Why is urobilinogen reabsorbed from the gut just to be excreted via the kidneys? The Wikipedia article on Urobilin states:

Bilirubin is... excreted as bile, which is further degraded by microbes present in the large intestine to urobilinogen... Some is reabsorbed into the bloodstream and then delivered to [the] kidney.

This process is puzzling to me since it doesn't mention any function or reason for urobilinogen to be absorbed into the body, aside from it being there so it can be removed by the kidneys.
The only reasons I can speculate are that:

Urobilinogen shares a transporter/receptor with a similar, useful compound.
It has a direct useful function when in the bloodstream, not mentioned on the wikipedia article or a few other sources I've skimmed.
High urobilinogen is harmful to the gut and it's necessary to remove it via the blood to the kidneys.
Urobilinogen is inherently able to diffuse across the intestinal barrier into blood as a result of its chemical structure

Is it one of the above, or some other reason I haven't taken into account?

I think that it is missing some details. Note that the vast majority of urobilinogen (~80%) is actually eliminated via fecal elimination. I would recommend looking at the article on enterohepatic circulation, which provides more context on this issue. Basically, bile salts can be useful (even or especially after metabolism by bacteria), so a fraction is reabsorbed by the large intestine and then dumped back into the digestive system:

However, just like bile, some of the urobilinogen reabsorbed is resecreted in the bile which is also part of enterohepatic circulation. The rest of the reabsorbed urobilinogen is excreted in the urine where it is converted to an oxidized form, urobilin, which gives urine its characteristic yellow color.

...

The net effect of enterohepatic recirculation is that each bile salt molecule is reused about 20 times, often multiple times during a single digestive phase.

Obviously urobilinogen isn't one of the salts recirculated that much if most of it gets excreted in feces, but apparently it still happens (possibly just because it is chemically similar to the other bile salts, as you suggest).
I think that the mechanism which is emphasized in the urobilinogen wiki page is a secondary mechanism for excretion when urobilinogen is at toxic levels in the bloodstream (e.g. jaundice). These high levels come for example from blood breakdown as pointed out in the article, which may be emphasized because it is a common medical issue (which is of course not a focus of SE Biology).
So, in other words, the wiki article is targeted towards the potential medical problems (toxic levels requiring elimination via kidney) rather than the normal physiology (mostly eliminated in feces, sometimes-useful salt that helps digest stuff), possibly leading to confusion. This flash card resource succinctly notes the functions of bile salts such as bilirubin and its derivatives and may be helpful for other basic info:

Functions:
(1) Digestion and absorption of lipids and fat-soluble vitamins
(2) Cholesterol excretion (body's only means of eliminating cholesterol)
(3) Antimicrobial activity (via membrane disruption)

More about (unfortunately medical focused) physiology of bilirubin etc. can be found here.


Interspecies competition and pathogen Following my answer to this question, a debate ensued on whether the loss in population of one species (namely red squirrels) due to its lesser resistance to a pathogen brought by a competing species (namely squirrel parapoxvirus and grey squirrel) should be labelled as a result of interspecies competition or not. Here I will try to state it as a question with in a more general setting. I'll give my own answer to it, and would welcome other views on the issue.

Assume the following: Species $A$ lives in a closed ecosytem and has reached carrying capacity $A=M_A$. At time $0$, a new species $B$ is introduced which is in competition with $A$, and additionally bears a pathogen to which it is resistant but which causes a high lethality rate in $A$.

It is observed that $A$ dimishes while $B$ thrives. Can we necessarily ascribe it to interspecific competition?

No, you cannot for certain ascribe it to competition, without further information. The mediation by a pathogen is similar to the effects on prey species that are indirectly caused by shared predators (e.g. Prey B increase -> Predator X increase -> more predation on Prey A). Such effects, which can be tricky to separate from direct competition, are usually called apparent competition (see e.g. the classic paper Holt. 1977. Predation, apparent competition, and the structure of prey communities. Theor Popul Biol 12).

However, to some extent, the terminology used may depend on what you view as "the environmental background". All species have lots of adaptations to certain aspects of their living environment, and these naturally differ between species. Some might be more resistant to a certain pathogen (of to drought or other abiotic factors), but this might trade-off against other traits. I that respect, you might view species B as outcompeting species A in a certain environment (e.g. in the presence of the pathogen). However, since you specifically know about the pathogen (which is the focal point of the question), and that species B will probably function as a host/source population of the pathogen, I think it is more useful and informative to label the effect as apparent competition. To partition the direct and indirect effects you will however need moe information.


Is it possible to cultivate cheek epithelial cells in a non-CO2 incubator? CO2 is important for maintaining constant pH in cell culture. Unfortunately, I do not have access to such incubator and buying a new one is expensive. I found a cheap incubator online, but it doesn't support CO2. I'd like to ask if I can cultivate cheek epithelial cells in such incubator and if it won't negatively affect my cell culture. Another option is building a small CO2 generator inside the incubator. I made some calculations - I know how much CO2 I need to generate, how many grams and mL of solutions I need, moreover the build-up pressure is so small, it should not negatively affect the incubator.

L-15 media does not require a CO2 atmosphere and according to Sigma-Aldrich this media is suitable for primary explants of adult human tissues.


Book request: systematics and evolution of vertebrates Would you recommend any good vertebrate systematics & evolution book?

The main goal is to teach a Master's level class - mostly focused on amphibia, reptiles and fish.

I really like Liem et al.'s Functional Anatomy of the Vertebrates: An Evolutionary Perspective.


How can the child and the mother have different blood types? As far as I know the fetus is fed by the umbilical cord which basically connects his/her circulatory system with the mother's in order to supply oxygen and nutrients. But how is this possible if they (the mother and the fetus) have different incompatible blood types?

It is possible that the father has A blood type, the mother B and the child A and thus incompatible with the mother's.

The blood of the fetus does not mix with the blood of the mother.  Instead, the placenta provides a system where the two separate blood streams flow past each other with thin separation allowing nutrients to flow between the two streams but the not the blood cells and other large components.


plant crossing for creating breeding population I read some material about plant breeding. For a self-incompatible plant with high heterozygosity, it said that after selecting the plant population based on phenotype/desired trait, a cross was done among plant with the desired trait to create the breeding population. However, as far as I know, the breeding population was usually phenotypically selected for desirable traits. I'm not experienced in this field, could you please kindly explain to me why crossing is conducted for creating breeding population?

Thanks in advance

A cross was done among plant with the desired trait to create the breeding population. The breeding population was usually phenotypically selected for desirable traits.

That phrase is confused. To phenotypically select from a breeding population, you first have to generate the breeding population, which requires an initial cross of desired plants. The generations are generally labelled as F1 F2 F3 and checked for statistics. They can back-cross the mother plant onto herself. The selection refines itself as the number of crosses of the most desirable plants increases in generations.

Hybrid populations are often stronger and have a wider gene base, so if you want big fruit for a tree, you can cross an asian one with a european one, it might be more resistant and vigorous, gain stronger roots, better low N performance, and better structre from one plant, which is then mixed with the desirable traits for example of yield or mould resistance. The wider the gene base, the more potential diversity of individuals can be chosen which also contain the alleles from the desired traits, and the selections start with more options. The goal is to maximize the desired pheno's.

http://www.nature.com/nature/journal/v537/n7622/full/nature19433.html?foxtrotcallback=true


Why is the thalamic reticular nucleus called a nucleus? In the Wikipedia article on nuclei I read:

  A nucleus is one of the two most common forms of nerve cell
  organization, the other being layered structures.

Is there a specific and plausible reason, why the  thalamic reticular nucleus is called a nucleus, even though it is - anatomically - a layer?

Has the TRN once been a somehow spherical nucleus and evolved into a two-dimensional layer? Or does the TRN play a functional role that normally nuclei play, but not layers?

The thalamic reticular nucleus (TRN) is a thin layer of GABAergic cells adjacent to the thalamus (Fig. 1).  Because of its strategic location between the thalamus and cortex, the TRN is often suggested to be important to attention and regulation of information flow between the thalamus and cortex (Lam & Sherman, 2011).

A nucleus is defined as a

  [p]ortion of tissue that are compact accumulations of neurons having roughly similar connections and functions

Reticular is defined as

  A fine network or net-like structure.

So reticular nucleus translates itself as a net-like accumulation of neurons.

In contrast to the wikipedia meaning, therefore, I interpret nucleus as more of a cluster of functional organizational units rather than a morphological characteristic of that cluster per se.

Fig. 1. Thalamic reticular nucleus. source: Dana Foundation

Reference
- Lam & Sherman, J Neurosci (2011); 31(18): 6791-9


When does Coelom form exactly? Related to my other question.
I know that the coelom is derived from mesoderm.

Coelom seems to form during organogenesis within 3rd and 8th week of embryogenesis.
However, that answer is not either enough exact or it is wrong.

I am reading the thing in Kimball 5e and Gilbert 9e, but cannot find an exact mention about the thing. I know for sure that the coelom develops within gastrulation and organogenesis, since it is forming from mesoderm.

When does coelom form exactly?

In humans, the coelom forms by the splitting of the lateral plate mesoderm, which occurs during weeks 4-5 (Sweeney, 1998).

Sweeney, LJ. 1998. Basic Concepts in Embryology. McGraw-Hill.


What sequences are between adjacent genes? The human genome has a lot of non-coding regions, which include regulatory elements, repetitive DNA, and introns. Suppose there are two adjacent genes on a chromosome, and their positions on the chromosome are, say,

For the first gene: 11,785,723 to 11,803,245 bp.

For the second gene: 11,806,096 to 11,806,143 bp. These values include their regulatory elements, promoter and introns as well.

So what sequence is present between bases 11,803,245 and 11,806,096? Are they satellite sequences? Is this non-coding, non-regulatory region 11,803,245 to 11,806,096 bp heterochromatin?

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

In short, there can be functional and/or non-functional DNA in-between the transcribed regions.

Repeat regions need not be heterochromatinized and conversely not all heterochromatic regions consist of repeats.


What is this flying bug in Denver, CO? It seems to be a flying insect about 2-3mm in length. It also doesn't seem like it's very good at flying. They seem to crawl around my desk until I try to hit them, which is when they'll start flying.

Location: Denver, Colorado, USA

They seem to come out more at night.

These are Scuttle Flies (Order Diptera, Family Phoridae) (the wing venation, best seen on the lower left individual of the top photograph, is characteristic); the group has several hundred species in America north of Mexico.  So far as I am aware, the generic key in Manual of Nearctic Diptera, Volume 2 (available online here, pages 25 to 48) will still yield useful results, but cannot be used on these photographs.  The 30 pages in bugguide.net's gallery (starting here) eliminate a few of these, but not nearly enough to go further on the evidence we have.


What animal / bird can be heard in this evening sound recording from Western Washington, USA? We heard this animal outside in Western Washington (Port Townsend area) during the late evening. I think it is a bird, but it honestly sounds sort of like some creepy woman singing or something. The audio is linked below. The sound (in the audio) was repeated for a long time at random intervals averaging probably every ten seconds.

https://clyp.it/tzybty1w

Anyone know for certain?

I asked the same question on another forum here: http://www.birdforum.net/showthread.php?p=3454684.

It looks like another possibility is a barred owl. It also sounds somewhat similar.


What is the formula to establish ec50 reproducibility with respect to dose response curves for some drug? The EC50 is determined by fitting a standard curve to the experimentally obtained control values for each dose response curve using some software that does trial and comparison until satisfactory(nonlinear regression).

In the literature, it is mentioned that experimentally obtained control values for the dose response curves, are EC50 reproducible. To my current understanding meaning that EC50's obtained for different for several dose response curves are actually 'close enough'(in some formal statistical sense) together. Is there some procedure or formula for formally establishing EC50 reproducibility?

Thank you :)

The different models that can be used to fit the curves do differ.  The linked paper and this website outline the differences; the discussion revolves around an R package called DRC but much of the information is generally applicable. Modelling can also be used to estimate ED50.

The parameters and models that are being used need to be consistent with the biology that is being studied. If it's appropriate, scaling the upper and lower bounds of your data can improve the consistency of ED50 estimates as this removes the requirement for the model to estimate those parameters. Something like this can be used for scaling;

(VALUE - topdrugmean)/(nodrugmean-topdrugmean)

The Akaike Information criterion can be used to measure the goodness-of-fit for different models (see the preceding links).


If targeting a certain daily water intake, do you have to compensate for beverages that promote diuresis? Please forgive my ignorance on the topic and I hope this is a "on topic" question here. It was a toss up between this SE and Physical Fitness SE but I want a more scientific answer.

I came at a impasse in a conversation with another fitness enthusiast. They stated that if you are targeting your water intake during the day then drinks with a diuretic effect (tea/coffee) count negatively towards that water intake total.

So, is it true that one should over-compensate if drinking these diuretics? Or does the water content of drinks like coffee and tea balance out or even positively hydrate you?

The notion that tea and coffee are diuretic and don't count in your daily waterbalance, is an urban myth. At most, both are mildly diuretic (if any).

The assumption is based from an old study from 1928 with only three participants. While the small number of participants alone is a good reason to reject the study (it would never get published today) because the findings would lack any statistical power, the design is also questionable. You can find this story in reference 1 if you want to read it.

It is known that large amounts of caffeine indeed have a diuretic effect by increasing the blood flow to the kidneys and inhibiting the reabsorption of sodium. This leads to the outflow of water and an increased production of urine. See reference 2.

However, reference 3 found that this diuretic effect (which is only present at high concentrations of caffeine) diminishes due to tolerance when people regulary drink tea or coffee. They do not see any diuretic effect from normal tea, coffee or caffeinated beverages.

The explanation for this effect is most likely a misinterpretation of our observation. We seem to produce more urine when we drank tea or coffee, but we wrongly compare it to a time when we drunk nothing. If we would compare it with a time, when we drank the same amount of water, the effect (you have to pee more when you drank something) would be the same.

Drinking tea and coffee will therefore help to keep our waterbalance, as would water, juice or softdrinks.

References:

TOLERANCE AND CROSS-TOLERANCE IN THE HUMAN SUBJECT TO THE DIURETIC
EFFECT OF CAFFEINE, THEOBROMINE AND THEOPHYLLINE
Caffeine and the Kidney: What Evidence Right Now?
Caffeine ingestion and fluid balance: a review.


Explanation of the ‘cherry red spot' in Tay Sachs disease In Tay Sachs disease, a hallmark symptom is a cherry red spot in the macula of the eye surrounded by a halo of white.

I understand that the ganglion cells, which are higher in numbers around the macula rather than in the macula, accumulate gangliosides due to the hexosaminidase deficiency, and thus cause the surroundings of the macula to appear white, but I don’t understand why the macula is red.

It is said that in Tay Sachs disease, the macula is the only normal region of the eye, but isn’t the macula supposed to be yellow, as it is referred to as the yellow spot?

Moreover, I’ve read that the red color comes from the choroid blood vessels, but isn’t the choroid black? It contains blood vessels, yes, but it is pigmented. The hindmost layer of the retina also happens to be a pigmented epithelium. So what is the explanation of a cherry red spot?

Short answer

The fovea centralis is colored red in both the healthy retina and Tay-Sachs affected retinae. The macular region around the fovea has a yellowish hue. You are confusing fovea and macula in your question.
The reddish hue from the fovea comes from the well-vascularized choroid layer below. The choroid is not black, it is colored red due to the presence of many blood vessels. You are confusing choroid with the retinal pigment epithelium, which is indeed black.

Background
The macula includes the fovea at the center, also called the fovea centralis, which forms the very center of the retina. The macular region around the fovea includes the perifoveal and parafoveal areas. The macular region around the fovea has a slight yellowish appearance to it due to yellowish pigments present in the cone axons (Fig. 1) (Kolb, 2012).

Fig. 1. Healthy retina. The macular region is seen in the center, The parafoveal region has a slight yellow/orange hue to it. Note that the landmark yellow circle at 4 o'clock, with the vessels sprouting from it, is the optic nerve head. source: Webvision.

Below a Tay-Sachs affected retina showing the hallmark cherry red spot (Fig. 2):

Fig. 2. Tay-Sachs affected eye. The fovea centralis appears red. source: Prezi

The only normal part is the fovea centralis, appearing in its native red color, i.e. the cherry red spot.

The choroid plexus is well-perfused and is, therefore, red. You are confusing it with the pigment epithelium, which is pigmented (Fig. 3).

Fig. 3. Layers of the eye. RPE = Retinal Pigment Epithelium. source: Retina Eye Specialists

Reference
- Kolb (2012), Simple anatomy of the retina. In: Kolb et al. (eds.), Webvision. The organization of the retina and visual system. Salt Lake City, UT, Moran Eye Center


Is NADPH unstable in UV light? I am working on an enzyme activity assay using NADPH as a cofactor. The MSDS for NADPH Tetrasodium Salt, tells to store it in a place away from heat and light. Does this include UV light or just visible light? I was told that a pure NADPH stock solution (with pH 7 phosphate buffer as solvent) could be re-used after absorbing UV light at 340 nm, but based on my understanding of the MSDS it seems that shouldn't be the case. So my question is: could I reuse a sample of pure NADPH stock solution that was exposed to UV for my enzyme activity assay?

In my experience, reuse of NADPH stock solutions maintained at pH 7.0 or above is perfectly acceptable. Taking an absorbance spectrum every half-hour or so will probably show that definitively.  However, NADPH is VERY unstable in acid, leading to a 'bleaching' of the absorbance at 340nm.  Try measuring a rate at pH  6 or below, 340nm,  with 100 micromolar NADPH and no enzyme or cosubstrate. There will be a very significant decrease in absorbance with time (ie a 'blank' rate) which will make estimation of enzymic reactions at low pH virtually impossible.


Why do we use DNA sequencing methods such as shotgun? I am learning about DNA cloning for the first time. What I understand is that, in order to clone DNA, we break-up the original gene into shreds. Then try to piece it back together.

Why exactly do we do this? Instead wouldn't it be better to clone one base at a time? Basically in pseudo code:

old_dna_strand = 'ACTCATGCGAGCGTCAGTAGTACGTACTG'
new_dna = ""
for base in old_dna_strand:
    new_dna+=base

That looks a lot more easier and a lot less prone to errors. Why do we have weird methods such as shotgun?

Thanks in advance. Let me know if i should clarify or update anything in this question.

This is a technique from the "old time" of genome sequencing. The underlying method for sequencing is the Sanger chain termination method which can have read lenghts between 100 and 1000 basepairs (depending on the instruments used). This means you have to break down longer DNA molecules, clone and subsequently sequence them. There are two methods possible.

The first is called chromosome (or primer) walking and starts with sequencing the first piece. The next piece of DNA (which is  and then uses a specific primer from the end of the sequence. The next (contigous) piece of the sequence is then sequenced using a primer which is complementary to the end of the first sequence read and so on. This technique doesn't require much assembling, but you need a lot of primers and it is relatively slow.

To overcome this problem the shotgun sequencing method was developed. Here the DNA is broken into different pieces (not all broken at the same place), cloned and sequenced with primers specific for the vector used for cloning. The leads to overlapping sequences which then have to be assembled into one sequence on the computer. This method allows the parallelization of the sequencing (you can prepare a lot of sequencing reactions at the same time and run them) which makes the process much faster and also avoids the need for sequence specific primers. The problems are to sequence repetitive sequences, as overlaps are not as clear here. To resolve this problems a first draft is made and then critical regions are resequenced using other techniques as primer walking. Have a look at the Wikipedia page about shotgun sequencing if you want to read more details.


Random Mutagenesis vs Directed Evolution as Strategies to boost expression Do people use random mutagenesis (say using UV) to generate host variants that have high expression of a metabolite / enzyme? I've seen it mentioned as a strategy but it confuses me as to why.

How does that compare to using Directed Evolution for the same purpose? Intuitively, random mutagenesis seems highly inefficient (since you have no control over which genes you mutate) given the combinatorial explosion even in something like E Coli's genome size. Am I making a mistake in this reasoning?

What are situations where one may prefer random mutagenesis over directed evolution? Are there any pros and cons to consider?

Well, you already mentioned it. Random mutagenesis (with UV or chemical mutagens) targets the entire genome and you select the organism for certain traits.

In a directed evolution experiment, you are just targeting a gene or a group of genes. With the progress of synthetic biology, it might be possible to synthesize small genomes (already shown by Craig Venter and group) and apply directed evolution methodology genome wide. This would still not be considered directed, as the mutations are actually random over the genome.

The pros and cons depend on what exactly you aim to do.


Why do NK cells not destroy bacteria, even though bacteria don't have MHC-I? Part of the function of NK cells is to destroy cells that are unable to bind their KIR receptors. Or in other words, cells that don't express MHC class I. This is why they can kill MHC supressed infected- or tumor cells, which other immune cells can't.

However bacteria also don't express MHC-I. Yet NK cells are said to have very limited influence one microbial infections. I do not understand why NK cells do not degranulate (kill) bacteria upon finding that they do not have the MHC-I receptor complex.

Could someone elaborate this?

While you’re correct that NK cells are often activated (in part) by the absence of MHC-I, they require other signaling events to become fully activated:

  The Molecular Mechanism of Natural Killer Cells Function and Its Importance in Cancer Immunotherapy. Paul & Lal. Frontiers in Immunology. 2017.

  Activating Receptors on NK Cells

  Lack of MHC class I on the target cell is not sufficient to trigger NK cell activation. Full NK cell activation also requires recognition of stress-induced molecules by NK cell activating receptors.

  Natural cytotoxicity receptors (NCRs) are another immunoglobulin superfamily of activating receptors that utilize extracellular immunoglobulin-like domain for ligand binding. Human NK cells express three distinct types of NCRs... NCRs recognize a wide variety of ligands on target cells ranging from viral, bacterial and parasite proteins to molecules from tumor cells and other host cells.

  Role of natural killer cells in antibacterial immunity. Schmidt et al. Expert Review of Hematology. 2016.

  6 Bacteria fight back and inhibit NK cell activities

  During evolution, many bacteria have developed survival strategies which counteract NK cell activity.

  Both Gram-positive bacteria such as Streptococcus pneumoniae and Gram-negative bacteria such as Salmonella spp and Escherichia coli are able to induce prostaglandin E2 (PGE2), which negatively affects NK cell functions at different levels. PGE2 inhibits the cytolytic activities of NK cells by suppressing their responsiveness to cytokines such as IL-12 and IL-15, and suppresses NK cell mediated activation of macrophages by inhibiting the production of IFN-γ. Similarly, PGE2 has a deleterious effect on homing, migration, and survival of NK cells, as it has been shown in Human Herpes Virus 8 (HHV8) infection.
  Thus, bacteria are able to inhibit both cytotoxic and immunoregulatory effects of NK cells in various ways.

  8 Conclusions

  In conclusion, there is a growing body of evidence that NK cells play an important role in the antibacterial host response. NK cells are able to kill bacteria directly, or to modulate the immune system via cytokines and interferons. Further studies are needed to characterize how NK cells are activated by different bacteria. In addition, the role of NK cells among the other arms of the immune system in the defense against bacteria is poorly understood. Last, bacteria are able to inhibit NK cell activities, and a better understanding of this impairment may be the basis to specifically strengthen the antibacterial host response. Therefore, additional in vitro and in vivo data may open new therapeutic strategies using NK cells to fight bacterial infections.

If you’d like a full-text copy of the Schmidt paper, I can share it with you.


Why don't phosphatases both add and remove phosphate groups if enzymes catalyze reactions in both directions? We know that Phosphatase is a type of enzymes that removes a phosphate group.

Why can't phosphatases add a phosphate group if we know that all enzymes reactions are reversible ?

I think the description of enzymatic reactions as 'reversible' is potentially a bit misleading. It might be better to think of enzymes as agnostic to reaction direction.

The big missing piece is the difference in free energy of the reaction itself. Reactions that remove a phosphate group are energetically favorable in biological conditions. A phosphatase will effectively never add a phosphate group back because one would have to supply additional energy to make the reaction proceed in that direction.

Phosphatases catalyze a reaction that results in a free phosphate ion. However, kinases that add phosphate groups are catalyzing quite a different reaction, where a phosphate group is lost from a molecule of ATP which becomes ADP. This reaction is also energetically favorable, and the reverse reaction does not occur.


Why is second pKa value of phosphoric acid different across different sources? Am I missing something very fundamental here for phosphoric acid's second pKa value?

I check the Wikipedia page and these are the values: (1) 2.148, (2) 7.198, (3) 12.377
Then I check Sigma-Aldrich website and it says: (1) 2.15, (2) 6.82, (3) 12.38

Why is the second pKa value different? Any ideas?

I need to prepare potassium phosphate buffer for my proteins and got stuck with this simple problem.

Someone will probably come along and move this to "chemistry", but here goes anyway.

The answer is: it depends upon how you measure it.

See:

  Jungas, RL (2006) Best literature values for the pK of carbonic and phosphoric acid under physiological conditions. Analytical Biochemistry 349 1-15

The author states that   "..the best value for the true thermodynamic second dissociation constant of phosphoric acid in pure water at 38°C is 7.180, rounded to the nearest 0.005."

He then goes on to re-analyse the data reported in:

  Cohn, EJ (1927) The activity coefficients of the ions in certain phosphate solutions: a contribution to the theory of buffer action. J Am Chem. Soc. 49 173-193

and concludes that under physiological conditions of ionic strength and pH the best estimate is 6.795.


Does translation have a way of preventing mismatching between mRNA codons and tRNA anti-codons? What happens in translation if a tRNA with an inappropriate (non-cognate) anti-codon binds to the A-site of the ribosome carrying mRNA?

For example, what would happen if an ile tRNA with the anti-codon 3'-UAG-5' occupied the A-site when juxtaposed to a met codon: 5'-AUG-3'? This would seem possible to some extent as two of the three  bases pair correctly.

Does something prevent this occuring or are incorrect amino acids removed or the protein degraded?

Summary

Non-cognate codon–anticodon interactions on the ribosome do occur, but do not normally result in misincorporation of amino acids into protein. This is because aminoacyl-tRNA binds the ribosomal A-site in an EF-1A–aminoacyl-tRNA–GTP complex, and hydrolysis of GTP must occur before the peptide bond can form. The non-cognate interaction appears to be unable to trigger this hydrolysis and dissociates from the ribosome.

More Detailed Explanation

The hydrogen bonding between the bases of the mRNA codon and the tRNA anticodon is the basis of the specificity of decoding. It is easy to see that a codon such as 5’-GGG-3’ would form nine hydrogen bonds with an anticodon 3’-CCC-5’, but none with an anticodon 3’-AAA-5’. However, as the question makes clear, the situation is not quite so simple if two of the codon bases form the correct hydrogen bonds. A more telling example is shown below (here with the same tRNA, but different codons), where the difference between a his-tRNA interacting with a His codon and a Gln codon is only the strength of a GU ‘wobble’ base pair, often reckoned to be that of a single hydrogen bond. Certainly there is a difference in energy of the two interactions, but not enough to prevent a significant extent of miscoding.

The answer to this conundrum turned out to be the solution to another long-standing puzzle — that of why GTP is required in the binding of aminoacyl-tRNA to the A-site of the ribosome, which is directed by EF-1A (originally known in bacteria as EF-Tu). The GTP is not required for peptide-bond formation — the energy for that is supplied by the ATP in the tRNA synthetase reaction. It transpires that the role of GTP is in maintaining the fidelity of translation. The hydrolysis of GTP only occurs when the correct tRNA is bound — presumably the conformation of the incorrect interaction does not allow this to occur — so the non-cognate tRNA will eventually dissociate from the ribosome.

It is interesting that the other elongation factor, EF-2 (EF-G), involved in translocation of the peptidyl-tRNA, binds to the same site on the ribosome in a complex with GTP, and that translocation and removal of the deacylated tRNA can only occur after hydrolysis of GTP. It is as if the requirement for GTP hydrolysis ensures that the system is in the correct conformation before the next step of the complex process proceeds.

References

Berg et al. provides a general account, freely available online. A more detailed structural consideration can be found in a review by Nilsson and Nissen, which requires library access.


How to estimate the DNA density in human sperm head? I have got an estimate of sperm head volume from internet.Like consider it as a disk of order 4-5µm. Now I wanted to find the DNA density in the sperm head. How to find that?

Find, or calculate, a value for the volume of the sperm head.

Find a value for the size of the human genome (haploid or diploid?)

Convert the genome size, which will probably in Giga basepairs, into mass (I suggest picograms).

Divide mass by volume to get a density, pg μm-3

Refinement - does the sperm nucleus take up all of the head volume? Do you need to factor this in?


Why does all life use the same macromolecules in their genetic code? There is no biochemical constraint of any sort, so why doesn't some other code work? Why is it specifically RNA/DNA?

Preamble
Any answer regarding the origins of our biochemical evolutionary origin will be reasonably speculative given that this is a very hard question to scientifically test and this field is generally understudied to say it is pretty much the most fundamental biochemical question. But there are a few reasons why RNA makes sense as the prime genetic molecule compared to other established macromolecules present in the primordial soup, and also there are good reasons why DNA superseded it as genetic storage for most cellular organisms.
In summary, the alternative abundant polymer macromolecules that came from the primordial soup aren't as versatile as RNA, and over time DNA was used more over RNA due to it being a more reliable information storage molecule.
We must remember though that the conditions that lead to the genesis of RNA is a much tougher question. There are an unfathomable amount of combinations of chemicals that could have facilitated an evolutionary process. @WYSIWYG made an excellent comment regarding why this is an almost impossible question to answer definitively:

...Why is there a phosphodiester backbone used rather than
ether, amide, carboxyl ester or any other kind of linkage? Or why
purines and pyrimidines, why not naphthalene ring heterocycles? Why
imidazole, why not oxazole or furan? You cannot reason this out in a
reverse manner.

Therefor in this answer we will be discussing RNA and other bio-polymers that were established in abundance from the very early primordial soup, not the original genesis of such biochemicals. What made each of them good vessels for an evolutionary process?
A genetic code macromolecule needs the following features:

Stable.
Variable structure.
Expandable.
Replicable.

RNA has all these and doesn't rely on a biological system for reproduction of the RNA molecule.
RNA world.
Let's not forget that DNA is probably not the first one along and there was an RNA world before the cell as we know it. Even today many viruses particularly make use of ssRNA.
RNA was a good molecule because it was a polymer made of 4 base monomers that could bind with other polymers to make any array of compositions of the base components and was spontaneously replicable. This allowed a primordial form of molecular evolution as we know it today. It is able to carry more varied information than other abundant macromolecule polymers.
RNA can also carry out functions in a similar way a protein might, including catalysis. No known sugars or other macromolecules are able to demonstrate the same level of variability and versatility as RNA, although deoxyribosymes have been artificially designed in laboratories.
This probably gave it a good chance at establishing itself as the first molecule to trigger biogenesis, and this lead to nucleic acids being established as the fundamental molecule of molecular evolution.

DNA chemical structure.
Eventually RNA evolved into more complex structures and DNA broadly superseded RNA as a storage device for genetic information in cellular organisms primarily due to the increased stability DNA offers over RNA. If we take a look at DNA specifically we see a very good data storage mechanism for a couple of reasons.

Intra-strand hydrogen bonding and different chemically structured sugar group makes a more stable overall structure.
More rigid grooves allow proteins to bind at particular sites.
Again, it's a polymer of variable composition.

Alternative coding macromolecules.
What are our other options from the biological polymers?

Carbohydrates. The glycocalyx coats most cells in our body, and clearly sugars (specifically polysaccharides and glycoproteins) are an expandable, information rich molecule. However it relies on proteins for assembly in the same way proteins do, so it never really got the chance to be that prime molecule.
Lipids. A brilliant expandable polymer, and many are spontaneously expanding in the right conditions, but generally lipids cannot carry as much "information" in the polymer (pretty much just varying lengths of CH2 groups).
Proteins. Too complex and not spontaneously replicable. They rely on other systems for production (except in some rare examples, although they arguably still rely on a complex biological system).


What is this woodlouse doing? I picked an apple from the ground, it was wet with dew and a woodlouse was stuck to it, with its back against the apple. When it got loose, it started flexing its "tail" like this for a while. Why?

It was moistening its respiratory and osmoregulatory organs:

Woodlice as all other terrestrial arthropods face the major challenge of preserving water balance. In their case the two systems that immediately suffer from desiccation are osmoregulation itself and respiration. In woodlice these two functions are carried out mostly by the pleopods: modified leaf-like appendages on the ventral side of the hind body part ("tail") (see here and here some annotated photos and drawings of ventral side of woodlice).

To maintain these structures in moist state woodlice have a number of adaptations, one of them being the ability to "pick up water from external sources via uropodal dipping, with the water moving upwards by capillarity" (see here). Uropods are the tiny rod-like appendages on the tip of the "tail", and dipping of the uropods is exactly what you were observing.


Help me identify this insect Over the last week or so as warmer weather has arrived, I've noticed small insects crawling around in the bathroom. I'm located in western Europe. They are perhaps 1mm in length, quite difficult to see without a magnifying glass. I used a macro lens to capture these pictures. What might they be? Ticks? Aren't ticks larger? Why are there so many?

Note: these pictures are heavily magnified (they are on an old wooden door with cracking paint), and I've applied lighting auto correction. Actual size of each insect is 1mm or less.

After a long hunt it seems they are Dermanyssus gallinae. It appears I have a pigeon's nest somewhere near my building.

http://en.wikipedia.org/wiki/Dermanyssus_gallinae


Do bacteria with capsular antigen always have a capsule? Assume some bacteria have capsular antigen.
Do these bacteria always have a capsule?
I think not, I think the antigen only makes it possible.

In short: It can depend on your definition of encapsulation.

According to the Oxford Dictionary of Biochemistry, a capsular antigen is defined as

  any of the antigens, usually polysaccharide in nature, that are
  carried on the surface of bacterial capsules. The term K antigen is
  used for those that mask somatic (O) antigens.

In general, capsule polysaccharides have complex structures and are produced by a the action of several enzymes, with the genes necessary for production of the capsule typically making up a gene cluster in the genome (see for example Chen et al.: http://www.biomedcentral.com/1471-2180/10/274). On the face of it, it would seem somewhat unlikely that a bacterium would produce a known capsular polysaccharide antigen without retaining the ability to produce a capsule, as the selective advantage of the capsule then would be lost.

In actuality, the answer might depend on how you define "have capsular antigen" and "capsule". Historically, several methods have been used for demonstrating encapsulation. Methods based on staining microscopy or colony morphology observations tend to identify fewer strains as encapsulaed than does serotyping (reaction of serum with antigen). With this in mind, strains that can be shown to be encapsulated without serotyping are sometimes referred to as "highly encapsulated" to distinguish them from strains that test positive for encapsulation through serotyping only.

For discussions of capsule detection methods as applied to Staphylococcus aureus, see Sutra et al. (http://jcm.asm.org/content/28/3/447.full.pdf) and O'riordan and Lee (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC321462/).  O'riordan and Lee writes

  Isolates belonging to the remaning serotypes produce nonmucoid
  colonies on solid medium, and their colony morphology is
  indistinguishable from that of strains lacking a capsule. Some
  investigators have referred to nonmucoid, encapsulated S. aureus
  isolates as microencapsulated to distinguish them from the atypical
  mucoid strains.

Thus, if both "have capsular antigen" and "have a capsule" is defined by a positive serotyping result for a capsular antigen, then all strains with a capsular antigen as detected by serotyping have a capsule per definition. If on the other hand you define encapsulation based on ink staining microscopy or colony morphology, there are definitely strains that produce K-antigens and don't qualify as "encapsulated".

Note that while bacterial capsules consist mostly of polysaccharides, capsule proteins make up a second class of capsule antigens. One example is the Caf1 capsule antigen protein produced by Yersinia pestis: http://en.wikipedia.org/wiki/Caf1_capsule_antigen


Is there a difference between ISH and ISHH? (In Situ Hybridization, In Situ Hybridization Histochemistry) I came across the term ISHH in my document and discovered that it stands for In Situ Hybridization Histochemistry. I's translating to Russian a document that uses this abbreviation.
Example from the PubMed:

We then validated these findings by using a combination of tools, including the analysis of an additional brain region in an independent subject cohort, cross-validation with an alternate custom microarray platform, and follow-up with in situ hybridization histochemistry (ISHH).

Is there any difference between ISH and ISHH, or are these just synonyms for the same method, in situ hybridization?

The term appears to be in use as a synonym.  PLOS ONE is a good journal, and in it Okubo, 2016 write "The protocol for ISHH was described in detail previously [22]."  Where [22] is Yamanaka, 2007, describing a classic ISH protocol.
Note that both papers use good old fashioned nuclear tract emulsion for S-35 labelled probes.  The ISHH protocol is in its own section separate from IHC.  It seems a bit odd because no literal "chemistry" is involved in recognizing the target - the RNA probe binds non-covalently and emits radiation.  However, as noted in the question discussion, IHC is formally defined (OED) as "the branch of science concerned with the identification and distribution of the chemical constituents of tissues by means of stains, indicators, and microscopy".  For example, though I have seen immunofluorescence and immunohistochemistry used to describe mutually exclusive visualization options, noncovalent binding of fluorophore-labelled antibodies is described as "fluorescent IHC".


Sodium-Potassium Pump From my understanding, in the sodium-potassium pump we have Na+ inside the cell and K+ outside the cell, thus forming a so called "salted banana." After reading my textbook I found many statements saying that "potassium ions tend to diffuse out of the cell...sodium ions tend to flow into the cell." I initially thought that when the action potential hits Na+ leaves the cell and K+ enters the cell, which to me contradicts the previous statement.

Can someone please clarify this and differentiate between the two?
I am trying to understand the action potential process as a whole.

Thank you !

Your confusion is caused by the assumption that Na+ always leaves the cell and K+ always enters. The Na+/K+ pump is there to maintain membrane potential and relative Na+ and K+ ion concentrations stable inside. When an action potential (AP) is generated, sodium channels open and sodium rushes inside to depolarize the cell( 1st phase of AP). Next, the sodium channels close and K+ begins to leave the cell (since the inside of the cell contains too many positive charges and the cell would remain depolarized if nothing was changed). Potassium leaves through leak channels. So in summary, Na+/K+ pump and the channels that are part of AP generation result in different movement of Na+ and K+ across the cell membrane.

Here is a nice review of Na+/K+ pump and action potential generation.
https://www.khanacademy.org/science/biology/human-biology/neuron-nervous-system/v/sodium-potassium-pump


What is the name for when genetic deviation results in an organism that doesn't work? There is a word for this, and it's escaping me. I want to reaearch more papers on it, but I can't find them or what the word is called.

It's typically used in the context of fitness and evolution. If there is a dead individual, it doesn't have a fitness and the mutation is called _____. ?? ( in some models could be given a zero or neg inf)

If you are referring to the mutation
I think the word you are looking for is lethal.
A lethal mutation is a mutation that causes the death of its carrier. Now there are recessive lethal and dominant lethal. For dominant lethal mutations, all heterozygotes are inviable. For recessive lethal, only double mutant homozygotes are inviable.
If you are referring to the individual
An individual that is not able to survive and reproduce is said to be inviable (I already used the term above). However, the reason for it is not necessarily genetic.


If a woman was fertilized with her own DNA, would it be her clone? Several questions:

1) Can human DNA fertilize an egg, without having been naturally packaged in a sperm cell?
2) If a female had her ovum fertilized with her own DNA, would the fetus be her clone?
3) If this technology of fertilizing ovum from arbitrary samples of human DNA were effective, would males be unnecessary for reproduction of the human species? (No political implications, just a thought experiment.)

Thank you for your insight!

1)
In principle yes, you could in theory use micro injection to inject haploid DNA into the egg. I don't think this has been used in practice though. However Dolly the sheep was created by exchanging haploid nucleus of a sheep egg with a diploid nucleus from a mammary gland cell.

2)
Not necessarily, DNA is packaged into chromosomes and diploid cells have two copies of the same chromosome (with the exception being the sex chromosomes MALE:XY FEMALE:XX). Remember that gametes are haploid (single copy of each chromosome) and that homologous recombination occurs during gamete formation, therefore the chance of obtaining two identical sets of haploid DNA that also match the females is extremely low, unless all chromosome pairs are completely identical.

3)
In principle yes. I could imagine that DNA extraction from eggs could be used for artificial fertilization and the result of that would be a race of all females.


Any relevant knowledge/studies about voluntary goose bumps I'm not entirely sure how normal this is, but since I was a child, I've been able to produce myself voluntarily a "chill" sensation that seems to start on my head and traverse the rest of my body, being least intense in the feet. Looking around the internet and forums, looks like other people but not everybody also describe this ability. However, unlike other people's reports, I don't see "goose bumps" on my skin, at least there aren't any visibly; it's just the sensation.

Does anybody know if there are any relevant studies or knowledge out there about "voluntary goose bumps"? Is there even a proper name for that?

Recent studies prove that this involuntary phenomenon must be untrue. Obviously this is false, in order for research like this to take place people need to spend money. It would be interesting if we could create a crowd sourcing account maybe on kick starter to find ways to bring money into the research. I wish I had more information for you, I've been able to do it as long as. When you go to the dentist, just curious, you don't happen to have two bones underneath your tongue that is an anomaly as well? I've been trying to think of correlations for years. I can get the medical terms, if you like. Find me on Facebook Chris Azzy


Why not produce protein based on condensation reaction? I'm fairly new learning about protein. As I know protein can be synthesis by condensation reaction. And the current method to produce protein is purify them from an organism. So why not produce protein based on condensation reaction instead of purifying it from an organism?

It is important to first remember that to do anything useful, the sequence of the amino acids in the protein must be exact. For example, sickle-cell anaemia is caused because one amino acid in a haemoglobin protein is incorrect. Because of this, peptide synthesis involves rather complex chemistry in order to ensure that amino acids are added in the correct order and number, and is only effect up to a chain of a few dozen amino acids.

Now it is possible to produce peptides of various lengths in a cell-free extract, which basically involves taking the cytosol out of cells (with all the ribosomes, tRNA's, and other factors therein) and adding the mRNA template to be translated and an ATP source. This way, a peptide can be prepared by using the cell's own machinery for protein synthesis without actually needing a viable cell.

Remember also that even if it were possible to chemically synthesize a correct peptide sequence, the protein would still need to fold into a correct 3-dimensional structure to work properly, which in some cases is impossible for any artificial method currently available.


Why similarities among organisms led scientists to believe that organisms are evolved? Theory of evolution states that organisms are evolved into other more advanced ones over time because there are some traits in modern organisms resemble with organisms existing before (from fossil record). But it might be possible that each organism has created independently of each other. why similarities mean evolutionary relationship?

I will answer by explaining some misconceptions in your original question:

  Theory of evolution states that organisms are evolved into other more advanced ones over time

Nope that's not what the theory of evolution is stating, mainly because the expression "more advanced" does not mean much and also is a loaded expression. You might want to start with an intro course to evolutionary biology to understand what the theory of evolution says. Understanding Evolution is a very introductory course you might like

  @Remi.b Alright I will have a look at what theory of evolution states but the basic thing is humans are thought to have evolved from chimpanzees. What I want to know is chimpanzees might resemble to humans but why chimpanzees are considered ancestor of humans? It might be possible that humans and chimpanzees created individually?

No, the theory of evolution does not state that humans evolved from chimpanzees. It says that humans and chimpanzees / bonobos have a common ancestor (about 6 millions years ago) that was not a human, nor was it a chimpanzee or a bonobo.

You can find an introduction to phylogenetics in this post and you can find online tools to visualize the tree of life in this post.

Philosophical issue in your question

The theory of evolution makes predictions that have been tested and demonstrated correct. You are asking why would creationism would not lead to the same predictions. For this purpose, one need to know what predictions would creationism make but this is very much undefined. If you can point to specific predictions that creationism would make, then we could tell you whether we have a counter evidence. The issue is that there is always a way to say, everything has been designed so that it looks like evolution is at play even if species were created anew. But this is not falsifiable.

So, maybe you might want to make specific predictions, that in your opinion, would be congruent with creationism but not with the theory of evolution and then we can tell you if we have evidence to support this prediction.

Related posts

While it does not directly answer your question (because IMO, for semantic issue, the question is unanswerable), you might want to have a look at Is evolution a fact? and Demonstrable and repeatable examples of evolution


Does neuroeconomics study the brain or study economics? I'm trying to understand what neuroeconomics is. There are two possibilities for what it might mean. (1) The study of cognitive processes in the brain by applying basic principles of economic theory like concepts of utility, decision making, etc. (2) The study of how a human behaves in an economic setting, somewhat like game theory and so on, which is more economics than brain science.

Which one is it?

As @Kyle beautifully summed-up,

  Neuroeconomics is the study of the neural basis of economic behavior.

The terms applies to studies concerning the appeal of new logos for marketing purposes to the understanding of the neural correlate of subjective value. The term neuroeconomics has been subject to some debate which made it sometimes unclear. In particular, the term is ambiguous with regards to its applications.

Are the theories that are built upon these studies used for marketing purposes (some would say "to optimize brain washing you in the necessity of buying a 7 blade razor") or for the sake of knowing how the brain may be better understood and to the therapeutical applications of these new theories.

My answer would therefore be this:

the brain is a complex system for which science often used analogies to make progress. It has been compared as steam machines in the 1800s, electricity in the 1900s, or to computers in the this century.
The complex interactions present in an economic system -as studied by game theory for instance- present a powerful analogy to understand the brain.
Of course, it thus impacts our knowledge on economics as these are often based on our knowledge of decision making. Thus, your two options are (1) and (2) are interconnected.


Found this spider in my bed last night.. can someone help ID? As I was going to bed last night, this little guy greeted me when turning the covers. Can someone help ID this for me? I'm located in Kentucky, USA.

Demonstrating size, compared to a bottle cap:

It seems like an Agelenopsis to me. According to www.spiders.us, the size, the description and the location (Kentucky) match your specimen.

Here is another image (also from www.spiders.us), for comparison:

The mentioned link lists 13 species in the Genus Agelenopsis. It shouldn't be difficult narrowing it down to species (if that's the correct Genus, of course).


Codon tables and the wobble hypothesis In E. coli, there are only 47 different tRNAs but 61 potential anticodons. This is because, from what I understand, the third base of the anticodon can pair by wobble rules.

However, it is known that there is some correlation between tRNA pools and expression levels.

So if, for example, GUA and GUG were covered by the same tRNA, why are their codon usages different in a codon table? If one were only concerned with expression level, shouldn't they theoretically affect translation rates similarly?

This is a good question as, although in higher eukaroyotes codon usage does not necessarily correlate with translational efficiency, it does to a large extent in Escherichia coli (see e.g. Boël et al., 2016). The answer is not simple, but the following may contribute.

To optimize the strength of base pairing

Although in particular circumstances ‘wobble’ allows one tRNA to decode more than one codon (see diagram in my answer to Redundancy and the Generic Code) the strength of base pairing will be less for the wobble base-pair:

It has been suggested this would generally disfavour (and hence reduce the incidence of) the degenerate codon that needs to be decoded by wobble. (In some cases a wobble interaction might be an advantage if the first two codon bases were G or C, so that the hydrogen bonding was not too strong.)

To utilize the spectrum of tRNAs able to decode degenerate codons

Although wobble enables a reduction in the total number of tRNAs necessary to decode the 61 amino-acid codons, additional tRNAs often exist that one might regard as unnecessary. Furthermore, where three codons are decoded by a tRNA with a 5'-I (inosine), the other tRNA sometimes has a 5'-G (rather than A) and can hence decode two codons. This is illustrated by the E.coli tRNAs for threonine:

Thus, the relative abundance of these three Thr-tRNAs could determine the codon usage, and Dong et al., 1996 reported that this is the case.

To reflect the overall GC-content of the genome

If the genome of a prokaryotic organism has a particular base composition, because there is so little non-coding genomic DNA the mRNA will necessarily reflect that base composition in its codon usage. Your might ask why doesn’t the base-composition of the genome just reflect that of the synonymous codons, but there are actually strong pressures on the GC-content of prokaryotic and viral genomes. In some bacteria this may reflect needs for thermal stability, but in others it seems to be random drift (see e.g. Biology SE questions on GC-content of genomes).


How does the bear mother ensure her cubs don't escape during hibernation? I have some questions relating to bears- more specifically, the brown bears we have in Scandinavia.

When they go into hibernation, do they fall asleep as we know falling asleep? If a bear mother brings her cubs into the den, how can she keep track of them? How can she make sure they don't wake up, leave the den and get lost in the snow?

She probably can't, but a bear that wanders out of the den away from it's mother probably won't be doing much reproduction.  Infant wanderlust will be strongly selected against.


Extinction of species with extant descendants From what I've seen, species such as Homo heidelbergensis which have extant descendants are classified as extinct, which makes sense as far as it goes.

However, given that species exhibit a continuum of development throughout time, does that mean that for any given extant species and their ancestors there is an "extinction line" which moves gradually forward as small changes in the "current" gene pool render the ancestors from a given time no longer capable of producing fertile offspring with the "current" species and thus shunts them out of the current species and into the extinct species immediately proceeding it?

Additionally, does that mean that there might have existed a species (say, for argument's sake, H. heidelbergensis) with a genetic distribution such that some of them would be capable of producing fertile offspring with the "current" descendant species (in this example, H. sapiens) and some of them not, thus rendering half of the species effectively extinct and the other half not (at least, not yet)?

You are right. Consider a population at some point back in time and ask how many of the individuals left descendants that are still alive today?, the answer will be between 1 and N (inclusive), where $N$ is the population size. We call this process coalescence

A tiny introduction to coalescence

Consider a population of constant size $N$ and to the previous generation and ask the question What is the probability of two random individuals to be siblings?. This probability is $\frac{1}{2N}$ (assuming no selection and diploid population). The probability of them not being siblings is $1-\frac{1}{2N}$. We can say that, with probability $\frac{1}{2N}$, two randomly individuals coalesce in the previous generation. What is the probability that 2 random individuals coalesce $t$ generations ago? It is the probability that they don't coalesce for $t-1$ generations and then coalesce, that is $P(t) = \left(1-\frac{1}{2N}\right)^{t-1} \frac{1}{2N}$. In words, the coalescent time follows a geometric distribution with parameters $t$ and $\frac{1}{2N}$.

Because coalescent times are independent variables (and I won't prove it here), one can extend this to not only 2 individuals but $n$ individuals. There is therefore, a point in time where all individuals of the modern day population coalesce into only one individual. At this time, this one individual was not alone in the population of course.

Coalescent theory: Usages and book recommendation

The simple calculations I just made are the very basis of coalescent theory. Coalescent theory is a very powerful set of mathematical tools that one can use to make detailed predictions of the genetic patterns to expect in a population. Statistical test such as Tajima D test is based on results from coalescent theory. Coalescence theory can be extended (through approximations) to structured population (structured coalescent theory), non-neutrality (selection) and recombination.

coalescent theory: an introduction (by John Wakeley) is a good book on the subject. However, it requires from its reader some basic knowledge in mathematics and problem some knowledge in population genetics.

What is the percentage of people living in England in 1500 AD whose lineage is still alive? is a recent post on Biology.SE that is relevant to the kind of question that could be answered with coalescent theory.


glossary of biotechnological engineering Similar to A good book for history of biology/biotechnology for lay people

but not for lay people.

Can anyone recommend an advanced dictionary of biotechnological engineering concepts in English (contemporary, not historical)?

There doesn't seem to be anything adequate at my research institution nor even country.  I have been looking for PDF's and e-books since they can be previewed more easily than ISBN #'s, but any suggestions are welcome.

I found this glossary of Biotechnology and Genetic Engineering off Wikipedia, what do you think?

Or The Facts On File
DICTIONARY of
BIOTECHNOLOGY
and
GENETIC
ENGINEERING

What concepts are you necessarily hoping to include? I'm hoping someone actually experienced in this field can advise.


What is the name of this insect? This insect was found in my garden in India on the evening of August 07, 2019. It's rainy season here.

This is a treehopper (an insect in the family Membracidae).
As Arthur J Frost mentioned in his comment above, it will be difficult to ID this specimen more specifically given the angle, lack of further info, and my personal lack of knowledge of Indian fauna.
However, you can view an at-least similar looking species by viewing Oxyrachis tarandus, which is found in India (see here and Sharma & Pati (2011)1).
You can find photos of O. tarandus here, with one copied below for reference.

 © www.NatureLoveYou.sg

 1. Sharma, A. and Pati, P.K., 2011. First report of Withania somnifera (L.) Dunal, as a new host of cowbug (Oxyrachis tarandus, Fab.) in plains of Punjab, northern India. World Applied Sciences Journal, 14(9), pp.1344-1346.


What's the point of glycolysis in fermentation? In order to initiate glycolysis, 2 ATP are necessary. In the glycolytic process, you generate an additional 4 ATP, which results in a net gain of 2 ATP.

If you don't undergo glycolysis, however, then you have an extra 2 ATP not being used. If you do glycolysis, you still got only 2 ATP. Am I missing something here?

Remember that glycolysis yields 2 NADH as well as 2 net ATP. This NADH can be used to a terminal electron acceptor to produce an end product with a net gain of ATP. End-products of fermentation can include lactate, acetate, butyrate, propionate and ethanol, all of which generate different amounts of additional ATP.

The exact pathways involved vary according to the organism, but anywhere between 1 (or even 0.5) and 4 additional ATPs can be generated, even without the involvement of oxygen. In the case of aerobic respiration of course, the NADH feeds into the electron transport chain and yields ATP.

EDIT: It's perhaps worth noting that the 2 ATP is gained. See @SatwikPasani's answer for the math.


Why do most organisms have negative supercoiled DNA? It has been observed that in nature most organisms have negative supercoiled DNA and that few organisms have positive supercoiled DNA. Some of the organisms that have the positive supercoiled DNA live in strong acidic environments but are very rare compared to negative supercoiled DNA. Why wouldn't all organisms have the same DNA supercoiling? Does it affect their survival in any way?

One important notion in DNA topology is the linking number ($Lk$) which is the sum of right-handed twisting # and left-handed writhing # ($Tw+Wr$). Say the $Lk = x$ for relaxed DNA. If $Lk<x$ then you have negative supercoiling while positive supercoiling happens when $Lk>x$.

The higher the $Lk$ value the higher the helical energy of the DNA and the harder it is to separate it meaning the DNA is now more stable. In so-called "extreme" conditions (e.g. high acidity or high T˚) the organism must protect his DNA from degradation. Therefore those organisms require a more stable form of their DNA which can be achieve by positive-supercoiling and/or high GC content.

Now why do the vast majority of the organisms have negatively-supercoiled DNAs? If you let the DNA by itself, it will adopt an $Lk=x$, i.e. it will be in his "relaxed"-form. Negative supercoiling arose because of the presence of Topoisomerases (type I and II), which are proteins that cleave the DNA and release the helical tensions and which cumulatively provokes the DNA to be slightly underwinded compared to it's relax-form. Is this good for the organism, if living in non aggressive conditions? Yes it is because a decrease of the $Lk$ will make the DNA easier to separate. This means replication and transcription can occur more easily or in proper terms, they now require less energy to perform their functions.

Here an excellent reference on this subject as well as a Youtube video that explains those concepts using strings. The latter is really helpful as those concepts are easier to understand visually than in writing.

I hope this helps.


Does red light preserve your night vision? A number of companies have started marketing LED lamps that can be switched to a red mode. The claim is that red light is less harmful to one's night vision. Given that our eyes are less sensitive to red light, though, I'm not convinced that that red light is any better than dim white light. So if "equivalent" luminosity is defined where it's equally easy to, say, read a book in both light types, is there some physiological reason that red light is better than the equivalent white light?

This is a very good question.  Red light is routinely used by scientific laboratories to do low light dissections of retinas, and of course it is used in other low light contexts such as printing plate development.

In both of the above contexts, you have a clear subject: the retina being dissected or the printing plate being developed.  In the case of the printing plate the film has been designed to be specifically non-reactive to red light, so red light is used because your eyes can see it, but the film doesn't react to it.  Similarly in some scientific settings it makes sense to use red light during dissections.  Mice lack a long wavelength opsin, and therefore using a dim red light allows the experimenter to have a relative sight advantage compared to the mouse when keeping the mouse dark adapted.

But in the case you're asking about, there is no film or animal to serve as a second party.  So is there any intrinsic advantage to using red light?  As it turns out, there is.  The fovea, which is in the center of our eye and used for high acuity vision, has no rods and primarily L- or red sensitive cones.  Note the high density center area which lacks blue sensitive cones and has 2:1 red to green cones.

So by having red light present, you stimulate this area.  But red light is present in white light, too, why not just use that?  Leonardo's answer comes the closest, but it's a little off.  Red light is used because it preferentially stimulates L cones more than rods, but you are definitely not able to preserve night vision by using red light.  Why not?  Well it may look like it is possible to exclusively stimulate cones from the chromatic sensitivity figure

But that figure is 1) normalized and 2) not indicative of synaptic signal processing.  1000's of rods can converge onto a single ganglion cell, where cone convergence in the fovea can be on the order of a single cone per ganglion cell.  When it comes to perception, in order to compare the black rod line above with the red L-cone line you'd have to magnify it dramatically in size.  Practically speaking, it is nearly impossible to stimulate cone pathways without stimulating rod pathways when using a relatively broad spectrum LED that you're powering with a battery.  Maybe with a high power infrared laser.

So the purpose of using red light is to attempt to balance the activation of high sensitivity (red insensitive) rods with that of the low sensitivity (but red sensitive) cones in the fovea.  While using a similar level of rod activation with blue light, you would perceive a "blind spot" where your fovea is.

Finally, instrinsically photosensitive cells (the melanopsin cells brought up) do not factor into this processing.  These cells are activated only with extraordinarily bright levels of light, and the therefore do not enter into conversations dealing with night vision.


Why is pith of Cucurbits hollow when mature? What is the evolutionary significance of pith in cucurbits? Does it serve a function by being hollow? Or is it an evolutionary vestige? What function would it have had in its ancestors?

Pith autolysis is a phenomenon due to which in some dicotyledonous plants like cucurbits, the pith gets hollowed.

Background: We all know that plants get their Carbon from atmosphere in the form of Carbon-dioxide, and fixes it by photosynthesis. During rapid growth Carbon requirement may not be in pace with rate of carbon fixed by photosynthesis alone, So some plants adopted pith autolysis.

This is useful for a  plant when it is in scarcity of carbon, Scarcity here implies that the plant is not able to get enough carbon for its growth with just photosyntgesis. So the plant autolyses it's pith to get required carbon to maintain its growth.Thereafter this carbon resulting from autolysis ,is transported to growing regions of plant.

Source:https://doi.org/10.1006/anbo.1995.1063


Do self-exciting neurons exist? I have two questions concerning self-exciting neurons in the brain.

Have directly self-exciting neurons been oberved, i.e. neurons with an axon terminal building a synapse with one of its own dendrites.
Does self-excitation work?

I guess that self-excitation can only work when the following time constants fit to each other:

refactory period of the neuron's membrane voltage (approx 1 milliseconds)
run time of the signal along the axon
refactory period of the synapse (approx 5-6 milliseconds)

I tried to estimate a typical run time by taking a not untypical axon length of 1cm = 0.01m and dividing it by a typical nerve propagation speed of 10 m/sec, getting 0.001 sec = 1 millisecond. Direct self-excitation would not work because the synapse would not be ready when the self-exciting signal arrives.

The other way around: Only when the run time is longer than the two refactory periods direct self-excitation might work.

Once again: Are there known examples of direct self-excitation in the human brain or nervous system?

Short Answer

Yes, autapses exist, though the role of excitatory autapses in particular is unclear.

Long Answer

A lot of your assumptions are wrong for biological neurons (I'm suspecting you have a background in artificial neural networks but that might be inaccurate). These don't directly impact your question of whether these connections exist, but I think they are important for understanding how they could function, which is just as important if not more so.

The 'refractory period' refers to a period in which a cell cannot or is less likely to fire an action potential. Cells can receive inputs freely during their refractory period.
Neurons are not single compartments. Action potentials are generated near the soma, and although they can propagate into the dendrites, synapses out on the dendrites can be fairly electrically isolated from the soma, and synaptic potentials in dendrites can take some time, easily a ms or two, to affect the soma, and they also last for several ms. They can also affect the potency of other nearby synapses.
Although axons can be cms or more in length, dendrites are rarely found and further than 1 mm from a soma in the CNS (there can be exceptions, of course; I am mostly thinking of neocortex), and most dendrites are within 100-200 um from the soma. So travel distances are much shorter than your estimate. However, synaptic transmission itself is somewhat slow, so you can add another .5 ms, and your estimate for speed is quite fast for the brain; the link you gave applies to peripheral fibers and spinal cord to brain transmission only (note they are talking about "nerves"), so your overall estimate of 1 ms from spike to autapse turns out to be reasonable, but for different reasons.
It isn't meaningful to talk about refractory periods for most synapses. Synapses can display short-term depression and/or facilitation but that isn't the same as a refractory period. Only at particular synapses containing a single release site does it make any sense to talk about refractory periods.
Cells are not activated by an individual synapse, with a few exceptions in very specialized brain areas. So just because a cell has been made to fire tells you nothing about whether a particular synapse was activated. In fact, unless that cell has fired previously very recently, you can be confident that an autapse would not have contributed to that particular firing event.

Evidence for excitatory autapses

You specifically asked about self-excitation, but it's important to know that inhibitory self-synapses also exist, and they are much more common between GABAergic inhibitory cells than between excitatory cells (Bekkers, 1998). Inhibitory autapses make a lot of functional sense because they serve as direct negative feedback.

However, excitatory autapses do exist and they may have function significance(Bekkers, 2009), rather than just being rare "accidents" that do little. In Aplysia, for example, there are autapses that cause an excitatory plateau potential during feeding behavior, maintaining activity for a long duration (Saada et al., 2009).

In mammalian neocortex, excitatory autapses have been observed but their function is unclear. Their properties can be a bit different from other synapses (Liu et al., 2013). Spike-timing dependent plasticity would suggest that autapses should shrink and go away, but they don't, which suggests they might have some functional utility, though it isn't understood yet. There are many computational attempts to find some function, which I won't list here but you can easily find by searching a reference like Google Scholar for recent articles about "autapses."

Experimentally, the role of autapses in vivo is difficult to study because there is no specific way to selectively suppress autapses outside of a computational environment, or a reduced prep where individual cells can be activated without activity in the rest of the network.

References

Bekkers, J. M. (1998). Neurophysiology: Are autapses prodigal synapses?. Current biology, 8(2), R52-R55.

Bekkers, J. M. (2009). Synaptic transmission: excitatory autapses find a function?. Current Biology, 19(7), R296-R298.

Saada, R., Miller, N., Hurwitz, I., & Susswein, A. J. (2009). Autaptic excitation elicits persistent activity and a plateau potential in a neuron of known behavioral function. Current Biology, 19(6), 479-484.

Liu, H., Chapman, E. R., & Dean, C. (2013). “Self” versus “non-self” connectivity dictates properties of synaptic transmission and plasticity. PloS one, 8(4), e62414.


Are there any plants that fix their own nitrogen? I know that most nitrogen is fixed through industrial processes and bacterial symbiotic relationships. However, are there any plants that can fix their own atmospheric nitrogen?

There are no known plants that fix their own nitrogen. However, there soon may be!

Because N is the major limiting factor in agricultural productivity, there is huge interest in plant systems which can fix their own. It's important enough that the Bill & Melinda Gates foundation have started a project aimed at reducing dependence on fertilisers by giving plants the ability to fix their own nitrogen. There are several potential strategies, the most obvious being encouraging more species to form symbioses with nitrogen fixing bacteria.

However, there's another proposal which builds on recent discoveries about the mechanism of nitrogen fixing in bacteria: we now know how the crucial enzyme complex is made (Rubio & Ludden, 2008). As a result, there are many people calling for efforts to engineer the system directly into a plant organelle (e.g. Beatty & Good, 2011; Godfray et al., 2010).

So, in 10-15 years time you can check back and the answer to this question might have changed! The most likely answer then will be "just the usual suspects: rice, maize, wheat".

References:

Beatty, P.H. & Good, A.G. (2011) Future Prospects for Cereals That Fix Nitrogen. Science. [Online] 333 (6041), 416 –417. Available from: doi:10.1126/science.1209467 [Accessed: 2 February 2012].
Godfray, H.C.J., Beddington, J.R., Crute, I.R., Haddad, L., Lawrence, D., Muir, J.F., Pretty, J., Robinson, S., Thomas, S.M. & Toulmin, C. (2010) Food Security: The Challenge of Feeding 9 Billion People. Science. [Online] 327 (5967), 812 –818. Available from: doi:10.1126/science.1185383 [Accessed: 2 February 2012].
Rubio, L.M. & Ludden, P.W. (2008) Biosynthesis of the Iron-Molybdenum Cofactor of Nitrogenase. Annual Review of Microbiology. [Online] 62 (1), 93–111. Available from: doi:10.1146/annurev.micro.62.081307.162737 [Accessed: 2 February 2012].


Transport mechanism in absorption of monosaccharides in small intestine In the cell membrane of the intestinal cells, there is a mobile carrier protein called Sodium  Dependent Glucose Transporter(SGLT1).It transports glucose and galactose to inside the cell using energy.The energy is derived from sodium-potassium pump (Primary Active Transport).How it is possible cause we need energy in Na-K pump too ?

From my initial reading on this, the SGLT1 does not itself directly use energy in the form of ATP. https://en.wikipedia.org/wiki/Sodium-glucose_transport_proteins It appears the uptake of the sugars by this protein are achieved by cotransport. In this case, they "hitch a ride" into intestinal epithelium by following the flow of sodium ions back into the epithelial cells. The reason the Na+ ions flow into the epithelial cells is because of their higher concentration outside the cells. This concentration gradient is created and maintained by the Na-K Pump. So, ATP is used to create a chemical gradient, higher [Na+] outside compared to inside. Then the natural flow of Na+ down its gradient "drags in" the sugars.


Does focusing on a certain part of the body increase electrical activity in that region? I am batting around ideas for master's thesis topics and was wondering whether or not just focusing on an area of the body would cause of boost of  neuronic activity? Not sure whether this would fall under the rubric of a self-fulfilling prophecy of the mind, or some other secondary body function. I though it might be interesting to examine the relative differences between varying parts of the body and their respective degrees of responsiveness to intentional cortical activity, as directed by a person. If anyone has an answer please respond soon as I can't quite nail down how to search for a question like this online (finding specific phrases, etc.) Also, feel free top point me to any readings related to this (would-be) phenom.
Thanks!

Gut reaction, I don't think this is a solid thesis idea. If you attach an EMG to my finger, and then I concentrate on my finger, and then my finger moves (due to stray thoughts), there will of course be a whole bunch of action potentials firing. However, that's kind of trivial and not really that interesting.

If your theme is "weird EM effects in the human body", one possible decent idea (and one that's gotten some quantity of buzz in the recent past) would be to focus on the role of electric fields in wound healing. You could even add in an intentionality/focus angle, if you really wanted to.


Tool for nucleotide alignment with all nucleotide codes (e.g. R, Y, W, S, etc.)? I have a vector sequence and would like to find the following nucleotide sequence in it.

AASYWSRA

This query sequence uses several degenerate symbols, defined as:

S = C or G (Strong)
Y = C or T (pYrimidine)
W = A or T (Weak)
R = A or G (puRine)

(See this page for a complete description of the IUPAC nucleotide codes.)

Is there a tool to align this sequence with the vector and find all the possible sites?

EDIT: I found this website but couldn't find any of the resources helpful. Maybe one of these will work but I found most of them too complicated. If you know which one will work and explain how to use it I will be grateful.

If you're looking for an exact match, you don't really need a complex aligner. Perl regular expressions are pretty powerful at string transformations or conditional matching of substrings. For example, to find all matches of AASYWSRA in a nucleotide sequence $seq, you can do:

@matches = $seq =~ m/AA[CG][CT][AT][CG][AG]A/g;

The [] brackets are known as Perl character classes, which allow different characters in a position.


Why does the sex of the parent species determines the species of a hybrid offspring I've read a little about hybrid animals, and have been amazed by the fact that the sex of the parent species determine the species of the offspring, in some hybrids.
A male horse and a female donkey will give birth to a Hinny, while a female horse and a male donkey will give birth to a Mule.

The same goes for tigers and lions, male lion and a female tigress will give birth to a Liger, while a male tiger and a female lioness mating will result in a Tiglon

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

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

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

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

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

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


Scientific name for the union point of a plant stem and root Is there a word that describes the meeting point of a plants growing stem and its root?
Is this the same term for aerial roots above soil level?

From Basconsuelo et al 2002:

"The zone of the plant axis where the arrangement of vascular systems changes from root- to stem-structure is often called “transition region”" (see also the refs they cite).

The idea behind it is that the organization of the vascular tissues is radically different in the root in comparison to the stem, such that the switch cannot occur in one point. This transition region (in general case) crosses the air-ground interface.


How long might a tick be on a body before biting? I understand that a tick must be attached for roughly 24+ hours before presenting a danger of transmitting Lyme Disease. However, I am wondering how long a tick might be on my body before actually attaching itself to me.

They wander the body for 30 minutes to an hour before inserting their feeding parts into the skin. Source.
It entirely depends what material you are wearing, i.e. fluffy wool is difficult for them to climb on. They can fall off somewhere in the home and bite another day.
2mm nymphs climb on human skin at about 10cm per minute, so it could find the back of the knee in about 5 minutes and search for a bite site. tick attachment site distribution is: 9% head-neck, 5% arm,
24% stomach-groin, 7% back, 18% chest-shoulder, 25% leg-foot, and 12% hip.


Choosing appropriate statistical test for ordinal data Ordinal response variables show up often in biology, but I'm not sure how they are best analysed. Some examples are qualitative assessments (little, many, a lot) or risk assessments (low risk, medium risk, high risk).

My study is about correlation between pain and depression levels. We are measuring pain on an ordinal Likert scale. This is a number scale running from 10 (severe pain) to 0 (no pain).

We will also measure depression on a similar scale (scale: 4 - 0).

What statistical test should I use?

You can use ordinal multinomial regression (also known as ordered logit) if the response is ordered. These methods are basically extensions of logistic regressions, but using e.g. a cumulative logit instead of the logit. However, there are a number of different assumptions you need to consider. For instance, are you going to use a proportional-odds assumption (which is commonly used), which means that there is an equal probability of going from e.g. class 1 -> 2 and class 5 -> 6? You can also evaluate the proportional odds assumption using plots or a score test. If the response cannot be ordered, there are multinomial nominal methods that you can use, and you can also evaluate the results from an ordered analysis by comparing the predictions with ones from a multinomial nominal analysis. I have used these kinds of methods for the analysis is Red list classifications, which are clearly ordered but cannot simply be transformed into a numerical response (similar to your situation).

The book Analysis of Ordinal Categorical Data (Agresti. 2010) is a really good starting point.

In R you can look at the packages polr and vgam for ways to perform different types of analyses on ordinal data. The author of the book above has also published some examples for categorical data analysis in R, using the packages I mentioned: Examples of Using R for Modeling Ordinal Data. In SAS similar analyses can be done using Proc Genmod and Proc Logistic.


Did Darwin ever reach the conclusion that selection will remove variation? According to simple models of selection the genetic variance in a population should be reduced by selection. (Fisher's fundamental theorem states that the rate at which a population can evolve is limited by its variance). If we select the next generation from one population we will only ever capture as much, and probably only a subset of, the variation that exists in a the first generation.

Did Darwin ever discuss this loss of variation? What did he conclude?

(For now lets ignore the potential roles of sexual antagonism, pleiotropy and such)

A little clarification on my question:

Darwin saw variation in phenotypes, and variation in fitness dependent on phenotype - an effect he called selection. He also saw that this variation was heritable (but did not know how). This is the basic concept of evolution, and is mathematically speaking, the breeders equation:

$r = h^2 s$

He also would have realized that life must therefore have started out as a simple unit, and new variance in traits (and whole new traits) must have arisen over time, i.e. that some kind of changes (mutations) were going on in the heritable information (genes). However, what I'm asking is, did he realize that selection would act to reduce the variation in a population? This would reduce the rate at which evolution can occur over time (Fisher's fundamental theorem - assuming no influx of variance or potential for pleiotropy to maintain variation). Or was it Fisher that first formally discussed the concept of lost phenotypic/genetic variance?

After reading your question, I had a vague memory that this subject was indirectly touched upon in "On the Origin of Species", so I did some text searches (in this pdf version I found online). From what I can see, Darwin never used the technical term 'variance' (I don't know how old this use of the word is), but 'variability' is often used, both with regard to accumulated variation but also meaning variation between individuals within a population.

All-in-all, I could not find clear support for the idea that selection will decrease the amount of variation. However, there are number of passages where the subject of variation vs selection comes up (often indirectly), but, to me, these just as often (most often?) indicate that Darwin saw no risk that selection would reduce variation as the opposite. Here are the most interesting passages I could find (searching for combinations of 'variab*', 'selection', 'decrease' etc), with page references referring to the pdf version and a short comment below each quote:

  A large number of individuals,
  by giving a better chance for the appearance within
  any given period of profitable variations, will compensate
  for a lesser amount of variability in each individual,
  and is, I believe, an extremely important
  element of success.
  (p. 44)

This is clearly discussing amounts of variation within species, where large numbers can compensate for a smaller amounts of standing variability, by increasing the chance of advantageous mutations.

  Nothing can be effected, unless favourable variations
  occur, and variation itself is apparently always a very
  slow process. The process will often be greatly retarded
  by free intercrossing. Many will exclaim that
  these several causes are amply sufficient wholly to
  stop the action of natural selection. I do not believe
  so. On the other hand, I do believe that natural selection
  will always act very slowly, often only at long
  intervals of time, and generally on only a very few
  of the inhabitants of the same region at the same time.
  (p. 103)

Not directly related to selection vs variation, but deals with the rate of evolution vs amount of variation.

  But what here more
  especially concerns us is, that in our domestic animals
  those points, which at the present time are undergoing
  rapid change by continued selection, are
  also eminently liable to variation. Look at the breeds
  of the pigeon; see what a prodigious amount of difference
  there is in the beak of the different tumblers,
  in the beak and wattle of the different carriers, in the
  carriage and tail of our fantails, &c., these being the
  points now mainly attended to by English fanciers.
  Even in the sub-breeds, as in the short-faced tumbler,
  it is notoriously difficult to breed them nearly
  to perfection, and frequently individuals are born
  which depart widely from the standard. There may
  be truly said to be a constant struggle going on between,
  on the one hand, the tendency to reversion to
  a less modified state, as well as an innate tendency
  to further variability of all kinds, and, on the other
  hand, the power of steady selection to keep the breed
  true. In the long run selection gains the day, and we
  do not expect to fail so far as to breed a bird as coarse
  as a common tumbler from a good short-faced strain.
  But as long as selection is rapidly going on, there
  may always be expected to be much variability in
  the structure undergoing modification.
  (p. 141)

This is maybe the most interesting passage, which to me indicates that he saw little risk that selection could/would limit variability (see especially beginning and end).

  For forms existing in larger
  numbers will always have a better chance, within
  any given period, of presenting further favourable
  variations for natural selection to seize on, than will
  the rarer forms which exist in lesser numbers. Hence,
  the more common forms, in the race for life, will tend
  to beat and supplant the less common forms, for
  these will be more slowly modified and improved.
  (P. 162)

Also on limitations for variation that selection can act on, and the value of large populations.

  ... firstly, because new varieties are
  very slowly formed, for variation is a very slow process,
  and natural selection can do nothing until
  favourable variations chance to occur, and until a
  place in the natural polity of the country can be better
  filled by some modification of some one or more
  of its inhabitants. And such new places will depend
  on slow changes of climate, or on the occasional immigration
  of new inhabitants, and, probably, in a still
  more important degree, on some of the old inhabitants
  becoming slowly modified, with the new forms
  thus produced and the old ones acting and reacting
  on each other.
  (p. 163)

On the limiting nature of variation, but does not connect selection to decreased variation.

  It cannot be asserted that organic beings
  in a state of nature are subject to no variation; it cannot
  be proved that the amount of variation in the
  course of long ages is a limited quantity; no clear
  distinction has been, or can be, drawn between spe-
  cies and well-marked varieties.
  (p. 425)

On variation over the long run.

These are the most interesting sections I found on the subject from my (quick and limited) searches. I hope you find them useful. However, this is only based on the first edition of "On the Origin of Species", and it is possible that it is is modified in later editions or that he touches upon this in his other writings. However, when looking at these particular passages in the sixth edition, I cannot see a major change in his thinking.