What is the point of Meiosis II, considering Meiosis I already produced haploid cells? Meiosis I is required so that the 2N cells become 1N, and so a 1N sperm and 1N egg can fuse to become 2N again.

But why is meiosis II required? Why does our body need to go from  2 1N cells to 4 1N cells? Can't it just use one of the 2N cells after Meiosis 1?

Source

After meiosis I, those n=23 chromosomes have two chromatides. Meiosis II just separates them into single chromatides.

befor a cell enters its division its heridity material is in a form of a coilled and condensed material called chromatin whose amount is 2N and is diploid 2n However when the cell enters its interphase  its chromatin dobbles but its no of chromosomes remain 46 so  when cell enters meiosis 1 it produces two daughter  haploid cells 2n having 2  same   sister chromatids attach to same centeromere as cells at the end of meiosis 1 are  haploid 1n but amount still remains 2N to half the amount of chromatin meiosis 2 occur so that 4 daughter cells with haploid no of chomosomes 1n as well as halfed amount of chromatin 1N o can be produced


How do painkillers prevent shock? I was reading about the Placebo effect and came across this little story:

  The roots of the placebo problem can be traced to a lie told by an
  Army nurse during World War II as Allied forces stormed the beaches of
  southern Italy. The nurse was assisting an anesthetist named Henry
  Beecher, who was tending to US troops under heavy German bombardment.
  When the morphine supply ran low, the nurse assured a wounded soldier
  that he was getting a shot of potent painkiller, though her syringe
  contained only salt water. Amazingly, the bogus injection relieved the
  soldier's agony and prevented the onset of shock.

https://www.wired.com/2009/08/ff-placebo-effect/

I also read that Morphine specifically lessened the effects of shock:

  Only when it is severe, or when a severely wounded or injured person must be moved quickly (as from a wrecked vehicle or aircraft) it is wise to give Morphine at once. It may not always relieve the pain entirely, but will certainly lessen shock.

https://web.archive.org/web/20140420133119/http://www.med-dept.com/morphine.php

So, how do painkillers prevent wounded soldiers from going into shock and dying? What physiological mechanisms are responsible? Is it something to do with blood pressure? Heart rate? Pain itself?

1) Pain can aggravate hypotension, so painkillers may help to prevent shock.

A severely wounded person with significant blood loss can develop hemorrhagic shock due to drop in blood volume and consequently drop of blood pressure and insufficient perfusion of vital organs.

It is known that pain can trigger vasovagal syncope, also known as neurocardiogenic syncope in which a person faints due to sudden drop of heart rate and arterial vasodilation resulting in drop of blood pressure and reduced brain blood perfusion.

Here is an example how carbamazepine, which prevented pain, also prevented the episodes of neurocardiogenic syncope (The Korean Journal of Pain):

  A 65 year-old male patient diagnosed with glossopharyngeal neuralgia
  complained of severe paroxysmal pain in his right chin and ear
  followed by bradycardia, aystole and syncope. We report a case
  successfully treated with a permanent pacemaker and carbamazepine in a
  patient with GPN who had syncopal attacks preceded by paroxysms of
  pain.

In an injured person who is at risk to develop hemorrhagic shock, severe pain could cause neurocardiogenic syncope that could proceed into shock, so, it sounds logical that painkillers could help to prevent shock.

From the first quote in the question (the patient was convinced he was receiving a strong painkiller), we cannot conclude that the painkiller prevented shock, because this has not even started to develop.

2) Analgesics for a person in severe pain who has lost blood and is in danger of developing shock.

According to Pain Control in Trauma Patients (Trauma Reports, 2011, fentanyl can be appropriate painkiller in shock since it does not aggravate hypotension:

  Fentanyl is the best known synthetic agent and is widely used in pain
  control. It is 50 to 100 times more potent than morphine and has the
  added benefit of not causing histamine release and peripheral
  vasodilation, as found with morphine administration. Based on this
  physiology, fentanyl should not impact blood pressure as much as other
  narcotics and, therefore, is preferential in the critically ill trauma
  population who may have tenuous cardiovascular status from hypovolemic
  shock.

Morphine can cause hypotension, so it may aggravate shock. According to prescribing information for morphine sulfate oral solution by FDA.gov, 2018:

  In patients with circulatory shock, Morphine Sulfate Oral Solution may
  cause vasodilation that can further reduce cardiac output and blood
  pressure. Avoid the use of Morphine Sulfate Oral Solution in patients
  with circulatory shock.

In conclusion, painkillers may help to prevent shock by reducing pain.


What is the function of E-coli bacteria in our gut? So, I recently came up with this question. I  googled it, but couldn't understand the proper functions of E-coli bacteria. A little definition would be wonderful.

Nonpathogenic E.coli are a component of the gut microbiome of humans and many other organisms.

They are commensals, meaning that when they remain in the areas they have evolved to live in, and when they do not acquire virulence factors, they are benign. They live in our digestive tract and basically do nothing to harm us.

In fact, commensal microorganisms like E.coli can be considered part of the multicellular organisms innate immune system. They take up space on the exposed surfaces of internal organs such as the intestines and prevent the colonization of pathogenic strains of microorganisms.

Along with the endothelial cells and mucous, commensals form the barrier defenses that are the first line of protection against pathogenic organisms. Basically they are the good neighbors that don't cause problems and they don't leave space for bad neighbors to move in.

Problems can occur if they gain access to areas that are normally sterile. If the intestine is perforated and E.coli gain access to the thoracic cavity, they can become an opportunistic pathogen, as they will not be interacting with the host in a way that can control their proliferation. They can also come in contact with cells that are not expressing the necessary proteins to protect them from the E.coli.

You can also end up with the situation where a pathogenic bacteria or a bacteriophage carrying a virulence factor can transfer that virulence factor to the commensal E.Coli, turning them pathogenic.

But for the most part E.coli are there to take up space that could otherwise be colonized by harmful bacteria.

E. Coli bacteria are present in the caecum region of large intestine and plays a major role in erythropoeisis i. e.  Formation of RBCs.


What causes the complementary copy of an RNA molecule to separate? I have recently read an article which explains that, in the RNA World hypothesis, an RNA molecule gets 'scanned' by nucleic acid, catalysed by a different specifically-folded RNA molecule, to arrange itself complimentarily to the original molecule. However, what causes the new, complementary molecule to detach from the original molecule? I always hear people say that this complementary base pairing allows the RNA molecule to reproduce, but I never quite understood: how? If complementary bases tend to bind together, shouldn't the newly formed structure then be stable? What causes the actual reproduction?

First, I want to point out that the RNA world hypothesis is just that - an hypothesis. While it has been shown that it's possible for certain RNA molecules to make copies of itself, this is not a 'normal' function of any RNA.

Edit - to give a clearer answer to the question itself:

After replication of an RNA molecule it may form a stable structure together with its template or it may dissociate. Due to the various possibilities and complexity of RNA structures its almost impossible to predict this, since both the (exact) sequence itself and environmental conditions especially temperature are very important.

More background from the unedited answer:

Whether two complementary strands or RNA (or DNA) bind together is not something that can always be easily answered. For DNA of a given length (in a given environment / buffer) one can more or less predict the temperature at which complementary strands will separate (often called melting temperature), because DNA forms relatively stable helices.
RNA, however, often forms complicated 3-dimensional structures, often involving self-complementary and is not restricted to the typical helices seen in DNA. Trying to predict the resulting 3D structure of RNA molecules is still an ongoing field of research. Some of these structure are quite stable (e.g. in tRNA) but in other cases they can also be very dynamic and change quickly.
In the end it always depends on the RNA sequence, temperature and many other environmental factors.


What is the big plant with white flowers on the photo? What is the 3m tall plant with white flower? It is from Central Europe and there is a creek near to it. I have a guess, but I want to know for sure...

Is the small one the same species?

More high res photos here:

https://ibb.co/cAaUMU
https://ibb.co/ih4Zo9
https://ibb.co/eJSyFp
https://ibb.co/gstS89
https://ibb.co/kQ2OWU

They both look like poison hemlock (Conium maculatum).  It can grow up to 3m tall and grows in moist areas including along creekbeds. One of it's common names is European Hemlock.  It is toxic to some domestic animals and humans.

Source: United States Department of Agriculture

Source: http://natureid.blogspot.com/2011/11/poison-hemlock-111211-elkhorn-slough.html


Which plant's part is this? I found this plant in Rajasthan, India.
This sample is 4-5 cm long.
This is an ornamental plant. It was a potted plant.
I put my fingertip in the photo to give an idea of size of the specimen.
I can't figure out which plant this part belongs to.
Please give the species name if you can.
I would be very thankful to anyone out there who will help me.

This is a bit hard to say exactly, since there is a number of possibilities. We can be pretty sure that these sample is from a Cypress, belonging to the family of Cupressaceae, but which subfamily or species this is exactly, can't be identified here. Therefore a wider image would be necessary, but since this is a potted plant, even this might not be enough, as a lot of these plants are used in gardening.

It is called Leyland Cypress. For more details, refer the following link. https://en.wikipedia.org/wiki/Leyland_cypress


Why aren't there any competing biologies on Earth? Why aren't there any competing biologies on Earth? I read sci-books about life based on silicon and I've read an article that said that other structures than DNA can encode genetic information.
So does physics allow for many competing biologies? What makes DNA-based biology the dominant biology on earth according to known laws of physics?

There are indeed almost certainly other potential alternatives to DNA-based biology and the RNA-based biology that may have predated it, which could be used to form viable organisms.
Many of them likely have some energetic disadvantage relative to DNA and RNA (e.g., requiring a higher bond formation energy, having a less flexible backbone) and those would naturally be expected to be outcompeted. But some probably aren't so different from DNA and could indeed have formed a viable alternative---if nothing else, the opposite chirality molecules are certainly candidates. Why aren't alternatives still around?
Surprisingly, it turns out that when time scales are long enough, we should expect a natural loss in the number of different independent lineages. Another more recent example of this is the fact that all modern humans are descended from Mitochondrial Eve and Y-chromosome Adam, despite the fact that these two individuals were members of thriving human populations at entirely unrelated times. Biodiversity is constantly being gained through divergence of existing lines and lost through lines that fail to reproduce. Over many generations of reproduction, this produces a random walk pattern that converges toward elimination of all but a single lineage in a given population even if all lineages are equally fit.
Now back to the origin of DNA-based life.  If abiogenesis is a rare and difficult event, then we would expect only one or a small number of life models to have emerged billions of years ago. Random fluctuations over all that time will tend to drive all but one toward extinction. With evolution at play as well, any lineage that randomly gains an advantage will be even more likely to outcompete the others.
And once there is life of any sort around? Well, potential alternatives to DNA are still nutrients, and therefore will simply be eaten by existing life forms before they have the chance to evolve into something new and interesting.

Directed Panspermia
Directed Panspermia occurred only once.  The principle evidence is that the genetic code is almost universal. To answer your question, one might hypothesize that the payload was designed to root only one phylogenetic tree.
While I have been unable to follow this paper's logic, the literature citations are very thorough: Biological Wow Signal
Here is some extreme speculation.
Unfortunately, Directed Panspermia has been considered by some to be part of the theist version of Intelligent Design, as you can see here.  That is in stark contrast to the actual WP article on Directed Panspermia, which is excellent.
As to why there is no competition, or parallel lineages, I am tempted to invoke the Anthropic Principle.
The answer to your question might fall out of a ToE, which Hawking thought would require a future, highly advanced AI to solve.
Obviously, the three Abrahamic religons saw a simultaneous creation of life, which theists would invoke to answer your question. But, that's a different forum.


What is the human ear's temporal resolution? What is the smallest sound duration that the human can hear? In other words, what is the lower duration limit for a sound to be translated into electrical signals by the ear?

Suppose the human ear can discern or distinguish between 18 kHz and 20 kHz sounds, this would mean that, if a single wave could  be processed at 20 KHz, the sound duration would be 1 / (20KHz) = 0.00005 second, which would be next to incredible (and probably impossible).

I am particularly interested in the lower duration limit as depending on frequency.

I am expecting something like this (I am not sure)

 Freq   Duration needed to be aware of the sound
 20KHz  0.05S (50 mS)
 10KHz  0.04S (40 mS)
  5KHz  0.03S (30 mS)
2.5KHZ  0.02S (20 mS)

I will provide an answer in 2 parts. The first part is a theoretical approach based on the absolute possible minimum (my original answer). The second part focuses on experiments in the peripheral auditory system (added edited answer).

PART I: Absolute theoretical minimum (original answer)
As you inquire about electrical signals in the auditory human system I have to say that electrophysiological data at such a fundamental level is scarce in humans. That having said, we can start off by looking at auditory clicks, which are generally the shortest possible well-defined auditory stimuli. The shortest auditory click I was able to find, and which was used in a psychophysical context (i.e., audible to a human) was 10 microseconds (Leshowitz, 1971).

Now, (1) assuming 10 microseconds is the lower duration limit of a click (it may well be lower), and (2) assuming this click duration is representative of the lower limit of a tonal burst duration limit (it may well not be), and (3) assuming you indeed wish to know about/use auditory tones and not clicks, and finally (4) assuming we need at least one wavelength of a tone to fit in this window, then we could present a frequency of 100 kHz, or higher. As 20 kHz is the upper frequency limit of the human ear, we would need at least 50 microseconds for one wavelength, i.e., basically what @Dustin concluded, but it does not end here:

Frequency splatter (Fishbach et al., 2001) limits the lower limit of tonal stimuli. To prevent spectral splatter one needs to incorporate rise and fall times (ramps) onto the tonal stimulus. Hence, again assuming you do want tonal stimuli, an onset and offset ramp of one wavelength each would be advisable (at the very least) and hence 3 wavelengths are needed, increasing the duration of a 20 kHz tone to 3 wavelengths, i.e., 150 microseconds (spectral splatter may not be prevented, but at least reduced).

On top of this theoretical approach, it has to be noted that I started off with taking a click as a starting point. A click, being an impulse signal, basically stimulates the entire cochlea (the inner ear), and hence represents the most powerful auditory stimulus. Pure-tone bursts are, as a consequence, weak stimuli as they stimulate a small proportion of the available hair cells. High sound levels may therefore be necessary for short tonal stimuli, in turn degrading the frequency resolution in the cochlea as excitation spreads away from the characteristic frequencies. Mostly, several milliseconds are used as tone bursts.

Moreover, taking 20 khz is kind of an upper limit, and many folks are not even able to hear 16 khz. An upper limit of, say, 12 kHz would be advisable when grownups are used. This means a wavelength of 83 microseconds and for 3 wavelengths (for ramp times) that means 250 microseconds.

If lower frequencies are needed, this number would increase further.

EDIT: PART II. Phsyiological experiments.
As you are also interested in electrical signals, we might take another approach and start looking at experimental (animal) data. The temporal limits of the auditory system are generally assumed to reside in the ribbon synapse that is situated between the inner hair cells and the auditory nerve fiber (Parsons, 2006):

This synapse is considered to be the limiting factor in the temporal characteristics of the auditory system (Khimich, 2005). By analyzing this synapse using very short tone bursts, it was shown that the vesicles of glutamate (the neurotransmitter activating the auditory nerve fibers that lead the signal to the brain) were released as shortly as 2 ms after tone onset. Tone bursts were 8 - 16 kHz, 10 ms plateau, 1 ms
rise/fall (Khimich, 2005). Note the tone burstduration and rise fall times mentioned in answer PART I.

Indeed, when first spike times in auditory nerve fibers were determined, spikes with the shortest latency occurred just under 2 ms (Heil and Irvine, 1997).

SR in the figure means spike rate, showing that higher spike rates are accompanied by shorter latencies. A1 means auditory cortex neurons, which obviously have longer latencies.

Hence, from these experiments I dare say that 2 ms would be sufficient to elicit at least one spike.

Why then leave part I of the answer? The problem is that the experimental data do not show that a spike wouldn't have been generated at shorter stimuli. The data merely show that with an ongoing stimulus the first spike appears at 2 ms. It does not show whether 2 ms of temporal summation is necessary, and that is why I have left part I of my answer in place, as a theoretical lower bound.

As a side note: the spike rates are highly dependent on loudness levels. Lower sound levels result in longer latencies. Specificaly, acceleration of the stereocilia on the inner hair cells in the cochlea is the primary parameter. The faster the cilia move, the faster the spike response.

References
- Heil & Irvine. J Physiol 1997; 78:2438-54
- Fishbach et al. J Neurophysiol 2001; 85:2303-23
- Khimich et al. Nature 2005; 434:889-94
- Leshowitz et al. J Acoust Soc Am 1971; 49, Suppl 2:462-6
- Parsons. Nature 2006; 444:1013-4

The average human auditory range is between $20$ Hz to $20$ kHz [1]. How this relates to time is by the definition of frequency.
$$
f = \frac{1}{\text{time in sec}} = \frac{\omega}{2\pi}
$$
where $\omega$ is angular frequency. So if a human can hear a sound frequency of $18$ kHz, then
$$
(18\cdot 1000)^{-1} = 0.000056\text{ sec}
$$
where $18$ kHz is $18000$ Hz.

  Abel (1972) reported duration DLs ranging from approximately 0.4 to 80ms for stimulus durations of 0.2 and 1000 ms, respectively. The lowest frequency on average is $20$ kHz but all people are different and some people may hear at a lower frequency.[1]

  A different type of auditory temporal resolution can be assessed by measuring the minimum detectable duration of a gap in a continuous sound. The gap detection is in the order of 2 to 3 ms for tones at moderate and high sound
  pressure levels (Exner, 1875; Ostroff et al., 2003; Plomp, 1964). Zwicker and Feldtkeller (1967) reported values of 1.5 ms and 5.0 ms for gap detection in tonal signals and noise, respectively.[1]

Reference:

http://www.usaarl.army.mil/publications/HMD_Book09/files/Section%2019%20-%20Chapter%2011%20Auditory%20Perception%20and%20Cognitive%20Performance.pdf


Antigen Antibody reactions during blood donation A person wih blood group O is called a Universal Donor. Well, his plasma contains antibodies A and B. During blood donation, if blood group O is given to a person with blood group A (since blood group O can be donated to all the blood groups) then wouldn't the antibodies of the donor with blood group O harm the recipient?
Although nowadays doctors prefer giving blood having 100 percent compatibility...

The key feature of type O blood as "universal donor" is that the incoming red blood cells have neither A nor B antigens and so the resident antibodies (anti-A , anti-B) will not react with them. Since transfusions are carried out with packed red blood cells the plasma antibodies of the donor don't matter - they will not be introduced into the recipient.

Since a person with blood group O does not express the A and B antigens, his blood does not contain antibodies to A and B. Therefore, it is safe to transfuse into someone with type A, B, AB, or O blood.


Is 100% antibacterial resistance possible? The quest to develop antibacterial and antibiotic substances has often been described as an arms-race, as bacterial life develops resistance, requiring us to develop novel agents which can effectively kill said microbes.

My question is: is it at all possible for a single microorganism to develop resistance to everything we can possibly develop?

There is only so much information-capacity in microorganism DNA to encode the means of resistance to various substances. If we climb the arms-race ladder high enough would a highly-advanced bacteria somehow "forget" how to defend against penicillin, for example?

...or are we utterly boned?

This is a theoretical question, which I can't answer, because genetics is not my favorite topic. In practice we only have about a dozen antibiotic classes. There are already panresistant bacterias, which are resistant (as far as I know) all of these classes of antibiotics, so we have already lost.

The causes of our defeat is more interesting I think:

Pharmaceutical industry does not have enough interest in the antibiotics research, since it is not as profitable as for example cholesterol reducers. Antibiotics are cheap, and you usually heal after the first treatment, while the research and the clinical trials are really expensive, it is hard to find working chemicals, which do not have severe side effects.

  “We  need  to  shift  from  the  concept  of  the  pharmacy  as  a
  ‘shop’  and  build  a  culture  of  pharmaceutical services. This is
  already happening  in some countries, but we need to make it  the
  rule  everywhere,”  says  Zsuzsanna  Jakab,  WHO  Reg ional  Director
  for  Europe.  “As  pharmacists  dispense  medicines  to  patients,they
  are   important  allies  in  our  fight  against  antibiotic
  resistance.  As  such,  they  need  to  be  ena bled  to  deliver
  accurate  information  and  counselling on proper antibiotic use.”

  Over  40%  of  antibiotic  prescriptions  are  inappropri ate,  recent
  studies  found.  This  relates  especiallyto antibiotics prescribed
  for the common  cold and sore throat; these most oftenresult  from
  viral infections,on  which antibiotics have no  effect. Further, in
  some countries, there is  atendency towards self-medication.
  Inappropriate an tibiotic use is the major driver of growing
  antibiotic resistance.

Pharmacists have decisive role in combating antibiotic resistance, says new WHO European survey
People with Mycobacter infections does not always do the treatment long enough, so Mycobacters can become resistant to antibiotics.

  Most people with TB are cured by a strictly followed, six-month drug
  regimen that is provided to patients with support and supervision.
  Inappropriate or incorrect use of antimicrobial drugs, or use of
  ineffective formulations of drugs (e.g. use of single drugs, poor
  quality medicines or bad storage conditions), and premature treatment
  interruption can cause drug resistance, which can then be transmitted,
  especially in crowded settings such as prisons and hospitals.

http://www.who.int/features/qa/79/en/
There is no global regulation of how to use antibiotics, so in some countries you can buy them without consulting a doctor and get a prescription. On top of this you can buy antibiotics without prescription on the internet if you want. This leads to overuse of antibiotics, and overusage leads to resistance.

  Self-medication is more common in developing countries due to factors
  such as ready availability of antibiotics without prescription, the
  unrestricted access to antibiotics,lack of regulation over drugs, and
  physicians and pharmacists prescribing and dispensing antibiotics
  without regard to the cause of infection

http://article.sapub.org/10.5923.j.cmd.20110101.02.html#Sec3.3.4

  We found 138 unique vendors selling antibiotics without a
  prescription. Of those vendors, 36.2% sold antibiotics without a
  prescription, and 63.8% provided an online prescription. Penicillins
  were available on 94.2% of the sites, macrolides on 96.4%,
  fluoroquinolones on 61.6%, and cephalosporins on 56.5%. Nearly all,
  98.6%, ship to the United States.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746509/

  These results demonstrate that, although illegal, the sale of
  antibiotics without a prescription continues in Spain.

http://cid.oxfordjournals.org/content/48/10/1345.full
Some of the antibiocstics are used by agriculture industry, which leads to antibiotics resistance as well.

  They identified bacteria able to shrug off the drug of last resort -
  colistin - in patients and livestock in China.

  It is likely resistance emerged after colistin was overused in farm
  animals.

http://www.bbc.com/news/health-34857015

  Nutritive and therapeutic treatment of farm animals with antibiotics,
  amounting to half of the world's antibiotic output, has selected for
  resistant bacteria that may contaminate the food produced.
  Antibiotic-resistant enterococci and staphylococci from animals are
  found in food when they survive the production processes, as in raw
  cured sausages and raw milk cheeses1. The broad host ranges of some
  plasmids and the action of transposons in many bacteria allow
  antibiotic-resistance genes to be communicated by conjugation between
  different species and genera2,3. A multi-antibiotic resistance plasmid
  from a lactococcus found in cheese provides a historical record of
  such events.

http://www.nature.com/nature/journal/v389/n6653/abs/389801b0.html

  About 2/3 of the antibiotics are used in animals.

https://youtu.be/iLJAleLjJv8?t=3m47s

So the problem is with not enough motivation in development and the lack of proper regulation of usage. Regulation is the business of the politicians, so its their fault as always. :D

A 100% antibacterial resistance is a very dangerous situation, which would mean that the age of antibiotics will be over. To achieve a total resistance the microorganisms would have developed new ways of mutation, transferring genes between them, rapid cell damage repair. It would mark a new step in the evolutionary process. There has been many questions as to whether the age of antibiotics have come to its end or not, but the demand has never been this high. its a very scary scenario, a ticking time bomb.


What happens if a non-diabetic receives an injection of insulin? If a person without diabetes or any diabetes-related issues receives an injection of insulin, what happens? Would the blood glucose level drop or does the body naturally compensate for the added insulin? What biological process occurs?

Blood sugar drops (Hypoglycaemia)
There are several other uses of insulin (other than diabetic treatment)

Some of those could be:

Diagnostics
Psychology (Narcoanalysis)
Parenteral nutrition
Cardiology (Glucose–insulin–potassium solution (GIP or GIK solution) is given   after a myocardial infarction)
Malignancy (Insulin potentiation therapy (IPT))
Psychiatry (Deep insulin coma therapy (DICT))

Sources:

Niazi, Asfandyar Khan, and Shaharyar Khan Niazi. "A Grand Dame
with Hidden Aces: The Non-diabetic Uses of Insulin." Indian Journal
of Endocrinology and Metabolism. Medknow Publications & Media Pvt
Ltd. Web. 06 Feb. 2016.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3354952/.
"Hypoglycemia." Hypoglycemia. Web. 06 Feb. 2016.
http://www.niddk.nih.gov/health-information/health-topics/Diabetes/hypoglycemia/Pages/index.aspx.

depends on how much injected, you could just feel lightheaded or you might get yourself into an insulin induced coma, serious cases, yeah, one could die. There's a certain blood insulin level that the body can naturally compensate to maintain homeostasis, like I said before, depends on the injected amount. sidenote - Watch 'A Beautiful Mind', it shows the usage of insulin shock therapy (insulin coma therapy (ICT)) to "reduce" schizophrenia.


Why do more complex DNA strands take longer to anneal? My textbook and several websites told me that more complex DNA strands take longer to anneal because it is harder to find the correct sequence. A simpler, repeating sequence like ATATATATA would be faster to anneal since it would be really easy to find a spot to reanneal.
I kind of get the logic here. Yet, this wouldn't always produce the exact complement strand. Consider the following:

The point is to illustrate that there could be matching of strands without correctly pairing the whole thing (i.e. there is a shift of the strands).
This means that if you want to fully anneal the strands, you need to find the correct spot in the second strand to begin annealing - which is no better than if these were completely random strands.
So then, why is annealing more complex strands slower? I've tried searching it up on the internet but all I get are people telling me it is true, and without much of an explanation.

What is meant by complexity?
This is the crux of the matter. As is often the case, confusion arises from not defining one’s terms. In this case the three possibilities we have to deal with are:

The extent to which a sequence is not homogenous. e.g. ATATATAT is more complex than AAAAAAAA; ATGCATGC is more complex than ATATATAT; ATGCTCAG is more complex than ATGCATGC. This would seem to be the definition assumed by the questioner (and also in another answer).
The length of the sequence. This is the definition given in the article quoted in the question: “Complexity - the total length of different sequences”. However it is not one that would have occurred to me on encountering the expression.
The extent to which a length of DNA (especially a chromosome) has regions present in multiple copies. This seems not to have been considered in the question, but is historically what was meant be genome complexity deduced from annealing experiments. This is shown in these extracts from a venerable text on nucleic acids, long out of print:

In human cells unique DNA has a Cot1/2 value of 1000 (moles nucleotide seconds litre–1)…Repetitive DNA includes all of the rest of the DNA. Among the repetitive DNA is a fraction which reanneals with a Cot1/2 value of between 100 and 1000…thought to be those [genes] coding for proteins which form major structural components of the cell… [some examples given of multi-copy genes like tRNA]…At the other extreme DNA with a Cot1/2 value as low as 10–3 consists largely of satellite DNA.

Explanation for Case 3 (complex because of multiple copies)
As the article quoted in the question correctly states, “Renaturation, or duplex formation requires random collisions between two single-stranded molecules”. However such experiments are performed with fragmented DNA in solution, not whole chromosomes, so the two molecules that must collide are gene-size or smaller in length. The more copies of geneX or sequenceX there are in the DNA, the greater the number of targets there will be containing geneX or sequenceX, hence the faster fragments containing such genes will anneal.
Explanation for Case 1 (complex because less homogeneous)
Assuming that one is comparing single-copy genes of different degrees of homogeneity, one can imagine that for something like ATATATAT there will be more ‘hits’ that give partial overlaps that may be detected as double-stranded:
A T A T A T A T A T A T A T A T
        T A T A T A T A T A T A T A T A

Alternatively, once bound imperfectly, there may be a greater chance of perfect binding after dissociation because of proximity.
However, it is also possible that writers are confusing or amalgamating this with Case 3, as simpler DNA may actually be present in more copies in a genome.
Explanation for Case 2 (complex because longer)
The explanation here is trivial. If you perform reannealing experiments with two geneomes — E.coli (4.6 Mbp, c. 4000 protein-coding genes) and Carsonella ruddii (0.16 Mbp, 182 protein-coding genes) — employing the same amounts of DNA as 300bp fragments, the fragments from the smaller genome will be approximately 20x more likely to make a random collision with a complementary fragment.

From physics point of view, annealing is about finding the lowest energy configuration of the two DNA strands. The configuration space of two strands has many minima, and after every annealing cycle the strands settle in one of them, which is not necessarily the lowest. One then reheats the DNA to allow it to explore teh surrounding minima and hopefully settling in the one of even lower energy. In a sequence containg many identical elements, such lower energy minima a readily available - in the OP language it would be really easy to find a spot to reanneal. On the other hand, if the sequence elements are very different, a large deviation from the current configuration is required to find a more favorable configuration.


What is the difference between drought resistant non-succulent plants and plants that cannot be allowed to dry out? What features make one plant able to withstand dry spells better than another with relatively similar structure? For instance, one of my Rudbeckias is wilting from drought at the moment, and an Oenothera next to it is not yet showing signs of dryness.

Or like jewelweed (Impatiens capensis), which wilts even while the soil is damp, in full sun, and ragweed (Ambrosia artemisiifolia), which will grow in very dry locations without being phased.

Is it caused by a faster transpiration rate in some plants than in others?

The difference may be related to how the plants fix carbon. While all plants convert CO₂ and H₂O to glucose and oxygen, there are at least three pathways that are used to do it. The C3 pathway is older and less efficient than the CAM and C4 pathways. Many drought tolerant plants use the CAM or C4 pathways because less water is needed. The C4 pathway is better than C3 in drier climates, hotter climates, and when CO₂ or nitrogen are limited. The hard part about this answer is that I'm not a botanist. Wikipedia lists some plants that use C4, CAM, and C3, but there is no comprehensive list, so I can't match up all the plants you mentioned in your question. In general, a higher percentage of monocots, especially grasses, use C4, but a wider diversity of dicots use C4. But you still can't draw conclusions about families of plants, because while corn and sorghum use C4, rice and barley use C3. Ragweed, a plant you say grows well in dry conditions, is a member of Asteraceae, which includes many plants that use C4. However, rudbeckias are also members of Asteraceae, but don't do as well in dry conditions. The C4 pathway has appeared and disappeared in several different plants, making any general claim hard to make. Here are some links that might help:

http://www.en.wikipedia.org/wiki/C4_carbon_fixation
http://www.en.wikipedia.org/wiki/C3_carbon_fixation
http://www.en.wikipedia.org/wiki/Crassulacean_acid_metabolism
http://www.brown.edu/Research/Edwards_Lab/reprints/sage_etal_2011jexb.pdf

If you know more about plants than me, that last link might be helpful, it's about the evolution of C4 pathway in plants and includes lists, but uses the formal species names I just don't recognize.

Plants in drier conditions usually have reduced surface area, thick waxy cuticle covering the epidermis, reduced number of stomata, and water storage tissues that presides in its roots and leaves.

This means that even if the plants are similar, one of them might express more of one of the features shown above.


What really causes cancer? A lot of things are claimed to cause cancer, eating red meat, eggs, smoking, using phones, deodorant, breathing.

Surely these can't all actually significantly contribute to the development of cancer.

I've heard smoking is a big one to lung cancer, with someone--I can't recall--saying that most patients with this cancer are smokers.

What kind of activities/foods are sure to, or have high chances to, lead to the development of cancerous cells and how do they cause them, at a molecular level?

Cancer is caused by the mutations in cells.

Cancer exists because of the failure of cell cycle checks which could actually allow cells to survive with erratic genomes. However, that alone does not cause cancer.

Cancer is the uncontrolled proliferation of cells. That only happens when cells have accumulated enough errors during cell division and each cell division goes undetected to the point that cells refuse to commit apoptosis; they are no longer receptive to the body's control mechanisms.

Cancer cells are also malignant. That means that cancer cells cannot be called cancer cells until they are invasive. That means a few cancerous cells cannot be caused cancer because they don't take nutrients from the body . Also, tumour  suppressor  genes can also cause cancer when they turn proto-oncogenes into oncogenes.


Why can't you just take a vitamin? Why you need a healthy diet on top of that? From what I understand, your body needs certain amounts of vitamins and minerals to maintain health. Why can't we just take enough pills to obtain these vitamins and minerals?

I think the piece of missing information here is the distinction between macronutrients and micronutrients. The info from Mayo clinic quoted in the another answer addresses some reasons why whole foods might be better than pills for obtaining micronutrients (i.e. vitamins and minerals).  While this may be true, most of it remains to be conclusively demonstrated (arguably). However, one clear reason “why….you need a healthy diet on top of that” is (unarguably) to obtain the fat, protein, and carbohydrates that your body uses to create energy. Unlike the minerals that act as cofactors, these macronutrients are the substrate. They are broken down to create the ATP that keeps everything running and they are built up to create the very structure of the body.

  The energy that is consumed in the form of food or drinks can either be stored in the body in the form of fat (the major energy store), glycogen (short-term energy/carbohydrate reserves), or protein. . . to be used by the body to fuel energy-requiring events. *

These are called macronutrients because they are required in gram quantities — hundreds or even thousands of times more massive than the requirements for most micronutrients. As such, they don’t fit in a pill. As tragic as it is, we must keep eating.

*Gibney, M. J., & Nutrition Society. (2009). Introduction to Human Nutrition. Chichester, West Sussex, U.K.: Wiley-Blackwell.

This is more of a biochemistry question and to be honest its a little bit out of my league because I have not had the necessary grad classes to explain nutrition but indeed I will try.
Unknown metabolite cofactors and things like ionization, oxidation and state of matter are the reason that straight up vitamins are rejected by the body and cause really expensive urine and a difficult time otherwise excreting.

Metabolism involves a vast array of chemical reactions, but most fall under a few basic types of reactions that involve the transfer of functional groups. This common chemistry allows cells to use a small set of metabolic intermediates to carry chemical groups between different reactions. These group-transfer intermediates are the loosely bound organic cofactors, often called coenzymes.
Each class of group-transfer reaction is carried out by a particular cofactor, which is the substrate for a set of enzymes that produce it, and a set of enzymes that consume it. An example of this are the dehydrogenases that use nicotinamide adenine dinucleotide (NAD+) as a cofactor. Here, hundreds of separate types of enzymes remove electrons from their substrates and reduce NAD+ to NADH. This reduced cofactor is then a substrate for any of the reductases in the cell that require electrons to reduce their substrates.
Therefore, these cofactors are continuously recycled as part of metabolism. As an example, the total quantity of ATP in the human body is about 0.1 mole. This ATP is constantly being broken down into ADP, and then converted back into ATP. Thus, at any given time, the total amount of ATP + ADP remains fairly constant. The energy used by human cells requires the hydrolysis of 100 to 150 moles of ATP daily, which is around 50 to 75 kg. In typical situations, humans use up their body weight of ATP over the course of the day. This means that each ATP molecule is recycled 1000 to 1500 times daily.

-wikipedia
If you did not like that explanation of cofactors maybe you will this:

Whole foods offer three main benefits over dietary supplements:
Greater nutrition. Whole foods are complex, containing a variety of the micronutrients your body needs — not just one. An orange, for example, provides vitamin C plus some beta carotene, calcium and other nutrients. A vitamin C supplement lacks these other micronutrients.
Essential fiber. Whole foods, such as whole grains, fruits, vegetables and legumes, provide dietary fiber. Most high-fiber foods are also packed with other essential nutrients. Fiber, as part of a healthy diet, can help prevent certain diseases, such as type 2 diabetes and heart disease, and it can also help manage constipation.
Protective substances. Whole foods contain other substances important for good health. Fruits and vegetables, for example, contain naturally occurring substances called phytochemicals, which may help protect you against cancer, heart disease, diabetes and high blood pressure. Many are also good sources of antioxidants — substances that slow down oxidation, a natural process that leads to cell and tissue damage.

-The great Mayo Clinic


how can a recessive allele become represented in a significant number of individuals in a population Darwin believed that individuals that are poorly adapted to their environment are less likely to survive and reproduce. This means that their genes are less likely to be passed to the next generation. Given enough time, a species will gradually evolve.

-individuals in a species show a wide range of variation
this variation is because of differences in their genes

-individuals with characteristics most suited to the environment are more likely to survive and reproduce. The genes that allow these individuals to be successful are passed to their offspring.

In genetic terms, evolution is any change in the allele frequency of a population.

A recessive allele can become represented in a significant number of individuals in a population, how?

A recessive allele is one whose phenotype can be masked by a dominant allele. A recessive allele is not necessarily deleterious, and the dominant allele does not necessarily have higher fitness than the recessive allele. Fitness and dominance are often confused, but they are not the same thing.

In some scenarios, the recessive allele indeed confers a fitness benefit, and when it does, it is predicted to increase in frequency rapidly because homozygous recessive individuals have higher fitness than both homozygous dominant genotypes and heterozygotes.

A recessive allele can also persist in a population if it is deleterious in homozygotes but confers a heterozygote advantage. The most famous example of this phenomenon is in Africa, where individuals heterozygous at the sickle cell locus have a fitness advantage because they are resistant to malaria. A higher prevalence of sickle cell phenotypes occur because selection for heterozygotes maintains a high frequency of recessive alleles in the population. For more, see Templeton (1982, http://www.indiana.edu/~curtweb/L567/readings/Templeton.pdf) and Allison (1954, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2093356/).

Recessive diseases are insidious because most of the time the dominant (healthy) allele masks them. Then every once in a while, someone in the village gets a wide range of chronic, unexplainable symptoms that the local shaman explains as a random curse.

While these are a no-brainer in the developed world, they are a daunting problem for primitive cultures and third-world nations where superstition is much more commonly practiced than science and no one knows what a "genome" is.

With even distribution, a quarter of the population has the disease and half of the population have 1 allele for the disease.


Why does histamine cause bronchoconstriction? What purpose does histamine-caused constriction serve in lungs during allergies and such, since it's vasodilator in other parts of body. Wouldn't it be more practical to vasodilate lungs so that white blood cells can arrive and toxins can be flushed more quickly.  Thanks in advance

Basics first: Crash Course

We will be introducing:
Autonomic divisions, Histamine and Vasoactivity (or Broncho-)
Starring: Innervation of the Lower Respiratory Tract

Lower respiratory tract is mostly innervated by the parasympathetic division, it has only scarce sympathetic-receptors there.

So, why it matters?

Autonomic divisions serve as fight-or-flight and rest-and-digest mechanism for the body as to respond for sudden changes.

You are having a good picnic, your body is in a state of rest. Your body is absorbing nutrient and enjoying your day. Blood isn't needed so much on your hands, or skin, or muscle.
This is the Parasympathetic Division

Suddenly a snake appeared in front of you, you scream, you panicked, and you flight away (or fight?). Your eyes dilate (where is that snake!), your muscles work, your respiratory tract dilates, as to prepare to avoid being killed by the snake. Blood rushs in to your muscles, but shunts on your digestion part, as what every you eat doesn't matter.
This is the Sympathetic Division

What matters?

Parasympathetic division only knows how to lock down things.
Sympathetic division can lock things, open things, and so, and so, and so.

How does sympathetic division work with so many things?
It has different receptors which reacts differently on input
Imagine people when reacting to clown: NOOOO and YAYYY

Histamine serves as modulation to outputs of autonomic division, directly or indirectly

Histamine is a broad-response chemical used to respond against an infection. As different cells have different ratio of autonomic division, it can cause dilation or constriction on different places.

One thing to note that, in a nutshell, histamine serves to buffer the work of autonomic innervation. It is entirely up to the regular function of the "autonomics" there to do their business.

Vasoactivity (or Broncho-) is achieved by state of balance between innervation by the autonomic division and local signals

Local signals play a part. A balance of signal determines the effect of innervation.
For bronchi, when histamine puddles, local signal sends stronger input than global innervation. Hence, the parasympathetic takes over.

  histamine-caused constriction serve in lungs during allergies

Histamine serves as to protect the lower respiratory tract from inhaled irritants. The lower respiratory tract is innervated by parasympathetic stimulation. Parasympathetic stimulation only knows one command: constrict and strike.
When histamine buffs up the signal, it constricts.

  vasodilator in other parts of body

Indeed it is. The vasodilation effect is achieved by GPCR-mediated sympathetic innervation.
Histamine buffs a diverse response of sympathetic division, hence dilates the blood vessels.

  Wouldn't it be more practical to vasodilate lungs so that white blood cells can arrive and toxins can be flushed more quickly

In line with WYSIGYG, vasodilation is different from bronchodilation (or constriction). We have noted above that the operators are different, and they serve different functions.

As a note, white blood cells can't just come anywhere they want. Ever seen your nasal mucus being very viscous? That will happen your lung when white blood cells arrive.
White blood cells also cause fibrillation, which succumbs people when does.

It has been a reason why pneumonia and lung-infection related diseases, tend to succumb people by drowning them in "their own mucus".

Another part of sending much things down your lower respiratory part is...
How could you clean the mess up?
The upper respiratory part is the defense capable of trapping irritants by mucus and send the mucus to your stomach.
Bronchus? Not so much. More mucus will eventually drown your lungs.

I invested 50 minutes for this.


What is the name of this tiny creature? Place: South India,

Metropolitan, Year: 2017; Night Time.

Size: 1-2 cm (Very Tiny)

From the posture, it looks like it can belong to Geometridae (Larentiinae). But I haven't been able to find a species that has that particular color.

It's 'Indian skipper'. Family :Hesperiidae.
Source: http://abeautiful-butterflys.blogspot.in/2010/04/hesperiidae-butterflies-of-india.html


What is this? Found in southern Illinois Found in southern Illinois in the driveway.  What is this?

Nice find! It looks to me like a Bush Cicada or scientificly Neotibicen dorsatus. It also looks like its injured, because we can see the white liquid around its wings and abdomen. Bush Cicadas tend to have a yellow or brown color but as shown here there is a wide variaty to the colourations that it might have:

Size (Adult, Length): 35mm to 57mm (1.38in to 2.24in)

Identifying Colors: yellow, brown, white, gold, black

North American Reach (Though Not Limited To*): Arizona; Arkansas; Colorado; Illinois; Indiana; Iowa; Kansas; Kentucky; Louisiana; Minnesota; Mississippi; Missouri; Nebraska; New Mexico; North Dakota; Oklahoma; South Dakota; Texas; Wyoming; Mexico.

Here are and some photos:

Adults:

It looks like a cicada of the Genus Tibicen, perhaps a "dog day" cicada (because of when they come out.)

Here are others of that genus; they're very similar.

Something is not right, though. I can't account for the white opaque liquid; even pictures of injured cicadas don't show it (at least that I can find.)

It looks like yours was dipped in Elmer's glue or something similar; the fluid is pooling under the wings and around the body. They usually hatch from a dry case, so I'm mystified.


Mushroom Identification (USA) I would like some help identifying this mushroom I found in my yard.
Location: Southeast Georgia
Near Pine trees after heavy rainfall
Color: Light brown to Dark Red, biggest is about 4 inches in radius

It is some type of boletus. You would need a spore print and a few more examples to decide which one. They are commonly found under conifers.The books say most are editable and good taste. The couple kind I have eaten had no flavor , not worth collecting. The tubes instead of gills on the bottom of the cap are an indicator of boletus group.


Geographic regions as subpopulations/demes I am developing a computational simulation for DNA barcoding. One of the parameters in my simulation is the number of subpopulation/demes, which I label as $K$. Most studies that use DNA barcodes tend to focus on a single geographic region.

My question is: is it valid to presume that a single geographic region is equivalent to a single subpopulation/deme?

For example, if the focus was on cichlids of Lake Malawi, would it be a safe assumption that Lake Malawi comprises a single subpopulation/deme?

Eventually, I would also like to incorporate migration rates into my simulation, but these are very difficult to estimate without accurate data on $F_{ST}$.

Any insight would be most helpful and is warmly welcomed.

It is impossible to answer your question in the general sense. Yes, detailed population structure may matter. It very much depends upon what your question is and what parameter space you are willing to answer but it is possible that assuming panmixis would be unrealistic.

Note that accurate data on $F_{ST}$ won't suffice to estimate migration rate $m$.

Note also that many simulation platform already exist and you might not have to reinvent the wheel (see Sequence evolution simulation tool).

For simulating DNA barcoding, it is valid to presume that a single geographic region is equivalent to a single subpopulation. Although there do occur cases where one or two nucleotides differ at the same location, that is rare, and these few differences would still cluster together in any analysis of barcode data.


Name of this kind of stain on fruits and how do they form Last year I made some photos with avocados touched by some stains. They were even more delicious than the regular ones.

What's the name of such stains and how do they form? My guess is that they form because the fruit was hurt but maybe that's just me.

Later edit: A farmer told me it's a disease. Then I've found that it looks quite similar with apple scabs. Is it correct to call this "Avocado scab"? Is it made by the "Sphaceloma perseae" fungus?

Here are the photos:

You never visited the avocado blemish identification fanpage? do you use google? it's quite good.

http://ipm.ucanr.edu/PMG/C008/m008fpfrtdmg.html
Causes of avocado Damage

Avocado thrips

Anthracnose

Caterpillars

Branch canker and dieback

Fruit and stem-end rots

Genetic mutations

Greenhouse thrips

Latania scale
Mechanical injury

Nutritional disorders

Off-season fruiting

Persea mite

Phytophthora fruit rot

Sooty mold

Sunblotch

Sunburn

Vertebrates

Weather extremes

Wildland fire

mosty they are insects, funghi, viruses, mechanical forces, and sometimes, like the woody avocado, the cause is unknown:

referenced.


Can humans' ability to dive with only breathing modifications tell us anything about our evolution? Can humans' ability to dive with only breathing modifications tell us anything about our evolution?

For example, it is possible to imagine a human anatomy that would be destroyed by the pressure of a few meters of water, and yet humans can, with scuba apparatus dive to several hundred meters.

This is not a complete answer to your question, but your question prompted me to research the Mammalian Diving Reflex, which is used, according to the article, as a survival mechanism rather than assisting us in day to day functioning.

Looking at the evolution of the diving reflex, and how it appears in varying degrees in all mammals, suggest that it has been around for a long time, this article suggests for over 125 million years.

Actually, there was a very interesting Animal planet episode (http://www.youtube.com/watch?v=Cm3XdC-p8_I) on the recent news about the probable discovery of a mermaid body. In the show, scientists suggest that may be our evolution has had some roots under water. First, our body structure is far more plastic and ergonomic than the structure of a monkey. We are great swimmers in our movements and as you mentioned - our ability to hold our breaths under water for a very long time - the record is about 20 minutes! We can easily control our breathing which is something usually connected with marine mammals. In difference of other animals, we are almost hairless. Just like other marine mammals, we are born with insulating fat distributed throughout our bodies. This keeps us warm in water. All this takes place in the "Aquatic ape hypothesis". This view claims that our alleged ancestors went through a watery stage in our evolutionary development.

Of course, although all those facts connect very conveniently, the theory has not been proven yet by experiments and is so far just an idea that should be considered and investigated more.

In addition, some people still have marks from gills as an atavism.


Can carnivores survive on a (processed) vegetarian diet? Why or why not? There are many differences in for example the digestive system between carnivores, herbivores and omnivores.

It seems that in certain kinds of species adaptability with respect to diet is possible. What I have heard is that it is impossible for carnivores to survive on a non-meat diet.

Therefore I wanted to ask: Is it really impossible for a carnivore to survive on a vegetarian diet, even when the fruits/vegetables/plants are processed? I could see how their digestive tract would not allow for them to survive on grass, but what about certain kinds of nuts, mushrooms, or even processed plant based foods?

If it is impossible to survive on these diets, why?(With respect to either causes in their digestive system or substantial differences between meats and any type of vegetarian food.

With arbitrarily broad meaning of "processed", yes. If absolutely nothing else, elemental purification and inorganic synthesis of something chemically resembling meat in nutrition is possible. Prohibitively expensive and stupid, yes, but possible. So then the question becomes exactly how much processing you need to do. Without clear bounds on that question and inadequate research on the metabolism of obligate carnivores, nothing closer than a broad stab at an answer makes sense. That said, here's a broad stab.

For instance, you'd probably need to synthesize vitamin D3, carnosine, DHA, and a handful of other things from plant extract, which is possible but difficult. Carnivores often have carnosine synthases, for instance. Cats have two distinct carnosine synthases. In terms of dietary sufficiency, that may or may not be enough. To be sure, you'd have to break it down to amino acids and build it back up again, essentially. Obligate carnivores are likely to have a number of other metabolic needs that aren't met with, for instance, pulverized soybeans. You're going to need at least one vat for fermenting raw amino acids into carnosine, and probably another for vitamin D3. Seawater microalgae contain lots of DHA, so that is probably something to look into. You could oversupplement alpha-linolenic acid instead of supplementing DHA, which might or might not work. There's not a lot of study into carnivore metabolism, so prepare to make some discoveries the hard way. Genetic studies can only take you so far, so don't try this on your favorite pet first.

In short: yes, you can raise carnivores on a diet made from plants and plant material. Rhetorical you, as in it is possible. It's probably not something you can do at home, even if you're wealthy.

(I'm assuming "feeding the vegetable matter to chickens" falls outside the domain of "processed" but it would be much easier than large-scale amino acid purification and fermentation.)

Of course it is possible for a carnivore to live with a vegetarian diet. Technically you could come up with a complete meal out of vegetables and make a carnivore pup live with it. Dogs and cats are good example of it. They can learn to eat vegi-processed food and as far the nutrients needed are present they will grow and live well. To make them eat raw vegetables is more difficult.

As correctly asked by the commenters, here some links where you can find some info about:

Vitamin D3 in plants (many thinks that only meat/fish contains it)

Carnosine also can be synthesise by the body, here the main references

DHA that is contained in several veg food

Vitamin B12 from cyanobacteria


Can our body adapt to periodic fluctuations in sleep? Suppose that if I've to attend a morning class then I must wake at 5 AM in morning. Next, if I don't (attend the class) then I wake up at 7-8 AM.

I've experienced that, since I do attend those classes almost regularly, my body has adjusted itself (sleep cycle) to wake at 5 AM almost precisely without a alarm set and has also decided when to sleep (it seems to demand 7-8 hour of sleep). This, I think, is common to most of us.

Now suppose that I attend classes only on alternate days. Put simply, I wake up at 5 on first and at 8 on the next day and so on. This implies that I am constantly switching my sleep cycle every day. Would my body, now, be able to adapt to this continuously varying cycle (which is but periodic).

I suppose no, and that is just a guess based on my experience. But provided I give my body enough time, I think that it may really adjust to this scenario.

On a side note, assume that (in case it matters) I take a sleep of 7 hours during class days and a sleep of 8.5 hours during holidays to make this data realistic. .

In the same way that it takes time to fully adjust to jet lag (~ 1 timezone/day), it is unlikely that the body can adjust to alternating patterns of 3hr gaps on wake time on a daily basis [Ref. 1].  We simply have not evolved to jump timezones.  The most healthy thing to do is to have one time to get up each day (5am) so that your body is in sync.

[Ref. 1]: Review about circadian rhythms

Definitely your body will adjust. All you have to do is make it a thinking point that you have to wake up early at 5 and trust me you will, if you don't think hard about it then you will wake up later than 5.


10 inch spider near Mexico City Four years ago I found a spider so big that I'll never forget. Unfortunately I don't have a picture but I guess there isn't a lot of big spiders in Mexico. So here are some things I remember:

It wasn't a brown spider, I think it had red legs with some parts black and others white.
Its legs were skinny and very long
The main body was tiny compered with the spam of its legs.
I found it at noon, after I moved to my new house. Unfortunately it wasn't moving when I found it
The spider didn't have any visibly hair.

That's all I can remember. I know that this may be impossible but I don't know what else to do.

It almost definitely wasn't 10 inches, but there are some pretty big spiders in Mexico. There is a species of spitting spider with a 9 inch legspan but it lives in South America not Mexico.
Scytodes globula

The cellar spider has a legspan of up to 3.6 inches and a comparatively small body with long skinny legs and no visible hair, but I can't see how that would be confused for 10 inches.
Pholcus phalangioides

The giant crab spider fits that description to some degree. It has a legspan of up to 4 inches.
Heteropoda venatoria

The golden silk spider is very large with long skinny orange and red legs.
Trichonephila clavipes

Sounds like a Mexican Red Knee Tarantula. they are kept as pets. not dangerous except for irritant hairs which they can project and which can get into eyes.

https://www.google.com/search?q=mexican+red+knee&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiJlvWuyvLgAhULlhQKHbfrD3IQ_AUIDigB&biw=1431&bih=734&dpr=1.65


What kind of mushroom is this in central Europe? I found some mushrooms in the forest and I'd like to know what kind it is, for being able to tell how to protect the trees from it.
Growing Info
growing location: central Europe, forest
host plant: beech tree, alive
season: late Summer (Sept. 15th 2020)
The area where the mushrooms were found is a typical beech forest with unusually low water levels, as the last few summers have been drier and warmer than usual. I presume the trees suffer more from these mushrooms because the trees are weakened due to the hot weather and little rain.
Some of the mushrooms dry out while on the host tree.
Picture Taking Conditions
The closeup pictures were taken at home. This was after transporting the mushrooms and storing them in the fridge for 2 days. They got a bit squeezed during this procedure.
Pictures
host tree:

host tree from below:

multiple mushrooms, pic A:

multiple mushrooms, pic B:

bright mushroom, pic A:

bright mushroom, pic B:

bright mushroom, pic C:

cream colored/older mushroom, pic A:

cream colored/older mushroom, pic B:

cream colored/older mushroom, pic C:

Could be oyster mushroom. Get some books. Look up Pleurotus ostreatus; a book I found it in is primarily for US,although mushrooms often have very wide distribution. One book I have says " The worst thing you can do is pick mushrooms ,then try to decide what they are ;if they are edible". The recommendation is to learn some local editable mushrooms and then hunt for them.


What type of Insect Egg is this? Can you please tell me what type of insect eggs these are? I found them in the corners of my office kitchen behind boxes and cardboard. Found them in between the broom bristles. Found them along the edge of the wall. There are quite a few of them.
If you could please provide me some tips on how to avoid getting these eggs or killing off the main insect would be helpful.

These are probably cockroach cases, or oothecae, that may contain up to 50 eggs, depending on species.

It looks like they are oothecaes of German cockroaches.

You can read more about baby cockroaches here.

perhaps it's a fly chrysalis. If you had a mouse that died, that would do it. put them in a jar and wait. https://www.insectes-net.fr/pieride/images/pier159gf.JPG


The alignment of fingers in our hand I noticed that in my hand the index and middle finger are aligned in one direction and the next two fingers somewhat in the opposite direction. My question is, why are our fingers aligned in that way?
Moreover, is it of any evolutionary significance?

For clarity, I am posting a picture of my hand.

This is normal, and the effect is accentuated dramatically if you pretend to be holding an imaginary round object (somewhat smaller than a baseball, for instance.) The fingertips will all approximately point towards the very end of the thumb.

(See upper right image.) If the stone were smaller, the effect would be more visible.)

This orientation of the fingers makes the hand and fingers extremely versatile, being able to grasp and manipulate objects of a wide variety of shapes.

It also allows fine manipulation of thumb and fingers. Touching each fingertip to the tip of the thumb quickly shows the same effect - the fingertips approximately align with the thumb. If they didn't align this way, we would lose some of our very fine (as in requiring great precision, not as in quality) motor skills.

I'm not going to hypothesize on why the hand evolved the way it did; it's very efficient and that seems reason enough.

Observation: The bend in the fingers gives the straight hand a more compact appearance so that we can actually tightly close the gaps between the fingers.

Hypothesis: Without the bend small gaps would remain between the tip and the first joint of the fingers unless we press the fingers together with force. Not having this gap could protect the fingers from injury while walking or running through tight underbrush because the likelyhood of entangling the fingers in some vine or branch is lower. Also, being able to compact the hand may help us to easier scoop up water with our hands.

(yes my hand show the same slight bend in the fingers)


What species is this? What the fruit? The berries of the fruit are sweet. The tree is growing in Israel.

Looks like it is Phytolacca dioica.  I found this by searching your first image in a phone app called Pl@ntNet (PlantNet).  Looking at Wikipedia confirms the ID.

Interestingly, you said the fruit was sweet.  The North American relative Phytolacca americana is extremely poisonous.  A brief search suggests your species is possibly poisonous, with reports about the leaves more common than the fruit.

Perhaps a white mulberry? See the Wikipedia: https://en.wikipedia.org/wiki/Morus_alba


Why does a worm's skin need to be wet for oxygen to diffuse across it? Pages I've read about worms' respiratory systems says that the skin needs to be wet (covered in mucus) or oxygen won't diffuse across the skin. Why? If there is more oxygen outside the worm's skin than inside, what prevents it from diffusing across the skin, even if the skin is dried out?

The quick answer: When the skin dries, the lipids in the cell membranes of the skin tissue undergo a phase transition which makes the membranes less permeable for oxygen.

Explanation: The lipids of the cell membrane can exist in different phase states. In the liquid disordered phase the lipids are relatively flexible and mobile, making this phase more oxygen permeable compared to the liquid ordered phase, in which the lipids are more rigidly packed.

The phase transition temperature of lipids increases upon dehydration (another reference), meaning that at the same ambient temperature, a dry lipid membrane is in the liquid ordered state and a wet lipid membrane is in the liquid disordered state.

Therefore, a dry cell membrane is less oxygen permeable than a wet one.

Respiration in aquatic organisms involves diffusion of dissolved gases present in the aquatic medium across their permeable cell membrane . In worms which lives in moist environment the skin functions as a respiratory surface and requires the surface to be moist to enable exchange of gases.


Why are bruises not lethal? Given the following:

bruises are caused by minor trauma which breaks blood vessels beneath the skin, causing bleeding
the mechanism by which bleeding stops is clotting
blood clots inside the body have an unfortunate tendency to get into the bloodstream and cause blockages, leading to severe problems such as strokes or heart attacks

why is it that people don't die from bruises?  What mechanism does the human body have to keep this from happening?

blood clots inside the body have an unfortunate tendency to get into the bloodstream and cause blockages, leading to severe problems such as strokes or heart attacks

This statement is primarily true only for blood clots within blood vessels, especially in the veins. When you are talking about bruising, you are talking about clots outside of the vasculature.

When a blood clot occurs in an artery, it can block that artery or break off, flow downstream, and block some smaller distal vessel. These events are most severe when they affect crucial organs like the brain and heart ("stroke" or "heart attack"), though of course any organ can be damaged in this way. However, blood clots in arteries can't ever directly affect a tissue that is not distal from where the clot starts, because they can never pass through capillaries or travel backward.

When a blood clot occurs in a vein and is dislodged, it can follow the increasingly larger venous system back to the heart, where it can cause a pulmonary embolism (blockage in the lungs) or, via a patent foramen ovale, travel to the left-side circulation and end up anywhere, including the coronary arteries or blood vessels of the brain. Similarly, clots that form in the venous return from the lungs to the heart or in the left side of the heart itself can travel anywhere (except the lungs) and create a blockage.

For a clot outside the vasculature, for it to have an effect somewhere else systemically it must re-enter the vasculature. This is simply not possible in most situations, because the vessels involved are very small, and during bleeding the blood is flowing out of vessels: there is no pressure gradient to push the clot back into the vessels.

In more severe cases of injury where major vessels are involved, clotting in those major vessels can indeed be a problem, but not for common occurrences of bruising.

(see also @anongoodnurse's answer that contains a good clarification of what exactly a bruise is, as well as how there are risks from very serious bruises but not the same way the original question implied)

Bruises usually damage capillaries (think of them as being side roads well away from the expressway and major routes). Just as closing down a few side roads in a lightly populated suburban or rural area a mile away from a major interstate is unlikely to cause a backup/traffic jam, blood clotting in capillaries at a bruise shouldn't generate dangerous blockages.


Are all genes transcribed in differentiated cells? My textbook tells me that it’s specific transcription factors that allow for a different set of genes to be expressed in different cells (differential gene expression). My book gives the example of liver and lens cells—liver cells contain the specific transcription factors (STFs) to activate the enhancer for the albumin gene, while lens cells contain the STFs to activate the enhancer for the crystallin gene. Liver cells do not have the STFs to activate the crystallin gene, and lens cells cannot activate the album gene.

However, my book also tells me that there is a basal level of transcription that arises from the binding of general transcription factors. Enhancers only increase the rate of transcription on top of that basal rate. Does this mean that in differentiated cells, all genes are indeed transcribed? I.e. a lens cell does transcribe the gene for albumin and the liver cell does transcribe the gene for crystallin?

(The wording of my book dissuades me: "Liver cell: The albumin gene is expressed, and the crystallin gene is not. Lens cell: The crystallin gene is expressed, and the albumin gene is not.”)

No
Not all genes are transcribed, repressor proteins and nuclear receptors can bind the DNA preventing transcription of particular genes. Even things like histone regulation can prevent transcription. There may even be epigenetic regulation of transcription.

Source 1

Source 2

I think genes are transcribed but either mRNA is not transcloated (moved) into the cytoplasm or they are not translated (maybe degraded).I think if you do RNA screening you will get same positive results in both liver and lens cells (as transcription occurred and if your procedure is not having any error) but if you do a western blot, the result will change as now we are seeing the things at the protein level.
So even though all of our cells have same gene composition depending upon the tissue and organ they have differential RNA selection so that they will not waste resources in making unwanted proteins.


Are there any papers arguing against vaccination in French? Disclaimer: This question is NOT about challenging the safety or efficacy of vaccines. It is only asking for tips on providing credible references that may show harmful effects of vaccination, if any.

In my French class, we were asked to debate an issue in current events. My topic is vaccines in children or adults.

The challenging part is that I was assigned to argue against vaccination, and I have to back up my arguments with credible sources (not blogs) that are in French. Hopefully some of you could point me towards some links to articles or research papers in French.

Please avoid discussion on safety and efficacy of vaccines, including local and global policies on their use. I just need help with this topic for my French class

I wish you good luck, as 99.99% of the anecdotal claims out there that conclude vaccination is bad are based on unfounded rumors.

Note that much of the negative public opinion is based on a fraudulent (and retracted) paper by Wakefield in The Lancet (1998). Unfortunately for you, however, it is in English.

My French is a bit rusty, but if you go to Google Scholar and type in a search term like vaccination results in autism (les résultats de la vaccination dans l'autisme) or Wakefield vaccination autisme something might pop up in French that advocates against vaccination.

The only angle I can think of that isn't "Haha, I can't believe these people are allowed to vote" is that the enemy we know is better than the enemy we do not know.

I see no reason why the classic argument of selection pressure doesn't apply. (See Warfrin(spelling?) resistance in rats, the resistant rats required more vitamin-k, thus more time out in the sun, so in a warfrin free environment are at a disadvantage, but thrive in an environment with warfrin)

Unfortunately (fortunately) evidence doesn't really support that, in fact we have eradicated several diseases already entirely and nothing replaced them.

(Long comment sorry)

By the way! Do tell us some of the arguments that come up!


How to interpret Glimmer scores? I am trying to find orfs with Glimmer. At the end, Glimmer gives me a .predict file with the orfs and a corresponding raw score.

When I look at the documentation, it says about the score, "This is 100 times the per-base log-odds ratio of the in-frame coding ICM score to the independent (i.e., non-coding) model score. It gives a rough quantification to how well an orf scores that can be compared between any two orfs." You can look here for the documentation-

https://ccb.jhu.edu/software/glimmer/glim302notes.pdf

But what does the score really mean in an absolute manner? How do I realize for an orf, if the score is significant or not?

The score is the log odds ratio, times 100, that the ORF that you input is a coding region. For example, if Glimmer thinks the log odds are 10 to 1 that your region is coding, then your score will be 10x100 = 10000. Log odds of 10:1 imply more than a million to one certainty.


Is a virus a poison? I've understood that a virus is not a living organism (like e.g. a bacterium). From Wikipedia I get that a poison is a substance that reacts physically or chemically with molecules in the human body. Since a virus is a protein that binds to certain cells in the body and alters the cell's function in a harmful way (resulting in the production of more viral matter), why is a virus not a type of poison? (Or is it?)
Additional info:
I'd like to understand the difference between them—if any—on a chemical and physical level, as well as the consequences for treatment. For example: we all know by now that viruses can only remain harmful/intact on surfaces for a certain amount of time. However, I would think that a poison on a surface does not have such a time limit (but I may very well be wrong). What's the difference, if there is one? Why is licking a banister with viral load older than 4 (or so) days not harmful, but is licking a banister with poison older than 4 days?

Although "Virus" literally means "Poison" in Latin, it would be a great over-simplification to regard a Virus as a Poison.
Now, most poisons are chemical compounds that interfere in some chemical pathway in our body. For example:

Carbon Monoxide: Binds with Haemoglobin, rendering it unable to transport oxygen
Sarin: Indirectly inhibits degradation of the  neurotransmitter "Acetylcholine"
at the synaptic cleft.   Mechanism of action of Sarin

Hence most poisons are quite "simple" in their actions. However, viruses can be considered as a complex machinery of functions that interfere with a multitude of processes in our body including cell transcription, receptor-mediated endocytosis, et.c
Hence, the best analogy would be to consider a virus as a tactical poison.
Now, as for last question, viruses are fragile assembled structures.  Viral Self-Assembly

Environmental factors like heat, uv-light, oxygen, etc may damage the assembled structure. Hence, viruses have a self life, and so do may poisons.
  Sarin (self life)
However, poisons tend to have a longer self life because chemical compounds are more stable than the capsid of viral proteins with weak hydrogen bonds.
As per David 's suggestion, poison is defined as "...substances that cause death, injury or harm to organs, usually by chemical reactions or other activity on the molecular scales, when an organism is exposed to a sufficient quantity."  Wikipedia
Viruses do work at molecular level, but not in the same sense as poisons do. Hence, viruses do fit into the description of poisons but not precisely.
Hope you find this helpful.

Is a virus a poison?
In toxicology, a virus is not classified as a toxic agent or a poison but as a biological agent (regardless of whether you consider it to be living or not). With the main distinction being the biological agents reproduce. You can find different definitions of "poison" in different sub disciplines of toxicology, but generally it's any substance capable of causing toxic effects in relatively small quantities. A "substance" in this case is considered to be a single agent. Just as salt-water is not a single substance but a mixture of substances, a virus is a structured organism made of proteins, nucleic acids, and other macro-molecules. Its often the case that none of these different parts are solely responsible for the toxic effects of a virus, but instead it's the action of viral replication which causes cellular damage leading to disease.
There are some biological agents which also produce toxins or poisons. One example is Clostridium tetani. This organism can infect an open wound, but it's toxicological effects are not a result of direct tissue damage caused by the organism, but of the tetanospasmin toxin it produces, which is a potent neurotoxin and the causative agent of tetanus. Again, in this case, C. tetani is the biological agent, but tetanospasmin is the toxin/poison.
we all know by now that viruses can only remain harmful/intact on surfaces for a certain amount of time. However, I would think that a poison on a surface does not have such a time limit
Neither statement is universally true. There are viruses that can remain infectious for months in the environment, and some bacterial spores that can survive for years. There are also some insecticides (poisons for insects) that breakdown in a matter of days in the environment. It just depends on the specific properties of each different agent, and on the environment they are in.


Value of r (intrinsic rate of natural increase) What is the current value of 'r' (instrinsic rate of natural increase) in India? How do we calculate it?

My book says that In 1981, the r value for human population in India was 0.0205. But this link (https://www.google.co.in/amp/knoema.com/atlas/India/topics/Demographics/Population/Rate-of-natural-increase%3fmode=amp) says it was around 22.50 in the year 1981. Such big discrepancies are a query.

NCERT shows per capita value is divided by 1000, not hundred (%). So the data you see is 22.50 per thousand! So, the per capita rate is 22.50/1000 = 0.02250 that is almost equal to 0.0205 given in book!

To make you understand better, remember that GDP and per capita GDP is different, the same way birth rate or death rate is calculated per 1000 but when we ask per capita we have to actually divide it by 1000.

Now in 2016 , it is 0.01019 i.e. 0.0102

I hope you understand!!

If we consider birth and death rates given by government in 2016 and 2017 , then the value ‘r’ is 12.0 . Per capita birth rate given is 19.3 and per capita death rate given is 7.3 so using the formulae dN/dt= (b-d)N.


What would happen if you combined the world's deadliest diseases & viruses? What would happen if you took the deadliest diseases/viruses in the world and combined them in a single medium (a solution of water or a test subject)? Would the strongest virus defeat the rest or would a  new deadly virus be created?

Viruses in the same cell can recombine (although they don't always do). This can happen by crossing-over of the genomic strands or reassortment of genomic segments. Therefore, you can get a new virus out of the fist two. The new one is not necessarily deadlier than the first two. If there's no recombination, the test subject will enjoy both diseases until the deadliest one kills him.

See viruses are made to destroy the host, not other viruses, so putting different types together really wouldn't have much an effect would it? as Manuella answer says, the host cell will simply suffer (or enjoy as he says) with both at once. Viruses don't mate so I sincerely doubt there would be a "combination". What some [evil] scientists are doing is that they take bacterium or viruses and they genetically modify them, and though this is a seriously tedious process, a bio-weapon could be created. Google bio-weapons and how they are made by governments.

Also, this would probably cost you a TON of money to do such a dangerous and complex project, and I doubt that anyone sensible would sponsor you.


Why does it hurt when water touches cuts? Why do we feel a burning sensation when water touches cuts/wounds? People suggest applying oil over cuts while bathing to prevent water touching it, but water is heavier than oil so it shouldn't work, but it does, Why?

Water changes the local ionic concentrations and therefore induces an electric
signal at exposed neuron membranes.Oil is used to prevent entrance of water to the cut because it is hydrophobic i.e. repels water but attaches to the tissue.
Gravity plays no role here.

Your nerves withold a solution that has an electrical charge, when water enters a damaged nerve and nerve membrane, it changes the electrical balance in the nerve. Wounds are supposed to be treated with physical cleaning and topical antisceptic.

Here is a more scientific account:

  Cells normally have a functioning
  ion pumps. Cells are surrounded by a membrane that acts as a wall with
  little holes that ions(sodium,chloride,potassium, calcium) can pass
  through with difficulty.  There pumps in functioning cells exchange of sodium, chloride and potassium.  This causes a
  difference in electrical potential across the cell membrane, in effect
  making the cell a battery. By exposing that tissue to water, which has
  no sodium or chloride, you immediately changed the concentrations of
  these ions surrounding these injured pain cells causing them all to
  fire at once.

Cleaning is normally water and soap or saline solution (9mg/L approx).
Non stinging antisceptics currently favored by doctors are Betadine, Merbromin, amonst others.

I like alcohol for reed cuts etc because it indicates when the exposed inner cell inside the cut and under the miasma have been well sterilized and attained.

https://www.quora.com/Why-do-wounds-hurt-more-when-they-get-wet


Why are diabetic people often overweight? I was looking at diabetes the other day, and I noticed something strange. Lower amounts of lipase are a symptom of diabetes, as is overweightness. However, since lipase is the enzyme that breaks down fats, shouldn't a lack of it mean that less of it enters your blood stream and is simply excreted instead? In that case, how come diabetic people are often overweight?

This question has been bugging me for ages, does anyone know why?

How are diabetes and obesity connected in light of low lipase activity?
Short answer: There's more than one type of diabetes.  (And to complicate things, there's also more than one type of lipase.  It's unclear from the question which type were mentioned in what you read.)

Diabetes mellitus is usually divided into Type 1 (insulin-deficient) and Type 2 (insulin-resistant).  Obesity is a risk factor for Type 2 diabetes, but not all diabetics are overweight. In fact, people with Type 1 are often lean.

Decreased lipase activity is not a major symptom of diabetes.  However, these two articles suggest that plasma lipase activity may be lower in cases of Type 1 diabetes but not Type 2.
Junglee, D. et al., Low pancreatic lipase in insulin-dependent diabetics, 1983.
Dendona, P. et al., Exocrine pancreatic function in diabetes mellitus, 1984.

People with type 1 Diabetes have a heritable defect in their genes. People with type 2 Diabetes eat too much. The prevalence of type 2 diabetes has increased by a factor of 2 since the 1970's. This means more patients for the endocrinologists and more insulin sales for the pharmaceutical companies.


Are chilies technically peppers? Nando's chain of restaurants (UK) refers to chili peppers as just "chilies". My friend and I had a discussion with regard to whether chilies can be called "peppers" or if they do not belong to the pepper family at all. In fact, my friend added that there are 2 types of this specimen - "chilies" and "chili peppers."
To what extent is this all true, and what exactly are chilies?

Chili is a common reference to chili peppers in an abundance of countries, but they fall within the same designation as other so-called "peppers" such as bell pepper, cayenne, jalapeno, etc. because they are all of the same genus Capsicum. They differ, however, from traditional real peppers (black pepper for example) of the Piperaceae family. Capsicum actually belongs to the nightshade family (Solanaceae), but so do potatoes.

The word pepper originates from a south Indian term for the long pepper plant which was used as spice at the time and is a member of the Piperaceae family. I think that people have generalized chili as a pepper in this case due to the heat component, but this section of the answer is also off topic for this site.

Chilis are from the New World, and as CMosychuk has answered, belong in the Capsicum genus. Their name derives from the Aztec Nahuatl word for the plant chilli, and this name has been used by the Aztecs to refer to the plant prior to Spanish contact and spread of the plant to the Old World.

The pepper, however, belongs to the completely unrelated Piper genus, and the plant originated in the Old World. Its etymology derives from the Sanskrit word pippali, also referring to the plant. As the Etymonline entry suggests, the word "pepper" was also used to refer to the Capsicum plants when they were first introduced to the Old World, perhaps due to their similar spicy taste.

Therefore, it is not the case that chilis are peppers, since the Capsicum genus has no recent genetic relation to the Piper genus.


A Brain Implant improves memory--but how? https://www.nytimes.com/2018/02/06/health/brain-implant-memory.html

A new therapy could improve memory by "sending electrical pulses to aid the brain when it is struggling to store new information." I'm trying to figure out how this works physically, in terms of how it actually helps the brain. I would imagine that it has something to do with the neurons getting past the threshold for firing a signal with more ease, but is this because the threshold is suddenly lower because of the presence of the current, or what?

Could anyone provide me with an explanation of the science behind this in lay terms?

Many many thanks

From what I understand, when we learn we go over things quite a few times, this is so that our brain goes over the memory cells where we store that information with electrical impulses. Thus when an electrical impulse travels over some branches they strengthen the branches, (I don't know the science behind this). This is what helps us memorise data. So if we ran lots of Impulses over the branches it could help strengthen them or fry your brain, just saying try this in a safe environment such as a lab and not in a homemade electric chair. Also like you said it helps them run easier over the brain which makes it a lot easier to remember things.

Hope this helps,

IbnJalal


Evolutionary chronology - if any, which species have evolved in the last 100 years I heared somewhere, I cannot remember where, that there has not been an evolution observed in our lifetime. In life science class, right at the start, we was doing the usual MRSGREN (how to tell if something is a living organism), and the tutor said that you can also tell something is a living organism if it evolves. So I asked if there has been an observed evolution in our lifetime. She said that there had been many but could not recite any off the top of her head, so the next week she handed me a piece of paper with 8 or so websites that aparrently corroborated her claim. I have not got the paper anymore but I recall there been on there the peppered moth or something. So I set out to look for a chronological list of evolution but could not find an authoritative one. I could only find something on wikipedia that indicated that species have been dying out for the past thousand years, but nothing saying that any have evolved.

Every single species in existence has "evolved" over the past 100 years. Evolution is a constant process. You are asking whether we can observe evolutionary change in a given species over a short time span, not whether evolution is occurring. I know this sounds like pedantry but it is a very important distinction.

That said, yes, of course we've seen evolution in action in short time spans. The classic example is the various bacterial species that have developed resistance to antibiotics. As very nicely illustrated by Garry Trudeau:

If you want more rigorous evidence than a comic strip, have a look at Wikipedia's page on antibiotic resistance or read Demerec, 1948(1).

Another example is described by Yona et al.(2) who show that subjecting yeast to high temperatures (heat stress) for a few generations causes genetic changes that help the cells deal with the stress. This is, clearly, evolution in action. In fact, they even show that the first response is the duplication of an entire chromosome (think of it as a crude, bludgeon-like solution) which is later suppressed by other, more subtle, compensatory mechanisms which arise to replace it.

Demerec, Milisav, "Origin of bacterial resistance to antibiotics." Journal of bacteriology 56(1), 1948
Yona et al., "Chromosomal duplication is a transient evolutionary solution to stress", PNAS, 109(51), 2012.

Short generation cycles

By definition, we shouldn't expect to observe within our lifetimes the evolution of any species with a generational cycle comparable to our lifetime (mammals and such) since species differentiation requires a multitude of generations.

The directly observed evolution thus is limited to short lived organisms such as bacteria, viruses, plants or insects, with an emphasis on the first two.

It is possible to directly observe evolution in an experimental laboratory setting by taking a strain of bacteria that doesn't possess a certain capability (e.g. resistance to some chemical compound), periodically introducing this compound and accelerating the mutation rate by e.g.  radiation, observing the formation of a new species of bacteria that is able to resist this chemical.


Neurons during Numb feeling We become numb when there is short supply of blood to some parts, as mentioned here.

If that is the reason, why don't neurons and other cells die at that part if they don't receive oxygen and other things needed?

A lower supply of blood does not mean no supply of blood, so my guess is there's generally enough to keep stuff alive for some time. But if the supply is restricted for long periods (think frostbite), then stuff starts to die.

Also, the sensory neuron endings in the skin are normally just one long projection from a cell body, the major components of the neuron are protected by being located in e.g. The Dorsal Root Ganglion.

Simply put, the cells and "other stuff" WOULD die if the blood flow and/or oxygen were too severe, and would be cut off for too long.

It would probably take some time though.


Why are sugars like mannose expressed on the outside of eukaryotic cell membranes? Bacteria are able to adhere to sugars (e.g. mannose) on the exterior of eukaryotic cells, leading to infection and disease. Why have eukaryotes not evolved so as to dispense with sugars on their cell surfaces? I assume there must be a positive aspect to having these sugars. What is it?

The “positive aspect” or reasons why the surfaces of eukaryotic cells contain sugars are various. Major ones appear to be cell adhesion and cell–cell interaction.

In fact, the variation of the sugars in certain cell-surface antigens (blood group antigens and histocompatibility antigens may represent the kind of evolutionary response to infectious agents mentioned in the question. The situation with the major histocompatibility antigen is complex, but variation in blood group antigens is thought to be a response to the malaria parasite — reviewed by Cooling.

I'd look on it from the other side. Thoose structures have certain purposes, such as stability or signaling purposes. Due to their short doubling time compared to most cells of more complex organisms, bacteria is able to adjust to changed condition rapidly and therefore adapts to it's environment. (Just think of mechanisms of resitance to antibiotics: plasmids for example with the information for β-lactamase ere exchanged even between differnet kinds of bacteria) It would therefore not make a lot sense for the slower cells to adjust their usefull structures in order to avoid bacteria, which change way faster.