What animal has the longest juvenile period? I just heard the following complaint from a comedienne.

  Humans are the only animal that is completely useless for the first twenty five years of life.

Obviously this is just a joke but it is true that primates and especially humans do have profoundly long juvenile periods compared with most animals. It's got me wondering whether humans really do spend the most time in sexual immaturity.

Unfortunately I have found this question hard to search because Google thinks I'm asking about the longest gestation period (which seems to be a much more popular question). To be clear, I am not asking about the longest gestation period.

As you indicate in your question, the average age of sexual maturity is probably the best way to approach this, since immaturity is usually how juveniles are defined. Age of puberty is also different in boys and girls (the same goes for many animals), and has also decreased in the 21 century. However, as an historical average for humans 15 years is probably fair, even though there is a lot of variance. That is high compared to most animals, but there are some that have similar or higher ages of maturation, e.g.:

Cicadas in the genus Magcicada, which can have a 17 year life cycle
Elephants reach sexual maturity at about an age of 8-15 years, but usually dont start to breed until they are at least 18-20 years (see e.g. elephantsforever.co.za and Association of Zoos and Aquariums). Males mature and start reproducing later than females, and in practice it is mostly older bulls that reproduce.
The Nile crocodile, which reach sexual maturity at at an age of 12-16 years (largely dependent of body size though).
Some species of Tortoise reach maturity at ages 13-16 years (e.g. Gopherus
sp, see Germano, 1994), and, again, which is largely due to body size and growth rate. Captive bred individuals can mature more quickly.

As you can see, there is a difference between sexual maturity and reproductive age. To actually be able to reproduce, especially in some male mammals, you often need experience and size, which means that reproduction is delayed in practice. Whether this period from sexual maturity (with respect to producing mature eggs/sperm) to reproductive age should be defined as least partially as "adolescence" will affect how humans compare to other animals. In my examples, I have focused on sexual maturity (which usually has less variation between individuals).

For other examples, you might want to look at insects other than Cicadas that have delayed larval stages. This does for many woodliving beetles, where development times can be very variable, and under poor conditions take up to 20-30 years. This is usually not the norm though.

When searching for other examples, use the terms "age of maturation, "reproductive age", "sexual maturity" etc, to focus on sexual maturation and not gestation.


The second law of thermodynamics and the cell (3 questions)? How is that the cell maintains internal order, yet it discharges heat (disorder) to the surrounding?
If the cell is supplied with materials for metabolism and growth by the surroundings (disorderly environment), then how does that disorder generate order inside the cell?
When we zoom out from a single cell to a multi-cellular organism, will the net value of internal order of cells decrease disorder which would contradict the 2nd law of thermodynamics?
Note:I would appreciate serious informative answers. The questions are important for me no matter how silly they may look like for you.

First question: the answer is actually contained within the question.  The cell maintains order precisely by discharging heat.  The second law of thermodynamics states that the tendency of a closed system is to proceed from ordered to disordered.  Since thermal energy is (to our knowledge) the most disorderly form of energy that exists, in any given system where energy is involved, some energy will always be lost to heat.

For instance, if your cell performs the break down of ATP to drive some chemical need of the cell, some of the energy released in the breaking of the bonds in the ATP to form ADP will be lost as heat.  This means that the cell's heat is going up on average, and it must export heat to the environment.  If the heat was held inside the cell, the cell would rapidly become extremely disordered as proteins de-natured, non-enzymatic reactions sped up, and the cell basically self-destructed.

Second question:  I think you've slightly missed something.  Autotrophs (producer cells, such as plants) are the cells to actually "create order" in the biosystem.  They do this by capturing Carbon dioxide and water from the environment, and using light energy from the sun to bond them together and form complex biomolecules - usually carbohydrates.

These carbohydrates are then sent into the rest of the biosystem, where heterotrophs (consumers like me, you and the lion in the zoo) break them down to release their energy for tasks their cells need to do (cellular respiration, catabolism).  As time passes, all that energy is converted to heat and radiated from our bodies, and ultimately by the atmosphere off the Earth (barring excessive greenhouse gases.)

Third question: Not necessarily.  If the multi-cellular organism were a closed system, you are absolutely right.  The chemical energy would rapidly be all converted to thermal energy, and the order would disappear entirely.  However, bodies are not closed systems: they are continually radiating thermal energy and absorbing chemical energy, either from the sun through photosynthesis, or from autotrophs through ingestion and digestion.

A picture is worth 1,000 words:

(Image courtesy of stephsnature.com)


Can you design a bacteriophage that attacks the part of the bacteria that makes them antibiotics resistant? I read in a newspaper about a case where they had found a virus that could attack a specific form of antibiotics-resistant bacteria and managed to save a girl from a certain death by "infecting her" with the virus.

See this article for instance.

I would like to know if it is possible to construct a virus that attacks the part of the bacteria that makes them immune to antibiotics?

I mean if you could combine a certain type of antibiotics with a virus that attacks any bacteria that is immune to that particular type of antibiotics the bacteria is in a bad place.

I have read before, now citing this answer

  "Bacteria usually gain resistance mechanisms through horizontal gene
  transfer (such as conjugation and phage infection)."

and that bacteria can be resistent by for instance:

  "produce beta-lactamase that inactivate many lactam based antibiotics
  such as penicillin."

then if you can construct a drug that somehow can attack the bacteria because of the specific genetic code that gives the bacteria the ability to produce beta-lactamase then you might be able to attack all bacteria that shares the same genetic code that gives them that ability and the bacteria can not mutate to escape without losing their resistance to penicillin.

Check out phage therapy. For more details check out the reviews by Levin & Bull (2004) and Skurnik & Strauch (2006). The idea was around for quite some time and there is active ongoing research in this field.

However, this idea just involves killing the bacteria using bacteriophages and not reducing their resistance to antibiotics. The bacteria that are immune to antibiotics can be killed by viruses (and vice versa). If you use them in combination then possibly there can be synergistic effects under a certain regime.

  Another clinical trial was conducted to evaluate a combination of the
  antibiotic enrofloxacin and intramuscularly administered bacteriophage
  (Huff et al., 2004). Both treatments individually provided effective
  treatments of the E. coli infection, but the synergy between the two
  treatments led to a total protection of the birds, thus suggesting a
  significant value of the combined treatment.

  Skurnik & Strauch (2006)

The combined treatment may not always be synergistic; they could also be antagonistic and therefore a good therapeutic strategy should be applied (Chaudhry et al., 2017).

  As suggested above for tobramycin, antibiotics can be antagonistic to
  phage because they reduce the density of the bacteria and thus the
  capacity of these viruses to replicate [43]. Worse, antibiotics may
  even interfere with phage replication within the cell, thereby causing
  a reduction in phage numbers [41, 44, 45]. One way to test the effects
  of this possible antagonism is to treat with phage first and
  subsequently treat with the antibiotic, comparing the outcome with the
  case of simultaneous treatment. Here, we used delays of 4 and 24
  hours. Results show substantial effects of delayed treatment with
  phage for some antibiotics but no effect for others (Fig 4). The only
  statistically significant effects of delay are for the 24 hours delay
  using gentamicin and tobramycin, but the magnitude of the effect is
  profound. These are two of the three drugs for which simultaneous
  treatment suppressed phage replication (Fig 4B). The third such drug
  that suppressed phage replication with simultaneous treatment
  (ciprofloxacin) also exhibited greater kill with phage-first
  treatment, but the statistics fail to reject the null hypothesis of no
  effect of delay. This case warrants further investigation.

Unfortunately, bacteriophages are very host-specific and are hence not as broad spectrum as antibiotics. They are just like viruses of animals: the virus that infects a cat would most likely not infect humans. Very few viruses have a broad range of hosts.

For your query:

  if you can construct a drug that somehow can attack the bacteria because of the specific genetic code that gives the bacteria the ability to produce beta-lactamase then you might be able to attack all bacteria that shares the same genetic code that gives them that ability and the bacteria can not mutate to escape without losing their resistance to penicillin.

the answer is that it is possible in principle. There are ways to knock out certain genes (CRISPR-Cas is one of the ways). However, the problem is the delivery of these molecules that mediate these knockout, to the bacterial cells. For that, you again have to rely on virus like particles for the delivery which gets us back to square one: how to make delivery machines/viruses that target all pathogenic bacteria. Moreover, the mechanisms of antibiotic resistance are diverse. Considering several other factors (that I am not going to list here), it is very difficult to make an efficient system for targeting antibiotic resistance genes in different bacteria.


Contracting muscles in humans I study biology at school, and unfortunately for me, my program skips the muscles in humans chapter.

I know (and mainly, feel) that the movement in one direction isn't created by the same muscle as the movement in the opposite direction, e.g the Triceps ("front") and Biceps ("back").

I know that the triceps straightens the elbow, while the biceps contracts the elbow.

I also know that, instead of actually moving the arm, I can contract these two muscles (when I show off, for example...) without actually moving the arm. That area becomes hard. Both muscles, as I feel, are contracting. I cannot statically contract only one of them.

My question is whether this action is something "special", or simply both muscles working against each other, resulting in zero movement?

The situation you are describing where muscles are situated on opposites sides of a joint and produce opposing movements is called "antagonism." Most joints are set up where one or more muscles on either sides will produce such movements (e.g., flexors vs. extensors). Here's a question about muscles without antagonists.

When you contract all the muscles crossing a joint (i.e., when you are "showing off"), the muscles balance each other. If not, the bones would move and the joint angles would change. So taking the elbow as an example, in the image below, Arnold is contracting the elbow flexors (biceps brachii, brachialis) as well as the elbow extensors (triceps brachii). In order for the bones to remain static, the forces must be equal and opposite.


Binding BSA to silver surface via large difference in isoelectric points of the two materials I would like to bind BSA to a silver surface so that I can utilize plasmonic sensing to detect the BSA. There seems to be two methods of doing this: 1) to rely on electrostatic forces or 2) to form a covalent bond. The former seems to be the easier route, especially for someone like me who does not have a background in chemistry/biology.
So I found a paper (https://doi.org/10.1016/0021-9797(91)90121-N), which has been cited 54 times, that determined a silver (oxide) surface has an isoelectric point (iP) of ~10 pH. So this should mean that it has a positive charge when a neutral pH solution covers the surface. In other literature BSA has been shown to have an iP of pH 4-5, so it should become negatively charged in a neutral pH solution. So the BSA should bond to the silver surface in a neutral solution, correct?
The reason I ask is two-fold. First, I found a more recent paper (https://doi.org/10.1021/am400909g) that has a conflicting value for the iP of a silver film (~3 pH). Second, I found a paper (https://doi.org/10.1016/j.vibspec.2003.09.003) were the authors adsorbed BSA onto silver films, but with the intermediate step of applying 2-mercaptoethanesulphonate to the silver surface. Why the need for this if the silver should attract the BSA electrostatically?
In addition, if BSA bonding to silver were to work in this way, am I correct in thinking that a neutral solvent such as phosphate buffered saline would hinder the electrostatic bonding process because the positive and negative ions from the salt solution would bond to the respectively charged molecules and neutralize the charge?

Concerning the apparent discrepancy between your first and second citations, the difference in values is addressed by the authors in the more recent work:

Perusal of the literature yields few IEP values for silver metal. Chau and Porter reported an IEP of 10.4 for an evaporated silver film as determined by contact angle titration.(6) The method employed in their investigation used only neutral and basic liquids, and the maximum contact angle achieved on the silver films was ∼35°, in contrast to the maximum we observe of 52° at pH 3.2 (Figure 1d). This dichotomy may be indicative of the amphoteric behavior of the native oxide at the surface.

Concerning your third citation where the authors bound BSA to silver via a 2-mercaptoethanesulphonate linkage monolayer, the authors give their reasoning in the abstract:

The direct adsorption of proteins on metal surfaces usually leads to loss of their enzymatic activity

So, to answer one of your questions

Why the need for this if the silver should attract the BSA electrostatically?

BSA here is a proxy for other proteins.  The purpose of the research was to examine how the structure of the linkage monolayer changed in response to protein adsorption, not how BSA specifically binds a silver substrate.


Is Homo sapiens the only extant species of genus "Homo"? Is Homo sapiens the only species of genus "Homo" that survived?

Is Homo sapiens the only extant species of genus “Homo”?

Yes, Homo sapiens is the only species left in the genus Homo. To be more accurate, some even consider all modern humans as being part of the same subspecies Homo sapiens sapiens. In those terms, Homo sapiens sapiens is the only subspecies left in the genus Homo.

There were other lineages before though but they got extinct.

Other Homo lineages that existed

There were other Homo lineages that went extinct. Consider the followings for example

H. habilis
H. gautengensis
H. erectus
H. neanderthalensis (sometimes called H. sapiens neanderthalensis)
H. heidelbergensis

Related posts

Here are two other posts that may be of interest to you

Does it make sense to classify all humans in a single species?
How could humans have interbred with Neanderthals if we're a different species?


Is the birds' decision to fly away congenital or learned behaviour? I see two possibilities how could the birds know what to do every fall:

The birds' migrations are driven entirely by the vertical memetics and today it is just a custom transferred from parents to offsprings.
There is a gene that causes birds to decide to fly to the warmer areas every fall, activated when it is appropriate time

Which of these hypothesis is closer to the truth?

This example proves IMHO that migration is largely nature and not nurture:
In the Netherlands, white storks were bred / reintroduced. A large part (about one third?) of the reintroduced birds do not migrate, but their offspring usually does migrate see. They couldn't have learned it from their parents, that's for sure.


Standard datasets for testing new multiple sequence alignment algorithms? Are there any open and freely distributed standard datasets for testing new algorithms for multiple sequence alignment?

I would suggest you PAcAlCI or Prediction of Accuracy in Alignments based on Computational Intelligence, though the acronym in wierd the tool is good for testing new Sequence Alignments. They

But before you start testing your algorithm, I suggest take a look at these papers:

[1] Who Watches the Watchmen? An Appraisal of Benchmarks for Multiple Sequence
Alignment

[2] Issues in bioinformatics benchmarking: the case study of multiple sequence alignment

PS: I haven't tested or used the tool myself.


Do Penicillin based antibiotics affect birth control? I wasn't sure whether to ask this question on Biology or Chemistry Stack Exchange, since it is really biochemisty, but this is something that's been puzzling me.

Most pharmacists (all that I've encountered) tell you that antibiotics decrease the effectiveness of birth control. There are side-effect warnings on all Penicillin based antibiotics that say they decrease the effectiveness of birth control, and advise you to use a back-up method when taking antibiotics.

However, most health organization websites (Planned Parenthood, Mayo Clinic, NHS) explicitly state that ONLY two antibiotics have been shown to sometimes decrease the effectiveness of birth control-- Rifampicin and Rifabutin.

NHS Website: http://www.nhs.uk/conditions/contraception-guide/pages/antibiotics-contraception.aspx

Yet websites of Pharmacies like Walgreens or CVS say that to a lesser extent Penicillin based antibiotics can decrease birth control effectiveness, or in general remain vague about antibiotics affecting birth control :

http://www.walgreens.com/topic/faq/questionandanswer.jsp?questionTierId=600006&faqId=600022

So--do Penicillin based antibiotics affect birth control?

Evidence on the association between antibiotic use and combination oral contraceptive (COC) failure remains controversial, with recent studies reporting no evidence to support decreased effectiveness of birth control with the use of antibiotics except rifampin and rifabutin.
The reasoning is antibiotics might interfere with the effectiveness of COCs by decreasing steroid hormone’s plasma concentrations by hepatic microsomal enzyme induction or inhibition, interference with enterohepatic circulation of
COC metabolites, interference with absorption from the GI tract, competition between two drugs for the same metabolizing enzyme, alterations in plasma protein binding, induction of an opposite physiologic effect, or increased urinary or fecal excretion of the contraceptive.
As you stated, the strongest evidence is for rifabutin and rifampin: a significant decrease in the hormonal levels was noted in women taking rifampin even after a single dose.  Dirithromycin slightly decreased plasma ethinyl estradiol levels, with questionable clinical importance. A recent study in the Netherlands did find a relationship between the use of antibiotics and breakthrough pregnancy in a population-based prescription database; also, individual patients do show large decreases in the plasma concentrations of ethinyl estradiol when they take certain antibiotics, notably tetracycline and penicillin derivatives.
Because of earlier studies, anecdotal reports, and the above (it's not possible to identify whose levels will drop with antibiotic use), a cautious approach is advised. Physicians and pharmacists (80-90% of both) still lean towards believing that broad-spectrum antibiotics decrease the effectiveness of COCs, and continue to advise the use of back-up contraception.
The tide is shifting, however, as new studies come out. Here are a few excerpts of recent studies:

Available scientific and pharmacokinetic data do not support the hypothesis that antibiotics (with the exception of rifampin) lower the contraceptive efficacy of oral contraceptives. (J Am Acad Dermatol 2002;46:917-23.)

Since dermatologists treat acne with antibiotics, and a significant percentage of these patients are young women of child-bearing age, they certainly have a vested interest in knowing if this is true.

Rifampicin and griseofulvin induce hepatic enzymes and do appear to have a genuine interaction with the COCP, leading to reduced efficacy. The situation with the broad-spectrum antibiotics is less clear. There are relatively few prospective studies of the pharmacokinetics of concurrent COCP and antibiotic use and few, if any, demonstrate a convincing basis for any reduced contraceptive efficacy.
We did not find an association between concomitant antibiotic use and the risk of breakthrough pregnancy among COC users. However, due to limited power and potential carryover effects, findings from this study cannot rule out an elevated risk of COC failure among antibiotic users. (2011)

So, the answer is (except with your noted exceptions) the penicillin-class antibiotics probably do not interfere with effectiveness of COCs. However, one unwanted pregnancy is one pregnancy too many, and the use of a back-up method is not a huge deal (just ~14 days).
Until more and larger studies demonstrate a lack of interaction between most antibiotics and COCs, this will likely be the advice people continue to receive. When you look at the risk to benefit ratio of back-up, it's probably the wisest course for people prescribed a short course of antibiotics. It is more significantly problematic for people prescribed continuous antibiotic use for acne, Crohn's and other conditions/illnesses.
Oral contraceptive efficacy and antibiotic interaction: A myth debunked
Interaction between broad-spectrum antibiotics and the combined oral contraceptive pill: A literature review
Antibiotics and oral contraceptive failure — a case-crossover study
Are antibiotics related to oral combination contraceptive failures in the Netherlands? A case-crossover study
Drug interactions between oral contraceptives and antibiotics.
Survey of pharmacists and physicians on drug interactions between combined oral contraceptives and broad-spectrum antibiotics.


How does guanidium denature DNA? Guanidium salts like (G-isothiocyanate) disrupt the hydrophobic interactions inside a protein or nucleic acid and denature it. What happens when hydrophobic interactions in DNA are broken? (I don't think it should get ssDNA because guanidium doesn't break hydrogen bonds within molecules)

Guanidium is a chaotrope i.e it increases the entropy in the solution. It doesn't disrupt hydrophobic interactions. Guanidium and urea act by forming hydrogen bonds. They can bond with both the dissolved macromolecule and water. The water molecules are arranged as a shell around the hydrophobic regions so as to contain it, which leads to the reduction of entropy. This containment causes hydrophobic regions to come together and give rise to a pseudo-interaction (hydrophobic interaction. See the figure below). Guanidium interacts with the water shell and disorders it, thereby reducing the hydrophobic effect.
Guanidium can also interact with macromolecules directly, by forming hydrogen bonds. In this process they can disrupt the normal H-bonds in the macromolecule.


Can a hemorrhage occur after death? Can a hemorrhage occur after death?

Specifically lung hemorrhages. Can an organ hemorrhage after death and, if so, how long for?

Usually,blood moves through the body by force from the contraction of ventricles, the contraction on muscles, gravity, or other forces. At death, the only force left is gravity, which is why we see lividity (or livor mortis -pooling of blood in dependent positions) after death. This continues for ~8-12 hours (depending in part on temperature).

The blood in the arterial system at the moment of death is still under pressure because arterial wall musculature has not relaxed yet. (I don't know how long this takes, to be honest.) If an artery is pierced (say, a bronchial artery, e.g. by a knife), blood will flow from a high pressure area to a lower one (e.g. into non-inflated lung tissue, the abdominal cavity, or the outside or the body) So post-mortem hemorrhage can occur until the arterial musculature has completely relaxed. After this relaxation, stabbing a corpse will produce a small amount of oozing at most, unless pressure is applied somehow, e.g. during CPR. CPR may make small petechiae larger.

Livor mortis can occur in the lungs post death as well.

  as the blood accumulates in the dependent areas, the pressure of the settling blood can rupture small vesslels, with development of minute hemorrhages (petechiae)... This usually takes 18-24 hours... and is more common in (asphyxia).

Hanging is death by asphyxia, and is known to be associated with lung hemorrhages, but very small ones.

Forensic Pathology, Second Edition By Dominick DiMaio, Vincent J.M. DiMaio, M.D., pp.22-25


Which sex of trees bears fruit? Which sex of trees bears fruit? The males or females? And what specifically cause that one to bear fruit. Is it the same as it is with blossoms in trees?

The distinction between male and female is not that clear in plants, at least at the level of individuals. Actually the details may be rather complicated (see [1]), but in general we can distinguish between plants that have:

male and female individuals (dioecy)
male and female flowers on the same individual (monoecy)
flowers that have both male and female structures (bisexuality)

In the first case, only female individuals produce flowers that -- when fertilized by the pollen from the flowers of a male individual -- develop into a fruit. Examples are Hazelnut, common nettle and a few other species [2]. However, dioecy is rather rare among extant flowering plants [3].

Monoecious plant species are somewhat different. A good example is maize. The male flowers of a maize plant are located in the tassels at the apex of the stem, wheres the female flowers are are in the leaf axils. Note that each corn developed from a single flower and that the cob is actually the infructescense.

Then there are bisexual plants. In these, every flower has the potential to be fertilized and develop into a fruit, which is why they are also called perfect flowers. Plants have developed several strategies to prevent self-fertilization, e.g. the temporally delayed expression of female/male structures within the same flower.

Resources:

[3]: Bawa, K. S. (1980). Evolution of dioecy in flowering plants. Annual review of ecology and systematics, 15-39.


Problems understanding membrane potential I understand that membrane potential is the difference of the extracellular and intracellular ionic charges, due to their concentrations. We say that the extracellular space has a charge of 0 and then take the membrane potential with respect to the extracellular space. The intracellular space is normally around -60mV due to more negative charges being in the cell than the extracellular space.

This is how I understand membrane potential.

From this understanding, it is hard for me to see why I can't get this right:

We work with a regular cell with potassium 120mM inside and 4.5mM outside.

Say that we increase the intracellular concentration of potassium by 10 mM, a +1 valence ion which contributes to POSITIVE membrane potential.

What I envision is that as we put more positive ions in the cell, the cell is now more positive in regard to the extracellular matrix. However the Nernst equation states that the membrane potential actually gets MORE NEGATIVE!!
http://www.physiologyweb.com/calculators/nernst_potential_calculator.html

What is it that I am misunderstanding? Thank you.

I think this question has more to do with kinetics / transport phenomenons than biology, but that's okay, everything is connected especially my computer to the internet. ;-)

The basic idea behind transport phenomenons is that there will always be a flux of quantitative properties (e.g. charges, particle number, entropy, volume, etc...) where the qualitative properties like (electrical potential, chemical potential, temperature, pressure, etc...) have a gradient in space (note that kinetics of chemical reactions can be described similarly without the space gradient part).

In this case we are talking about electrochemical potential gradient and ion flux. It is very important to recognize that the electrochemical potential is not the same as the electric potential. It has a chemical component, so the result will depend on both charge and concentration gradients. By a single ion channel system (e.g. Na⁺ channel only) you can count the potential of each side of the membrane using the Nernst equation, by a system with multiple ion channels it is more complicated, so in that case you have to use the Goldman equation. So at the end you can say something like one side has a potential of x[mV] and the other side has a potential of y[mV] and so the difference is:  d[mV] = x[mV] - y[mV]

The sign of d depends on x or y has a greater value. By single ion channel systems this expresses an x → y direction so by positive d the cation flow direction is x → y and by negative d it is y → x. By anion flow it is the opposite.

By cells we use the out → in direction by counting the membrane potential. We can count the potentials using the

Nernst equation:
$$E_m = \frac{RT}{zF} \times ln \left(\frac{c_{out}}{c_{in}}\right)$$ or the
Goldman equation:
$$E_m = \frac{RT}{F} \times ln \left(\frac{p_{K^+}.[K^+]_{out} + p_{Na^+}.[Na^+]_{out} + p_{Cl^-}.[Cl^-]_{in}} {p_{K^+}.[K^+]_{in} + p_{Na^+}.[Na^+]_{in} + p_{Cl^-}.[Cl^-]_{out}}\right)$$
where

$Em$ is the membrane potential
$z$ is the ion charge
$[X]$ is the ion concentration
$p_X$ is the relative membrane permeability for the actual ion

and so on...

So for example by an average human cell in blood plasma, assuming that the inside of the membrane has a small negative charge

the Na⁺ has a positive effect (positive charge, high out → in concentration gradient, low out → in charge gradient),
the K⁺ has a negative effect (positive charge, high in → out concentration gradient, low out → in charge gradient),
the Cl¯ has a negative effect (negative charge, high out → in concentration gradient, low in → out charge gradient)
the Mg⁺⁺ has a small positive effect (positive charge, low out → in concentration gradient, low out → in charge gradient)

on the membrane potential. It is hard to find an ion in this case which flow is charge gradient dominated instead of concentration gradient...

  I understand that membrane potential is the difference of the
  extracellular and intracellular ionic charges, due to their
  concentrations.

The (sign and) value of the membrane potential is not determined by the charge gradient because the concentration gradients usually have a much bigger effect on it. The cells maintain these concentration gradients by using up energy.

  We work with a regular cell with potassium 120mM inside and 4.5mM
  outside.

  Say that we increase the intracellular concentration of potassium by
  10 mM, a +1 valence ion which contributes to POSITIVE membrane
  potential.

In your case K⁺ has a negative effect on the membrane potential, because of the high concentration gradient with reverse direction. So decreasing the concentration gradient will increase the membrane potential.

If you want to learn more about how to count membrane potentials, you should read this and its next section instead of wikipedia...


What is a "pan-specific" antibody? I am new to biology. I searched a lot to find an article that explains what "pan-specific" antibody is but I could not find anything substantial that would help me understand what it is.

An example from an article

  In this report, we address this long-standing analytical deficiency by
  developing a pan-specific antibody against the pHis modification. We
  show that this antibody can be used to detect protein histidine
  phosphorylation in vitro and in vivo.

Another definition

I appreciate if someone helps me with finding a scientific explanation (article/ book) on what "pan-specific" antibodies are.

Kind Regards,

What does pan-specific antibody mean?

The combining prefix pan- means "all" or "every".

Antibodies are specific because they bind specifically to an epitope ('target') on a molecule. A pan-specific antibody is one that binds specifically to all desired targets, within a defined range.

Here are three correct examples of how the word could be used, to help you understand. Only the first two are relevant for your particular case:

In your case, there is an antibody for the phosphoprotein, the unphosphorylated protein, and both. The antibody that targets both is pan-specific because it binds both ("all", or "every") forms of the protein.
Another possible use for pan-specific is that some antibodies bind to some members of a protein family, but not all, so they are not comprehensive enough. Other time, antibodies bind to all members of a protein family, but bind additional targets, so they are not specific enough. Pan-specific is a great way to describe an antibody (monoclonal) or set of antibodies (polyclonal) that are both specific and comprehensive enough to adsorb an antigen of choice.
An antibody that binds specifically to a protein called pan.


Is casein hydrolysate the same thing as casamino acids? Probably a dumb question, but these seem identical. If a protocol calls for one, can I use the other instead?

Roughly, yes they are similar, but there are processing differences- the real difference is filtering. A product containing simply casein hydrosylate will only be roughly filtered with lots of peptides (like body builder products). Whereas casamino acids should be primarily clean/free amino acids (like nutrients for bacteria).

The actual manufacturing methods will be proprietary for the manufacturer... but you can trust that they are basically doing whatever works best to obtain the individual amino acids and/or whatever is cheapest for obtaining a useable product.

I have used bodybuiling and several other grades of casein products for growing bacteria. I have found that although various products may get the job done there are some serious drawbacks to casein products not intended for growing bacteria.

Differences include clarity of media, cleaning of glassware/fermenter/bioreactor, sudzing of aerated media, and the microorganism. Some microorganisms won't grow very well, and generally, those that can may still not grow quite as well or as fast... so that extra 10% or 20% cfus may be important (or maybe not since the price for quality may be 10 times higher).

The quality-features vs price must be weighed by the grower. Personally, I sometimes autoclave a cheap casein product in one (easy to clean) vessel then rag-filter it into another (then autoclave it again) for growing bacteria... but that's because I have about a thousand pounds of rough casein hydrosylate, and only a kg or so of casamino acids (for particular studies). This method does not eliminate all of the problems but it does reduce some of them.


Question about the expression of MHC Is it possible to express both the MHC class-1 and MHC class-2 both in one cell?

Sure generally any cell that expresses MHCII will also express MHCI. Most cells in the body express MHCI as a self-identifier and to present intracellular proteins to T cells as a sort of a status update i.e. the cell will constantly be presenting peptides (pieces of endogenous proteins) on its surface bound to MHCI, if the cell becomes infected it could also present viral proteins on its surface with MHCI, which can potentially be recognized by a T cell specific for that particular epitope. B cells and antigen presenting cells such as dendritic cells and macrophages express MHCII but also need to be able to be identified as self through their basal level of MHCI presentation of self-peptides. The two MHC molecules are recognized by different cell types, MHCI by CD8 T cells and MHCII by CD4 T cells. So you could consider them to work independently from one another. The source of antigens (peptides here) and process for presenting them via MHCI and MHCII are somewhat different from one another.


What species of snail is this? I found it in Washington state, in a city south of Seattle. I found it next to a bush after it rained on someone's driveway. Here are two pictures of it:

( originally posted in instagram )

If anyone can identify this species, kudos to you.

It resembles Cepaea nemoralis, or commonly called Grove Snail, belonging to the family Helicidae.

Image Source: WikiMedia Commons

According to Wikipedia, these snails were introduced to North America from Europe. These fascinating creatures occur in diverse forms of shell color as well, as shown below.

Image Source: Metodologie di Programmazione

Here I have found a very detailed shell and body markers for Cepaea nemoralis.

Image Source: ResearchGate


Why was Achromobacter xerosis removed from the NCBI taxonomy? The Global Catalogue of Microorganisms lists a bacterium called Achromobacter xerosis which is mentioned in several papers and patents. It once existed in the NCBI taxonomy database, with ID 216898. However, it is no longer there - going to https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=216898 just yields a "No result found" page.

Why was this species removed from the NCBI's taxonomy? I haven't managed to find any documentation on why the NCBI would purge a species from their database, nor can I see any obvious reason to do so.

For whatever it's worth, I queried NCBI support about this and got a reply:

  To: info@ncbi.nlm.nih.gov
  Subject: Reason for removal of a species from the taxonomy?

  Hi,

  I notice that the species Achromobacter xerosis used to be listed in the NCBI taxonomy at https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=216898 but no longer is. I haven't been able to track down any documentation hinting at why a species would ever be removed from the taxonomy. Is there any such documentation that I've missed, and are you able to explain why this species in particular was removed?

  Thanks in advance for your time,
  Mark

Reply:

  Dear Mark Amery:
  The NCBI Taxonomy database records exist to support data that are in other NCBI databases. A review of the Taxonomy database must have identified that we have no records for which Achromobacter xerosis
  is designated as the organism name.

  regards,
  Bonnie L. Maidak, Ph.D.
  NCBI Help Desk
  DHHS/NIH/NLM/NCBI


Effect of 2,3-bisphophoglycerate (2,3-BPG) on haemoglobin When 2,3-bisphophoglycerate (2,3-BPG) binds to haemoglobin, a higher partial pressure of oxygen is needed to bring about 50% saturation of with oxygen.

What is the physiological significance of this and its molecular basis?

How would this affect the oxygen dissociation curve of  haemoglobin and would it alter the Bohr effect?

Note regarding editing
In its original form this was a multiple choice question that had remained unanswered for a year, possibly because the detractors are very bad. Because the topic it covers is thought to be of general interest it has been reformulated as a standard question. For the record, the original question asked which of the following were correct: (1) 2,3-BPG in red blood cells causes the oxygen dissociation curve to shift to the left. (2) The binding of 2,3-BPG to haemoglobin lowers the affinity of the haemoglobin for oxygen. (3) Binding of 2,3-BPG to haemoglobin reduces the Bohr effect. (4) When 2,3-BPG is absent, oxy-haemoglobin is less likely to unload oxygen. The ‘correct’ answer was given as (2), but the poster thought that (4) was also correct.

The oxygen dissociation curve for haemoglobin (Hb) in the absence and presence of 2,3-BPG is shown in (i) below:

It can seen that the curve has shifted to the right (MC-1 incorrect) and the oxygen affinity is obviously decreased, as it takes a higher concentration (pressure) of oxygen to achieve the same percentage saturation (MC-2 correct — and so is option MC-4 as far as I and @JM97 can see, agreeing with the poster. MCQs are an educational abomination!).

The physiological significance of this is  considered in detail in my answer to another question, but, in short, it ensures that an adequate proportion of the (smaller) amount oxygen taken up at the lower pressure in the lungs is released in the tissues (3 minus 4, cf. 1ʹ minus 2).

To address the interaction between the effect of 2,3-BPG and the Bohr Effect one needs to consider the corresponding curves for the effect of hydrogen ions (falling pH), shown in (ii), above (see also my detailed answer to this question).
It can be seen that the effect of hydrogen ions is similar to that of  2,3-BPG. Can these two have independent (additive) effects? It is known from molecular studies that they both interact with and stabilize deoxy-haemoglobin at different positions (see ii, below), and in one model of the allosteric mechanism they can be considered as shifting the equilibrium from the tense (deoxy-) to the relaxed (oxy-) state of haemoglobin:

(i) Generalized diagram of allosteric equilibrium of tetrameric protein between relaxed state (where it can bind substrate/ligand) and tense state. Negative effectors favour the tense state. (ii) Illustration of this for haemoglobin, where H+ ions protonate His-146 of the β-subunits and 2,3-BPG forms ionic bridges between the two β-subunits.

So it would appear that Bohr effect can still augment the 2,3-BPG effect, but I would imagine that the extent of this augmentation would depend on the initial position of equilibrium, and I would not expect it to be additive — I may be wrong. (Is MC-3 correct or not? A school student can hardly be expected to know unless he had been fed the ‘correct’ answer. Perhaps he is intended to interpret the option as meaning “does the 2,3-BPG effect work in the opposite direction to the Bohr effect”. You may now understand why I loath MCQs.)

Bibliography

The diagrams are my own, based on various sources I have used over the years. To check whether what I have written is correct, the reader may wish to check any of the many accounts online, including the following which have references to original material:

Wikipedia article on haemoglobin
Proteopedia article on
haemoglobin


Studying changes in DNA for causes of cancer First of all let me say that I'm not into Biology myself... but I have a question for those of you who are.

From what I've read, cancer is caused by 'faulty' DNA that behaves abnormally. Mutations can occur for various reasons, ranging from simple 'copying errors' to environmental factors.

I was just wondering whether current research has dealt with storing DNA of people or animals (e.g. rodents) and observing how it changed, especially for cases where it eventually resulted in cancer. Something along the lines of this, but I'd like to know what research has actually been done so far.

I tried to comment but what I wrote is too long, so here it is as an answer of sorts.

If I understand the question, you are asking: has anyone done a prospective study where they store the DNA of individuals and then later, when some of these individuals get cancer, have a look for mutations that are associated with that cancer. In fact this is done all of the time, but it isn't necessary to store any DNA because the cancer patients will have the normal sequence in all of their non cancerous tissues - only the cancer cells will have the relevant mutations. See here for a recent example of this type of study that made the news.

Your BBC link is to a story in which the genomes of people will be analysed to determine if there are genetic factors which predispose them to cancer (and other diseases), but these won't be the mutations that actually create the cancerous cells.


MTHFR recessive alleles and B-vitamins I know that being heterozygous or homozygous recessive for the MTHFR gene prevents that person from being able to process and use folate and B-12. It causes an unhealthy level of homocysteine to accumulate in the bloodstream which can cause more serious problems. Taking methylated B-vitamins, specifically Methylfolate and Methylcobalamine will prevent homocysteine from building up, but I am not sure why.

Can someone explain how this process works? I am wondering how the body uses folate and B-12 (cobalamine) normally and how the recessive MTHFR genes interfere with this process.

Folate, or rather its active form tetrahydrofolate (THF), is a coenzyme that carries a 1-carbon group. The carbon group can occur in various redox states: CH3-THF (methyl-THF), CH2-THF (methylene-THF), CH-THF (methenyl-THF) or CHO-THF (formyl-THF). These can be interconverted by a variety of enzymes, and are used by cells to synthesize a number of products, including nucleotides and methionine.

MTHFR (methylene-THF reductase) converts CH2-THF into CH3-THF. The CH3-THF form is the most abundant folate in blood, and is therefore considered the "transport" form of folate. CH3-THF is also the form used to synthesize methionine, in the reaction

CH3-THF + Homocysteine $\rightarrow$ THF + Methionine

catalyzed by methione synthase (gene symbol: MTR). This enzyme requires cobalamin (B12) as a cofactor. Actually, the reaction occurs in two steps,

CH3-THF + Cobalamin --> THF + CH3-Cobalamin
CH3-Cobalamin + Homocysteine --> Cobalamin + Methionine

Loss of MTHFR leads to deficiency of CH3-THF, causing methionine synthase to run out of substrate, and homocysteine to accumulate. Lack of the B12 cofactor also blocks methionine synthase, and it should be clear from the reactions above why supplementing with either CH3-THF or CH3-cobalamin can alleviate the problem (at least in theory). I would guess the phenotypes seen in this condition is mainly due to lack of methionine though, rather than excess homocystine, since methionine is required for a variety of methylation reactions in cells.

This is a simplified view. There are many other interactions between B12 and folate; for example, the methinine synthase reaction is needed for cells to take up and store folates, and therefore B12 deficiency can create a folate deficiency as well. See for example http://www.ncbi.nlm.nih.gov/pubmed/6115113 and http://www.ncbi.nlm.nih.gov/pubmed/10466189 for further reading.


What is/are the molecular differences between HDL and LDL cholesterol? Why exactly is HDL-cholesterol good for us and LDL-cholesterol bad for us. It has been well-established that LDL-cholesterol is associated with atherosclerosis and that HDL-cholesterol helps remove excess LDL-cholesterol from the circulation. From a biochemical view, however, what is the difference between the molecules that causes this difference?

First of all, we should specify that there is no such thing as "HDL-cholesterols" and "LDL-cholesterols". On the same note there is no such thing as "good cholesterol" and "bad cholesterol": cholesterol is just one molecule, with this chemical structure

What blood tests generally report is HDL-C and LDL-C, that is the amount of cholesterol in HDL or LDL respectively (again, cholesterol is always the same molecule, whether in an HDL or in an LDL).

HDL (high density lipoprotein) and LDL (low density lipoprotein) are lipoproteins, aggregates of proteins and lipids that can carry, amongst other things cholesterol.
There are 5 major types of lipoproteins, called chylomicrons, VLDL, IDL, LDL, and HDL and are distinguished by their size, density and the proteins they are composed of.

The main function of lipoproteins is that of carrying lipids (=fats) around the organism in the blood. The problem is that lipids are not soluble in water (try to pour some oil in a glass of water) and blood is mainly composed of water. Lipoproteins, on the other hand, have a hydrophilic (="water-loving") exterior and a lipophilic (="fat-loving") interior, like this:

In the picture, the "balls" represent proteins, called apoproteins, and the C represent cholesterol and T tryglicerids, which are both lipids.
As you can see, all the fats are inside the lipoprotein, but the exterior, being soluble in water can be easily dissolved in the blood.

The biochemistry of lipoproteins is quite involved and I will not go into details here (but please leave a comment if you want further explanations) but, to simplify things:

HDL bring lipids from the periphery back to the liver
LDL bring lipids from the liver to the periphery

It is very important, at this point, to note that lipids are a physiologically important part of our organisms. All the cells in our body contain lipids: the membrane of each cell in the body is made up of lipids (called phospholipids) and also contain cholesterol. In fact, cholesterol is extremely important for the correct functioning of the body as, for instance, it is used as the base to make many hormones (the so-called steroid hormones, such as estrogen, progesterone, cortisol, testosterone etc).

However, too high levels of lipids, particularly cholesterol, are not beneficial, as high cholesterol levels have been in fact linked to many cardiovascular diseases, which we hear a lot about these days.

So, because HDL tend to remove the lipids from the circulation and bring them back to the liver they can be considered as some sort of "cleaners", that remove excess cholesterol from circulation.


Layman definition of genetic polymorphism? I am reading an article about Genetic Polymorphism and there are lines in the article about genetic polymophism that I don't quite understand like.

  In this area, there are six different chemotypes that are the expression of a genetically controlled polymorphism in T.vulgaris(24).

Can someone explain genetic polymorphism and morphic distribution in layman terms.

Thanks

Polymorphic sites

Consider the following sequence of DNA

ATTTGC

Now consider that in a population of 5 haploid individuals (in reality populations are larger of course) you have the 5 following sequences

ATTTGC
ATTTGC
ATCTGT
ATTTGC
ATCTGC

Looking at those sequences you can identify two sites (site 3 and site 6) for which the nucleotides vary throughout the population. For example, at site 3, 3 individuals have a T while 2 individuals have a C. Sites 3 and site 6 are said to be polymorphic sites (a.k.a. segregating sites).

Statistics of genetic variance related to polymorphic sites

Note that there are all sorts of ways to describe the genetic diversity in this population. You could calculate the total number of segregating sites or the average number of pairwise difference between any two sequence. Or the average expected (and not observed) heterozygosity (which is sometime refer to as genetic diversity). One could calculate the frequency distribution of the number of individuals carrying a given variant (called the site-frequency spectrum).

Other polymorphism

Note that I emphasized on polymorphic sites for the moment but there are a whole bunch of different reasons that two genomes may differ. Two sequences may differ in their length as well (insertions and deletions of nucleotides). Genomes may differ in the number of copy of a given sequence (copy number variation). Genomes may differ in the number of copy of very very long sequences or in the order of those sequences (synteny). Genomes may differ in their number of chromosomes or in their ploidy level.

About the citation

  In this area,there are six different chemotypes that are the expression of a genetically controlled polymorphism inT.vulgaris(24)

It is hard to say anything without the link to the article.

There are six different chemotypes (found in the population). Not all individuals have all chemotypes (eventually each individual has one or two chemotypes). Having one or another chemotype depend on your DNA sequence.

Assuming that the difference is due to polymorphic sites (which is impossible to say for sure without reading the paper), there is therefore one (or several) polymorphic sites that explain the variance in chemotypes in the population.


Yellow/Orange Fungus on Oak Tree What is the fungus pictured below? The photo was taken October 6, 2013 near San Antonio, TX.

I have Googled it and my results suggest Laetiporus root rot (Laetiporus sulfureus).

According to this website the presence of this fungus indicates the tree should be removed.

Is there any chance that this is something else? I would hate to remove such a beautiful oak tree.

I can't say for sure but it looks like a species of the Laetiporus mushrooms. Please refer to its wikipedia page for the full info.

edit: I did not read your question fully and now I see that you reached the same conclusion. Just ignore my answer. As to the second part of your question asking if it could be anything else, that is quite hard to visually determine as there are many look alikes in the mushroom kingdom. Read this for some imposters.


Could this Francobelgian comic book woman really have these 4 diseases at the same time? I'm doing an archive binge of a paper comic "The Kiekeboes". One of the characters is an elderly woman currently at the doctor, and she says the has the following illnesses:

Erythema Exsudativum Multiforme;
Necrobiosis Lipoïdica;
Phlegmasia Alba Dolens;
and Metropathia Haemorrhagica.

now, I googled these, and these are apparently real diseases (which actually makes sense, since she said she found them in her medical dictionary), namely 3 skin diseases and 1 menstruation problem. However, I find it hard to believe an elderly woman could have 3 different skin diseases and a menstrual disorder at the same time, especially since she already stopped menstruating.

Is it possible for a patient to have all 4 of these illnesses at the same time? Or do the causes interfere with each other too much for that? I don't want to know how to cure it, I just wonder how much they're talking out of their anuses.

Image I just took with my camera:

Kiekeboe 21: the Piri-Piri Pills, Page 17, strip 30. Author: Merho. Publisher: J.Hoste NV (currently part of Standaard Uitgeverij). Picture taken by Nate Kerkhofs on 16 september 2014.

It is in Dutch, but the names of the illenesses are clearly readable (since they're Latin anyway).

The doctor asks "what are you here for, madame? a cold, reumathism, headache?" right before this. The woman answers "no, doctor, I'm struggling with ... and also ... not to mention ... and a really annoying .... The doctor then replies "but madame, where did you get all those illnesses?" the woman replies "in my medical encyclopaedia!".

Erythema multiforme (minor) can and does occur in a lot of people; while it is usually self-limited, it can recur, especially when the trigger is an unsuspected food.[1] How common is it? It is very common.

Necrobiosis Lipoidica is not uncommon in diabetics, less common but still found in non-diabetics. It can occur at any age, including the eighth decade. It also shows a sex predilection, being 3 times more common in women than in men.[2] How common is it? It is not rare.

Phlegmasia Alba and Cerulea Dolens[3] is serious and associated with deep vein thrombosis, which is an acute event. It is not uncommon, but it's not chronic. (More than 600,000 cases of venous thromboembolism are estimated to occur each year in the United States, all of which can lead to Phlegmasia Alba and Cerulea Dolens. How common is it? Luckily, not very. If the author is referring to garden-variety thrombophlebitis, though, that's a chronic problem, and not uncommon in the elderly. Thrombophlebitis is chronic and common enough.

I'm not going to address Metropathia Haemorrhagica, because, as you have noted, it's found in menstruating women.

Diseases generally don't really interfere with each other; some diseases can't co-exist (you can't have hyperthyroidism and hypothyroidism at the same time, for example, or have an active pituitary gland tumor and empty sella syndrome at the same time), but diseases don't interfere with each other exactly. Some diseases have common underlying foundations, so can occur co-morbidly, for example collagen vascular diseases can manifest with skin, joint, and lung findings, which might not be diagnosed as several manifestations of one disorder if it's not obvious. A better example might be diabetes, where similar underlying pathologies cause, say, heart disease, skin disease, eye-problems and kidney disease together.

Whatever, the likelihood of a little old lady having all four of your diseases are nil. The first three all the time (assuming not garden variety thrombophlebitis) - nil. Once, not impossible once, but not chronically. Of the first two - not far fetched. The first - common as dirt (comes and goes, though.)

I hope this helped.

[1] Erythema Multiforme on Medscape
[2] Necrobiosis Lipoidica on Medscape
[3] Phlegmasia Alba and Cerulea Dolens on Medscape


Measuring sugar content of a tree I would like to grow mushrooms on oak trees I can harvest from my property.  I've read that the best results will be when the sap is rising but the tree hasn't budded yet.  The mycelium feeds on the sugars in the logs.

I would love to be able to measure the sugar content so I could accurately asses the sugar content.  Here in Southern Oregon the winters are mild and the leafing out of the oaks varies quite a bit from year to year.

How can I measure sugar content of the sap in a tree?

The difficult step will be getting samples of sap: have a look at the WP page for maple syrup for ideas about methods of tapping into the xylem of your trees.

You will then need to assay sucrose in the sample of sap. There are many commercial assay kits available (Google: sucrose assay), which rely on an enzyme, invertase, to convert the sucrose to glucose + fructose. The released glucose is then measured by a glucose oxidase assay. You would need some kind of colorimeter/spectrophotometer for quantitative results but there is a visible color change, so you could probably get a rough idea of what is going on by visual comparison with a set of glucose standards.

Supplementary
An alternative would be to measure sugar concentration by refractometry: see here and here.


How does alum help in blood coagulation? I recently came across a test in my chemistry book which says that potash alum, $\ce{K_2SO_4.Al_2(SO_4)_3.24H_2O}$ is used on cuts and bruises, because it coagulates the blood quickly. The explanation it gave, was that blood is a colloid of proteins in water and the $\ce{K^+}$, $\ce{Al^{3+}}$ and the $\ce{SO_4^{2-}}$ ions coagulate(=precipitate) them, causing a blood clot (quickly). However, from biology, I know that blood coagulation(=clotting) is brought about by formation of fibrin network which traps the WBC and RBC in blood. The formation of fibrin from fibrinogen involves a series of reactions with many factors like $\ce{Ca^{2+}}$ , but not $\ce{K^+}$ or $\ce{Al^{3+}}$.

So, I was wondering what the actual explanation might be.

Do people actually use alum to stop bleeding, or only as a disinfectant? Does alum have any disinfectant effects?
Does precipitation of proteins in blood help clotting?
Does alum contribute in any way to the process of blood clotting?

Note: This is a question involving both chemistry and biology, but I posted the question here as I thought that this is more of biology than chemistry.

I will answer the three questions one at a time. Lets begin with the first one:

  Do people actually use alum to stop bleeding, or only as a disinfectant? Does alum have any disinfectant effects?

Yes, alum is also used as a disinfectant, and it works in the same way as it does in blood coagulation. In aqueous solution, potash alum dissociates as:

$K_2SO_4.Al_2(SO_4)_3.24H_2O \rightarrow 2~K^+ + 2~Al^{3+} + 4~SO_4^{2-} + 24~H_2O$

Now, as is known, blood is a colloidal solution, in which the plasma proteins are charged (see Rügheimer et al, 2008). These ions from alum neutralize the charges on plasma proteins, causing the blood to coagulate. Similar effect is observed in disinfectant where these ions react with the free organic acid and thiol groups of proteins on microbes and free proteins, resulting in their precipitation (Williams, 2001). Thus alum can act as disinfectant.

  Does precipitation of proteins in blood help clotting?

Coagulation of both plasma proteins and RBCs takes place on application of alum, since both of them are charged (Fernandes et al, 2011) as is discussed in next point. However, it is difficult to say whether coagulation of plasma proteins plays a significant role in clot formation or not.

  Does alum contribute in any way to the process of blood clotting?

Yes, alum does contribute in the process of clotting: it makes clotting faster. Although the term 'clotting' is generally used for formation of what is called as platelet plug, the actual process of clotting also depends on coagulation of colloidal particles in blood. When the blood is exposed to the extracellular matrix (due to damage to blood vessel), platelets activate and, via a cascade of reactions, lead to formation of a platelet plug. Red Blood Cells get tapped in this plug (which is actually a fibrin meshwork) and lead to formation of clot. A nice and simple representation of this process is below (from here):

Without alum, RBCs would take longer to coagulate due to mutual repulsion. By neutralizing them, alum makes this process easier and faster. Hence, alum helps in the formation of blood clot via coagulation of red blood cells.

I hope this helps.


What physiological processes within a muscle cause the latent period in a muscle fiber? This is a lab question I cant find the answer in the lab manual or in the text book.
What physiological processes in a muscle cause the latent period in a muscle fiber?
Please help.

Edit:
The latent period is the short delay between the muscle action potential and the beginning of muscle tension development. This is what I'm talking about. I'm sorry I didn't make that clear.

The action potential causes Ca2+ ions to be released in the cells, that is needed for muscle fiber contraction. There is a small time delay from the arrival of the action-potential until the Ca-ions are released and reach the required concentration in the cell for contraction. On the molecular level there is a protein called troponin (this is bacically located on the actin filament along with tropomyosin and obscures the myosin binding site(s)), that bind calcium and then undergoes conformational change - this also adds up to the delay. After this - the conformational change of troponin - myosin and actin can bind together and contraction can occur through conformational changes. All these binding and conformation changes take a small time to be completed, and thus causes a small delay. Below is a picture about the molecular mechanism ofof muscle contraction taken from this wiki page. The linked wiki page has real good detailed information.

I found this article and where they exactly measured things. To clarify my answer (taken from the linked article):

  Electromechanical delay (EMD) was described as a time elapse between the onset of muscle electrical activation and onset of force production, reflecting both electrochemical processes [i.e., synaptic transmission, propagation of the action potential, excitation-contraction (EC) coupling] and mechanical processes [i.e., force transmission along the active and passive parts of the series elastic components (SECs)]

So as for the whole muscle, not for just one cell the delay is caused by the things listed in the above quote - although excitation-contraction (EC) coupling and force transmission (things I have described earlier) take place in every single muscle cell that is in a specific muscle fiber.

Edit 2: I found a good and simple ppt/pdf about AP propagation and muscle contraction here.


Is high metabolism linked to high evolutionary turnover? I recently read The Dinosaur Heresies by Robert T. Bakker, a 1986 popular science book presenting arguments for an active lifestyle and high metabolic rate in dinosaurs.

One of the arguments that Bakker presents relates to the pattern of species and genera in the fossil record over time.  He states that "warm-blooded" animals (i.e. animals with high metabolic rates) are expected to have higher turnover of taxa and faster rates of diversification.  Dinosaurs have high species and genus turnover and rapid diversification, which Bakker interprets as evidence for a high metabolism.

This argument rests on the claim that high metabolism is correlated with high evolutionary turnover.  Setting dinosaur physiology aside, I wonder how reliable the underlying assumption really is.

Is there good evidence that metabolism and evolutionary rates are causally linked, perhaps due to the ecological strategies that warm-blooded animals tend to adopt?

Metabolism and evolutionary rates are linked, but not in the way you describe.

First consider that metabolism is intrinsically linked to body size. The larger an animal is, the smaller amount of energy per unit mass it takes to maintain that body. This can then be extended to many things about an organism, such as life span, gestation time, population growth, etc. (see Brown et al. 2004 for more detail).

Next consider that metabolism changes with temperature. Take an ectotherm (an organism who's internal temperature is the same as the ambient environment, traditionally called cold-blooded creatures) like a lizard, which will go thru temperature fluctuations throughout the day. It will have higher metabolism when the temperature is higher. A lizard living in a warm environment like the tropics will have an overall higher metabolism than a lizard of the same size living in a temperate climate. With that higher metabolism comes a different life span, gestation time, population growth, etc. even though their body sizes are the same.

When temperature is considered and corrected for, all organisms have attributes that scale directly with body size. A plant literally has the same metabolic rate as a lizard if they are a similar mass and live at the same temperatures. (Seriously, see the Brown paper).

Now onto evolution. Rates of evolution depend on many things, but primarily two. Generation time (the time for 1 generation of a population to reproduce) and mutation rates of DNA.
A longer generation time decreases the rate of evolution. For example a single celled organism reproducing every month will evolve faster than an elephant reproducing every decade.
Larger rates of mutation in DNA increase the rate of evolution. If DNA does not change then evolution cannot happen. So the faster DNA changes (thru mutation rates) the faster the potential evolution can be.

Generation time increases with increased body size/metabolism (Brown et al. 2004). Mutation rates decrease with increased size/metabolism (Gillooly et al. 2005).

With those two general patterns, one can say that the rate of evolution decreases with increased metabolism.

Now onto dinosaur evolution. You said that R. Bakker observed that dinosaurs had a higher rate of evolution than expected. With the hypothesis that a higher metabolism caused this. I'll assume they had the same physiological constraints as animals of today, which is reasonable considering they are ancestors of birds. Which everything I just laid out I would propose R. Bakker hypothesis is false, since a higher metabolism means a higher generation time and lower mutation rates, which would lead to decreased rate of evolution.

The latest science says that dinosaurs were endothermic (regulate their own temperature) up to a point (Witze 2014), so their internal temperatures were not as warm as mammals, but probably warmer than most fish and reptiles.
So when accounting for size they likely had lower evolutionary rates than mammals, and higher rates than fish, reptiles, insects, or other ectotherms.

Why then does R. Bakker observe higher evolutionary rates in the fossil record then? I can think of just a general reason why. The timescale of dinosaurs is on the order of 10's of millions of years. Much longer than the tiny amounts of evolution that we have observed in the past 100 years of science. There could easily be processes happening at those long time scales that we aren't considering.

References

Brown, J. H., Gillooly, J. F., Allen, A. P., Savage, V. M., & West, G. B. (2004). Toward a metabolic theory of ecology. Ecology, 85(7), 1771-1789.Link

Gillooly, J. F., Allen, A. P., West, G. B., & Brown, J. H. (2005). The rate of DNA evolution: effects of body size and temperature on the molecular clock. Proceedings of the National Academy of Sciences of the United States of America, 102(1), 140-145. Link

Witze, Alexandra  (2014). Dinosaurs neither warm-blooded nor cold-blooded. Nature. 2014 Link


Is it possible to create a restriction map using python? I have some fragments of DNA from single and double digests using three different restriction enzymes. I'm trying to construct a restriction map of a linear fragment of DNA. The map needs indicate the relative positions of the restriction sites along with distances from the ends.

Can this be done using python at all?

DNA Sizes of Fragments (bp) - uncut DNA = 900

DNA cut with EcoRI = 500, 350, 50

DNA cut with HindIII = 600, 300

DNA cut with BamHI = 400, 300, 200

DNA cut with EcoRI + HindIII = 350, 300, 200, 50

DNA cut with EcoRI + BamHI = 300, 250, 200, 100, 50

DNA cut with HindIII + BamHI = 300, 200, 100

First I'll answer this question on the assumption that you are learning or about to learn python (perhaps because you have heard it's become popular in bioinformatics) and you wish to know whether it can be applied to this problem. The answer is: almost certainly, yes. Python is a programming language of the type that can be used to automate the solution of this sort of problem, just as C, C++, Java, Perl could.

How would you go about it? You would first solve the problem by hand, analyse the logic of your solution and then try to devise a general algorithm based on this logic that can deal with a variety of cases. Then you would code this in python (or whatever). The program would have to deal with inaccuracies in real values of fragment lengths (your data are obviously contrived) and the possibility of more than one fragment of the same length (see below).  If you used python and wanted graphic output you would need to use a library that provides graphics as python does not come with graphics like Java does. I gather there are some. However this is certainly not the easiest of programming tasks for a beginner, as you'll see when you try to analyse the logic of manual solution. And of course the data might be insufficient to provide a unique solution.

However as this is a homework assignment you may also be wanting to find a program to check your answer and perhaps be unsure of how to go about it. I don't know of any packages to do this — it's perhaps not 'cutting edge'. So how to go about it?

What I would do is start with the single digests and draw a set of diagrams for each of the possible arrangements of the restriction sites in each case (pencil and paper work well here). Then I'd look at the simplest double-digest, identify unique fragments that were also present in the single digests and thus not cut by the second enzyme, and again draw diagrams of the possibilities for the pairs of restrictions sites. Be careful; the HindIII/BamHI double-digest doesn't add up to 900, so there must be two fragments of the same size here. When you have all the possibilities drawn out, there is presumably only one final restriction diagram that is consistent with all the data.

On second thoughts, devising an algorithm for solving this general case would be quite a demanding task. If you are starting programming I'd tackle easier algorithms first. And an effective algorithm might adopt a brute force approach rather than the semi-intuitive way we solve these by hand. For example your algorithm might generate all possible maps for each of the the three single digestions, and then generate all possible maps for the double-digestions, together with a calculation of the size of fragments the double-digestions would generate. These would be compared with the size of the actual fragments from double-digestions, eliminating those possibilities that don't fit. Coding it would involve writing methods/functions (or whatever they are called in python) to generate these maps, storing the coordinates of the sites in a data structure such as an array, and writing other methods to make comparisons etc.


Why do musk deer have the smallest red blood cells and amphibians have the largest? What is the reason that musk deer have the smallest red blood cells and amphibians have the largest? Should they not be proportionate to the size of the organism?

In the abstract of (Duke, 1963) we see that mouse deer (Tragulus) have the smallest erythrocytes, not musk deer (Moschus). The paper also explains the origin of the confusion. Mouse deer have 1.5 µm erythrocytes but those of musk deer are 3.6 µm (p. 240). In fact musk deer erythrocytes are the same size as goat erythrocytes at (2.5-3.9) µm (Weiss, D. (2010). Schalm's Veterinary Hematology. 6th ed. pp. 836–842). Whether smaller erythrocytes have since been found, I can't say.

I don't have a definite answer why mouse deer erythrocytes are the size they are but I'd posit a few factors. The size of the erythrocyte needs to approximately match the size of the capillaries so they can press tightly to the epithelium and increase the efficiency of gas exchange. Another factor affecting erythrocyte size is cell number. If you have smaller cells, you need a larger number of them to keep the same sum total volume (as in the figure below). So then factors affecting blood vessel size and the rate of erythrocyte production could possibly affect erythrocyte size.

Size also changes surface area to volume ratio (sa/vol) by the square-cube law and this changes characteristics of diffusion over the cell membrane. A larger erythrocyte may have more plasma membrane, which would allow more diffusion and transporter activity but this may also increase the erythrocyte's volume, which would limit the rate of gas exchange due to solutes needing to work their way out of the middle of the cell. Having a high sa/vol is dependent on morphology (hence, our erythrocytes are biconcave) but Duke claims that mouse deer erythrocytes are actually spherical. So, in theory, the cells' small size could be a compensation to keep their sa/vol high, despite not being biconcave.

Interestingly the size of the cells might not affect the sum total intracellular volume of the cells. In fact, sphere packing density is independent of the size of the spheres. If the cells were made larger, this would increase the size of the gaps between them by the same amount. This could indicate that the the total amount of solutes in the blood is independent of the size of the cells, which could explain the great variation in the size of erythrocytes.


Criteria for compound action potential thresholds As opposed to action potential thresholds (which are binary yes/no events), electrophysiological thresholds of compound action potentials are arbitrary. Mostly a certain noise level is picked and when the neural signal crosses this 'threshold' it is said to be 'above-threshold'. I have come across various definitions of this threshold, such as SD-based values (2xSD, 4xSD etc), 'visual' thresholds (a bit iffy from my point of view) among other things. Is there a rule of thumb as to define threshold? Alternatively, a review article, book chapter, or a primary research article with considerable impact explicitly dealing with this matter would be very helpful.

Action potentials of single neurons (APs) are the building blocks of compound action potentials (CAPs). While each of the individual APs is a yes-or-no response with a clear-cut defined threshold, CAPs are not. CAPs are build up of hundreds or thousands of neuronal contributions in, e.g., the auditory nerve. Decreased responsiveness as well as desynchronization of the neuronal responses can decrease the amplitude of the CAP.

It all depends on the amount of background noise and stimulus artifacts versus the amplification factor (the gain) whether a CAP can be recorded and identified yes or no. Typically, gross-potential recordings do not allow for single APs to be measured. CAPs are therefore stochastic phenomena and hence the CAP threshold should either be defined by visual examination (subjective), or through noise-dependent threshold criteria (objective). Therefore, unlike AP thresholds, CAP thresholds are arbitrary and heavily dependent on the noise level.


Minimum amount of RNA for cDNA conversion and qPCR I searched several protocols for reverse transcription of RNA and all suggest using RNA concentrations of 1ug. Could a lower amount result in inferior transcript representation and therefore decreased quality of the qPCR results?

We use the SensiFAST SYBR Lo-ROX kit from BIOLINE. I was thinking of using 500ng instead of the suggested 1000ng. In order to accommodate the protocol, I would use 0.5ul of RTase to maintain the 1:1 (m/v) ratio. Buffer, DNase, water, and RTmix concentrations for the reaction I would keep the same. For the final dilution of the cDNA, I would dilute 5x instead of 10x to maintain equal concentrations.

Does anyone have experience with this? Does transcript representation suffer?
Do the suggested protocol adaptations seem reasonable?

Thanks for the help in advance.

Two answers follow:

Technical experience of many: it should be no problem to have the same protocol with a twice-lower starting concentration, without making any adjustments whatsoever. The suggested 1ug is very much on the safer side of things, 2-fold fewer transcripts makes almost no difference. Maybe at 1 or 2 orders of magnitude (10 to 100s) less will you run into problems or a need to correct your reactions.
Scientific orthodoxy: the most scientific piece of advice anyone can offer you would be to try it both ways and compare your results using qRT-PCR. I'm guessing both approaches will show very similar results.


What is the significance of cysteine in a protein sequence? What is the importance of cysteine-cysteine in amino acid sequence? What can I infer if I get a high percentage of C from a protein sequence?

What can I infer if I get a high percentage of C from a protein
  sequence?

A highly stable structure that is likely found in the extra-cellular space.

Cysteine can form a disulphide bond with another cysteine. Cysteine can be found as a lone cysteine, but is often paired with another cysteine in the tertiary structure to form these bonds.

Disulphide bonds play important roles in protein folding and stability (60 kcal/mol compared to around 1 and 5 kcal/mol for a hydrogen bond depeneding on the environment). Notably though, cysteine disulphide bonds are usually only used in extracellular secreted proteins, as they are unstable in the cytoplasm.

As an example, take the structure 2ksk. Look at how the structure is held together by cysteines that are distant in the sequence. If you see cysteines in a sequence, expect interesting folding!

The cartoon is going from blue to red, whilst cysteines are shown with sticks and the S-S bonds are in yellow.

Side note, they are annotated as SSBOND in the PDB.


Do Traits Have to be Adaptive in Order to Survive? I'm reading Michael Pollan's book 'How to Change Your Mind', which is largely about psychedelic mushrooms. In discussing the biology of the mushrooms, he writes:

'Even if psilocybin in mushrooms began as 'an accident of a metabolic pathway', the fact that it wasn't discarded during the course of the species' evolution suggests it must have offered some benefit.'

I'm wondering if this is actually true. In general, I'm wondering if it is true that traits that do not confer advantage will eventually be weeded out.

Being ignorant of the finer points of evolution/natural selection, I can make arguments both ways. On the one hand, it seems that the intense competition would make investing any resources at all in a trait that was not beneficial a totally losing proposition. Therefore no traits that weren't positively adaptive would survive. On the other hand, there seem to be all kinds of traits that are 'neutral' in fitness terms but which survive anyway. E.g. coccyx, male nipples, appendix, whale legs, etc.

I am not talking about information encoded in the genome, which can be present but not expressed. I am talking about phenotypes, i.e. traits that get expressed in interactions with the environment, such as the psilocybin chemicals in these mushrooms. (Though I suppose unexpressed genetic info could never be selected for or against by natural selection by definition.)

So to put a very fine point on my question: Is it possible/likely that psilocybin mushrooms produce a chemical that happens to engender hallucinations, not because doing so is adaptive, but just incidentally? So that this property would be something like the redness of blood, i.e. not adaptive in itself but just a matter of happenstance?

Good question. And good analysis. I have little to add! I'll simply provide my own list of thoughts to complement your ideas, which are not mutually exclusive.

  The fact that it wasn't discarded during the course of the species'
  evolution suggests it must have offered some benefit.

This statement is speculative. The key word here is suggests. i can think of several speculative scenarios, of course the list is by no means exhaustive:

Traits that are not adaptive can still exist in the organism as vestigial traits. This can be because the trait was recently useful but no more, over evolutionary time scales, and not enough time has passed for the trait to be lost.
The trait may also be floating, i.e. has not been selected against, and acts as a neutral trait. It therefore remains as a phenotype. Traits are theoretically unlikely to float for very long periods of time, as I will describe later.
Some traits can very indirectly affect other traits. In practice it is often difficult to completely describe or understand which traits are a result, or cause, of other traits.
Many traits can also be byproducts of other useful traits. With nipples it might have something to do with early exposure to hormones; developing a way to bypass male nipple formation could be difficult and costly. With psylocibin, it may be a side-effect of a particularly useful biochemistry to the fungus, perhaps metabolic, that is completely unrelated to its neuroactivity in humans. It may be that a biochemical pathway might form psychoactive intermediates or products that are difficult to remove or metabolize, and find themselves in the mushroom co-incidentally.
The trait may simply be very useful, but we don't understand why it is useful. Humans often overlook this possibility; for instance, I assume you have not considered that psylocibin may have unknown effects on non-human or even non-vertebrate life.
I am not an expert but filamentous fungi sometimes/often have very complicated sexual reproductive strategies. Psylocibin may be maintained through sexual selection, rather than natural selection. This is probably far fetched, but hey- we're speculating about our ignorance.
Lastly, but very importantly, all organisms face pressure to survive and replicate. It is expensive to maintain useless features and traits, or to produce excesses, or to overdevelop or harbor chemistry that is not doing anything. Natural selection is ever-active in limiting in which traits are maintained within a population. This I think is the most convincing argument; the principle of economy. This argument fares well in all discussions on biology; life is difficult, and the costs of survival are very important to consider, always. It is expensive to store or maintain constituent chemicals, even if they are not toxic, nor if they have no use for the survival of fungi. It is more economical, and less costly, to lose such traits; selection will favor fungi that save or spend this energy elsewhere. This is a very important point, and I think it is the most salient to understand the quote you provide.

I think it would also be a good idea to study the number of times psylocibin arose. If it occurred ('was invented') multiple times independently, it must have had some functionality for the organism, like wings, or vision. If it occurred only once, one can ask whether the majority of descendant strains has lost it, or whether they maintain the trait. That could also shed some light on whether it is maintained through positive selection. Lastly, psylocibin may be a chemical that allows to explore a very specialist niche of the ecosystem. If few descendant strains contain it, that can mean it is still selected for, though only by fungi that rely on it as a strategy. This would also mean that psilocybin-less fungi would have found no need to maintain it, and may point to the occurrence of negative selection. Hope that makes sense.

Mandatory reading for you on relaxed selection.

tl;dr yes, psylocibin may be maintained by happenstance, though likelier via positive selection, at least in specialist fungi


What is the pathogenuc mechanism of brown pigment lipofuscin in muscle atrophy? I think it is autophagy. Lysosomal degradation. Autophagocytosis.

Example of the brown pigment (lipofuscin) here:

I am not sure if autophagy is the right answer to the "pathogenic" mechanism of atrophy.

Is autophagy the pathogenic mechanism of atrophy?
Or what pathogenic mechanism is involved if you see lipofuscin in the histologic slide?

Simple answer: Atrophy through autophagy.


What is the difference between vegetable and animal fats? I often hear from many people saying to waiters - "Please, don't put oil to salad". They probably believe the fat from vegetables has the same impact on the weight as an "animal" fat (meat, eggs, butter).

My questions are -

Are these two types of fat have equal influence considering their converting to fat tissue in humans?
What are the pathways for conversion of vegetable oil fats to adipose tissue storage, in humans?
If one eats $X$ grams of either saturated or unsaturated fats, will they (in equal conditions) gain equal weight ($Y$ grams) in both the cases ?

There is a subtle difference between oils and fats- oils are generally unsaturated (Carbon-Carbon double bonds) whereas fats are saturated (all single bonds).

  Are these two types of fat have equal influence considering their converting to fat tissue in humans?

No. There are some kinds of fatty acids that are synthesized only by plants (Essential fatty acids). However, these can be obtained indirectly from animal sources such as fish.

Fats have multiple roles- not just storage. They are also critical for making up the cell membrane.

  What are the converting pathways for vegetable oil fats to adipose tissue in humans?

The fatty acids in oils are absorbed in the intestine and esterified (wit glycerol) to form triglycerides. Then, they are incoporated in lipoprotein complexes. There are different types of lipoproteins- VLDL (Very Low Density Lipoprotein), LDL (Low Density Lipoprotein) and HDL (High Density Lipoprotein) which have different sizes and compositions.

When lipoprotein comes in contact with lipoprotein lipase in capillaries, the free fatty acids are liberated from trigycerides, which is taken up by adipose tissue.

The fats stored in adipose tissue depends on diet. This has been studied in rabbit but similar principles may apply to humans too. Fats can also be synthesized in the body. It is always saturated fat and is synthesized by the fatty acid synthase complex. The starting substance is Acetyl-CoA which is produced during catabolism of both carbohydrates and fats.

  if one eat Y of 2 meal if saturated and unsaturated fats, he/she (in equal conditions) will gain X gram if they were saturated fat and Z in a case of unsaturated fats?

By principles of mass balance, if both have equal rates of absorption and degradation then there will be equal gain. According to this study, absorption rate of unsaturated fats is higher. In that case if you eat $X$ grams of both types then the absorbed amount should be $Y_{sat}$ < $Y_{unsat}$

I am not sure about the degradation rates but I think it is higher for saturated fats because unsaturated has to be reduced to saturated before metabolizing via $\beta$-oxidation. Determining the exact steady state values will be tricky without a mathematical model.

NOTE: Dont confuse this with body weight gain (in the sense of obesity); it is a complex phenomenon. You have to consider a lot of things when predicting weight gain.


What is synaptic clearance? Please explain what the term synaptic clearance means. For example, what would dopamine synaptic clearance be? It is important to me in context of dopamine signaling variation due to difference in synaptic clearence level.

Some gene alleles are associated with greater synaptic clearance in dopamine pathways. It used to explain dopamine level variation and throught it some brain areas activity (for example Nucleus Accumbens) difference among people with different genotypes. For more information see for example. Also, reduced synaptic clearence related to greater dopamine signaling levels. So I was interested in this term from prespective of brain activity in areas with dopamine receptors

"Synaptic clearance" is referring to the clearing of a neurotransmitter from a synaptic cleft.  A synapse is a place where one neuron can stimulate another neuron. The tiny gap between the neurons is called the synaptic cleft. The presynaptic (stimulating) neuron releases a neurotransmitter (such as dopamine) into the cleft and some of the neurotransmitter is recognized by receptors in the membrane of the postsynaptic (stimulated) neuron.  In order for the synapse to stimulate the postsynaptic neuron a second time, the concentration of the neurotransmitter in the cleft must be reduced to its original levels.  This reduction is called clearance, and can occur in several ways (mainly dependent on the type of neurotransmitter).  The neurotransmitter may be transported back into the presynaptic neuron for reuse; this is called reuptake.  The neurotransmitter may also be degraded (broken down chemically) into an inactive form.  To a lesser extent, neurotransmitter can also be absorbed by astrocytes or simply diffuse away out of the cleft.


Interesting Insect, possibly a beetle (Northern Indiana) I happened across an interesting looking insect, that I've never seen before.  In Northern Indiana, late spring around 5 PM CST.  I tried a reverse image search, with no luck.  It is approximately 3/4 inch long.

Any ideas?

That is a carrion beetle. Family Silphidae, in the genus Necrophila
https://www.insectidentification.org/insect-description.asp?identification=American-Carrion-Beetle


Is there a detectable amount of bacterial DNA in the blood of infected persons? With which bacterial infection in humans has it been shown that bacterial DNA can be found in the blood?

If any is found it is likely not to be very much, and even difficult to distinguish from human DNA, but presumably recent advances in sequencing should have made it possible.

Everything depends upon the infection and on the general immune status of the patient.

Generally, the prerequisite for DNA to freely circulate in the blood is the presence of bacteria themselves in the blood (bacteraemia). This means that the infection left its original site (where it is usually kept isolated from the blood flow by the immune system). Depending upon the body reaction to this breakthrough, sepsis and/or SIRS can be the consequences.

Under these conditions (not necessarily as severe as sepsis, but in case of proven bacteriemia), the bacteria cells get attacked by the immuno cells, that leads to their eventual lyzing and releasing their content to the blood.

PCR can be used as a method to prove the existence of bacterial DNA. (Here is a publicly available paper on this topic).


How is circadian rhythm of gastric acid secretion regulated? Gastric acid secretion shows a circadian rhythm where acid production in the morning is minimal and it reaches a maximum towards the evening.

How is this process regulated?

I'd suggest reading wiki first.

Autonomic nervous system, the one that regulates breathing rate, heart rate and other physiological processes as a function of circadian time, regulates secretion of gastric acid. Vagus nerve, part of parasympathetic nervous system (the one responsible for "rest and digest" part of behavior, opposite to sympathetic "fight or flight") stimulates secretion of gastric acid and regulated through circadian mechanism.

See also here, Circadian variation in gastric vagal afferent mechanosensitivity:

  Thus, gastric vagal mechanoreceptors display circadian rhythm, which may act to control food intake differentially at different times of the day.

This is another interesting review: Gut clock: implication of circadian rhythms in the gastrointestinal tract. It states that GI tract has its segments set their own circadian clocks, different for various segments. But all of them are operating and adjusted by main clock, regulated by, as I know, melatonin and orexin hormones.

Surprisingly, not much seems to be known about this connection. Pineal gland seems to be very important in this process, because it produces melatonin.


How do prodrugs exactly work? Are there multiple varieties of prodrugs? I have been reading about a (new?) prodrug of LSD, 1CP-LSD, which is being synthesized in the body to LSD.
However, I don't know how exactly. I read somewhere, that another prodrug of LSD, 1P-LSD was put  into a vial of human blood, and it was synthesized to LSD. Which is kind of hard to belive, that just exposure in blood synthesizes 1P-LSD to LSD. What processes in the body are responsible for this, are there another processes for synthesizing another prodrugs to their respective drugs?
Are there multiple varieties of prodrugs? By that I mean that they synthesize themselves using another method instead of one another.

Prodrugs are extremely common; we often don't even think of some of them as prodrugs unless we're also familiar with the metabolite. Psilocybin, for example, is a prodrug; the active molecule is psilocin. Aspirin is a prodrug of salicylic acid (though there are also other active metabolites).
Prodrugs can be categorized according to where they are converted to active forms: intracellularly in target tissue or other organs like the liver, or extracellularly like in the gut or in the bloodstream. The Wikipedia link at the beginning of this answer includes a table with some examples.
Prodrugs may be converted to active forms by enzymes or by environmental conditions in the body, like pH. I'd argue they are diverse enough that it doesn't make all that much sense to study them as a category, rather that in any pharmacological class of drugs you should be aware that they may be administered in a modified form, often to improve bioavailability or storage stability.


Should we be looking for extra-terrestrial life on comets? I have just read What elements are a possible basis for life? and I find myself wondering whether instead of seeking advanced life-forms at remote locales a La SETI, and perhaps fundamentally differently, we ought to be looking for similar microscopic life forms on comets that pass off-and-on.

Granted, a comet may be near absolute 0 for a lot of the time, but microscopic life-forms are known to be capable of surviving lean periods by using a cyst, for instance. As far as the rest is concerned, comets probably contain some amount of ice, and hence water, too. Similarly a comet's sprint around the sun could provide some limited amount of gravity/mass too.

So, should we be looking for life on comets?

Yes we should be and we are! Scientists have been analysing cometary material - but its a challenging task. The problem with looking at meteoritic material from comets on Earth is that it is generally contaminated with material from Earth. In addition, meteorites get physically altered during their passage through the Earth's atmosphere due to the high temperatures of re-entry.

So, the trick is to send missions to the comet. However, then the difficulty is in designing a mission that can analyse samples in situ. NASA's Stardust mission got around this by sample return to Earth. The probe visited comet Wild-2 and found the amino acid glycine among other interesting organic compounds. However, no evidence of life was found (metabolic products, organisms etc.) Further missions to comets (and asteroids) are planned, but they are not going to explicitly look for life.

Elsila, J.E., Glavin, D.P., & Dworkin, J.P. 2009, Meteoritics and Planetary Science, 44, 1323