Why do people with Down syndrome get fewer cancers? I'm coming across some conflicting information regarding the correlation between cancer incidents and trisomy 21. I read a report from nature that discusses how Downs are only a tenth as likely to develop cancers, but at the same time are 20x more likely to develop certain B cell malignancies.

One of the more prominent findings show that a regulator of angiogenesis, DSRC1 plays a significant role.

What I'm trying to find out is what gene(s) on 21 contribute to the associated risk for lymphoma?

And does there exist a good list of those genes on 21 that suppress or enhance tumor genesis.

This is a great question. Just to make it clear people with DS do have a reduced risk of solid cancers and an increased risk of blood cancers, (B-ALL and AML).

You are correct in picking out DSRC1 because of its angiogenic implications. The current hypothesis centers around people with DS being less capable of driving angiogenesis, and therefore having an internal environment that is less nurturing to metastasized or even developing solid cancers. Current unpublished work I have recently seen shows this very clearly in the eye, where the vasculature in DS is far less branched than in the wild-type population.

Why however they show an increased risk of leukemias is a largely unanswered question, with one exception being AMKL (Acute Megakaryocytic Leukemia). People with DS are at a ~500X increased risk of AMKL over the unafected population, and it appears to be entirely driven by the in-utero introduction of a stop mutation in codon 2 the transcription factor GATA1. This transcription factor is important in driving differentiation of progenitor cells in the bone marrow to become erythrocytes and megakaryocytes. Thus inactivating this transcription factor plays a large role in disrupting normal hematopoiesis such that megakaryocytes are overproduced and become a leukemia.

All that being said, and as you mentioned people with DS have around a 20-50X increased risk of AML and B-ALL. There are certainly some chromosome 21 genes that have been implicated in this like Bach1 (important in DNA repair) Ifngr2 (plays a role in cell death) Usp16 (epigenetic regulator Really important recent Nature Paper) and Runx1 (important in stress response) but the field is entirely unsure why this directly leads to increased risk of leukemias. Many current cancer biologists favor the direct gene-dosage problem that people with DS face in that a some ~120 genes are overexpressed when they shouldn't be, and assume that these gene level cocktail directly leads to this increased risk of leukemogenesis, and this very well may be in part the answer. There is however a great 'contrarian' view, in that hematopoietic stem and progenitor cells will become pro-apoptotic and pro-differentiative when faced with certain stresses like aneuploidy. The effect of this on a global scale would be that many of the stem and progenitor cells in the bone marrow would die or differentiate prematurely. This would then result in teenagers with DS having far fewer blood stem cells then they should, and these cells would then be tasked with pumping out more blood per cell than originally meant for them quite possibly leading to an exhaustive phenotype. In this way the blood systems of people with DS will 'prematurely age', and might thus rapidly increase the risk of cancer.

Make sense?


Is there a certain environment where all cellular functions (or at least some) increase their rate? Is there a certain environment in which all the functions (or some) inside a cell increase in their rate? Would the increased rate cause any damage to the cell?

There are optimal temperature, pressure and substrate concentration for each biochemical process. The optimal temperature and pressure for two or more (but not all) processes may overlap. So there is no SINGLE temperature or pressur where ALL of them will be at their maximum. Please note, by mentioning "cellular processes"  I meant all the biochemical(e.g glycolysis), physiological (cellular micro-transport) as well as physiochemical(transcription) processes. But we can try to provide substrates at reasonably high concentration ( keeping in mind negative feedback phenomena); we may reach the maximum achievable rate. All the above conditions follow bell-shaped curve; so I put the word 'resonably', as after the optimum condition is reached further increasing that condition will lead to decline in "speed" of reaction. We have to create an artificial enviornment using that substrate combination at proper concentration; as there is no such natural condition where that happens(cell always decrease one process while increasing another).

But it may seem to be a paradox - does anabolic and catabolic reactions both will increase simultaneously! E.g glycogenesis and glycogenolysis at the same time......well, as I already said this is not a natural condition; we are forcing substrates of one reaction at "reasonable" concentration keeping in mind the 'opposite' (is it??) reaction. E.g glucose produces glycogen by glycogenesis and that new glycogen is used in glycogenolysis; so we have to consider the concentration of glucose only. Isn't that easy! well, not so soon. Doing this requires lot of ATP, of course we'll get some from the glucose breakdown, but the need is even higher. So we have to provide additional ATP. Then there are second messengers (cAMP, DAG, IP3 to name a few of them). We have to nutralize them all( they favours unidirectional process).....this is a very complicated thing(just for example, we are supplying ATP, so cAMP will be automatically produced; so we should select all the enzyme blockers of cAMP production). But then electrolyte concentration will be disturbed and we need to monitor & regulate that also.

Thus it is clear that such condition requires sofisticated laborarory instruments.

N. B.
1. I considered only a single cell while discussing this.
2. The word "exhausted" was taken as progressive deterioration of cellular architecture, that leads to death.


How do Gram + bacteria use a proton gradient for F-type ATPase? Does anyone know of any papers showing how Gram positive Fermiculates or Actinobacteria use  a H+ gradient for an F-type ATPase, It seems impossible since there is no outer LPS membrane to maintain the protons in a periplasmic space. Is the use of ATPase for production of ATP exclusively a Gram negative thing?

I found this question "Production of ATP in Lactobacilli" but no answers:
https://biology.stackexchange.com/questions/14669/production-of-atp-in-lactobacilli

Protons are pumped out of the bacterial cell by the electron tansport chain. This creates a protonmotive force with two components, one due to the difference in proton concentration, the other due to the membrane potential that is created. In bacteria and mitochondria it is the membrane potential component that provides most of the driving force to pull protons back in through the ATP synthase. Thus the fate of the protons outside the cell doesn't matter too much. Even if you were to buffer the exterior absolutely, the fact that charge had moved out would drive ATP synthesis.


Is there a realtime molecular clock within the genome to co-ordinate the developmental sequences in an embryo? It is difficult to assume that the massive number of co-ordinated developmental sequences in a developing embryo is controlled by molecular signalling alone. Is anyone aware of a molecular or developmental clock within the genome which control the on off states of the genes concerned with developmental sequences? If it has not been reported is it likely to exist? (This is not about the molecular clock in evolution.)

Assuming there is a molecular clock, is it possible that the clock is switched on at the time of fertilization, and the zygote transfers the elapsed time to the progressive generations of the cells?

I think that the "molecular clock" that you refer to and the "molecular signaling" that you are skeptical of are one and the same thing.

In the 1960s, nuclear transplant experiments established that molecular signals in the cytoplasm can dedifferentiate terminally differentiated nuclei, "resetting" your molecular clock, or in the more common terminology "rerunning" the "developmental program" to yield viable animals.

This "developmental program" metaphor has been frequently used to describe this process, seeing development as a series of gene regulatory cascades; they called it a program because they were thinking of procedural computer programs. It isn't really a clock so much as a complex process by which different sets of genes are turned on and off in a concerted fashion, where one step depends on what happens in the previous step. An undergrad course discussing some of the mechanisms of this is posted here.

We've known for many decades that interrupting cellular processes such as transcription, translation, and DNA replication tend to arrest development at different points (for one early example see here).

A good example of a step/series of steps in the developmental program is the maternal-to-zygotic transition in metazoans, where embryos transition from using maternally deposited mRNAs as molecular raw material to de novo transcription of their own mRNAs.

From the linked review:

  As development proceeds, two processes are triggered that together form the maternal-to-zygotic transition (MZT): first, a subset of the maternal mRNAs is eliminated; second, the transcription of the zygotic genome begins. Initially, the destruction of maternal mRNAs is accomplished by maternally encoded products. However, zygotic transcription leads to the production of proteins and microRNAs (miRNAs) that provide feedback to enhance the efficiency of maternal mRNA degradation. In addition, among the earliest mRNAs synthesized de novo in the embryo are transcriptional activators that enhance the efficiency of zygotic transcription. The net result is that the control of development is transferred from the maternal to the zygotic genome.

  Figure 1. A comparative overview of the maternal-to-zygotic transition (MZT) in several model organisms. Key embryonic stages for each model organism are depicted schematically above the corresponding cleavage cycle and time after fertilization. The red curves represent the degradation profiles of destabilized maternal transcripts in each species. The light and dark blue curves illustrate the minor and major waves, respectively, of zygotic genome activation. The last embryonic stage presented for each organism is the developmental point at which there is a major requirement for zygotic transcripts.

This transition requires that the developmental steps based on maternally-deposited mRNAs have completed successfully before de novo transcription of embryonic RNAs can begin.


What is this crawling next to my house? I just found this outside my house while walking the dog. I was thinking it's some kind of slug? It's been raining a lot lately and today, so maybe that has something to do with it being on the pavement. I live in South Central Indiana, US. When it wasn't stretched out, I'd say it was 2-3 inches long.

It looks as though it has a keel along it's back (the area behind the mantle shield.)

If so (and I think it is), it would be a keelback slug, the coloration strongly suggesting a leopard slug (Limax maximus):

Coloration varies but the general pattern is a spotted spotted mantle sheild about a third of its length in size, with a striped tail.

The major doubt I have is the size. It looks smallish in the photo. Leopard slugs are very large. Perhaps it's a juvenile.


What is ischaemia exactly? I think it is decreased blood supply to organs and tissues.
I also think it is the stopped circulation.
However, both ones cannot be right, I think.

What is ischaemia exactly?

Ischaemia is lack of sufficient perfusion to a tissue.  Reduced perfusion could therefore mean decreased blood supply to organs and tissues and could also mean a complete cessation of blood flow to an area - therefore both can be correct as they are on a continuum.  Infarction is tissue death due to hypoxia which can result from ischaemia that is not swiftly resolved.


Do alleles, by definition, code for the same trait? A trait is defined as an inherited characteristic, like eye color and height.
A phenotype is defined as the specific physical manifestation of a trait, like blue eyes and 6 feet, respectively.

Now, genes code for traits. And because alleles are different versions of the SAME gene, they must code for the same trait. Let's say gene A codes for hair color (trait). Gene A(1) (allele) codes for brown hair (phenotype) while gene A(2) codes for blonde hair. Therefore, alleles code for the same TRAIT, but differing PHENOTYPES.

Here is the problem. When I google: "heterozygous", I get a bunch of websites defining it as "referring to a gene pair in which the two alleles do not code for the same trait"

This is not correct because a gene-pair refers to genes located at the same locus on a chromosome. In other words, they are alleles of the SAME gene and code for the SAME trait. They only code for different phenotypes associated with that trait.

So. Either my definition of traits is wrong. My definition of alleles is wrong. My understanding of alleles being different versions of the same gene is wrong. OR. The internet loves to be imprecise with their language and interchangeably use terms that mean different things.

Which is it?

I fear you won't get a definitive answer on this. A survey indicates both usages of trait all over the Internet. As a teacher, I generally used trait to apply to the gene. This made teaching the "central dogma" clear: DNA -> RNA -> protein -> trait. Of course this simplification gets added to later as the course progresses.

One interesting question this poses is in the case of skin color. Is that a trait? Last I read, at least four different genes interact to produce skin color.

I'd side with you on this but acknowledge the fact trait doesn't seem to have the consistent, well-defined meaning that allele does.

On the other hand, a visit to UC Berkeley's evolution site shows them applying trait to the variations due to allele combinations.

Hope that helps! :)


Why is statistical mechanics relevant to RNA and protein folding? This is a very naive question. As far as I understand the folding of a molecule is governed by the electromagnetic forces between its atoms and also between its atoms and the atoms in the surrounding environment (so basically a many body problem). So I don't understand how statistical mechanics, such as Boltzmann's law, come to play.

To my knowledge statistical mechanics and thermodynamics exist when we have an ensemble of particle such as in a liquid or a gas. So what is this ensemble for the RNA or protein folding problem?

I’m no physicist, but your statement “To my knowledge statistical mechanics and thermodynamics exist when we have an ensemble of particle such as in a liquid or a gas” is surely incorrect. The problem of protein folding is one of thermodynamics — finding the structure of lowest free energy, and the path by which it is reached from a random coil.

One of the difficulties relating to the path is that of getting ‘stuck’ in a position in the energy landscape from which the protein cannot escape. This is called ‘frustration’ and there is apparently a quantitative treatment of ‘minimal frustration’ using the statistical mechanics of spin gasses. This is mentioned in a review by Onuchic and Wolynes, available on-line, which you will probably be able to understand better than I can.


How to give a biological interpretation to this phase portrait? Consider the following system and analyze its behavior.
$$\begin{array}{rl} \frac{dA}{dt} &= A \left( 2-\frac{A}{5000}-\frac{L}{100} \right)\\ \frac{dL}{dt} &= L \left(-\frac{1}{2}+\frac{A}{10000} \right)\end{array}$$

The analysis
It has $3$ equilibrium points. I know the stability of the three points but I am not sure if I interpret the meaning of them correctly according to the phase portrait. $x_1, x_2$ are saddle points and $x_3$ is stable point they are
$$\overline x_1=(0,0)$$
$$\overline x_2=(10000,0)$$
$$\overline x=(5000,100)$$
According to the phase portrait I think the behavior of the system is described as:
For every point $(A,L)$ given in the first quadrant, where $A$ is the number of aphids at time $t$ and $L$ is the number of lady-bugs at time $t$, we'll have that in the future, the maximum number of lady-bugs and aphids it's going to be $(5000,100)$ respectively. This also means that both population will never going to extinct.
Even in the case where there were just a few number (near 0) of lady-bugs, their population will grow and will be establish also.
My question
Did I miss something important in the biological description to the phase portrait?

I don't think you missed anything important!

You could investigate the cyclic behaviour around the equilibrium. For example, looking at the variable aphid population size can start above its equilibrium point, then overshoot it and overshoot it again to finally reach the equilibrium point. If you zoom close to the equilibrium point, you might see long cyclic behaviour before ever reaching the equilibrium.

You sure could do all kind of further analyses such as a stability analysis or searching for cyclical equilibrium but it is easy to see with this simple model that nothing very complicated will arise. You could also investigate for what parameter values this classic pattern breaks up if it does.

Another option is to make the model more complex by introducing a carrying capacity (and then investigate under what aphid growth rate the behaviour becomes chaotic), or population structure, or whatever.

You might learn much from it but you might still want to have a look at the post What prevents predator overpopulation?.

I highly recommend the book A Biologist's Guide to Mathematical Modeling in Ecology and Evolution by Otto and Troy. It will show the typical kind of analyses that can be done for this kind of systems.


Are evolutionary mutations spontaneous? My question is whether mutations which lead to evolution occur by any environmental force or it occur spontaneously? I have read in genetics that x-rays, ultraviolet rays and chemical mutagens are the causes of mutation but how are they responsible for evolutionary mutations?

Mutations occur spontaneously because all molecular processes are stochastic in nature: DNA replication is an imperfect process. However, certain external factors can increase the probability of a mutation to occur or even cause specific types of mutations.

Both spontaneous mutations and this kind of externally driven mutation contribute to the genetic variability that is the basis for evolution. It is sufficient that variation exist for evolution to be possible, no matter the origin of this variation. X-rays are probably not common in nature, but there is plenty UV on the surface of earth, and there probably exist chemical mutagens that are formed without human contribution.


Can anyone tell me what type of snake this is? I found this snake in my garden and I'm wondering what type of snake it is! It was around 1 metre long and I'm in Lincolnshire UK.

I believe this is a Barred Grass Snake, Natrix helvetica. There are only a few snakes naturally found in the UK, and the Grass Snake matches the size, color, and pattern (bars on the sides but not on the back). The "N. helvetica" designation is relatively new, 2017, following genetic testing that showed that the previous name of Natrix natrix was not correct. "The newly distinguished snake is grey, not olive green like the N. natrix and does not have the same bright yellow collar."

Youtube video
Stock photo from Alarmy
Publication describing geographical distribution: Phylogeography and taxonomy of the barred grass snake (Natrix helvetica), with a discussion of the subspecies category in zoology. Figure 1 (below) includes a photo

Smooth Snake is another possibility but seems much less likely to me.

  Smooth snakes are slender and normally grow to around 55 cm (2 ft). They are grey or grey-brown with darker markings along their back and usually a 'butterfly' shape on the top of their head. They are very rare in the UK but can be found in heathland habitats in Surrey. It would be very unusual to find a smooth snake in your garden. They are very secretive and would normally be found underneath objects.

--Which snake is it?
 (My emphasis)


What causes the cardiac ventricular pressure change during the isovolumetric part of the cardiac cycle ? Why does the cardiac ventricular pressure change during isovolumetric contraction and relaxation. The volume ( both valves are closed)  is constant, Does Boyle's Law not apply?  P1V1= P2V2 at constant temperature.

Boyle's law doesn't apply to all fluids: only gasses, not liquids. Liquids like blood are (mostly) incompressible, so their volume does not change substantially when you add pressure.

During isovolumetric contraction, the ventricular walls are pushing in on the blood contained in the ventricle, causing the increase in pressure, but there is not yet sufficient pressure to force the blood out the pulmonary/aortic valve.

Source:

Hillegass, E. (2016). Essentials of cardiopulmonary physical therapy. Elsevier Health Sciences.


Junk DNA and "random" mutations I'm somewhat irritated by "mutation" generally being described as a fully random factor in evolution: pure randomness does not seem like something that can survive in a long evolutionary process.

And some basic evolution in some long-lived organisms appears to happen in quite fewer generations than one would consider plausible considering just natural selection over an unbiasedly mutated genetic base.

So I'm wondering whether there have been attempts to view mutation itself as a process influenced by evolution.  For example, couldn't "junk DNA" result in a susceptibility to certain mutations that is determined by environmental factors, like amount and constitution of nutrients, ambient temperatures and others.

The overall discussion of mutagenesis I can find focuses entirely on "damage", again basically assigning all mutations a negative or at least undirected character (like more mutations occuring under stress, with the "aim" being more likely to have more random mutations where one offspring might be more successful than the stressed parent by chance).

In a similar vein, I don't see not much of anything about evolution and competition of gametes: how different environmental factors influence which of an abundance of eggs mature and which of the (asexual) male gamete reproduction mutation in the testes will be favored over time or under environmental conditions.

Basically all of evolution and natural selection seems about how to survive into fertility and select a partner, and that's it as genes are constant apart from random cosmic radiation or toxic substances.

I think that this kind of viewing the message in the DNA as isolated from its medium just does not sound like something that would survive billions of years without something less random replacing the pure randomness.

So are there any major studies trying to figure out whether certain mutations leading to better adapted phenotypes occur in a non-random manner (namely not just affecting mutation rate but also direction) in response to environmental circumstances?

pure randomness does not seem like something that can survive in a long evolutionary process.

I think this is because you don't quite understand (no offense) the interplay between mutations and natural selection. You should have a look at Understanding Evolution.

  The overall discussion of mutagenesis I can find focuses entirely on "damage"

This is because the vast majority of mutations are deleterious (=damaging). But obviously, not all mutations are deleterious, otherwise no adaptation would be possible (only purifying selection would occur).

  In a similar vein, I don't see not much of anything about evolution and [..]

I don't understand this paragraph.

  Basically all of evolution and natural selection seems about how to survive into fertility and select a partner [..]

No! There is much more to evolution than that. Note that the semantic of evolution and natural selection is wrong as they are used in your sentence. Again, check out an introductory course.

  I think that this kind of viewing the message in the DNA as isolated from its medium

No! The environment is a fundamental tenet in evolutionary biology. The association between genotypes to fitness is a function of the environment as well.

Are mutations random?

The mutation rate varies dramatically among species and along genomes (roughly speaking from $10^{-2}$ to $10^{-10}$). For example microsatellites (repeated sequences) are highly mutable. Note also that the probability of a given nucleotide to mutate depends also on the exact nucleotides that are around it (Rob Ness; Personal communication). The mutation rate is also a plastic trait (and is therefore under selection) in some species (of plants typically). The environment affect the mutation rate and the environment can be chosen by some species (avoidance) or even constructed in some species (niche construction). In multicellular organisms, the age of the father correlates with the number of new transmitted mutations as well. However I have never heard of any studies showing such behaviours in order to affect the mutation rate. Epigenetic changes (does not concern all species) can also the mutation rate and even into what new nucleotide the old nucleotide will be mutated into (with a given probability). Mutations are more likely to be transitions than transversions. If a specific region is under environment-depend selection, then a mutation that would allow to drastically increase the mutation rate at this nucleotide whenever the organism has a low fitness (or even whenever the trait of the organism is unfit for the specific environment) could reach fixation. This process (and maybe others I am not aware of) are I think encapsulated within a hypothesis called (and it is a horrible name as it can yield to confusion) adaptive mutation hypothesis. But really don't start studying any field of science by jumping into an advanced subject (or even worst, a controversial subject). You should start with an introduction.

However, the impact on fitness (and on phenotype) of a new mutation is essentially random. An organism has absolutely no way to know what protein will be caused by a given new mutation. Selection then select upon the variance created by the mutations, the variance decreases and adaptation occurs. The impact of new mutations seem to follow more or less two weighted gamma distributions (added to which a bump of probability density for lethal mutations).


What kind of insect can this be? This appears to be just a shell after and insect went through a metamorphosis process What kind of insect can this be? This appears to be just a shell after an insect went through a metamorphosis process.

It's a carpet beetle larvae (family Dermestidae).
See here fore more info.

Example:

 Anthrenus verbasci from Wikipedia


How does transpiration help in sucking water up? How can transpiration help in sucking water up as the amount of water that is sucked up by the evaporation of water equals to the amount of water evaporated. (Correct me if I am wrong). Then how it helps?

The benefit is not in taking up more water but in transporting the things that water contains.
Plants rely on bulk transport in water flowing though specialized tissue (xylem), somewhat analogous to blood flow in an animal. Water flows through the xylem using capillary action; when water is lost at the top, capillary action pulls water into the vacated space and the flow continues down the entire height of the plant. Water removed for other uses like photosynthesis also contributes, but transpiration is important for many plants to increase the flow rate.


Why should or shouldn't we allow the human body to take its natural course? For example, when you are sick but don't feel thirsty, this could be due to baroreceptor reflex that is attempting to readjust salt and water balancing.

Why shouldn't a patient be left thirsty and let the body to adjust until he or she feels thirsty again?

I am assuming that your question is: "why can a human intervention improve health?". Let me know if I misunderstood your question.

Why can a human intervention improve health?

Let's first avoid going into the details of your example. It is quite obvious that human intervention can often improve health in a way that your body alone cannot. To me, an intuitive way to classify the reasons why human intervention are important to improve health into two categories.

The body does not always react in an adaptive manner.

Example: Anaphylaxis is a serious and sudden allergic reaction that may cause death. An allergic reaction is what is happening when your immune system recognize a chemical as a infectious element while it is not. The reaction of the body is not adaptive and taking medication such as an anti-histaminic can force the body to stop this "stupid" reaction.
Note: There are reasons why the body cannot be always perfect but it is a bit long to make an overview here. There is stochasticity in the developmental processes, there is genetic variation for example due to always occurring deleterious mutations, there is also an arms race between parasites and host. This arm race leads parasites to take advantage of normal host physiological pathways. There are tons of other reasons that relate to the stochasticity and to the physic and physiological constraints of evolutionary processes.

The body sometimes cannot (physical constraint) produce the action that is required to be performed to improve health.

Example:  If you have an important wound, then a human-made compression can by far improve your chance of the survival. The body is not able by itself to simulate this external compression to prevent blood to exit the body through the wound.

You might easily find semantic issues with these categories though such as the question of cancer and its removal for example and some may argue against this categorization.

Dehydration and thirst

Your example would fall into the first category. It is not so uncommon that the body needs water while not causing thirst. Because after 50 years old, the sensation of thirst start to diminished, dehydration without the sensation of thirst is common among old people. Dehydration along with hyperthermia is a relatively important cause of death during hot weather in summer. It is especially true in old people as the sensation of thirst diminishes with age. Dehydration following diarrhea is also a common and important issue in old people sometimes leading to death.


Does taking a shower have the same effect on muscles as warming up? When playing sports, coaches and trainers are always very clear that it is necessary to warm up and stretch. But sometimes athletes sometimes want to get an extra stretch in and don't want to go through the hassle of warming up.

Will taking a hot shower warm up muscles or does an athlete sctually have to do physical exercises like jogging in order to be ready to stretch?

I know this sounds like a question I could go on the physical fitness SE, but I'm really hoping for an answer involving thermodynamics and I doubt I'll get that there.

Hot shower will definitely affect your muscles health. Hot water shower results in Vasodilation,which will decrease the vascular resistance and allows blood to flow easily through the blood vessels. As the vasodilation (increase in diameter of blood vessels) allows blood to move without resistance and which in turn nourish the tissues with sufficient oxygen and nutrients. Also it affects in the removal of metabolic wastes from cells. There is another process called  Vasoconstriction (decrease in blood vessel diameter) which makes the blood vessels to contract and may lead to increased blood pressure.

There is a technique called as Heat therapy which will be effective in muscle and body health.

  Heat therapy, also called thermotherapy, is the use of heat in
  therapy, such as for pain relief and health. It can take the form of a
  hot cloth, hot water, ultrasound, heating pad, hydrocollator packs,
  whirlpool baths, cordless FIR heat therapy wraps, and others. It can
  be beneficial to those with arthritis and stiff muscles and injuries
  to the deep tissue of the skin. Heat may be an effective self-care
  treatment for conditions like rheumatoid arthritis.

  Heat therapy is most commonly used for rehabilitation purposes. The
  therapeutic effects of heat include increasing the extensibility of
  collagen tissues; decreasing joint stiffness; reducing pain; relieving
  muscle spasms; reducing inflammation, edema, and aids in the post
  acute phase of healing; and increasing blood flow. The increased blood
  flow to the affected area provides proteins, nutrients, and oxygen for
  better healing.Reference

While taking a hot water bath we are just making our muscles and tissues nourished, which means the muscles will be in a healthy state for expansion and contraction. So it is recommendable to take a hot bath before exercising.


Why is alcohol such a weak drug? Most day to day drugs such as caffeine and paracetamol require a dosage in milligrams to have the desired effect.

Why then, does it take many tens of grams of alcohol to have a tangible/noticeable physiological impact on the body? What is it about the composition of alcohol that makes it so weak, gram for gram, compared to other recreational and medicinal drugs? Are there any other psychoactive drugs that require similar dosages to alcohol to have an effect?

For clarification, as per the comments

For example, as a 90kg adult I can consume 30g of alcohol (3 UK units) before it has any noticeable impact, whereas a coffee containing just 100mg of caffeine (300 times less than alcohol) produces a noticeable reaction.

As Christiaan already pointed out, this depends on the pharmacokinetic and pharmacodynamic parameters. The effective drug concentration depends on the drug-receptor association constant and the drug degradation constant (for a highly simplified model). The degradation/removal depends on the abundance of the enzyme catalyzing this reaction.

Ethanol is primarily thought to cause intoxication by activation of GABAA receptors. However, only a very specific subclass of these receptors are activated at the levels of alcohol that one consumes during "social/moderate" drinking. Others require very high alcohol concentrations (Hanchar et al., 2006). Basically alcohol is not a very specific agonist/antagonist of any neurotransmitter or neuromodulator receptors. In other words, it does not have high affinity to any of these receptors. There is no answer to "why". I would guess that since ethanol is a very common molecule (and is also used as energy substrate by some organisms, to a certain extent), high sensitivity to ethanol would have been evolutionarily selected against.

  Although many proteins show changes in their function at very high
  alcohol concentrations (>50 mM), the molecular basis for behavioral
  alcohol effects at low to moderately intoxicating doses experienced
  during social alcohol consumption remains elusive (1). GABAA receptors
  (GABAARs) and the inhibitory GABAergic system have long been suspected
  to be targets for acute alcohol effects (2–4). For example, the GABAAR
  agonist muscimol potentiates the sedative actions of alcohol, whereas
  the opposite effect, a reduction of ethanol (EtOH)-produced sedation,
  is detected with the GABAAR blockers picrotoxin and bicuculline (5).
  Although most GABAAR subunit combinations can be activated by high
  (anesthetic) alcohol concentrations (6), only very specific GABAAR
  subunit combinations (containing the δ as well as the β3 subunit)
  exhibit dose dependencies that mirror blood alcohol levels that are
  associated with mild to moderate intoxication in humans (7, 8) (≈3–30
  mM, because the legal drinking limit is 17 mM or 0.08%).

  From Hanchar et al., 2006

Other psychoactive drugs are highly specific and have high affinity to their corresponding receptors. For example, caffeine acts on the adenosine receptors at µM concentrations (Daly et al., 1983). This is because of caffeine's high affinity to these receptors.

Moreover, ethanol is readily metabolized to acetyl-CoA by alcohol dehydrogenase and aldehyde dehydrogenase enzymes which are quite abundant in the body. Some people who have mutations in these enzymes leading to their reduced activity, "get drunk" and experience hangovers even with a low level of alcohol consumption.


Insect (I hope) identification Look, let's get something straight.  I am not the worlds biggest sissy when it comes to bugs, but I'm not David Attenborough either.

Now that that's out of the way, down to business.  Living in Michigan as I do, I was quite surprised to find what looked like the spawn of Predator and a cicada living in my back yard.   Suffice to say it made me nervous.  In one of the pictures below, I have included a cigarette with about 3 drags smoked off of it for sizing.

Please offer insight into the true nature of this animal.

In the absence of someone more qualified, I believe this to be a prairie crayfish, based on where it was found (land) and what it is (decapod of some kind that looks like a crayfish). Therefore it is unfortunately not an insect.

It's in the right range and roughly the right terrain.

I welcome entomologically qualified advice!


How to interpret this cuffcompare result? Sensitivity over 100? I run a cuffcompare:

cuffcompare -r transcripts.gtf TransStandard_1.0.gtf

I got the following result:

#= Summary for dataset: /home/tedwon/Sources/QA/data/trans/TransStandard_1.0.gtf :
#     Query mRNAs :     165 in      78 loci  (157 multi-exon transcripts)
#            (69 multi-transcript loci, ~2.1 transcripts per locus)
# Reference mRNAs :     165 in      78 loci  (157 multi-exon)
# Super-loci w/ reference transcripts:       77
#--------------------|   Sn   |  Sp   |  fSn |  fSp
    Base level:     100.0   100.0     -       -
    Exon level:     110.6   110.6   100.0   100.0
  Intron level:      99.6    99.6    99.6    99.6
Intron chain level:     100.0   100.0   100.0   100.0
  Transcript level:     100.0   100.0    99.4    99.4
       Locus level:     100.0   100.0   100.0   100.0

 Matching intron chains:     157
          Matching loci:      78

      Missed exons:       0/872 (  0.0%)
       Novel exons:       0/872 (  0.0%)
    Missed introns:       3/756 (  0.4%)
     Novel introns:       0/756 (  0.0%)
       Missed loci:       0/78  (  0.0%)
        Novel loci:       0/78  (  0.0%)

 Total union super-loci across all input datasets: 78

What I don't understand is that why the sensitivity and specificity for the exon level are over 100? The values in this example are both 110.6. Shouldn't it be from 0% to 100%? The website doesn't address it.

I don't know if this is still needed but I went through the source code of cuffcompare to see if this phenomenon is indicative of the false positive rate or an issue with the tool (and to provide a more thorough answer). It seems like it may be a bug in the code for cuffcompare (which is a massive amount of code). If you look at line ~1518 in the source code at this URL:

https://github.com/cole-trapnell-lab/cufflinks/blob/master/src/cuffcompare.cpp

There are several statements that suggest Sn values > 100% would be possible and should be reassigned to 100%. These results may occur from keeping "redundant" transcripts if they start with the same 5' intron. How do your "fuzzy" Sn and Sp compare to this result? are they are similar?

The developers are no longer maintaining this software in favor their new faster version, Hisat/Stringtie. However I find the output to be more complete from Tophat and Cufflinks. To get a better understanding of the output, you could compare the number of potentially novel features in your cuffcmp.combined.gtf to the total number of features in your new cuffcmp.combined.gtf using overlapping and contained features as a proxy for false positive rate. Comparing these values with the total number of lines in your reference annotation may provide you with another Sn estimate without performing qPCR.

# to count the number of potentially novel
grep -c "\"j\"" cuffcmp.combined.gtf

# to count the overlapping and contained features
grep -c "\"[c,o]\"" cuffcmp.combined.gtf

# to count the number of exact matches
grep -c "\"=\"" cuffcmp.combined.gtf

# To count how many features are identified for each gene
cut -f4  -d ";" cuffcmp.combined.gtf |   uniq -c

# To count how many known genes gene were identified
cut -f4  -d ";" cuffcmp.combined.gtf |   uniq -c | wc -l

# To count number of features in the reference gtf
wc -l reference_annotation.gtf

or if you prefer to use Bioconductor packages like rtracklayer in an R environment, you could read the cuffcmp.combined.gtf file and analyze the data further

library(rtracklayer) # if you have the package installed
rtracklayer::readGFF("~/full/path/to/cuffcmp.combined.gtf")


Did modern alligators and caimans come from prehistoric crocodiles? I know that crocodilians have been here since the time of the dinosaurs. I also know that crocodiles came first. But alligators have been here for a good 37 million years. Did alligators come from crocodiles when the crocs swam into freshwater areas?

And since the alligators and caimans are 2 groups in alligatoridae did they have a common ancestor?

And also if alligators came from crocodiles (which might or might not be true), why isn't it more like this:

Crocodylidae $\rightarrow$ Alligatoridae $\rightarrow$ Alligatorinae $\rightarrow$  Alligator

for alligators and

Crocodylidae $\rightarrow$ Crocodylus

for crocodiles?

This is the phylogeny of the Crocodilia, as best as we currently know it:

The order Crocodilia is a monophyletic group including all living crocodile and alligator species. That means that all of these species share a common ancestor and all descendants of that ancestor are part of Crocodilia.

Within the Brevirostres, three superfamilies exist - the now extinct Borealosuchus, the Gavialoidea, within only two species not already extinct, and the Brevirostres.

The Brevirostres are the monophyletic group containing the crocodiles and alligators (that includes the caimans).

  Did alligators come from crocodiles when the crocs swam into freshwater areas?

That very much depends on what you mean with "crocodile". If it's Crocodylidae, then no, these are sister groups. If it's only the true crocodiles (Crocodylids), no, those evolved after the split with alligators. If it's Crocodilia, then yes, alligators evolved from crocodiles.

  And since the alligators and caimans are 2 groups in alligatoridae did they have a common ancestor?

Yes. However, saying that is rather boring - all life has a common ancestor. If you mean whether they have a common ancestor and all descendants of that ancestor are either alligators or caiman, then yes.

Additional source: Crocodilian phylogeny inferred from twelve mitochondrial protein-coding genes, with new complete mitochondrial genomic sequences for Crocodylus acutus and Crocodylus novaeguineae


How do mosquitoes orientate in the darkness? An annoying mosquito (Culicidae) which kept me awake nearly the whole night lead me to this question.

I have heard that mosquitoes can smell CO2 which could help them to orientate in the darkness, but how do they avoid obstacles and know where to land? I was browsing the wikipedia article but did not see an explanation for this, can somebody explain this to me?

I also wonder about the purpose of their loud, annoying sound (afaik only females produce it), which i would think as an evolutinary disadvantage, but this would be another question...

What is the purpose of their loud, annoying sound?

Both males and females produce a sound when flying but not at the same frequency. I would think of the male sound as mainly an artefact of flying and don't really know if it has any usefulness. I would note though that before mating both gender tend to synchronize their sound (Gibson and Russel 2006). On the other hand males are very attracted toward the sound of females.

In nature, mosquitoes make swarms. Male's job in the swarm is find find female, courtship and mate. This means that males need a cue to detect them from far away and this cue is their sound. Males evolved large and fluffy antennas (with which they hear) while females only have small antennas Charlwood and Jones 2008.

  How do they avoid obstacles?

They have eyes! It is never complete darkness and they just move around, see things and sometime bump into something and keep flying until they reach their goal.

I can't offer you a citation for that but as I worked with mosquitoes in the past, I think it is a good description.


What does the difference between GPP - NPP represent? Overview

Researchers have been studying a temperate grassland ecosystem with the view to understand it's current status with regard to carbon inputs and outputs and to identify whether the grassland is currently a sink or source of carbon.

The aim of this self-study is to become more familiar with different energy fluxes within the terrestrial carbon ecosystems.

The idea is to calculate energy fluxes in various scenarios, and I am feeling a little confused about the scientific theory of gross primary productivity (GPP), net primary productivity (NPP), net ecosystem production (NEP), net ecosystem exchange (NEE), RT = Total respiration, RA = animal respiration, and RS = soil respiration,

If anyone can help, I would be deeply appreciative.

The relationship between production fluxes and other fluxes summarised by these key equations:

NPP = GPP - (plant respiration)
NEE = NPP - (heterotrophic respiration)
NEP = NEE - (carbon losses from leaching, disturbance, and other inputs, and outputs)

Table of flux values

Questions:

What does the difference between GPP - NPP represent? In other words, what is GPP-NPP equal to (see table for values)? Is the value of 800 equal to respiration?

GPP - NPP = R

1400 - 600 = 800

I understand that GPP is the overall rate of biomass production by producers at the rate at which solar energy is captured as carbohydrate molecules during photosynthesis and NPP (energy captured per unit error per unit time). Producers such as plants use this energy respiration and growth.

I also understand NPP is the rate of energy lost to metabolism or maintenance or the energy stored as biomass by plants or primary producers in the ecosystem.

I am making the assumption that this value of 800 is associated with the respiration of plants; although, I am still confused with what this value represents. From my way of thinking, the difference between GPP-NPP equals the extent of CO2 lost from plant respiration within the ecosystem. Since the value of GPP (1400) is larger than the value for NPP (600), more energy has been used during the intake of carbon during photosynthesis rather than plants using glucose or the energy stored in the system to photosynthesise for the emission of CO2.

Therefore, this value represents the amount of CO2 that is lost from plant respiration or from metabolic activity.

Am I on the right track? Do I have the right ideas about energy fluxes?

Diagram

What does the difference between GPP - NPP represent?

The answer is in your overview: it's plant respiration.

  Is the value of 800 equal to respiration?

That is the unavoidable consequence of the equation you presented and the numbers you plug in, yes.

  I understand that GPP is the overall rate of biomass production by producers at the rate at which solar energy is captured as carbohydrate molecules during photosynthesis and NPP (energy captured per unit error per unit time).

That sentence was fine until "and NPP". What is it doing there? Did you misquote something or are you thinking NPP is a process like photosynthesis?

  Producers such as plants use this energy respiration and growth.

Yes.

  I also understand NPP is the rate of energy lost to metabolism or maintenance or the energy stored as biomass by plants or primary producers in the ecosystem.

No. NPP is the energy stored as biomass by plants or primary producers in the ecosystem (or rather the rate at which such energy is stored, if it's productivity you're talking about and it's in gC/m-2/yr-1). Respiration is the energy lost to metabolism or maintenance. GPP is what that sentence seems to be describing, as it's the total carbon captured by plants, i.e. whether it's used to build up the plant's biomass or used by the plant in its metabolism (i.e. respired).

  I am making the assumption that this value of 800 is associated with the respiration of plants;

Correct.

  although, I am still confused with what this value represents.

Maybe you should study the metabolic processes of plants and life in general to better understand this. All life consists of chemical reactions that build up structures; in order to build them up you need energy (because of the second law of thermodynamics), and all living things create that energy by breaking down complex molecules into simpler ones. (as such it would be more accurate to say that all life consists of chemical reactions that build up and break down various structures). You might be wondering "but what about the difference between autotrophs and heterotrophs I heard about"; the difference between those is where they get the complex molecules from in the first place. Autotrophs use a different source of energy to build them up while heterotrophs get them from their environment. As such, you can think of every living thing as being made of two kind of molecules: those that actually form their structure (in humans, the molecules that make up cell membranes, bones, muscles, etc) and those that are stored in order to be broken down to power the whole system (in humans that's fat, glycogen, glucose, etc). Of course a molecule can do both; if you're starving your body may start to break down structural molecules for power. There are many different ways of breaking down those big molecules for power; the most efficient one, that starts with a big chain of carbon atoms and cuts it down into individual CO2 molecules using O2 molecules, is called aerobic respiration (i.e. respiration that uses oxygen).

Because those complex molecules are required to power all life, autotrophs (the organisms that actually make them) are very important, and the processes they use to make them are very important too. The process that makes almost all of the molecules that power almost all life on earth is photosynthesis, which uses the energy from the sun to power a reaction that converts CO2 from the atmosphere into big carbon-based molecules we'll call carbohydrates. This is called "fixing carbon", since the carbon atom is the most important one; measuring how much photosynthesis is happening is another way of measuring how many carbon atoms move from being part of a CO2 molecule to being part of a plant.

GPP is the measure of that exact process: how many grams of carbon per square meter per second (or year in your graph) move from being in a CO2 molecule to being part of a plant via the process of photosynthesis.

You might think this is also a measure of how much the plant grows, but it ignores the fact that as I said, all living things contain molecules that make them up and molecules they break down for power; obviously the plant's growth will involve the former, and the latter just goes back to being CO2 through the process of respiration. Another way of putting it is that in the flow of carbon, there is a huge flow of CO2 to plant molecules via photosynthesis (GPP), but a huge proportion of that flow goes right back the other way (the plant molecules are broken back down into CO2 via the plant's respiration); the remaining flow that's actually still in plant molecules at any given time is NPP.

NPP is the proxy for plant growth; it's basically how much of the carbon the plant fixed via photosynthesis it actually contains in its body, while R (respiration) is how much of the carbon it fixed it broke back down for energy, releasing it as CO2 into the atmosphere. Hence, GPP = NPP + R, and GPP - NPP = R.

  From my way of thinking, the difference between GPP-NPP equals the extent of CO2 lost from plant respiration within the ecosystem.

Indeed.

  Since the value of GPP (1400) is larger than the value for NPP (600), more energy has been used during the intake of carbon during photosynthesis rather than plants using glucose or the energy stored in the system to photosynthesise for the emission of CO2.

I don't understand this sentence at all. The fact that GPP is larger than NPP shows that plants don't keep all of the carbon they convert from the atmosphere to make up their physical structure; they also use a lot of this carbon to power their metabolism through the process of respiration, which results in said carbon turning back into CO2 and being released back into the atmosphere (as opposed to staying in the form of wood, leaves, starch, etc).

  Therefore, this value represents the amount of CO2 that is lost from plant respiration or from metabolic activity.

That is correct, with the two caveats that it's the amount of carbon fixed in organic molecules that is lost by being released into the atmosphere under the form of CO2, and that there is no "or" - all plant metabolism is fuelled by respiration, and the only metabolic activity that releases CO2 is respiration.


Why human cannot stand still in one place? When a human stands in one place, he cannot stand still but we can see the body slightly swings.

Is this due to the Earth rotation or it has something with biology and muscles relaxations?

I have not been able to find a concrete documents on this thing.

Although at first sight this might seem to be biology rather than physics, maintenance of human posture is an example of control theory. Indeed a quick Google will find many publications on it - I found a good review here.

A standing human is a dynamical system that is not in equilibrium so it requires a (closed loop) feedback system to maintain it. This means sensors in your body detect deviations from your desired posture and muscles contract to return you to it. The problem is that there is a lower limit to the movements you can detect i.e. you body moves a certain distance before your muscles respond and move it back. The result is that even when we try to stand absolutely still we are actually continually moving then correcting that movement.

Some people are better at maintaining posture than others, so some people can stand stiller than others. Plus the ability declines with age, as I can testify from personal experience :-)


What slope do I need to prove a hypothesis? I am conducting an experiment for school in which I am measuring people's heart rates as music plays at different tempos. My hypothesis is that as the tempo of the music increases, so will the subject's heart rate. After recording data from many subjects, I will use linear regression to find the overall function to represent my data.

What slope would I need on my function to prove my hypothesis correct?

You will get a much more complete answer on a statistics forum, or by simply consulting some basic tutorials on linear regression.

But a little intuition should tell you that setting a cutoff on the value of the slope does not make sense. For instance, suppose you measured heart rate in beats per second instead of beats per minute. All the y-values would be 60x lower, your slope would be 60x lower, but intuitively, nothing should change about your interpretation.

When you calculate your linear regression, you'll be able to obtain a correlation coefficient and a p-value, which tell you how well your data fits the line and the probability of obtaining such a result if there was no relationship between the data. These will be based not on the slope, but rather on how well your data fit the line and the number of points you have (the more data you have, the more confident you can be of the effect).

But you will never prove your hypothesis. The best you'll be able to say is "if my hypothesis were false, the probability of obtaining the result I got is less than X%". The clearer your data, the smaller X will be.

You would also do well to consider sources of systemic bias, not just statistical power. For instance, could the music affect the accuracy of the measurement? Do you always gradually increase the tempo of the music, or do you randomize the order? Just some examples off the top of my head, I'm sure you can think of others more relevant to your setup.


Validation by PCR of a lowly expressed gene in microarray I am interested in validating the precence of a gene (FETUB) whose expression is in the lower quartile of the microarray (see figure in link).

https://drive.google.com/open?id=0B82aQne0d_mYWlFiMjRlb05CUVU

Do you think this gene would be detectable by PCR?

Thanks

If it was detectable in a microarray, the odds are very good for RT-rtPCR. If you are designing your own primers, make sure they span an exon junction, or if the gene is intronless, then span the UTR to exon junction to avoid amplifying DNA.


Effect of Ethanol on Brain Volume Measurements I want to compare the brain sizes of two populations of fish. However, all the samples I have were fixed in 95% ethanol. As far as I know, 4% formalin is the normal fixative for soft tissues. Can I conduct my study, or do I need to obtain samples in formalin? I've scoured the literature, and I can't find any useful recommendations.

I just spoke with my histological colleague about your question. He said that you should be fine for gross examination but not for microscopy. Why? He says, "When working with specimens, the higher resolution microscopy you try to achieve, the more 'potent' the fixative needs to be. A preservative will preserve what tissues are there. However, fixatives (like paraformaldehyde or glutaraldehyde) bind proteins together and, thus, are used to try to 'fix' a tissue posthumous in the manner that it was structured in life. For gross examination, a preserved specimen (without prior fixation) can act as a decent voucher for macroscopic evaluation of its internal organs; however, it will not suffice for any type of detailed histology at the light microscopy or electron microscopy level."

So, the short answer is that it depends on the type of work you need to accomplish.


Reseach on feeling pain of other people I'm more of a tech than bio kind of guy, but I have read and learned a lot alongside of my girlfriend's education. Which is very interesting!!

Currently I want to investigate : people claiming to feel another persons pain when they are touching them.

I cannot seem to Find any papers about it. I guess I'm using the wrong search terms.
Or does nobody research about it ?

I believe what you are referring to is called 'sympathetic pain,'and the reason you can't find any papers on the subject is because it is not really a well studied concept. That is primarily due to the lack of robustness in the sensation and idiosyncratic nature of the phenomenon. Personally, I'm not too familiar with the concept beyond placebo treatment of patients with such pains.

HOWEVER, I will explain the different types of pains briefly, their biology, and where the pain you have described fits roughly. There are three categories of pain (scientists sometimes argue four, but for our sake let's say three): nociceptive, inflammatory, and neuropathic. Nociceptive pain is the immediate pain reaction you get when you sense something harmful. It's that jerking sensation you get when you touch something hot or you feel something hazardous coming your way. This pain comes from peripheral nerves that link your senses of touch or perception directly to your spinal chord for an immediate knee jerk reaction. Thus, there is no central nervous system (or brain) processing of the pain, just a reaction. You end up feeling the pain more intensely later once the moment has passed. Then inflammatory pain is the pain you get when you cut or bruise yourself, have allergies, stuffy nose, etc. It is the more common and treatable types of pain and is easy to detect. It comes with redness, swelling, and sensitivity to the general area. Biologically your body is stimulating this pain because your inflammatory system is trying to attack any invasive particles or repair damaged sections of the body. There has been much research done in this type of pain (see sources) and is treatable with non-steroidal anti inflammatory drugs (NSAIDs) such as aspirin, Tylenol, etc.

The last type of pain, which is the sympathetic pain falls into, is called neuropathic pain. This pain is more abstract and is often described as constant and idiosyncratic (non standard intervals). In research it is often modeled by inducing diabetes and doing damage to the nerves to cause constant pain signals to the brain. However, the method is controversial in both practice and in efficiency of modeling. This because there are often many different biological ways to induce cognitive pain and it is primarily central nervous system based (aka in the brain), whereas this type of pain is specifically induced by nerve damage (hence neuropathic). This type of pain is often tested using cognitive based test parameters to see if a drug can relieve some of the mental struggles either caused by the pain or causing the pain. There are also such cells called "mirror neurons" that fire when you sense (visual, audio, touch) something and then cause a similar behavior or sensation to occur within the person. It is possible that seeing or feeling someone else's pain causes these mirror neurons to fire for certain people, perhaps due to associate learning or a memory that person has that reminds them of pain they once had. I've attached some literature on the subject for your leisure, but it is a poorly understood science that we are trying to grasp in modern research. Hopefully that answered your question!

Sources

The Principles of Neuroscience by: Kandel, Schwartz, Jessel, Siegelbaum, and Hudspeth (most indepth source)
Pyschopharmacology by Meyer and Quezer
From Mice to Men: Jacqueline Crawley
Pathology Based Pain
Inflammatory Pain Review
Neuropathic Pain Review
Mirror Neurons


Mode of Enzymatic Inhibition via R-Allele The photo above shows the effects of the R allele of the pea shape gene on the synthesis of an enzyme that converts unbranched starch into branched starch. The r allele of this gene determines an inactive form of the enzyme, leading to a buildup of linear, unbranched starch that ultimately causes seed wrinkling. My question is, How does the r allele specifically prohibit the activity of the enzyme?

Does the DNA/Gene sequence simply code for proteins that create an enzyme which cannot bind to its respective substrate ?
Is the substrate in the above illustration the unbranched starch itself ?

Bhattacharyya M, Martin C, Smith A. 1993. The importance of starch biosynthesis in the wrinkled seed shape character of peas studied by Mendel. Plant Mol Bio 22(3):525-531

Abstract:

  The wrinkled-seed mutant (rr) of pea (Pisum sativum L.) arose through mutation of the gene encoding starch-branching enzyme isoform I (SBE1) by insertion of a transposon-like element into the coding sequence. Two isoforms of starch-branching enzyme have been documented in the developing pea embryo. The second isoform, SBEII, is expressed towards the later stages of embryo development while SBEI is expressed highly in the early stages. Due to mutation of SBEI the total amount of starch and the proportion of amylopectin, a branched starch polymer, are greatly reduced in the wrinkled (rr) line as compared to that in the wild-type, round (RR) line. Consequently, the level of sucrose in the rr line is nearly two fold that of the RR line. Increased sucrose concentration in the developing embryos of this mutant line causes increased uptake of water and thereby increases the cell size and fresh weight. During seed maturation in these mutant seeds a greater loss of water occurs. As a result, the wrinkled seed phenotype develops. Besides this morphological variation, the mutation also causes changes in the amount of lipid and of one storage protein, legumin. This review article discusses the role of the SBEI enzyme in causing such metabolic changes in the developing embryos with the implication that metabolism can play a central role in plant development.

These authors claim that the mutant protein is not present in peas, so the wrinkled phenotype is not due to an inability of the protein to bind its substrate (amylose and amylopectin - the linear and branched components of starch, respectively) but rather its complete absence. The mutant is due to an 800 bp transposon insertion into the coding sequence of SBE1. If it was expressed, it would be reasonable to expect that it wouldn't be able to bind its substrate. The authors also discuss mutations at other loci that have been shown to be responsible for the wrinkled phenotype, but it is believed that these are relatively newer and would not have been observed by Mendel.


How does the body repair extracellular damage caused by glucose? So we know that glucose is an aldehyde that can cause cell damage to the lysine and arginine residues on proteins through the Maillard Reaction (among other damaging reactions that glucose participates in). Since everyone needs glucose to survive, though - I'm wondering - how does the body repair damage to its proteins+blood vessels that are caused by all this glucose? I'm especially interested in the blood vessels, as the damage to blood vessels is common in diabetics.

The Wikipedia article on "Advanced Glycation Endproducts" (or AGE) is quite nice and in this case especially the section on "Clearance", which also contains a few references.
In short the AGE which are inside of cells are taken up by the lysosome and then broken down until AGE-amino acids are left. These are secreted into the blood stream and excreted with the urine. Bigger extracellular AGE which cannot pass through the cell membrane are taken up by special receptors first and then processed, here macrophages and Kupffer cells are included. An involvement of the liver is also discussed.

The following articles are also interesting:

Advanced glycation end-products: a review
The biology of the receptor for advanced glycation end products and
its ligands
Pathogenic effects of advanced glycosylation: biochemical, biologic,
and clinical implications for diabetes and aging.


Why do different bacteria have different shapes? Why do different bacteria have different shapes? Is it only related to their function?

Reasons for Bacteria with different shapes as given in Wikipedia/Bacteria:

  The wide variety of shapes is determined by the bacterial cell wall and cytoskeleton, and is important because it can influence the
  ability of bacteria to acquire nutrients, attach to surfaces, swim
  through liquids and escape predators.

There is an article based on research by Kevin D. Young Bacterial morphology: Why have different shapes? which highlights 3 main points which defines the shape of Bacteria:

Nutrient uptake: Cell shape, in and of itself, affects nutrient acquisition and argues that other nutritional situations may create conditions that favor one bacterial shape over another.
Motility: Motility imposes a heavy selective pressure on cell shape. Fast cells are better off as rods with a certain length-to-width ratio, chemotactic cells must adopt shape ratios in line with their environments, and cells that forage near surfaces or navigate viscous environments may do best if they are slightly curved or spiral.
Predation: In their struggle against being eaten, bacteria have adopted morphological defenses that may have produced the wealth of shapes we now observe.

These factors play a role in shaping bacteria. Further he explains what in general gives the shape to bacteria:

  Bacterial morphology is affected by a combination of selective pressures - access to nutrients, cell division, attachment/dispersal, predation and motility (among others). Among these different factors, our understanding of the relationship between motility and cell shape is most complete; for example, highly motile bacteria are usually rods with a specific (optimal) shape and size, and movement through viscous fluids seems to a favor spiral shape. But since multiple selective forces are always in play, there is at the moment no way to predict cell shape based on the environment or vice versa.

Shape Matters: Why bacteria care how they look - This article highlights Kevin's work explaining why shapes matter for bacteria and they take it seriously for survival.

So adaptations to various environments could be possible but depending upon the environment we can not predict the shape of bacteria because some other factor might have played major role in giving shape to it. But the above mentioned 3 main factors gives some explanation.


Are any genes over a billion years old? Are there any genes (for any organism) for which we can say with confidence that they are over a billion years old?

Ribosomal RNA (rRNA) genes are shared among all living organisms, including lineages that have diverged from one-another well before a billion years. Bacteria, Archaea, and Eukaryotes diverged over 3 billion years ago, and their rRNAs are virtually identical to one-another. http://www.biologyreference.com/Ar-Bi/Archaea.html
Any genes that are shared between plants, animals and fungi would also be over a billion years old.


Do vitamins protect you from common cold? Do vitamins (taken as pills) boost your immune system, and make you less likely to contract diseases such as common cold or flu?

There are two answers to your question, "emphatically yes" and "sort of."  Vitamins play a critical role in immune function, and a deficiency of certain vitamins can lead to a higher risk of developing an infection.  Specifically, vitamin A, B2, B6, C, D, and E deficiency are linked to depressed immune function.  However that is deficiency, not supplementation above what most people need.

There's a popular idea that megadosing with vitamins, usually vitamin C, lowers the risk or length of common upper respiratory infections (eg the common cold).  The evidence on that is much less convincing.  A metanalysis of studies finds weak or no evidence that it is effective, but may be associated with a small effect.  More study is recommended by the researchers, but they don't go as far as recommending large doses of vitamin C.  (It is also worth noting that large doses of fat soluble vitamins, A, D, E, and K, can be quite toxic and should be avoided).

The magnitude of the first effect is quite large: people with a vitamin deficiency certainly have a depressed immune system.  However it is not clear that larger doses are helpful.


What is the right spelling for this agar? I could not spell the agar [gonoline-uroline] which I heard yesterday.
My spelling is so wrong that I could not find it in Google.

What is the right spelling for this agar?

The first word is ok, there is agar called Gonoline, the second one is probably Euroline and there is an agar with this word too (Liver IgG Euroline).

I've found both of them on the Italian site, probably the are not one, but two agars.


Is there a way to examine amount of red/white muscle fibers without biopsy? I want to conduct some research on red and white muscle fibers, why do some people tire during certain movements while others do not. Obviously I can't get a biopsy on the subjects so I wanted to hear if anyone here maybe had a suggestion to a reliable method to test for amount of red vs. white muscle fibers?

Maybe some strength measurements, endurance tests etc. I'm looking for something that is documented to work.

Indeed, a paper was published in 2011 regarding the same for humans by using a magnetic resonance spectroscopy to measure carnosine content.

A significant positive correlation was found between muscle carnosine, measured by 1H-MRS, and percentage area occupied by type II fibers. Explosive athletes had ∼30% higher carnosine levels compared to a reference population, whereas it was ∼20% lower than normal in typical endurance athletes.
Muscle carnosine content shows a good reflection of the disciplines of elite track-and-field athletes and is able to distinguish between individual track running distances. The differences between endurance and sprint muscle types is also observed in young talents and former athletes, suggesting this characteristic is genetically determined and can be applied in early talent identification. This quick method provides a valid alternative for the muscle biopsy method. In addition, this technique may also contribute to the diagnosis and monitoring of many conditions and diseases that are characterized by an altered muscle fiber type composition.

Baguet, Audrey, et al. "A new method for non-invasive estimation of human muscle fiber type composition." PLoS One 6.7 (2011): e21956.


Why is LH level much higher than FSH level at ovulation? My teacher showed us an elaborate collection of graphs with one of them showing FSH and LH plasma levels during the menstrual cycle. LH level was almost 3 times higher than FSH level. Why?

Does this have anything to do with their synthesis or cellular responses?

It is not the absolute plasma levels that are important, it is about their relative differences during the cycle. The steep rise in FSH during the first days induces follicle stimulation. The LH surge at day 12 induces maturation of the egg and stimulates its release (see wiki page). The fact that LH's absolute plasma levels are higher may theoretically have to do with the fact that more LH is needed to elicit its physiolocal response. However, the differences of their relative levels is way more important from a physiological point of view.


Can an influenza virus carry other infectors with it? This idea came to my mind when thinking about how many people become ill in many locations with similar symptoms (fever and rough cough) from Influenza.

There are of course different types of influenza virus.

Can Influenza A virus work as a vector for other upper respiratory infections?
That is, much the same as the mosquito being a vector of malaria, can an influenza virus carry other infections with it?

If so, how? If not, why do some people get so sick from viral influenza, and not others?

I wouldn't call influenza a vector here, but yes, an infection with the flu virus which results in a full infection can have secondary infections as complications. There are often caused by bacteria which usually live in the respiratory pathway and kept under control by the immune system.

This includes pneumonia (either viral or bacterial), inflammation of muscles and the heart muscle (myositis and myocarditis) as well as pericarditis. Less severe complications include infections like ear infections and sinusitis.

See the references for more details:

References:

Complications of Viral Influenza
Double trouble: Bacterial super-infection after the flu
A Mouse Model of Lethal Synergism Between Influenza Virus and
Haemophilus influenzae


Can pets catch the cold? Last night I was drying my cat with a towel after shenanigans in the rain and she sneezed!

Questions

Can cats/dogs/hamsters or other pets catch the cold?
How quickly do they recover?

Yes they can. The viruses that cause a cold include rhinoviruses (up to 80%), coronaviruses and influenza (together accounting for much of the remaining 20%) and a small percentage of adenoviruses. When discussing cross species transfer, influenza is the most important to discuss as it is a fairly common cause of the "common cold".

Influenza A has humans, pigs, bird and horses as its host. Different influenza strains have different hosts. Influenza can recombine if two strains infect the same host (antigenic shift) and also mutate (antigenic drift). With a combination of these influenza can and has numerous times crossed the species barrier which has caused the major flu pandemics as well as swine and avian flu. It's this reservoir that makes these viruses so hard to eradicate. When we are the only host such as in polio virus, it is a lot easier. Pigs don't adhere to national flu guidelines.

Comparing recovery times, all mammals are roughly similar although due to our slightly more evolved immune system as well as social factors of knowing what to do when we are ill we recovery very slightly earlier.


Why is free ribose not reduced to deoxyribose rather than the reduction occuring on ribonucleotides I cannot understand why deoxyribonucleotides are not synthesized directly from deoxyribose, but ribonucleotides have to be synthesized first, and only then can deoxyribonucleotides be synthesized.

Clarification

I assume that question is posed in the knowledge that ribose is an intermediate in the dark reaction of photosynthesis and can be synthesized in the hexose monophosphate shunt in animals. Hence I assume that the question is not why ribose precedes deoxyribose in the metabolism of mammals and other living things. Rather, the question would seem to be why ribose is not converted directly to dexoyribose, but only after ribonucleotides have been formed (in the ribonucleotide reductase reaction).

Possible Answer

Question as to why a metabolic pathway has one form rather than another can sometimes have a chemical explanation, but in this case I suggest answers can only be speculative.

Thus, one possible answer could be:

  There is no need for free deoxyribose in the cell, and that if free
  deoxyribose were produced there would be potential competitive
  inhibition of enzymes that catalyse reactions involving ribose.

If an ‘RNA world’ preceded the modern ‘DNA world’, then one could argue that:

  The simplest way for the shift from an RNA genome to a DNA genome would by the introduction of a
  specific reaction for the reduction of the ribose in nucleotides. The
  fact that the base that differentiates DNA from RNA — thymine —
  is also synthesized as a nucleotide (see my answer to this
  question)
  is consistent with (but does not, of course, prove) this idea.


What are the effects of muscle and fat mass on survivability? If we have humans A, B and C who are different:

A is thin (skinny) without significant muscle or fat mass.
B is muscular
C is fat

Which one of them has the best body for survival in accidents like car crash, aircraft crash, fall from the ladder, fall down the stairs, being hit by a car, slip in the bathroom, etc?

What are the effects of muscle and fat mass on survivability?

For car crashes, it's a mixed bag:

Better
Better
Worse
Worse

Basically, it looks like, if wearing a seat belt, slightly overweight is more likely to survive a car crash, but if no seat belts are worn they are at a disadvantage; the very obese are always more likely to die, however.  Also, some of this was found only for males, not females.


Would BMP7 introduced to a Petri dish with cartilage cause chondrocytes to replicate? Chondrocytes are the cells that make up cartilage. As I understand it, the best growth factor that signals replication of chondrocytes is Bone morphogenetic protein 7.
If supplied with a sufficient source of nutrients and a growth factor, would those chondrocytes begin to replicate?
If you prepare a Petri dish full of blood and cartilage and add BMP7, would the cartilage start to grow? Are those two questions the same?

Hello and welcome Delaney Fitzpatrick.
BMP7 - Bone morphogenetic protein 7 - Plays a role in cartilage homeostasis.
Chondrocytes - A cell which has secreted the matrix of cartilage and become embedded in it.
Chondrocytes therefore make cartilage. Cartilage unfortunately has a poor regeneration capacity.
BMP7 stimulates Chondrocyte division
Naturally the question then becomes, does BMP7 also increase cartilage production?
A paper from 2009 - Chondrocytes that expressed increased levels of BMP7 in defected rabbit knees showed statistically significant repair when compared to controls.
Although an early study, it does suggest that BMP7 may improve cartilage repair.


Why isn't acetyl-coA an entry point for gluconeogenesis? The process of gluconeogenesis starts from various possible precursors - plausible entry points like, Pyruvate, OAA, Fumarate, Propionate (as succinate) and alpha-KG. It is important to note that, acetyl-coA is not an entry point for Gluconeogenesis.

Entry points shown as blue circles.

The most common reason cited for this is the irreversibility of the enzyme, pyruvate dehydrogenase. Since it is irreversible, Acetyl coA can't get back to pyruvate to go on forming glucose.

But, Acetyl CoA naturally enters the Krebs cycle, so why can't it go ahead and form glucose via gluconeogenesis using one of the Krebs intermediates?

I have had this doubt for very long and tried to come up with an explanation to satisfy myself but I still don't know if it is valid.

So here it goes. All the entry points to gluconeogenesis (mentioned before) are an addition to the Krebs cycle. They get on the boat, sail along, get off at oxaloacetate and leave. They don't bother the boat in any other way. Even Pyruvate, forms oxaloacetate via pyruvate carboxylase and then gets on the boat for gluconeogenesis.

On the other hand, Acetyl coA would be a part of the Krebs cycle itself. It is not adding anything to it (2 carbons that are added are lost as CO2). So an Acetyl CoA added, can't leave as OAA. It would be analogous not sailing on the boat but eating it down itself. Slowly, it would lead to a decay and loss of the intermediates Krebs cycle and it would come to a standstill (?)

Is this explanation right? Are there any other ways to explain why irreversibility of PDH results in this?

Although acetyl-coA can enter gluconeogenesis via pathways like glyoxylate cycle (not in humans) and pathways to make pyruvate from acetone (not economical) to form glucose, the question is why it can not do so directly via the Krebs cycle.

Image: Harper's Biochemistry, 29th Edition.

The problem is that acetyl-CoA enters the TCA cycle by condensing with oxaloacetate in the citrate synthase reaction. Therefore, you need 1 oxaloacetate for each acetyl-CoA added. Now, if the citrate formed goes on to oxaloacetate which is then removed for gluconeogenesis, there is no oxalocatete left for the next citrate synthase reaction. The reactions do not balance. Therefore, an anaplerotic substrate like glutamine or asparate is needed to replenish the lost oxaloacetate.


What is the effect of Montelukast on the amount of IgE in blood? I know that it decreases the amount of leucotrienes in blood.
I saw a patient with high IgE altough under Montelukast medication.
This suggests me that Montelukast does not affect the immunoglobulins, but somehow restrict the allergic reaction indirectly.

What is the effect of Montelukast on the amount of IgE in blood?

I was interested in this question because I have always been a little confused about allergic responses, so I did some rather superficial research (i.e. I looked at some Wikipedia pages). As far as I can see there is no reason to think that Montelukast will have any effect upon IgE levels.

Montelukast is a leukotriene receptor antagonist. It is used to treat allergies and asthma.

Leukotrienes are lipid signalling molecules that are used by cells to regulate immune responses. One role of leukotrienes is to promote contractions in the smooth muscles lining the bronchioles. If they are over-produced they can cause inflammation in the airways leading to symptoms of asthma. Since leukotrienes act through a receptor, an antagonist of that receptor such as montelukast can reduce their effect.

IgE is involved in allergic responses because it interacts with Fc receptors on the surface of certain cells such as mast cells. If the IgE molecules are associated with one another through Ig-antigen interactions this leads to clustering of the Fc receptors which triggers an intracellular signalling pathway leading to mast cell degranulation - the release of histamine by fusion of storage vesicles with the cell membrane (i.e. exocytosis). Histamine causes constriction of the bronchioles via effects on smooth muscle, just like leukotrienes.


Dogs bark at familiar person in Santa costume. Why? Don't dogs trust smell over vision? Last night 10 humans and 2 dogs spent Christmas together. At some point, one human dissappears for a few minutes and comes back wearing a full Santa outfit. Upon respawning, the dogs start barking aggressively until they are calmed down by non-Santa humans. They remained attentive of Santa until he left after a few more minutes.

Why is this? Did the dogs not recognize the human because of his fake full beard and altered body shape (pillow under coat for fattening)? The human didn't shower or put on perfume or anything. I'm stumped by this and I'd love to learn the reason for this odd behaviour.

The dog was probably freaked out by the weird costume.  Humans do it all the time (I've been seeing Halloween decorations for sale since early August, which is terrifying) but we generally comprehend what's going on.  Dogs may not fully understand the idea of a costume, much as a human infant might be scared by masks or beards (or the sudden removal thereof).

Anyway, this 1997 article titled Canine fears and phobias; a regime for treatment without recourse to drugs is kind of a fun read and has some interesting tidbits about, go figure, canine fears and phobias.  One thing it discusses is the importance of the primary associations brought on by sight, smell, and hearing.

  However with a fear of hot air balloons the dog will hear the propane burner and see the balloon but a primary (coming from the balloon), olfactory cue will be missing.

Missing out on that is enough to freak 'em out.  This research article from the 1950s is a little more exact/thorough and has what you want.  It's worth reading in more detail if this topic interests you, but the part that answers you is here (emphasis added):

  Some at least of the test objects could not have been discriminated by smell, as with the bronze deer, or the mechanical turtle, and in the course of the work it was frequently clear that visual cues were affective before olfactory ones could have been. Vision also can dominate olfaction: fear of a modelled human head was observed although the model was completely wet with dog urine.*

Likely what happened was the dog saw a weird/scary/new person and, were upset that their vision and smell didn't match up, and continued being freaked out.

(*The urine experiment comes from this article out of 1944 Germany, in what is now known as Ethology, in case you feel like reading German.)


Is a stab wound to the back lethal? How deadly is a stab in the back?

Video games, movies, and other fiction would have us believe that a backstab against a foe with a modestly-sized blade leads to immediate and certain death, having a 100% success rate and causing death virtually instantaneously.  How close is this to reality?  How does the lethality of a puncture wound to the back compare to such wounds delivered to other areas of the body?  What is the primary target in such an attack in terms of internal organs, and what variables effect its projected success?

Check out the sources of Wikipedia article: the mortality rate is up to 4%.

The main causes of "immediate" death in penetrating trauma are shock (low blood pressure due to external/internal hemorrhage, especially arterial hemorrhage), pneumothorax, penetrating heart injury (with resultant hemopericardium) and other less frequent causes.
The same causes account for "later" lethal case plus some specific causes like infections, emboly etc.

The overall mortality rate of stab wounds is far from 100%, and according to different studies is between 1% to 4%, but rarely more. The morbidity depends on depth of wound, place of injury, overall health status etc, thus multifactorial analysis is required to get an overall image of the penetrating wounds of the body.

Some sources:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2627025/ -
 (4.3% mortality in stab wounds to the anterior abdomen, back, and flank).

http://www.ncbi.nlm.nih.gov/pubmed/3798182 - the mortality in back/flank stab wounds was 1.3%.


Can jellyfish sting outside of water? According to my understanding of the Wikipedia page on the stinging cells of the jellyfish, the mechanism of delivering the toxic missile is largely due to water pressure. Does that mean that a jellyfish on land (or brought out water) is unable to, or perhaps less efficient at, delivering its stings?

Short answer
Jelly fish can sting out of the water and even when they are considered to be dead.

Background
I do not have detailed scientific literature available. However, popular sources generally and equivocally warn against touching jelly fish, even on land and even when they appear to be dead. In fact, dead box jelly fish can be as dangerous as live ones (ABC News).

Credible sources
 - National Poison Control Center
 - UK Telegraph
 - ABC News


Can anyone identify this bird? Can anyone identify this bird: it looks like a zebra finch but they are not native to UK  are they?

Photo taken from my garden in Shoreham, West Sussex on 16/8/2014.

This looks pretty much like a female zebra finch to me (the male have a more prominent feather pattern). See this picture:

These birds are not native in Europe, this is correct. But it is always possible that birds escape captivity (or are released) and the live in countries where they originally not belong. I think this is the case with the zebra finch here. Since the birds are able to live in a pretty broad range of habitats, they can also survive in England.

According to this Wikipedia page (thanks to @Orethrephes) zebra finches which escaped from captivity are quite common in Britain although they usually not survive for long.


What's the opposite of a thermophile? Thermophiles, heat-loving organisms, have been a popular topic of research for decades due in large part to the utility of their enzymes in various chemical reactions (Taq Pol single-enzymedly made PCR practical). One of the signatures of thermophiles is that their proteins resist heat denaturation up to much higher temperatures than their mesophilic (middle-loving) homologs.

Is there a corresponding group of extremophiles whose proteins resist cold denaturation down to much lower temperature than their mesophilic homologs? If so, could someone please point me towards a few good literature reviews on the topic? Or at least give me the proper name for this group of cold-loving extremophiles?

The term you are looking for is psychrophile or cryophile. There are examples of microbes adapted to very cold conditions in Bacteria, Archaea, and Eukarya. There are also fairly complex animals capable of surviving very low temperatures -  Tardigrades, for example. There are multiple issues that organisms face in withstanding extremely low temperatures - protein denaturation, membrane fluidity, intracellular ice-formation, just to name a few.

There is this review that might be useful to you.

D'Amico, S., Collins, T., Marx, J.-C., Feller, G., Gerday, C. Psychrophilic microorganisms: Challenges for life (2006) EMBO Reports, 7 (4), pp. 385-389. link


Troubleshooting SDS-PAGE of trypsin-treated BSA I am currently working on SDS-PAGE technique having 20% acrylamide concentration for hydrolyzed BSA protein. Here I attached a gel photo for trypsin hydrolyzed BSA. I don't know , is it a good result and how do I interpreted this result?

I'm going to treat this as a partial homework question but provide some guidance as to how you can potentially address your question and have solid theory to back it up. Chymotrypsin preferentially cleaves peptide amide bonds where the carboxyl side of the amide bond (the P1 position) is a large hydrophobic amino acid (tyrosine, tryptophan, and phenylalanine). So one solution which is often used by experimental biologists (such as myself) performing mass spectrometry (MS) is to put their protein sequence (in this case BSA) in an algorithm such as PeptideCutter (from ExPASy), which performs a theoretical digest of the protein sequence having chosen the desired enzyme or combination of enzymes) and see what peptide fragments are expected to be produced and work out their length/molecular weight and compare that to your experimental data.

Having had an initial look, I noticed that your protein marker/ladder is missing, which is quite important in figuring out the peptide sizes produced! Also what is 1-8 lanes? are they different concentration of enzymes? if so then it looks ok to me since the higher the enzyme concentration from left to right, the higher the amount of digest products you have. If the peptide sizes obtained are not the ones expected then perhaps increase or decrease the digestion time since you could have a problem due to either incomplete digest or unspecific digestion, depending. I guess since BSA MW is ~ 66kDa your gel concentration is appropriate since you have a problem with the 15% gel as the products are too small and too abundant to resolve.


What is this insect seen in Northern Italy? I am from Northern Italy, close to the border with Slovenia.

I saw this thing today on the window, and was sure it was a piece of a dry rosmarine branch carried there by the wind - until it started to move.

It looks like a cocoon of some kind, on the top of it there is an opening from which a head of something like a caterpillar comes out, sometimes together with some portion of its body with two (?) tiny legs on each of its body "segments". But I imagined cocoons as something attached to a branch, not moving.. While this thing moved from one point of the window to another, always attached to the window (not using what I think are the caterpillar's legs). (I must admit I am reluctant to open the window and examine it from a closer range :) ; the photograph is taken from inside the house).

What can this insect be? (the length is around 4-5 cm)

This looks like some kind of bagworm moth. Their larvae would use silk and plant debris to construct a protective case around themselves. It’s hard to tell the exact species unless you open up the case or wait for it to emerge as an adult moth.

There are species on pretty much every continent and definitely some in Northern Italy. You can check out a list of observations and photos here: https://www.inaturalist.org/taxa/61415-Psychidae


Minimum age to reproduce How old does one (male and female human) have to be in order to reproduce
Im thinking that it's 13 for a boy and 3 for a girl, is that right?

The youngest fathers recorded were 11 years old (see wikipedia >
List of youngest birth fathers).

The youngest mother recorded is L. Medina was 5 years, 7 months and 21 days old when giving birth, which is rather astonishing! Of course, she gave birth by a caesarean section. She had an extremely early puberty; she appears to have had her period when she was 3 years old only. You might want to have a look at wikipedia > List of youngest birth mothers. According to this article, a mother (L. Gryshchenko) became a mother at 6 years old and gave birth "naturally" (not by cesarian section).


How to compare two RNA transcripts? In this paper, the cuffcompare RNA package is reported:

  Because of the stochastic nature of sequencing, assembly of the same
  transcript in two different samples may result in transfrags of
  slightly different lengths. A Cufflinks transfrag was considered a
  complete match when there was a transcript with an identical chain of
  introns in the combined annotation.

What does this mean in terms of comparing two transcripts to see if they are the same? Does that mean two transcripts are considered equal if they have the same introns, even some exons are missing in one of the transcript? What do they mean by transfrag? Is there an example?

If some exons are missing in one of the samples then the introns will, by definition, be different. What this allows is for the bounds of the outermost exons to vary a bit. This is particularly useful for exon 1, which often has lower coverage.