The antiquity of man What are the oldest fossils of modern man? What is the evidence until now? I do not ask to know the evolutionary
chain that led to H. sapiens, but I wouldn't mind to hear it, nevertheless.

What are the official sources, like peer reviewed journals, confirming it?

I wish for reference and rigorous scientific analysis.

Try this article as a starting point;

Stringer, Chris B., and Peter Andrews. "Genetic and fossil evidence for the origin of modern humans." Science 239.4845 (1988): 1263-1268.

It is old, but it has been cited 918 times to date. That should be more than enough of a breadcrumb trail to find what you are looking for. Also if you click through to the Science Magazine page, it also has a list of relevant articles below the abstract. You may need a membership to AAAS or library access to get a copy of the actual article.

Also try a Google Scholar search for Modern Human Fossil Record. The above article is the second article referenced in this search.


What is this insect in this picture? I recently found this insect  near our veranda wall. What insect is this ?
Is it poisonous?

As you can see, it has multiple legs fine as hair, but it is not like a common millipede or centipede.
I searched for this insect by reverse Google image search without result.

Location: Kolkata, India

Nature: fast-moving, aggressive.

Unlike earthworms, this insect loves basking in sunlight.

I think it's Scutigera coleoptrata.

Source of the image.


Why are P and T waves curved and not straight (ECG) The P and T wave are in shape of a curve while the QRS complex is in straight lines.
What is the reason this is happening?

P wave represents atrial depolarization (hence atrial contraction).

Atrial depolarization takes only a split second, therefore its corresponding wave will be smooth and rounded.

Variations from this shape could be consequences of various heart diseases: for example,a spiked P wave is called P pulmonale and suggests right atrial enlargement.

T wave represents ventricular repolarization: a normal T wave looks like an

  upright low amplitude broad hump following the QRS complex.

Abnormalities in T wave could be the signs for multiple heart diseases, varying from myocardial ischemia to hyperkalemia.

In particular, peaked T waves suggest an hyperkalemia diagnosis.

T wave abnormalities are well documented here

The QRS complex corresponds to ventricular depolarization, which is faster and more intense than atrial or ventricular repolarization: hence a normal QRS complex is peaked.

In conclusion, P wave and T wave are rounded because these correspond to low-intensity electrical events while the QRS complex is provoked by an intense electrical event.


What is the difference between second and third generation sequencing I am writing the section about history of DNA sequencing in the introduction chapter and after reading quite a few research papers, I am still confused about them. Here I compile some questions to make sure that I understand it correctly.

Is second generation sequencing the same as next generation sequencing?
Is Sanger sequencing the first generation?
As of today, is there any commercial 3rd generation sequencing technology in use (or is it still in development)?

If there is any paper reference that could explain all of the above then it would be really great.

I'm assuming you mean DNA sequencing (excluding things like RNA-seq).

Is Sanger sequencing the first generation?

From Metzker 2010:

  The automated Sanger method is considered as a "first-generation" technology

Some of the technology that was in development when this review was written is no longer in development, but this is still an excellent review and a great place to start.

Is second generation sequencing the same as next generation sequencing?

Also from Metzker 2010:

  and newer methods are referred to as next-generation sequencing (NGS).

The "newer methods" in the review are:

Emulsion PCR based like Roche/454
Solid phase amplification like Illumina/Solexa
Single molecule like Helicos BioSciences and Pacific Biosciences

As of today, is there any commercial 3rd generation sequencing technology in use (or is it still in development)?

The development of single molecule methods (third item in the above list) has historically taken longer than the other two, so sometimes they are referred to as third generation. However, note how Metzker above considers them all "next-gen".

A recent paper from PacBio itself makes the distinction of halting:

  Second-generation sequencing (SGS): Sequencing of an ensemble of DNA molecules with wash-and-scan techniques.

  Third-generation sequencing (TGS): Sequencing single DNA molecules without the need to halt between read steps (whether enzymatic or otherwise).

Ultimately, I think the "generations" are more useful to make the "Sanger vs. Not Sanger" distinction. Sanger sequencing is very different than next-gen in terms of what kind of experiment you can do and what sort of data you obtain.

Past that, the number of a generation is more of a marketing term. For instance, at the bottom of the PacBio paper:

  Conflict of Interest statement. All authors are employees of Pacific Biosciences and own stock in the company.

In practice, PacBio competes with second generation platforms. It is in their interest to say their technology is on "another level" compared to what's available on the market, but in practice, this is debatable.

Anyhow, to answer your question:

There is a technology in use and commercially available which has been referred to as third gen (PacBio)
There was a technology in development that falls under most definitions of third gen (Helicos), which went bankrupt in 2012
There is a technology in development (ON MinION) that is single-molecule based and was introduced after PacBio, so if PacBio is third generations, so is MinION (although the MinION is apparently very different from PacBio)


How can facultative anaerobes exist without catalase? Catalase-negative bacteria may be anaerobes, or they may be facultative anaerobes that only ferment and do not respire using oxygen as a terminal electron acceptor

  A facultative anaerobe is an organism that makes ATP by aerobic respiration if oxygen is present, but is capable of switching to fermentation or anaerobic respiration if oxygen is absent

But if facultative anaerobes can be present in oxygen rich environments, don't they have to have catalase in order not to die?

There is another class of peroxide decomposing enzymes called peroxidases. These enzymes can catalyze the reduction of $\ce{H2O2}$ to water using an electron donor. However, unlike in the catalase reaction, the electron donor is not another $\ce{H2O2}$ molecule and no molecular oxygen is produced. Thus their presence would not be detected by the typical spot catalase test (which looks for gaseous oxygen generation). For example, NADH peroxidase catalyzes the following reaction to protect cells from oxidative damage:

$$\ce{NADH + H+ + H2O2 -> NAD+ + 2H2O}$$

Thus catalase negative organisms can still have a means of protection against $\ce{H2O2}$. You can read more in this textbook, specifically the section titled "Oxygen Toxicity".


How can Taenia solium (tapeworm) lay 35,000 eggs per proglottid? As far as I know TAENIA SOLIUM is an acoelomate which basically means that the space between the alimentary canal and the gut is completely filled [or] occupied by the mesoderm and they do not have primary body cavity as well as secondary body cavity then from where does the space comes in taenia to store that huge amount of eggs

The eggs are very small compared to the proglottid.

According to this site:

  T. saginata can be up to 4 to 6 meters long and 12 mm broad; it has a pear-shaped head (scolex) with four suckers but no hooks or neck. It has a long flat body with several hundred segments (proglottids). Each segment is about 18 x 6 mm with a branched uterus (15-30 branches). The egg is 35 x 45 micrometers, roundish and yellow-brown. It has peripheral radial striations and contains an embryo with 3 hooklets.

  T. solium is slightly smaller than T. saginata. It has a globular scolex with four suckers and a circular row of hooks (rostellum) that gives it a solar appearance. There is a neck and it has a long flat body (0.1 meter in length). The proglottids are 5 x 10 mm with a 7-12 branch uterus. The eggs of T. solium and T.  saginata are indistinguishable.

I assume that the measurements given for the T. solium proglottid relate to the dimensions of your diagram, and since this is a tapeworm it is thinner than either of these values, so let's assume 2 mm to make the arithmetic easy.

volume of proglottid = 5 * 10 * 2 * 10-9 = 100 * 10-9 = 10-7 m3.

The egg approximates to a 40 µm sphere = 33,500 * 10-18 m3

So, volume of 35,000 eggs = 1.2 * 10-9 m3

So, volume occupied by eggs = (1.2 * 1010-9 * 100)/1010-7 % of proglottid = 1.2 %

So, not much of an accommodation is required for the volume of the eggs, even allowing for errors in this approximation (e.g. I neglected spherical packing which would add somewhat to the volume occupied by the packed eggs).


Does one need to perform two Chi-square tests? A question from my University's Question paper 2016:

  A newly identified fruitfly mutant, cyclope eye –large and single in the middle of the head is hypothesised to be autosomal dominant. The experiment started with homozygous wild type females and heterozygous cyclopes males. The data from the F2 generation was 44 wild type males males, 60 wild type females, 110 cyclops males and 150 cyclops females. Does this support or reject the hypothesis$^1$? Use chi square to prove.

I think the following should be a proper approach at solving it:

H0= The proportion of cyclope eyed male and female is not that same,i.e. the gene responsible is not autosomal. $or$ There is an association between the sex of fruitfly and the phenotype.$^2$

H1= The proportion of cyclope eyed male and female is the same, the gene is present on autosome $or$ There is no association between the sex and the phenotype.$^2$

Chi square contingency test with Male and Female (in the columns) and Wildtype and Mutant phenotype (in rows).

Once the H0 is proved wrong (if it is proved wrong), we consider a next Chi-square test, goodness-of fit, where :

H0= The proportion of mutant phenotype is the same as the wildtype i.e. 1:1 ratio is followed

H1=The proportion and the mutant phenotype is greater i.e. the allele responsible is dominant.

When the final H1 is accepted the $^1$hypothesis is correct or else wrong.

$^2$ I'm not sure which one is better / proper.

Is it alright?

You should just have 1 chi-square test to test the hypothesis.

Note that the problem is asking about F2 generation, not F1.

H0 in a chi-square test is your prediction based on a model; H1 is that the real outcome differs from what is expected, so you have that a little backwards. H0 should be the expected counts knowing the initial proportions and expecting autosomal dominant inheritance.

Start with your prediction:

F1 generation will be half heterozygous males/females, half WT males/females, so F2 generation has 3 types of mating events:

Cc x Cc occurs 25% of the time, and 75% of offspring are affected

Cc x cc occurs 50% of the time, and 50% of offspring are affected

cc x cc occurs 25% of the time, and 0% of offspring are affected

Multiply these probabilities and you should have 43.75% expressing the phenotype; your prediction for the chi-square test is that you will see this same percentage regardless of sex.

From there, doing a chi-square test is simple and there are many many resources online for this (here is just one).


Why have parasites not evolved to be harmless? I have yet to understand why so many viruses or bacteria haven't evolved to be harmless (specifically, I don't know of any harmless virus). I think it would be greatly beneficial for a virus to control his population and use natural transfer channels that dont cause discomfort(like feces), since it would be allowed to stay in an organism indefinitely and would have a lifetime channel for transmission, hopefully getting to be the most common strain.

So, why have viruses not evolved to be harmless to their hosts?

There are actually many examples of viruses that have integrated into the human genome and were rendered harmless, perhaps even helpful.

This New Scientist article referencing this Nature article describes endogenous retroviruses, which are ancient viruses which have integrated into the human genome.

  About 9 per cent of our genome is thought to have come about this way.
  Until recently, these viral relics were largely dismissed as inactive
  “junk” that ceased to have any impact on their host many thousands of
  years ago. The discovery that HERVK, the most recent ERV to make
  itself at home in our DNA – probably around 200,000 years ago – is
  active in human embryos challenges that notion.

  Joanna Wysocka and her colleagues at Stanford University in California
  made the unexpected find while they were analysing gene activity in
  3-day-old human embryos, which are bundles of eight cells. Besides DNA
  from the parents, they found genetic material from HERVK. “The cells
  were full of viral protein products, some of which had assembled to
  form viral-like particles,” says Wysocka.

  Further experiments revealed that the virus appears to produce a
  protein that prevents other viruses penetrating the embryo, suggesting
  it protects the embryo from dangerous circulating viruses, such as
  influenza. It also seems to play a crucial role in the genetic
  activity of the embryonic cells, helping to genetic instructions to
  the cellular protein factories.

Additionally, the endosymbiotic theory is also another possible example. It is thought that mitochondria and chloroplasts are previously free-living, possibly parasitic organisms that ended up integrating into the host cell and living as an organelle.

In short, parasites absolutely can and do evolve into harmless versions of themselves. There are already discovered examples, and as the human genome is better understood, doubtlessly more would be discovered.


Derivation of Michaelis-Menten kinetics for discrete stochastic simulations According to this article,

  [...] the propensity function for the conversion reaction S → P in the
  well-mixed discrete stochastic case can be written $a(S) = \frac{V_{max}\cdot S}{K_m + S/\Omega}$ where $\Omega$ is the system volume.

I don't quite understand how this formula is derived from the non-discrete Michaelis-Menten kinetics $v = \frac{V_{max} \cdot [S]}{K_M + [S]}$ (see Wikipedia). According to my understanding, $[S] = S/\Omega$. If we apply this to the formula from Wikipedia we get
$$
\frac{V_{max} \cdot[S]}{K_M + [S]} = \frac{V_{max} \cdot S/\Omega}{K_M + S/\Omega} = \frac{V_{max} \cdot S}{\Omega \cdot K_M + S}
$$
which is not the same as $\frac{V_{max}\cdot S}{K_m + S/\Omega}$. So, how can one derive the formula from the quoted article (if it is correct)? If not, how can we correctly get to a discrete propensity function from the Michaelis-Menten kinetics?

I think I figured it out myself. Since $a(S)$ is in $\frac{mol}{s}$ and $v$ is in $\frac{\frac{mol}{l}}{s}$, we have that $a(S)= v * \Omega$.
Therefore
$$
a(S) = \frac{V_{max}\cdot [S]}{K_M + [S]} \cdot \Omega = \frac{V_{max}\cdot S / \Omega \cdot \Omega}{K_M + S / \Omega} = \frac{V_{max}\cdot S}{K_M + S/\Omega}.
$$


Is telomere shortening consistant over consecutive cell divisions from zygote to a differentiated cell? Considering the complexity of embryogenesis, a temporal referance would be helpful to coordinate the developmental sequences during embryogenesis and fetal development which is to be completed within the gestation period. Can telomere shortening if consistant be used as a reference by every cell to do what it is destined to do at particular time frame? This is without considering the influence of telomerase etc.

This is also without prejudice to the role of DNA directed molecular signalling.

To repeat the question is telomere shortening consistant over consecutive cell divisions from zygote to a differentiated cell? If so can it function as temporal control of embryogenesis?

It is not consistent, and so cannot function as a temporal or generational signal. Not because the telomere shortening is unpredictable, but because of telomerase activity in the embryo.

If it did, gamete production in specialized tissues like the ovaries or testes would have shorter telomeres than the zygote they originated from. Each generation would have shorter telomeres than their parents. They would be genetically 'older', which can't go on forever.

Development is incredibly complicated and mediated by a large number of genes. Try homeobox genes for developmental layout.


Replacing, instead of repairing, DNA I've been doing some light reading on DNA damage theory of aging. One of the main ideas from that theory that I got is that the accumulation of damage in our DNA is one of the biggest causes of why we age, which is quite intuitive for a non-biology major like me. Furthermore, there has been research on DNA damage repair pathways and ways on how nanotech can help repair DNA. The technicalities are beyond me. My question is

  If accurate DNA repair is such a difficult mechanism to sustain over a
  lifespan, then why not catabolize DNA and replace it with a new one?

It seems very feasible to synthesize human DNA (please inform my ignorance, if I'm wrong. lol.) and it looks very promising after reading this: https://www.wired.com/story/live-forever-synthetic-human-genome/.

EDIT: It was pointed out to me in the comments that my question is too broad, please do tell me how to make it more specific, if you agree that's the case here. I'm very happy to accept technical answers, since I can always retrace it to the basics.

It seems very feasible to synthesize human DNA (please inform my
  ignorance, if I'm wrong. lol.) and it looks very promising after
  reading this:
  https://www.wired.com/story/live-forever-synthetic-human-genome/.

It is certainly possible to synthesize human DNA, but it's another thing to create a functional chromosome. In fact, in the article you link to, they are discussing a research effort to synthesize a human Y chromosome. As far as I can tell they haven't actually done this yet, they are just proposing to attempt it. George Church is a highly regarded genomicist, but the article is very sloppy about distinguishing what they think they can do from what they've actually done. There has been work with human artificial chromosomes (HAC), but these have been special purpose constructs that successfully replicate and divide in cells, but don't duplicate an entire natural chromosome.

Synthesizing a human genome would just be the start of the therapeutic process. You then face the question of how to place the synthesized genome in the cells of the recipient. Current approaches to gene therapy involve inserting a single "repaired" gene into a virus, and then infecting the relevant tissue with that virus. This doesn't insert the gene into all cells of the body, just the ones infected with the virus. For some simple genetic diseases this is enough to relieve the symptoms of disease. You can't insert an entire human genome into a virus though.

It's also been proposed to harvest stem cells from the recipient, modify them with the repaired gene, and re-insert them in the diseased tissue. Again this would affect only a portion of a single tissue, not all the cells of the body. It's also one thing to insert a short sequence into a stem cell, but nobody knows if you could swap out a stem cell's entire genome and still maintain it as a stem cell. Also, this would only work for tissues that are still actively dividing. Many important tissues (in the brain for example) have stopped dividing or divide only slowly in adults.

Even gene therapy involving single genes has been approved in only a handful of diseases. It's sill almost entirely experimental. What you are suggesting is still in the realm of wild speculation. Speculation can be inspiring and motivates research programs, but don't starting counting chickens yet.


Can you recharge without sleeping? Sometimes it's difficult falling asleep for almost an entire night. You might feel like getting up and being productive instead, or 'pull an all-nighter'.

Or you can try to simply lay in bed to relax and rest, even though sleep does not kick in. In this situation, you may eventually fall asleep, only to be woken by your alarm just an hour or two later. Upon waking from such short sleep you can feel completely wrecked.

It leaves me wondering if you would feel more rested if you didn't sleep for just one hour. Maybe if you could relax throughout the night without really sleeping, you'd feel more rested by the time your alarm goes.

But is it physically possible to recharge as if you were sleeping without actually sleeping?

No, you cannot. Although we don't know how sleep works, we know that lack of sleep is very devastating to the body, and nothing (including laying in bed relaxed but awake) can replace it. If a rat experiences 100% lack of sleep (somebody keeps it awake all the time), this will kill it sooner than 100% lack of food would. There are no wake-until-you-die studies in humans, but even reduced sleep has very bad effects, both cognitive (it impairs you similarly as if you were drunk) and physiological (metabolic changes: you need more energy for the same actions, and food intake increases disproportionally).

If you have insomnia (and yours sounds severe), you need to get it treated. There are different options depending on whether an underlying cause is found, and whether behavioral therapies turn out to work for you. There are no alternatives which replace sleep.

The above is just a summary. For a dry but very reliable source on sleep, see Principles of neural science (ed. Kandel et al), Chapter 51 written by David McCormick and Gary Westbrook. For a very good popular science book on the subject, see Sleep thieves by Stanley Coren, I can recommend it for anybody with insomnia.


Knockdown of long noncoding RNA (lncRNA) - how is it done? I don't work at the wet lab and don't know all the details about the knockdown techniques.
My question is:
How lncRNA knockdown is done?
For example - you have lncRNA that is functional in the nucleus. How is it possible to do knockdown using iRNA if interference happens only in the cytoplasm?
Sorry if there is biology related misconception in my question.

Knockdown of lncRNA in mammals is not done via RNAi. Instead, one transfers antisense DNA oligos which bind to the RNA. This triggers the action of the RNase H enzyme, which degrades RNA-DNA duplexes. It degrades the lncRNA.

UPDATE: For reference, I learned about this from a seminar, and it is not very well documented, but after some literature search I found this paper to quote:

  Although we (Fig. 3A) and others (42, 49) have used siRNA to knock down NEAT1 lncRNA and although the knockdown of strictly nuclear RNAs has been well described (53, 54), we remained concerned that because NEAT1 is mostly a nuclear RNA (55), it may not be very efficiently targeted by the RNAi machinery. Nuclear RNAs, however, are proficiently targeted using complementary antisense (AS) oligodeoxynucleotides that recruit nuclear RNase H activity to degrade the RNA (56). Hence, we also employed complementary AS oligodeoxynucleotides to knock down NEAT1 lncRNA in HIV-1 NL4-3-infected Jurkat cells (Fig. 4C, left). The AS approach reduced NEAT1 (Fig. 4C, left) and increased HIV-1 p24 production (Fig. 4C, right), providing results consistent with those from siRNA-mediated knockdown of NEAT1 (Fig. 4A and B).


Why are plasmid genes not already incorporated into bacterial chromosomes if necessary for stressful situations? If plasmids are important for bacteria to express specific genes under stressful conditions, why are these genes not already incorporated into their chromosome to begin with? What is the evolutionary significance for this?

Plasmids do have the advantage that they replicate independently of the cells chromosome and that they can be transferred between different bacteria. This spreads the gene encoded by the plasmid to other bacteria, which then can also survive.

Think about antibiotic resistance. Bacteria which have a plasmid which allows protection against the antibiotic will survive. They can transfer this protection to other bacteria which then also become resistant. This can either happen through pili which develop between bacteria or also via the uptake of plasmid DNA from the environment in a process called horizontal gene transfer.

Additionally mutations on the plasmids are not as dangerous on the plasmids than on the chromosomal DNA, where essential genes might be damaged. Plasmids can also get lost, if they are not needed by the bacteria due to a missing selection pressure, which is also much harder for genes encoded on the chromosome.


Can Taq polymerase be stored with PCR primers? I don't think it's possible for TAQ to be stored with the primers, but I'm not sure. This storage wouldn't be long-term (a few days, or a week at most). Thoughts?

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

Thermo Fisher
Sigma-Aldrich
BioRad
Promega
Qiagen

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


Can you eat enough to make your stomach explode? Background

After eating a large meal last night, I noticed that my tummy had significantly enlarged. After that, I started wondering if eating too much could cause a stomach to explode. Could this actually happen?

Question

  Are you able to explode your stomach by eating too much? Can it pop or break?

I assume your body would just regurgitate the extra food.

  What if you held in the regurgitation? Then would you explode?

Here's a simple cross-section of the stomach (from here):

The stomach accomplishes much of its function by mechanically breaking down the swallowed food particles and mixing them with acid and enzymes into a sort of slurry. To do this, there are three major layers of muscle surround the stomach - from the outside, the longitudinal layer, the circular layer, and the oblique layer. The stomach also has two holes in it - the gastroesophageal opening, coming from the esophagus with the swallowed food/saliva mix, and the pylorus, where the food/acid/enzyme slurry exits into the duodenum, which is the beginning of the small intestine.

Due to the three layers of (rather strong) muscle, the stomach doesn't have a lot of expansion capability once it is filled completely to capacity. Fortunately, this almost never occurs (despite how we may feel after a large meal) because material is always leaving the stomach on its way to enzymatic digestion in the intestines. Additionally, once the stomach is filled to a certain extent, hormones such as leptin are secreted that give you the feeling of being sated, or full, triggering the brain to make you stop eating.

Of course, as we can see with the current epidemic of obesity around the world, the stomach can change its size over time. However, this is a rather slow process (weeks to months to years) of adapting to continuously consuming large meals.

But what would happen if you completely ignored these internal warnings, or were being force-fed, or whatever? Instead of rupturing (the biological equivalent of "exploding"), food would most likely be expelled either into the small intestine or back into the esophagus and back up the way it came down, i.e. causing vomiting.

For this answer to be complete, however, I should point out that stomach or gastric rupture is technically possible, although it is an extremely rare occurrence. Cases have been described in the literature (1, 2, 3, etc.), but they are rarely correlated with overeating or eating disorders like bulemia. In cases that are, other pre-existing conditions such as gastric ulcer have been found on autopsy that likely weakened the stomach wall in the first place. The bottom line - if you're an otherwise healthy person, a single instance of massive binge eating is very unlikely to end in stomach rupture, as vomiting will most likely begin well before you are in significant physical danger.


Animal reproduction when resources are scarce (This question is aimed at animals that take care of their young, e.g. dolphins.)

As I understand it, most animals reproduce if possible. The only way they don't is because they run out of resources. I'm wondering how this shows up in practice:

Do they simply not have sex? If so, does this mean they don't have sex drive?
Do they conceive and then let their children starve to death?
Do they fail to conceive (that is, are there biological changes to a mother who's not getting enough food such that she is no longer fertile)?

Option #2 seems the least likely to me because presumably pregnancy involves a cost to the parent, and with resources already scarce this would be a waste; however the plot of White Fang does indeed involve this situation (I have no idea how scientifically accurate that book is however).

This is actually a comment, but was not allowed to comment.

I think what you're interested is more in population dynamics and I think what you're really asking about is more in line with what system of  differential equations explains a network of animals and how their populations grow and decrease with the amount of resources and the species population.

I think the problem is that, there's actually no good model, because there are so many factors which seem to contribute to shifts.

@ MIT this year, they had a visiting prof from Tufts give a talk on this, and they're working on models, to try and describe this, and even HE- the prof said, yeah, it gets complicated even for two species.

I would recommend, that if you have time to read up on this?

https://sites.tufts.edu/hening/publications/ <--- a link to his publications

https://arxiv.org/abs/1710.01220

Also, this is probably more a question for the mathematics stack.


Larvae appearing after many rainy days After a few days of raining, I found these larvae in a puddle. What animal are they from?

They are the final stage of a mosquito larvae, called "pupa".


Pyruvate oxidation - where did the hydrogen come from? As shown in the diagram above, NAD+ is reduced and becomes NADH by gaining two electrons

Now, where did the hydrogen come from?

In the diagram, pyruvate has 3 hydrogen, but it still has 3 hydrogen in acetyl CoA.

The Wikepedia page has a really good diagram of the reactions involved. The Pyruvate Dehydrogenase Complex facilitates the removal of CO2, and the addition of two hydrogen atoms to the overall reaction come from the FADH2/FAD molecule.


Retrieve the associated annotation from Uniprot I have a dataset that I extracted using Cytoscape and STRINGAPI
Hoz can I retreive the annotation of that network from uniprot  as it has more than 1k proteins . and doing it manually is not possible

You can upload your list of accession numbers to the batch retrieval service for the UniProt Konwledgebase, http://www.uniprot.org/uploadlists

A video tutorial for this service is available at https://www.youtube.com/watch?v=kLdgjqWoMZc

Once you have retrieved your proteins, you can click on "Columns" to customize your output and add columns, e.g. for function annotation. See also http://www.uniprot.org/help/customize or http://insideuniprot.blogspot.ch/2015_03_01_archive.html
Results can then be downloaded in tab-separated format.

If you have any additional questions, please don't hesitate to contact the UniProt helpdesk.


Warburg effect in lung carcinoma, the logic? Outside of 'purposefully' removing mitochondria to diffuse cytochrome C's apoptotic threat, I would assume that lung carcinomas, and their proximity to high oxygen levels, would have the lowest rate of cells entering the Warburg effect. Would this be a correct assumption?

Thanks

As far as I can tell, there are no data to support your hypothesis. Someone correct me if I'm wrong.

There's actually some data to support that aerobic glycolysis occurs in lung carcinomas despite their proximity to oxygen (ref). There's even an article on the prolifertative pathway behind lung microvascular endothelial cells (ref), alluding to this requirement for anaerobic glycolysis in rapid proliferation.

T cells exhibit a similar pathway, switching to aerobic glycolysis in the effector phase where T cells are rapidly expanding (see clonal expansion). The general trend is that the Warburg effect lends itself to the rapid accumulation of biomass, supporting rapid cell division, instead of energy production to support cell survival (ref). You could rationalize it like cancer is already a failure in cell death, and so the cancer cells need to worry more about carbon compounds that support rapid division. There was also a paper by Cai et al. in 2014 that described their hypothesis behind aerobic glycolysis in cancer, whereby the Warburg effect helps tumors resist anoikis and thereby promote metastasis (ref).

It may be that the Warburg effect is a means to a required end for cancer cells, but as far as I know there's is no correlation between proximity to oxygen and incidence of Warburg metabolism. There are papers out there that continue to ask: is the Warburg effect a cause or consequence of cancer (ref? My thought is that cancer cells will undergo the Warburg effect at a given stage regardless of histology or behavior because it's beneficial.


Uncompetitive inhibitors In Uncompetitive inhibitors , the Km decrease .
With uncompetitive inhibitors , the affinity of the enzyme for the substrate (E+S) increases .

I've searched up on the net and it says that the substrate has now been taken up to form E-S and E-S-I , therefore consuming more substrate than the original inhibitor-free equilibrium .

E + S -> ES (equilibrium position shifts to the right)

I've read up on all these and more doubts form in me .

Why is substrate needed to form ESI ?

I understood what it meant by equilibrium position will shift to the right . It is harder to form E + P as more substrate will form ESI.

Thanks !

An uncom-petitive inhibitor doesn't compete with the natural substrate of the enzyme for active site i.e. it binds at a site distinct
from the substrate active site and binds to the $ES$ complex.

$K_I$ is the equilibrium constant for inhibitor binding to $E$ and $K_I^{'}$ is the equilibrium con-
stant for inhibitor binding to $ES$. Uncompetetive inhibitor lowers the value of $V_{max}$ and $K_m$.


is left brachiochephalic vein and left pulmonary artery is same? I am reading about ligamentum arteriosum which connects the left pulmonary artery and descending aorta. But I am seeing that if any figure shows left brachiochephalic vein it does not show left pulmonary artery (and vice versa). Are they both the same?

No, they are not the same.  The left brachiocephalic vein receives de-oxygenated blood from the left subclavian vein (draining the left arm) and the left internal jugular vein (draining the brain and parts of the face).  The brachiocephalic vein then joins with the superior vena cava which flows into the right atrium.

The left pulmonary artery carries the deoxygenated blood that has just passed through the right atrium and ventricle, through the pulmonary trunk to the left lung for oxygenation.

In the foetal circulation, the ductus arteroisus (before it closes into the ligamentum arteriosum) allows blood to bypass the lungs, which are not oxygenated in the uterus!

Please see this diagram (which shows the foetal circulation including PDA for you).  The left brachiocephalic vein is circled in yellow, whilst the left pulmonary artery is circled in green.

Image from public domain edition of Gray's.


Best tail for swimming? I understand that the vertical tails of fish and the horizontal flukes of cetaceans evolved due to the spinal movements of their ancestors but I was just wondering if there has been any investigation into which was the most efficient for swimming (speed, required effort etc...)?

For lift-to-drag ratio (so, hydrodynamic efficiency), high aspect ratio semi-lunate tails are most efficient-- leading edge suction is implicated in their ability to produce lift (which provides the thrust for high economy swimmers) while minimizing drag. Convergence of multiple animals (tunas, swordfishes, jacks, pomfrets, whales, ichthyosaurs, etc.) on that tail shape is considered indirect evidence of it's hydrodynamic benefit. So, for speed and energy economy, a tuna like tail, independent of orientation in the water.

NB: other aspects of morphology and physiology are also very important in predicting performance, and a semi-lunate tuna-like tail has often coevolved with these other traits.

More info:
http://rspb.royalsocietypublishing.org/content/280/1756/20122071.short
http://jeb.biologists.org/content/213/1/89.short
https://academic.oup.com/icb/article/24/1/107/104211/Body-Form-Locomotion-and-Foraging-in-Aquatic


Genes related to senses and their variation across animals Animals often have very different numbers of active genes related to any sense. For instance, most fish or even aquatic mammals have very few olfactory receptor genes, whereas this is higher in terrestrial animals. Even among them, there is huge variation; compare dogs and humans, for instance. But this comes at a cost; for instance, dogs are dichromatic, the blind mole is, well, blind. So there is a compensation across the senses which is not merely a plastic change. I was wondering if there is any way to reconcile this with some notion of conservation of the total proportion of active genes involved with sensation.

There are two notions I could think of

There might have a trade-offs about where to spend ressources (energy and nutrients). If an organism spend a lot of ressources in, say, vision (incl. the part of the brain that deal with interpreting the input), then there won't be much left for other things.
When a sensory system is well enough developed that the other sensory systems would bring up only marginal benefits, it is better to just not spend unecceesary ressources on building these other sensory systems.

Please note that

The above two hypotheses are just guess work from me and I did not support any of what I said with an actual evidence.
I assumed that there is a negative correlation between the "quality of the different sensory systems" (whichever way that would be defined) but I don't know whether this is true or not.


How big can cold-blooded animals get? It seems impossible to have reptiles the size of dinosaurs, just because they are really big! Did they have different systems of maintaining body temperature or maybe they weren't the exact type of animals that we today call reptiles?

Answer is quite simple as from @Alan Boyd link. They are cold blooded and thus, can go out for hunt in cold, they need to stay put till they get some prey.

So, it mainly depend on the temperature of the outside, I found this interesting paper on relation of body sizes and latitude.

  Body sizes of poikilotherm vertebrates at different latitudes

  Maximum sizes of 12,503 species of poikilotherm vertebrates were
  analyzed for latitudinal trends, using published data from 75 faunal
  studies. A general trend appears which may be summarized by the rule
  "among fish and amphibian faunas the proportion of species with large
  adult size tends to increase from the equator towards the poles". The
  rule holds for freshwater fish, deepsea fish, anurans, urodeles, and
  marine neritic fish arranged roughly in order of decreasing clarity of
  the trend). In general the rule applies not only within these groups
  of families but also within single families. In reptile groups, the
  rule holds weakly among snakes and not at all among lizards or
  non-marine turtles. Possible explanations include an association
  between small size and greater specialization in the tropics; the
  possibility in poikilo-therms of heat conservation or of some other
  physiological process related to surface/volume ratio; selection for
  larger size in regions subject to winter food shortages; and an
  association between large adult size and high reproductive potential
  in cold regions. Other suggestions can be advanced, but all are
  conjectural and few are subject to test. Global size - latitude trends
  should be looked for in other living groups.

  Cite: Lindsey, C. C., 1966: Body sizes of poikilotherm vertebrates at
  different latitudes. Evolution: 456-465

Now lets compare some of the largest cold blooded Animals:

Reptiles
Amphibians
Fishes (Pisces)

Reptiles:

The smaller size of Reptiles give them more agility to hunt andsave them predators but some times when they are top of food chain they can grow as giants.
Anacondas (Eunectes), gigantic snakes from South America, are undoubtedly the largest living snakes.
The largest species, the green anaconda (E. murinus), likely only rarely exceeds 9 metres (30 feet) in length; nonetheless,
persistent but unsubstantiated reports have been made of anacondas that are 12 metres (40 feet) long.
The reticulated python (P. reticulatus) of Southeast Asia and the East Indies has been recorded at 10.1 metres (33.3 feet).

Others:

King Cobra(Ophiophagus hannah) 5.5 meters (18 feet)
Keeled rat snake (Ptyas carinatus), at about 3.7 metres (12 feet).
Nile crocodiles (Crocodylus niloticus) 6 metres (20 feet)
American crocodile (C.acutus) 4–5 metres (12–15 feet).
Marine leatherback sea turtle (D.coriacea) 2.7 metres (9 feet)
Galápagos tortoise (Geochelone nigra) 255 kg (560 pounds).
Komodo dragon (Varanus komodoensis) 3 metres (10 feet)
Green iguana (I. iguana) 2 metres (7 feet)

Green Anaconda http://www.wallshq.com/wp-content/uploads/main/2013_01/green_anaconda-wide.jpg
Green Anaconda

Amphibians:

According to Wikipedia:

  "The Chinese giant salamander (Andrias davidianus) is the largest
  salamander and largest amphibian in the world, reaching a length of
  180 cm (5.9 ft), although it rarely—if ever—reaches that size today"

Others:

West African goliath frog, 30 cm (12 inches) 3.3 kg (7.3 pounds)
Caecilia thompsoni 1.5 metres (5 feet)
Axolotl(Ambystoma mexicanum) 30 cm (12 in)

Chinese giant salamander

African goliath frog

Axolotl (Small 12 inch)

Fish:

West Indian Ocean coelacanth, (Latimeria chalumnae), is 80 kg (176 lb), and they can reach up to 2 m (6.5 ft)
African lungfish (Protopterus aethiopicus), 2 m (6.6 ft) and may weigh as much as 50 kg (110 lb)
Ray-finned bony fish (Actinopterygii)
Ocean sunfish (Mola mola) 4.3 m (14 ft) from fin-to-fin, 3.1 m (10 ft) in length
and weighed about 2,300 kg (5,100 lb)
King of herrings or oarfish (Regalecus glesne) 6 m (20 ft)( The longest
known king of herrings, which was hit by a steamship, was measured as 13.7 m (45 ft) long)
Bowfin (Amia calva)  109 centimetres (43 in) in length, and weigh 9.75 kilograms (21.5 lb).
European conger (Conger conger) 3 m (10 ft) and a mass of 110 kg (240 lb)
Lancetfish (Alepisaurus ferox) 2.1 m (7 ft) long and can weigh up to 11 kg (24 lb)
Houndfish (Tylosurus crocodilus) 1.5 m (5 ft) and a weight of 6.35 kg (14.0 lb)
Giant Tigerfish (Hydrocynus goliath) 1.5 m (5 ft) and 50 kg (110 lb)
Golden Dorado (Salminus brasiliensis) 1 m (3.3 ft) in length and weigh 31.4 kg (69 lb)
Tambaqui (Colossoma macropomum) 1 m (3.3 ft) and 32.4 kg (71 lb)
Giant barb (Catlocarpio siamensis) 3 m (10 ft) and a weight of as much as 300 kg (660 lb)
Muskellunge (Esox masquinongy)  1.8 m (6.0 ft) and 45.4 kg (100 lb)
Atlantic tarpon (Megalops atlanticus) 161 kg (350 lb) and length is up to 2.5 m (8.2 ft).
The Atlantic cod (Gadus morhua) grows to 2 m (6.7 ft) long and 96 kg (212 lb)
milkfish (Chanos chanos) 22.7 kg (50 lb) and 1.84 m (6.1 ft) long
Electric eel (Electrophorus electricus) 2 m (6 ft 7 in) in length, and 20 kg (44 lb)
Opah (Lampris guttatus) 2 m (6.6 ft) in length and weigh up to 270 kg (600 lb)

Source: http://en.wikipedia.org/wiki/List_of_largest_fish
Source: Britannica.com

Mola mola

Oarfish

West Indian Ocean coelacanth

Bowfin


Difference/similarity between adaptive radiation and species divergence? I've been reading various answers on different sites but I still don't know whether adaptive radiation and species divergence are different or similar.

My questions:

1) On some sites, it says that adaptive radiation is a form of species divergence, while on others it says that they are different. Which one is correct?

2) Is the main difference that adaptive radiation occurs relatively rapidly and species divergence takes longer?

3) Darwin's finches is used as an example for adaptive radiation, but is it also an example of species divergence?

4) Are the finches on the galapagos islands all difference species (one species diverged into many)? Or are they all the same species, just with different characteristics (e.g size of beak)?

Adaptive Radiation

A radiation refers to the process by which one species rapidly speciate into a number of different species. A radiation can be adaptive or non-adaptive. An adaptive radiation is a type of radiation when new species are formed through selection into new ecological niches. Such adaptive radiation typically occurs after the raise of a key mutation that allows for further specialization such as a mutation causing a change in the Pharyngeal jaw as observed in cichlids (Albertson et al. 1998).

You can learn much more on adaptive radiation in the book The Ecology of Adaptive Radiation by D. Schluter

Species divergence

Species divergence refers to the process by which two existing species diverge through time, either through the accumulation of neutral (or non-neutral but equally selected) mutations or by selection on different trait values.

Species Divergence and Adaptive Radiation

Because of the semantic difficulties behind the concept of species (see here), it is unclear from which point can we talk about species divergence and by which point the observed process of divergence is only divergence within a metapopulation.

Ignoring the eventual detail of the definition of species, and considering species divergence as referring to the divergence between any two lineage (whether or not in reproductive isolation), then it is clear that species divergence is part of the process of adaptive radiation.

To answer your multiple questions directly

1) On some sites, it says that adaptive radiation is a form of species divergence, while on others it says that they are different. Which one is correct?

Adaptive radiation is a little more than a form of species divergence as it includes also the event by which divergences starts.

2) Is the main difference that adaptive radiation occurs relatively rapidly and species divergence takes longer?

mmhhh... not exactly as the concept of radiation also refers to the event allowing the divergence to happen

3) Darwin's finches is used as an example for adaptive radiation, but is it also an example of species divergence?

Yes, indeed! No radiation, without species divergence. On the other hand species divergence will occur between any two existing species regardless of whether they speciated through a radiation

4) Are the finches on the galapagos islands all difference species (one species diverged into many)? Or are they all the same species, just with different characteristics (e.g size of beak)?

The Darwin's finches refers to about 15 (different) species. The different species of Darwin's finches do NOT refer to intra-species variation but to different species. In other words, there is some reproductive isolation between these different species. Again, you might want to make sure you understand the concept of species and you might want to read this post (same as the one linked above) on the subject.


Why do we use an autoclave at 121°C (250F)? (Origin) Let me start by saying I know why, but I am inquiring more about the origin.
My question is more related to literature that I cannot seem to find.
I've found some helpful papers and information on the origin of the using 121°C for sterilizing equipment, and killing bacteria but I wanted to ask the question anyways and see if anyone knew something more about it.
So to restate my question, I want to see data as to why 121°C and not 120°C?
Originally I though it is because the experiments might've been conducted in F and the inter-conversion from F to C yielded 121°C which is an odd number.
From what I could gather it started in the food industry with a company that made canned products and their canned products were exploding. This company approached MIT and after some research they found that at 121°C (250F) for 60 min in retort would kill the spores surviving the previous processing. (further exp. reduced the time to 10 min, for canned clams)
This is detailed in the paper which was published in 1897
https://www.jstor.org/stable/1623441?seq=1#metadata_info_tab_contents
The autoclave was invented in 1879 (18 years prior to the publication).
At the end of the publication it says:

Detailed descriptions of the organisms and of many more experiments will be given in our full paper on this subject to appear in a forthcoming number of the Technology Quarterly

I have not been able to find this specific issue of Technology Quarterly
The authors (S. C. Prescott and W. Lyman Underwood) also say:

As we have shown in our previous paper, in order to insure
sterilization in practice, it is necessary to obtain and maintain a
temperature in excess of 121°C (212F) throughout the contents of the
can. Intermittent sterilization may be employed, but is less efficient
and is not practicable upon a large or commercial scale. We have found
by experiment that sixty minutes at 121°C (250F) is sufficient time for
sterilizing corn, and it seems probable that this can be shortened
somewhat or the temperature reduced.

They are using °C, but since it's 1890's retorts (autoclaves) used in food industry might be F and the authors probably converted retort eqipment readings to °C for scientific community.
Also, this was what pioneered thermal death study and if you look at the temperature that they used for the study they are kind of sporadic. Probably because they wanted to see what temperature + time would reach the center of the can. The length of heating, or processing, and the pressure which is given vary somewhat in different factories and that might’ve been what led them to the 121°C and not 120°C.
Further research was done in this field:
In 1956 and 1958  F. H. Deindoerfer & A. E. Humhrey found that 250F (121C) is the optimal temperature to avoid damage nutrient media. They also discussed analytical methods for heat sterilization times.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1057515/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1057690/
What I've been specifically looking for is the first thermal death study with D&Z values that led to the widespread usage of 121°C. Andy why the time and psi required for sterilizing biological samples. I know and found papers on what is used to validate Autoclaves.
Geobacillus sterothermophilus (known as Bacillus sterothermophilus also) is used for validating autoclaves and that is due to it being very heat resistant, making a good biological indicator of microbial life post sterilization. The one paper I found which had some graphical data about its thermal death rate uses °C instead of F. I cannot seem find any information on the bacterial Log reduction at 120°C comparing it to 121°C. This answer might as well as be a mathematical equation leading to the that temperature, but that is only venue I haven't explored
Paper on Geobacillus sterothermophilus: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1057891/
If anyone can find that Technology Quarterly paper I mentioned at the start that'd be great.

The reason for 121°C and not 120°C is due to how autoclaves work and how they were developed. They sterilize with saturated steam under pressure.  Historically, we measure the pressure generated by the steam. Which leads directly to the answer.
Steam power was the basis of industrial process in the 19th century, and to use it safely required monitoring and controlling boiler pressure. Boiler explosions were not uncommon in the early days of steam power. The Bourdon pressure gauge was invented in 1849 and was a robust technology that yielded reliable and accurate measurement of steam pressure.
https://journals.sagepub.com/doi/pdf/10.1177/002029408702000803
When Chamberland invented the autoclave in 1879 from Papain's earlier pressure cooker, it relied exclusively on pressure measurement for control. Not until 1933 were autoclaves produced that monitored temperature at the drain line to confirm that air was exhausted and the steam was truly saturated.
https://www.steris.com/healthcare/knowledge-center/sterile-processing/everything-about-autoclaves
Study of steam engines was the basis for the development of thermodynamics and the kinetic molecular theory of gasses. Although steam is far from an ideal gas, there is a predictable relationship between temperature and pressure in saturated steam as well as well established properties of heat transfer. These can be found on standard engineering steam tables.
Examples: https://www.engineersedge.com/thermodynamics/steam_tables.htm
Saturated steam is very efficient in transferring heat. This is why scald injuries are so severe compared to simple burns at the same temperatures. It is also how saturated steam kills even heat resistant microorganisms in an autoclave. https://learnaboutgmp.com/good-manufacturing-practices-cgmp/saturated-steam-efficient-sterilization/
One earth atmosphere of pressure at sea level is defined as 14.69 pounds per square inch (psi), though in reality it varies a little bit due to temperature and weather. Because of this variation and because humans using Arabic numerals, arithmetic, and algebra like integer units in 5's; engineers often think of 1 atmosphere of pressure as 15 psi. This amount of saturated steam pressure is well within the capacities of typical steam boilers. This nice round of 15 psi saturated steam will kill even highly resistant bacterial endospores in about 15 minutes. A very reasonable time frame, and a nice mnemonic: 15 psi for 15 minutes.
The temperature of that 15 psi of saturated steam? 121°C.
And that is why we use a very unusual 121°C for typical autoclaving. It's because we are really using a rounded one earth atmosphere of steam pressure. And we did so without concern for direct temperature measurement for the first 50 years of autoclave use. In many ways the temperature of the autoclave was of secondary importance.


What the difference between an inverted and everted retina? I'm looking specifically for examples and comparisons, because the definitions of inverted and everted are remarkably similar; e.g. from Dictionary.com/Reference.com:

  everted
  verb (used with object)
  to turn outward or inside out.

http://dictionary.reference.com/browse/everted

vs. (esp. #5)

  inverted
  verb (used with object)
  1. to turn upside down.
  2. to reverse in position, order, direction, or relationship.
  3. to turn or change to the opposite or contrary, as in nature, bearing, or effect: to invert a process.
  4. to turn inward or back upon itself.
  5. to turn inside out.

http://dictionary.reference.com/browse/inverted

I'm curious because of this:

  Structurally, the cephalopod eye differs from the vertebrate eye.
  Cephalopods do not have a cornea, and the retina is everted so that
  the distal end of photoreceptive cells lies directly behind the lens
  and points toward incoming light. As a result, photoreceptor cells
  connect to the optic nerve behind the retina (Packard 1972).

From: Evolution: Education and Outreach
October 2008, Volume 1, Issue 4, pp 439-447

http://link.springer.com/article/10.1007%2Fs12052-008-0084-1
http://link.springer.com/article/10.1007%2Fs12052-008-0084-1/fulltext.html

via

https://en.wikipedia.org/wiki/Cephalopod#cite_note-Serb2008-12

If you have the rep please tag this with cephalopod; the tag doesn't exist and I don't have enough rep to create it. Thanks.

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

Hope this helps!


Why did life not evolve to use radio? We use electromagnetic communication everywhere these days. Cell phones, wifi, old-school radio transmissions, television, deep space communication, etc.

I'm curious about some of the possible reasons we have never seen biological systems having evolved to use electromagnetic, i.e. radio, for communication. The one obvious exception to this are organisms that generate their own light, i.e. bioluminescence. Cuttlefish are masters of this, and many other species as well.

It seems like bio-radio could have offered all kinds of evolutionary advantages for animals capable of using it.

Are their basic physical limits in chemistry, or excess energy requirements or something that would basically have made this impossible? Or was this perhaps just something that life never evolved to use, but would otherwise be possible in evolution?

There is a very different mechanism for generation (and detection) of ultraviolet, visible and infrared light vs radio waves.

For the first, it is possible to generate it using chemical reactions (that is, chemiluminescence, bioluminescence) with a typical energy of order of 2 eV (electronovolts). Also, it is easy to detect with similar means - coupling to a bond (e.g. using opsins).

For much longer electromagnetic waves, and much lower energies per photon, such mechanism does not work. There are two reasons:

typical energy levels for molecules (but it can be worked around),
thermal noise has energies (0.025 eV) which are higher than radio wave photon energies (<0.001 eV) (it rules out both controlled creation and detection using molecules).

In other words - radiation which is less energetic than thermal radiation (far infrared) is not suitable for communication using molecular mechanisms, as thermal noise jams transmission (making the sender firing at random and making the receiver being blind by noise way stronger than the signal).

However, one can both transmit, and detect it, using wires. In principle it is possible; however, without good conductors (like metals, not - salt solutions) it is not an easy task (not impossible though).


Which class of animals constitute the largest biomass? I found here that species-wise it is cow. But, collectively, insects may exceed even mammals. So, which class of animals constitutes the largest biomass?

Following from MarchHo's comment, I have not been able to find class-specific (in the formal sense) estimates, but if you meant 'class' in an informal sense, the following may be useful.

A nice infographic covering the relative biomass of all land mammals is here, and a full table for species groups (at the level of domesticated vertebrates, invertebrates, etc) is here (reproduced below).

Short answer: amongst animals, invertebrates are where the mass is.


What stops messenger RNA from binding to itself? Since mRNA is single-stranded, and (mostly) floats freely within the cytosol, what stops it from folding onto itself (like DNA) and preventing transcription?

It does fold on to itself. There are secondary structures in RNA and some of these secondary structures also have regulatory functions (for example, riboswitches). Some of these structures can also inhibit translation (by different mechanisms such as the masking of the ribosome binding site or analogous eukaryotic sequences, or stalling of ribosome etc). Other non-coding RNAs like tRNAs and rRNAs fold into specific structures that are essential for their function.

Many assays have been developed to study RNA secondary structure in vivo. SHAPE and DMS-seq are some examples.

The translation initiation factor eIF4A has a helicase activity that helps in resolving some secondary structures and facilitate translation (despite this, some structures can impede translation).

Also check out ribosome profiling experiments.


Could the growth rates of Vibrio vulnificus be affected by an oil spill? I live on the Gulf Coast, and Vibrio vulnificus has recently made the news due to an increase in the number of reported infections. Naturally, it has people around here worried. I live in an area that was affected by the BP Deepwater Horizon oil spill, and many people are concerned that the oil or byproducts of the clean-up could be fueling the growth of this and other bacteria.

I know that bacterial species which are capable of metabolizing the components of crude oil exist, but are rare. I also know that Vibrio vulnificus thrives in warm salt water, and since it is a "flesh-eating" bacteria that infects shellfish, it must be capable of "eating" organic material.

I can think of several possibilities that might explain an increase in reported infections:

The amount of bacteria and the number of infections is actually the same, but reports have increased due to more awareness in the public and in the medical community.
Warmer water temperatures in the Gulf in recent years have led to more bacterial growth.
The bacteria is capable of metabolizing crude oil, its degradation products, or one of the other cleanup chemicals (Corexit, for example).
The oil spill has compromised the immune systems of the organisms that are typically V. vulnificus hosts, which has led to higher infection rates and therefore, more bacteria.

There could of course be other explanations, but these are the ones I came up with off the top of my head. I imagine that if bacterial populations actually have increased, then any of these scenarios that are possible would likely contribute something.

However, in the short amount of research I have done, I haven't been able to find any concrete data that shows whether populations have increased at all, or whether they could be affected by the oil spill.

My questions are:

Are there any studies that show the population of V. vulnificus over a time period covering the BP Horizon spill (this happened in April 2010, and oil products are still washing up on beaches in small amounts)
Is it possible that it could be metabolizing oil or other chemicals related to the spill?

I found these article, which show exponential increase in population of Vibrio in BP oil spill region (published in 2011 supported in 2013).$^{1,2}$
There is evidence that Vibrio representatives can metabolize oil-derived compounds $^{3,4}$. There is a sizable amount, more than 31%, where found in the Deepwater Horizon Spill.$^5$. Though the reason is still to be proved $in\ vitro$, but studies shows they can persist in the presence of oil.$^6$
Source:
[1]:
High Numbers of Vibrio vulniﬁcus in Tar Balls Collected from Oiled Areas of the North-Central Gulf of Mexico Following the 2010 BP Deepwater Horizon Oil Spill
[2]:
Associations and dynamics of Vibrionaceae in the environment, from the genus to the population level
[3]: West 1984, Numerical taxonomy of phenanthrene-degrading bacteria isolated from the Chesapeake Bay.
[4]: Moxley K., Schmidt S. (2010). Preliminary characterization of an estuarine, benzoate-utilizing Vibrio sp. isolated from Durban Harbour, South Africa. Curr. Res. Technol. Educ. Top. Appl. Microbiol. Microb. Biotechnol. 1249–1254
[5]: Hamdan L. J., Fulmer P. A. (2011). Effects of COREXIT® EC9500A on bacteria from a beach oiled by the Deepwater Horizon spill. Aquat. Microb. Ecol. 63, 101 10.3354/ame01482
[6]: In situ and in vitro impacts of the Deepwater Horizon oil spill on Vibrio parahaemolyticus.


What do the Clustal Alignment Symbols Mean? Occasionally I will run protein alignments on peptide families and I can never remember what the symbols mean to show degrees of identity. What do they mean?

From the FAQ for the Clustal-W2 program:

An * (asterisk) indicates positions which have a single, fully conserved residue.
A : (colon) indicates conservation between groups of strongly similar properties - scoring > 0.5 in the Gonnet PAM 250 matrix.
A . (period) indicates conservation between groups of weakly similar properties - scoring =< 0.5 in the Gonnet PAM 250 matrix.

Therefore the hierchy of conservation using these symbols is * (identical) > : (colon) > . (period).


By what mechanism does an obstructed bile duct cause excess fat in the stool? By what mechanism does an obstructed bile duct (for example gallstones) cause steatorrhoea (excess fat in the stool)?

The function of bile produced by the liver and concentrated in the gall bladder is to aid in fat digestion.  Bile acts as an emulsifier to allow the fat to be packaged into small droplets, micelles.  The breakdown of fats into small micelles greatly increases the surface area for lipases produced by the pancreas have to act on.  These are then absorbed across the intestinal wall.

Bile breaking down large fats into small micelles

If this first step of bile production and transport is lacking (due to liver dysfunction or obstruction anywhere in the biliary tree), the fats are not packaged into micelles and are consequently very hard to digest.  They pass through the entire alimentary canal virtually undigested causing steatorrhoea, fatty, bulky and foul smelling stool.

The Biliary Tree


Hepatitis Lab diagnosis based on serology HBcAg which can't be detected in serum can be detected in hepatocytes , why is it so that they become detectable in hepatocytes?

HBcAg is capsuled by HBsAg and therefore can't be detected, while within the cells it's still free (before assembly of the virus).
The test checks for presence of antibodies (IgM) against HBcAg. It does not try to detect HBsAg anyways.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC154683/


How can DNA profiling be used to determine the number of organisms from a specific species that is within a certain area? Here is the tedious exam question that asks this: question 8(b).
https://drive.google.com/drive/folders/0B23NLD5L6099VWJya3dfLVJpbmc
The question states:

In 2007, the brown bear was a threatened species in Alberta, Canada. A study was carried out to determine the number of bears in the area. Fur wascollected from trees that the bears had rubbed against and their DNA analysed.
(i) Explain how DNA analysis would help the scientists to determine the number of bears in the area.

The answer simply states:

idea of comparing bands

idea that each bear has unique {DNA / banding patterns}

idea that the number of different banding patterns would equate to the number of different bears

My question is: How does the entire process fit into together?
I am absolutely baffled as to how the entire investigation would fit into each other, and I've been trying to articulate it for hours. It seems like if I'm just going to be collecting fur samples off trees there are going to be cells belonging to different species, then the DNA pattern produced will include a different number of bands from all of the different species. To overcome this problem, I think 'would we somehow separate the different cells into different groups with each group belonging to a specific bear by some technique that isn't DNA profiling and I don't need to know about at high school level? I then reason that we would have accomplished our task of identifying the number of different number of bears present within the sample. How would one identify the different numbers of bears?
The second part of my question is that I don't understand how the different samples from trees and fur will be used in order to estimate the overall population size within the area? The only animal sampling technique that I know of is that capture-recapture method.

The general process of DNA profiling (I prefer calling it "DNA fingerprinting", but that's just me) generally involves developing PCR primers specific for a particular region surrounding some sort of highly polymorphic region. So in this case one would need primers surrounding VNTRs (or other polymorphic regions, have a look at the wikipedia article for an overview of some other methods). Presuming the PCR primers are specific for bears (one could blast them to get an idea of this), then regardless of what other animals were mixed in, the resulting bands would predominantly be from bears (after all, PCR results in an exponential amplification of favored species). This would be answer part (1).

For part 2, one needs to find a sufficient number of sufficiently variable regions for profiling to work. A single site might not be informative enough, but a couple of them together will be.

Part 3 is the logical outcome of parts 1 and 2. If you can amplify a bunch of mixed samples together and the repeats are of variable length (thus the use of VNTRs or similar repeats), then you'll see those as different sized bands on a gel.


How far does eardrum move? Sound waves move human eardrum back and forth, like the peak to peak excursion of speaker driver, how much is it though? Ofcourse this movement depends on sound pressure, frequency and even location on eardrum, the edge moves less than center just like rubber surround around driver diaphragm.

I am interested in center of eardrum, the part of it that moves the furthest. The SPL is 100db at the eardrum and I would like to know how far it moves at 20 Hz and 20 KHz. I know this is hard question without specific answer becose every person have different eardrum but I believe there must be some rough average, some decent estimation about how much is it.

Is it micrometers? Is it nanometers? Or does it exceed 1 milimeter?

Tympanic displacement measurement (TMD) is a well studied field using hi-tech tools (i.e. stroboscopic holography), and complex units:
Vm = volume displacement in nl nanoLiters.
μm/pa (UDTF) = Linear tympanic membrane displacement is known as the umbo displacement transfer function.

The graph on the left gives you a value of 0.8-0.6 = 0.2 microns:

The graph above can be seen as resonances in an images sequence of stroboscopic holograms of tympanum (cool name to call your band) https://i.stack.imgur.com/fD6E9.jpg

According to this graph a 94dB sound wave gives you 0.1 micron displacement and a 100dB sine wave gives you 2pa, 0.2 microns.
https://i.stack.imgur.com/O7nQL.jpg

The first research document on google gave me a volume displacement from -120 to -700 nl.

1000 nano Liter = 1mm3

So the TMD volume displacement when very loud can be 1-2mm3, and eardrum rupture probably occurs from 10 to 100 mm3.

There are even muscles in the ear that can modify the way that you hear, i.e. the stapedius muscle which protects against low fequencies, and perhaps which can focus your eardrum elasticity modulus to let hear different frequencies, perhaps conciously? fascinating, I don't know.

See also pages describing elastic measurement of the eardrum, energy transfer by the tympanum by the cone, through these two google search phrasings: "eardrum response measurement" and "tympanic membrane displacement measurement"

Here is research comparing the eardrum to microphone design which is written easily.


The detail about the exact time of heart attack Storage of cholesterol in coronary artery tends to heart attack. But in which phase heart attack occurs? Why only a definite time is called heart attack? Why this is the extreme point of coronary block?

Acute myocardial infarction (MI) usually happens when a coronary artery is abruptly occluded, typically by a blood clot. The clot can be an embolus that forms elsewhere (such as in the heart itself) and then happens to flow into a coronary artery, or more often it occurs when an atherosclerotic plaque (containing cholesterol) ruptures. Because a ruptured plaque looks a lot like tissues outside the blood vessels, the clotting machinery in the blood responds like it would to stop bleeding from a wound.

MI can also occur in other situations where blood flow is reduced to a level insufficient to supply the cardiac muscle with oxygen, without complete blockage, either from vasospasm or when increased activity (such as exercise) demands more flow than can be delivered through a narrowed atherosclerotic coronary artery.


Gene frequency problem 1/330 of white people in south Africa have a disease called Porphyri.

What is the frequency of the gene if it is inherited autosomal recessive?

This one I understand. The genotype frequency is $q^2 = 1/300$ so the gene frequency has to be $\sqrt{1/300}$ as it is inherited aa.

What is the frequency of the gene if it is inherited autosomal dominant?

Here's where I run into trouble. So if $p$ is the dominant allele and $q$ is the recessive allele the allele frequency has to be $2pq+p^2$ right? As we can either see them as $Aa$ or $AA$

But my book says it is $2pq+q^2$ and then solves it algebraically by pretending $q^2$ is so close to 0 that it's not in the calculations. I strongly disagree that $p^2$ is very small if I am right with my assumption. Which one is right and why?

I think you pretty much nailed the problem. If I understand correctly, you are just confused about the approximation that your textbook does, an approximation that is correct but not needed. Let me restate the solution to the problem first.

Resolution of the problem

As you said the frequency of sick people $\frac{1}{300} = 2pq + q^2$ in this case, where $q = 1-p$ is the frequency of the (dominant) allele causing the disease. It is a simple quadratic equation with one unknown so one doesn't even need to make any approximation to solve for $q$ (or for $p$). Rearranging the equation and expressing $p$ in terms of $q$ (p=1-q), you'll find that $q ≈ 0.00167$.

Are the results intuitive?

Note that the frequency needed to create a frequency of $\frac{1}{300}$ sick individuals is $\sqrt{\frac{1}{300}} ≈ 0.05$ if the allele causing the disease is recessive while it is only about $0.0016$ (31 times less frequent) if the allele causing the disease is dominant. It shows that indeed a lower frequency of a more dominant allele is enough to create more sick people.

Is the $q^2$ term negligible?

Given that $q ≈ 0.00167$, the term $q^2 ≈ 10^{-6}$, while the term $2pq ≈ 10^{-3}$. So, indeed the term $q^2$ is rather negligible compared to $2pq$.


Identify this beetle from Bangladesh Location: Bandarban, Bangladesh

This appears to be some species of beetle (order Coleoptera) in the Bostrichidae family.

Commonly called auger beetles, false powderpost beetles, or horned powderpost beetles.

 Xylopsocus capucinus

Identification to species can be difficult, but fortunately for you Sittichaya et al (2009) created an illustrated key for IDing species associated with South Asia.

Based on their key and visual characteristics of your specimen, my guess is that your specimen is Xylopsocus capucinus

 Source: Sittichaya et al 2009 . a. lateral view; b. elytral declivity; c. intercoxal process of the 1st abdominal ventrite; d. dorsal view.

Description: 3-5.5 mm long; 1.4-1.7 mm wide. Shape is cylindrical and similar in general appearance to other common species of the family Bostrichidae.
Distribution: throughout South and Southeast Asia from India to the Indonesian archipelago.
Hosts: apparently polyphagous attacking almost any woody plant in suitable condition.
Phenology: adults emerge mainly
between May and November.

Like most false powderpost beetles, the head cannot be seen from above as it is downwardly directed and hidden by the thorax:

 Source: UFL IAFS

Sources:

Sittichaya, W., Beaver, R., & Ngampongsai, A. (2009). An illustrated key to powder post beetles (Coleoptera, Bostrichidae) associated with rubberwood in Thailand, with new records and a checklist of species found in Southern Thailand. ZooKeys, 26, 33.
Woodruff RE, Gerberg EJ, Spilman TJ (2005). A False Powder-post Beetle, Xylopsocus capucinus (Fabricius)
(Insecta: Coleoptera: Bostrichidae). University of Florida, IFAS Extension Publication No. EENY-179.
Institute of Food and Agricultural Sciences, University of Florida, 4 pp


Quantitative Traits Genetics Can someone please help with this question? I'm not so sure whether part A should be 11 inches or something else. Also, is part B correct

Question a

The only possible genotype that brings a phenotype of 12 inches is: $AABBCC$. Similarly the only possible genotype that bring a phenotype of 6 inches is: $aabbcc$. In consequence the offsprings can only be: $AaBbCc$ which measure $2+1+2+1+2+1 = 9$ inches.

Question b

Now the question is: if we breed two $AaBbCc$ how many offsprings measure 11 inches? Because there are three bi-allelic genotypes you have $2^3=8$ possible gametes and therefore you have to draw a 8x8 punnett square. Doing so, just count the proportion of offsprings that measure 11 inches. You can reason slightly more logically and get a faster answer. To measure 11 inches you need to have only capital letters in your genome except at one position. In consequence, if your father gives the gamete $ABC$, you mother should give the gamete $ABc$, $AbC$ or $aBC$. You can inverse the role of the father and the mother and it works as well. Therefore, you have 6 possible combinations that give rise to an offspring that measure 11 inches. Because there are $8 \cdot 8 = 64$ possible combinations, the proportion of offspring that are 11 inch-long is $\frac{6}{64} = \frac{3}{32} = 0.09375 ≈ 0.1$. About 10% of your F2 individuals are 11 inch long.


Cat's tail movement as an indicative of tension It appears to me that tail's twitching in the cats indicates how much tension the individual is under. During a hunt, when a cat tries to stay invisible, while approaching a target it is almost immovable, yet the tip of the tail keeps on moving restlessly.

Is there an explanation for such a behavior? How does it help?

According to Desmond Morris in Catwatching: The Essential Guide to Cat Behaviour, a cat wags its tail when...

  The cat is in a state of conflict. It wants to do two things at once, but each impulse blocks the other. (emphasis mine)

Then, some pages after that, Morris talks about what he called the dilemma of the suburban cat hunting a bird on a lawn:

  To start with, the open, manicured lawn robs the cat of all its natural cover, exposing its whole body to view. This is doubly damaging to its chances. It makes it almost impossible for the cat to creep near enough for its typical, close-quarters pounce without being seen. This puts it into an acute conflict between wanting to stay immobile and crouched, on the one hand, and wanting to rush forward and attack, on the other. The conflict starts its tail wagging furiously, and the same lack of cover that created the conflict then cruelly exposes the vigorous tail movements to the frightened gaze of the intended prey. (emphases mine)

That being said, your observations are probably of urban cats in this kind of conflict, in a situation where a successful attack is almost impossible. It's the conflict that makes the cat wag its tail and, as you can see, this behaviour doesn't help the cat at all.

A feral cat in the wild, in a effective attack, will not wag its tail.


How do our sensory organs work automatically without our conscious effort? I wonder how our different sensory organs (e.g., eyes, nose, ears, etc.) work automatically without our conscious efforts or without our command. We don't have to tell our eyes how to see, our ears how to hear, etc. How does this work?

Because consciousness evolved much much later than sense organs, and consciously seeing does not make much sense evolutionarily speaking.
We can consciously direct some sense organs, like the eyes, but signals sent sense organs by their very nature have to activated by outside stimuli otherwise they don't work as sense organs. If I could command my taste buds to taste cheese pizza while eating hay or poison it kinda defeats the purpose of having taste buds in the first place.
You really don't tell most of your body to do anything it happens automatically, becasue there is no benefit to doing it consciously, humans have more ability for fine motor control of some muscles becasue they help with things like speech or tool making, but having to learn to consciously control pupil dilation would take much longer and likely result in quite a bit of damage to the eye.
Now our eyes do have to learn how to see (or at least how to focus) and our brain has to learn how to interpret the impulses from our sense organs, but this is not really conscious learning. there is a cool experiment you can to to reteach your brain wrong see the inverted vision experiment but all the learning is without you being aware of it.


How close are we to having phages take over the role of infection control from antibiotics? What developments need to occur? The discovery of, and research in, the field of phages was overshadowed by the discovery and implementation of antibiotic treatments for infectious disease control.  With the rising concern of antibiotic-resistant microbes, is there a serious effort to refocus research and development to master the science and technology of phages?

This is a very interesting topic. Indeed, historically, it might seem that "phage therapy" research is in a dormant state. But there are some groups actively doing theoretical research on the synergy between phage treatments and the immune system, as well as research on how the appearance of antibiotic resistance could be attenuated by the use of phages.

Nevertheless, this research is not what the field is trending towards, since there is still hope to find new antibiotics (for which, then, we will see other types of resistance evolving), and most of the funding agencies are still privileging this instead of the alternatives.

A colleage of mine is working on this very same theme. Here is one of his recent research papers on a specific type of infection.

Cheers,

Pedro


For people who work in microbiology labs, what software do you use to manage your strains? It's just a small microbiology lab that currently records everything on paper, and there's quite few mutants as well. Is Excel commonly used for this sort of thing? Or is there a better software to manage a lab?

Thanks for any help

I would go for StrainControl Laboratory Manager. Works perfect and covers all needs of a lab. Do not go for all the "free" stuff since they rely on a active sponsor and your data is never safe.

StrainControl is free for 3 months and if you want to continue use it you simply purchase the Admin password and all your data is saved.


Why can't humans drink sea water? Why can't humans drink sea water?

It would seem to be a huge evolutionary advantage for an animal to be able to drink sea water rather than have to rely on fresh water, and it's provably not impossible due to the existence of sea mammals that must filter the sea water somehow.

Could someone explain to me any likely reasons that this is the case?

For humans, our blood and other tissues have a salinity which is less than that of sea water. The osmolarity of blood is 275-299mOsm/L, while the osmolarity of seawater is ~1000 mOsm/L.

The major reason we need to drink and excrete (sweat, breath and urine) water is to rid the system of waste- i.e. water soluble chemicals or heat we do not need.  The kidneys do a lot of this work and they need a reasonable osmotic potential to help them.

The osmotic potential is the tendency of molecules, for instance salts, to diffuse from one reservoir of liquid to another.  The kidneys burn metabolic energy (food) to create a slightly higher concentration of waste chemicals into the bladder/urine.  Other organs will fail or also work to maintain a local salt concentration (e.g. any nerve cell which depends on Na+/K+ concentrations to transmit their signals.  But the kidneys are the gatekeepers of salinity in the body.  They work hardest (and can get injured) when there is more salt in the water we drink. If you drink sea water you will quickly find your kidneys overworked and not really functioning.

That's why salt water will tend to make you thirsty (if you can drink any at all). Most people will gag when they drink even a little sea water, much less a glassful.

Sea mammals actually eat their fresh water. They rely on the fluid they get from fish to keep their salt balance.  Its true that some animals like fish and molluscs etc have adapted other means of keeping their salt balance in check.  Its just also true that its a lot of work to keep this ability and when animals move away from the oceans, they quickly lose that ability.


Why is an A-U bond less stable than an A-T bond? I have encountered the following fact many times, but have not yet encountered a possible explanation for it. Will you please help me understand the molecular mechanism by which the bond between Adenine and Thymine is more stable than the bond between Adenine and Uracil?

Thanks in advance

I was not previously aware of this assertion, but on doing a little searching found it discussed in the following paper (I'm not sure whether it is open access or not).

  Kamya PR and Muchall HM  (2011) "Revisiting the effects of sequence and structure on the hydrogen bonding and π-stacking interactions in nucleic acids" J Phys Chem A. vol 115 pp. 12800-8

From this it emerges that the claim relates to the effect of substituting U for T in DNA, and the paper references previous claims for a stronger AT hydrogen bond. It also references other studies which did not find any difference, so the question was/is contentious. All studies were made on particular stretches of DNA duplex, and the authors' own studies were on a wider range of duplex structures from the protein data bank and (apparently) used more sophisticated analysis. To quote, they concluded:

  "H-bonding in AT can be stronger or weaker than that in AU base pairs, depending on the particular choice of nucleic acids used for comparison"

They explain this in terms of the influence of neighbouring bases in the duplex on base stacking, which, depending on the bases (i.e. the sequence), can be enhanced by interactions with the methyl group of T. (There may also be other effects caused by distortion of the base-pairs from planarity in particular cases.) So it would appear that AT base-pairs are not intrinsically stronger than AU base-pairs, but can be stronger in certain three-dimensional contexts.

As a generalization, the premise of the question would therefore appear to be false.


What is the name of the bug that emerging from a wood chip like cocoon? We found it on the wall of a home at West Palm Beach Florida. Is this a kind of infestation or a sick tree near the house fall on the wall?

That is a bagworm moth, in the family Psychidae. https://en.wikipedia.org/wiki/Bagworm_moth


What is this animal looking like an Axolotl? My friend caught a strange looking animal and he's saying it is an axolotl. I keep telling him it's almost impossible, since they are almost extinct in their natural environment and he caught it in St-Larent River (Quebec, Canada)

Anyone have any idea what it is ?

Based on the size and location that appears to be a Common mudpuppy (Necturus maculosus). (Photo © Brian Gratwicke — CC BY)

The four toes visible on the front foot are also consistent with this identification.

This species is found throughout eastern North America and you can learn more about them from the Canadian herpetological society and iNaturalist.


Does body mass have a bearing on reflex speed? A reflex is an unconscious action in response to some specific stimulus, e.g., blinking an eye, or pulling the hand away from a hot pin

I know from school biology, and reading online that withdrawal reflexes are quick because

CNS is involved
Danger receptors send impulses to prevent inhibition of flexion

When a person is extremely obese, do these flexion impulses take longer?

Is a withdrawal reflex in an obese person noticeably slower than in case of a reasonably fit person?

I went into this with the same assumptions that jello did, but I found two studies that had some interesting results.

Isojärvi (2010) found that in obese and under-exercised adults, physical fitness level predicted, among other things, a significant proportion of the variance of nerve conduction velocity and F-wave latency.  So, these individuals may theoretically have a slower response to noxious stimuli.

While Type II diabetes is not always a result of obesity, there is often a high correlation between the two.  Oltman (2005) found that, in "Zucker diabetic fatty" rats (an animal model of Type II diabetes), motor nerve conduction velocity in the sciatic was significantly slowed.  This effect, too, would affect the rate with which an individual could withdraw a limb from a noxious stimuli.

So, I don't think that anatomical changes in the bodies of individuals who are obese would have any effect, but clearly there are physiological changes in the neurons of these individuals.

References:

Isojärvi H, Keinänen-Kiukaanniemi S, Kallio M, Kaikkonen K, Jämsä T, Korpelainen J, Korpelainen R. (2010). Exercise and fitness are related to peripheral nervous system function in overweight adults. Med Sci Sports Exerc. 42(7):1241-5.

Oltman CL, Coppey LJ, Gellett JS, Davidson EP, Lund DD, Yorek MA. (2005).  Progression of vascular and neural dysfunction in sciatic nerves of Zucker diabetic fatty and Zucker rats. Am J Physiol Endocrinol Metab. 289(1):E113-22.


Names of nerves in hands, shins and face I am looking for the names of the nerves in 3 specific locations of the human body:

The nerve running along the "top" (opposite side of the palm) portion of the thumb, from knuckle to fingernail (see 1st picture below); and
The nerve running along the anterior tibia (also see 1st picture below); and
The nerve(s) of the face running along the eyebrows and outer edges of the eye sockets (see 2nd picture below)

After looking here, here and here, the best I could muster was:

The median nerve is the nerve that carries sensory signals from the top of my thumb; and
The superficial peroneal nerve is the nerve that carries sensory signals from my anterior tibia

But in every diagram of the face's nerves, there are simply too many for the article/blog/diagram to enumerate, and I can't discern which specific nerve or nerves runs outside of the eyes and across the brows.

Any ideas? Here are the pics to solidify the specific areas I'm looking for:

Please note: this is not homework! And although it may be considered by some to be a rudimentary question, I have actively tried to research this myself and have come up short. Below, I explain all the failed methods I attempted to figure this out on my own. So all this to say: if you do down/closevote this, please don't do it because you think it's homework or because you think it shows a lack of research!

You are looking for the Trigeminal nerve, the largest nerve in the face. Here it is with its branches.

It is both afferent and efferent.

Afferent and efferent components of the facial nerve in the bullfrog (Rana catesbeiana)
Cranial Nerves Illustrated: Figure V-4 General sensory component of the trigeminal nerve, ophthalmic (V1) division.
General sensory afferent (blue-green)


Do organs or any structure in the human body shrink/shorten if it's function is no longer useful? Charles Darwin was one of the first scientists to theorize on the function of the appendix, which in his day had been identified only in humans and other great apes. He hypothesized that the distant ancestors of these animals survived on a diet of leaves, and so they required a large cecum, a portion of the gut that houses bacteria that can break down stubborn plant tissue. Later, he speculated, these ancestors shifted to a largely fruit-based diet that was easier to digest. A large cecum was no longer necessary, and it began to shrink...Darwin thought the appendix, which juts off of the cecum, is one of its former folds that shriveled up as the cecum shrank. Consequently, he thought it carried no function.

I recently read a source which states the above. It made me wonder that if there is some other organ/part in our body which may shrink as further evolution progresses and it's use diminishes, just like our appendix. I'd like to know if this 'theory of shrinking' applies to any organ that may become useless.

First of all, our appendix isn't 'useless'. Their is a high concentration of lymph nodes (higher than anywhere else in your gut), so it might not be needed for digestion anymore, but it's function somewhat shifted to a more immunological role.
Secondly, yes there are other organs/body parts that shrink over time. In evolutionary time, look at our tailbone. In monkeys it's still a full tail, in apes it's almost nothing, and in humans it's still present in the skeleton, but not visible on the 'outside' anymore. Probably in a few (hundred/thousand/..) years it will be completely reduced until it is no longer present in the human skeleton (because since we don't have a tail anymore, it doesn't have any function anymore).
Over a much shorter timescale it is also possible. For example the thymus expands in puberty, and afterwards it shrinks until it is almost completely gone.


How do the antibodies in colostrum survive the infant’s digestive system? What happens when the antibodies in colostrum reach the infant's stomach? Why aren’t they destroyed by digestive enzymes?

There are two main differences between adults and newborn babies which allow the passage of antibodies (while maintaining the activity) through the stomach and the resorption in the gut.

The digestive activity of the stomach in newborns is still immature and needs to develop. This results in almost no production of hydrochloric acid (which is responsible for the very low pH in the stomach). It can take up to two years to until the pH in the stomach of children reaches the level of adults (see chapter 5 in reference 1).  Because of this higher pH much more proteins (and other components of the milk like anti-microbial proteins, carbohydrates and lipids) can pass the stomach unaltered.
The other really important feature of newborns is their much greater permeability of their intestine. This allows an efficient transport from the antibodies into the blood stream and where they provide protection. See references 2 and 3 for more details.

References:

Breastfeeding and Human Lactation
Antibodies in  Milk
Intestinal permeability in the newborn


Does osmosis require a protein channel? Earlier today, I undertook an exam which featured a question regarding the stickiness of mucus in a person diagnosed with CF's. We had to explain why they had stickier mucus than a 'normal' person, given that CF changes the protein channels used for chloride ions to move through osmosis. This confused me, becuase I thought osmosis was through a permeable membrane, and active transport used a protein channel. I have googled it and I have been proved neither wrong nor right.

Basically, I want to know if osmosis requires or uses a protein channel, or the exam board wrote the question wrong and should have put active transport instead.

(Sorry for the waffle, I just felt some clarification is needed)

Normally, epithelial cells of mucous membranes express a chloride ion channel that allows movement of Cl- down its electrochemical gradient and out of the cell. This increase in extracellular electrolytes draws water out of the cells by osmosis, hydrating the mucus.

In cystic fibrosis, this protein is defective, most commonly caused by misfolding and subsequent degradation. Cl- cannot diffuse out of the cell and thus water is not drawn out, leading to thick mucus.

  ...given that CF changes the protein channels used for chloride ions to move through osmosis.

Water flows by osmosis, not ions.

  I thought osmosis was through a permeable membrane...

Osmosis does occur through permeable membranes, but large, bulk flow of water can be mediated by protein channels called aquaporins. Read more here.

  ...and active transport used a protein channel.

Active transport of solutes does use protein transporters, but they are not strictly "channels": "channel" is the term used for passive transport, also called facilitated diffusion when a channel is involved.


What is a regulable promoter? And how does one regulate it? I'm reading a patent where they (in S. cerevisae YNP5 strain):

  downregulate the ERG9 gene by replacing the native ERG9 promoter with
  the regulable MET3 promoter

What's a regulable promoter and how does one regulate it? Must one add something to the broth to down-regulate the expression?

I don't see anything special in the culture medium.

Regulatable promoter means that the expression of the gene downstream of this promoter can be either induced or repressed. Met3 is an example of such regulatable promoters and it is regulated by the addition of methionine to the media. In yeast, Met3 gene encodes for ATP sulphurylase, an enzyme in the methionine biosynthetic pathway. Upon the addition of methionine, the gene driven by Met3 promoter is repressed, as its expression level is reversely correlated with the concentration of methionine added to the media (Figure from this paper):


How does reversibility of lactic acid fermentation work? For the production of lactic acid we need pyruvate from glycolysis.
This process is known as lactic acid fermentation. One of the features of this process is reversibility. How does this reversibility work?

The enzyme catalysing this reaction in mammals is lactate dehydrogenase of which there are two major isoforms: LDHA and LDHB. The general reaction scheme can be shown as:

In muscles LDHA reduces pyruvate to lactate consuming one NADH. This gets rid of the electrons which would normally go through the respiratory chain. The lactic acid is then transported to the liver where it is turned back into pyruvate by LDHA producing one NADH. This is know as the Cori cycle.

Both enzymes however are very similar and can catalyse the reaction into either direction, they are just slightly different in structure which make them have a greater affinity for pyruvate or lactate.