Software to model and analyse protein–ligand interactions I am currently trying to model a certain protein (Golgi Mannosidase II) and compare the induced fit of the inhibitor swainsonine. I would like to be able to analyse the distances between bonding interactions and the strengths of bonding regions. I was wondering if there was any type of software that would allow me to analyse this protein and its interactions with swainsonine? I have seen many images like the one below in research papers, but I’m never sure what software the researchers are using to generate these models.

Liberato, M. V. et al. Molecular characterization of a family 5 glycoside hydrolase suggests an induced-fit enzymatic mechanism. Sci. Rep. 6, 23473; doi: 10.1038/srep23473 (2016).

I don't know precisely what you mean by "analyze", which could be anything from simply "view" or "measure distances", to evaluating an energy function on a crystal structure or molecular dynamics simulation, to prediction of binding sites de novo. The tools are different for each case, though some can do several things.

For simply viewing, measuring distances, and creating "pretty pictures" like the ones you included with the question, PyMOL and UCSF Chimera are the most popular tools. Chimera is highly scriptable and can perform molecular dynamics simulations (i.e. simulate movement of atoms based on an energy function), though its capability in this regard is somewhat limited. The NAMD/VMD software suite (which was used in the study cited in the question) is more full-featured, as is CHARMM (the latter of which is also the name of an energy function). For prediction of binding sites de novo (without a bound experimental structure), i.e. "docking", there are DOCK and AutoDock (both with long academic histories) as well as more industry-oriented ones like Glide.

Be careful though what you're getting into — while simply viewing structures and making geometric statements by direct observation is well within reach of the average biochemist with reasonable knowledge of protein structure (provided you trust the lab that solved the structure in the first place!), simulation of proteins using energy functions requires considerable computational expertise, though the "black box" nature of some software glosses over this. It may be relatively easy to run a simulation using questionably appropriate parameters, but the adage "garbage in garbage out" applies very much here. This is somewhat true with docking as well.


What is the role of Homocysteine in cognitive function? I'm looking at this link : Homocysteine and cognitive impairments and am looking for more information on specific cognitive impairments associated with elevated levels Homocysteine. That article is not very clear on that point. I've seen some research papers about the study of this in elderly people and cardiovascular studies. I'm interested in average adults.

I've been fascinated with the effect/lack of thereof of vitamin B6 on dreaming and Homocysteine is the first thing that I've stumbled upon in quite some time that is directly related to the B family of vitamins. Has there been any research about what Homocysteine gets metabolized to if exposed to B-Complex vitamins versus Vitamin B6 alone?

Thank you for your input!

I'm not sure if this answers your question, but I'll give it a try anyway. Here's a diagram of homocysteine metabolism. Vitamin B12 is a cofactor for homocysteine methyltransferase, and folic acid is required for tetrahydrofolate (THF). As both vitamins are involved in homocysteine metabolism, the symptoms of folate and vitamin B12 deficiency are similar. Vitamin B12 deficiency can result in neurological symptoms due to abnormal myelin, but folate deficiency does not. Vitamin B12 also metabolizes methylmalonyl-CoA to succinyl-CoA as seem here, so the methylmalonic acid level is often measured to test for vitamin B12 deficiency.

Hyperhomocysteinemia is the condition of high levels of homocysteine, but it is usually due to low vitamin B12 or folate.


Is it possible for a child to grow taller than their tallest parent? I have heard that offspring can't grow taller than either of their parents but I've also heard that sometimes some gene activation can skip generations. Is it possible for a child to grow taller than their tallest parent?

People can grow taller than their parents. Anecdotally: I'm 185 cm, my parents are 155 cm and 178 cm. Joakim Noah, an NBA basketball player is 211 cm, his dad was 193 cm and mother was 175 cm... how?

Genetics and environment play a role in determining height. First of all, a more nutritious environment during development can lead to increased height, this is one reason why more recent generations appear to be taller.

Height is also an example of a quantitative trait - this means many genes (or loci [singular is locus], locations in the DNA) affect the phenotype (the physical measurable result i.e. a persons height). It is infact how the vast majority of traits are determined. At each locus that affects height there may be polymorphism (when more than one allele, or variant of that gene, exists).

Example:

Suppose height entirely is determined by 2 additive loci, $A$ and $B$, and no environmental effect occurs, and there is diploidy (two of each locus, one from each parent, determines height in a person).

Each locus has two alleles denoted by $A_1$, $A_2$, $B_1 $ and $B_2$. Each copy of alleles $A_1$ and $B_1$ add 40 cm to a persons height, $A_2$ and $B_2$ add 50 cm to a persons height.

Now a man who is $A_1 A_1, B_1 B_2$ (remember, humans are diploid) and a woman who is $A_2 A_1, B_1 B_1$ have children. Both parents are 170 cm tall. The theoretical limits for the population would be 160 cm and 200 cm. The children will inherit one copy of $A_1$ from the father and $B_1$ from the mother, but they could inherit either $B_1$ or $B_2$ from the father and either $A_1$ or $A_2$ from the mother. If a child inherited both of the taller alleles then they would be taller than the parents ($A_1 A_2, B_1 B_2$ = 180 cm). Likewise some offspring could be shorter.

Of course the reality is much more complex; height is determined by many more than 2 loci, by the environment, and gene * environment interactions. This principle was a hugely important because it meant that reproduction did not necessarily remove variation from the gene pool (a fundamental problem with early evolutionary theory was the thought of "blending" - when offspring are the average of their parents)


Why do tears fall from our eyes when we ride a bike too fast? When we ride a bike too fast why do tears fall from our eyes. What is going on biologically and what may the evolutionary story be behind this?

This quora Q&A gives a few ideas, none of which satisfy my question fully.

This is similar to a response to smoke.

But this is clean air? Why doesn't this happen all the time?

Our eyes always need to be lubricated.

But why the need for excess tears?

Our eyes need to be covered with a thin film of liquid all the time. When riding fast, the wind flow pushes the liquid away from your cornea. Your eye compensates for that by producing more tear.


How specific are CRISPR-cas9 cuts? CRISPR-cas9 uses a string of RNA that matches with DNA and makes a double stranded cut at that point.

If the RNA is just a few letters in length, the enzyme would cut DNA in many places. It would be unspecific. But if you can make the RNA string very long, it would only cut at the exact place where you want to cut.

So how long can you make the RNA sequences?
And is this enough to avoid unintended cuts?

The problem of off-targets in CRISPR/Cas is often discussed. It was shown that the system allows mismatches up to five basepairs. For your question, if it is helpful to elongate the gRNA: it was shown that truncating the RNA enhances the specificity more than elongating (see also here).

So what can we do? Well, there are different methods to improve the specificity. The simplest may be the usage of lower dosages of the CRISPR/Cas system. Another method is to use altered PAM motifs.

A more complicated method is to convert the Cas9 into a nickase. In this strategy you would use two different gRNAs for two different target sites and introduce ssbreaks. A modification of this method is to completely knock-out the enzymatic activity of Cas9 and fuse it to a FokI nuclease which will cut the DNA only when it dimerizes.

There are several advantages in these methods, however, you may also loose on-target effects.

There is another method which, in my opinion, is really awesome. It is possible to alter the energetics of the DNA binding site resulting in high-fidelity variants of Cas9 (HF1 and HF2)

So, I hope I could help you. There are other and even more effective ways to increase CRISPR/Cas specificity instead of altering the gRNA. If you're interested, have a look on the references.


Explain a transpiration graph The solution is A, but I think both A and C are correct. For choice C, stomata that protected by hairs will have a greater amount of water vapour around them, hence lower water potential gradient. Hence, this results in the reduction in the rate of transpiration, as well as choice A.

Though I don't come across graphs like these too often, I guess the answer should be A because...

From the graph, it is clear that Leaf 1 has more mass than Leaf 2 after 5 hours. This means there is a lower rate of transpiration in Leaf 1, which can definitely be explained by a thicker cuticle (since the thicker the cuticle, less is the water lost). Hence choice A is correct.

Now, look at choice C. Like you said, in leaves where stomata are protected by hairs, there will be lower rate of transpiration. Then, obviously Leaf 2 should have a higher mass than Leaf 1, right? But this is not the case (as per the graph). Hence, choice C is incorrect.


Why don't phagocytes eliminate mutualistic foregin organisms residing in our body? Many organisms residing in our body and have a symbiotic mutualistic relationship with our body e.g. organisms in our small intestines. How come our body does not activate an immune response against them? Is it that the organisms have self antigens, or do the immune cells have no antibodies for these organisms? Also, how come our immune system is able to respond to these same organisms if they cause an infection in our body? E.g. Entamoeba histolytica causing amoebic dysentery.

Molecular context is important here. E.coli in your colon is OK with the body, it is taken up by phagocytes as part of normal "surveillance". Your immune system will learn and gain "tolerence" to these mutualistic bacteria as long as they are in the correct environment.

If that same E.coli is a pathogenic strain or finds a way into the blood stream (sepsis), your body will recognize that it does not belong and mount a immune response. There are different classes of antibodies with different properties including where they are predominantly found. For instance IgE is found in mucosa but not in serum.

On top of that there are the 'Danger/Pathogen associated molecular patterns' (DAMPs or PAMPs). Cells can 'sense' general molecular patterns such as LPS, unmethylated CpG DNA, double stranded RNA through a class of molecules called Toll-like receptors (TLRs). Different TLRs are found in different cells or cell surfaces and they are the 'first line' response against inappropriate bacteria or viruses.

Once the TLRs are activated the cells will produce 'Danger Signals' called cytokines which initiates an immune response. In the absence of 'Danger Signals' present in the microenvironment, our immune system won't really begin mounting an immune response but just 'surveys'.

In this 'danger' context, you get robust phagocytic response.

If you'd like to learn more about this Mucosal Immunology is what the topic is called. All in all, the vast majority of our immune system is mucosal, it's just less studied relative to humoral immunity since it's harder to study.


What exactly is meant by the expression "differentially expressed"? As far as I've seen, this expression is almost always used in relation to gene expression profiling. Unfortunately, I have no background in this area. Can someone please explain this in layman terms?

Although each cell of your body essentially contains the same DNA and the same genes, cells in different tissues express (turn on) different genes under different conditions. Measuring differential gene expression involves looking at the amount of expression for a gene (or set of genes) in two contrasting scenarios. The contrast could be across different times, different tissues, different conditions, different related species, etc.

When, you say a gene is "differentially expressed", this is very context-specific. The phrase means nothing by itself, and it is only useful in terms of the applicable contrast. For example, the statement "gene A is differentially expressed" is uninformative, while the statement "gene A is differentially expressed in liver and muscle tissue" is descriptive--it tells you that liver tissues and muscle tissues have a significantly different level of gene A products. Often the terms "up-regulated" and "down-regulated" are also used to provide additional detail. In the context of the previous example, the statement "gene A is up-regulated in muscle tissues" tells you that the level of gene A products is higher in muscle tissues than in liver tissues.


Does thyroxine increase BMR or metabolic rate? I know that thyroxine increases the metabolic rate, but my teacher said it increases the metabolic rate, not the basal metabolic rate, the basal metabolic rate is always the same. What's the difference between BMR and metabolic rate??

The definition of BMR from wiki is :

  Basal metabolic rate (BMR) is the rate of energy expenditure per unit time by endothermic animals at rest.

When BMR is calculated for a volunteer some conditions are taken into account:

complete physical rest
sitting upright
at a comfortable room temperature usually around 25 centigrade
at the post-absorptive phase of digestion

On the other hand metabolic rate may be calculated even when one is exercising, at high or low room temperatures, during digestion etc. So it is more generalised.

When you are talking about thyroxine or thyroid hormones, you must keep in mind what (factors) stimulates its secretion.
One such factor is coldness.

So that definitely indicates temperatures below the 25 centigrade mark at which BMR is usually calculated.

So in my opinion it was quite prudent of your teacher to advise you to use metabolic rate instead of basal metabolic rate for the thyroxine effect description.

REFERENCE BOOK:
Biochemistry by Debajyoti Das 14 th edition
Academic publishers P-677 to 680.


Vo2 of the brain is 21% of Q=13% or of the entire blood? I am reading now the book which states that the Q (blood flow per unit of time) of the brain is 13% while the Vo2 (relative Oxygen used per unit of time) is 21%. Now my question is if the Vo2 of the brain (21%) is taken from the entire blood or from the part the brain gets (Q=13%)?  It is not clear on the book. I've attached the picture with the explanations.

TL; DR 21% of the whole body.

The VO2 numbers add up to 100%. You are looking at the way six major compartments of the body split the oxygen consumption. The brain takes 21% of the whole oxygen brought into the body by the arteries.

The Q numbers add to 100% too. The brain takes 13% of the blood coming out of the heart.

The picture is meant to contrast high-flow and high-metabolism organs. The kidneys take 20% of all the aortic blood, but use only 7% of the oxygen consumed in the body. The coronaries take 4% of the blood leaving the ventricles, but use a large 11% of the oxygen take in by the whole body.


Identifying internal structures of dissected fish Note : Images displayed below might be disturbing to some people.

I have dissected a fish for the first time ! I have some idea of what some of the structures might be but I am not sure and so would like your help.

1.Here is the fish I dissected. Are the white structures (towards the dorsal surface) muscles ? They are beautifully arranged.

2.I want to know what the yellow coloured structure (towards the ventral side) is. I guess it's the intestine. It looks "noodly". Here is a close up.

3.I have pointed at two different parts in the following images. I want to know whether they are part of the same structure - ie swim bladder or whether they are two different structures altogether. When I poked one of the parts the other part increased in size ,so I guess it's one structure but I just wanna make sure.

Since I can't actually look at and handle the yellow structures, it is difficult for me to provide any information on them.

As far as the white structures you mention on the first picture, I believe those are most likely muscles.
As for your third question. That does appear to be all one structure; and yes, going on that assumption, the entire structure would be the swim bladder.


How does aspirin "thin" blood? As we all know, aspirin doesn't actually thin the blood, as it has been explained to me, it makes it "slippery". Slippery blood doesn't stick to itself hence this helps prevent internal blood clots (or allows blood to pass more easily around an existing clot). I also understand that having your blood too "slippery" can lead to the body attempting to counteract that and making it too "sticky".

Anyhow, my question regarding that is this, how does aspirin work? How does it make the blood "slippery"? (If there is a more medically correct term for "slippery" and "sticky", I'm all ears).

P.S. I paid the Mayo Clinic's website a visit before coming here, the information about aspirin's mechanism wasn't particularly helpful to me.

Aspirine irreversibly inhibits the enzyme cyclooxygenase. This enzyme facilitates the reaction from arachidonic acid to prostaglandin G2/H2. The further reaction leads to the generation of Thromboxane A2 which is important for the activation and aggregation of platelets. See the figure (from here) for an overview:

Thromboxane A2 usually stimulates the activation of new platelets and increases their aggregation, with a shortage of this compound these activations are not possible and the coagulation of blood is reduced.


Why is sheep erythrocyte lysis considered as classical complement activation pathway, and rabbit as alternative one? Any suggestions are highly appreciated.

The complement system is an innate immune response which has three pathways - as shown in the image below.
The breakdown of red blood cells assesses the functional capacity of the complement system. This experiment is titled: "Total complement activity", "CH50" or "CH100". Is this what you're referencing?
Hemolysis of sheep red blood cells occurs via the classical complement pathway.

More information: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4360204/


How hot can a beverage get without burning the tongue? What is the maximum temperature that a beverage can be without burning the tongue?

I suspect there's a maximum temperature that the surface tissue of a tongue can withstand without being damaged (causing the burning feeling that lasts even after the heat goes away). So let's say I want to setup a device to keep my coffee to the right temperature to drink without damaging my mouth - I'm interested to know the highest possible temperature that will not damage the surface tissue of the tongue in a way that will result in lingering pain after the heat is gone.

Afaik the tongue is not more heat tolerant than other parts of the body, so the minimum temperature to cause burn is about drinking a beverage having 45°C temperature for a long time (more than 5 minutes). The pain threshold of tongue is around 47°C, so you will feel when it really burns.

According to studies the hedonic value of coffee has a maximum by 60°C, and it is significantly lower by safe levels (45°C). Frequent burns of mouth increases the risk of oral cancer. So I think this will be a hard choice... ;-)

  A burn is an injury which is caused by application of heat or chemical
  substances to the external or internal surfaces of the body, which
  causes destruction of tissues. The minimum temperature for producing a
  burn is about 44°C for an exposure of about 5-6 hours or about 65°C
  for two seconds are sufficient to produce burns.

Thermal injuries

  I. With the object of producing standard low-temperature burns in
  animals, and of studying the area of tissue only partly damaged in a
  burn, a burning iron has been made capable of applying temperatures
  from 45°-80°C. to the skin; with this the amount of heat and
  temperature causing skin damage has been studied, and the macroscopic
  and microscopic damage due to graded temperatures have been
  delineated.

  Graded temperatures of 45°-80°C. have been applied to the skin of shaved, anæsthetised guinea-pigs, and in some cases rats, for times
  varying from 10 sec. to 6 and 10 min. Observations have been made of
  the development of erythema, flare, blanching, blueing, heat fixation,
  incipient blister formation, œdema, and edge wheal, as also upon the
  later scab formation and rate of epithelium regeneration.
  Applications of 47°C. up to 6 minutes produce no visible change.
  At 50°-55°C. applied for 1 minute and over, there is a critical temperature for the development of permanent and irreversible damage;
  in animals good scab formation occurs after burning at this
  temperature.
  After temperatures of 60°-65°C. the epidermis can be peeled off from the exposed area, leaving a punched-out exposed surface area
  somewhat like the exposed human blister.

1943 - EXPERIMENTAL THERMAL BURNS, ESPECIALLY THE MODERATE TEMPERATURE BURN
According to Green the pain threshold of tongue is around 46-48°C.

1985 - Heat pain thresholds in the oral-facial region

  In all experiments, the chosen mean preferred temperature for drinking
  was around 60 °C (140 °F). Black coffee drinkers chose a slightly
  higher mean temperature than drinkers with added creamer, and they
  also chose a slightly lower mean temperature when the flavor was
  stronger. In all cases, consumers tended to choose, on average,
  temperatures for drinking coffee that were above the oral pain
  threshold and the burn damage threshold.

2006 - At What Temperatures Do Consumers Like to Drink Coffee?: Mixing Methods

  Overall, the available results strongly suggest that high-temperature
  beverage drinking increases the risk of EC. Future studies will
  require standardized strategies that allow for combining data, and
  results should be reported by histological subtypes of EC.

High-temperature beverages and Foods and Esophageal Cancer Risk -- A Systematic Review


Could habitat selection pattern be deformed in environment with low variability? It is possible that strong (clearly visible) pattern of selection towards particular parameter is detectable only in environment with high variability (difference between used (red) and non-used (grey) space will be significant) whereas in sub-optimal environment used and non-used space do not differ due to low variability.

And if this is possible, is there any relevant study which focuses on such issue?

P.S. It seems to be very basic idea, however I could not find any relevant sources on this topic.

If I understand your question correctly, I've seen this idea in many papers, sometimes stated clearly and sometimes in more implicit terms. After a quick look I found a paper which should be relevant as a starting point for you: Mayor et al. 2007. Spectrum of selection: new approaches to detecting the scale-dependent response to habitat. Ecology 88(7).

In my mind, there are two questions here. First, to what extent will low population size in sub-optimal environments (leading to a smaller sample to work with) lead to more uncertain inferences of preferred habitat/substrate; basically saying that noise might swamp signal in sub-optimal environments. Second, to detect selection for a particular habitat/substrate, you must sample a wide enough range of environments so that you capture both preferred and unpreferred habitats and transitions between them. In the paper I linked to this issue is touched upon in the discussion:

  Second, evidence of habitat selection depends on the scale of analysis. To understand scale dependence, investigations must encompass a spatial scope sufficiently wide to uncover scale domains of selection and the thresholds or transitions between them. In both cases, spatial scale is the empowering principle, and scaling continua are the means of application.

I've seen similar ideas as this show up in papers on habitat choice in birds living in agricultural landscapes as well, where some species are often found in rather poor environments (because these environments are common). Looking at habitat preferences only in these environments might then give a misleading view, since individual choices are constrained. Also relevant, even if not mentioned in your question, is the concept of maladaptive habitat selection (sometimes called ecological traps), where you can have situations where species use environmental cues that used to indicate high fitness habitats, but might now result in maladaptive choices, see e.g. Pärt el al. (2007). However, in this case you will still have a clear preference/selection (as in your high variability environment), the problem being that the organism is selecting suboptimal habitats from a fitness perspective.


How can inbreeding be used for selecting mutations? I understand that inbreeding, after a number of generations of crossing genetically related individuals eventually yields homozygotes, however I can't seem to understand how it can be used for selecting mutations.

Consider a sibling-sibling mating system, the simplest inbreeding situation, with a simple Mendelian trait.

Step 0:
Let's start with heterozygotes, Aa x Aa.

Step 1:
Their offspring will be a collection of AA, Aa, Aa, aa, in roughly those ratios assuming equal survival.

Step 2:
Now we breed siblings. If we happen to breed Aa x Aa, we are back to the original starting point. Return to Step 1.

If we happen to breed AA x AA or aa x aa, and then continue to breed those offspring with their siblings, all of the following generations will be homozygous unless there is a mutation. Stop here, you have homozygotes.

If we happen to breed AA x Aa or Aa x aa, the next offspring will match those parents: AA, Aa or Aa, aa. If we breed Aa x Aa, return to Step 1. If we breed AA x AA or aa x aa, stop here, you have homozygotes.

Of course, theoretically you could end up with heterozygotes doing this forever, but the odds get lower and lower the more generations you breed.

For selecting a particular mutation, it is often simpler to genotype for presence of an allele rather than zygosity (i.e., just use simple RT-PCR). For example, if you want to eventually produce aa, you can test for the 'a' allele, and not breed any offspring that do not have any 'a', therefore they are AA. If you do this, you will always eventually end in a path with aa homozygotes.

If you have an easily produced model organism, you can also do this simply by phenotype (depending on the trait): once a strain settles into a consistent phenotype, you know you have a homozygote of one type or the other. If your model organism is easy to produce, it's okay if some don't end up carrying the mutation.

For selecting a random mutation, the same is true, except you have many genes instead of just gene "A". Any random mutation in just one individual early in the breeding could potentially be fixed in the inbred population somewhere down the line, following the steps above. If you breed BB x Bb, where Bb has a random mutation, you have a chance to breed a Bb x Bb pair in the next generation, which starts you at Step 0 for that particular random mutation.


Why do cells divide (or copy themselves)? What I know

I learned about cells (not too much, but I've studied them a little bit. So don't feel offended when I say something which isn't really true. If something I write is wrong, please correct me (if it's not too much of effort).

Question

Imagine the first cell on earth.

Why would this cell "think" of dividing itself? How would a cell come up with the idea of dividing itself? The process of dividing itself isn't that simple, so ... how could that be? I don't really see a reason for devision from the "standpoint of a cell".

One of the solutions would be, that there's an intelligent creator, but I want to know the answer from the point of view from science.

Layman explanation would be appreciated

Just don't go too deep in the answer, I really just want to know if there is a solution to my questions. And if scientists really found out something, please just give me a very (VERY VERY) easy explanation.

The "Why" question

Why do organisms replicate?

Given that there is (extrinsic and also eventually intrinsic) sources of mortality, organisms that did not replicate just ended up disappearing. Those that did replicate eventually ended up giving rise to important lineages.

In other words, replication occurs because those who did not replicate disappeared. It is also because unique instance of things may disappear that you regularly backup your computer (if you do).

The "How" question

By what mechanism did early replication occur?

You actually did not really ask about it but here are a few words anyway.

The mechanism by which first replication occurred are mainly unknown as it is hard to investigate specific processes that occurred such a long time ago. The field that studies the origin of life is called abiogenesis. You might especially want to read the section on Self-enclosement, reproduction, duplication and the RNA world. You might also want to read about Autocatalysis.

I am afraid that a summary of existing hypothesis on early reproductive systems are 1) out of my capacity and 2) would hardly fit into the wish to receive a very (VERY VERY) easy explanation.


Why are trichomes important for both the roots and shoots of plants? In what ways are trichomes vital to the plant?

Why have them on the plant shoots as well?

Plant leaf hairs, or trichomes are vital for many reasons.
Interestingly in 1975 researchers were correct when they stated:

"It can be argued that essentially the same genetic system should be required for both root hairs and trichomes." [1](Pay-wall)

For example:

C. salvifolius, there are more adaxial trichomes present to avoid UV light from injuring the abaxial surface.[2](Pay-wall)
Increased transpiration [3](Pay-wall)
Protecting against insect herbivores [4](Pay-wall)
Increasing tolerance to freezing [5](Pay-wall)


Why are turtles classified as reptiles and not amphibians? I understand that turtles are reptiles because like all reptiles, they have scales on their body. But turtles (specifically sea turtles) live on both land and water, very much like amphibians. Also, don't sea turtles have more of a moist skin unlike reptiles? So is there any anatomical difference which makes turtles different from amphibians?

Amphibians are not defined for having a moist skin, neither are reptiles defined for having scales on their body.

In biology, organisms (elements) are grouped according to their evolutive history in monophyletic groups, also known as clades. Basicaly, a monophyletic group is

  A group consisting of an ancestral and all its descendants.

"Tetrapoda" is a monophyletic group, formed by vertebrates with four limbs. Inside Tetrapoda, there are two groups: "Amphibia" and "Amniota". Amphibians are non-amniotes tetrapods, and we have some doubt if they are a monophyletic group. Amniotes, on the other hand, are tetrapods having an amniotic egg, including you and me, and they form a monophyletic group.

The amniotes are divided in two monophyletic group: "Mammals", which are amniotes with a synapsid skull, and "Reptiles", which are amniotes with diapsid skulls (I'm using "reptiles" as synonym of Sauropsida).

Reptiles include turtles, lizards, snakes, alligators and dinosaurs (which include the birds: all birds are dinosaurs). It doesn't matter if a animal has or has not scales, or if it lays eggs or if it is viviparous, or if it has 5 fingers or 3 fingers: All the descendants of a given ancestor are included in the monophyletic group that contains that ancestor.

Turtles, despite being strange or somehow different, are descendants from the same most recent commom ancestor of Reptilia... that's why turtles are reptiles (and that's why birds are reptiles as well).

To make this more clear, have a look at this cladogram (from Hickman, Integrated Principles of Zoology):

The apomorphy that defines the tetrapods is "paired limbs". You have Amphibia to the left and Amniota to the right, whose apomorphy is " egg with extraembrionic membranes". Inside them, you have Reptilia, whose apomorphies are "skull with upper and lower fenestra and beta-keratin in epidermis". Turtles came from an ancestor with these characteristics. So, turtles belong to the monophyletic group of "Reptiles".

Post scriptum: You wrote that "turtles (specifically sea turtles) live on both land and water, very much like amphibians". Just a curiosity: the reason why sea turtles leave the water (sea) from time to time shows exactly that they are not amphibians! Amphibians, being non-amniotes, have eggs that survive under water (actually, with few exceptions, they need to be under water). Turtles, on the other hand, are amniotes, and the amniotic egg cannot be laid under water. That's why the turtles have to leave the water to lay eggs: because, contrary to the amphibians, they cannot lay eggs under water.


Hamilton's derivation of direct fitness from his 1970 paper In his 1970 paper "Selfish and Spiteful Behaviour in an Evolutionary Model", Hamilton uses Price's equation to derive his well-known rule $rb -c >0$. My question is about one of the steps in his derivation.

Hamilton considers a population of $n$ individuals. Let $s_{ij}$ be the effect of individual $i$ on the fitness of $j$. The fitness of an individual $j$ is defined as $w_j = 1 + \sum_i s_{ij}$, $w=1/n \sum_j w_j$ is the mean fitness in the population, and $q=1/n \sum_j q_j$ is the average frequency of a certain allele. Using Price's equation, we get

$w \Delta q = Cov (q_j, \sum_i s_{ij})$.

So far so good. But Hamilton then says that this equation can be rewritten as

$w\Delta q = \sum_i 1/n \sum_j (q_j - q)s_{ij}$

Based on the definition of covariance (i.e., $Cov (X,Y) = E((X-E(X))(Y-E(Y)))$, this seems to only be the case if $E(\sum_i s_{ij}) = 1/n \sum_j \sum_i s_{ij} = 0$. But this would imply that the average fitness wouldn't change over time, which sounds odd for me. In sum, I don't understand this step in Hamilton's paper. What am I missing?

Actually the derivation is pretty straightforward. It's easier to use the fact that $Cov(X,Y) = E(XY) - E(X)E(Y)$ to derive this result. Suppose
$x_{j} = \sum_{i} s_{ij}$.
\begin{align*}
  Cov (x_j, q_{j}) &= E (x_{j}q_{j}) - E (x_{j}) E (q_{j}) \\
                    &= \frac{1}{n}\sum x_{j} q_{j} - \frac{1}{n}\sum
                      x_{j} q \\
                    &= \frac{1}{n} \sum x_{j} (q_{j} - q)
\end{align*}


Are all pathogens parasites? If parasites are organisms that feed on other living organisms, then aren't all pathogens parasites?

I've emphasised on 'feed' because I guess the pathogens just eat us (i.e. take nutrients to reproduce and sustain their lives), right?

But then there's another question.
If, pathogens need us (a host) to survive, then why do they eventually kill us? I mean, why did they evolve to become an organism that exploits their food to the extent that even they, themselves die? Isn't it disadvantageous for pathogens to kill their hosts, because they will eventually die?
Or I'm totally wrong, do those pathogen sustain their lives even when host has died?
Or perhaps they don't care if they, as individual organisms die, because they can survive as an species by infecting other.

Not all pathogens are parasites. Many opportunistic infections can be caused by organisms that are normally commensal or even mutualistic.
For example, this paper describes how multiple bacteria species can be pathogenic as well as mutualistic.

Despite its generally innocuous nature, over the past 20 years S.
epidermidis has emerged as a frequent cause of nosocomial infections.
Several extrinsic factors contribute to the conversion of S.
epidermidis from a member of the resident microflora to an infectious
agent. The bacteria primarily infect compromised patients including
drug abusers, those on immunosuppressive therapy, patients with
acquired immune deficiency syndrome (AIDS), premature neonates and
patients with an indwelling device.
...
Recent studies can be interpreted to suggest that S. epidermidis is a
mutualistic organism, much like the bacteria of the gut. Many strains
of S. epidermidis produce lantibiotics, which are
lanthionine-containing antibacterial peptides, also known as
bacteriocins (Fig. 3). Among the several identified bacteriocins are
epidermin, epilancin K7, epilancin 15X, Pep5 and staphylococcin
1580.37–39 Additional antimicrobial peptides on the surface of the skin have recently been identified as originating from S. epidermidis.
...
The removal of S. epidermidis (i.e. through overuse of topical
antibiotics) may be detrimental to the host for two reasons. Firstly,
removing S. epidermidis eliminates the bacterium’s endogenous
antimicrobial peptides, allowing potentially pathogenic organisms to
colonize the skin more effectively. Secondly, without bacterial
priming of the skin, the host may be less efficient in warding off
infection.


Why can't we use plasmids to add genes to ourselves? Reading these answers I wonder, why doesn't "gene therapy" use self-contained plasmids instead of trying to splice a length into a chromosome?

First, plasmids do not usually integrate into the chromosomes of human cells. In the laboratory, plasmids can be introduced into the cytosol of cells, and plasmid DNA will then be "read" by the host cell and used to make new proteins, for example. But plasmids usually remain separate from the cell's own DNA, and in that sense they are not effective for gene therapy.

Second, our cells are quite good at detecting and destroying plasmids, as well as other foreign DNA. This is a self-defense mechanism, evolved to get rid of viruses and other nasty parasites that might be trying to hijack the cell. In the lab, where we are working with isolated cells in a culture dish, with no immune system, plasmids are typically tolerated. But in a human being, immune cells that have specialized in detecting intruders are very competent at detecting such manipulations, and they will quickly sound the alarm and wreak havoc ... So if injected into the body, plasmids are quickly detected and destroyed.

Research in gene therapy aims to find more efficient ways of "editing" the DNA of human cells, ultimately in a way that can be safely applied in the body. Such a technique does not exist yet. The latest CRISPR-Cas9 gene editing system is a phenomenal tool, and is very efficient at getting into the DNA of human cells; but the CRISPR-Cas9 proteins must themselves be delivered into the cell, for which a virus is typically needed, and this would again cause immune reactions if attempted in a human body.


The move from RNA to DNA and the necessity of reverse transcriptase In this piece about giant viruses and the origin of life, in the context of the move from RNA world to DNA world, virologist Valerian Dolja states:

  In order to move from RNA to DNA, you need an enzyme called reverse transcriptase

Is this true though? Don't many DNA polymerases work with both, ssDNA and ssRNA templates, i.e. they function as reverse transcriptases although they're not "true" reverse transcriptases. So, in order to move from RNA to DNA, a reverse transcriptase was not a necessity like ribonucleotide reductase was for RNA to Uracil-DNA and thymidylate synthase was for Uracil-DNA to DNA?

Yes, this is true. This flow of information is called the "Central dogma of Molecular Biology". It basically describes the flow of information from DNA to RNA to proteins. Since a virus needs to amplify its genetic information before it can take over the infected cell and make only viral proteins and its genetic information, it has two possible options.

DNA viruses can use the cells replication and transcription machinery to make copies and express proteins. RNA viruses either have to use a reverse transcriptase to make DNA from its RNA genome to go on like the DNA viruses. Or they have to have a special, RNA-dependent (works only on RNA templates) RNA-polymerase (our RNA polymerase are all DNA-dependent and work only on DNA templates) to make more copies of their genome. Our DNA polymerases are dependent on DNA, the same is true for our RNA polymerases. So if the virus is not encoding (and actually bringing a few molecules with it in the virus) of the RT-polymerase or the special RNA-dependent RNA polymerase it will not be able to spread.

Using ribonucleotide reductases would theoretically be possible, but it is not the way nature went. And since a cell contains huge amounts of RNA, I doubt this would be a feasible way, as the enzyme would reduce all RNA. And later on the new viruses also needs new (not reduced RNA) to be packaged into new viruses. This would also be problematic.


Beautiful blue enigmatic insect (mantid?) in Kenya This beautiful insect was found in Kenya today - and we don’t know what it is. We think it may be a mantid of some sort?!
Nairobi kenya, croton trees, cape chestnuts, bougainvilliea, there is quite a lot of lichen on the trees.
Despite looking to be the size of someone's arm, it's about 2” long!
Needless to say, no-one had a good camera at the time. Just phones!
The colour of the insect is very similar to the lichen on the trees (hence the mention above).
Someone suggested it was a 'grizzled mantid' Gonatista grisea (Fabricius), but we didn't think they are found native to Kenya - and likewise, we don't see a protuberance on the back of grizzled mantids... Still hoping for an answer.
You can see it also has very small wings, which I hear is a feature of some mantids - micropterous mantids.
I don’t know anything about these - someone said ‘some sort of bark mantis’ - which, for insects would probably mean that it’s bite is worse than its bark...

I'm converting my numerous comments into an "answer" -- I don't currently know the exact species, but I can at least explain some of my thoughts more completely.
Your specimen looks a lot like Gonatista grisea, a tree mantis that mimics a lichen -- as you mention in your post. However, G. grisea, is native to the southeastern USA. I could find no evidence of any reports finding this species in Africa, so we will rule it out.
If we examine some other species of the Gonatista genus (e.g., G. jaiba, G. major, G. phryganoides, and G. reticulata) we find that they are all neotropical and not found in Africa. Therefore, let's look elsewhere.
So, I would recommend examining other close members in the same family that are found in Africa.

I originally recommended reviewing Patel et al (2016) because they provide a checklist of the global distribution of other members of the Liturgusidae family. Using this guide, we could examine known African genera.

They list Dactylopteryx, Majanga (Madagascar), Theopompella, and Zouza as African genera.

However, I had not realized that there had been some taxonomic rearrangements, and Gonatista is now in the family Epaphroditidae.

The other genus in the same subfamily as Gonotista, Gonatistella, is monotypic, and G. nigropicta is not your species.

The other genera in this family, Epaphrodita and Callimantis, (as well as the now-moved genus Brancsikia) also do not seem to contain any species I could find that are morphologically similar to yours.

So maybe we should look elsewhere in the previous Liturgusidae...

Subtribe Humbertiellina in the Gonypetidae  family are just one example of another group perhaps worth investigating because it too was once contained within the original Liturgusidae family along with Gonatista and because some online evidence suggests some members of this subtribe (e.g., Humbertiella and Theopompa) share some similar physical characteristics to Gonatista.

Some non-reputable sources (e.g., here for Humbertiella and here and here for Theopompa servillei) show specimens similar to yours with labels as one of these two genera. I couldn't find consistent imagery or reputable sources with imagery to support either one as correct...
(Also, Patel et al. (2016) suggest these genera are recognized as Asian genera, and so they may be geographically unlikely anyway like Gonatista).

However, perhaps trying to solve your unknown specimen using taxonomic and trait-similarity approaches could be misleading.

According to Rivera (2010): "Whereas the monophyly of Mantodea is well supported, the evolutionary relationships within the order are still contentious. Several classification systems for mantids have been proposed...However, the natural affinities among supraspecific taxa have been extremely difficult to discern due to the highly variable and derived morphology of these insects."

According to Schwarz & Roy (2019): "As already noticed by previous authors, external morphology is highly homoplastic and does not provide useful systematic tools above subfamily level."

Schwarz & Roy (2019) do suggest that the morphology of male external genitalia may be useful for relating individuals as these traits tend to be fairly congruent with more recent molecular phylogenies. You could start there for further research.

(I myself can't discern meaningful detail of the genitalia in your photos, nor am I any type of expert on mantises, so this route of inquiry might be too much in the weeds for me...)

If you find a good key for your region, you might want to check out Brannoch et al (2017) for a "Manual of praying mantis morphology, nomenclature, and practices" to help you with all the mantid jargon. [it appears to be a very thorough and excellent resource!].
I will update this post if I find anything more definitive for you...

Citations
 Brannoch, S.K., Wieland, F., Rivera, J., Klass, K.D., Béthoux, O. and Svenson, G.J., 2017. Manual of praying mantis morphology, nomenclature, and practices (Insecta, Mantodea). ZooKeys, (696), p.1.
 Patel, S., Singh, G. and Singh, R., 2016. A checklist of global distribution of Liturgusidae and Thespidae (Mantodea: Dictyoptera). Journal of Entomology and Zoology Studies, 4(6), pp.793-803.
 Rivera, J., 2010. A historical review of praying mantid taxonomy and systematics in the Neotropical Region: State of knowledge and recent advances (Insecta: Mantodea). Zootaxa, 2638(1), pp.44-64.
 Schwarz, C.J. and Roy, R., 2019, March. The systematics of Mantodea revisited: an updated classification incorporating multiple data sources (Insecta: Dictyoptera). In Annales de la Société entomologique de France (NS) (Vol. 55, No. 2, pp. 101-196). Taylor & Francis.


Identifying this spider I think this is a spider. 8 legs, 2 body sections, and 2 really long Palos? Anyways, can anyone identify this bug, or point me to a resource where I could classify it?

It's camel spider, they have large pedipalps, big chelicerae, and their body is covered by little "hairs". As far as I know, there are only 2 families of that order in North America


Among primates, is it true that homosexual behavior is extremely unnatural and uncommon? I was recently reading a book published by some anonymous biologist known as Lynn Saxon, in which she appears to want to refute Christopher Ryan's thesis in Sex at Dawn that prior to the invent of agriculture, humans were presumably far more promiscuous and had sex not just for reproductive purposes.

In order to do this, she then goes on to show how, in the animal world, the great majority of all sexual activity is directed only towards reproduction. Another author, David Barash, says similar things: namely, that "evolution is very much about reproduction—variation in reproductive success is evolution".

However, homosexual behavior is anything but reproductive. Saxon appears to suggest indirectly that all such "non-reproductive" behaviors that are "useless from a evolutionary point of view" are rare and unnatural among primates, who are our closest relatives.

One more biologist, known as Antonio Pardo, says:

"Properly speaking, homosexuality does not exist among animals…. For reasons of survival, the reproductive instinct among animals is always directed towards an individual of the opposite sex. Therefore, an animal can never be homosexual as such."

Is this true? Is homosexuality really uncommon and unnatural among our closest relatives who are primates? Is sex mostly for reproduction?

First Antonio Pardo is not a biologist, he is a professor of bioethics and his degrees are in medicine and philosophy.

Second, Clearly he does not know anything about primates, since there is one famous great ape that has sex even more often than humans do, the Bonobo. Bonobo have sex for everything, hello, goodby, conflict resolution, social bonding, ect. Bonobo engage in homosexuality and a hundred other sexual practices, including some things humans can't do, like penis fencing. Bonobos along with chimps are also our closest living relative.

As for other animals there are hundreds of examples of homosexuality in nature. I hate using all these wiki links but this is such general biological knowledge I would need either dozens of links or a link to a textbook.

As for Lynn Saxon, first let me say she does not have a degree in anything, It is possible Lynn Saxon is not even her real name.

Now for her argument, it is true that in nature sex is most often directed towards reproduction (that is why it evolved in the first place* and just consider how many sexual animals have very simple behavior), but as I have pointed out there are notable exceptions one of them our closest relative. And not just homosexuality, masturbation is observed in nature as well. Also consider monogamy is also extremely rare in nature with the exception of birds, arguing humans should behave based on how other animals act will not help their argument. It is also a common fallacy, what is natural and what is ethical are not related, Sanitation, science, religion, medicine and reading are also not natural.

If you want to read more about humans and our relatives I suggest the book (the Third chimpanzee" by Jared Diamond as a t least a good starting book.
"Wild Connection" by Jennifer L. Verdolin is even better, both have actual degrees in biology.

*Of course your legs originally evolved as fins,  so what something starts as is not necessarily what it is used for now.


Which colourful insect is this? I found it on my plant this morning while watering it. Location: Hyderabad, Telangana, India. Any ideas?

Nice find! That most definitely is a Poekilocerus pictus, also known as a "Painted Grasshopper".


How does the stomach handle continuous eating? In biology class, we learned this familiar story:  Food enters the stomach, the stomach churns it with acid and enzymes, and then, somehow, the stomach senses when the stew is ready and releases it into the small intestine.

But this simple narrative implicitly assumes that all the food of a meal comes into the stomach at about the same time, and only then does the digestion process begin.  This is often not the reality.  What happens when we eat continuously over many hours, such as at a Super Bowl party, or an all-day summer barbecue, or a long afternoon at an all-you-can-eat crab shack?

Does every new bite cause the stomach to reset its process to zero?  "Uh oh, detecting fresh, undigested food...  better start over..."  But if the stomach resets to zero with every new bite, wouldn't it eventually grow overfull?

Or does the stomach eventually get fed up with all the new introductions and just start releasing whatever it has into the small intestine, ready or not?  In that case, when and how did it decide to proceed with incomplete processing?

First of all, the stomach releases the digested food continuously. Simply put, during digestion the pylorus regularly opens a bit so that small food particles (< 1-2mm) are able to leave the stomach – it's not a batch process (see also this question).

However, because humans tend to ingest a lot of indigestible materials (e.g. bones), there is a need to pass the larger indigestible particles – and this process only happens after all digestible food has left the stomach and thus is "reset" every time you ingest new digestible food.

So if you would continuously ingest food that contains indigestible parts (e.g. mice or other small mammals), the larger bones of those mice would accumulate until you take a longer break and the stomach could complete it's digestion – but for normal food, this does not matter since it will be broken down enough to leave your stomach continuously.

Source: According to Estimation of gastric residence time of the Heidelberg capsule in humans: Effect of varying food composition, 1985 (PDF), the  interdigestive migrating myoelectric complex (IMMC) is responsible for the emptying of of large undigested particles:

  Recently, Hinder and Kelly (1), using radiolabeled techniques, demonstrated differences in the gastric emptying patterns of a liquid, a digestible solid, and an indigestible solid in dogs. Based on such experiments, it has been suggested that the emptying of large (>1 mm) indigestible objects from the stomach
  is dependent on the interdigestive migrating myoelectric complex (IMMC)

Furthermore the study shows that the IMMC gets triggered only after all digestible matter has leaved the stomach:

  The longer GRT of the Heidelberg capsule compared with the t1/2 of the 99mTC-DTPA is consistent with the finding that large nondigestible solids are emptied by the IMMC once all of the digestible materials have passed through the pylorus into the duodenum

and

  the interdigestive migrating myoelectric complex can be markedly delayed by frequent feedings with solids, and the interdigestive migrating myoelectric complex is delayed by both liquid and solid meals

and

  Feeding has been shown to interrupt the IMMC; resumption of myoelectric activity is necessary for the passage of large nondigestible particles such as the Heidelberg capsule


I don't wash my hands and never get sick. Any theories? I have only been sick a few times in my life(I'm 21 and probably 3-4 times) and even when I am sick I don't feel that bad and I am over it within a day or two. My family has always given me slack for never washing my hands but I see no point unless they physically look dirty. Unlike me though my family gets sick around the same amount as other people(a couple times a year).

I have this theory that since my body is always exposed to germs and other bacteria that it is stronger and able to fight off most colds before they ever happen. This theory obviously contradicts popular opinion and what doctors recommend but I have always felt fine not washing.

What do you guys think?

You may very well be strengthening your immune system, but there are microorganisms that you don't want to get, which can have longer term health consequences. For example, there seems to be a significant increase in developing MS if you've ever had the Epstein-Barr virus. But this is just one case. You also don't want Salmonella, tape worms, etc.

So there may be a price to pay for a stronger immune system: namely higher probability of exposing yourself to the more dangerous things out there.


Why is the rough ER necessary to make extracellular proteins? It is my current understanding that free ribosomes synthesise proteins to be used inside the cell, and the rough endoplasmic reticulum is necessary to make proteins that are to be secreted by the cell. Is this correct - and more importantly, if so, why?

Extracellular proteins are proteins that function outside the cell, meaning they are made in cells (transcribed from ribosomes) and then are transported to the plasma membrane to be delivered to the extracellular space. The proteins that need to be secreted aren't secreted as free proteins, rather they are packaged into vesicles. Vesicles are membrane-enclosed structures. When ribosomes are translating mRNA and come across a specific sequence called a signal peptide (wiki), the ribosome goes to the ER and delivers the peptide into the ER. From here, the peptide gets packaged into a vesicle-- first a membrane budding off from the ER.
 source(NCBI)

This is also how secretory proteins get into the Golgi, by vesicle trafficking. From the golgi, proteins are packaged into vesicles. It is a hotly debated topic whether proteins are sorted into specific vesicles or proteins within vesicles (that do not belong in that vesicle) are sorted away (and degraded by the lysosome).


Species Identification: Snake, New Mexico The snake is about one and a half inches in diameter at its widest, a half inch at the head, and about two feet long. I found it in central New Mexico. It's hard to see the head in the pics, but it wasn't triangular or any bigger than the body/neck

It's difficult because the image quality is low, but there are some key features that can be made out which suggest it to be a Western Coachwhip, or "Whip snake", Masticophis flagellum testaceus.

There is not a huge number of species in New Mexico, and most have quite clearly different patterns and coloration, which brings it down to just a couple of species. With respect to colour and pattern, the main candidates are Western Coachwhip, New-Mexico Ridge-Nosed Rattlesnake, Mojave Rattlesnake, and Prairie Rattlesnake.

We can rule out the rattlesnakes because of the shape of the pupil; like most poisonous snakes, the rattlesnakes all have a "cats-eye" pupil, while in the second picture of yours it's fairly clearly a round pupil, which is a feature of the Western Coachwhip.

The slender head is a very telling feature that suggests Coachwhip.

The length is also about right (I'm going to suggest though that the one in your photo is perhaps more than 2 feet/60 cm - it looks bigger to me using the surroundings as relative measures); Coachwhips are in the region of 1-2 metres (3-6 feet) when fully grown.

The range is also perfect for the Western Coachwhip, though Sonoran Coachwhips are also found in southern areas of New Mexico. However, you list this as central New Mexico, so that virtually rules them out.

It seems, given that your picture is in the daytime, that it is diurnal (unlike many species in New Mexico which are nocturnal).


What caused the Mesozoic-Cenozoic radiation? The Phanerozoic eon has had 5 major extinction events and 3 major radiation events. After the Cambrian and Ordovician radiations came all five of the major extinction events, the last of which (Cretaceous-Paleogene) occurred during the last major radiation event (Mesozoic-Cenozoic). This timeline suggests the freeing of previously occupied ecological niches isn't the primary driver of major radiations. (However, the Cretaceous-Palaeogene extinction freed niches during the Mesozoic-Cenozoic radiation, and this may be part of why it continued for so long rather than being a purely Mesozoic event.) Although Wikipedia generally gives a good account of suggested reasons for major extinctions, and also for the Cambrian and Ordovician radiation events, it provides no real such detail for the Mesozoic-Cenozoic radiation. What are its conjectured causes?

There is no real start to a radiation event.

First there are many mass extinctions and many radiation events, what you are referring to are just the most notable ones. also the big five do not occur after the odrivian the first occurs directly before.  Radiation events happen after every mass extinction even minor ones, the amount of radiation corresponds well with the severity of the extinction. The big five and the big three are just the ones we find the most interesting, not the largest, note graph below). The ordovician radiation event happened directly after the cambrian–ordovician extinction event for instance. And there was a massive diversification after the P_T extinction, it just does not get as much press because almost all the major players become extinct in later extinction events and becasue there are  fewer fossils from that time period. Every extinction event is followed by a radiation event. the Mesozoic-Cenozoic radiation is a large radiation because of the KT mass extinction otherwise it would just be the normal background biodiversity turnover.

Essentially radiations are always happening, there is always some radiation going one in some clades.  But if you suddenly wipe out a large number of species and organisms, many of those what survive will be the ones that were radiating simple becasue they were small fast breeding generalists which is also the group that radiate a lot. Small fast breeding generalists are what what best survive mass extinctions and a group that does a lot of radiating. There is also a large anthropomorphic component to this, if you take the tree of life and make a radom slice across it anywhere it sill look like many of the groups that survive are radiating becasue all the other radiation events are cut off, while we ignore stable groups becasue they are stable. You can even notice that the radiation of different groups start at different times but then explode after the event. Almost as if our artificial lines between groups is not a great predictor of diversification events. Radiation events are not one off occurrences with clear cut beginnings and ends but a prolonged uptick in an ongoing system with a lot of variation. there is no clear cut start to radiation events imagine trying to pick the exact second summer or winter begins using nothing but temperature data, there is just to much noise due to local and daily condition to make any such point anything but arbitrary.

So the large scale radiations is still caused by the extinction event, it however will almost always look like it was happening earlier becasue on a small scale it never really stops, and where we draw the lines for groups does not correlate well with radiation events, yet we still use it to decide which "groups" are radiating.

Sources

If you look at this paper and its graph you can see this effect in angiosperms. The group originates and begins to diversify before the KT but a massive upswing in diversity happens after (actually fairly long after, once the climate/extinction has stabilized)


Interchromosomic vs Intrachromosomic Recombinations What is the difference between interchromosomic and intrachromosomic recombinations?

I did a research about them and saw some videos (e.g. this and this) with animations on YouTube. But I'm still lost between them and can't differentiate between these two expressions.

The prefix inter- means "between two or more", and the prefix intra- means "within one".

So interchromosomal recombination means recombination between two different chromosomes (for example, it normally and often occurs between each homologous paternal and maternal chromosome pair during the Prophase I stage of meiosis).

Intrachromosomal recombination would mean recombination within a single chromosome.


colocalization by IFA? I have done IFA (immunofluorescence assay) previously but i targeted only one protein or i tagged my endogenous protein with GFP/RFP then i performed IFA. I want to do the IFA in parental cell line (HEK cells). My aim is to show the two proteins are co-localized or not?

Protein-1 (secondary antibody Mouse)
Protein-2 (secondary antibody Rabbit)

How can i co-localize two different proteins in the same sample? Which primary antibody do i have to add first?  can any one please suggest me something?

If you search the web or Google Scholar, you should be able to find plenty of examples of colocalization protocols.
In general, though, for each target you're going to want to have an unstained control sample (you can use one for all targets), a secondary-only sample to look for non-specific background staining, and a single-color sample (primary plus secondary). Then, you'll have a sample with both primaries and both secondaries. You always add the primaries at the same time, and the secondaries at the same time.
As you start getting into higher numbers of colors, you'll also need an FMO (fluorescence minus one) control for each color so you can test for signal bleed-over from one channel to another. This sample will combine all the colors except for one.


Is Insulin-Glucose dynamic Lotka-Volterra? From Wikipedia:

The Lotka–Volterra equations, also known as the predator–prey equations, are a pair of first-order, non-linear, differential equations frequently used to describe the dynamics of biological systems in which two species interact, one as a predator and the other as prey. The populations change through time according to the pair of equations:

\begin{align}
\frac{dx}{dt} = \alpha x - \beta x y \\
\frac{dy}{dt} = \delta x y  - \gamma y
\end{align}

This looks very similar to how Insulin and Glucose interact with each other in the body.

Glucose uptake release insulin and glucagon offsets the effect of insulin through glycogenesis.

Can the Glucose-Insulin dynamic be described as Lotka Volterra?

Is the standard Lotka-Volterra (LV) model an exact fit for insulin-glucose (IG) dynamics? No. Can a similar model built on the same principles capture most of the essential features of the IG dynamics? Absolutely.

How to capture most of the insulin-glucose dynamics using a slightly modified Lotka-Volterra model

We can figure out how to change the LV equations to fit the IG dynamics by figuring out how our assumptions have changed. Like Daan mentioned, neither insulin nor glucose undergo self-reproduction. So we'll drop those terms from the equation, and we'll represent an influx of glucose (as from, say, a meal) as a simple time-dependent linear spike. Your rate equations will now look like:

$\frac{dx}{dt} = \alpha[t_{gi} < t< t_{gf}]-\beta x y$

$\frac{dy}{dt} = \delta x-\gamma x y$

where $x$ is glucose concentration, $y$ is insulin concentration, and $[t_{gi} < t< t_{gf}]$ is equal to 1 if the current time $t$ is greater than the time when the glucose spike starts $t_{gi}$ and less than the time when the glucose spike ends $t_{gf}$, and is equal to zero if the time $t$ does not meet this condition.

Simulation of insulin-glucose dynamics using the above LV model

I ran a simulation of the above model in Matlab, and here's what it looks like:

The basic features of the insulin-glucose dynamics from the example graph the OP posted are present. Just like in the real system, first the glucose spikes, then the insulin spikes after a short lag, then they both return to baseline.

With some small improvements, the LV model can capture the dynamics of the infamous "sugar crash" phenomenon

Now for the really cool part.

As can be seen on the OP's graph, glucose levels tend to fall somewhat below their baseline following a large glucose spike. This is the physiological basis for the sugar crash that people sometimes get a little while after eating something really sugary like a candy bar. Regardless of whether the psychological symptoms actually occur, the dip in glucose levels is a real thing.

In order for a model to be considered "good", it has to be able to capture these kinds of complex but important phenomena in their underlying systems. The glucose dip did not show up in my original LV model, so the question is, can the model be modified in a simple way so that it will capture the dip? Let's take another crack at it!

Part of the problem with trying to study phenomena related to baseline levels using the previous model is that the baseline levels of both insulin and glucose are effectively fixed at 0 in that model. We can set the baseline levels by adding what's called a zeroth-order production term (essentially a fixed constant that isn't multiplied by the concentration of anything) to each of our rate equations. The rate equations now look like:

$\frac{dx}{dt} = \alpha[t_{gi} < t< t_{gf}]+\epsilon-\beta x y$

$\frac{dy}{dt} = \delta x+\eta-\gamma x y$

where $\epsilon$ is the 0th order glucose production term, $\eta$ is the 0th order insulin production term, and everything else is exactly the same.

Simulation of insulin-glucose dynamics using the "dip-enabled" LV model

Again using Matlab, I ran a simulation of the "dip-enabled" LV model:

and this time the dip shows up.

Notes:

-The term with the times in it is called an Iverson Bracket.

-You could make this model more physiologically relevant by using a more complex function for the glucose spike, but for simplicity's sake we'll stick with a linear function. A smoother function, like for example a Hill function, would probably help to reproduce your original graph of the IG dynamics.

Matlab code

function dxdt = insulin_glucose_birth_death_dxdt(t, x, kip, bip, kid, kgp, bgp, kgd)
dxdt = [kip*x(2) + bip - kid*x(1),
    kgp*(t>1 && t<2) + bgp - kgd*x(1)*x(2)];
end

function [t,x] = insulin_glucose_birth_death_odesol(tspan, x0, kip, bip, kid, kgp, bgp, kgd)
opts=odeset();
[t,x]=ode45(@(t,x)insulin_glucose_birth_death_dxdt(t, x, kip, bip, kid, kgp, bgp, kgd), tspan, x0, opts);
end

function [t,x] = insulin_glucose_birth_death_plot(tspan, x0)
%run with:
%   tspan = [-10, 5];
%   x0 = [0,0];
%   [t,x] = insulin_glucose_birth_death_plot(tspan,x0);

kip = 2;
bip = 0;  % set to .01 for the "dip" simulation
kid = 1;
kgp = .1;
bgp = 0;   % set to .1 for the "dip" simulation
kgd = 50;

[t,x] = insulin_glucose_birth_death_odesol(tspan, x0, kip, bip, kid, kgp, bgp, kgd);

figure(gcf)
hold on
plot(t, x(:,1), 'b', t, x(:,2), 'r')
legend('insulin','glucose')
xlabel('time')
ylabel('concentration')
axis([0 inf -inf inf])
hold off
end


Which function do nicotinic receptors have in the periphery? I came across this question today, it says:

  Nicotinic receptors stimulation is directly responsible for …....

I should fill the spaces by one of the following choices:

Increasing the excitability of sympathetic postganglionic neurons.
increasing the the force of stomach contraction.
delaying the emptying of liquids from the stomach.
decreasing the excitability of sympathetic postganglionic neurons.

The only article speaking about the nicotinic receptors in my physiology book says that they are cholinergic receptors found in the autonomic ganglia, i.e., they are found on the postganglionic neurons.

So when I tried to solve the question, I thought the upper three answers are correct. Specifically, because stimulating the receptors on the postganglionic neurons will increase their excitability, option 1 seems to make sense.

But if that postganglionic cell happen to be sympathetic it may provoke the emptying of the liquids from stomach to be delayed (choice 3)?

And, if it was parasympathetic the force of stomach contraction would also increase (choice 2)?

I am confused as all three answers 1) 2) and 3) seem to be correct and the question asks specifically for one correct answer. Could someone help me find the correct answer, but put simply please, as I'm just a first-year dental student.

Short answer
1

Background
Nicotinic recepeptors (nAchRs) are widely distributed in the central and peripheral nervous system. Your question seems to focus on the peripheral nervous system. Taken from (Taylor, 2012):

In the periphery, nAchRs are found in:

Innervated skeletal muscle, especially postsynaptically in the motor end plate;
The presynaptic nerve ending in some motor neurons to control Ach release;
Ganglia at the postsynaptic dendrite and nerve cell bodies, and presynaptically to control Ach release.

Now in your answer the options 2 and 3 are incorrect, as muscarinic Ach receptors regulate gastric fluid secretion (Aihara, 2005) and contraction (Kitazawa et al., 2006). Given that nAchRs are excitatory receptors. In muscle cells, the binding of Ach leads to an opening of the associated ion channel, in turn producing a rapid increase in the cellular permeability of sodium and calcium ions, resulting in the depolarization and excitation of the muscle cell, thereby producing a muscular contraction (source: EMBL-EBI). This leaves only one opion left, namely 1). Since this was basically answering the question by exclusion, below Fig. 1 shows that answer 1) is indeed the correct one through a more positive approach - the top panel clrearly confirms that the sympathetic pathway deploys Acetylcholinergic neurons to stimulate its postganglionic adrenergic neurons.

Fig. 1. Ach in the peripehral nervous system. source: Austin Community College

References
- Ayhara, Gastroint, Liver Physiol (2005); 2886): G1199-207
- Kitazawa et al., Eur J Pharmacol (2007); 554(2-3): 212-22
- Taylor, Primer on the Autonomic Nervous System (3rd Ed. ( 2012}


How many transcription factors are there? In molecular biology and genetics, a transcription factor is a protein that binds to specific DNA sequences, thereby controlling the flow (or transcription) of genetic information from DNA to messenger RNA.

My question is simply how many transcription factors are there in the genomes of:

Humans
Anopheles gambiae (or it's close taxonomic relatives)
Less prioritized: any other species

This is the Curated database of mouse and human transcription factors. And this is the paper in which they describe how they curated the database. In summary, there are 3230 putative mouse TF, 1200 of which are described in scientific papers.


What type of movement is "spontaneous movement" if it isnt reflex movement and it isnt purposive movement? According to Spontaneous and induced fetal activity

  Spontaneous motor activity of the foetus depends significantly ot the
  foetal age; during the period between the 12th and 16th week it was
  recorded in 94.4%

By spontaneous, correct me if I wrong, I understand non reflexive movement and by induced I understand reflexive movement, since

  A reflexive reaction or movement occurs immediately in response to
  something that happens.

But also, according to this other article Fetal movement

  purposive movement begins at about 18 weeks, gradually replacing
  reflex movements

If "spontaneous movement" it isnt reflexive movement since it isnt an automatic reaction to something, and it isnt purposive movement, what is it exactly, and what does it generate it?

Although I can't read the original article in Czech, from their abstract it is clear that all they mean in differentiating spontaneous versus induced movement is whether the experimenter manipulated the uterus to induce a movement. Movements they observe could still be reflexive, they make no distinction of the type of movement (and do not intend do) except indicating whether the movement was purposefully caused by the experimenter.


How long can I store extracted RNA? If I extract RNA from a (leaf tissue) sample using a one-step phenol:chloroform extraction, how long can those samples be stored at -80°C? And how many times can I defrost and refreeze them before they will become degraded?

I've found that extracted RNA using commercial kits has stayed stable for many years at -80 C. I would certainly aliquot it before freezing however as RNA is particularly sensitive to freeze-thaw cleavage.


Should heart-to-body energy consumption ratio equal oxygen consumption ratio? The human heart pumps oxygen to the body, and the heart itself requires oxygen.

Both the body and the heart use energy, usually expressed in calories or ergs.

If we look at the energy consumption (in Watts) of the heart as a fraction $F$ of the energy consumption of the body as a whole it is about

$F \approx \frac{1.3}{91.3}=0.014.$

Humans consume about 550L of oxygen per day per this website and the heart itself consumes about 8 ml of $O_2$ per 100g per minute at rest according to this site. Assuming an average global human heart mass of about 310g (Google) the daily total heart oxygen consumption is about  (8ml x 3.1 x 1440 min) = 35712 ml or 35.7L of oxygen. The ratio $R$ of heart to body oxygen consumption is thus about

$R \approx \frac{36}{550-36} = \frac{36}{514} =0.07$

These figures are rough at best but not rough enough to account for a discrepancy of a factor of 5 in the ratios. Can someone suggest what might account for the difference?

The calculation seems to show that the heart's proportional consumption of oxygen is a lot higher than its proportional consumption of energy. My understanding is that the respective oxygen consumption of the heart and body are a good reflections of their respective energy consumption. Is that a sound assumption?

Thanks for any insights.

At first glance there are a few major issues with your calculation and assumptions.

You're comparing the energy output in work (pumping action) with the energy consumption of the rest of the body in input (oxygen consumption). I don't know how efficient the heart is, but I'd guess only somewhere from 20-40% of input energy is actually converted to pumping action.
Oxygen consumption is correlated with energy consumption, and would be a good way to measure energy consumption if you know exactly what the subject is burning. However, if you have a big difference between the preferred fuels between the heart and the rest of the body, this doesn't really apply  anymore. A quick google leads me here: https://www.ncbi.nlm.nih.gov/pubmed/17081788, showing that the heart prefers to burn fat over glucose, and this creates a significant difference:

  Carbohydrate oxidation typically generates approximately 120 kcal per mole of respired oxygen, whereas fatty acid
  oxidation typically generates only approximately 100 kcal per mole of oxygen.

This means that the heart needs more oxygen than the rest of the body to generate the same amount of energy.

I think combined this could explain the 5-fold difference.


How will rising carbon dioxide levels in the troposphere affect photosynthetic producers? Much discussion has been had about the affects of climate change on plantlife, but how will rising carbon dioxide concentrations affect the photosynthetic process itself? Since CO₂ is a reagent in photosynthesis, would we expect higher CO₂ to mean an increased rate of photosynthesis in a real-world context? Has there been any research on this?

I am thinking more of large-scale field tests rather than lab plants.

There are several key ways in which rising atmospheric CO₂ concentrations will affect photosynthesis, and these are related to the different types of photosynthesis. In order to properly answer your question, I'll provide some background about photosynthesis itself.

Photosynthesis evolved in a high-CO₂ atmosphere, before the oxygen-enrichment of the atmosphere (which actually happened as a result of photosynthesis). Most plant species operate C3 photosynthesis. In these plants, carbon dioxide diffuses into the cell where it is fixed by Ribulose-1,5-bisphosphate carboxylase oxygenase (RuBisCO) into a 3-carbon molecule (hence C3), which is then polymerised to make sugars. A crucial fact about RuBisCO is that it has both carboxylase (carbon-fixing) activity and oxygenase (oxygen-fixing) activity. This means that oxygen and carbon dioxide compete for the active site on the enzyme complex, leading to RuBisCO being quite inefficient and slow at fixing carbon in higher oxygen concentrations. That didn't matter in the high-CO₂ atmosphere of the early Earth, but in todays atmosphere O₂ concentrations are high enough that they severely limit the productivity of C3 plants.

However, plants haven't just been growing slowly all that time - several mechanisms for increasing photosynthetic efficiency have evolved. The most influential systems involve concentrating carbon dioxide in a particular area, excluding oxygen, and concentrating RuBisCO in that same area. This avoids the oxygen competition for the active site and allows RuBisCO to operate more efficiently. The key adaptation here is C4 photosynthesis - the system which is present in most grasses and many of the most productive plants on Earth (e.g. maize, sugarcane, Miscanthus). It has evolved at least 62 times independently. It works by having RuBisCO concentrated within 'bundle sheath' cells which are surrounded by a layer of suberin wax. This layer prevents CO₂ escaping and O₂ from getting in. CO₂ from the atmosphere is then fixed in different cells - 'mesophyll cells' - by another enzyme - Phosphoenolpyruvate carboxylase (PEPC), resulting in a four-carbon molecule (hence C4). This 4-carbon acid, (malate or oxaloacetate depending on the system) is then shuttled into the bundle sheath cells. There, the CO₂ is released again by a variety of enzymes depending on the system, creating a high CO₂ concentration in the cell where RuBisCO can then work efficiently.

In general, C4 plants are much (about 50%) more efficient than their C3 counterparts, and they are particularly well adapted to high temperatures and moist environments. So, to answer your first question: as atmospheric CO2 levels continue to rise, C3 plants will gradually be able to photosynthesise more efficiently. Interestingly though, C4 plants are predicted to also benefit from increased atmospheric CO₂. If global temperatures rise as predicted, both C3 and C4 plants will be able to operate more efficiently than they currently do, up to a maximum temperature beyond which enzymes will begin to denature faster and efficiency will drop. One consideration is that the difference in efficiency between C3 and C4 systems will decrease, which may significantly alter the makeup of plant communities around the world.

This is a vast oversimplification, but it is accurate for the predicted overall effects. Localised effects (i.e. productivity changes in a particular region or for a particular crop) will depend on habitat, physiology, etc.

Some key papers to launch you into the literature:

Leakey, A.D.B., Bernacchi, C.J., Dohleman, F.G., Ort, D.R. & Long, S.P. (2004) Will photosynthesis of maize (Zea mays) in the US Corn Belt increase in future [CO2] rich atmospheres? An analysis of diurnal courses of CO2 uptake under free‐air concentration enrichment (FACE). Global Change Biology. [Online] 10 (6), 951–962. Available from: doi:10.1111/j.1529-8817.2003.00767.x [Accessed: 31 January 2012].
Morgan, J.A., LeCain, D.R., Pendall, E., Blumenthal, D.M., Kimball, B.A., Carrillo, Y., Williams, D.G., Heisler-White, J., Dijkstra, F.A. & West, M. (2011) C4 grasses prosper as carbon dioxide eliminates desiccation in warmed semi-arid grassland. Nature. [Online] 476 (7359), 202–205. Available from: doi:10.1038/nature10274 [Accessed: 31 January 2012].


Do invasive species survive in the long run? If an invasive species preys on native species, spreads widely and becomes dominant, should it not become extinct soon enough because of a lack of food?

This potentially depends on what species you are referring to.

In the case of plants, photosynthesis is used to as their source of energy, so will never run out of food as such. Assuming the conditions are favourable in terms of water and temperature (likely, otherwise the species wouldn't have flourished in the first place) and they stay that way, the only limiting factor is going to be nutrients in the soil. These are returned to the soil when the plant dies, so this is fairly self-limiting, when there's not enough then plants will die and the nutrients will return to the soil.

Animals face a slightly different situation, in that they need to eat to survive. As such, if the population that was introduced was large enough to eat all the prey (whether plants or other animals) in the area and carnivorous animals didn't partake in cannibalism even when times were tough, then the animal may die out.

In general however, predator and prey regulate fairly effectively, a decrease in prey causes a decrease in food availability which leads to a decline in predators. This allows an increase in prey, which gives a higher availability of food to predators so their numbers increase. This causes a decrease in prey numbers and so on. In general once an invasive species has been established, it will require intervention for it to be removed and it will not die out naturally.


Translation of mRNA? We inserted an insulin gene from human into bacteria. Will translation of the gene (protein formation) occur in bacteria? If translation occurs then why does it occurs, give a reason for this?

Yes, bacteria will produce human (or any organism's) proteins if you introduce their genetic material but there are a few things to consider.

First, the introns must be removed from the human genetic sequence. Bacteria do not have the machinery to splice out introns after transcription. This is typically done by using a viral protein to reverse transcribe mRNA, which already have the introns removed, into DNA which you can use to transform bacteria.

Second, you need to insert a Shine-Dalgarno sequence. This allows the bacterial ribosomes to bind to the mRNA they will produce, and translate the protein you desire. This sequence is not found in eukaryotic genes, so you have to make sure it was included either in the vector or in the PCR primers you used to amplify the gene sequence.


How long can a bee surive in a jar? So, some people and I encountered an adventure game where you have a bee in a jar and need to move it from place to place before it suffocates, and someone tried to find out how long a bee would actually survive in the jar. We've found three relevant papers:

Oxygen consumption in the foraging honeybee depends on the reward rate at the food source [1]
Oxygen consumption and body temperature of active and resting
honeybees [2]
Physiological Correlates of Foraging Efforts in Honey-Bees: Oxygen
Consumption and Nectar
Load [3]

which has given us what we think is a good high-end guess of 40µl of oxygen per minute consumed.

However, we don't know at what point the oxygen level would get too low for the bee, or if carbon dioxide poisoning  would occur. Does anyone have a source for the minimum oxygen levels a bee needs to survive, or the point at which CO₂ toxicity becomes a problem?

Assuming the jar is airtight--

I think your oxygen consumption rate may be too high and that 40$\mu l$ per hour$^1$ might be closer but since it's a high figure anyway we can use it. 40 $\mu l$ per minute would be about 2400 $\mu l $/hr.

A 12-ounce jar is about 0.355 liters. At sea level, air contains about 20% oxygen so the volume of oxygen in the jar is about 0.0709 liters.

At altitudes which are considered high for humans (17000 feet or higher) the percentage of oxygen falls to about 15%. If a bee is able to get 2400 $ \mu l$ of oxygen per hour from a jar, the volume of oxygen will fall to about 13% after ten hours.$^2$

Based on oxygen consumption alone I think a bee would be stressed at this level, especially at temperatures exceeding 32C. I would guess the bee would be stressed well before this, maybe after 5 hours (16.6% oxygen). If we factor in the likelihood that the bee's respiration is up due to the agitation of confinement I think we can shave another hour off.

Depending on the age, size, species, variety, temperature, location, etc. I think an outside limit of 4 hours in an airtight jar is a good guess.

Toxicity from CO$_2$ may be a problem but bees have a much higher tolerance for CO$_2$ than humans, according to one set of entomology notes. At 0.04% the concentration will only increase marginally due to a drop in oxygen alone but the bee itself will produce CO$_2$ and in far greater quantities under stress. A chart here shows production of CO$_2$ in reaction to a light being turned on. 400 ppm is 0.04% but in this case it is due to the bee. If the bee during respiration returns CO$_2$ as quickly as it consumes oxygen the jar could reach 7% CO$_2$ in four hours, a level that may be toxic for humans. But we have already suggested the bee is under stress from oxygen depletion at that point.

There are many assumptions in this note. A conservative estimate might be an hour in an airtight jar. I would not bet on more. There are probably other issues I haven't thought of. Bees are very fragile and the chart linked above suggests they would not fare will in such an environment.

$^1$ Respiration of Worker Honeybees of Different Ages and at Different Temperatures, Allen, 1958, J. Experimental Biology 36, 92-101. At page 97 Allen gives a chart showing log $\mu l$ $O_2$/mg body weight/hr. For a 14-23 day old bee at 32C he appears to give about .5 which means 1.65/mg/hr or about 115 $\mu l$ per hour for a 70mg bee. It may be a typo or perhaps I am misreading the chart. Also the study uses an older method of measuring respiration.

$^2$ This is a simplification. The bee will start breathing a mixture containing falling oxygen levels and this may slow the oxygen depletion a little. But if we say the bee needs what it needs this saves us a differential equation.


Why am I getting low transformation efficiency with DB3.1 E.coli cells? I am making competent cells using DB3.1 E. coli cells. Even after following the exact protocol (Inoue method for ultracompetent cells) given in 'Sambrook and Russel', I am not getting transformation efficiency of more than 104. I am using a 5.1kb plasmid for checking transformation efficiency.

I will be thankful if any of you can share your experience in this experiment.

How are you storing the cells?  Competent cells can be very finicky.  In my lab, we usually flash-freeze them with ethanol/dry-ice and store at -81 degrees (long-term use) or we store them surrounded by ice at 4 degrees (short-term use).


Do larger multicellular organisms have an increased risk of mutation and thus cancer? So I was thinking that if each cell has P(X) of becoming cancerous, then the chance of cancer is 1-((1-P(X))^n) where n is the number of cells in the organism.

Since larger organisms have more cells than smaller organisms (I'm guessing that larger organisms simply have more cells than smaller organisms as you can't have larger cells since there is an optimum surface area to volume ratio), does this mean then that larger creatures are more likely to have cancer cause they have more cells?

As mentioned in the comments, this question is quite complicated. If the chance of a single cell from different organisms getting cancer was the same, then you would be correct, but this is not the case.

Different organisms have evolved to live different lengths of time. This is rather obvious when you think about it: mice have a maximum lifespan of ~3 years, humans ~80years (these figures are of course massive generalizations - but it doesn't really matter). Yet 'old' mice (> 2 years) still get age-related diseases such as cardiovascular disease, and cancer. It should be fairly clear that the risk of a 2 year old mouse getting (age-related) cancer is much higher than a 2 year old human.

The explanation for this isn't exactly concrete, but it goes something like this; mice invest a lot more resources in growing very fast and reaching a reproductive age very early, whereas humans develop much more slowly, and invest a higher proportion of their resources in maintaining tissue function, thereby reaching reproductive maturity much later than the mouse. The Hayflick limit for a mouse is about 10, whereas for humans this is closer to 60.

Thus the rate of aging in humans is much lower than that of the mouse, and it comes back to evolution: mortality in the wild is very high for the mouse, and thus mice that invest heavily in reaching early reproductive maturity are selected for - and those that invest in anti-cancer mechanisms take longer to reach reproductive maturity, and thus have less chance of actually doing it!

So to answer your question - smaller organisms tend to have higher risks of getting cancer because their lifespans are comparatively shorter, and thus they 'age' at a faster rate and invest less resources in maintaining function (e.g. genome integrity).


Why isn't the p16-INK4a gene involved in apoptosis expressed in heart or liver tissues? New York Times article explains how killing p16-INK4a positive senescent cells can help keep the surrounding cells vigorous.

So here's my question: why is p16-INK4a expressed in most cells other than heart and liver cells? What would happen if we knocked it out everywhere?

p16-INK4a is a part of a very important checkpoint mechanism. It's the "bad guy" in the context of aging because it induces senescence, and too much senescence leads to aging-related  tissue degradation.

But senescence is important. It's one of the responses cells take when something goes wrong-- DNA damage, viral infection, telomere depletion, that sort of thing. Senescent cells have stopped proliferating. We have a word for cells that don't stop proliferating, and that word is "cancer". So, p16-INK4a is a major tumor suppressor. A universal p16-INK4a knockout would have a much harder time shutting down the proliferation of cells that had undergone DNA damage, and would therefore be much more prone to cancer. You'd have very young-looking tissues filled with tumors.

So, the headline question is why INK4a is not expressed in the heart or liver if it's so important. This is speculation on my part, but I think it's because those tissues are especially prone to being damaged by fibrosis, and a build-up of senescent cells would lead to increased fibrosis. Senescence is just one possible response to DNA damage, though. Another is apoptosis. If the senescence-induction pathways aren't active in heart and lung tissue, I'd expect the apoptosis-induction pathways to be pretty active.


Does the brain consume more energy when a person is stressed or anxious When a person is anxious or stressed or suffering from chronic depression, it is observed that the person is usually tired.
Is there there a connection between fatigue and racing thoughts/obsessions.
Also I want to know what damage can anxiety do to brain and body over time.

The tiredness associated with depression/stress is not due to the 'brain power' increasing but due to a change in what parts of the brain are active and/or disrupted sleep. Anxiety can cause issues to the brain and body over time.
Brain power is relatively constant
For the average adult in resting state the brain consumes about 20% of the body's energy. It has been shown that the brain requires about as much energy at night when you are asleep as during the day. The increase of energy for 'hard thinking' is about 8% which is very little compared to the baseline usage (leg muscles can have a 300-400% increase when walking compared to sitting).
See this paper for more analysis.
Tiredness and Mental Health
Depression affects neurotransmitters associated with alertness and reward systems thus making you feel less awake, less motivated, and more tired even if you might have sufficient sleep. However depression and anxiety often also lead to disrupted sleep (trouble falling asleep, nightmares/poor quality sleep, waking up too early etc). This would lead to a feeling of constant fatigue. Unfortunately, the feeling of fatigue can also worsen feelings of depression and anxiety though it is often not the root cause of depression.
Effects of Anxiety Over Time
Repeated activation of the stress response (a cascade of stress hormones colloquially known as the 'fight-or-flight' response) takes a toll on the body. Research suggests that chronic stress contributes to high blood pressure, cardiovascular disease, and causes brain changes (including differences in the volume of gray matter versus white matter, as well as the size and connectivity of the amygdala paper) that may contribute to anxiety, depression, and addiction. Preliminary research also suggests that chronic stress may also contribute to obesity, both through direct mechanisms (causing people to eat more) or indirectly (decreasing sleep and exercise). Chronic stress keeps levels of cortisol in the body high.
Source
Another important factor is the effect of stress on the cortisol levels.
Stress leads to an increased release of the steroid hormon cortisol, which can lead to reduced bone formation, favoring long-term development of osteoporosis (progressive bone disease) source.
It transports potassium out of cells in exchange for an equal number of sodium ions. This can trigger the hyperkalemia of metabolic shock from surgery. Cortisol also reduces calcium absorption in the intestine source. Cortisol down-regulates the synthesis of collagen source.
Sustained stress can lead to high levels of circulating cortisol (regarded as one of the more important of the several "stress hormones"). Such levels may result in an allostatic load,which can lead to various physical modifications in the body's regulatory networks source.


Are there any studies on the fertility levels of humans/mammals as a function of their stay at Antarctica? Wikipedia, and Space.SE seem to indicate humans become infertile in space due to the increased exposure to cosmic rays. Knowing as we do that Antarctica is holey, and subject to increased radiation (atleast UV if not broad-spectrum), I find myself wondering whether any studies on fertility were ever conducted on that continent.

So ... Are there any studies on the fertility levels of humans/mammals as a function of their stay at Antarctica?

I haven't been able to find a study on fertility, but it would be important to note the difference between radiation considered.  The dangerous radiation discussed in both of your links are cosmic rays as you noted.  Our main defense against this sort of radiation is the earth's magnetic field.  The hole you are talking about is in the ozone layer, which is much more important in UV protection than cosmic ray protection.  The amount of incident cosmic rays is slightly more at latitudinal extremes due to the deflection away from the equator by the magnetic field, but this is only 1.5 to 2 times greater, see fig. 8.

Unless we figure out how to punch a hole in the magnetic field as well, the main threat in the arctic is skin cancer from UV, not infertility from cosmic rays.


Grasshopper identification I found this grasshopper (although I'm not sure if it was really one) near a lake in Bangalore, back in mid April. This is the only picture i could get and since it's so well camouflaged I would like to point out that it's right in the middle. It had those very conspicuous green bands on either half of the dorsal side with longitudinal white pinstripes. It was around 10 cms in length. Can i get an ID please?

This is known as a "long-headed grasshopper", and belongs to the species Acrida sp. Of the species I've been able to find images of so far, I think is most closely resembles

Acrida conica

and

Acrida bicolor

A full list of species for this genus can be found here.