreceptors are way faster than rod cells. Check out reference I provided in question.


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What is a subspecies?
Within a species there may be subspecies that are named using trinomial nomenclautre. For example the Grizzly Bear, Ursus arctos horribilis is a subspecies of the Brown Bear Ursus arctos.
The dictionary definitions of subspecies seldom expand beyond this:

A taxonomic category that ranks below species, usually a fairly permanent geographically isolated race.

I'm assuming redefining species into subspecies is not a completely arbitrary process as the definitions would imply, but is based on biology. What are the biological criteria for a group within a species to be "upgraded" to a subspecies?

This is the definition by ICZN which is equally un-informative "The species-group rank below species; the lowest rank at which names are regulated by the Code. (2) A taxon at the rank of subspecies."

@WYSIWYG The definitions are all very tortological rather than insightful. Of course it's below a species rank! What else could 'sub' mean in this context? There must be criteria that make some strains, or groups biologically different enough to be subspecies, but that threshold is apparently hard to come by if you're not 'in the know'.

The wikipedia article is more helpful, if accurate: "a polytypic species has two or more subspecies, races, or more generally speaking, populations that need a separate description" and "A monotypic species has no distinct population or races, or rather one race comprising the whole species. A taxonomist would not name a subspecies within such a species."

@jzx It sounds better until you realise that it's still missing that nugget of information; specifically what factors warrant the 'need' to be separately described?

To clarify, it might be better to refer to subspecies on equal footing as Ursus Arctos Brunneis (brown) and Ursus Arctos Horribilis, both of which would be members of species Ursus arctos.

I think the answer is that it is whatever taxonomists agree to. So we have Canis lupus familiaris to identify our lovable friends and C. lupus dingo for the baby eaters. These are holdovers from Linnaeus et.al. But in all seriousness, this comes from an eLS article on genetic differences of Chimpanzees. "The researchers also used demographic history models to identify the values of different population and evolutionary parameters for all four populations of subspecies (i.e. effective population size, divergence and rates and directions of migration)." It sounds like there are a lot of factors.

There are likely many changes to come, and a rethinking of classifications, as we learn more about genomes and have access to whole sequences for organisms, tools that were not available to taxonomists when many of the classifications were first made.

Your assumption is wrong. Subspecies taxonomy is highly arbitrary. There are no clear criteria. On the other hand species are frequently constituted by an array of loosely defined races.

@RobertMcFetridge - Welcome to Biology.SE. Please provide references for your claims and explain answers in good detail. You can take a look at what is considered a good answer on this site here.

@RobertMcFetridge - Welcome to Bio. I've converted this answer into a comment. AlexDeLarge has given fruitful details on how to improve your post.

This post is related as it talks about the concept of species.

In practice, subspecies are often fairly loosely-defined, reflecting a degree of uncertainty and ambiguity at this level of taxonomy. There are systematists who take the view that subspecies-level classifications should not be used as they are not rigidly definable.
In general, a subspecies will fulfil the following criteria:

it will occupy a distinct geographic range from other subspecies
within its species,
it will have limited gene flow to other subspecies within its species, while still being capable of interbreeding
it will have some recognizable shared character, used to distinguish it from other subspecies within its species

Subspecies classifications, and their usefulness, are discussed in the Turtle Taxonomy Working Group's 'Turtle Taxonomy: Methodology, Recommendations, and Guidelines', for those interested in further reading.

Great answer, albeit not what I was hoping for! I'm with the systemists on this one. I can't understand the usefulness of unsystematic subspecies nomenclature.

There can be good pragmatic reasons to hold on to subspecies labels. For instance, imagine you're after old DNA samples from museum specimens, and the species falls into two subspecies, one in the Pacific Ocean and one in the Indian Ocean. However, the old specimens do not have a lat/long of collection associated with them. In that case, you can get geographic subsets of the museum's catalogue by searching based on subspecies, and there may not be any other useful way to get that geographic subset.

There are also conservation reasons for wanting a "subspecies" designation. If a species is cosmopolitan, but a local unique population is threatened, being a "subspecies" may provide for governmental protection. For instance, many freshwater fish species on the US endangered species list are subspecies.

Subspecies are useful becasue species are not uniform homogenous populations, subspecies, may gave different behaviors, gene ratios, morphology, ect. For example there are several subspecies of Canus lupus including dogs, dingoes, and a variety of wolves ranging from the high tundra to the equatorial desert with adaptations to those environments.


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What is a mechanical cue?
I was attending a talk related to neurogenesis. So one professor was asking a question related to biochemical cues and mechanical cues (related to signaling pathways I believe). Cue as far as I understand is a signal, right? Biochemical cue is understandable for me.
But what does mechanical cue mean?

Mechanical pressure, stress, strain or distortion are mechanical cues. In general, cues sensed by mechanoreceptors are mechanical cues!

It is not necessary that mechanical cues are sensed by mechanoreceptors. These cues can also be relayed via the cytoskeleton and the adhesion proteins.

I doubt adhesion proteins can transduce mechanical signal. They can only recognize specific molecule or protein on opposite cell (or ECM). They are sending chemical signals not mechanical.

Adhesion proteins relay the mechanical stress as they are directly connected to the cytoskeleton. They are not really like signalling receptors. See this abstract:  "Experimental evidence confirms that cell differentiation or proliferation can be regulated according to the extracellular matrix stiffness...". So adhesion proteins are involved in relaying these signals.

In given paper, there is no clear indication of any adhesion protein. Given study is mathematical model with correlations. However I found this line in that paper's conclusion, "α5β1-integrin could switch between relaxed and tensioned states in response to traction forces generated by a cell.". This gave me this reference. Which suggest that 'a5b1' is 'most likely' candidate who changes confirmation by mechanical stress. In that case 'a5b1' will be mechanoreceptor by definition :P

Well they are not classified as mechanoreceptors, if you are getting what I am trying to say. I am not refuting what you are saying, but you cannot call integrins as mechanoreceptors. This is just like the equilibrium- steady state argument. It is a matter of classification and not an all pervasive superlogic :P


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Is studying complete mitochondrial genome need biological lab work?
The research complete mitochondrial genome study done on species:

Juema pig Sus scrofa (Suina: Suidae) from southern Gansu
red rainbowfish
speckled dace, Rhinichthys osculus
white char Salvelinus albus (Salmoniformes, Salmonidae)
Himalayan honey bee, Apis laboriosa

Did they need to do any work in biological laboratory?
More specifically, Are they related to bioinformatics completely?
Most of them just wrote length in bp (base pair), percentage of ATGC and several combinations of them and some special behavior. These seemed to me as expressing some statistics.
So, how could it be a research work?

All papers you mentioned have involved biological lab work. They all have sequences specific mitochondrial genome and then have analyzed it with the help of bioinformatics. Sequencing genome requires lot of bench work (wet work or "biological lab work"). Even one of them have mentioned it in abstract itself.

The complete mitochondrial genome of Himalayan bee Apis laboriosa, from Mizoram, India, has been sequenced using Illumina NextSeq500 platform and analysed.

Yes, obviously there should some biological lab work. but is it possible to do this types of thesis without doing the biological lab work practically? say collecting the lab work data from any open source gene bank or something. You know, a lot of bioinformatics thesis could be done without doing any biological lab work. can it be done that way? (Sorry for my bad English. I asked one question here, but several questions appearing to make you understand the question)

@manetsus Someone needs to do the lab work to generate the data for analysis by bioinformatics. That's not always the person doing the analysis, but even then they must have a very strong understanding of biology in order to create relevant conclusions. The best way to learn biology is by doing.

@MattDMo I fully agree with you. but my question is the one who just doing analysis on the basis of lab work available on the internet is producing knowledge or not?

@manetsus if you are making novel insights into biological phenomena, then of course you are producing knowledge, regardless of whether you have a pipettor or a computer mouse in your hand. Just look at the fields of mathematics and theoretical physics - a lot of work is done without ever being able to do experiments at all.

@manetsus, Yes that is possible. You can join any theory, bioinformatics, systems biology or computational biology lab. These don't required wet work. These fields are also in demand now a days.


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Why don't the apples seeds from grafted trees produce the same kind of apples?
As Wikipedia says:

Grafting is a horticultural technique whereby tissues from one plant are inserted into those of another so that the two sets of vascular tissues may join together.
In most cases, one plant is selected for its roots and this is called the stock or rootstock. The other plant is selected for its stems, leaves, flowers, or fruits and is called the scion or cion. The scion contains the desired genes to be duplicated in future production by the stock/scion plant.

So why I don't get the apple-tree of the scion kind if I plant the seeds from an apple which has grown on such a tree? I would expect that the genes in the apple seeds must be the same. However if I plant the seeds, I have to graft the new seedling again.

The reason most apples are produced from grafted trees is that apples don't breed true.
In a large number of crops, you have "lines" of crops. Basically, if you breed two plants of the same cultivar together, their offspring are similar enough to both parents that it performs like the parents. The reason for this is that these crop lines have been interbreed with each other for long enough that the population is self consistent, and the important alleles are present in frequencies that mean all progeny are likely to inherit them.
However, the types of apples which are sold commercially are not from these sorts of cultivar lines. Instead, they've been obtained from "sports". That is, the chance production of either a particular hybrid gene set, or sometimes from random mutations that happened on an adult tree of another apple variety. For example, the Granny Smith occurred from a chance seedling which was discovered by Maria Ann Smith.
These apples don't necessarily have "consistent" alleles. For example, it may be heterozygous for certain genes. If you have Aa alleles at one gene, if you self-pollinate the plant, you're going to get a mix of AA, Aa and aa genes in the offspring, the last of these isn't going to be the same phenotype as the parent. Now recognize that this is happening at multiple genes across the entire genome, so there are many chances to get non-parent-like allele combinations. Add to this the issue of co-dominance, where the heterozygote has a different phenotype than either homozygote (that is, BB isn't like Bb), and the chances that an offspring has a gene with a non-parent like allele combination is pretty high.
There's a further complication that some apple varieties like Honeycrisp are self-sterile. Even if Honeycrisp could theoretically breed true, there's no way for it to fertilize itself, meaning that all fertilization events are hybridizations.
Now you can certainly grow apple trees from seed. The planted seed will grow up into an apple tree, but the chances are that the combination of alleles it received by random chance from its parents will not result in an genotype that produces any commecial apple phenotype. Instead, you're likely to get regression to the mean, meaning the apple tree will be like the ancestor of apples - a crab apple, or at least crab apple-like. - But there's a small chance that it will have commercial apple-like properties, which may or may not be like the parent. This is how new apple varieties are formed, after all.
The only way to guarantee that the genotype of an apple tree is close to the parent plant is to propagate it by cloning, and the easiest and cheapest way to clone trees (at least apple trees) is by grafting.
(As a final note, remember that the seeds get their genome from the flowers and the cells which produced the flowers. The genotype of the rootstock - grafted or not grafted - has no bearing on what genes are present in the seeds. You'd have the same issue with apples breeding true even if the parent tree was on its own rootstock.)

According to such sources as North Dakota State University Ag Department (https://www.ag.ndsu.edu/hort/info/fruit/graft.htm) one primary reason for continued grafting is unaltered reproduction. Apparently some fruit stocks (scions, in grafting terminology) will produce true fruit, but the seeds within the fruit will not be genetically identical to the original fruit. This makes sense in the idea that fruit reproduction is sexual in nature and requires separate genetic stock from another plant in the form of pollen.
The original fruit would be true to form, but the seeds within it could be adulterated with foreign genes.
Another factor (that comes from more personal than referenced sources) is that often hybridized plants are not able, either intentionally or inadvertently, to reproduce from their own seed. This requires purchase of new material every year for planting or new scions for additional grafting.

Grafting is not always the answer.
My persimmon grafting was successful, but the produced fruit is the fruits of the stock (from seedling), not the scion, when I used the own seeds from the scion; while the same scion is grafted onto a wild persimmon stock, it produces desired fruits of scion.
Let's say: A is grafted persimmon imported from Asia
           B is stock grown from the seed of fruit of A
When A (scion out of A) is grafted onto B, the fruit is different from A.
But, when A is grafted on wild American persimmon, the fruit is the same as A.


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Was site-directed mutagenesis used to study the effects of sickle-cell anemia?
The title says it all. I am inquiring whether or not site-directed mutagenesis was used to study the effects of sickle-cell anemia/figuring out that specific amino acid mutation was the problem.

Why mutagenesis? You can simply genotype and see what the mutation is.

Mutagenesis was brought up in my lecture and how it can be used to see the affects of single amino acid changes. I asked the professor whether or not they could apply it to sickle cell anemia and there wasn't a clear answer.

The cause of sickle-cell anemia to be a molecular defect was discovered in 1949 by Linus Pauling. In his experiment hemoglobin molecules were broken down to smaller fragments, which were then subjected to electrophoresis and chromatography. The results of these measurements were compared between healthy and affected samples, allowing the identification of a mutated fragment.
The amino acids in the mutated fragment were analyzed in 1956 by Vernon Ingram, identifying the single mutation. The process in a bit more detail is described on this webpage.
Site-directed mutagenesis is used primarily in research aimed at finding a gene therapy based treatment for sickle-cell disease, such an attempt is described in this publication.
Also, the technique was used on recombinant hemoglobin to create and study some properties of naturally not occurring mutations. [Link]


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How does a garlic clove thrive inside a closed refrigerator?
A garlic clove has been growing very well inside a closed refrigerator.
It has developed beautiful green stalks, which I think are the equivalent of leafs.  Since they are green, I assume they contain chlorophyll.
Without any source of sunlight (for photosynthesis) or soil (for nutrients), how can such a plant thrive so well?
Is it simply growing off the internal stored energy of the clove itself?
Will it continue to grow without sunlight and soil?

You called it, it is using stored energy to do this, and will continue for some time but will eventually run out of energy. An analogous but common example is when a tree or bush is cut down so it has no more branches/leaves and will re-sprout after some time.

Your garlic was likely purchased as a bulb, not seed, and stored in the fridge.  The garlic 'clove' is not frozen, so your fridge readily mimics underground conditions in the temperate late winter or spring season. The bulb is generally buried underground, and the subsequent initiation of plant development and growth uses the stored energy. In a garden, the garlic would, however, begin photosynthesizing soon thereafter. Bad news: in your fridge, the plant is certain to become etiolated, because the lack of light, and yes, eventually run out of the stored resources--and die. Good news: you can eat or transplant it.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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What is the meaning of oIMR
In reference to genotyping primers, often some are labeling with 'oIMR'. It seems that this often refers to internal positive control primers, but I'm not sure. What does this stand for?

it stands for oligo Induced Mutant Resource.


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Blood after death
After the heart stops beating, do the red and white blood cells and the other cellular elements in the blood become non-functional immediately? Or does it take time? Would clotting occur after death?

Not immediately, but clotting will happen within a matter of minutes. When I do blood draws from cardiac puncture in mice, the blood in the heart is coagulated enough that I cannot get a draw within about 10min.

I don't exactly know what you meant to say by "non-functional".

Red blood cells are delivering oxygen to tissues, but they cannot do this anymore in the lack of blood flow.
White blood cells degenerate and after about 84 hours are no longer existing as cells (Babapulle CJ, Jayasundera NP, 1993). Neutrophiles degenerate first and lymphocytes last.
Platelets follow an apparent increase in number due to hypostatic phenomena (Thomsen H et al, 1999). Then thrombolytic activity is increased and platelet-platelet aggregates form. Some also adhere to fibrinogen and erythrocytes.

Overall, due to increase of acidic metabolites concentration, the pH of the blood decreases. It takes about 20 hours to reach a blood pH of 5.5 (Andrea E. Donaldson and Iain L. Lamont, 2013)

References:

Babapulle CJ, Jayasundera NP. Cellular changes and time since death. Med Sci Law. 1993 Jul;33(3):213-22.
Thomsen H, Kaatsch HJ, Krisch B. How and why does the platelet count in postmortem blood change during the early postmortem interval? Forensic Sci Int. 1999 May 17;101(3):185-94.
Andrea E. Donaldson, Iain L. Lamont. Biochemistry Changes That Occur after Death: Potential Markers for Determining Post-Mortem Interval. PLoS One. 2013; 8(11): e82011. doi:  10.1371/journal.pone.0082011


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What is the reasoning behind the Drake Equation?
I've read a bunch on how the Drake Equation is constructed, but I'm not able to understand some of the reasoning behind it.
$$
N = R_* \cdot f_p \cdot n_e \cdot f_l \cdot f_i \cdot f_c \cdot L \cdot f_d
$$
Why does $f_c$ represent the fraction of intelligent life able to communicate? Isn't communication (in some form) part of what defines intelligent life itself? Or is this term included just to break the number down further?
I'm asking this here and not elsewhere because I'm wondering specifically about this term and not the entire equation.

Geez this so called "equation" is about us being able to get signal from them - fc is for telecommunication, not speech.

This question is not off topic because it is about astrobiology.

The second half of that sentence on Wikipedia says it all: "the fraction of these civilizations that have developed communications, fc, i.e., technologies that release detectable signs into space"

Humanity has had roughly the same level of intelligence for tens of thousands of years, and as the Drake Equation estimates the number of civilizations capable of extrasolar communication - we only met that criteria ourselves within the last century.


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Open database of medical images
Does anyone know of an open repository of medical images (e.g., CT scans) organized by disease category? I'm working on some computer vision software that requires a large set of controls from which to learn.

Try this -- http://www.nlm.nih.gov/NIHbmic/nih_data_sharing_repositories.html

Similar: What are good sources of free-to-use images and diagrams

Searchable database of Point of Care Ultrasound (POCUS) Images: https://www.grepmed.com/?q=POCUS

https://opendata.stackexchange.com/questions/6661/open-source-mri-image-dataset/13565#13565

Open-access medical images:

MedPix (by keyword, organic system, pathology and diagnosis A-Z)
Radiopaedia (by keyword)
PEIR Radiology (by keyword, organ or anatomic region)
Ultrasound Cases (by keyword and organic system)
Open Access Biomedical Image Search Engine (Openi) (by keyword)
Wikimedia Commons (by keyword)
Google image search (using the filter "creative commons," "public domain" or "open access")
Google image search (using filters: black/white, noncommercial, photo)

More:

Gray's Anatomy
Dermatology Atlas

+1 Nice collection. I won't add google image search in the list though.

I have used that search extensively with good results, because you can find pretty much all free images available on Internet in one go. And it's easy to narrow the search down.

Here's a good start: http://www.aylward.org/notes/open-access-medical-image-repositories. I understand that this question was somewhat googleable, but perhaps amassing a collection of curated resource links is constructive here since a search through the exchange revealed no prior inquiries into this topic.
Update:
For those who are interested in understanding the current landscape of tools available for analysis of medical images: Check out this list of open source tools (http://www0.cs.ucl.ac.uk/opensource_mia_ws_2012/links.html).

Like I already referenced on an early post, there are several options on the DICOM Library. It is easy to find whatever image modality you want and also whatever disease category.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Evolution of blood types
What are the popular theories regarding how our blood divided into 4 groups. Particularly I'm interested in whether this was originally linked to disease.
Thanks for your answers, useful articles and further reading would also appreciated.

Hi and welcome. Your question is very interesting, however, the general expectation of SE is that you demonstrate that you have researched the topic of your question and have hit a wall in that search, or you are looking for expert advice to explain an advanced topic that you have found that you are having a difficult time explaining. Review How Do I Ask a Good Question for tips and general expectations for the site. Though I personally hope someone can provide an answer as I would be interested in this as well.

Possible duplicate of http://biology.stackexchange.com/q/31920/3340

yep, sorry for duplicating and thanks for your answers!


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Are eukaroytic promoters located in the 5' UTR region?
I was wondering if promoter sequences are located on 5'UTR region in eukaryotic organisms?

as i understand, UTR is part of mRNA (UnTranslated Region), whereas promoters are part of DNA, sequences where DNA-dependent RNA polymerase binds. So by definition, promoters can't be in UTR. More than that, since RNA Pol binds to promoter, only part of promoter sequence can be transcribed if any at all

Most promoter elements are not a part of the mRNA sequence. They are upstream (towards 5') of the transcription start site. However, a certain class of promoters called downstream promoter elements (DPE) can overlap with the geneic region. These elements have been reported to lie at 29-33bp upstream of the transcription start site and widely employed, in Drosophila [1]. Mapping of DPEs has been done for mouse human genes as well [2]. However, a detailed analysis supported by good sequencing data is yet to be done.
So, though DPEs are present in the transcript, I am not sure if they are retained in the exon. This can be confirmed by mapping the splice sites but this analysis is not presented in these papers.
You can see from the below figure [3] that most first exons in humans are big enough to harbour the DPE.

I do not think promoter sequences are on 5'UTR region. 5' end of 5'UTR is the transcriptional start site and the general transcription factor binds to immediately upstream of the 5' end on the genome (about 30 to 40bp upstream).
https://en.wikipedia.org/wiki/Promoter_(genetics)


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Expected dS/dN ratio for exome
I am trying to determine whether or not my sequencing data has more/less non-synonymous mutations than would be expected. My understanding is that there is some fixed ds/dn ratio for the human exome that I can use to calculate this. Is this true? And how might I calculate this?

The page linked behind the anchor "ratio" has gone stale. Can you fix that?

There isn't a fixed value for the human exome AFAIK, nor would it be a good idea to have a fixed value for the exome because different regions and genes can be under different selective pressures.
The norm is to compute the ds/dn ratio and then test against a null hypothesis of the ratio being 1 to infer if your region is under selection or not. If it is greater than 1 it indicates positive selection and if it is less than 1 purifying selection.
You can find a  decent introductory treatment here.


text:
Caterpillar identification
It has since cocooned I think but it was a weird circumstance. I kept adding leaves for it to eat, and it decided it was done, and cocooned under a wilted leaf.  I'm wondering if anyone can ID the species, and the following: I think it is a real cocoon, as there is no dead or rot smell.
But the cocoon was under the wilted leaf, and is now quite firmly attached. In the pics below, I've turned the leaf and cocoon over. Does the cocoon know "up"? And does it know it before or after making the cocoon? If it was stuck on its "up and out" direction, can turing it over be harmful? I.e. I turned it over so now it's trying to emerge towards the ground, can it figure out how to find 'up'?
Locale: Southwestern United States
Found in: found it in a moist garden bed (tomatoes, radishes, peppermint, basil) eating radish leaves
Description: About 2 inches long, 1/2 inch long hairy, black/grey hairs, body is black/grey with yellow striped markings
Cocooning position: wilted leaf / \, stick |, cocoon (), ...
 /|\
/()|\

Summary: It made the cocoon with the leaf on top of it, and it would never make it out in that case, so I turned it over. Is that okay? Can we still see the winged form come out? Like I said, it doesn't smell dead... in fact smells better than when the caterpillar was pooping everywhere.
Aside, this is the only tag I could find that might fit. Please feel free to edit tags to get this answered. TY
Caterpillar

Cocoon after being turned over, you can see it's kind of wrapped in the leaf

Till you put your pics, can we keep this question on hold? Because your textual information is also insufficient. Describe the caterpillar: colour, size texture etc. Describe your geographic location and local landscape.

@WYSIWYG added images and more description

From an unrelated answer, I think it might be a saltmarsh caterpillar. Can anyone confirm this?

This question is still open probably because the quality of the image is not good. Why don't you take it outside the jar for making picture? Like this it could be anything.

@ruffp because it's been over a year since I had the caterpillar, and I confirmed a few days after posting that it was, indeed, dead. I should probably just delete the question

Although a definitive ID will likely never be possible with such low quality photos, you probably have a Western Tent Caterpillar (Malacosoma californicum).

According to the USDA Forest Service, mature larvae are about 2 inches (4.5-5.1 cm) long and are highly variable in color and markings.

This insect is the most variable of the North American species of Malacosoma, in which six subspecies and several unclassified forms have been recognized.

Although this species eats primarilly trees and shrubs (e.g., see here and here), the Minnesota DNR suggests that garden plants can also be targeted.
Cocoons are of white silk dusted with a white to yellow powder. Your image appears to show that.
The Western Caterpillar is found throughout western North America:

 [Source: USDA Forest Service]


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Plasmid copy number and Rop protein
If i want to transform a bacteria (E. coli) with a particular plasmid (in my case pBR322) will the presence of the Rop gene affect the production of it ?
Is it desirable to use a plasmid without that gene to increase plasmid copy number ?
I found some informations about the protein cited on these links:
https://en.wikipedia.org/wiki/Rop_protein
http://www.proteopedia.org/wiki/index.php/Rop_protein

Since the pBR322 is derived from the pMB1 plasmid (which is closely related to the ColE1 plasmid, it does indeed contain the coding information for the rop gene. It's expression will limit the copy numbers from the plasmid, so if you are looking for high copy numbers, the usage of a plasmid without the rop gene should be preferred.
If it is only for the yield in a plasmid preparation, you could also simply scale up your production and make a midi prep instead of a mini or a maxi instead of a midi. It also depends, what you are planning with the plasmid. For cloning purposes mini preps with pBR322 have always given enough yield for me.


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Does the human body convert water?
I just read Andy Weir's "The Martian" (which was very good) and one line made me wonder:

[...] a human body only borrows water.

Is that true? Does all water "that goes in, go out"?

Water is "created" and "destroyed" in biochemical reactions in the body all the time. The overall water balance, as described below, stays at a relatively steady state, but any one water molecule entering the body may be used as a proton (Hydrogen) donor, to make a hydroxyl (-OH) group, etc.

Yes, the human body "converts" water.
Out of the hundreds of chemical reactions going on in the human body, there are reactions which take water as an input and "react it away" into something else. There are also reactions which create water out of other molecules.
Example 1: Hydrolase reactions. They have the form of

A–B + H2O → A–OH + B–H

You get water as input, and something else as output.
Example 2: Peroxidases "defuse" the highly reactive hydrogen peroxide, producing water. For example, look at the L-ascorbate peroxidase, which catalyzes

L-ascorbate + H2O2 → dehydroascorbate + 2 H2O

Beside these reaction, there is also a lot of water which doesn't react and is simply excreted after having served its purpose. So, while some water is "converted", some other part "passes through".
The reactions are balanced in such a way that normally, you excrete the same amount of water as you drink, as explained in Amory's answer. But despite this balance of the amount, you cannot claim that the water just passes the body unchanged. Some molecules of it are used up, and others are created de novo.

Yes, essentially, but in practice you need to consider the context of the novel.[1]
Your body needs water every day - somewhere around 3 liters is sufficient for baseline activity - in order to maintain balance due to obligatory losses.  Here's a figure that sums it up (it has a few errors, see below):

That whole online textbook chapter might be of interest, but that figure has a few errors.  If you look, the numbers at the bottom for output aren't summed up correctly, and the value for transpiration is repeated.  Doing the math on the correct numbers gives 2500 ml output for the 2500 ml input.
So yes, input and output are roughly equivalent.  You and I need new sources of water every day since our urine isn't something we'd like to drink, but Watney has a "water reclaimer" and lives in a sealed environment[2]; his entire world is one small, well-balanced water cycle.

[1]: For the uninitiated, "The Martian" is a novel and soon-to-be-movie about Mark Watney, an astronaut stranded on Mars who must use his ingenuity to survive as long as he can.  The context of that quote is the need for hydrogen, which Watney will get by hydrolyzing his urine.
[2]: Well, most of the time anyway.

So all the $H_2O$ that goes in, comes out as $H_2O$?

Actually, more comes out than goes in: metabolic water is synthesized by the organism.

@NickRussler no, that's wrong. There are several metabolic reactions which require water as input, for example the esterase activity comes to mind. So, when looking at a specific water molecule, it is very much possible that it is consumed, and then reacts to something else, without being excreted as water. What this answer says is that the amount of water going in and out is balanced, not that all water passes through the body unchanged.

@NickRussler As rumtscho said here and in the other answer, it's not the same water molecules, but it's the same amount.  If you look at the diagram, you'll see that plenty of the input water is from food that we eat, not just liquid water.


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Normalised gene counts to edgeR/DESeq2?
Both very popular differential expression packages assume a raw gene matrix count. This makes sense because the statistical model models the library depth.
But what if I normalize my counts with say, the ERCC RNA spiked-in standard? Would that affect the statistical power? False-positive? Why exactly is it not recommended to give a normalized count matrix?

This question should have edgeR and deseq2 tag, but I don't have enough reputation (require 300). Would somebody else add the tags for me?

No need for specific tags. There are hardly any DEseq/edgeR specific questions.

The advice is to not generally use ERCC spike-ins at all because of variations introduced by pipetting at the volumes they recommend.
The thread also explains how to use DESeq and EdgeR with spike-in normalisation, with the process being easier significantly with DESeq, where you can use the calcSizeFactors on a count matrix of spike-in reads alone. With edgeR you will have to pass values using the lib.sizes parameter in the apposite functions.
If you want to use fractional counts through limma-voom should work, I think; I've had good results using voom on RSEM counts, which are fractional.


text:
Is blood pressure in the aorta and brachial artery the same or different?
Does the blood pressure at the root of aorta equal the blood pressure in the brachial artery?
I've heard it does, but it doesn't quite seem to make sense as I'd think the blood pressure would be lowered the further it travels?

Blood pressure is mostly dependent on the height from the heart. Therefore, if it is below the heart it will have higher blood pressure and if it is above the heart it will have lower blood pressure.
Here you are asking from two parts of body that have same height as the heart,

so they will have approximately the same blood pressure.
For more see:
Netter's Anatomy Page 136 and Campbell Biology

You can quote Pascal's law too :)

Hmm. Right , Thank u for every thing , for editing my posts , for helping me to improve my knowledge  and for many other things, Thank U...      :)

But I'm confusing , Why no one vote up my posts?????

It is up to the community.. If someone finds your post useful then they'll vote, don't worry.. If you can add some references or calculations in your post then I'll be happy to upvote..

I think I did. :)

U know since I joined this community I just want to be active as u are but that was a little bit hard, But I'm always trying to be . :)

Well done @M.Y.Ard.Ir - much better!

Thank u my friend , U taught me and u helped me ...   :)


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Do spinal cord reflexes (such as the knee-jerk reflex) continue to function under general anaesthesia?
The knee-jerk reflex (patellar reflex) is an example of a stretch reflex (myotatic reflex). Stretch reflexes are monosynaptic reflexes happening in the spinal cord without involvement of the brain.
Does it mean that this reflex will continue to function in an unconscious person, e.g. under general anaesthesia? Does it depend on the "deepness" of anaesthesia? Does it depend on a specific drug? I would also be interested to know if spinal reflexes keep working in unconscious states such as e.g. alcohol poisoning or a knockout.

The issue is complicated. In general it depends on the specific spinal reflex and on the specific anaesthetic. But it seems that the modern general anaesthetics usually do NOT block monosynaptic spinal reflexes (such as knee-jerk).
Here are two figures from Baars et al. 2009  that show that propofol and sevoflurane strongly inhibit withdrawal reflex (spinal two-synaptic reflex) but have almost no effect on the H-reflex (spinal monosynaptic reflex closely connected to the stretch reflex):

See below for many more details. Disclaimer: I know very little about anaesthesia and am simply writing down what I found after a couple of days searching and reading.

Withdrawal reflex
As @AliceD wrote, withdrawal reflex (a two-synaptic spinal cord reflex) usually disappears under any anaesthesia and this disappearance is used as a clinical sign of anaesthesia being deep enough for the surgery. As an example, this handout on monitoring anaesthetic depth in rodents has the following entry on the list of criteria for surgical anesthesia:

Withdrawal    reflexes    are absent! Try at  least   2   toes    and the ears    so  that    you are  sure   that    this    reflex  is  absent.

Knee-jerk reflex: early history
On the other hand, it is known from the XIX century that stretch reflexes such as knee-jerk (note that they are monosynaptic) are very persistent. They can be abolished under some drugs (such as e.g. chloroform and ether) that act directly on the spine, but keep working under others. I am quoting from three old papers on the topic (here and below emphasis is mine).
Horsley, 1883, Note on the patellar knee-jerk:

In 1881, while experimenting (on myself) with this gas [nitrous oxide] for
a different purpose, it occurred to me to contrast the conditions of the superficial and deep "reflexes," taking the
plantar reflex as an example of the former, and the patellar
phenomenon to illustrate the latter. Being aware of the fact
that deep chloroform-narcosis abolishes all the "reflexes,"
superficial and deep, and yet that with ether-narcosis, however deep, ankle-clonus frequently, appears, I was scarcely
surprised to find that the knee-jerk persisted in the deepest
anaesthesia from nitrous oxide, while the superficial reflexes
all disappeared.

Sherrington, 1892, Notes on the arrangement of some motor fibres in the lumbo-sacral plexus (p 671):

With regard to the effect of anaesthetics on the "jerk," a better proof of
the action of chloroform being rapid and direct on the nervous mechanisms of
the cord itself could hardly be found than in the speedy abolition of the
"jerk" by chloroform inhalation when the cord has been previously divided
in the thoracic region.

Simpson & Herring, 1905, The effect of cold narcosis on reflex action in warm-blooded animals:

The knee-jerk is a very persistent phenomenon. It is known to disappear in deep anesthesia produced by ether or chloroform [Sherrington 1892]. [...] The knee-jerk is as a rule easily elicited, and we find it present when
all the reflexes have disappeared. [...] The lower the
temperature the smaller the jerk. [...] In several animals that died at a low temperature the disappearance of the knee-jerk was simultaneous with death [...] The lowest temperature at which we found the knee-jerk present was 15° C., and this
was also the lowest temperature at which any of our animals were
still alive. [...] Pinching the skin does not provoke any response till the temperature is 25° C. [...] We have compared these results with similar ones obtained from
cats in recovery from deep ether anesthesia and find that the order of
reappearance agrees very closely.

Modern studies in animals
Hara & Harris, 2002, The Anesthetic Mechanism of Urethane: The Effects on
Neurotransmitter-Gated Ion Channels mention in the abstract that

Urethane is widely used as an anesthetic for animal studies because of its minimal effects on cardiovascular and respiratory systems and maintenance of spinal reflexes.

(they don't specify which reflexes specifically).
Ho & Waite, 2002, Effects of Different Anesthetics on the Paired-Pulse Depression of the H Reflex in Adult Rat study the effect of five different anaesthetics (ketamine, halothane, etomidate, saffan, and nembutal) on the Hoffman reflex (H-reflex), a monosynaptic reflex similar to the stretch reflex. They report that it keeps working under all five drugs, but the drugs modulate the decrease of the reflex under repeated stimulation (this decrease depends on the descending controls and is affected differently by different drugs):

The  results  suggest  a  preferential
action  of  some  anesthetics  on  descending  pathways
involved in reflex modulation [...]

Strangely, Ho & Waite do not describe how anaesthesia affects the reflex strength following an unrepeated stimulation, but in any case it is clear the the reflex keeps functioning.
Propofol etc.
What about the anaesthetics widely used in humans, such as e.g. propofol? Matute et al., 2004, Effects of propofol and sevoflurane on the excitability of rat spinal motoneurones and nociceptive reflexes in vitro:

We used an isolated spinal cord in vitro preparation from rat pups and superfused the anaesthetics at known concentrations. [...] Applied at anaesthetic concentrations, [...] sevoflurane produced a large depressant effect on the monosynaptic reflex whereas propofol was ineffective. [...] Sevoflurane produces large inhibitory effects on nociceptive and non-nociceptive reflexes which are likely to contribute to immobility during surgery. Compared with sevoflurane, propofol appears to have much weaker effects on spinal reflexes such as those recorded in an isolated preparation.

Kerz et al., 2001, Effects of Propofol on H-reflex in Humans:

Previous studies of motoneuron excitability using H-reflexes or F-waves during general anesthesia found significant depression after administration of halothane,  enflurane, isoflurane, desflurane, or nitrous oxide. [...]
Recommended propofol doses for induction and maintenance only had a transient effect on the H-reflex and were no longer demonstrable after 10 min of propofol anesthesia. [...] Immobility during propofol anesthesia [...] does not seem to be caused by a depression of spinal motoneuron circuit excitability.

So why is then the withdrawal reflex so easily abolished and the stretch reflex is so persistent (e.g. under propofol)? This does not seem to be well understood. Baars et al., 2009, Effects of Sevoflurane and Propofol on the Nociceptive Withdrawal Reflex and on the H Reflex write

Both H reflex and nociceptive withdrawal reflexes are reduced dose-dependently by propofol and sevoflurane in humans. [...] We have shown a striking difference of the degree to which both reflexes are reduced by the two anesthetics. The relative reduction of the polysynaptic RIII reflex amplitude was more than four times higher than that of the H reflex. This difference can probably be attributed to the higher number of neurons interposed in the RIII reflex pathway in comparison to the H reflex.

Note that the last sentence is very vague; it says that the difference is "probably" due to monosynaptic vs. polysynaptic mechanisms of these two reflexes but does not offer any explanation. Withdrawal reflex is mediated by an excitatory interneuron and propofol acts on GABA (which is inhibitory transmitter), so it remains unclear. This study is from 2009 and I did not find anything relevant in the papers that cite it.

From an animal-experimentation perspective, the absence of functional reflex arches are often used to assess adequate anesthetic depth. For example, in rodents  a toe-pinch is often used to assess whether the animal is sufficiently anesthetized to commence surgery. The absence of a withdrawal reflex marks the point to proceed after initiation of general anesthesia. Hence, in these cases, pain-induced muscle reflex arches are suppressed. Note it is a two-synaptic process (nociceptor to spinal chord, spinal chord to muscle).

Thanks, Alice! +1. This is interesting; withdrawal reflex is polysynaptic, but nevertheless a spinal reflex. So what is your intuition then: would a knee-jerk also disappear under similar anesthesia? By the way, by now I think that the answer might depend on the specific drug and dosage, but I am actually not interested in anesthesia per se. I will now update my question to specify that I am rather asking about any "unconscious" state, such as e.g. after an alcohol intoxication or after being knocked out.

My intuition is that these reflexes will be absent. I will try to ping @anongoodnurse here in the hopes she can shed light on this. After your edits it is outside the realm of my expertise. Note that alcohol, being quite related to ether, may be considered a general anesthetic, in a way. I think that the question is becoming quite broad as of now and I'll not attempt another answer. Good luck and nice question nonetheless, +1'd.

I guess you are right to say that the question becomes quite broad because "unconscious states" can (I presume) be quite different and can have distinct properties. I am not asking for a lot of details here and would be happy to accept any answer that gives a short overview. Also, I have just updated my question with some quotes from several XIX - early XX century papers that I found on the topic, I think you might like them.

I have posted my own answer with a lot of citations; it seems that modern anaesthetics such as e.g. propofol do eliminate the withdrawal (as you say) but do NOT affect the stretch reflex (contrary to your intuition). Even though the effect seems to depend strongly on the specific drug. I have no idea at all why the withdrawal is so much more susceptible than the stretch. Neither can I make any general claim across various anaesthetics, because I only found some isolated information about several specific ones.

I am not a surgeon.
However, I might have some insight:

General anesthesia often (most of the time ?) include curare derivated drugs (such as pancuronium) that will effectively block any muscular response (by interfering in the neuromuscular junction: they block nicotinic Acetylcholine receptors). So this will effectively inhibate any reflex by blocking the final effector.
Spinal anesthesia might also inhibit reflex arc, for the same reasons, but only for a specific zone.
Other kind of anesthesia might be conservative regarding reflex arc.

You will find informations on wikipedia:
https://en.wikipedia.org/wiki/Neuromuscular-blocking_drug
https://en.wikipedia.org/wiki/Spinal_anaesthesia
If you want me to give you a more elaborate answer, just say so, I will try to improve a little bit.

Thank you for your answer! +1. As far as I understood, neuromuscular blockers such as pancuronium are often used in anaesthesia (to prevent possible movements) but do not have an anaesthetic effect themselves. I guess you are right, and neuromuscular blockers would block spinal reflexes too, but my question was rather about unconsciousness/anaesthesia without an additional muscle paralysis. Your third bullet suggests that spinal reflexes will be unaffected in this situation (and I agree that it sounds plausible) but I would like to have some direct evidence or reference.

My intuition is that, if there is no neurological lesions, or muscular pathologies, and you're just in presence of a person that is under anesthesia, spinal involving reflex won't be affected. But I will ask to the folks at the hospital tomorrow, whether this is true or false and get back to you.

Maybe that will also interest you: https://en.wikipedia.org/wiki/Lazarus_sign

General anesthesia is not induced by muscle blockers. They are given to block muscle activity to enhance ease of operation.

I couldn't get anyone at the hospital to answer me.

I cannot add commentaries for other posts, but inhibition of withdrawal reflexes is kinda logical speaking of anesthesia. You are aiming to block nociception signal and responses as well as to provoke unconsciousness. I think if you do not administer morphine, or any other kind of analgesic and only use propofol to knock someone down, this will not abolish reflexes.

Abolition of all reflexes necessitates blocking every signaling way involved in those. This can be achieved either by drugs, which have either a broad or narrow spectrum, either by nerve damage (either by some mechanism I wouldn't be aware of, like brain inhibition of reflexes if that exists)

Thanks, @OvoiDs. I have just updated my answer, putting my earlier update to the question in there (to have it everything together). It seems that you are right, and propofol does not abolish stretch reflexes. My remaining confusion about withdrawal reflexes is that those are also entirely spinal, so I don't understand why a drug (such as propofol) would affect two-synapatic withdrawal reflexes but leave monosynaptic stretch reflex unaffected. Does it have anything to do with the number of synapses? Or is it just that the modern drugs are selected to abolish specifically withdrawal?

So, I've looked a little bit on pubmed. Propofol acts by linking to GABAa receptors (so it tends to inhibit neuronal signals). In the case of a monosynaptic reflex, there is little to no regulation (this is purely hypothetical). In case of polysynaptic reflexes, regulation can occur. For withdrawal reflex, if there are inhibitory GABAergic neurons, these will be affected by Propofol and this inhibit the signal leading to reflex abolition.

I haven't read the entire paper, but at least the introduction of this paper might be of interest for you: http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.325.4279&rep=rep1&type=pdf

The more neurons you have, the bigger the chances of regulatory systems, either with an excitation cascade, either with inhibition. Inhibitory neurons are for most part GABAergic or Glycinergic neurons, and those are widely spread in the spine's dorsal horn. However, I wasn't able to find a clear answer in any book i've looked, so I guess this should all be considered as hypothesis. Sorry !

Thanks for your replies! Withdrawal reflect seems to be meditated by an excitatory interneuron, not an inhibitory one... I found this paper from 2009 that explicitly measures the effect of propofol on withdrawal/stretch in humans and reaches the same conclusions. In the discussion they say that "This difference can probably be attributed to the higher number of neurons interposed in the RIII reflex pathway in comparison to the H reflex". Note the word "probably"... I have updated my answer to include this study.


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How do DNA-binding proteins recognize the correct DNA base pairs?
My professor posed this question to the class today - "How do DNA binding proteins specifically bind to base pairs?"
He alluded to the different arrangements of hydrogen-bond donor and acceptors in A-T, T-A, C-G, and G-C base pairs. However, they are not always significantly different in some pairs (i.e. the minor groove of the C-G and G-C base pairs have the same acceptor - donor - acceptor pattern).
So how would a binding protein know the difference between C-G and G-C on the minor groove of a DNA base pair? How does a DNA binding protein know it's reached the right base pair, more generally?
Thank you!

The major groove contains more information and can distinguish between C-G and G-C

Lock and key mechanism. Isn't?

There are different kinds of DNA binding domains; the ones involved in base identification in the major groove can differentiate between different base pairs of the same nucleotides i.e. AT vs TA because they bind to functional groups on a nucleotide and not the base-pair per se. The stereochemistry i.e. which nucleotide is in the major groove, is important. The location of the nucleotides in the major groove also is a factor (Figure 1).

Figure 1: DNA sequence identification by Helix-Turn-Helix transcription factor. This is the example case of the Engrailed protein in Drosophila. Reproduced from Paro and Sauer (1992) [1].

You can see that Adenine is recognised differently than Thymine. In many cases such as that of zinc finger proteins (ZF), sequence identification usually happens for dinucleotide pairs such that each finger (a modular unit) can identify a di/tri-nucleotide (Figure 2,3). An array of fingers in case of ZF and helices in case of Helix-Turn-Helix motifs can recognize a unique stretch of DNA sequence (which is certainly more unique than individual base pairs). Usually the binding of the fingers are co-operative which leads to increased affinity and specificity of the protein-DNA binding [2,3]. Analogous mechanism may exist for other kinds of DBD too (I haven't specifically looked for that). Moreover, many DNA motif binding proteins oligomerize, which is again co-operative. This increases the specificity and the overall binding kinetics becomes sigmoidal and thresholded (see Hill kinetics).
Binding mechanisms are best understood for ZF proteins that led to the development of zinc finger nucleases which was one of the first modern methods of targeted genome editing [4] (though they have now been obsoleted by CRISPR-Cas system).

Figure 2: DNA sequence identification by zinc finger proteins. This example considers the Zif268 protein. Reproduced from Paro and Sauer (1992) [1].

Figure 3: A more detailed depiction of Zif268-DNA interaction. Reproduced from Durai et al. (2005) [4].

References:

Pabo, Carl O., and Robert T. Sauer. "Transcription factors: structural families and principles of DNA recognition." Annual review of biochemistry 61.1 (1992): 1053-1095.
Krishna, S. Sri, Indraneel Majumdar, and Nick V. Grishin. "Structural classification of zinc fingers SURVEY AND SUMMARY." Nucleic acids research 31.2 (2003): 532-550.
Lee, Juyong, Jin-Soo Kim, and Chaok Seok. "Cooperativity and Specificity of Cys2His2 Zinc Finger Protein− DNA Interactions: A Molecular Dynamics Simulation Study." The Journal of Physical Chemistry B 114.22 (2010): 7662-7671.
Durai, Sundar, et al. "Zinc finger nucleases: custom-designed molecular scissors for genome engineering of plant and mammalian cells." Nucleic acids research 33.18 (2005): 5978-5990.


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How to understand certain protein names
I am looking for a reference to help me understand what is meant by acronyms such as : H3K9me1, H3K9me2, and H3K9Ac.
I know that these are all histone proteins, but is there a general nomenclature algorithm for all cellular proteins? Are H3K9me1 and H3K9me2 just different proteins that methylate the same region? What is meant by H3K? Etc.
Thanks!

For H3K9me1:

H3: name of the histone
K9: amino acid and position (K = lysine, position 9) of modification
me1: modification (me = methylation, ac = Acetylation), and number of modifications

So H3K9me1 means that the 9th residue (lysine) of histone H3 was monomethylated. Similarly H3K9Ac means that same residue was acetylated.
Wikipedia gives a decent explanation of the nomenclature of histone modifications, and there is also a more detailed table in Nature Structural & Molecular Biology.

Thanks! This is great, now when we say H3K9me1 vs. H3K9me2, is there a different protein that performs this single vs. double methylation, or can chIp-Seq or western blotting techniques somehow differentiate between when the same protein adds one or two methyl groups?

@NaiveHalmos I don't know offhand but there are a number of histone methyltransferases (see https://en.wikipedia.org/wiki/Histone_methyltransferase). It looks like there are a number of methods to differentiate between different modifications, e.g. see http://www.ncbi.nlm.nih.gov/pubmed/22130888

There is also a cool table at Cell Signaling Technology's website that lists all the known or suspected histone modifications, the modifying enzymes (again, if known), and known or suspected functions.

@NaiveHalmos if an appropriate reagent is available, yes you can differentiate between mono-, di-, and tri-methylation by Western or ChIP/ChIP-Seq. My lab uses a lot of CST's stuff, so I know they have a bunch of specific antibodies, but I'm sure other vendors do as well.


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Do any predatorial animals attempt to appear smaller?
There are many animals that have behaviors or characteristics to make themselves appear larger than they are as a defense mechanism, such as butterflies have large eye patterns on their wings.
Are there any animals that do the opposite? That attempt to appear smaller in order to lure their prey closer?
I'm more interested in physical characteristics but behavior that does this, also counts.

Many carnivores crouch closer to the ground with ears flattened when stalking prey

@ScottStensland yes that's correct however that's in order to remain unseen, I'm more interested in behavior/characteristics that are meant to be seen by prey to lure them, similar to the angler fish's light

In order to answer your question, two things must be demonstrated: First, we must demonstrate that the prey animal has perceived the predator. Second, we must demonstrate that the prey animal believes that it has perceived a small animal (which poses no threat).
There are several ways that a predator might achieve these outcomes. The first way is to present a small part of its' body as an independent animal, and the rest of its body as something innocuous, like a rock. There are many examples of this type of deception: you've already identified anglerfish lures. My personal favourites are frogfishes. Several other examples are discussed in the Wiki on Aggressive Mimicry.
Another way is to present the whole body in a way that makes it appear small, for instance by presenting a silhouette with a small apparent area to the prey. This has long been thought to be part of the foraging strategy of some ambush predators which have bodies with a small cross-section, such as pike and dories.
In addition to visual deceptions, some predators may use other signals to be perceived as animals that are smaller than themselves. Atkinson (1997) suggests that predatory Northern Shrikes impersonate the songs of smaller Passerine birds in order to lure them into striking range. This behaviour would also qualify as a predator attempting to be perceived as something smaller than it really is in order to gain prey.

This kind of deception can happen at various levels. Mimicry (which you already mentioned), Camouflage, distractions, deceptions, display behaviors. These are not just for predation or avoiding predator but also for reproduction and avoid conflicts. There are many examples of this kind of behavior, I know few of them. All are not exactly reduction in size but something similar to lure prey.

Hunting Strategy of the Margay to Attract the Wild Pied Tamarin
Zone-Tailed Hawk a Mimic of the Turkey Vulture
Fireflies who mimicks flash responses of the prey's own females.
Motion camouflage of dragonflies
Fake death by opossums
Assassin bug's fake vibrations to lure spiders
Octopuses occasionally stroll around on two arm
Tactical concealment in primates


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What factors cause males to be more common than females in humans, from an evolutionary perspective?
Fisher's principle states that there should be a 1:1 ratio between males and females born on average for a population.  However, if you look at birth statistics your find that boys are slightly more likely to be born then girls.   This article talks a little about how it happens
If it was truly advantageous for an even sex ratio to exist at birth I imagine we would have evolved to make that happen, by slightly favoring more female sperm or by having the processes that decides which embryos to spontaneously abort be stricter for males embryos then females.  For that matter since it's more important for males to be exceptionally healthy then it is for females, since males have to compete for a mate while females don't, you would think more strict filtering for 'bad' embryos in the case of males then females would make sense anyways.
Thus I'm inclined to think that the increased number of males to females is not random evolutionary fluke, but adaptive.  I'm wondering what would cause there to be a benefit for males to be slightly more common then females.
I know males are more likely to die in childhood, due to risk taking activities to impress the females, so could it be that the increase in males is due to the expectation that more males will die before reaching sexual maturity?  I'm not certain I buy this logic, it doesn't seem you should favor a sex any more because it's likely to take higher risks.
I know that strong/healthy mates would prefer males and weak ones prefer females, since strong males would out compete weak males for mates it's good to have strong males that can achieve multiple mates and weak females since their guaranteed to have at least one mate.  Is it possible that our increased nutrition and health of recent generations simply results in more males because our bodies judge each of us as 'healthy' compared to the standard that existed for 99% of our evolution, ie, evolution hasn't caught up with technology when judging health to decide which sex to favor?
Is there some more obvious explanation for why favoring males slightly would be adaptive in humans?
Edit: I want to stress again, I'm not asking how the bias happens.  The article I linked clearly explains what causes males to occur more in terms of pregnancy.  I'm asking why the bias happens.  This could be evolved away in the past if it was disadvantageous,  Whatever mechanisms cause there to be a bias this bias is presumably adaptive for it not to be evolved away.  Both the possible duplicate and the current answer only address what causes the bias to happen today, not why it would be evolutionarily adaptive to have.

Answers to this question are also relevant, and one of them directly addresses Fisher's principle: Are human fetuses more likely to be male?

Nice question! The answer is in your linked article. I quote:

When you put this all together, it turns out more males are born because more female fetuses are lost during pregnancy.