What is the biological reason for a burst appendix being potentially lethal? Given that the appendix does not seem to be used by the human body, what is the biological reason that it is potentially lethal when this organ bursts?

Also, what would cause the 'burst'?

Necessary conditions

In order for the process culminating in appendiceal rupture to begin, there must first be proximal obstruction of the lumen (the inside cavity of the appendix) that prevents normal communication with the bowel.

  Obstruction is most commonly caused by a fecalith, which results from accumulation and inspissation of fecal matter around vegetable fibers.
  The bowel wall inside the (now closed) appendix continues to secrete muscous, and bacteria continue to multiply, producing the distention that is often perceived as nausea, vomiting, and poorly localized abdominal pain.1

The process leading to rupture

As the pressure in the appendix increases, venous pressure is exceeded. This means blood can no longer exit the venules of the appendix normally. In the presence of ongoing arterial flow, this leads to vascular engorgement, worsening the distention and increasing pressure further. The inflammatory process spreads from the lumen (inside) of the appendix to the serosa (outside) and then to the parietal peritoneum (lining of the abdominal cavity). This last step is what causes the characteristic shift in pain from poorly localized visceral pain to focal right lower quadrant pain.

As distention worsens, arterial pressure is eventually exceeded, and the most poorly vascularized areas of the appendix (generally just beyond the point of obstruction on the antimesenteric border) infarct first. Dead tissue has very little structural integrity, and once infarction happens perforation is likely to follow quickly.

Why this is (sometimes) lethal

There are several possible mechanisms, more than one of which is probably operative in most cases.

The three I have listed below all converge on the same final common pathway: In the absence of adequate systemic blood pressure (shock), the heart is not able to pump normally and will eventually deteriorate into a non-perfusing rhythm (a.k.a death).

Bacteria in the peritoneal cavity:
As in bowel perforation of any cause (e.g. perforated peptic ulcer, perforated diverticulum, traumatic perforation), bacteria in the peritoneal cavity (the “free space” outside the bowel within the abdomen) triggers an intense inflammatory reaction and fluid sequestration. Fluid pulled from the circulation into the peritoneal space causes hypotension and (hypovolemic) shock.
Infarcted bowel: Dead tissue connected to the body is never a good situation. Intracellular contents are released into the bloodstream – electrolyte release can cause hyperkalemia and other electrolyte imbalances; reactive oxygen species can lead to hypotension and (distributive) shock.
Sepsis: Bacteria (generally gram negative rods from among normal gut flora – most commonly Escherichia coli or Bacteroides fragilis)
may enter the bloodstream due to compromised vessels during the process of infarction and rupture. Lipopolysaccharides in the cell wall of gram-negative bacterial organisms lead to activation of monocytes and macrophages. This results in increased levels of interleukin-1 and tumor necrosis factor and eventually of IL-6 and IL-8. These cause widespread endothelial injury leading to diffuse alveolar damage in the lungs and activation of the coagulation system leading to disseminated intravascular coagulation. These cytokines also lead to systemic vasodilation and (distributive, septic) shock.

References

1. Silen W. Chapter 300. Acute Appendicitis and Peritonitis. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J. eds. Harrison's Principles of Internal Medicine, 18e. New York, NY: McGraw-Hill; 2012.

2. Kemp WL, Burns DK, Brown TG. Chapter 8. Hemodynamics. Pathology: The Big Picture. New York, NY: McGraw-Hill; 2008.

3. Charles Brunicardi, F. Acute Appendicitis. Schwartz's Manual of Surgery; 2006.


Identify the pink mold infecting refrigerated lemons I made lemon juice 6 month ago.

I just washed the lemon using brush and then cut them into pieces.
Then I put one layer of lemon in the bottle followed by one layer of
sugar
Again one layer of lemon and one layer of sugar.
Then I close the bottle and put it in the refrigerator.

When I opened it, I observed some pink colored mold on the lemon slices.

Can anyone can identify the mold or tell me how to identify it?

PS: in the 6 months, I never opened the bottle. The bottle was clean and I did not add water; just lemon and sugar.

I checked citrus diseases on wikipedia, then "ctrl+f" and typed in "pink mold". The result was Gliocladium roseum which is really a pink mold, but it is hard to find any image of it, where it is on fruits... So this is just a guess. Btw. I think it is rarely possible to identify microorganisms just by checking an image of them.


Measure of diversity, accounting for known species I'm interested in measuring the diversity of each sample out of many independent samples. I know a priori all possible species that could appear in a sample, and expect the counts of species to be from 0 to about 10, although often times there will be none of a particular species within a sample. For example, some data might look like:

Sample # | Species A | Species B | Species C
--------------------------------------------------
1          0           4           0
2          1           1           1
3          0           1           1
4          2           2           2
5          0           1           0

The most diverse sample here is #4. The least is #5. Theoretically, #5 would also be the least diverse ever encountered (assuming there is at least one of some species in each sample).

I encountered trouble when using Simpson's Index of Diversity since that formula would make the diversities of Sample 2 and Sample 3 both 1.0. Intuitively, with this data, I am confident that #2 is more diverse. This is because I know all possible species that may show up.

I'm relying on this definition:
$$
D = \frac{\sum n(n-1)}{N(N-1)}
$$

Are there measures of diversity which account for a priori knowledge of possible species (and perhaps their bounds) and expect near-zero counts?

Simpson's estimator, which assumes that sample frequencies are not population frequencies, is unbiased on the probability scale. As @fileunderwater noted, it can be helpful to quantify diversity in terms of effective number of species, or Hill numbers. On this scale (the reciprocal of Simpson's concentration in this case), Simpson's estimator is no longer unbiased. Chao and Jost 2015 recently proposed some estimators for Hill diversity that formally rely on the total richness (of the sampled community) to estimate the true diversity of the community based on the sample, and argue that they have reduced the bias.

I sense, however, this is not exactly the same as your question. If I understand correctly, you have a known maximum diversity but not a known true cardinality/richness/total number of types within a given community/corpus whatever the pool you're looking at is called. In this case I might use maximum richness as a Bayesian prior; I might still use a Hill number as your metric but use the model to estimate that metric.

This 2014 review paper gets into these ideas a bit, or to take an Alan Turing perspective, you might find Zhang 2017 helpful.

Most diversity indices that ecologists use are not sensitive to total abundance, only relative abundance, so as Remi.b noted, classic indices (including Hill numbers) would all rank even communities with the same cardinality/richness identically; the only reason you're getting a difference between {1,1,1} and {2,2,2} with Simpson's estimator has to do with Simpson's solution to the bias in estimates of the community's diversity arising from using sample frequencies.


If bortezomib, a cancer drug, inhibits cell proteasomes, wouldn't resulting protein aggregate in normal cells further increase the risk of cancer? Bortezomib is an anti-cancer drug that inhibits the proteasomes of cancer cells, allowing proteins that stop cell growth to fold and perform their function.

However, wouldn't bortezomib also affect the proteasomes of normal cells? If the proteasomes of normal cells are inhibited, the major factor in the regulation of unfolded and damaged proteins is gone. The resulting protein aggregate would lead to cell damage and diseases such as cancer, Alzheimer's and Parkinson's.

What is stopping bortezomib from affecting normal cells? Does it?

Proteasome inhibitors do affect normal cells to some extent, but the whole point of using them as cancer treatments is that (some) cancer cells are far more sensitive to proteasome inhibitors than are normal cells.  For example, multiple myeloma cells (the first clinical targets of Bortezomib) that overproduce immunoglobulins are dependent on proteasome degradation to eliminate them and are therefore sensitive to Bortezomib.  There are many other aspects of cancer cells that may make them more dependent on proteasome; see for instance

Proteasome inhibitors in cancer therapy: Treatment regimen and peripheral neuropathy as a side effect for some examples.

But of course there are effects on normal cells as well, such as the peripheral neuropathy mentioned in that review.


ID a shell from Puerto Rico I recently found this in Rincon Puerto Rico on the beach.

I assumed it was a baby sea turtle shell or some kind of turtle. Someone that frequents Puerto Rico said it was not. Does anybody know what this is?

This is the shell of a marine mollusk called a chiton.

They are also sometimes known as sea cradles or "coat-of-mail shells", or more formally as loricates, polyplacophorans, and occasionally as polyplacophores.

In Puerto Rico, they call these animals "Quitones."

All chitons bear a protective dorsal shell that is divided into eight articulating aragonite valves embedded in the tough muscular girdle that surrounds the chiton's body.

My initial guess as to the species is: Chiton tuberculatus.
 (Disclaimer: I know almost nothing about these animals, so this is at best a guess).

 Source: NATURAL HISTORY MUSEUM ROTTERDAM

 Source: NATURAL HISTORY MUSEUM ROTTERDAM
You can find additional images that look even more like your specimen here and here
According to Wikipedia:

This species can be found under rocks and in spray zones of rocky shores, in the intertidal, shallow subtidal zone of Western Central Atlantic (USA, Colombia, Bermuda, Mexico, Venezuela and the West Indies)

This includes Puerto Rico

Based on Fig 1 of Crozier (1918) showing typical sizes of various ages of C. tuberculatus, you have a fairly young specimen (likely only a few years old).
The Quitones of Puerto Rico by Cedar García Ríos (ISBN: 1-932271-16-3) is probably a good tool for definitively IDing your specimen to species.


metabolism in kangaroo rats Many documents (e.g., this, this, and this) state kangaroo rats are special because they can use water produced by metabolism. Is the metabolism of kangaroo rats more efficient in producing water than that of other organisms?

Or the metabolism mechanism of kangaroo rats is the same as other organisms, but kangaroo rats can subsist with little water produced by metabolism because they conserve water from various mechanisms?

Various adaptations help desert animals survive in dry and hot environments. These adaptations are not specific to Kangeroo rats in particular.

From Wikipedia :

  Metabolic water refers to water created inside a living organism through their metabolism, by oxidizing energy-containing substances in their food. Animal metabolism produces about 100 grams of water per 100 grams of fat, 42 grams of water per 100 g of protein and 60 grams of water per 100 g of carbohydrate.

  Some organisms, especially xerocoles, animals living in the desert, rely exclusively on metabolic water. Migratory birds must rely exclusively on metabolic water production while making non-stop flights. Humans, by contrast, obtain only about 8-10% of their water needs through metabolic water production.

  In mammals, the water produced from metabolism of protein roughly equals the amount needed to excrete the urea which is a byproduct of the metabolism of protein. Birds, however, excrete uric acid and can have a net gain of water from the metabolism of protein.

Also see Xerocoles - Water Conservation


Who and when was the first human diagnosed with hemophilia, or considered a carrier? The earliest case I can find is Queen Victoria of England, who ruled from 1837-1901. Is this the first hemophilia case on record?

The disease hemophilia has been known for much longer than that. At the time the Talmud was written, for example, it was known that if some boys in a family died from circumcision, the next were also at risk. This might have been because physicians recognized an inherited blood disorder.

Abulcasis, an Arab physicians of the 10th century, wrote about families in which male members died from bleeding out after injury.

In 1803, John Conrad Otto wrote about

  a hemorrhagic disposition existing in certain familie

Tracing the condition back three generations in that family named Smith, who lived in  Plymouth, New Hampshire. So there were definitely earlier cases where we even know the names of the patients, eben before the disease was named.

The word haemorrhaphilia, later shortened to hemophilia was first used in 1828 by Friedrich Hopff, before the birth of Queen Victoria.

Queen Victoria herself did not have the disease, though, she was a carrier. At least one of her sons had the disease and at least one of her daughters was also a carrier.

The history of hemophilia

History of Bleeding Disorders


Why we do not get hurt from HCl secreted in the stomach? I read in my book that during digestion our stomach secretes hydrochloric acid ($HCl$). Why we do not get hurt from it? It was also said that mucous provides protection, but from where is it coming?

Goblet cells.

These are specialized epithelial cells whose job it is to produce mucins. Mucous role is not only important in protecting the epithelium of the digestive tract from HCl, it is also a very important substance in the innate immune system, acting as a barrier defense to trap pathogens and/or prevent them from breaching the epithelium and gaining access to sterile parts of the body.


Why don't fish get hurt with so many sharp fish bones? Why don't fish get hurt with so many sharp fish bones? And why don't fish feel pain when they swim? Don't those sharp fish bones stick into the flesh while swimming?

Connective tissues prevent fish from being hurt by its bones. They surround the sharp bones so that the bones do not hurt its organs/flesh.

However Of course the bones can hurt the fish, but the situation is quite imaginable.

If a fish is smashed or gets too much force, its connective tissues cannot protect its organs much(like our clothes cannot protect us from bullets, or our broken bones penetrating our organs when we encounter a serious car accident despite our connective tissues covering the bones - the bones just damage our connective tissues and organs, and so on...) and its organs get hurt.

Your worry can happen in human case too (but much weaker version), we can think of our hip bones sometimes pressing our flesh between the bones and the chair we are on.


Can a color-deficient person be made to visualize the missing colors? Hope this is within the scope of this site.

Color-deficient persons lack the cells in their retina needed for differentiating some (or all) colors.

However, the part of the brain that actually processes images is not deficient.

Is it possible to somehow make a color-deficient person "see" the missing colors by directly activating that part of the brain responsible for processing colors?

It is a very interesting question and I did some efforts to investigate the literature on this topic, but yet I don't have a definitive answer for you. But let's start from the beginning.

First of all, the reason for color deficiency can be not only lack (rare) or impairment (more often) of certain types of color-perceiving cells (cones) in retina, but also brain injures: the central color blindness can develop after head trauma or as a result of some neurodegenerative deceases, like Parkinson's decease. In case of brain origin of the color blindness it is usually the complete color blindness (no color is percieved), whereas congenical primary color blindness (receptor-based) is usually just the unability to distinguish one or two colors, whereas the rest can be more or less separated.

I searched Pubmed for the literature on the topic and found a recent PNAS paper about the simulation of primary and secondary visual cortex on humans using intracranial electrodes. As they describe their results (bold font by me):

  When percepts were elicited from late areas, subjects reported that
  they were simple shapes and colors....

But the paper investigated only healthy humans, no color impaired subjects were used for the tests, so cannot conclude from here whether we can elicit the perception of the color the person is incapable to see with the eyes using these stimulations.

I took this paper as the starting point and did some reference research, looking for the paper referenced there and for newer publications referencing this one: PNAS is one of the top journals in this area with very high impact factor and if there were a publication about brain stimulation and color blindness I would have definitely identified it.

During my investigations I came accross a series of interesting articles devoted to "cortical visual neuroprosthesis for the blind" (read this paper<1> from 2005 for review on this topic), but this is the treatment of conventional blindness, not the color blindness. There was no intersection in keywords or titles for color blindness and brain stimulation, both in the referenced articles and in the complete article database.

So, I would suggest that you address some talented experimentalist with your question and maybe one day, who knows, we will read your name under the Nature article dedicated to the novel way to cure color blindness.

<1> -- unfortunately not available publicly for free, I am sorry.


What is this insect? 6 legs and black spots What is this bug?

Details:
 - Georgia, (Southern) USA
 - Maybe 1-4cm in size
 - Seen near an open area/crack between an outer door-frame and door where it could have come from outside, or going from inside to outside since the temperature difference was noticeable in this area.

Thanks in advance!

(Note: I'm going to be using the British English "ladybird" instead of the US English "ladybug" in this answer.)

This is a clearly a species of ladybird. Going by the number of spots, their size and not-perfectly-round shape, the positioning of the four central spots relative to the others, and the fact that its background colour isn't bright yellow... I'm pretty sure it's Harmonia axyridis, the species that us Brits refer to as a "Harlequin ladybird". I think Americans refer to it as an "Asian ladybug" or "Asian ladybeetle".

The spot patterns for this particular species vary a lot, as to some extent do the colours, so I've googled for images to support this answer. The below picture was posted to:

https://en.wikipedia.org/wiki/File:Harmonia_axyridis01.jpg

and is the IP of a user or organisation called Entomart. On the Wikipedia page and on their homepage, Entomart grant permission for the use of the image as long as they are given proper attribution, so I'm able to include it in this answer:

For more pictures of the Harlequin (again, showing how much the spot pattern and colouration vary), see:

https://scx2.b-cdn.net/gfx/news/hires/2018/amechanismof.jpg

For pictures of other ladybird species to compare the Harlequin with - as also one more of the Harlequin:

https://www.naturespot.org.uk/taxonomy/term/19357

Thanks for posting this question! I didn't expect to see a ladybird on Christmas Day :-)


Why does mouldy food make you sick? Bread gets mouldy pretty quickly. My parents (both of whom are nurses) throw out a loaf of bread after a spot of mould is seen (because "if you can see one spot, it means the whole thing is covered in mould spores") because they say you'll get sick if you eat it. The USDA also has a handy chart on it's mould page telling you when you should discard food with mould on it.

Is it the mould itself that makes us sick or is it something that the mould is releasing?

What are the mechanisms that cause us to feel sick after eating mouldy food?

The USDA says that there can also be bacteria along with the mould on the the food - is this what is really making us feel ill?

One of the most common toxins in mouldy food/bread is aflatoxin.

The exposure to high amount of aflatoxin can lead to acute aflatoxicosis with fulminant hepatic failure and even death.

While mild exposure to aflatoxin could be asymptomatic, it is better not to take a chance considering possible complications (citation from the link above):

  Aflatoxins produce acute necrosis, cirrhosis, and carcinoma of the
  liver in a number of animal species; no animal species is resistant to
  the acute toxic effects of aflatoxins; hence it is logical to assume
  that humans may be similarly affected. A wide variation in LD50 values
  has been obtained in animal species tested with single doses of
  aflatoxins. For most species, the LD50 value ranges from 0.5 to 10
  mg/kg body weight. Animal species respond differently in their
  susceptibility to the chronic and acute toxicity of aflatoxins. The
  toxicity can be influenced by environmental factors, exposure level,
  and duration of exposure, age, health, and nutritional status of diet.
  Aflatoxin B1 is a very potent carcinogen in many species, including
  nonhuman primates, birds, fish, and rodents. In each species, the
  liver is the primary target organ of acute injury. Metabolism plays a
  major role in determining the toxicity of aflatoxin B1; studies show
  that this aflatoxion requires metabolic activation to exert its
  carcinogenic effect, and these effects can be modified by induction or
  inhibition of the mixed function oxidase system.


The role of duration of infectiousness in SIR models I refer to J.H. Jones' Notes on R0.

The basic SIR model - as described in Jones' Notes - considers three factors that make up the reproduction number:

$\tau$ = the transmissibility (i.e., probability of infection given contact between a susceptible and infected individual)
$\overline{c}$ = the average rate of contact between susceptible and infected individuals
$d$ = the duration of infectiousness

The (basic) reproduction number then is

$$R_0 = \tau \cdot \overline{c} \cdot d$$

The duration of infectiousness enters the basic SIR model as the so-called removal rate $\nu$ which is nothing but the inverse of the duration of infectiousness: $\nu = 1/d$:

$\frac{ds}{dt} = -\beta s i$

$\frac{di}{dt} = \beta s i - \nu i$

$\frac{dr}{dt} = \nu i$

with

$s$ = the fraction of susceptible persons
$i$ = the fraction of infected persons
$r$ = the fraction of removed persons (recovered or died)
$\beta = \tau \cdot \overline{c} = R_0/d$ = effective contact rate or infection rate

  My question concerns the way that $d$ enters the SIR model, because I
  find it not so plausible:

  to consider all persons that are infected today and take a fraction $\nu$ of them that will have recovered tomorrow.

  Wouldn't it be much more plausible

  to consider all persons that became infected $d$ days ago and let these be recovered tomorrow?

The latter approach would be especially valid when the death rate can be neglected, i.e. when "removed $\approx$ recovered".

My impression is that most papers using a variant of the basic SIR model let enter the duration of infectiousness in the first way - leading to significantly different predictions than in the second case.

I implemented both and this is the difference (only due to the different ways that $d$ enters the progression formula, i.e. the values of $\beta$ and $d$ are fixed):

(In case that you wonder why the curves oscillate: I have modelled some sort of acquired immunity with finite duration of only some month - but in the very same way in both cases.)

My question concerns the way that $d$ enters the SIR model, because I
  find it not so plausible:

  to consider all persons that are infected today and take a fraction $ν$ of them that will have recovered tomorrow.

Well, it is in fact not very 'realistic' as you point out, but in the assumptions of the model, we see that the population has no structure (it is well-mixed, constant) and there are no birth-death events. So, in this case, it is not so problematic to take $v$ as a constant across the entire simulation, because what you are trying to calculate is the rate at which the three sub-fractions of $N$ ($s$, $i$, and $r$) change, not really which individuals are moving from one class to another (which you cannot really know anyways, if you talk about fractions of $N$).

  Wouldn't it be much more plausible

  to consider all persons that became infected $d$ days ago and let    these be recovered tomorrow?

So, considering my previous comment, it would not make much sense really to take a time-delay form on $d$, because you cannot really know which individuals got infected at any given point, you can only talk about fractions of $N$ (there is no population structure, as they say in the model formulation). So, the fact that your formulation seems to have a slower dynamics might not be very informative, because what you did is simply applying $d$ to a fraction-of-the-fraction of the population classes, so it makes sense mathematically that it runs slower, but as per the model formulation it does not make much sense, unless you have population structure defined from the beginning (which in this case is not), and unless you can explicitely know individual-per individual class transitions. In fact, I believe that taking the fraction-of-the-fraction would lead to an artifactual 'undercounting' of these individuals that actually needed to be in the $i$ class (and overcounting of the other classes).


Detect which antigen binds to IgE Assume that a patient has chronic hives (itchy) on the skin. I understand that he has an antigen, which binds to IgE and eventually triggers histamine release, causing an allergic reaction. So is there any method to detect which molecule/antigen has bound to his IgE? (can we capture it with like what we do to obtain a 3d protein/molecule structure?)

From what I understand most allergies are detected by a scratch test. from the link below:

"A skin prick test, also called a puncture or scratch test, checks for immediate allergic reactions to as many as 40 different substances at once. ... After cleaning the test site with alcohol, the nurse draws small marks on your skin and applies a drop of allergen extract next to each mark. He or she then uses a lancet to prick the extracts into the skin's surface. A new lancet is used for each allergen. ...About 15 minutes after the skin pricks, the nurse observes your skin for signs of allergic reactions. If you are allergic to one of the substances tested, you'll develop a raised, red, itchy bump (wheal) that may look like a mosquito bite"

More information on scratch tests can be found here:

http://www.mayoclinic.org/tests-procedures/allergy-tests/basics/what-you-can-expect/prc-20014505

After a quick google search,I found a paper from 2014 [1] that seems to speak to the essence of what you are asking, link below.

http://www.tandfonline.com/doi/abs/10.1586/14737159.4.4.539 [1]

In the paper above they propose using a protein microarray technology to find allergies.

I am not sure if there is any way to extract the igE-antigen complex from the patient. But I think it could probably be done with the microarray technology. Although it would be cool to see a picture of the complex.
I hope I have helped answer your question.

[1] Harwanegg, Christian, and Reinhard Hiller. "Expert Review of Molecular Diagnostics." Taylor and Francis Online. Expert Review of Molecular Diagnostics, 09 Jan. 2014.


How did the first self replicating organism come into existence? When people try to explain evolution, they tell me that evolution is a cumulative result of mutations & natural section of the more superior individuals of a particular species. I think I'm fairly convinced with this explanation.

But when I think about it, all of them assume that there was an organism, however simple, that was capable of self replication & occasionally mutate. How did such an organism come into existence? Can anyone explain this?

An answer I found on Reddit didn’t really convince me.

Evolution or (as Darwin called it) "descent with modification" is a theory which explains the origin of the species NOT the origin of life.  How the first life arose is completely irrelevant to the theory of evolution.  What evolution does explain is how and why we have such variety of life on earth all descending from the same organism.

What you're asking about is not a theory of "evolution" but rather a theory of "abiogenesis."  Although there are many interesting hypothesis for how abiogenesis happened (e.g. the RNA world, the "metabolism first" theory, etc.), the fact is we simply do not know yet how life first arose.  What we do know is that life first arose between 3.5 and 3.9 billion years ago.  That's a really long time ago compared to lots of other important events in natural history (even the Cambrian explosion where modern animal phyla evolved was only half a billion years ago), and so it shouldn't be surprising that it's a hard problem.


What causes humans to be sleepy? Is there a hormone or group of hormones that regulates when we feel sleepy late at night, or in the morning?  Or is sleepiness caused by some other non-hormonal mechanism?  (e.g. pure psychological, or neuronal.)

The release of the hormone melatonin is responsible for the feeling of sleepiness. It is released by the pineal gland and production starts when the light fades, as it's production is inhibited by light stimulation of the retina, the onset of the production is called dim-light melatonin onset. Artificial supplementation can increase sleep quality and regularity related to some sleep disorders and is often administered as pills or patches.

Adenosine is an inhibitory neuromodulator, ie it inhibits neural activity. Neural activity can be either excitatory or inhibitory and adenosine more strongly inhibits the excitatory neural activity. Thus, increased adenosine levels should decrease excitatory effect of nervous stimuli and make you feel more relaxed & sleepy.

Other hormones & neural pathways may be involved (serotonin and the serotonergic neural pathways for example) as well as other stimuli like other people's behaviours (yawning, stretching etc.).

This page and the wiki entry on melatonin have much more information.

From sleepfoundation:

  Melatonin is a natural hormone made by your body's pineal gland - a
  pea-sized gland located just above the middle of the brain. During the
  day the pineal is inactive. When the sun goes down and darkness
  occurs, the pineal is "turned on" and begins to actively produce
  melatonin, which is released into the blood. Usually, this occurs
  around 9 p.m. As a result, melatonin levels in the blood rise sharply
  and you begin to feel less alert. Sleep becomes more inviting.
  Melatonin levels in the blood stay elevated for about 12 hours - all
  through the night - before the light of a new day when they fall back
  to low daytime levels by about 9 a.m. Daytime levels of melatonin are
  barely detectable.


Why did the Brain develop in the front in most organisms? I was wondering: why most, well, pretty much all organism with a brain have it right in front of their bodies or at the top.

TL;DR Visual and auditory systems are crucial for survival, especially in higher animals. Also, visual/auditory systems have great number of cells. For processing to be effective, it should be performed closer to data acquisition (eyes).

First of all, for example, in mouse or human, central nervous system includes brain and spinal cord. Since spinal cord is extremely important at regulating different physiological processes as well as in performing complicated motor tasks, it would be unjust to not think about CNS as a whole.

If you talk only about brain part of CNS, it makes sense to locate important processing pathways near sensitive organs for two reasons. First, it saves material on running long axons from many sensory cells. Secondly, longer axons deliver information slower. If there is a sense that is important for survival, than information in that modality must be delivered and processes as quick as possible.

In comments to the question @anongoodnurse mentioned that "butterflies 'taste' with their feet". I would argue that a) taste in butterflies is not vital for immediate survival and b) number of taste buds is very limited, whereas retinal cells are count up to more than thousand per eye.

But what about humans? We also able to "taste with our feet", e.g. feel temperature. For survival it is crucial to be able to escape hot surface as fast as we can. And we do, thanks to a direct reflex arc going from sensory cells to spinal cord and motor neurons. Which brings back point about CNS as a whole system. Crucial information and immediate decisions are made closer to sensitive organs.


What is this vinca like vine? What is this vinca like vine? Is it poisonous? 62521 USA Illinois

Wintercreeper, Euonymus fortunei

Given that you're just over in Illinois, here's the page from our Plant Finder database.

In regards to your second question, this factsheet from UMich mentions (and gives citations) for its use as a medicine. Given that, I'd avoid eating it if I were you, but there's not mention of it being especially toxic.


Larva of Halyomorpha halys? I just found these small insects on a Saponaria.

After search, it could be Halyomorpha halys, but I am really not sure.

Can anyone confirm? If so, should I kill them as they are considered as agricultural pest?

They are about 3-5mm. I am living in the south of Paris (48.814766, 2.334659)

This is an instar (nymph) of a shield or stink  bug (order Hemiptera, family [Pentatomidae])(https://en.wikipedia.org/wiki/Pentatomidae).

This appears to be similar to the 2nd (or possibly 3rd) instar of Halyomorpha halys.

European and Mediterranean Plant Protection Organization; Credit: Matteo Maspero

UTIA suggests the 2nd instar begins to develop an almost black appearance, where that blackness gradually shifts to browner shades in subsequent instars. According to Medal et al. (2013)1 the 2nd and 3rd instars have median lengths of ~2.75 and ~4.25 mm, respectively. According to WSU Extension, instar nymphs of H. halys are spiny (including on the shoulders) and possess light bands on the antennae.

 Source: WSU Extension

This University of Wisconsin Extension site provides a fairly similar photo to your specimens, which can be found at bugguide.com:

 Source: bugguide.com; Credit: Yurika Alexander

 Citations

1  Medal, J., Smith, T. and Santa Cruz, A., 2013. Biology of the brown marmorated stink bug Halyomorpha halys (Heteroptera: Pentatomidae) in the laboratory. Florida Entomologist, 96(3): 1209-1213. PDF


Bacteriophages and their role in genetic editing? I know how plasmids and restriction enzymes work to change the dna of a bacteria cell, but I do not really understand how a bacteriophage works to edit the genome of a cell. Is it related to crispr since its a virus which inserted genetics in bacteria? Also, is it during the lysogenic or lytic stage that the bacteriophage alters the DNA?

As explained in the Wikipedia page that you have linked to, transduction is the name given to a particular phenomenon whereby phage can be used to move bacterial DNA between cells.

Depending upon the phage, some aberrant or infrequent process can result in the packaging of host cell DNA into a phage particle during a lytic cycle. The resulting defective phage particle is still infective however, and when it infects a new host cell it injects the bacterial DNA that it is carrying. This DNA can then recombine with the host DNA.

So, for example, if the second host was a lacZ mutant but the parent host was lacZ⁺, then it would be possible to select lacZ⁺ in the second host.

Transduction was an important tool in E. coli genetics. Phage P1 can be used for general transduction, which means that any piece of DNA can be moved. As I said in my comment: anything that can happen will happen.


When is an ant colony at its loudest? I want to make a sound recording of an ant colony located in a wood pile in a German forest (I don’t know the exact species).
To optimise this, I would like to select a time for this when the ant colony is at the height of its activity, i.e., loudest.
My naïve guess would be that noon in summer with some time after the last rainfall is best, but I could find anything to confirm or go beyond this.

Thus I am asking: When is an ant colony loudest, more specifically:

What time of the year?
What time of the day?
What weather conditions?

I believe you speak of some species of Formica spp., such as Formica polyctena (nest example)

You should mind that (i) ants are not particularly noisy insects; (ii) ant nests are 3-dimensional structures within which ants are heterogeneously distributed. So considering a microphone somewhere on the nest where you happened to see more ants, mostly you will be picking up noises from foragers stumbling into debris while moving around. And that only when that region of the nest happens to be most active, which was your original concern. In case I am wrong and you're interested in some smaller ant species (e.g. Solenopsis fugax or Lasius flavus) then you will probably record few if any significant sounds resulting from ants' activities.

Thus my first advice if you're focusing on foragers moving around the nest surface is that you record them in the afternoon of your hottest days, particularly if they're refurbishing their nest or upon disturbance. If you leave the microphone for extended periods try to find out where most foragers are coming out from (and pray they'll not damage the equipment) and leave it there in the afternoon of a dry, hot day.

Now, I am not sure about your ultimate goal, but in case you want to actually hear the ants instead of their stumbling around, then you should focus on having a tiny (protected) microphone inserted into a nest chamber. It is hard to say when the insides of a nest of unknown species will be particularly active, but usually during a fair day, under the sunlight exposure following a wet night. Finding the best region to record ants stridulating inside their nest will depend on finding the best nest location(s) and equipment.

Good luck!


What is the state of automated quantitative analysis? Quantitative analysis of microscope images is essential for many types of studies, but the techniques used most often are very labor-intensive. I have been able to find some literature about using computers to perform the analysis, but do not have a good picture of the state of the art.

Is there a good literature review on the topic?
Is there much use in practice which I have not yet seen?

The word to look for is 'Image segmentation'. But also here, it very much depends on what you're looking at. Segmentation and quantification of simple fluorescence images is relatively easy and widely used. It can get very complex depending on how complex the structure is you're looking at. There are machine-learning approaches which are able to distinguish complicated structures from each other, such as different mitosis states.

Segmenting Hematoxylin-Eosin (HE) stained specimens is subject of intensive bioinformatical research. One goal is to assist pathologists in grading tissue lesions, such as in prostate cancer, but this is as far as I know not used clinically yet. Whole-slide scans of histological specimens are becoming more widely used clinically. These images are very huge (1 GB per specimen), so a research focus is also to provide a large-scale analysis of these whole-slide scans.

Also, take a look at CellProfiler (http://www.cellprofiler.org), this free open-source software saved my PhD project.

Literature I found:

Tabesh, A., M. Teverovskiy, et al. (2007). "Multifeature prostate cancer diagnosis and Gleason grading of histological images." IEEE Trans Med Imaging 26(10): 1366-1378.

Petushi, S., F. U. Garcia, et al. (2006). "Large-scale computations on histology images reveal grade-differentiating parameters for breast cancer." BMC Med Imaging 6: 14. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1634843/

I cannot provide you with a recent review, though...


Needing help in order to infer the statistical hypothesis tests performed in an old paper I am in great need of help in order to infer the statistical hypothesis tests performed in an old paper. However I need to make some reasonable guesses only from the abstract of the paper since the original text is in chinese which i can not understand (after extensive search i was also unable to find the original text even in chinese)

The title of the paper is:
“Detection of sister chromatic exchange in workers exposed to coal tar pitch and to coke oven volatiles"

The abstract of the paper (which was published in 1998 is the following):

In order to know the changes of genetic toxicological effects on workers occupationally exposed to polycyclic aromatic hydrocarbons (PAHs), sister chromatic exchange(SCE) was detected by the methods of peripheral lymphocyte culture in 23 workers exposed to coal tar pitch (CTP) and in 19 workers exposed to coke oven volatiles (COV) and 12 normal controls. The results suggested that the SCE in occupational workers was significantly higher than that in controls (11.31 vs 6.37, P < 0.001). The SCE in workers exposed to CTP and to COV was higher than that of control (10.27 and 12.58 vs 6.37) respectively. In workers exposed to CTP and COV, there were no differences of SCE for smokers and nonsmokers (P > 0.05). It is indicated that CTP and COV caused strong genetic toxicity and injury to chromosome.

In your opinion how do you think that the above reasarch was organized

For example: a) What types of statistical hypothesis testing was performed by the reasearchers b) What kind of data was collected and used for each statistical hypothesis test c) What methods were employed for the each hypothesis test ?

Someone else can probably elaborate on how "peripheral lymphocyte culture" works, but this is what the statistical results suggest to me:

  The results suggested that the SCE in occupational workers was significantly higher than that in controls (11.31 vs 6.37, P < 0.001).

This is a two-sample t-test. Occupational workers were pooled into one group and the mean value of SCE for those workers (11.31) was compared to controls (6.37). The null hypothesis is that the means are not different. They reject the null hypothesis. It would be nice if they included the standard errors for the means, so that you would have a sense for the amount of variation within the groups.

  The SCE in workers exposed to CTP and to COV was higher than that of control (10.27 and 12.58 vs 6.37) respectively.

This is likely an ANOVA with three groups (CTP, COV, and control). This test is kind of redundant with the first test, since the appropriate post-hoc test will tell you that CTP and COV are both significantly higher than control. But since they report only one P-value, then this is probably the overall F-test for the ANOVA. So all they can say with this test is "at least one group is different." You don't know if, for example, CTP and COV are different from one another. It's not clear from the text that they did a posthoc test (Tukey's HSD, for example), but I doubt it.

  In workers exposed to CTP and COV, there were no differences of SCE for smokers and nonsmokers (P > 0.05).

Considering only the occupational groups, the sample is divided into smokers and non-smokers. There was no significant difference in mean SCE between the groups. This is a two-sample t-test like the first one. The null hypothesis is that the means are not different. They fail to reject the null hypothesis.

It's also possible (but impossible to determine from the abstract alone) that they did a single, larger multiple regression. Properly coded, they would be able to, at once, test for occupational vs. control, CTP vs. COV vs. control, and smoker vs. non-smoker. It would be pretty dicey with such a small sample, so they probably didn't take that approach.

Why do we perform t-tests?

The null hypothesis of a two-sample t-test is that the means of two groups are not different from one another.

How do we know that our data follows a normal distribution? Shouldn't we perform tests in order to decide whether our data follows normal distribution and is of equal variance?

Assumptions of t-tests include normal distributions within groups and equal variance between groups. These should be checked prior to carrying out the test. We can assume that the authors did these tests, but they are very rarely reported.

In case the criteria needed to perform a t-test are not fulfilled should we choose a non parametric equivalent?

Non-parametric alternatives should be considered when the assumptions are not met. That being said, t-tests are pretty robust to violations of these assumptions.

Also the anova mentioned in the answer above is an N-way anova?

ANOVA in general is a test of equality among N groups. So you could think of a t-test as just a special kind of ANOVA on two groups (indeed, they are numerically equal).


Can ribosomes read ssDNA? My question is whether translation can be done, either naturally or artificially, through a ribosome reading (single-stranded) DNA directly. If not, I would like to know what allows ssRNA to be translated but not ssDNA.

Summary

Messenger RNAs that are recruited to the ribosome for protein synthesis in vivo, need to satisfy particular structural requirements and must interact with the protein initiation factors that deliver them to the ribosome. Generic single-stranded DNA (ssDNA) does not have these structural characteristics and so cannot be translated on ribosomes under natural conditions.

A single reported attempt to translate deoxyribose-based analogues of these mRNAs under conditions equivalent to those within the cell was unsuccessful. Thus, although experiments suggest that ssDNA may be able to bind transfer-RNA and allow some polypeptide synthesis under non-physiological conditions, this reflects only those aspects of protein biosynthesis that involve base-pairing interactions between the message and other RNAs involved in translation. In contrast, the stages involved in the selection of the first initiation codon and the recognition of termination codons involve interactions between protein factors and the message, where recognition of a hydroxyl group in the 2ʹ-position (and discrimination between thymine and uracil) may well occur and would prevent translation of a synthetic ssDNA message.

If, in fact, no discrimination against DNA has evolved for the ribosomal- and transfer-RNA components of the translation apparatus, this may be because the system arose in an ‘RNA World’ before DNA evolved, and because free ssDNA in the cell has never been a competitor with mRNA for ribosomes, especially after sophisticated protein-based systems arose for the selection of the appropriate initiation codon.

Contemporary physiological interactions of mRNA with ribosomes

Translation of mRNA by ribosomes (protein biosynthesis) is a complex process which can be divided into a number of stages, each generally involving a variety of RNA and protein molecules — initiation factors (IF), elongation factors (EF) and termination or release factors (RF). The reader who is not familiar with this is advised to read a text-book account such as that in Chapter 29 of Berg et al.. However, to summarize briefly, they are: selection of the correct AUG (usually) on the mRNA for initiation, IF-dependent binding of the initiator-tRNA to the P site, EF-dependent and codon-directed binding of an elongator-tRNA, peptide bond formation catalysed by the large ribosomal subunit, EF-dependent translocation, and eventually stop-codon directed and RF-dependent release of the completed polypeptide chain.

The first step, is crucial for the binding of natural mRNAs — the subject of this question. Under natural cellular conditions prokaryotes and eukaryotes have different methods of ensuring that the ribosome interacts with the correct mRNA codon to start translation. In prokaryotes a specific ribosome-binding signal (Shine and Dalgarno sequence) must interact with the 16S rRNA and a particular initiation factor protein is involved in this step. In eukaryotes the main method is recognition of a modified 5ʹ structure on the mRNA and unwinding of secondary structure, also modulated by protein initiation factors.

I am aware of one report of an attempt to translate a DNA-based analogue of such natural mRNA structures under any conditions. This was by Damian et al.  (Biochim. Biophys. Res. Commun 385, 296-301 (2009)), and was unsuccessful, even though physical methods indicated binding to the ribosome. I imagine that recognition by the protein initiation factors did not occur but I cannot be sure that base-pairing to the 16S rRNA was also hindered.

Regardless, one can answer the question posed:

  The fact that ‘random’ single-stranded DNA would lack the structural features for selection of the correct initiation codon
  explains why it would not be translated under natural
  conditions — it could not bind to the ribosome.

Artificial systems of protein synthesis

The full details of the reactions on the ribosome only emerged gradually. Nevertheless the lack of understanding of the features of natural mRNA required for binding to the ribosome did not prevent either the dissection of subsequent steps of protein biosynthesis, nor the use of ribosomal systems to decipher the genetic code. This is because it was possible to bypass the initial steps by using suitable unphysiological conditions, that allowed polynucleotides or oligonucleotide triplets to bind to the ribosome, where further reactions were possible, albeit generally less efficiently than in the cell. Such conditions included high concentrations of magnesium ions and certain antibiotics that affect the accuracy of protein synthesis. It has been suggested that the neutralization of the charge on the backbone phosphates of the RNA by Mg2+ enhances (non-specific hydrophobic interactions at the mRNA-binding channel, and that the antibiotics stabilize a state of the ribosome in which amino-acyl tRNA can bind more easily (and hence promote the binding of polynucleotides by base pairing). Once bound with the codons hydrogen-bonded to the cognate anticodons of tRNA, subsequent elongation reactions depended on components of the ribosome other than the artificial messenger.

Thus, it was that the genetic code was deciphered using bacterial cell-free systems to which were added simple synthetic polynucleotides, lacking Shine and Dalgarno sequences or start (or stop) codons; and by experiments in which amino acyl-tRNAs were bound to triplet codons in the absence of both IFs and EFs. Other partial reactions of protein synthesis were similarly dissected artificially — the peptidyl transferase reaction was studied on isolated 50S subunits using just a fragment of tRNA and puromycin by conducting the reaction in 50% ethanol!

Experiments with single-stranded DNA

Understanding that ribosomes can be induced to bind and translate ‘non-mRNA’ oligo-ribonucleotides under certain artificial conditions, we are in a position to consider the significance of reports of translation of oligo-deoxyribonucleotides — ssDNA.

The original experiments in this area by McCarthy and Holland in 1965 showed that denatured DNA from various sources (including animal cells) could stimulate the incorporation of radioactive amino acids in a bacterial cell-free system, but this depended on the presence of antibiotics. Furthermore, it was shown in Khorana’s lab that only certain synthetic poly-deoxynucleotides  (analogous to the poly-ribonucleotides he used to decipher the genetic code) were active. Thus, it would appear that under the non-physiological conditions that favour promiscuous binding of poly- and oligo-ribonucleotides, there is some binding of ssDNA, and subsequent translation.

A paper by Ricker and Kaji mentioned by @Mesentery — reports that oligodeoxynucleotides could function in some partial reactions (fmet-tRNA binding) although not in others. In particular it was not possible to perform RF-dependent termination reaction with oligonucleotides containing termination codons, but — in the presence of antibiotics — termination independent of release factors did occur.

It is, thus, obvious that these experiments in which ssDNA is translated on ribosomes have no physiological significance. However it is still pertinent to ask the complement to the question of the poster, why does the system work at all?

Why are deoxyribose (and thymine) not discriminated against under artificial conditions?

Enzymes of synthesis and degradation of nucleic acids — RNA and DNA polymerases; ribonucleases and deoxyribonucleases — are specific for either RNA or DNA (or in some cases DNA/RNA hybrids). This is both important to ensure they fulfil their specific functions, and perhaps an inevitable consequence of the nature of their reactions — the making or breaking of sugar–phosphate bonds. Here we are dealing with catalysis by a protein enzyme that binds these structures at its active site.

In contrast, those reactions of protein synthesis for which certain requirements may be relaxed under non-physiological conditions involve base-pairing interactions. In modern ribosomes they may be optimized by associated proteins, but it is thought that the latter only evolved later. Artificial conditions, such as high concentrations of magnesium ions or antibiotics, may be thought of as allowing the essential interactions that existed in ‘ur-ribosomes’. And, of course as DNA/RNA hybrids readily form, the participation of DNA in such interactions is not so surprising. (In the RNA world of ‘ur-ribosomes’ — or even an RNA/protein world — there would be no need to discriminate against DNA, because it had not yet arisen. And chemically, the substitution of a hydrogen for a hydroxyl group could not hinder an interaction — at the worst it would only weaken it.)

It is pertinent that the contemporary AUG-selection and termination reactions depends on RNA–protein interaction. These might well involve recognition of ribose as well as base sequence, explaining the observations by Ricker and Kaji, and by Damian et al., mentioned above.


Why do we have two eyes? Humans, animals and birds all have two eyes. Why? In addition to why two instead of one, why aren't there more than two?

First, it's not true that all animals have two eyes. For example many spiders have four, six or eight eyes whilst worms have none, but all are animals.

In simple terms, the reason typical mammals have two eyes is probably similar to the reason that cars usually have four wheels, the reason houses keep out the rain and why coffee cups have handles. It's because that's what works.

Each time an organism develops, there is a high chance that the genetic information that built it will include something new. When that happens, most often the phenotype (essentially, the organism's appearance, such as how many eyes it has) does not change. The organism looks the same as its parent(s) did. If something significant does change, it is most likely to be bad news for the new organism. The chances are the organism will not survive and the particular genetic information that built it will not used again. Hence, organisms don't tend to be that different to their parent(s). Dogs don't give birth to cats.

But just rarely, this new combination produces something different and useful - useful enough that the organism is particularly successful and a good fit for its environment. In that case, simply because it can, the organism has more offspring and more of those offspring themselves survive to have offspring of their own. The genetic information that built the organism is thus used to create more, similar organisms.

So, the first eyes were produced by accident. When eyes turned out to be useful, subsequent generations from the first organism with eyes were more likely to have eyes themselves. As it turns out, analysis of genomes shows that eyes have evolved like this multiple times.

We can only assume that since mammals typically have two eyes, either the random genetic accident that would produce different numbers of eyes in mammals has never happened, or if it did happen, the result was not a good fit to the environment.

Why not no eyes? Human beings are occasionally born without eyes and the cause may be genetically inherited. One might reasonably imagine that for much of human history such a child would be unlikely to survive into adulthood and thus pass on this mutation.

Why not one eye? One reason in the case of primates is that two eyes are useful for estimating distance, which is difficult with one eye. A two-eyed animal has an advantage against predators, making it more likely the next generation is going to have two eyes.

Why not more than two eyes? Perhaps a larger number of eyes requires a larger head making childbirth impossible, or perhaps it requires too much energy to sustain. Who knows? What we observe today - humans typically have two eyes - means that, if that mutation for more than two eyes did happen at some stage, then more than two eyes wasn't optimal for the environment in which the resulting organism found itself, so it didn't get passed on to the next generation.


Why does walking mitigate the urge to urinate? When feeling a strong urge to urinate humans tend to walk around when e.g. waiting for the current bathroom occupant to get out. Why is that?

This is what we call a displacement behaviour (or displacement activity, the term used by Konrad Lorenz - see below). Funnily enough, that's exactly the same general mechanism involved in the behaviour described in my previous answer here at Bio SE.

In short, a displacement behaviour is a behaviour that occurs when the animal (human beings are animals, of course) faces itself in a situation of conflict: you want to urinate, but you are inside a train, or in a concert, or in the theatre during the best moment of that movie, or the bathroom line is simply too huge.

In that moment, you realize that you need to hold it a bit longer. That's when you start your displacement behaviour.

When people need to hold a very strong impulse to urinate, the most common movements/behaviours are:

stamping the feet
squirming
walking, as you said
humming

Therefore, walking is just one among several behaviours we show when we need to urinate but we can't: there is nothing special with walking in this situation.

Another common displacement behaviours that humans show in other situations are scratching the head, rubbing hands, drumming the fingers or biting the nails.

Konrad Lorenz explains displacement behaviours in his The foundations of Ethology:

  When two conflicting motor patterns are activated simultaneously, it can happen that the organism performs a third pattern which may belong to an altogether different system. This curious effect was first described in avocets, Recurvirostra avisetta, by G. F. Makkink, the Dutch ornithologist who called the movements thus elicited "sparkling-over" activities (Über-sprungbewegungen). The accepted English translation is "displacement activities". Although "displacement" means something entirely different in the psychoanalytical literature, this term will be used here.

Further down, giving examples of displacement behaviours in human beings, he says:

  Locomotion, too, is often disinhibited in conflict situations; some people tend to walk restlessly to and fro while delivering a speech, and so on.

Sources:

En.wikipedia.org. (2017). Displacement activity. [online] Available at: https://en.wikipedia.org/wiki/Displacement_activity [Accessed 1 Jul. 2017].
Lorenz, K. (1981). The foundations of ethology. New York: Springer-Verlag New York.


Identification of an unusual tree Location : Lyon, France

I think it's one of the laziest trees I've ever seen XD

As Sudachi has commented it has been pruned, probably over many years, to take on this form. It is not natural shape.

I would say that it is not possible to identify the exact species of tree without a close up of the leaves. From zooming in it looks like it could be a Lawson Cypress (Chamaecyparis lawsoniana) although it could be a Leyland Cypress (x Cupressocyparis leylandii), or a number of other possibilities.

One way to investigate this further if you want to know for certain, apart from posting a close up of the foliage which may help, would be to find some specimens of cypresses that you can find the name of. Perhaps in a garden centre or an arboretum, then compare the smell of the foliage when you pinch and crush it between your fingers. Different species have a characteristic smell that is a useful method for identification.


Why does milk contained in cartons of milk expand? In the morning, I went to the fridge to drink some chocolate milk. At night, when I took out the same carton of milk, the packaging seems expanded, like some kind of air is inside. Explain please !

The likeliest culprit here is fermentation carried out by bacteria present in the milk. Fermentation of a sugar, for example glucose, releases carbon dioxide (a gas) :

$$C_{6}H_{12}O_{6} \rightarrow 2 C_{2}H_{5}OH + 2 CO_{2}$$

Since this reaction produces a gas, the gas builds up in the milk carton causing it to bulge. This is not, generally, a good sign, make sure to smell the milk before drinking it!


Are bees positively phototropic One day I had found some bees have come around the light source like other positively photo tropic insects, I hadn't seen any bees coming over light before. I think bees are diurnal and they don't leave their nest at nights, I also read from an article that parasitic wasps may attack bees and these attacked bees would lose their mind and leave their nest at nights.

Is this possible or any other reason behind the night travel of bees and their positive photo tropism ?
http://en.wikipedia.org/wiki/Apocephalus_borealis

Honey bees rely on the position of the sun (and the ephemeris function) to navigate and communicate (i.e. the waggle dance). If they are out too late in the day to return to the hive (occasional), or if they are disturbed at night in the hive, they will fly towards a light.

Beekeepers and bee renters have learned that if you are going to disturb a hive at night, do so with minimal light so as not to lose bees. Also, they avoid lights in the vicinity of the hive in general.

There are a number of parasites and insecticides that cause bees to behave erratically. Colony Collapse Disorder is a major threat to the honeybee's survival.

Why are bees attracted to light? I don't know if anyone knows that.

Dinner and Dancing: Bee Navigation
The Cause Of Colony Collapse Disorder, Disappearing Bees Becoming More Clear


What evolutionary reason is there for hemolytic disease? Nowawadays we have methods which allow us to overcome hemolytic disease of newborn or to prevent it to onset. The Rh or Kell conflict, but how is it possible that it is present? Why it haven't disappear due to natural selection?

A hemolytic disease occurs for example when mother have Rh- and the unborn child have Rh+ after his father. Then when the blood of the child gets to mother circulatory system she creates anti-Rh+ antybodies which will attack and eventually kill her next baby with Rh+. Thus we can assume that hemolytic disease is genetically dependent and cause lethal effect.

So i'm looking for any explanation. I know, that there can be none, i'm just asking.

Hemolytic disease is not a genetic disease. It is a drawback of how the immune system works. In general, the overall benefits of having the immune system as it is right now are way higher than sporadic disadvantages, like the Hemolytic disease, that is why it is not counter selected. If instead of being a rare condition it would be a common one, then I would expect it to be indeed counter selected.


What is the primary cause of death for small animals in urban and suburban areas? Small birds (sparrows, robins, jays, finches) and mammals (squirrels, rats, opossums, raccoons) are a common sight in many urban and suburban communities with green space. However, I observe carcasses of these animals relatively infrequently.
I imagine that the following are some of the most common causes of death:

Predation (the species I mention are small, and somewhere in the middle of the food chain)
Age-associated decline in foraging ability, leading to starvation
Disease
Fatal contact with infrastructure (collisions with buildings or wind turbines, contact with electricity lines)

I can think of two reasons why we don't see carcasses very often:

predation is the most common cause of death
individuals that succumb to disease/starvation end up in their nests/dens

Is this plausible? Has this been studied systematically, e.g. in populations of birds with tracking bands?

Cats, windows, and cars appear to be the leading causes of avian (bird) deaths:

 Major sources of anthropogenic bird mortality in the USA [from Fig 2b, Loss et al. (2015)]
Cats and vehicles are likely leading causes of death for many small non-avian animals as well.

Loss et al. (2013) estimated that 6.3–22.3 billion mammals are killed by free-ranging domestic cats in the USA each year.

The Wikipedia article for roadkill provides the following discussion of vehicular deaths:

In 1993, 25 schools throughout New England, United States participated in a roadkill study involving 1,923 animal deaths. By category, the fatalities were: 81% mammals, 15% bird, 3% reptiles and amphibians, 1% indiscernible. Extrapolating these data nationwide, Merritt Clifton (editor of Animal People Newspaper) estimated that the following animals are being killed by motor vehicles in the United States annually: 41 million squirrels, 26 million cats, 22 million rats, 19 million opossums, 15 million raccoons, 6 million dogs, and 350,000 deer.

I welcome others to corroborate these claims with a more reputable source in the comments. (I will try to do so myself and will update as I find them.)

DISCALIMER: I was previously only aware of Loss et al.'s work, so the emphasis of my post is on their papers. I did not otherwise search exhaustively for data. Noticeably absent from my post is mention of deaths caused by pest control (trapping and poisoning). I may update this post with more info as I come across it.

 Citations
Loss, S.R., Will, T. and Marra, P.P., 2013. The impact of free-ranging domestic cats on wildlife of the United States. Nature communications, 4(1), pp.1-8.
 Loss, S.R., Will, T. and Marra, P.P., 2015. Direct mortality of birds from anthropogenic causes. Annual Review of Ecology, Evolution, and Systematics, 46, pp.99-120.


An online tree of life with extinct species present? There are awesome online phylogenetic trees such as OneZoom.

But they all only list living species.

I want to see dinosaurs between birds and crocodiles.

I wanna see that humans are reptiliomorphs and eupelycosaurs.

species.wikimedia.org seems to contain this info, but it's not presented in a navigable tree structure.

The tree of life project is your best bet, its not 100% complete but it is more complete than any other project I have ever seen, and unlike most actually includes many if not most extinct taxa. http://tolweb.org/tree/phylogeny.html
It also includes citation and brief descriptions of links and groups to make it easier. Some extinct lineages suffer from unresolved phylogenies but many of those are in constant flux or are actually unresolved in the fine scale so I can't blame them, especially considering they were originally based entirely on genetics, and is updated constantly.


Non competitive inhibitors and Uncompetitive Non competitive inhibitors affects the function of enzymes and slows the rate of reaction. Can I say the same for uncompetitive inhibitors ? Because Vmax decreases and it takes longer to form products .

However when I plot the graph both gradients needs to be the same ? So I'm a little confuse here to whether for uncompetitive inhibitors, it does affect the function of enzymes and slow down the rate of reaction .

I am not really sure to understand completely your question, but both non competitive and uncompetitive inhibitors affect the rate (Vmax) of the reaction by decrease it. In fact in both case, the enzyme (E) takes longer to transform the substrates (S) in to products (or to release it).
To better allow you understand I put below two mechanism of action for uncompetitive inhibition and non competitive inhibition.
Uncompetitive inhibition

Uncompetitive inhibition is unique in that the inhibitor binds to the enzyme-substrate complex. This could imply that the binding site for the inhibitor is accessible only after the enzyme has bound to its substrate. This reduction in the effective concentration of the E-S complex increases the enzyme's apparent affinity for the substrate through Le Chatelier's principle (Km is lowered) and decreases the maximum enzyme activity (Vmax), as it takes longer for the substrate or product to leave the active site.

Non competitive inhibition

Non-competitive inhibition models a system where the inhibitor and the substrate may both be bound to the enzyme at any given time. When both the substrate and the inhibitor are bound, the enzyme-substrate-inhibitor complex cannot form product and can only be converted back to the enzyme-substrate complex or the enzyme-inhibitor complex [...]
This type of inhibition reduces the maximum rate of a chemical reaction without changing the apparent binding affinity of the catalyst for the substrate.

Hope this could help.


Transition/Transversion ratio I'm taking a bioinformatics class and at this point we are just going over basic stuff about molecular biology. Half of the class is doing reading/research on our own, so there isn't much class time to ask questions or go over examples. One topic is transition/transversion ratio, and I'm not 100% sure I'm understanding it. Do you just compare the first symbol of string 1 to the first symbol of string 2? What if the two symbols you're comparing are the same? Do you just ignore it? Let's say string 1 is ACGATG and string 2 is TCAGTG. Would the ratio be 2/1?

Here are the comparisons I made.
Transitions: G-->A, A-->G,
Transversions: A-->T,
Neither: C-->C, T-->T, G-->G

Is this correct or am I completely on the wrong path?

You are almost on the right path.

This schematics from Wikipedia is quite clear in my opinion.

Slightly more chemical explanation (which you do not necessarily need to do bioinformatics, however I think it is always better to know exactly what you are dealing with outside of the computer!)

The idea is that you have four basic nucleotides: cytosine and thymine are called pyrymidines and adenine (A) and guanine (G) which are called purines. Pyrymidines are characterised by a 6 carbon azo-ring which is called a pyridine, while purines have a larger double ring, formed by a pyridine ring + an imidazole ring.

A transition is defined as the passage purine -> purine or pyrimidine -> pyrimidine.
A transversion is the passage purine -> pyrimidine, or viceversa.

These mutations can be caused for instance by certain chemicals, such as alkylating agents, or by ionizing radiations.

In your specific example, given the sequences

 ACGATG
 TCAGTG

You have 3 mutations:

A -> T
G -> A
A -> G

So you have 1 transversion (from the purine A to the pyrimidine T) and two transitions (between the purines A and G).


How did these apples grow together? I came through this pic while scrolling through facebook, and it was a bit strange to me.

As far as I know apples have a corymbose type of inflorescence, in which a single pedicel ends in a single thalamus.

And I am totally sure that the edible part, which is fleshy in the apple, is thalamus. How did this fruit came into existence?

I want a biological answer for this query.

They are basically conjoined apples which share a common stalk. They are rare but do happen. Here is an article of one discovered in a backyard.

conjoined apple discovered in a store (reference)

It apparently happens because of bad weather conditions, stress and insect damage. Fused fruits are also found in the case of cherries, watermelons, peaches etc.

  Inadequate pollination because of heat and other adverse growing
  conditions causes that section of the fruit in which the seed did not
  develop to not grow and fill out. Also, the fruit primordium
  (embryonic growing point) can be damaged or altered by environmental
  factors and cause strange growth forms. Of course, Siamese twins or
  two fruit growing together is also rather common(reference).

Read more about them on article 1 and article 2.


Identify the fluff that I have found in tea I have just opened a new pack of a black Pu'er tea that I've bought at the local store selling it by weight, and found a piece of fluff in there. To me it looks much like some kind of a bird fluff. It might also actually be a plant fluff, but somehow I doubt it. Probably it was white originally, but being so long in contact with the tea made it a bit browner.

Of course it spoiled all the impression of the tea. Now I wonder if I should drink it, or even keep buying at the same store. The worst thing is that their supplier is one of the major suppliers of Chinese tea in our country, and this is not the first time I find something hairy in it. The last time it was a human hair.

The questions:

Please help identify what it is (I don't mean a particular species of whatever it is, but at least what is it? Bird fluff, plant fluff, synthetic fluff?)
Would you still drink your tea if you'd find such things in it? Like, should it be safe, or is there any risk in contracting some terrible infection or a virus in case if it comes from a bird?

Here are some photos that I've made:

It also very much looks like this picture I've found in the internet, but failed to find a proper description of what is it actually (the most bold one was that its a swan fluff, but I can't imagine how a swan would come in contact with the tea):

It's kind of hard to tell from the picture, but maybe it's a variety of Milkweed seed-pod that got into the tea?


Success of computer simulations in biology, new discoveries In an interview with Tim Hunt, Hunt makes the following comment:

  There are some people nowadays who think you can sort of model everything on a computer. But I'm not one of those. I don't think anyone has actually discovered anything modeling something on the computer because there are so many different way of doing things...how Nature herself actually chose to do it.

The claim starts at 4'25'' in the link interview.

Have biological simulations ever led to biological discoveries? What purpose have they served?

In my opinion, this question is a question of philosophy of science, not Biology but here are my thoughts anyway.

Science by definition is a methodology that requires the creation of a hypothesis under a specific model and testing the prediction of this particular hypothesis.

Such modelling can be done either analytically (math) or numerically (with a computer). Typically, numerical modelling is being used when there the mathematical tools fail to offer a solution for the system analyzed. To me rejecting, numerical modelling is like rejecting modelling and is therefore like rejecting the scientific method altogether.

Computational modelling has brought a lot in pretty much any field of biology (and pretty much any field of science), so much so that it is hard to know where to start to fully address this claim. There are many models that were only verbal as mathematical tools were not sufficient to bring more quantitative predictions. For many of these models, computer modelling could offer quantitative predictions that could then be further tested.


How to determine the probability that a mutation is lost / fixed? I have a question about how to determine the probability that a mutation is lost or fixed after 1 or 2 generations in population genetics.

Let's say we have a randomly mixing population, with N diploid individuals (N=5), and there is one mutation that appears. I know it should follow a binomial distribution, but I also heard it may follow a Poisson distribution... and all I feel like saying is that the probability to get fixed is the same as the frequency at time 0, which is 1/2N, or here 1/10.

Furthermore, how do you calculate the probability that it exists in 2 copies?

How to determine the probability that a mutation is lost / fixed?

The probability that a neutral mutation gets fixed after an infinite amount of time is equal to its frequency $p$ as you said. Therefore the probability of being lost is $1-p$. This post offers an explanation but there many ways to make the demonstration. You might want to have a look at any good book in population genetics for this demo. Here are book recommendations.

  how do you calculate the probability that it exists in 2 copies?

A probability always depends on a priori. What are your a priori? Let's assume that we know that the allele frequency was $\frac{4}{10}$ in the previous time step.

Under the Wright-Fisher model the probability of having 2 copies in the next generation is given by the binomial distribution. Let $N=5$ and therefore $2N=10$ and let the frequency of the allele of interest be $\frac{4}{10}$, the probability of having two alleles in the next generation is ${10 \choose 2} \left(\frac{4}{10}\right)^2 \left(\frac{6}{10}\right)^8 ≈ 0.12$.

Under the Moran model this probability is zero. Moran's model is a birth-death  model (Markov model) and therefore transition between time steps can only add or subtract (or make no change) a single allele. You will note that the time step does not mean the same thing for the two models. Loss of heterozygosity is twice as fast under the Wright-Fisher model but this discussion is definitely not what you were asking for!


Speed of reaction vs equilibrium Does increasing the speed of a reaction (say by introducing a catalyst) shift the equilibrium of the reaction? I assume it does not, as Gibbs free energy is not changed, but I am not sure.

The equilibrium constant $K$ is the quotient of the rate constants of forward ($k_1$) and backward reactions ($k_{-1}$) (for elementary reactions).

E.g., for an  equilibrium
$$\ce{A + B <=> C + D}$$
we get
$$\frac{[C][D]}{[A][B]} = K = \frac{k_1}{k_{-1}}$$

So,

If both rate constants are affected in the same way (multiplied by the same speed-up factor) so that the quotient doesn't change, then also the equilibrium constant does not change, no shifting, no change in Gibbs free energy.
That would be the case with your catalyst as that facilitates both forward and reverse reaction by lowering the energy of the transition state in the elementary reaction leading to just such a multiplicative increase in reaction rate - but no effect on the energy of educts or products (thus, no change in $\Delta G$).

This has an interesting link to the impossibility of constructing a "chemical" perpetuum mobile by use of a catalyst.
If the rate constant of either forward or reverse reaction (or both, but not by the same factor) change, the equilibrium shifts.
But, yes, that also means that Gibbs free energy has changed.
Thus, there must be a change in free energy of educts and/or products as the energy of the transition state does not affect $\Delta G$, it only affects the reaction rates.
Whether this is possible hinges on the question whether we consider it still the same reaction $\ce{A + B <=> C + D}$ or whether we say that now we have another equilibrium, say, $\ce{A' + B <=> C + D}$ or $\ce{A' + B' <=> C' + D'}$ which of course can have different equilibrium constants. An example where I think one may argue either way would be the dependency of equilibrium constants on solvent.
(And, btw, we still cannot build a perpetuum mobile: solvation energy makes the difference)


What chemical or biochemical agents do plants use to inhibit each other's growth? As I just learned, allelopathy is the action by which plants regulate the growth of other nearby plants.

I have hear of ethylene is a general signal for growth and fruit ripening in particular, but I would like to hear about more specific compounds or proteins that are known to be allelopathic agents and how specific can they be - lots of plants ignore each other and just grow over each other.

@AlanBoyd has pointed me to a journal, but as its not open content, I'm hoping for a next level review of the mechanisms and actors in this topic...

thanks in advance!

As with the massive variety of compounds that serve to protect plants against insect and animals, resulting in a wide range of poisons, antibiotics and other natural insecticides, allelopathic compounds are highly varied with different methods of action: some merely prevent germination while others are effectively herbicides.

One example is Alliolaria petiolata. In that species the allelopathic substance is not known, but is thought to ahve a fungicidal effect that impedes mycorrhizal development, which would seriously affect the development of many species.


cloning and blue white screening in pet21a I am using pet21a as a carrier vector for my gene, with R.E BamHI and XhoI,in reverse primer I haven't added any extra nucleotide sequence so that it should code for the histag towards C-terminal. Am I doing so correctly?

Another question: after transformation to DH5alpha, I am getting only white colony(X gal stock was 20mg/ml about 200ul and IPTG 100mM stock about 40ulon surface of plate)... why I am not getting blue colonies?

pET21A doesn't encode the lacZ α-peptide necessary for blue-white screening by complementation. Since DH5α has the lacZΔM15 background, only the lacZ ω-peptide is produced and thus β-galactosidase is inactive.


Can two proteins have equal primary structure but different secondary structure? I've been reading lately about primary (which I understand completely) and secondary (which I do not understand that well since I'm not very good at chemistry) structure of proteins. My question is: Can two proteins have equal primary structure but different secondary structure?

By equal I assume you mean identical.

Yes, in fact several known proteins have different folding patterns for the same primary structure as part of their function. but most proteins can take on more than one folding pattern, in fact specialized proteins called chaperones exist to encourage (force) a particular folding pattern in some other proteins, especially ones that are essential or in which the other foldings can be dangerous.

The easy way to understand the difference is the primary structure is the amino acid sequence and the secondary is the first stage in how the protein folds (the other being the tertiary). the primary creates the secondary (and tertiary) but there is usually more than one stable folding.

this video contains a further breakdown of the different levels of structure.


Identify this black dragonfly with bluish coloration along its flat top, yellow on it's mid-body and green on its head I took these photos around noon in late July in Hsinchu county Taiwan. This particular stick in this particular pond is visited by many dragonfly species. I have seen this kind of dragonfly very regularly, in different nearby ponds, they seem to me to be far more active than other dragonfly species in the same area at the same time.
Its body is about 5 cm long and mostly black. However it has light "power blue" to white markings on the flat top surface of its "tail" and "mid" sections and the front part of its body before the head, and it seems to have some smaller yellow bands on the sides of its fore body and greenish markings on its head.
Wings are mostly transparent but are tinged orange or brown near the body.
Question: Is it possible to identify this particular species of dragonfly?

This species of dragonfly is Brachydiplax chalybea. Colloquially known as blue dasher.
General information
More information


What does it mean to "map the human genome" I know some elementary chemistry and biology. I also think I know what a gene is (it's a sequence of DNA which encodes a particular protein). I also know that on a chromosome there are sections of DNA which are kind of junk and do nothing. But being armed with this information, doesn't seem enough for me to understand what it means to "map the human genome".

Some possibilities:

a. It tells me the entire sequences of nucleotides that make up a particular human's chromosomes (it could not possibly do this for humans in general because of course the sequence is different from one human to another).

b. It tells me the entire sequences of nucleotides that make up a human's chromosomes... with some annotations along the lines of "at this point in the molecule, we could optionally have nucleotides A, B or C".
It tells me the start and stop points for each of the genes along the chromosome.
It tells me the function of every gene.
Something completely different!

So, the very first map of the human genome was of a few pooled samples with a single nucleotide called at each position.

This is basically okay, though, because humans are 99.9 (with possibly a few more 9s) % similar to one another. So you can get a lot of broadly-applicable information out of a single individual's DNA.

Further genome-mapping efforts brought data from new individuals and started to give us information about variants, like in your option 1b. At this point, there are projects like the 1000 Genomes Project that are trying to get 1000 full human genomes from a variety of ethnic groups sequenced and to characterize all the common variations.

Your point 2 was a different project, but was also part of mapping the genome. It's mostly complete now-- in that we know almost all of the RNA sequences that are produced by most cell types and mostly where they come from on the genome, with a few mysteries left around the edges.

Point 3-- no. Lots about the genome we still don't know. We're pretty good about where genes are encoded, but how they're regulated, how they interact... and remember that the part of the genome that codes for genes is a very small percentage of the overall sequence. Something like the the ENCODE Project is trying to figure out the various biochemical interactions present at every position of DNA, but even if that data were complete and reliable, which it's not, it still wouldn't tell us the "purpose" of all DNA.

So, when we say we've "mapped" a genome, we generally mean (A) we have (something pretty close to) full sequence of at least one individual's DNA (or a consensus sequence from a pool) and (B) we know where genes are on it. That's a huge step but only the beginning of understanding genetics. In the case of humans, we're adding on to that understanding by learning where variants are and how common they are.


Why do oncogenes show genetic dominance? As we know that tumor suppressor gene causes cancer only when both the alleles are recessive in nature.But in case of oncogenes if only one allele is dominant it can cause cancer.Why in case of oncogenes to become a cause of cancer both allele aren't recessive?

A tumor suppressor is an essential gene that regulates the cell cycle at different checkpoints. If one allele is lost due to a mutation then the function of that gene can be carried out by the other allele (There might be a less expression of that gene because of copy number reduction but it is not necessary in all cases- cases where there are feedback controls).

An oncogene is a gene that promotes cell division. Different kinds of mutations will have different kinds of effect.

Mutation leading to loss/reduction of function: Nothing is likely to happen unless both alleles are affected.
Mutation leading to hyperactivity: In this case one rogue allele will always remain active leading to uncontrolled growth stimulation.

So, it is the second type of mutation that you are referring to as in the case of Ras.
Note that any mutation leading to formation of a toxic or hyperactive protein (rogue allele), will show genetic dominance. Also see the case of Huntington's disease.


What causes sodium channels to open? What triggers the opening of sodium channels in a neuronal membrane? Is it acetylcholine that activates sodium channels in the postsynaptic membrane?

Are sodium channels like receptors that have to bind to something (like a protein or an ion) to open? If so, what is the substance that forces Na+ channels to open?

Sodium channels are primarily voltage-gated - these are the channels responsible for action potentials.

Many other receptors are ligand-gated, and these are typically the signal that causes the initial voltage change that opens the voltage-gated sodium channels; however, these channels are less selective cation channels and are permeable to ions like potassium as well as sodium. Still, their permeability to sodium is quite important and so they may also be thought of as sodium channels sometimes.

These include neurotransmitter gated channels like nicotinic acetylcholine receptors and AMPA (glutamate) receptors, and transient receptor potential channels like the TRPV1 receptor that is sensitive to painful heat and the chemical capsaicin which makes chili peppers "hot."


How long do your eyes need to adapt to darkness and reach full contrast? I heard you should wait some time until your eyes adapt to darkness and are able to see smallest luminosity differences, otherwise you might overlook faint objects in the ocular. Are there any rules of thumb here?

What about looking for 5 minutes on your bright laptop, do you have to wait again the same time or wear some sunglasses? ;)

Actually, the US Army and Air Force (and I assume the Navy) teach their life support troops about this (as well as the aviators), since so many missions are conducted at night.  It is actually some very interesting physiology involved in this.  This Army Instructional manual should be of help (PDF File).

  On an average it takes 30 to 45 minutes for your rods to be fully dark adapted to night vision.

It also covers things such as Mesopic vision and Scotopic vision, eye health, and how to actually dark adapt.  I suggest it as a good read.  It's less than 14 pages.


MHC-I presentation during infection Which cell type cannot process and present antigen peptide in association with MHC-I when it is infected?

All nucleated cell (cells with defined nucleus) are able to present MHC-1 on their surface.  Since red blood cells do not have nucleus, they are not able to represent antigins in MHC-1 molecule.

Hope that helps check wikipedia for reference


Properties of Satellite Chromosomes I have some questions regarding Satellite chromsomes which could not be resolved by a google search.

Does the satellite consist of telomeric sequences ?
If not, What is the function of a satellite ? And where will the telomeric sequences be present - in the main body ? On the secondary constriction ?
Satellite chromosomes are also known as SAT chromosome which stands for Sino Acid Thymidine. I read in some sources that SAT means without thymidine. But how is that possible, if there is A then obviously there has to be T ? ( in dsDNA)

If by "satellite chromosomes" you mean "satellite repeats", then:

Not always. There many types of satellites, such as telomeric, centromeric (like gamma, alpha, beta satellites), simple repeats (CT)n.
It is still an open question. Some say they are important for chromosome structure (e.g., centromeres). Sometimes satellites get transcribed as might act as lncRNAs. And of course, most of them are just junk DNA.
If there is T then there is A too.

Edit

Satellites contain telomeric repeats at their ends as all chromosomes do. But they are more about NOR repeats.
They are important for the nucleolus functioning. But shorts arms of acrocentric chromosomes are not crucial, take Robertsonian translocation as an example.


How do I effectively visualize data showing change in a lot of samples over two time periods? I've tallied the number of glands in a plant this year and last year. My full data set has about 20 plants in it (I've reproduced the data from 10 of the plants here). I want to show that the plants this year have had consistently lower gland counts than they did last year, but I don't want to bog readers down with too many data points in their faces. What kind of graph/chart should I use to best show this trend?

        Gland Count
PlantID  2015    2016
1        22.92   19.50
2        11.67   7.12
3        19.67   15.33
4        22.33   12.00
5        20.92   18.58
6        25.83   23.83
7        25.67   32.17
8        22.83   17.00
9        28.42   26.25
10       17.92   16.92

Two styles of graph come to mind.

A simple 2 layer histogram showing the distribution of gland counts for each year. This is a kernel density as opposed to a histogram, but it gets the idea across.

Line graph with year on the x-axis and gland count on the y-axis, with a colored line for each plant. This would show a little more detail, and would be better if the mean gland count overall did not change much, but decreased significantly among individuals.


Question regarding Rate of Photosynthesis AP Biology Lab We are doing a lab on the effects of light intensity/wavelength on the rate of photosynthesis in AP bio and we were asked to visit this website here: http://mhhe.com/biosci/genbio/biolink/j_explorations/ch09expl.htm

The link takes you to a shockwave applet in which you can change the wavelength/intensity and record the ATP production (%). We were supposed to try out as many different combinations of intensity/wavelength and record the respective intensity, wavelength and ATP production (%) in a chart. Now the problem I'm having is that we are to graph this data. How should I go about graphing this? One problem is that for some values in the data, the intensity might be the same with different wavelengths or the wavelength maybe the same with different intensities. Can I do two graphs? One graph? Which one would be best and how should I go about doing so? And here is the chart just in case you want to see the data:

https://drive.google.com/file/d/0B4A27kix-0naMk4wNmNQejd3cGc/edit?usp=sharing

Your task is to determine how light intensity and wavelength affect ATP production. Therefore, we know for sure that your dependent variable (or response variable) should be ATP production. It is customary to depict the response variable on the vertical axis (Y-axis), so let's trying doing this.

Now we need to sort the other two variables. I suggest that you make one variable a control variable -- a variable that you don't change and keep constant, and the other then will be an independent variable (or explanatory variable). Then you swap them around, producing at least two plots.

In a nutshell:

You pick one value of wavelength and don't change it. Then you change the light intensity and record ATP with constant wavelength. You plot ATP (vertical axis) vs the light intensity (horizontal axis).
You pick one value of light intensity and don't change it. Then you change the wavelength and record ATP with constant light intensity. You plot ATP (vertical axis) vs the wavelength (horizontal axis).

Make sure to generate enough data points in order to be able to fit a smooth curve.

Another option would be to make a 3-D graph, with 3 axes: Y for ATP, X for wavelength and Z for light intensity. Initially, this might seem like a better approach, however 3-D graphs are not very common in science, and maybe there is a reason for it. Your goal is to make your data intuitive, easy to read and straight to the point. Science can be rather complex even without additional effort to complicate it with confusing graphs.

I would try it out as well, and see which one of two approaches shows you the trend more clearly. If I had to pick one straightaway -- I would probably go with the previous option that included a control variable.


Modelling insecticide net efficacy loss I am currently doing some work on modelling the effects of treated nets usage on mosquito populations. Nets do not retain their maximum efficacy forever. They lose their chemical efficacy after about three years and all that is left is the physical protection offered by the net which I estimate to be 20% of the original efficacy.

I am trying to model this behaviour. I need continuous function over the interval $[0,1095]$ which decreases slowly  from 1 when $x=0$ and asymptotically approaches 0.2 when $x \rightarrow 1095 $.

I tried an ellipse of the form $y=\sqrt{1-\dfrac{x^2}{(1095)^2}}$, but i realized the function is equal to zero when $x=1095$ which is not what i want.

Any help will be appreciated. Thank you.

As @WYSIWYG suggested, this is probably more suitable for Math-SE.

From you question, it is unclear exactly what shape you are looking for, and there are many functions that could describe the behaviour you're after, i.e. a continuous, smooth decrease towards an asymptote. However, two possible options could be the negative exponential and a negative gompertz function. Possible forms of these could be:

Negative exponential

$y(x)=e^{−ax+ln(1-b)}+b,$

where $b=0.2$ and a is a rate parameter.

Negative Gompertz

$y(x) = 1-\alpha e^{-\beta e^{-\gamma x}},$

where $\alpha=0.8$ (describing the asymptote), $\beta$ in an inflection parameter (given a displacement along the x-axis), and $\gamma$ is a rate parameter.

These functions can give results such as:

In these examples, $a = 0.005$ for the negative exponential and $\beta = 150$, $\gamma = 0.008$ for the gompertz v1 and $\beta = 5$, $\gamma = 0.005$ for the gompertz v2.

An alternative parametrization of the Gompertz, which might be easier to understand, is:

$y(x) = 1-\alpha e^{-e^{-\gamma (x-\beta)}},$

where the inflection point ($\beta$) is directly related to the scale of the x-axis (so $\beta = 400$ would give an inflection at x = 400).

Are these examples interesting for your application? Hopefully they can provide a starting point for you.