What is the oval shaped bone in the heads of some fishes? I had a dish of fish and found 2 oval shaped nearly 1cm long bones in its head.What help does it do to the fish? what is its name?
I have clicked the picture myself .

I am a professional fish biologist and those are otoliths; I have aged thousands of them. They are primarily used in maintaining equilibrium, hearing, and balance. The details of the shape of the otolith can vary between species but generally look very similar. They are located in the skull of the fish, usually at the back.

Here is an image of other otoliths:
Photo source: Examples of common fish otoliths found at archaeological sites in Florida. Images from the Florida Fish and Wildlife Conservation Commission http://www.flickr.com/photos/myfwc/sets/72157625872804969/

Otoliths are calcium based structures located within otolithic organs (the sacule, lagena, and utricle) and make up the inner ear of boney (teleost) fishes. They come in pairs and there are three of them: Sagittal (within the saccule), lapillali otoliths (within the utricle) and asterisci (within the lagena). They are made of calcium carbonate and are generally composed in two different crystalline formations, aragonite and vaterite; crystalline form and amount depend on the otolith and stress induce metabolic processes. Otoliths are formed as the fish grows. In periods of fast growth (warmer months) the otolith forms faster and in periods of slow growth (colder months) the otolith forms more slowly. Given the cyclical pattern of warm and cold months in the year, the otolith form annuli (growth rings); annuli can be used to age fish just like rings on a tree. Additionally, they are metabolically inert and cannot be reabsorbed as calcium reserves like other boney structures in the fish; thus, they are a permanent record of the fish's age. This permanent record can also be used to evaluate the life history (i.e., movement patterns) using trace element analysis.

Specifically, how do they work/help the fish? Within the sacule, lagena, and utricle the otoliths are suspended in endolymphatic fluid within their respective organs. The organs have hair-like sensors in them that detect vibration or movement of the otoliths within, triggering an associated nervous stimuli. The nervous stimuli are then interpreted as movement and orientation.

Here are some sources:

https://dfo-mpo.gc.ca/science/aah-saa/otoliths/info/introduction-eng.html

https://en.m.wikipedia.org/wiki/Otolith#Description

https://www.sciencedirect.com/topics/earth-and-planetary-sciences/otolith

https://www.daf.qld.gov.au/business-priorities/fisheries/monitoring-compliance/monitoring-reporting/commercial-fisheries/species-specific/estimated-fish-age

This book is also an excellent resource for a much more in-depth look:

https://fisheries.org/bookstore/all-titles/professional-and-trade/55078c/


Is this a flowering plant? I just received a small plant as a gift from a friend.

Here is its leaf:

I tried looking it up on flowers of India, but their database is too much to read manually.

Physical description:

It's short, around 5 inches, probably a flowering plant as per my experience (She says it is a cactus but I don't think so). The leaf is around 1.5 cm and has a cone+cylinder like structure.

Which species is this plant, and is it a flowering one?

Any help would be great.

Crassula tetragona, also known as mini pine tree (for its extreme use in bonsai technique), native to South Africa.

It is a succulent; a xerophyte (a kind of plant which needs very less water for survival), characterised with fleshy leaves developed due to evolution for storing water, this plant attains a height up to 3 meters.

Flowering in this plant usually take place in summer season, the flowers are yellowish orange and white.


Why do most theories assume "only" sexual reproduction can cause genetic diversity? The reason cited for sexual reproduction trumping over asexual reproduction broadly relies on the advantages of genetic diversity.

This completely overlooks the fact that a mutant which is able to reproduce asexually with some amount of genetic variation (editing, randomizing etc) would have more inclusive fitness?

This is a pretty big question so I'm going to focus on the core points.

It's not nearly so either-or, and really a range of two things: trait diversity and stability. Sheer diversity isn't sufficient to improve rate of adaptation. Stability in the sense that it's a good idea to hold on to successful traits.

In sexual reproduction, you have two sets (one set of traits from each parent) of proven survivable traits to draw from. Very roughly, it doubles the amount of positive feedback toward maximizing fitness for the environment the pair finds themselves in - of which pathogens are a major and quickly changing component.

In asexual reproduction, you have a single tested set of traits. Asexually reproducing organisms thus depend on things like horizontal gene transfer - proven traits from another organism. This has the effect of prolonging the amount of testing that takes place (one organism vs two), causing asexual organisms to be more adaptable to the circumstances they find themselves in compared to sexually reproducing organisms and vice versa.

Where I have written "proven" here, I am referring to the fact that the traits in question have survived in combination with the organism's other traits, as opposed to a totally new mutation that could have consequences before the organism has a chance to reproduce.

Related literature

Genetic variation in organisms with sexual and asexual reproduction
"With realistic environmental changes small alterations in any particular measurement or trait are usually sufficient to keep up with the changes, but fitness, since it depends on a large number of traits, will be selected with greater intensity, which may be enough to confer a distinct advantage on sexual reproduction." An advantage of sexual reproduction in a rapidly changing environment.
Bacterial adaptation to pathogens: What antimicrobial resistance has taught us about horizontal gene transfer.


Why do people have darker skin in sunnier climates? I don't understand why darker skin is advantageous in hotter climates. Wouldn't it absorb more of the heat? I have heard that it reduces the incidence of cancer, but I would think absorbing more radiation would increase the risk?

One of the important pigments that the earlier answer hinted at is melanin.  Melanin is a brown pigment with photoprotectant properties.

As you correctly identified in your question, exposure to EM radiation (particularly UV and shorter λ waves) is damaging (indirectly) to DNA, which can cause mutations and therefore possibly cancer.  Melanin production is one of the defence mechanisms the body has evolved to deal with this threat.

When DNA is damaged by the UV-B radiation, melanogenesis (the increased production of melanin pigment) is induced.(1)  Therefore, people often exposed to more UVB (i.e. in sunnier climates) are likely to have more melanin in their skin, which makes it appear darker in colour.  It is likely to be the increased incidence of melanin proteins in your skin which leads to the formation of a tan.

Melanin and its derivatives work as photo-protectors (protecting the body from the damaging effects of ultra-violet exposure) by absorbing UV-B photons and converting them into much less damaging infra-red wavelengths (heat energy).  It does this extremely rapidly by internal conversion and extremely efficiently - efficiency in excess of 99.9% has been reported.

As the melanin removes the danger posed by the UV within a few femtoseconds (x10-15 s), the more melanin that is present in skin tissues (and consequently the darker the skin), the lesser the chance of the UV damaging molecules in the skin so the lesser the risk of developing skin cancer.


What is a good review book/source for microbiological diagnosis? I am trying to find the diagnosis figure for different bacteria where phases are illustrated.

I am using at the moment: 1) First Aid for the USMLE Step 1 2013 and 2) Medical Microbiology by Murray et al, 7e.

What is a good review source for basic microbiological diagnosis?

I would suggest:

Koneman's Color Atlas and Textbook of Diagnostic Microbiology

by Elmer W. Konema


Can you tell me what species of insect this is? I live in Verona, Italy.
Today I found this black insect and I don't know what species it is. My mom claims it's a kind of mint but I don't think so.

This looks like a horsefly (family Tabanidae, in Italian "tafani"), maybe Tabanus bromius but I'm not sure. If it's so, be careful: they bite and their bite is painful. Here you can find some quick suggestions about horseflies and their bite.

However, as you live in a city, don't worry too much: as the female horseflies feed on horse and cattle blood, they are normally present in the countryside, so those that you saw are exceptions more than the norm!


Why does having cold hands hurt? (1). Why does having cold hands create a painful sensation?
Is it a physical effect, maybe a protection mechanism from evolution?
(2). Why, if one's hands are cold, does it feel as if they are more susceptible to pain?
Note: I have (2) as a separate question because the painful sensation in (1) refers to that from the coldness, whereas in (2), I mean that certain 'ordinary tasks' would feel painful, for example, holding a shopping bag.

For question 1 it's just a biochemical response from thermoreceptor nerves in the skin, temperatures that are likely to cause lasting damage from prolonged exposure cause a neurological response - in this case it's pain.

In address to question 2 it is most likely down to the physiological response of vasoconstriction.

When the body is cold the body undergoes constriction of the blood vessels in the extremities to preserve core temperature where it is more essential for the proper functioning of vital organs. By constricting blood flow to the extremities (in this case the hands) there is less volume of blood present, because of this nerves present in the hand are closer to the surface and thus more sensitive to pain.


What is the effect of temperature and carbon dioxide on the opening and closing of stomata? I am teaching biology in an academy. The question which I had asked above had been raised by on of my students. I tried my level best to search out the answer to this question but I could not find the answer. I had read a number of answers to different questions from this website. So that's why I thought to Post my question on your website

I like the reference book Plant Physiological Ecology for stuff like this. I know one of the authors is Thijs Pons.

When temperatures become high, plants may close the stomata to conserve moisture. When the stomata are open, usually in daylight hours, the open stomata allow $CO_2$ to enter the leaf. This carbon is needed to form glucose and many other products a plant makes from photosynthesis. Most plants will not open the stomata in the absence of light.

(I use the above text as the reference. I can't give you pages right now, but I was reading this a couple of days ago.)


Bird Identification: New Delhi, April 2018 I've looked in Birds of the Indian Subcontinent (BNHS version, not Inskipp) and two phone apps and still can't find this, although I am a newbie tourist so am probably making a basic mistake. Seen today, 2018-04-07, 9:00 local time, in a New Delhi urban garden.

Maybe 25cm long. Uniform grey above, mottled grey below, grey legs with slight orange tinge. Orange-yellow bill, very slim light eye ring. I wondered about a large grey babbler, but all the pictures I can find seem less grey.

Thanks!

It looks like you're on the right track.  Here's a photo of a Jungle Babbler (Turdoides striata).  They are found on the Indian subcontinent.

Source: https://en.wikipedia.org/wiki/Jungle_babbler


Does the lung absorb organic food? Imagine you swallow something up and not everything gets out of the windpipe (this is possible right?).

Would it be possible for the lung to handle with the rest implying that it is organic? Would it slowing absorb it?

When we eat the architecture makes sure most if not all the food ends up in our foodpipe rather than our windpipe. This is aided by a structure called the epiglottis.

However frequently foods may be inhaled, for example if a drink is sucked through a straw more if it gets into the lungs compared to if we drink it. Occasionally we will inhale a peanut or something else which typically occurs due to abnormal relaxation or muscular problems in the structures involved. This may be due to a neurological disease (e.g. myasthenia gravis) or because simply drinking too much and inhaling peanuts or vomit (aspiration).

If the inhaled substance is small and lipid soluble e.g. alcohol, it can pass through the alveoli at the end of the lung to the rich blood supply. If it doesn't we rely on macrophages to digest the food. They aren't frequent enough to digest anything substantial. Bacteria however are great at munching this up and increase substantially in number. Typically your lowest airways are sterile but food can interfere with clearance mechanisms and provide a home. The part of the lung blocked (distal to the foreign object) can collapse and frequently does. In the long run this may cause bronchiectasis, where an infection recurrently affects the area due to permanent damage done during the initial event resulting in widened airways and an ongoing inflammatory response. The inflammatory response reveals even more receptors for bacteria to latch on to.


Is it possible that there are unknown vitamins? Is it possible that there are vitamins or other essential nutrients about which we still do not know?

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

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

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

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

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

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


Is hair made of protein or dead cells or both? Some sources say hair is made of dead cells:

it's mentioned in many titles of Google searches, so I'm linking the Google search search

Other sources say hair is a protein filament:

Protein filament that grows from follicles found in the dermis, or skin

I don't think protein and dead cells are the same thing. Where am I mistaken?

I found the answer while trying to write the question. Hopefully this helps others

  We usually say that hair is “made” of a protein called keratin—that’s a bit of a simplification. As hairs become part of the shaft, they undergo a process called keratinization, in which they become filled with keratin. So, technically, instead of being made up of pure keratin, hair is made up of dead cells that are filled with and surrounded by keratin.

Source

I'd say some visualisation would be helpful, please add a new answer or propose edits to this answer


What is the most up-to-date CRISPR/Cas9 protocol? I am collecting literature to start a new project on CRISPR/Cas9 gene editing. I must put together a protocol to start and am intending to use the following paper as guidance:

"Genome engineering using the CRISPR-Cas9 system". Nature Protocol 8(11):2281-308 · November 2013

Could you please indicate whether this is the most reliable and recent published general protocol for the CRISPR/Cas9 system.

It really depends on what you want to do with it. Sticking to genome engineering in Human cells, Nature Protocol 8(11):2281-308 · November 2013 is the de-facto standard. One improvement I suggest is to replace the "Surveyor Assay" with deconvolution analysis of sequencing traces using TIDE.


What percentage of human capillaries are located in the skin? As in the subject line, what percentage of capillaries in a human (expressed in terms of total length, I suppose) are located in the skin, as opposed to internal organs?  Google scholar has not turned up anything obvious, but I'm an outsider so I may have missed the appropriate term.

Another followup question would be:  if we're considering the amount of energy expended by the heart in pumping blood throughout the body, what's the percentage of that energy that is devoted only to (1) transporting blood to the skin and (ii) circulating blood through the skin via capillaries?

The first part of your second question permits a rough calculation.

The second question ( i ): For humans the skin has been defined as ending at the hypoderm, which is 2-3mm deep. The average human skin has been estimated to cover an area of 1.5-2 m$^2.$ We can use 2.5 mm and 1.7 m$^2$, respectively. This gives a volume of 0.00425 m$^3$ or 4250 mL in fluid volume. The information for this calculation is at the Wiki site on human skin.

One estimate of the average total volume of fluid in a human body is 40L. Of that, 5L is blood. So roughly 1/8 of the body's fluid is blood. To a good approximation, the body is about 60% water by weight. This is presumably a little less than the percentage of fluids generally but since these are rough numbers we can use it. So 60% of the skin is fluid/water, and 1/8$th$ of this is blood.

Of the 4.250 L of skin, 60% is fluid, of which 1/8 $^{th}$ is blood, so $(4.25) \cdot (0.60) \cdot \frac{1}{8} = 0.3188$ liters of blood at any given moment in the skin, subject to considerable variation no doubt. This sounds a little low but the definition of skin sort of forces this--it is only skin-deep.

One source gives an estimate of the energy expended to pump blood in a normal adult heart as 0.5-1.0 Joule per beat which at 70 beats/minute amounts to 100.8 kJ/day using 1 Joule.

So the heart is handling about 5 L of blood of which 0.3188 L is blood in skin, so very roughly we could estimate that $0.3188/5 = 0.0638$ or 6.38% of the work above goes toward supplying skin, i.e. 6.43 kJ/day of energy.

As a sanity check, if someone burns 1200 [nutritional] calories a day, which is about 5 MJ, we can see that keeping skin supplied with blood represents a small fraction of daily energy expenditure.

The title question: Like you, I found no study on point but that does not mean one does not exist. I can't see why anyone would do/fund such a study as the answer is unlikely to inform further work, answer any current questions, or solve any problems.

The last part of your second question (ii) Transporting blood to the capillaries and circulating the blood through capillaries are aspects of the same job. Dividing the work of the heart into skin/non-skin was already artificial. To further divide the work into segments this way requires some motivation because any answer would be a bad approximation.


What causes peanut allergies? Surveys show that 0.6 percent of the US population has an allergic reaction to peanuts. This prevalent allergy has even prompted some to ban peanuts from schools altogether.

I am completely unfamiliar with the topic, and can't seem to find any specifics in the literature. Thus my question is:

What specifically causes the the allergic reaction associated with peanut consumption, and why is it so prevalent in comparison to other foods?

Ara H 1, Ara H 2, and Ara H 3 are the three main peanut allergies. AH1 and AH2 are typically higher-acuity anaphylactic type reactions. The molecular cause for this is that some Immunoglobulin E develop a serum sensitivity and bind directly to vicilin and conglutin (the active proteins in AH1 and AH2). There are actually 7 or 8 Ara H complexes, but it is believed the remaining ones have a lesser affinity for IgE, reducing the frequency of allergic reactions and thus their availability for relevant studies.

The prevalence of the allergy is generally attributed to a combination of exposure and genetics. Many people have a genetic predisposition to certain allergies, but to a certain extent the body must be exposed to the allergen before an allergy will develop. The high use of peanuts in the food industry, and even to a lesser degree in skin care products like lotions, can account for early exposure resulting in allergies.

From the other direction, some research suggests that early and frequent exposure from infancy through childhood (albeit the choking risk) can reduce the demographic prevalence of an allergy in a given population.


How does your body know when it is infected so it can invoke a fever? How does your body know when it is infected with a virus or bacteria so it can invoke a fever or ramp up the immune system?

During infection certain macromolecules present in the pathogens (pathogen associated molecular patterns) such as lipopolysaccharide launch the innate immune response, through toll like receptors. This leads to production of pro-inflammatory cytokines and also other inflammatory mediators like prostaglandins, thereby causing inflammation and fever.


Looking for a gene in my raw genetic data. What are the possible causes for this? Obviously, I barely know what I am talking about.

But I want to find the "MUC5B promoter polymorphism rs35705950" in my RAW genetic data from 23andMe. (see this paper  http://www.ncbi.nlm.nih.gov/pubmed/23695349)

I think rs35705950 is the SNP number...   When I search I get no results.

When I search for MUC5B I get 9 results, but the SNP numbers doesn't match.

My question(s)

Is it possible that I just don't have this gene (rs35705950)?

Does 23andMe not have ALL of my genetic information?

Am I doing something wrong or misunderstanding what I am looking for?

Let's set things straight. The genomes of humans are highly similar and in general everyone shares the same genes. SNPs, or Single Nucleotide Polymorphisms, are single basepair positions in the genome in which there tend to be differences between people. This means, that instead of measuring the whole genome sequence for a person, which is very expensive and difficult, we can just examine a subset of the genome (the SNP positions) and capture most of the unique characteristics of that genome.

23andMe do exactly that. They measure a large set of SNPs (but not all of them), and thus give you some useful information about your unique DNA sequence. So you would need to look in the output given to you by 23andMe and see if they measure the SNP in question (rs35705950).

What do SNPs have to do with genes then? Well, if one of these SNPs occurs inside a gene, it could affect the gene, for example by producing a slightly different protein that could lead to some phenotype. So, studies link SNPs to different phenotypes such as disease or hair color. Usually the link is not one-to-one, but given as a probability.


Polymorphism in cnidarians? To me, the phenomenon of polymorphism in cnidarians is particularly troubling. I gather that it essentially refers to existence of various different forms or  kinds of individuals, i.e. zooids and polyps in one species. But when we refer to the cnidarian Physalia, as an animal, aren't we actually referring to a colony of individuals? Physalia consists of several "entities" including gastrozooids, dactylozooids, and the float, and since each of these is a distinct "organism", therefore is what we refer to by saying Physalia is actually a colony of phenotypically distinct forms of the same species?

Therefore, can "animals" like Physalia or Gorgonia or Pennatula be thought of actually as "colony-beings" which always contain several individuals in group?

It seems like your question might contain two separate and linked issues, both of which are perhaps equally confusing and equally interesting. They're both really discussion questions in a sense, but they've also both been dealt with in the literature in thoughtful ways, so here's a stab at an "answer".

Issue One: how does your species concept deal with polymorphism?

This may depend on which species concept you're using. And, to some extent, the choice of which species concept you use depends on what kind of organism you're dealing with (for instance, organisms that reproduce asexually have a whole different set of issues and challenge several species concepts).

Various papers by Kevin de Queiroz deal very well with species concepts. In 'The General Lineage Concept of Species'  (which is also summarized on this page), he argues that although there are many different species concepts that can be better applied to different situations, they all share the basic tenet of defining a "segment of a population-level lineage". In other words, each concept is attempting to put a continuum into slightly different categorical bins, but they all recognize the existence of the same continuum (the lineage). (Also see his 'Species Concepts and Species Delimitation'.)

I think most species concepts have no trouble dealing with polymorphism because the different morphs are all part of the same lineage, that is, "a series of entities forming a single line of direct ancestry and descent" (de Queiroz 1999).

Issue Two: how does your concept of the individual organism deal with colonialism?

In 'Does Biology Need an Organism Concept?'  Pepper and Herron make a similar point to that of de Queiroz. They argue that multiple definitions (concepts) exist, and that these concepts all attempt to categorically bin what is in fact a continuum. Like de Quieroz, they argue that most definitions recognize the same underlying continuum, and that the difference is in the categorical bins.

In the case of the organism concept, this continuum is based on two criteria: increasing genetic homogeneity, and increasing physiological integration.

So, for instance you could have two organism concepts (in the picture below, lighter yellow and darker yellow) that agree that Physalia falls in the same location along these axes, but disagree on exactly where to draw the boundary between their "multiple organisms / colony" zone (yellow), and their "individual organism" zone (white).

I'll finally get to my point, paraphrasing both de Queiroz and Pepper and Herron. For both concepts of the species and of the organism, arguing about whether one concept is better than another is endless (especially on a site that aims at answers rather than discussion). However, recognizing that there are different concepts, understanding that what these concepts do is to bin the same continuum in different ways, and being clear about which concept you decide to use is very useful.


Cosmid genomic library, or genomic cosmid library? Which usage is better for referring to a "cosmid library of genomic DNA fragments"?

I've always used Cosmid Library but Cosmid Genomic Library is better than Genomic Cosmid Library.


What mammal or creature dropped this? (Warning: Gross Pictures) I'm at a loss to explain what creature dropped or created this. This giant pile showed up virtually overnight.  If someone could point me in the right direction, I'd greatly appreciate it.

The geographical area is Sparks, Nevada.

You can see a similar pile of bird poop seen below a barn swallow nest:

 Source: deepmuckbigrake

Alternatively, if it really did appear overnight, perhaps a pile pf pigeon poop was pushed out of a nesting area in the soffit?

 Source: Scranton Times Tribune

If it's pigeon poop, you might want to be careful.


Tools to find miRNA ID How can I get accession numbers of bread wheat miRNAs by their sequences? What are the tools or website that can be used?

If you have a sequence, run a nucleotide BLAST search at NCBI, specifying Triticum aestivum (taxid:4565) as the organism.
The miRBase page for Triticum aestivum has details of wheat microRNAs, and a page where you can do a sequence search with either BLAST or SSEARCH (as @WYSIWYG kindly pointed out).
Perhaps the Triticum aestivum page at PlantGDB may help.


Transmission of epigenetic regulation through surrogate mother I know the basics of epigenetics, but I do not know how epigenetic mechanisms are transmitted from parents to children (or if there is even enough literature to derive a consensus). My question is relates to surrogate motherhood, in which an egg is fertilized in vitro and then implanted in the womb of a woman other than the egg donor.

Are all the factors that affect epigenetic mechanisms encoded in the genome? Is it possible for the surrogate mother's epigenetics to influence the epigenetics of the child/children?

Epigenetic information is information that can be inherited through cell division that is not encoded in the DNA sequence. This includes, but is not limited to, DNA methylation and histone modifications (there is also non-chromatin based epigenetic information). A nice example is the centromere, the chromosomal region that binds the kinetochore and is important to attach chromosomes to the mitotic spindle during cell division. The location of the centromere on the chromosome is encoded by a specific nucleosome composition and does not seem to rely on the DNA that wraps around those nucleosomes: The DNA sequence at centromeres is not even conserved from chromosome to chromosome (with the exception of budding yeast), and there are several known examples of people and families where the centromere is in a different place. However, all the mechanisms for maintaining this epigenetic mark are encoded genetically.

As epigenetic information is transmitted through cell division, it is directly inherited from the biological mother (with the exception of e.g. the centromere, most epigenetic marks from the father's chromosomes are removed when sperm is created).

However, (some) epigenetic information can be modified. This is obviously important during development where gene expression patterns of a liver cell need to be stable but different from gene expression patterns of a neuron, even though both descend from the same cell.

There is evidence that the metabolism of the mother will influence the epigenetic program of the child; diet being one of the determinants. It has also been suggested that epigenetic changes may influence behavior. Thus, it is indeed possible for the surrogate mother's epigenetic state to influence the epigenetic information of the children.


Is the heterotroph hypothesis universally accepted? I was wondering whether there are hypotheses that take a different approach that is contrary to the heterotroph hypothesis.
The heterotroph hypothesis states that autotrophs evolved from heterotrophs because of the lack of food.
Is this issue still debated by scientists or is the heterotroph universally accepted?

I would say the the topic is still very much under debate. This paper by Ferry and House (2006) briefly review the heterotrophic vs chemoautotrophic hypotheses. They include citations from proponents of each hypothesis. Interestingly, Ferry and House propose an "energy conservation" hypothesis that attempts to merge ideas from the other two hypotheses.  Overall, much work remains to be accomplished in this field before we have a clear understanding of the origins of life.

Literature Cited

Ferry, J.G. and C.H. House. 2006. The stepwise evolution of early life driven by energy conservation. Molecular Biology and Evolution 23: 1286-1292.


After how many hours water drunk is expelled from the body? If one drinks a liter of water at 7 am when (in what span) will that water be eliminated through uresis?

Is that process influenced by any factors such as empty stomach, sleep or other?

The time from drinking to urination depends mainly on your hydration status and the presence of food in the stomach.

Scenario: You have drunk enough fluid in the previous days, so you are normally hydrated. In the morning, you get up from the bed, urinate, drink 1 liter of water in 5 minutes and eat nothing.

Some water can come through the stomach and can be absorbed in the small intestine in about 5 minutes; the entire liter may need more than 2 hours (sweatscience.com).

When some water is absorbed into the blood it can immediately trigger diuresis - the excretion of the urine through the kidneys into the bladder. It may take about 3 hours for the entire amount of water drunk to be excreted. So, the approximate time span (from start to end of water excretion) could be 5 - 180 minutes. But not likely the entire liter of water will be excreted, because, in the morning, you are in a slightly negative water balance, so some water will stay in your body.

If you are dehydrated before starting drinking, much less urine will be excreted in the first few hours.

If you drink after eating, the food in the stomach can delay water absorption and excretion by more than an hour. This also happens when you drink nutritional fluids, such as milk or juice.

This is from my experience and understanding basic physiology. I'll try to find some references.


Why didn't people taking up the Ice Bucket Challenge die? I recently came across Vagal Inhibition. That article says,

  (5) Sudden immersion of body in cold water.

can cause vagal inhibition and ultimately death.

Recalling the Ice Bucket Challenge. Going by what the above article says, shouldn't many of the participants have had a vagal inhibition ?

Theoretically, any treatment can cause death. Drinking water can be lethal and oxygen is highly toxic and a strong oxidizer.

To quantify toxicity we usually use Median Lethal Dose (LD50) metric. That is a dose at which half (50%) of test group is going to die.

To answer "Why didn't people taking up the Ice Bucket Challenge die?":

Dose that people used was not high enough to cause any significant increase in mortality. Maybe some people did die, but it was just masked by other news (to some degree)


First RNA polymerase-mRNA We know that RNA polymerase produces mRNA by reading DNA strand. Which enzyme produces the first RNA polymerase if other RNA polymerases are synthesized in the same way like other enzymes(proteins) ?

The RNA world hypothesis states that self-replicating RNA (that is, an autocatalytic RNA polymerase) was the first form or precursor of life. So, in that context, your question is basically asking how life originated. The obvious answer is that we don't know (currently anyways), but I'm going to take this opportunity to describe a few really neat experiments which might give you some insight over a possibly contributing mechanism of how self-replicating molecules may have developed. I won't go over the Miller-Urey or Oró experiments, but let's assume that the early Earth contained organic molecules (especially nucleotides for our purposes). It's also important to keep in mind the immense time scales over which these processes occurred (the Earth is ~4.5 billion years old).
Anyways, let's talk about in vitro evolution, also known as systematic evolution of ligands by exponential enrichment (SELEX). SELEX is a procedure whereby an initial library of random RNA sequences (flanked by known sequences to be used as primer sites) undergoes a selective process followed by amplification and mutation of the selected molecules. This is repeated several times. As an example, this process can be used to create aptamers, which are small RNA molecules which bind a specific ligand. A pool of random RNA is passed over a column containing the immobilized ligand. By chance, some RNA will have some amount of affinity to the ligand. Poorly bound RNA is washed off non-stringently and then slightly better bound RNA is eluted. This RNA is reverse transcribed and amplified by PCR. The PCR primers contain the T7 RNAP promoter which allows transcription of the cDNA to produce a new  RNA pool. Somewhere in this regeneration process, mutations are introduced so that the new pool contains randomly modified copies of the RNA which had some affinity. Through repeated steps of increasing stringency, an aptamer with high affinity can be developed.

(Ellington, 1994); Outline of the SELEX process.

So how does this apply to the origin of the first RNA polymerase? It just so happens that Bartel and Szostak (1993) used in vitro selection to produce a ribozyme (a catalytic RNA molecule). This ribozyme was a ligase, that is it catalyzed the formation of a phosphodiester bond between two RNA molecules that are aligned on a template.

(Bartel and Szostak, 1993); Methodology of the selection used to generate a ribozyme ligase.

While the ribozyme created was not autocatalytic, the experiment had implications on the origin of self-replicating RNA and life in general, which were discussed in the paper:

The ribozymes that we have isolated from a pool of random sequences catalyze a chemical transformation similar to that catalyzed by polymerases. Their abundance in the random-sequence pool is therefore relevant to the hypothesis that life began with an RNA replicase that originated from prebiotically synthesized random-sequence RNA. We detected about 65 sequences (Fig. 8, pools 3 and 4) capable of carrying out a particular ligation reaction in a pool of more than $10^{15}$ initial sequences, or a frequency of occurrence of one in about $2*10^{13}$ sequences.
[...]
Presumably, sequences capable of acting as efficient template-directed RNA polymerases are more rare than this, and sequences capable of acting as an RNA replicase are even more rare. Evidently, catalysts of moderate activity could arise spontaneously from relatively small quantities of RNA (and perhaps related polynucleotides); however, a catalyst with the activity, accuracy, and dual functionality (enzyme and template) of an RNA replicase would be so rare that it could only arise spontaneously and in a single step from a truly enormous amount of RNA. The problem is compounded because two such sequences would be required for autocatalytic replication to begin, one to act as the polymerase and a second to act as the template. Therefore, an RNA replicase could only have arisen from primordial sequence pools that were not truly random. Joyce and Orgel anticipate this difficulty and propose that nonenzymatic, template-copying reactions may have had a dual role in generating primordial sequence pools that are more likely to give rise to a replicase (21). The initial pool may have been biased in favor of local secondary structure by a mechanism involving intermittent use of intramolecular sequence as the template. In addition, some sort of nonenzymatic catalysis was probably necessary for the initial copying of the replicase sequence to generate a molecule that could be used as a template, the copying of which by the replicase would generate more replicase molecules, thus initiating the autocatalytic explosion of life.
[...]
The ribozymes that we have selected provide a new starting point for the evolution or design of RNAs with RNA polymerase and replicase activity. A series of issues including sequence-independent primer-template binding, the use of mononucleotide triphosphates as substrates, fidelity, and product-template dissociation now need to be addressed before an RNA replicase activity, an activity that has probably been extinct for over 3 billion years, can be fully resuscitated.

Johnston et al. (2001) took this experiment even further: starting with a pool of slightly mutated ribozyme ligases developed in a previous SELEX experiment, they were able to generate a ribozyme polymerase. This polymerase was able to catalyze the addition of nucleotides to a growing oligonucleotide chain up to 14 bases long and based off of an RNA template. The polymerase was also quite accurate.

(Johnston et al., 2001); Excerpts from the in vitro evolution of a ribozyme polymerase.

However, the authors are skeptical of this being the sole mechanism behind the rise of an autocatalytic ribozyme:

How could general polymerase activity have arisen on early Earth? If emergence of the first RNA replicase ribozyme coincided with the origin of life, it would have had to arise in a single step from prebiotically synthesized RNA, without the benefit of Darwinian evolution. Our shortest construct retaining activity was 165 nt, with about 90 nt involved in important Watson-Crick pairing and at least another 30 critical nucleotides (23). Ribozymes with the efficiency, accuracy, and other attributes of an RNA replicase might have to be even larger than this. However, current understanding of prebiotic chemistry argues against the emergence of meaningful amounts of RNA molecules even a tenth this length (1). This difficulty is anticipated by those who propose that life, and Darwinian evolution, began before RNA. Some speculate that in this "pre-RNA world," life was based on an RNA-like polymer, yet to be identified, that possessed the catalytic and templating features of RNA but also a more plausible prebiotic synthesis (1). The pre-RNA life forms presumably later developed the ability to synthesize RNA, facilitating the emergence of an RNA replicase ribozyme, which in turn enabled the transition to the RNA world.

There are other, similar experiments where people have made self-replicating ligases (Paul and Joyce, 2002) or a system of two, cross replicating ribozymes (Lincoln and Joyce, 2009). While the question still remains unanswered, perhaps from all of this you can get a sense of the plausibility.
References:

Bartel DP, Szostak JW. 1993. Isolation of New Ribozymes from a Large Pool of Random Sequences. Science. 261(5127):1411-1418.
Ellington AD. 1994. Aptamers achieve the desired recognition. Curr Biol. 4(5):427-429.
Johnston WK, Unrau PJ, Lawrence MS, Glasner MR, Bartel DP. 2001. RNA-Catalyzed RNA Polymerization: Accurate and General RNA-Templated Primer Extension. Science. 292(5520):1319-1325.
Lincoln TA, Joyce GF. 2009. Self-Sustained Replication of an RNA Enzyme. Science. 323(5918):1229-1232.
Paul N, Joyce GF. 2002. A self-replicating ligase ribozyme. P Natl Acad Sci USA. 99(20):12733-12740


Clownfishes and Sea anemones Relation between clownfishes and sea anemones is a classic example of mutualism. I wanted to list the species of sea anemones that are involved in this mutualism but I got lost.. Could you help me with that?

How many species of sea anemones which host clownfishes are there? Could you list them?

I only found this two references, but these are only secondary sources at the moment.
Look here "Clown Fish Anemone" and here "Choosing Clownfish and Anemones for Your Aquarium". It seems that there are only around two handful of anemones capable of supporting clownfish.
Here are some primary sources which confirm the 10 anemone species: "The anemonefish symbiosis: What is known and what is not." and "Field guide to anemonefishes and their host sea anemones". The last two links point to PDFs which contain a lot more references.


Why is gene finding in Eukaryotes such a difficult task? Why is gene prediction in eukaryotes such a difficult task? Every gene starts with a codon and the non coding regions in between a coding region also has some specific base sequence(which are used by enzymes to recognize non coding regions during splicing). A computer program could simply search for start codon and then for stop codon. In between it could also search for those non coding regions since they start with specific base sequences. Why does gene finding need such complex things such as HMM?

The main problem is that while most of the things you describe are necessary to have a protein coding gene (introns, the non-coding regions within a coding region, aren't actually per se, even though they're common), they are not sufficient. Additionally there are also genes for non-coding RNAs (including tRNA and rRNA), which obviously don't have a 'coding region' (and also usually no introns).

In order to classify something as a functional gene we usually require that is actually made into (at least) RNA, which requires regulatory sequences that lead to transcription of the gene, these are called promotors. In eukaryotes there are many different promotor sequences, so its very hard to predict them computationally, additionally there are evolutionary remnants in our genomes, which are called pseudo-genes, and while they still have the general structure of a gene, they are not actively used any more.


Is it common to have multiple recessive traits in humans? I just started thinking about my phenotype and realized I got multiple recessive traits. I have attached ear lobes, my blood type is O-, I got green eyes (I think eye color in polygenic but still somewhat recessive), a few years back I was in the control group of a study that was looking for a link between an allelic variant and the development of diabetes mellitus in patiences with another disease I forgot which, I was the only homozygous among all control patients! so you get the point. I am just wondering if anyone has any notion of how often humans present multiple recessive traits, maybe in terms of allelic frequency or something like that, or where can I find information about it. And maybe if there is something health related that may be worth knowing. I mean apart from a minor allergy I'm a really healthy person, but I may have predisposition to something.

It depends on how long a population in your dominant heritage was genetically isolated, how common certain recessive traits are.

However, you might reconsider about the "green eyes".  Iridologists claim that there are only blue eyes, and light brown eyes.  All other colours are indicative of bioaccumulation of various substances (evidenced by a return to blue or light brown when the body is supported in excreting these substances), and health issues in certain tissues.

While there is argument about how scientific a technique iridology is, all medicine begins as observation of patterns, and development of models based on those patterns.  Models in medicine are constantly undergoing upgrading and replacement, as old models no longer explain new and well-observed patterns.


Organism and plants reduce radioactivity? I would like to ask if there are organisms or plants that could help in reducing any one of types radioactive contamination?

Your magic search word is 'phyto-remediation'

There a bunch of plants used for this.

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

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

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

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


What is the difference between abiogenesis and spontaneous generation? As we all should know, abiogenesis and spontaneous generation are far from identical. For one, spontaneous generation was disproven with Pasteur, and abiogenesis seems to be a solid scientific theory. However, one can loosely summarize both as "the emergence of life from non-living materials" which, at the very least, is confusing for the layman.

My question is: What truly differentiates abiogenesis from spontaneous generation? For example, if abiogenesis were to happen again, how would we differentiate the two terms?

Is time the most contributing factor (abiogenesis happened over hundreds of millions of years)? Or the fact that abiogenesis generates "primitive organisms", while spontaneous generation assumes the generation of evolved, complex organisms?

One important difference is that spontaneous generation is a form of "mechanism" by which a certain species is "born", so it is repeated many times. For such complex organisms this would be part of their "life cycle". It would also need to be a regulated, robust process.

Abiogenesis, on the other hand, would create an organism which from that point on does not rely on abiogenesis in any way, so it would be a unique event. Abiogenesis is highly probabilistic which is why it would result in very simple organisms.


Why only heterogeneous SNVs for validation using genotyping arrays? I am trying to validate the variants I found using whole genome sequencing . The standard practice, I have seen in the two publications below were to check for the number of heterozygous SNPs called by the SNP array.

1) Performance comparison of whole-genome sequencing platforms

  To further assess the accuracy of the variant calling, ... Of the 260,112 heterozygous calls detected with the Omni array, 99.5% were present in the entire SNV data set, 99.34% were concordant calls and only 0.16% were platform-specific SNVs. This demonstrates that both platforms are sensitive to known SNVs and that few known single-nucleotide polymorphisms (SNPs) are detected by only one platform.

2) Optimised filtering reduces the error rate in detecting genomic variants by short-read sequencing

  To confirm that shared SNVs are indeed true variants, we used Illumina single-nucleotide polymorphism (SNP) arrays and selected all SNPs heterozygous on the SNP array.

My question is - why are only heterozygous SNPs chosen for validation when using Illumina Omni arrays?

The purpose of validating is to find genuine SNPs and not those caused by sequencing or amplification errors. It is extremely unlikely you will have a false homozygous SNP as a result of error. Just think about it. The same error, at the same base, occuring 80%+ of the time? Its not going to happen unless you have low coverage, and these SNPs should be thrown out anyway. You may have some cases where a genuine heterozygous SNP is called as a homozygous SNP. But that isnt much of a problem. It is still a genuine SNP. It would only be a problem if you were only interested in homozygous SNPs, in which case you will just need to validate everything biochemically, which you will need to do anyways.


Spores bacillus subtilis in milk I need to inoculate spores into milk and then count on the plate. I never see a spore, so how i recognize it from the germ cell? does anyone know the procedure and if there are differences from a normal count in agar colonies?

If you need to inoculate milk with a known number of Bacillus subtilis spores then you will have to go follow a "sporulation" protocol - (going by your question I am not 100% certain whether this is what you want to do).

However, please find a sporulation protocol, developed by the Universities of Bonn and Freiburg, below:

Sporulation

Overnight culture

Inoculate your culture of Bacillus subtilis in 4 ml LB-medium
Let them grow overnight at 37°C, 200 rpm

Exponential growth

Measure the OD600 of your overnight culture and dilute it in LB-medium to an
OD600 off around 0.1-0.2/ml in 10 ml LB
Let the cells grow to an OD600 of 0,8/ml (37°C, 200 rpm)

Sporulation

Centrifuge 10 ml of the cells at 13,000 x g for 1 minute
Wash the pellet with 1 x PBS
Re-suspend the pellet in 5 ml DSM (Difco Sporulation Medium)
Let the cells grow for 24 hours at 37°C (200 rpm)

Lysozyme treatment (additional for spore purification)

Treat the samples with lysozyme (15 mg/ml) at a dilution of 1:6
Incubate for 1 h at room temperature
Wash 6 times with 1 x PBS

Additional:

count spores using a Neubauer improved counting chamber and make aliquots
with a defined number of spores per aliquot (e.g. 100 Million spores per 500 μl)

(Note: always use fresh DSM since the FeSO4 is rusting when it is in dilution)

May I make special mention of the Bacillus subtilis Manual here which was put together by the iGEM team and has proved as an excellent resource. The protocol above was taken from it.

Once you have your spore counts you can then inoculate the milk to your liking. However, please be aware that milk, unless completely pasteurised prior to inoculation, is not a sterile product. This means that other organisms might grow on whatever agar you decide to plate out on.


What does the empty space in the bamboo stem do? Is the empty space inside a bamboo stem a xylem? And why is the space so large?

No, its not xylem. Bamboo is a grass, and the stem (culm) of many grasses are hollow in the middle (see e.g. Grass Structures from Oregon state for some more info).

The exact reason for why Bamboo have hollow stems is most likely due to evolutionary contingencies. However, from a mechanical stability point of view, a hollow stem is much more rigid and stable than a solid (but much thinner) stem composed of the same amount of biomass (Niklas & Spatz, 2012, p. 191ff). So from the perspective of efficiency, the hollow stems of grasses are very useful. The solid node discs found in grass stems (and in other plants with hollow stems) are however really important for increasing overall stability and ability of stems to resist deformations, while only contributing to a very small amount of the total biomass.


What are important temperature breakpoints for plant distributions? I am working on a climate classification system. Some previous works like Koppen and Trewartha use temperature breakpoints of 18℃ monthly minimum of daily average to delimit tropical climates, and 0℃ monthly minimum of daily average to distinguish subtropical from continental (Koppen only).

The first question, is there any scientific basis for these specific temperature breakpoints?

As an example of what I am looking for, I want to point out something in plant distributions in the area of the world I'm most familiar with; the South of the US. In Atlanta, where January averages are 6.3℃ and lows are 1.3℃, most of the natural trees you see around are either conifers or deciduous hardwoods (Oaks, hickories, yellow poplar (Liriodendron tulipifera) and sweetgum (Liquidambar styraciflua). However, towards the coast in New Orleans 11.9℃/7.1℃ or Savannah 9.8℃/3.7℃, there are a lot more evergreen non-coniferous trees. If you look at the (very similiar) distributions from Wikipedia of evergreens such as southern magnolia, live oak, or swamp laurel oak, you can see that there is a cline where the coolest month-averaged daily temperature goes below around 6-8℃ where these evergreen plant no longer grow.

So the general second question is, are there temperature breakpoints that are significant in controlling what sorts of plants can actually grow in an area?

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

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

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

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

Climate imposes other limits.

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


Exon skipping in mammals I've heard from several sources that the predominant form of alternative splicing (at least in mammals) is exon skipping. However, my personal evidence is only anecdotal: I've heard it and read it, but have not seen references to literature. Is there a seminal paper or set of papers establishing this finding that I can cite?

You can see this review.

  There are several different types of alternative splicing (AS) events,
  which can be classified into four main subgroups. The first type is
  exon skipping, in which a type of exon known as a cassette exon is
  spliced out of the transcript together with its flanking introns (see
  the figure, part a). Exon skipping accounts for nearly 40% of AS
  events in higher eukaryotes [17, 111] but is extremely rare in lower
  eukaryotes.


Evolution of umbilical cord and reason of its elongation To answer a question myself, recently I've read that

  Years and years ago, a long umbilical cord enabled a woman to grasp her baby after birth and run away from predators"

Update:

$Question:$ How umbilical cord is evolved and what's the reason behind it's elongation?

There is at least one position that supports this claim:

  So why 61 cm? Umbilical cords of whales, porpoises, goats and other
  mammals are rela- tively shorter than the human cord. Walker and Rye
  of Cambridge surmised in the British Medical Journal in 1960 that
  prehistoric humans evolved length for protection. Nature's purpose was
  to allow the mother to pick up the newborn without disturbing the
  placenta. The event of breast feeding would then separate the placenta
  - an event which could attract predators. Having the fetus in tow would allow escape for mother and child.

(title: Silent Risk, auth.:Jason H. Collins). Well, right now I feel confused a bit...

The woman running bit is obviously a myth but that is genius.. Other than that the length of the umbilical cord has been found to be highly variable depending on each individual. Characterizing it as just long would therefore not be right. According to Wikipedia,

  The umbilical cord in a full term neonate is usually about 50
  centimeters (20 in) long and about 2 centimeters (0.75 in) in diameter
  (reference).

Some complications during birth are

  A number of abnormalities can affect the umbilical cord. The cord may
  be too long or too short. It may connect improperly to the placenta or
  become knotted or compressed (reference).

Why does it become too long has been associated with these factors.

  Long umbilical cords, defined as total length over 70 cm, have been
  significantly associated with:

  Maternal factors:

  Systemic diseases. Delivery complications. Increased maternal age.

  Fetal factors:

  Non-reassuring fetal status during labor. Respiratory distress. Vertex
  presentation Cord entanglement. Fetal anomalies. Male sex. Increased
  birth weight.

  Placental features:

  Increased placental weight. Right-twisted cords. Hyper-coiled cords.
  True knots (reference).

In conclusion, length of the umbilical cord has an average as mentioned before and being too long or short can lead to complications during birth. Regarding evolution of the cord, you could read this discussion.


How much nucleoside triphosphate is required to form one peptide bond during protein synthesis? I'm trying to find out how many molecules of nucleoside triphosphates (ATP, GTP, UTP and/or CTP) it takes to release enough energy to link two amino acid monomers together with a peptide bond, specifically during the process of mRNA translation.

I've tried to do some research online, but I could not find a reputable source that will say definitely how much energy is consumed in the process. The best answer I could find is formulated based on 'Molecular Biology of the Cell' 4th edition by Alberts B, Johnson A, Lewis J, et al., which is that at least one molecule of ATP is consumed for every peptide linkage. Is this correct?

I've also read on a science forum that the amount of ATP consumed during translation is different for every amino acid, but I could not find a reliable source to back up that claim. Is this true?

Although the question shows considerable effort to achieve clarity, the way it is phrased as:

  How many molecules of nucleoside triphosphate… [does] it take to release enough energy

still allows ambiguity, as I would not really regard the NTPs involved in protein synthesis “releasing energy”. So let us consider two reformulations of the question, as the explanation of the answers is of more scientific interest than the actual answers.

1. How many molecules of NTP are hydrolysed in the reactions causing the formation of one peptide bond on the ribosome?

  Answer = 3

Formation of each peptide bond involves a cycle consisting of the introduction of a single new aminoacyl-tRNA to the A site of a ribosome carrying a growing polypeptide chain (or initiator tRNA for the first peptide bond), the peptidyl transferase reaction, and than translocation of the extended peptidyl-tRNA from A- to P-site. (See, e.g. Berg et al. online — Ch. 29)

1 ATP is hydrolysed in the aminoacylation reaction:

                Amino Acid + tRNA + ATP → Aminoacyl-tRNA + AMP + PPi

1 GTP is hydrolysed in the aatRNA binding reaction catalysed by EF-Tu/EF1.

1 GTP is hydrolysed in the translocation reaction catalysed by EF-G/EF2

No NTP is consumed directly in the peptidyl transferase reaction — the energy for bond formation comes from the ‘activated’ aminoacyl-tRNA.

2. What is the total energetic cost in molecules of ATP for the formation of one peptide bond?

Here one might argue that:

  Answer = 4+

The additional ATP occurs if one considers the total energetic cost of the aminoacylation reaction as 2 ATP, not 1 ATP. This arises from the fact that the ATP is hydrolysed to AMP (+PPi) and not ADP. Recycling of the AMP involves first the use of 1 molecule of ATP in the adenylate kinase reaction to produce ADP:

                                 ATP + AMP ⇄ 2ADP

followed by the energy (from membrane ATP synthase) to regenerate ATP from ADP:

                                 ADP + Pi ⇾ ATP

Why 4+? Certain amino acids (e.g. val and ile) are sufficiently similar to one another that the aminoacyl-tRNA synthetases have evolved a proof reading capacity, in which any incorrectly aminoacylated tRNA is hydrolysed. This only occurs for certain amino acids and at a rate that is difficult to determine, so the wastage of the ATP in this manner cannot be calculated precisely.


Can Omega 3 Fatty Acids prevent chest pain in periodic Atrial Fibrillation? It is debated if omega-3 polyunsaturated fatty acids (N3PUFa) may be effective in preventing AF (atrial fibrillation), meta-analysis here.

However, much less has been considered this: Do N3-PUFAs prevent acute symptoms of periodic Atrial fibrillation?

The meta-analysis concentrate only in the long-term effects of prevention.
My proposal focuses on the short-term i.e. the fact that the user can recognise AF first and then uses N3-PUFAs.

Please, assume that there is a validation method by which the user can easily detect that he has AF - he does this if he suspect it, i.e. feels special discomfort and special wave-like-pain the chest.

He takes each time in this case 20 ml of Müller omega-3 oil which has also vitamin D.
The effect of recovering is immediate in prophylaxis.
Assume the user has less than < 20 ng/ml vitamin D in blood each case, most of the time, 9 ng/ml so avitaminosis.

My conjecture is that N3-PUFAs can prevent the acute symptoms of periodic AF.

How can N3-PUFAs prevent the acute symptoms of periodic AF?
What is the role of vitamin D here?

Omega 3 Fatty Acids cannot prevent the the acute symptoms of periodic A Fib, nor is there a role for vitamin D in the treatment of acute symptoms of periodic AF.

Atrial Fibrillation with the symptom of chest pain is very worrisome and requires urgent or emergent treatment. The most common treatments are heart rate control via IV antiarrhythmics, or cardioversion, either electrical or chemical, usually done in the emergency room.

There has never been a study wherein AFib accompanied by symptoms of chest pain was treated by Omega 3 Polyunsaturated Fatty Acids and there never will be, because N3PUFA does not cardiovert arrhythmias nor does it effect heart rate in AFib.

No medical body of any kind would support such a study.

Finally, there is no convincing evidence that N3PUFAs decrease the incidence of AFib, and this has been studied often, because eating 4-5 servings of fish per week has been shown to have a beneficial effect on A Fib. That gives reason to hope that N3PUFA supplements might be similarly beneficial. However:

  The role of omega-3 polyunsaturated fatty acids in the setting of AF is controversial. Although some studies demonstrate a lower incidence of AF recurrence with omega-3 polyunsaturated fatty acids use, others have shown an increased risk. Further studies are needed to assess the role of N3-PUFAs in the prevention of AF.[1]

If N3PUFAs have not been proven to help AFib long term, there is no hope whatsoever that studies will be undertaken to shown their effect in the acute treatment of symptomatic AFib, which is the scenario you have described.

Atrial Fibrillation becomes symptomatic when the arrhythmia results in decreased perfusion of various organs. If there is decreased perfusion to the heart, the presenting symptoms may be of ischemia (usually chest pain or pressure) or shortness of breath due to decreased cardiac output and decreased oxygenation in the lungs. If it is severe enough, fainting may occur from decreased blood pressure, and decreased perfusion of the brain. If it is not severe, it may result in a sensation of flip-flopping in the chest, or palpitations (irregular, thumping, or pounding heartbeats). There are other symptoms of A Fib but since you mentioned chest pain, I won't elaborate.

[1] Atrial Fibrillation in the 21st Century: A Current Understanding of Risk Factors and Primary Prevention Strategies


How does (action potential) hyper-polarisation work? I understand that after depolarisation, repolarisation and then hyperpolarisaiton occurs and that an area in hyperpolarisation is in its "refractory period".

Why does this prevent Na+ ions diffusing "backwards"? Since an area of the neurone membrane in hyperpolarisation will have a very negative charge so surely positive Na+ ions would diffuse towards them rather than away from them - "forward".

Similarly, why does this prevent another action potential firing too soon?

(I know this is kind of 2 questions in one, but as they are so very related I thought it more prudent to combine them).

I'll borrow a diagram from another answer to a similar question, but not quite a duplicate (I hope @AliceD won't mind my laziness):

Fig. 1. Refractoriness. source: University of British Columbia

One important concept to understand about the refractory period is that it has two components. One is the hyperpolarizing part, which is due to open voltage-gated potassium channels. Because there is more potassium conductance than at rest, the membrane voltage gets closer to the reversal potential for potassium.

If you were to open a sodium conductance during this period, you would indeed get a larger sodium current than you would get at rest (because you are further from the sodium reversal potential), however it will also be accompanied by potassium leaving the cell (because there is more potassium conductance), such that the net current and net change in voltage may not be much larger than at rest. Voltage-gated sodium channels that open to cause an action potential are gated by voltage, not by sodium. However, this type of refractory period is referred to as a relative refractory period because you can overcome it if you open a large enough sodium conductance (or inject a bunch of current with a patch clamp amplifier).

However, there is also a second part to the refractory period, the "absolute" part, which is shown in the diagram above. The voltage gated sodium channels themselves are not only closed but they are also inactivated. While inactivated, those channels will not open even in response to depolarizing voltage. It takes some time for the channels to return to the 'closed' state where they can be opened by voltage.

Summary

To speak to your question more directly, nothing prevents sodium from diffusing 'backwards', but action potentials travel quickly, sodium channel inactivation prevents them from traveling into axon segments where the sodium channels were just recently open, and the open potassium channels that cause hyperpolarization will 'shunt' current out of the cell while they remain open. Lastly, voltage-gated sodium channels are gated by voltage, not sodium.


How do messenger RNAs regulate each other's expression levels? I know that researchers learn gene regulatory networks from microarray experiments that measure the mRNA expression levels. However, I do not understand how mRNAs regulate each other's levels. Do they affect the transcription step or the translation step? I know that there are transcription factors which affect the transcription step, but those are not mRNAs but proteins. How does an mRNA (the product before translation) affect another mRNA's expression level? Is this regulation process very similar to the regulation by microRNAs?

Typically, these experimenters aren't thinking that the mRNAs directly regulate each others' expression levels, but rather that the proteins they code for affect expression. They're just mRNA as a proxy for the corresponding protein.


Solving Hardy Weinberg problems I really fail to understand Hardy-Weinberg equilibrium and can't find an easy enough source of information.

Can you help me to understand Hardy-Weinberg equilibrium?

My goal is to be able to solve the following kind of problem

  In a population with two alleles for a certain locus, B and b, the allele frequency of B is 0.7. What is the frequency of heterozygotes if the population is in Hardy-Weinberg equilibrium?

Here is a tutorial to perfectly understand Hardy-Weinberg Rule! If you feel like you just need a brief reminder, you can skip the text until the section In short... and try out the exercises just to check your understanding.
Terms you should know a priori
I will not define the following terms, so make sure you understand them

locus
allele
(relative) frequency
Homozygosity and Heterozygosity

What is the Hardy-Weinberg rule?
Hardy-Weinberg rule (HWr) describes a relationship between allele frequency and genotype frequencies. I will present the maths later.
Alleles and Genotypes frequency
Let's assume we have a bi-allelic (two alleles) locus. The possible alleles are called A and B.
Notation for genotype frequencies
Note that I will use a slightly unusual notation on purpose.
Let $f_{AA}$ be the frequency of the homozygous individual caring the allele A on both haplotype (both chromosome). Let $f_{BB}$ be the frequency other homozygote. Let $F_{AB}$ be the frequency of heterozygote which inherited the A allele from the mother and the B allele from the father. Finally, $F_{BA}$ is the frequency of heterozygotes which inherited the B allele from the mother and the A allele from the father.
Most of the time people write $f_{AB}$ (or similar notation) to designate all heterozygotes irrespective of whether the A allele comes from the father or the mother. In this answer, I make the difference of which parent gave which allele. I will instead note $f_{het}$ the frequency of all heterozygotes. Therefore $f_{het} = f_{AB} + f_{BA}$. Similarly, I will note $f_{hom}$ the frequency of all homozygotes. Therefore, $f_{hom} = f_{AA} + f_{BB}$.
Notation for allele frequency
Unlike the above, I will use a class notation here.
Let the frequency of the A allele be $p$ and the frequency of the B allele be $q$.
All genotype frequencies must sum to 1
Of course, if you add up the frequency of all types of individuals in a population, you should reach 1 (or 100% if you prefer). Per consequence,
$$f_{AA} + f_{AB} + f_{BA} + f_{BB} = f_{hom} + f_{het} = 1 $$
is our first important result.
Problem 1

There is 20% of heterozygote in the population, what fraction of the population is homozygote?

Answer: (hover to see the answer)

 $f_{hom}=0.8$ (or $f_{hom}=$80%)

Problem 2

There are 10% of AA individuals and 15% of BB individuals in the population, what fraction of individuals are heterozygotes

Answer:

 $f_{het} = 0.75$ (or $f_{het} =$ 75% )

All allele frequencies must sum to one
The same is true for the allele frequency, they must sum to one. This is even easier than before. Using the above notation it means:
$$p + q = 1$$
You will note that an obvious consequence of this result is that $1-p = q$ is also true. This is the second important result.
Problem 3

The frequency of alleles which are the A allele is 0.3. What is the frequency of the B allele?

Answer:

 $q = 0.7$

Hardy-Weinberg equilibrium
Let's now talk about HWr.
HWr assumptions
HWr makes a number of assumptions that I will not detail them here. Please have a look at the post Assumptions of Hardy-Weinberg rule for more information.
HWr exercice without explanations
Here are exercises that one may consider they come too early in my explanations. Don't worry too much if you can't solve them but please take the time to try solving them. Please do not try to apply known formulas about HWr, only use your logic and the above formulas (allele frequencies must sum to 1 and genotype frequencies must sum to 1)
Problem 4

In a population, one observes that 20% of the population is homozygote for the A allele and that there are no heterozygous individuals at all. What is the frequency of the A allele?

Answer:

 $f_{A} = 0.2$

Below is a drawing of the population (assuming N=20 individuals) to help understand the answer.
AA | AA | AA | AA | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB | BB
Problem 5

In a population, one observes that all B alleles are present in heterozygote only. The frequency of heterozygotes is 0.1. What is the frequency of the A allele?

Answer:

 $f_{A} = 0.95$

The hard part here is to first calculate $f_{B} = 0.05$. Let's draw the population (assuming only N=20 individuals) and that will likely help you out.
AA | AB | AA | AA | AA | AA | AA | AA | AA | AA | AA | AB | AA | AA | AA | AA | AA | AA | AA | AA
HWr formula
As said above, HWr describes a relationship between allele frequency and genotype frequency
Without much explanations, here are these relationships
$$f_{AA} = p^2$$
$$f_{AB} = pq$$
$$f_{BA} = pq$$
$$f_{BB} = q^2$$
Therefore,
$$f_{hom} = p^2 + q^2$$
$$f_{het} = 2pq$$
To build your intuition, you should try to consider for yourself extreme cases where one allele is fixed (fixed=reached a frequency of one). For example, what are the expected genotype frequencies when

$p=1$ and $q=0$?
$p=q=0.5$?
$p=0$ and $q=1$?

How HWr is often expressed
Mixing up the idea of the above relationships and the fact that all genotype frequencies must sum up to one, one can also write
$$p^2 + 2pq + q^2 = 1$$
As by definition $q = 1-p$, it is also common to replace write
$$p^2 + 2p(1-p) + (1-p)^2 = 1$$
Why do these relationships make sense?
Problem 6

Imagine you are drawing alleles in a population of alleles like you would draw cards from a deck of cards! You draw a single allele. If the frequency of A allele is $p$, what is the probability of drawing an A allele?

Answer:

 $p$

Similarly, the probability of picking a B allele is $q=1-p$.
Problem 7

Ok, now. Assuming that the fact that you already drew an allele does not change the allele frequency in the population (because the population is very large), what is the probability of drawing two A alleles in a row?

Answer:

 It is $p$ for the first draw and $p$ for the second draw. The overall probability is therefore $p \cdot p = p^2$

Here we go! You just solved why $f_{AA} = p^2$. You can apply the exact same logic to find out $f_{BB} = q^2$.
Now the probability to first draw a A allele and then a B allele is $pq$. Therefore, $f_{AB} = pq$. The probability to first draw a B allele and then a A allele is $qp=pq$ as well. Therefore, $f_{BA} = pq$.
Exercise
Problem 8

In a population with two alleles for a certain locus, A and B, the allele frequency of A is 0.7. What is the frequency of heterozygotes if the population is in Hardy-Weinberg equilibrium?

(You will note I renamed the alleles to match my above notation)
Try to solve this problem yourself now!
Answer:

 It is a given that $p=0.7$. The question is what does $f_{het}$ equals to?
 Let's start by calculating $q$. $q=1-p=0.3$.
Then, let's calculate the the genotype frequencies.
$f_{AA} = p^2 = 0.49$.
$f_{BB} = q^2 = 0.09$.
$f_{het} = 2pq = 0.42$.
Here we go! We've got the answer. Let's make sure the answer makes sense by summing up the genotype frequencies to ensure we get 1.
$f_{hom} = f_{AA} + f_{BB} = 0.58$
$f_{hom} + f_{het} = 0.42 + 0.58 = 1$
All good!

Problem 9

At a bi-allelic locus, the allele A is dominant over the allele a. The phenotype associated with the dominant allele is present in 10% of the individuals of the population. What is the frequency of the allele A?

Answer:

 The genotypes coding for the phenotype associated with the dominant alleles are AA and Aa. Therefore, $f_{AA} + f_{Aa} = 0.1$ and therefore, $f_{aa} = 0.9$.
 The frequency of the allele a is $p = \sqrt{f_{aa}} = \sqrt{0.9} ≈ 0.95$.
 To conclude the frequency of the allele A is $q = 1 - p = 1 - \sqrt{0.9} ≈ 0.05$

Problem 10
You will find a HW problem involving selection at this post.
Problem 11
You will find a HW problem involving a population of triploids individuals at this post.
Problem 12
You will find a HW problem for sex-linked loci at this post

In short...
Here is a summary for a bi-allelic locus
Allele freqs sum up to one
$$p + q = 1$$

Genotype freqs sum up to one
$$f_{AA} + f_{AB} + f_{BA} + f_{BB} = f_{hom} + f_{het} = 1 $$
You will note that most often when people write $f_{AB}$, they just mean $f_{het}$ and therefore don't make the distinction between $f_{AB}$ and $f_{BA}$.

Hardy-Weinberg rule
Note that Hardy-Weinberg rule holds only under a number of assumptions (such as random mating, panmictic population, no selection, ...) that I have not detailed here (see Assumptions of Hardy-Weinberg rule for more information).
$$f_{AA} = p^2$$
$$f_{AB} = pq$$
$$f_{BA} = pq$$
$$f_{BB} = q^2$$
Therefore,
$$f_{hom} = p^2 + q^2$$
$$f_{het} = 2pq$$

Putting all together
The whole thing put together is often expressed as
$$p^2 + 2p(1-p) + (1-p)^2 = 1$$


Question about the Derivation of the cable equation for neurites I read in Wikipedia how the cable equation was derived (here) and had a specific problem regarding one of its equation:
At the start of the derivation it states that we first need to pretend that the membrane is perfectly sealed (Rm=∞) and that the capacitance of the membrane equal zero. Then we can say that the change in voltage over distance depends only on the resistance of the axoplasm, by the equation:
 and from that, the current equal:
But later when they derive the last equation, , they set  as in the equation above, which seems to me incorrect, since the resistance of the membrane also affect  . What did I get wrong?
Thanks!

The part you are quoting is about helping you conceptualize the cable equation by starting from some approximations that let you remove most of the terms. See the sentence beginning (emphasis mine):

  To better understand how the cable equation is derived, first simplify the theoretical neuron even further and pretend...

They then walk you through how, because these approximations are just pretend, one needs to include terms to account for the actual permeability and capacitance of the membrane. This means that you do not have a constant internal current with distance as you travel along; instead, the current decays with distance because of leak through the membrane and membrane capacitance.

This is what the last equation you quote from says: the change in internal current over distance x (written as dil/dx) is equal to the current lost to the membrane, which includes two parts: leak through the membrane (V/rm) and charging the membrane capacitor (cm*dV/dt).

Another correction that might be tripping you up: you write

  change in voltage over time

in your question, but that is not what the equations are representing, they are representing change in voltage over distance x.


Why does it matter to predict protein structure? And how do you predict it ? What is your input data (sequence of amino acids, temperature, pH, ...) ? Is there a "standardized" input that scientists agree on ?

Moreover, I've read that knowing the structure of a protein helps predicting its function, but is the prediction [Structure -> Function] reliable ? Should't we predict directly the function if that's our interest (I don't mean we should not take into account predicted structure, but I don't understand why the structure IS the purpose instead of the function)
I also read the structure helps predicting affinities with other proteins and how it will bind : same question here, is this prediction [Structure -> Affinity] reliable and why don't we predict directly affinities.

To sum up a bit, I have the impression that the structure in itself is not important to know except that it is a good predictor of other protein properties (like function of affinity) and that the structure is kind of an 'intermediate' ? What am I missing ?

How do you want to predict function and binding partners without knowing how your protein looks like? The sequence itself contains only limited information. Similar sequences might fold into similar structures with similar functions. These motifs can be used to transfer your knowledge from one protein to another, which might have similar e.g. binding abilities. But the motif might be nonfunctional in the second protein, because it is hidden in an inaccessible part of the protein due to its folding structure.

Interactions between proteins are weak compared to intramolecular bonds and dynamic. Different amino acid side chains have different characteristics (like polarity, hydrophobia etc.) which make specific interactions possible. Specific amino acids have to be accessible and while they might be far apart in the sequence, the folding of the protein brings them close together in its final shape.

Even small modifications like phosphorylation can alter the structural conformation significantly and e.g. change the enzymatic activity. Therefore, for analyzing protein function, finding binding partners or designing binding compounds (drug development), we need to know its three-dimensional structure. With the structure you can simulate binding affinity/dynamics. Scientists also try to resolve the protein structure in its different states to clearly see the differences.

Keep in mind that complex diseases can be caused by a single mutation, which exchanges only a single amino acid in the sequence but can have severe implications for protein function. Knowing the structure, the position of the amino acid and how the change affects the characteristics of the protein domain (e.g. charge), we can fully understand what's happening on the molecular level.

Since it is far from trivial to analyze the structure of a protein, predictions bridge the gap for functional predictions until the molecular structure of the protein has been reconstructed. But only with atomic resolution you will be able to properly identify interactions.

The question of how to do structural prediction might be beyond the scope of this answer. Pubmed lists around 400 papers each year on this topic. Depending on the amount of information you have about the protein or its family members (proteins with very similar sequences), you can use other known structures to predict an unknown structure:

https://medium.com/@HeleneOMICtools/a-guide-for-protein-structure-prediction-methods-and-software-916a2f718cfe


Current human behavior as a genetic heritage People: I have doubts about genetic heritage, but let me explain the context which has shown up this doubt for you: I was debating about sexism and the following question were put on the discussion: What kind of behavior, most of them come from men, is cultural and social, and what is a genetical heritage from our ancestry? Because I have a feeling that plenty of these behaviors that can be considered, maybe not correct, but at least justifiable. If you have some literature about this subject I would greatly appreciate it.

All phenotypic traits have some part of the variance which is explained by the environment and  some part that is explained by the genes. The heritability is then defined as:

$$H_N = \frac{V_{genetic}}{V_{phenotype}} = \frac{V_{genetic}}{V_{genetic}+V_{environment}+V_{interaction. gene.environment}}$$

where $V_{genetic}$ is the Variance in phenotypic traits due to genes, $V_{phenotype}$ is the total phenotypic variance, $V_{environment}$ is the variance due to environment and $V_{interaction. gene.environment}$ is the variance due to interaction between genes and environment.

So your question (if I understand it correctly) should rather be a list of phenotypic traits (behavior) and ask what is the heritability of each trait in the world-wide human population (or on a given subset of the human population).

I think, there is no objective manner of defining a given phenotypic trait. You should chose subjectively, some behavior, define it accurately and then ask the question what is it's heritability.

Moreover, it is quite hard to measure a behavior. It is much easier to estimate the heritability of height in humans.

There are several different methods in order to estimate heritability of a trait. See this wikipedia article

Some of these experiments are not feasible on humans for ethical reasons. Some others are quite limited and are quite expensive. I don't think we have many studies that quantify the heritability of behavioral traits in humans but I might be mistaken.

As said by @AlanBoyd, there is a field called evolutionary psychology that deal with this kind of question. To my knowledge this field is mostly a purely theoretical field and therefore, it does not quite allow to measure heritability.

A good start into this science would be the wikipedia article which seems quite complete.  I can give you some books but I haven't read most of them. Here and here are introductory books in the field. I think this book is a classic in the field. I read this book and it is quite interesting. There are actually many books in this field. The best think you can do is maybe to typewrite "evolutionary psychology" in amazon.

As a sidenote: If you enter in the field of evolutionary psychology you might as well be interested by memetic evolution (evolution of culture). Here is a classic book on the subject.

Be careful in these fields, I think that some ideas do not deserve to be considered as part of science while other do!


What type of immersion oil should I buy? I have an old Nikon Alphaphot microscope that came with a 100x oil immersion objective, but no manual. I've seen plenty of sources that explain that you need to place a drop of oil between the slide and objective, but when I went to order immersion oil I discovered that there are several different types. There's Type A, Type B (apparently similar to Type A but more viscous), and a number of specialty types. My plan is to use the microscope for projects like looking at blood cells, pond water, and other high school science project-type investigations?

Which type of immersion oil is right for all around, general purpose use?

For the best image (where you lose the fewest photons and get less refraction), you want the immersion oil to have a refractive index as close to the refractive index of the coverslip you intend to use.  In my experience, this is not much of a consideration on the oil-side, but rather on the coverslip-side.

There is little difference between type A and B oil, although for other types of oil see here.  If I were you, I would just use some type A.

For a lesson on the impact of immersion oil on optics, see this Zeiss website (similar sites for Nikon and other scope manufacturers exist too I'm sure!)


Continuous (yeast) culture system satisfying multiple criteria There are multiple ways yeast cells can be grown in liquid cultures.

Batch cultures are easy to prepare but cell density, medium composition and physiology change over time
Chemostats allow to maintain cells in physiological steady-state, but growth rate is limited by nutrient availability
With a turbidostat, cell density is kept constant and cells can grow at their maximal rate, with excess of nutrients, but medium composition changes over time
Cells in a microfluidics chamber can attain maximal growth rate with constant conditions, but with extremely low numbers.

I cannot think of a way to get (a) maximal growth rate, (b) constant medium composition, (c) constant cell density and (d) a decent culture volume (>50 mL). Am I missing something?

A chemostat should satisfy your criteria.
The cell mass balance around a chemostat is the following (assuming no biomass in the feed):
$$F-FX+V_RX\mu_g-V_Rk_dX=V_R\frac{dX}{dt}$$

At steady state there is no change in parameters with respect to time so we set the derivative equal to zero. If we also assume that the death rate ($k_d$) is negligible (for example cells in exponential/log phase) and let:
$$D=\frac{F}{V_R}$$

Where $D$ represents the dilution rate (how quickly the volume in the tank is being replenished). Then rearranging the above equation you get:
$$D=\mu_g$$

This says that the growth rate will be equal to the dilution rate. In other words you can set how fast the cells grow by modifying the flow rate and/or volume of the tank. But there is a limit. Cells grow as fast as they can use the limiting nutrient ($S$) and this relationship is often modeled as:
$$\mu_g=\frac{\mu_mS}{K_s+S}$$
Where $\mu_m$ and $K_s$ are unique parameters for every cell type. $S$ is the concentration of the limiting substrate in the tank (which is also equal to the concentration of the substrate in the outlet stream). The maximum growth rate is $\mu_m$ and if the dilution rate is higher then this value, the cells get washed out of the chemostat. This can be troublesome if you need a flow rate higher than $\mu_m$. In this case a recycle is useful.

To answer your question in the comments regarding medium composition. You probably want to operate at steady-state. Steady state means that there is no change of parameters with respect to time. So if you write the substrate mass balance:

$$FS_0-FS-V_RX\mu_g\frac{1}{Y_{\frac{X}{S}}}--V_RXq_p\frac{1}{Y_{\frac{P}{S}}}=V_R\frac{dS}{dt}$$

And set the derivative to 0. Then you will find the outlet substrate concentration is a function of other constants (biomass, volume, product yield, etc.). You're right in that some substrates get used more than others, but when steady state is reached. They stop changing and the medium composition stays constant in the vessel.


The genetic and physiological origins of laughter? This Wikipedia article  defines laughter in many terms, such as...

  "a visual expression of happiness, or an inward feeling of joy"

and

  "a part of human behavior regulated by the brain, helping humans clarify their intentions in social interaction and providing an emotional context to conversations".

Note: the emphasis was added by myself.

The article also states that laughter is "probably genetic", and that

  "Scientists have noted the similarity in forms of laughter induced by tickling among various primates, which suggests that laughter derives from a common origin among primate species."

According to this report which the Wikipedia referenced, the expression of laughter in general is present among other great apes. Phylogenetic trees were reconstructed to represent the evolution of this trait among primates (which concludes that the ability to laugh must have a genetic basis, at least to some degree).

Note: I also found this WikiAnswers post, but it clearly can't be that reliable.

A search on the OMIM database yielded this result, where children with Angelman syndrome were characterized with "excessive laughter", this result, in which Charles Bonnet syndrome was characterized with "inappropriate laughter", as well as many other genetic mutations which resulted in some sort of uncontrollable laughter.

I understand that laughter is a complex psychological expression of emotion likely associated with more abstract thought, and that there simply can't be "a laughter gene", but my question is:

Is there any known genetic or physiological origin of laughter? What is biologically different in great apes which allows for laughter, in comparison with a panoply of other animals? I'm looking for more of a molecular answer rather than an ecological or psychological one.

I recommend this article: The Evolution and Functions of Laughter and Humor: A Synthetic Approach by M Gervais and DS Wilson, 2005, University of Chicago Press.

For your question about the origin, firstly they explain that all laughter is induced by stimuli which are unexpected or unpredictable, experienced in a non-serious (unthreatening, safe) context. Given examples include peek-a-boo, which can make a child laugh but also cry if the child is not perceiving the situation as safe. Also that we can't tickle ourselves and tickling is induced by stimulating vulnerable body areas. Similarily, apparently in apes laughter is mainly induced by "tickling in conjunction with mock aggression and chasing".

They explain the function of (Duchenne, that is stimulus-driven "honest" as opposed to voluntary) laughter to be propagation of "positive affect" in a group, as it utilises the chameleon effect (it is contagious) which apparently has been shown to exist for its "cooperative value". Other studies seem to have shown that a) we are thirty times more likely to laugh in a social context than by ourselves and b) the contagiousness of laughter response increases with group size, making it an efficient tool for coordinating a group and getting everyone into the same emotional state.

As for other animals, the article doesn't address that. It does seem like a different question to me so I would consider separating that into a second one.


Suspensory ligaments: why are they ligaments? Don't ligaments connect bone to bone? In the eye for example, the suspensory ligaments connect the ciliary muscle to the lens, which obviously aren't bones. Is this just one of those instances where the terminology isn't that precise and you just have to memorize the exception?

"...The suspensory ligaments connect the ciliary muscle to the lens..."

You must be referring to the Zonule of Zinn (Such a great name).
You are absolutely correct, the definition of Ligament varies across texts which can create confusion.
For example:
Merriam-webster:
A tough fibrous band of tissue connecting the articular extremities of bones or supporting an organ in place.
Wikipedia:
A ligament is the fibrous connective tissue that connects bones to other bones.


What is possibly wrong in my gel electrophoresis when I didn't see bands of DNA ladder on gel? What was possibly wrong in my gel electrophoresis when I didn't see bands of DNA ladder, and genomic DNA sample on gel ? I could see bands of genomic PCR and RNA solution.

Edit

Thank you all of guys for sharing your opinions. From some opinions, I found out the possible error that my genomic DNA didn't show up because it was not pure (I forgot the detail that our group used a sample of DNA which was extracted from a previous lab and we didn't obtain an expected ratio for the purity of DNA. Then, we also used the impure DNA sample to do PCR, and finally used the amplified DNA for gel electrophoresis lab). However, the reason for DNA ladder didn't show up I'm not sure. I just can suppose that my groupmate who handled with DNA ladder solution possibly contaminated it.

Possibly You don't mix ladder containing microtube by Sampler. You should slowly Fill and emptying Sampler for several times when pick it for use, mix it well, but do it without creating a bubble.one more thing, check your ladder by "NanoDrop"


Are mutations the cause of alleles? For example, some leopards have a mutation which causes black fur. So Black fur and normal fur colour (orange-white) are both alternate forms of the same gene, right? So does that mean that mutations cause alleles?

Thanks

That's correct. Alleles are alternate forms of a gene that occur at the same locus and arise by mutation.
Another example might be sickle cell anemia where a SNP (a single base change) is the cause of the disease.