text:
What will happen when humans are injected with plant growth hormones
Will plant growth hormones (PGHs), (let us consider auxins for example) poison our body or not?
I do realise that when you eat a shoot, auxins get digested and are less likely to be poisonous but when taken as an intravenous injection can auxins cause some changes to the body?
I mean even if they do not poison a body, some osmotic changes are bound to happen.
According to this link, if the water was injected in not so little amounts it is bound to cause cells to burst.
EDIT: Now according to this link, plant hormones are actually beneficial to human body.
How is it possible if they don't have any receptors in humans or any other vertebrates?

There are no receptors for auxins or any other plant hormone in humans or other vertebrates. Of course they are not poisonous otherwise people would die of eating shoots. Please show some research effort from your side. A one line question without any research effort or suitable background is not appreciated.

You can improve this question; why delete it? This can be a good question. Just explain it a bit. Specify the plant hormone etc. Interestingly a study says that auxins can have anticancerous effects.

As a lead to satisfy the bullying mod @WYSIWYG (wink) - every compound gets toxic at certain levels. What dose are you talking about? How do you know what level is toxic and which may have a more physiological effect, if any?

@Christiaan I have edited the question a bit.

@WYSIWYG Yes, I noticed one such study and included it in the question. If they don't have any receptors how to they bring about such effects?

Interesting question, but still needs work. I see that it's actively being extended and improved, but a bit of re-formatting is needed to make it more clear.

cytokinin has age reducing effect on skin. It helps in rapid cell division.

"What type of questions should I avoid asking?" — "an open-ended, hypothetical question: “What if ______ happened?”". Please, let's follow the guidelines and close this question.

I will only give an outline based only on auxins otherwise the question may be deemed too long.I hope this helps a bit.
The first auxin was isolated from the urine of pellagra patients.
Most natural auxins are indole derivatives which are the intermediates or final products of tryptophan metabolism.Both vitamin B3 and auxins are consequences of tryptophan metabolism. [source]
POSSIBLITY 1-
Thus, auxin injected may be eliminated through urine.
We already understand that substances that are excreted via urine are either toxic to the body or above threshold.Perhaps this idea was harnessed by researchers to construct researches which proved that auxins have anti-cancer properties.

given that the chemical structure of plant and human auxin is identical and that cytokinin IPA is found in human cells bound to tRNA assisting protein expression, presumably supplied by the consumption of vegetables in the diet, and that we observe a positive effect of plant hormones on pluripotency and key anticancer gene expression levels in mammalian cells [1],[2]

POSSIBILITY 2-
In proper dosage may be utilised for its anticancer properties.
Cytochrome and a series of enzyme system in liver cells are known to detoxify indole
Protein putrefaction in the large intestine results in formation of indole.This indole is carried by the portal system to the liver where it is detoxified to indican  with the help of the cytochrome P450 isoenzyme system and consequently eliminated via urine.
POSSIBILITY 3-
Thus auxins (being indole derivatives and moderately hydrophilic) may be detoxified in the liver and then excreted.
REFERENCE:[1],[2],[3]


text:
Why is alcohol such a weak drug?
Most day to day drugs such as caffeine and paracetamol require a dosage in milligrams to have the desired effect.
Why then, does it take many tens of grams of alcohol to have a tangible/noticeable physiological impact on the body? What is it about the composition of alcohol that makes it so weak, gram for gram, compared to other recreational and medicinal drugs? Are there any other psychoactive drugs that require similar dosages to alcohol to have an effect?
For clarification, as per the comments
For example, as a 90kg adult I can consume 30g of alcohol (3 UK units) before it has any noticeable impact, whereas a coffee containing just 100mg of caffeine (300 times less than alcohol) produces a noticeable reaction.

It is an interplay between pharmacokinetics and pharmacodynamics. The question is superbly broad; you talk about overdose first and next to "being hammered". You won't get 'hammered' by paracetamol. You can get battered by it, as an overdose mostly ends through internal bleeding. In contrast, heroine OD is characterized by respiratory failure. What exactly is your question and could you focus it? I think I know where you are heading, but I'd rather not make drastic edits on such a vague question, given the risk of missing the point.

Alcohol is easily metabolized to acetyl-CoA.

Plus: a regular paracetamol dose for an adult is a gram. Which is 1000 mg, but I would call it also the gram range. Likely it's just the worst kind of example drug in the light of this question.

Fats or sugar are even "weaker" drugs. In any case, don't forget that The dose makes the poison. As a consequence, water is a very "weak" drug.

Perhaps because alcohol is fairly common in nature (e.g. in overripe fruit), so fruit-eating creatures with a low tolerance to its effects would have been selected against.

@jamesqf One would think drunk monkeys would be more likely to reproduce :)

@jiggunjer: But also more likely to be eaten by leopards &c.

As Christiaan already pointed out, this depends on the pharmacokinetic and pharmacodynamic parameters. The effective drug concentration depends on the drug-receptor association constant and the drug degradation constant (for a highly simplified model). The degradation/removal depends on the abundance of the enzyme catalyzing this reaction.
Ethanol is primarily thought to cause intoxication by activation of GABAA receptors. However, only a very specific subclass of these receptors are activated at the levels of alcohol that one consumes during "social/moderate" drinking. Others require very high alcohol concentrations (Hanchar et al., 2006). Basically alcohol is not a very specific agonist/antagonist of any neurotransmitter or neuromodulator receptors. In other words, it does not have high affinity to any of these receptors. There is no answer to "why". I would guess that since ethanol is a very common molecule (and is also used as energy substrate by some organisms, to a certain extent), high sensitivity to ethanol would have been evolutionarily selected against.

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

From Hanchar et al., 2006

Other psychoactive drugs are highly specific and have high affinity to their corresponding receptors. For example, caffeine acts on the adenosine receptors at µM concentrations (Daly et al., 1983). This is because of caffeine's high affinity to these receptors.
Moreover, ethanol is readily metabolized to acetyl-CoA by alcohol dehydrogenase and aldehyde dehydrogenase enzymes which are quite abundant in the body. Some people who have mutations in these enzymes leading to their reduced activity, "get drunk" and experience hangovers even with a low level of alcohol consumption.

Good, nicely formulated and concise answer +1

It has to do with the general genetic makeup of most humans (I believe it differs from a a population to another [Genetic polymorphism]), but in general:
There are much more receptors (both in quality and quantity) effected by the active ingredients in alcohol, than there are for other molecules like Heroin or Cocaine, so it takes more dosage to "lay the weight" over it's receptors in compare to those of these material.
To better understand this whole concept you could further read on articles about Physiological addiction, Psychological addiction, and the difference between these two types of addiction:
Alcohol addiction, like Heroin addiction is much more physiological than psychological, but it requires much more material, as I have explained very generally above.

Is it (your answer) only "maybe/I think" one or does it contain facts? If yes (contains facts), please put some reference to those facts.

@another'Homosapien' OP certainly homes in on the question, but in the q's current state, I wouldn't put a lot of research effort in an answer either.

I agree @Christiaan and that is why I aksed OP whether question contains research effort or not. Excuse me if my comment was too rude.

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Mechanism behind energy generation
I recently read about methanogens and methanotrophs. One converts CO2 to methane and vice versa respectively.
I can't get exact mechanism for the methanotrophs and I know they can't be reversed because this would result, in both directions being unable to produce energy.
Any information elaborating on the mechanism responsible for the generation is greatly appreciated.

"Methanotrophs oxidize methane to CO2 via a series of two electron steps with methanol, formaldehyde, and formate as intermediates."  from https://link.springer.com/chapter/10.1007%2F978-1-4020-3163-2_7 (link to a book that I can't access right now).

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What happens during the fermentation process of the eco-enzyme?
introduction about the eco-enzyme
I have tried to make several ones at home, no matter what I am using, lemon or pineapple peels with brown or white sugar, the final products all show the similar brown colour.
It seems to me that no matter what type of fruit peel or sugar used as the material, would all lead to a similar brown colour.
So I am curious about:
Why the colour of the final product is different from normal homemade fermentative fruit or vegetable?
Are the microbes  involved in fermentation have some difference between the both? Is this because of the difference between enzymes that are produced by bacteria?
I have tried to find the appropriate and availible resource about microorganisms that may take part in the fermenting process of fruit and vegetables, but I am still not sure which one would take part in which step of the eco-enzyme.
(In my observation, some white tiny spots and big speckles began to float on the the surface of the liquid after a week, before opening the container to release gas and make it become aerobic).
What could be the role of fruit peels aside from being the source of microbes,if it will also produce enzymes to influence the chemical reaction?
Is the eco-enzyme really an enzyme?

Why do you keep asking the same question again instead of making the old one better?

I am sorry,perhaps it's because my limited biological knowledge limited the way I ask ,but don't you think the questions this time focus more on the microbes and the enzymes it may produce?

The recipe is using yeast to convert the sugar into alcohol (ethanol). All of the proposed cleaning effect is from the dilute alcohol (and also some vinegar).  The citrus peel provides some aromatic oils. There may be low levels of some particularly hardy enzymes released from the rotting fruit and dying microbes, but it is difficult to imagine that any of those proteins have any effect on removing dirt from clothes, dishes, or surfaces. The solution is also acidic from the fermentation and the dissolved CO2 gas--just like if you used grape pulp and skins you would make a primitive wine with this recipe, and that wine would then turn into vinegar (acetic acid, HOAc).  Mixing some vinegar and alcohol would give you the same cleanser.
The enzyme concentration should be similar to the amount of active enzymes present in homemade beer or wine--would you use either of those for cleaning?


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Original paper about the all or none law for neurons
I am looking for the original paper about the all or none law for neural activity.
I know that there is a very old article about the all or none law for mammalian heart muscle fibers, but I'm specifically interested in when this idea was first stated about neural activity.
In A logical calculus of the ideas immanent in nervous activity from 1943 this law is already mentioned like an established hypothesis, so it is probably quite old.

I would guess on the Hodgkin-Huxley paper.

Hodgkin-Huxley seems to be too new.

This probably goes back to Lucas (1909), Adrian (1912), and Bernstein (1912). But the idea might have started from Helmholtz (1850).

Lucas, K (1909). The ``all or none'' contraction of the amphibian skeletal muscle fibre. Journal of Physiology; 38: 113--133.
Adrian, ED (1912). On the conduction of subnormal disturbances in normal nerve. Journal of Physiology; 45: 389--412
Bernstein, J (1912). Electrobiologie. Braunschweig: Vieweg.

See also: Galvani's Spark: The Story of the Nerve Impulse and The great Era of English Electrophysiology:
from Francis Gotch to Hodgkin and Huxley


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Are high sounds worse for your hearing than low sounds?
From about 80 dB it is possible to suffer loss hearing after a couple of hours. But does it make a difference what frequencies those sound waves are or is it just the volume of the sound in dB that matters?
In your ear the first sounds you lose in case of hearing loss are the high sounds because they are at the beginning of your ear. So are high sounds also more dangerous?

Loudness is a very subjective measure. What is loud to you may be very quiet to someone else who has had much more exposure to it. Decibels are the main measure of sound, measuring the intensity or level of the sound. Anything over 85 decibels can start causing hearing loss after some exposure, so it really does not matter how "loud" you think what you are hearing is. It only matters how "intense" the sound waves are.

Relevant: https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/335014/RCE-14_for_web_with_security.pdf (Health effects of exposure to Ultrasound and infrasound)

Yes.  http://american-hearing.org/disorders/noise-induced-hearing-loss/#causes  Most of the discussion of noise-induced hearing loss talks about the loudness of the noise, only rarely mentioning that higher-pitched noise is more damaging.  Probably because it is much easier to measure the amount than the frequency.

Measuring the frequency of a noise is fairly trivial these days, so I don't think that's the whole story.


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Is the knee locking mechanism present in animals?
We study in human anatomy that when the knee is in full extension, the femur slightly medially rotates on the tibia to lock the knee joint in place. This reduces the work required to be done by the hefty thigh muscles. This happens in the knees in humans since they are the weight bearing joints.
So, is the mechanism of locking present in other animals? If yes, is it even in the fore limbs or just the hind limbs?

Could you please paste in a link here? of an appropriate result? @Fang

https://en.wikipedia.org/wiki/Stifle_joint Equids use this stifle joint to stay standing while they sleep.

@fang thanks a lot! It happens to be similar to humans, the mechanism. But locking happens only in the knees in bipeds. This makes sense since our liwer limbs are the ones that are wt bearing. is there a similar mechanism in quadrupeds in their fore limbs as they too are weight bearing.

Yes, the mechanism of patellar locking does occur in quadrupeds too. Although they are 4 limbed, a major portion of the weight is borne by the hind limbs. This is known as the stay apparatus and includes the mechanisms of Patellar locking, reciprocal mechanism and check apparatus.
On the other hand in the forelimb, although there is no locking mechanism as such, there exists a neat difference from the human anatomy. Human forelimbs are majorly adapted for manipulation but for quadrupeds, they are weight bearing. There exists what is called the stay apparatus - which includes the suspensory apparatus and the check apparatus.
For a detailed explanation for the interested reader, heres a helpful link - https://en.wikivet.net/Stay_Apparatus_-_Horse_Anatomy


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Cellular specific mass (in grams-dry-weight per pico liter)?
What is the cellular specific mass, in units of pgDW (pico-gram dry-weight) per pL (pico liter)?
I suspect there is some variability between cell types, but this variability must be limited. Perhaps bacteria and mammalian cells are different, but the number shouldn't change much among bacteria. This is just intuition, I could be wrong.
So, what is the cellular specific mass, for different cell types (assuming there is limited variability, so this is not an infinite table)?

Density of a variety of cell types is rather well known. It can been measured directly by examining buoyancy (tendency to float) in liquids of known density, and also by microfluidic methods. But the results depend on the osmolality of the solution in which the cells are kept, since cells tend to "swell" (take up water) in low osmolality (hypotonic) medium.
Using a microfluidic technique, this paper reports a density of 1160 $\pm$ 1 pg/pL for E.coli at 290 mOsm, and 1139 $\pm$ 3 pg/pL for red blood cells. At comparable osmolality and using a gradient centrifugation method, this paper gives a density of 1095 pg/pL for E.Coli. So the results clearly differ a bit depending on experimental conditions (possibly the medium composition was different). For budding yeast, this paper estimates a density of 1103 $\pm$ 3 pg/pL, compared to 1113 pg/pL by gradient centrifugation.
In all cases, cells are heavier than pure water (1000 pg/pL), and larger eukaryotic cells seem to be slightly more dense. As macromolecules are more dense than water, this would suggest that eukaryotes have lower water content.

The most common opinion about this is a bacterium weighs about 10^-12 g. Here is a link with different results found using different techniques: http://hypertextbook.com/facts/2003/LouisSiu.shtml
This link also has useful relevant numbers, good to keep alongside: http://kirschner.med.harvard.edu/files/bionumbers/fundamentalBioNumbersHandout.pdf
Assuming a bacterial cell has a volume of 1 um^3 (10^-18 m^3; 0.001 pL) and 1 pg in mass, the density should be around 10^3 pg/pL. Similarly you can find out for other cell types.
Cheers!

Can you confirm that those are dry weights?

What becko means is that you should add a reference for each value that you mention. If you have taken them from BioNumbers then you can provide the BioNumbers ID or even better (and highly recommended) the actual reference (Pubmed IDs given in BioNumbers).

Also, a number for mammalian cells would be nice.

As per dry weights: E. Coli has an avg. dry weight of 0.28 * 10^-12 g. (BNID: 103904, link: http://book.bionumbers.org/what-is-the-macromolecular-composition-of-the-cell/). So, multiply the result above by 0.28. For mammalian cells, total weight per cell varies but on an average it is 3-4 ng. (Pubmed ID from Bionumbers: 17389958; BNID: 108454). The cell vol. varies: 100-10^4 um^3.(http://www.rpgroup.caltech.edu/publications/SnapShot2010.pdf). There is no concrete literature about the ratio of dry weight to total weight, but it is thought to be around 50-70%. Again these are avg. estimates.

Thanks for pointing out the calculation mistake @Roland .Of course for an accurate analysis you may need direct density measurement data, and also in that sense you will only get an average density of the cell as cells are highly heterogeneous. What I mentioned along with the specific references are some of the evidences of what have been done so far.


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Is receptor antagonism just long-term binding?
By my understanding, a substance that binds to a receptor and activates it is called an agonist, while a substance that binds to a receptor without activating it is called an antagonist. (Wiki) What is the fundamental difference between binding to a receptor and activating it?
EDIT: I guess the receptor is a complex enough beast that fitting into it and staying there can be accomplished by some sections of the interface being completed, without necessarily completing the "usual" interfacing process between the receptor and its agonist -- thereby blocking the receptor geometrically without imparting the proper energy to it chemically.

This is similar to competitive inhibition of enzymes.

The details of activation vary by receptor of course, but talking in the popular key-lock picture:

An agonist is a key, that fits the lock and opens ("activates") it.
An antagonist is a key that you can put into the keyhole, but it does not open the lock. What this means is: while the "wrong" key is in the keyhole, you won't be able to open the door, even if you have the correct key, as long as the wrong key is in the keyhole.

As far as Wikipedia goes, the articles for Agonist (and the links contained therein) might be more informative than the one you quoted.
https://en.wikipedia.org/wiki/Agonist


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Freestyle Libre's Glucose's Specificity and Accuracy?
I am studying the Continuous Glucose Monitoring devices i.e. glucose sensors with continuous monitoring.
Here one good presentation about the topic.
They are considering interstitial fluid in their analysis, which I think is risky, probably more risky than Theranos product, discussed here.
Characteristics

measure oxygen in interstitial space and estimate blood glucose
sensor current average efficacy 10-14% which is good but not enough

Sources

Sandeep Kumar Vashist, 2013. Continuous Glucose Monitoring Systems: A Review.

How can FreeStyle Libre glucose test's be specific and accurate compared to conventional blood-glucose devices?

Interstitial glucose sensors can be reasonably accurate, but there are two main concerns: the sensor response time, and calibration.
Glucose diffuses from blood into the interstitial fluid, and it can take some time during periods of glucose change (e.g. after a meal) for an equilibrium to be reached. Hence, the sensor measurement will lag behind the true blood glucose level. The blood glucose is what people are generally interested in, so measurements of interstitial fluid are used to estimate the blood glucose level, and so are only valid during periods of stability. With careful management of sugar intake this can be an acceptable compromise however.
Most CGM sensors require calibration against a reference instrument such as a test strip-based device using a finger-prick blood sample. As long as this is done during a period when the interstitial glucose level is stable, the sensor can hold calibration for several hours and indicate the trend in the blood glucose concentration.
The Theranos product is something completely different, and isn't suitable for day-to-day monitoring of blood glucose levels. The samples are sent away to their lab, so there is a delay in receiving results. They will measure your blood glucose level but this would generally be a fasting measurement to provide a background level. Nevertheless, this (should be) a more accurate test, as it is laboratory based and takes a physical blood sample.
CGM sensors have been shown to be accurate to within clinically useful ranges, when used with the above considerations in mind. Specificity (and sensitivity) are only really considerations when test results are compared against cut-offs to determine a positive/negative result. This paper is a good summary:
http://ceaccp.oxfordjournals.org/content/8/6/221.full


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Why does the affinity of haemoglobin for oxygen decrease at high altitudes?
My class 12 NCERT book says, Pg 226

The body compensates low oxygen availability by increasing red blood cell production, decreasing the binding affinity of haemoglobin and by increasing breathing rate.

Why should the haemoglobin binding capacity decrease at high altitude?
I think it should increase for better oxygen transfer and uptake from air. The concentrtion of oxygen in the atmosphere decreases with height. Hence, if the haemoglobin binding increases, we will be able to draw more oxygen from the air and transport it to the cells.

Haemoglobin's job is to transport oxygen and not store it. Therefore it should also be able to release oxygen effectively. When the differences in partial pressure of oxygen between the tissues and blood are low then oxygen will not be transported to the tissues from blood, leading to hypoxia.
2,3 Bisphosphoglycerate (2,3-BPG) stabilizes the T- (taut; oxygen unbound) form of haemoglobin thereby reducing its affinity to bind to oxygen. 2,3-BPG is found to be elevated in people living at high altitudes. The production of 2,3-BPG is controlled by a negative feedback (Mulquiney et al., 1999; also see wikipedia) so that it does not overdo its job.
David's answer explains the dynamics in details and addresses the non-linear (sigmoidal) nature of Hb-Oxygen binding which is a critical point for understanding how the effect of 2,3-BPG is actually favourable.
However, haemoglobin content also increases so that higher amounts of oxygen can be captured. This is a fine balance and as you may notice (even if you do not read it to great depth) in the linked paper, there are many mechanisms that are working towards this.

The answer to this question is yes, a decrease in oxygen affinity will decrease the oxygen taken up by the haemoglobin (Hb), but it is an appropriate response because it will have a greater effect in increasing the release of oxygen to the tissues.
This is not intrinsically obvious. It happens because of the (sigmoid) shape of the oxygen binding curve, and can only really be appreciated if you examine the curves for the normal situation and that in which there is increased 2,3 Bisphosphoglycerate (2,3-BPG) producing the change in oxygen affinity. I have devised a figure to demonstrate this, although it is not based on actual data, so should only be regarded as illustratative.

At sea level the lungs pick up oxygen at 1 (say 100% saturation of
Hb) and when the oxygen pressure drops to 40 mm Hg in the tissues (2)
the Hb will be 55% saturated. Hence in this example they have
released 45% of a full complement of oxygen.
If we look at the same curve for high altitude, in this example the oxygen pressure at the lungs (1') will be such that the Hb is only 80% saturated. Thus at 40 mm Hg in the tissues (2) when Hb is only 55% saturated it will only have released and made available 25% of a full complement of oxygen.
Now consider the effect of high altitude acclimatization with increased 2,3-BPG production changing the equilibrium and the oxygen binding curve (red). At the lungs (3) the Hb will be less charged with oxygen — only 70% saturation — but at 40mm Hg in the tissues (4) it will be much less saturated than on the black curve — 30%. Thus it will have made available 40% of a full complement of oxygen.

This is not a perfect solution, which is why over a longer term there is increased production of red blood cells to provide more haemoglobin to compensate for the smaller amount of oxygen it can bind.

+1 for the graph and pointing out the effect of non-linearity in the dynamics. That is a critical point that I missed.

beautiful answer

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text:
Headshot = instant kill?
While whatching a film, I've been thinking about how does a headshot kill someone, and how long does it take?
For example let's say you've beeing shot by a normal (police) handfired weapon - no shotgun or sniper weapon.
I know that the rhombencephalon regulate the most important vital functions like breathing and if the shoot goes throught it, that there will be no change.
Question:
But if the bullet passed the brain throught the telencephalon, which function is mainly thinking, and don't hurt any
brain regions who handles life keeping functions (like the rhombencephalon)  do you die instantly (like in movies) or have any change (fall into a coma)?

Depends on which part of the head is hit (and bullet ballistics). Headshot=instant death only happens in Counter Strike :P

Of course I know, that it depends on which way a bullet go, but in case of it passed the lobus frontalis and damage not the highly critical functions whould there be a change?

Heard of the famous case of Phineas Gage? He survived but apparently his entire personality changed.

Yes, that makes sense to me, because the lobus frontalis handles emotions, personality, humor, ... and when it gets damaged some variables can be changed.

IMO this question is less about biology than ballistics. The effect of destroying a particular structure in the brain is probably known, including the likelihood of instant death (whatever that means). The likelihood that a bullet causes such damage is a separate question.

On my first day of an ER rotation (Charity Hospital in New Orleans), a man walked into the ER with a chief complaint of "I was shot in the head." Sure enough, he had a bullet hole directly in the middle of his forehead. On his review of systems, his only complaint was "headache". The only physical findings were the hole in his forehead and blood in the back of his throat. Luckily it was a small caliber bullet, it went right down the middle missing everything important, and he had swallowed it after it exited the base of the skull. So... no. He didn't die.

@anongoodnurse this is really an interesting case !! Hope he's recovering well.

@anongoodnurse He ate the bullet after it had exited his skull? Or did it exit into his throat? Or am I misunderstanding you? Thanks for sharing either way - really interesting to hear.

@fileunderwater - It had exited the base of his skull at the back of his throat and he swallowed it (presumably in the gush of blood.) I found the bullet in his stomach when I did a pre-op chest xray along with xrays of his head. (This was a long, long time ago!) He stated he had never been shot before, so with the bone fragment locations and the history, that was the conclusion. I'm still amazed by the whole thing.

@anongoodnurse Ok, that makes more sense than eating it. Amazing story either way. Do you know if he recovered fully?

@MauroM - Charity was the busiest ER in the country when I was there. He didn't die while I was there, but he was kind of "lost to follow-up" (hard to keep track of.) I think he was fine, though.

@fileunderwater - As fully as we could tell. He was discharged to home without complications by neurosurgery/neurology. Can you imagine how easily it could have hit his spinal cord? Just amazing.

According to this article appearing on the website of the American Association of Neurological Surgeons, gunshot injuries to the head are fatal in 90 per cent of cases. Many victims die before reaching the ER, and the 50 per cent who survive the initial trauma die in the ER.

The comments on this question have pretty much covered everything I had to say. Generally, you're more likely to cause brain damage than an instant kill by shooting someone in the head, though it does depend on what part of the brain is hit and the kind of projectile being used.
Normal small-caliber weapons pierce bone and tissue and that's about it. Small arms marksman training teaches you to focus on center of mass because you're more likely to get a kill by bleed-out or organ trauma than the considerably-more-difficult headshot.
WYSIWYG mentioned Phineas Gage in the comments, who survived having an iron bar driven through his skull thusly. He suffered a severe change of personality but was otherwise fairly functional. (Full wikipedia article contains sections on various studies about brain damage).
The idea of a headshot being an instant kill most likely comes from use of hollow-point bullets and/or high caliber weapons like sniper rifles. Hollow-points expand on contact with or shatter inside the target, causing much more damage than a normal bullet. The larger impact area of a hollow-point or the higher velocity of a powerful rifle are what cause the familiar "exploding skull" visual.
(An additional personal theory: since headshots are much more difficult to achieve due to the small target, I believe they are used as an instant-kill reward in a lot of video games, adding to the myth. Realistically the victim is severely disabled, making it equivalent to a kill in game-terms, but would likely recover given proper medical attention.)
The extent of the damage, however, depends on what part of the brain is hit. I'm not an expert on neurology so unfortunately I can't answer that aspect of the question. Blood and/or fluid entering the brain through the wound, however, could very likely be fatal.
In summary: small arms like a police handgun wouldn't likely cause an instant kill with a head-shot. For practical purposes, the probable instant debilitation of the target may count as a "kill" without technically being immediately lethal.

Small arms are perfectly capable of killing via headshot. You have to take the caliber, velocity, type of bullet, location of impact, distance from gun to target, and path of travel of the bullet into consideration. A shot just above the bridge of the nose will kill with anything from a 9mm on up, and would likely kill with a hollow-point .22 with sufficient velocity to pierce the frontal bone. Most police sidearms these days are relatively high-velocity 9mm, larger but slightly slower .40S&W, and the even larger .45, which while relatively the slowest can still easily penetrate and kill.


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Reason Non linear Lineweaver–Burk plot
V vs S plot looks like hyperbolic but 1/V vs 1/S plot is not linear at all. Looks like some kind of exponential growth. What can be the reason?

It is supposed to be linear as per the model. Are you talking about your experimental observations?

Without a graph and the data this question makes no sense. Like, 'my pcr didn't work, how come?'

The linearity of a Lineweaver–Burk plot assumes that your system follows standard Michaelis–Menton kinetics.
Not every enzyme system follows Michaelis–Menton kinetics with all the assumptions made in its derivation. There are a number of reasons for non-linear behavior, including cooperativity, substrate inhibition, substrate activation, limiting cofactors, isoenzymes, and non-steady-state kinetics.
Further reasons for a non-linear plot involve experimental issues. Depending on your experimental setup, you may not have accurately measured the initial rates of some of the faster conditions, which can lead to non-linearity of your Lineweaver–Burk plot. If you're operating under conditions which may lead to product inhibition, you might also see non-linear behavior.


text:
A career in synthetic biology
So I am thinking about a career in synthetic biology, but I am not sure what route should/needs to be taken. I don't want to do technician work--I want to be involved in the planning. Y'know, the exciting stuff. :)
I'm wondering whether I should go for a Master's or a PhD (or is a Bachelor's enough?)
It's a young field, so I'm having trouble finding this kind of information online. Any help would be much appreciated!

this is off topic here, and is more suitable/appropriate on academia.SE

I'm voting to close this question as off-topic because it's a career question.

Sorry, I was torn on where to put it and thought that academia was more for questions about how academia works. But will move there!

I think that "career in synthetic biology" and "involved in planning" both express very vague ideas. There are significant differences in what you will be able to do with a Bachelor's, Master's or PhD, depending on what exactly you end up doing.
I entered a PhD program in biology for no better reason than that I felt awed and fascinated with science and had done really well in science subjects as an undergrad. Grad school seemed like a natural extension of that effort.
In retrospect, my motivations for pursuing a PhD were horribly naïve and easily the greatest challenge that I faced as a grad student was that of defining why I was there and where I wanted to go with my degree. So, to address the issue of vagueness in your question, my first piece of advice is to have a firmer idea of what you want to do. Plans will change, but simply having a plan (a real plan) might provide an anchor when you need one.
As to what you can do with the various degrees, I can't precisely answer your question, the way you've phrased it, but I can give you a general idea.
A bachelor's degree in biology will not get you far in a lab setting. Among the lab techs I've worked with, even most of them have master's degrees. From what I've seen, this holds just as true for academia as for industry.
It's a little unclear what you mean by "planning", but most of the admin that I work with, who are involved in planning our various projects also hold advanced degrees, typically in science, business or public health. I see a strong representation among the management at my institution (Columbia University) of PhD scientists, who left the bench for something less life-consuming, while still wanting to have a hand in research. These people are frequently grants managers or program directors.
As I mentioned earlier, the lab techs around me generally hold master's degrees. When I was considering quitting my PhD program after the master's component, a friend in industry advised me against it, if I ever thought that I might seek work in industry. The picture that he painted was that in industry, a master's degree makes you overqualified for many of the tasks that you can expect to be hired for, but underqualified for significant future career advancement.
Obviously, you shouldn't feel limited to academic vs industrial research tracks. There are plenty of other options out there. Maybe look up people's blogs that involve synthetic biology or whatever other topics of interest you might have to get a wider view of what people who have expertise in the subject are doing.
Good luck!

Thank you so much! This was very good. (And for clarification, by 'planning' I mean things like, for example, looking at symptoms (assuming we are looking at a person), pinpointing underlying causes, designing a molecule that stimulates X, modifying it to avoid inadvertent binding to Y, etc.)


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Do other animals have similar blood types to humans?
I am interested to know if there are any animals having blood groups similar to human blood groups? Is it possible to transfuse blood between humans and those animals?

You might want to have a look at wikipedia > Blood Type (non-human).

One of my cats needed several blood transfusions due to low hematocrit levels, and, yes, blood typing was involved.

I have now added an answer to the 'original post' which includes some information about cats. You will see from that that if your cat is cat-type B any human blood will contain antibodies to the N-glycolylneuraminic acid on its erythrocytes and so will be rejected. I'm not sure what the situation is if your cat is cat-type A. Also I'm not sure if cat erythrocytes have one of human-H, -A or -B antigens (they are not polymorphic but they have the ABO gene), which would also have ramifications with different human blood types. Somebody must know, but I can't find it on the web.


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Is there an equivalent to a refresh rate for the brain and consciousness?
Computers have a clock rate that synchronizes their processors. In spite of tempting analogies, the brain is clearly not simply an organic computer. It is constantly changing, rewiring and pruning its pathways, awash in changing nutrients, hormones and other chemicals in a manner that dwarfs any computer ever built.
But is there a biological equivalent to a refresh or clock rate in the brain that organizes perception, cognition and reaction? Is there a timing signal that creates the fleeting now of our consciousness? Or are the various sensory inputs, internal processing, memory storage and accessing, cognition, and signal output only loosely coordinated?

First of all you should understand how exactly a brain works. Brain is modular- there are some signals that are continuously fired whereas others are situational. The "clock rate" would apply only to continuously oscillating circuits. It is fine to draw analogies but as it is written, your question appears quite broad. Please read up some basics on how brain and neurons work and narrow down your question to a specific issue.


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Can multiple overt/covert intentions produce identical EEG readings?
With sophisticated techniques likes ERP, it is possible to correlate certain EEG activity with certain overt/covert actions.
What I'm wondering is: is there a risk for 2+ overt/covert actions producing identical EEG activity? Meaning:

Perhaps when I go to open/close my right hand, I produce certain neural activity (lets just summarize this as A1); where A1 is a specific set of wave signatures
Perhaps when I go to open/close my left hand, I produce neural activity A2 (a specific set of wave signatures that is distinctively/mathematically different than A1)
Perhaps there are 10,000 other movements I could make that produced their own distinct set of wave signatures (A3 - A10002), etc.
But perhaps when I think of sea turtles and pat my stomach at the same time, I produce the same set of waves as A2 (opening and closing my left hand)

My question is: is this a concern/possibility with EEG/ERP? In other words, can multiple overt/covert intents produce identical wave activity (hence, identical EEG readings)?

Why the downvote? This question is not a dupe, shows some basic research, is on topic, and is an SSCCE.

EEG/ERP are methods applied with a goal in mind. Your question asks for a concern, without defining the purpose to measure EEG/ERPs in the first place. That makes the question open for interpretation, vaguely defined and hence making the answer pob. That may explain the downvote, but I can't really speak for others

Thanks @Christiaan (+1) - but I (respectfully!) disagree, I don't think this is vague. All I'm asking is: is it possible for two distinct thoughts to produce the same electrical signature on an EEG?

That makes sense.  I +1d already.

Also,  don't worry too much about a downvote or two. It's all in the game. Upvotes give you more rep than downvotes take away anyway.

I know! I've been on various StackExchange sites for many years now and know that - typically - one lone downvote/closevote can often trigger a "Mob Lemming Effect" and cascades into multiple users mindlessly repeating the down/closevote. And I've found that defending a question with my above boilerplate response usually helps prevent this Mob Lemming Effect from continuing any further :-)

That's an interesting point. The herd effect is indeed a common one. I often have the tendency to do the opposite. Comment and upvote after edits.

The close votes are for "unclear what you are asking".. You can add some background to your question if possible. Plus, I guess EEG may not clearly resolve between two "thoughts" that well. fMRI is something that you can have a look at. People have done experiments like the ones that you are suggesting using fMRI.

To curtly answer your question: given the sheer amount of different thoughts possible (billions I guess) and the limited spatial resolution of the standard EEG as well as the restricted number of characteristic parameters to describe EEGs (frequency, amplitude, latency) it is safe to say EEG is not suitable to characterize all of the brains processes. In fact, no state-of-the-art technique can do so, as far as I can see.

Thanks (as always) @Christiaan (+1) - however I feel like you might not be understanding my question. Let's take a concrete example: is it possible that blinking my left eye might show up (analytically-speaking) to have an identical "wave signature" as, say, wiggling my big toe? By "identical wave signature", what I really mean is "identical results/outputs on an EEG reading." Does that make more sense? Thanks again!

What christiaans Answer means is: Yes it is possible that different intents show up with the same EEG signature. This is due to the fact that the resolution of an EEG is not large enough to distinguish all possible intents simply because the parameter space resolved by an EEG is much smaller than the space of all possible intents produced by the brain.

Thanks for the clarification @Thawn (+1) - unfortunately since you are only leaving a comment I can't qualify you for the bounty, but your comment is immensely appreciated!


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I know why phototaxis happens but why did those bees die?
There is a tube light in front of my veranda. This is just spring. So at night when I turn on the tube light many bees gather around the tube for phototaxis. But in the morning I see many of them are lying dead on the floor.
Why does this happen?

Are you sure they are bees? You should post a picture of the insect that you are talking about. Some insects actually have a short adult lifespan.


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Any books/publications about what life was like before antibiotics?
Just wondering. We've been discussing antibiotic resistant bacteria a bit in lecture, and how we're slowly sinking into a pre-antibiotic era again.

Any medical literature before 1928 is about "life without antibiotics". Please add some details to your question. Have a look at the tag-wiki for [tag:book-recommendation]

A google search with "life before antibiotics" gives a nice list of sources.


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de novo gene synthesis vs cDNA library creation from plant RNA: Pros & Cons
What are the relative pros & cons of the following two approaches when one wants to insert a known, sequenced plant gene into a target host organism:

de novo gene synthesis vs
plant matter extracted RNA converted to a cDNA library

Specifically my gene of interest is approx. 2000 base pairs so de novo gene synthesis cost works to about $350. (please correct my estimate if I'm wrong)
While this isn't cheap, collecting plant samples, cryopreservation, digestion, extraction etc. aren't easy either.
Any other considerations when / why one may favor one approach over the other?

Isn't "collecting plant samples, cryopreservation, digestion, extraction etc." also expensive? Think about cost and time. How long would it take to isolate the DNA vs synthesize it?


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What is the length of the centromeric repeat sequence in a human?
I'm looking for the lengths of the centromeres of human chromosomes.
The best I could come up with so far has been: The length of individual centromeric arrays was found to range from an average of 680 kilobases for the Y chromosome to 3000 kb for chromosome 11.
Here they say that "Human centromeres are located at repetitive alpha satellite DNA arrays that compose approximately 5% of the genome." Which unfortunately is not the same as saying the centromeres compose 5% of the genome. (Or maybe it is? Biologists to the rescue!)
Ideally an answer would contain the length of the centromere in each chromosome, but a precise percentage for the whole human genome would be good enough.

No specific length for centromeres. Actually in a real chromosome in a cell, centromeres are usually very condensed sequences of DNA, they are winded and folded (if you know about the DNA structure). Thus you cannot measure the length of the centromere unless you decondense the chromosome first.

My question is about the length in base pairs. My understanding is that you can sequence centromeres, you just cannot assemble them. But the sequencing reads might be enough to give an estimate of the total base count.

@BlindKungFuMaster There's not much genes in centromere region. So it is hard to design a RNA primer for sequencing. Sequencing cannot be done on the entire DNA molecule due to the the vulnerability in the structure of macromolecules. By the way, why does total base count matters? What triggered this question? And what do you mean "cannot assemble them"?

My question is in the context of whole genome assembly. I wanted to know how much of the human genome cannot be reconstructed, when treated as a DeNovo Assembly. The centromeric region is a big chunk of the unassembled regions in the human genome, I just wondered how big.

There is no fixed length of human centromeres.
As the paper you cited says in its introduction, there are array-length polymorphisms in centromeres. A polymorphism can be described as two or more forms of the same DNA sequence existing; which one you have depends mostly on which one you inherited from your parents. There are also polymorphisms that are created by imprecise DNA duplication during meiosis. Array-length polymorphisms can be explained by the latter.
As the DNA in centromeres is highly repetetive, it can happen that during replication, the number of repeats is decreased or increased. This leads to many different copy numbers in different individuals. Therefore, your answer cannot be answered with a specific number.

I would settle for an average number, a range, or the specific number of a specific individual.


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Using PGAL10 promoter to overexpress specific yeast genes: How to?
I was reading a poster about expression boosting for Artemesinin production in yeast and it had this line:

PGAL1
  and PGAL10 have been used for the
  overexpression of all genes from the mevalonate
  pathway.

What exactly does this mean? I suppose these are promotors? http://www.yeastgenome.org/locus/S000000224/overview
But how exactly does one use them during cloning to boost expression?
Say that you wanted to over-express ERG10, the gene coding for the first enzyme in the MVA pathway. How does one go about using PGAL10 to do this during the cloning steps?
Link to the poster: https://ddd.uab.cat/pub/tfg/2014/119349/TFG_narcisferrerledo.pdf

You're right about them being promoters, although it would be useful if you posted the link to the source of the sentence that you cite, so that we can read exactly how they are being used.
A fairly common way to study genes that aren't consistently highly expressed is to place them under the control of a strong promoter; that is, a promoter that is recognized by transcription factors in such a way that its linked gene is almost always expressed.
This is exactly what this group did in this paper, to study some features of yeast metabolism. In this case, the genes that they were interested in studying were cloned into a vector that was then inserted into yeast cells that lacked that gene. This way, the researchers knew that any expression of their gene of interest came from the vector and was driven by the pGAL1 promoter.
Similarly, if ERG10 was your gene of interest, this might be a strategy that you could adopt to study it.

I added the link to the source. It's a poster not a review, sorry. https://ddd.uab.cat/pub/tfg/2014/119349/TFG_narcisferrerledo.pdf

And this is a related paper: http://www.nature.com/nature/journal/v496/n7446/full/nature12051.html

From the poster, it looks like they're doing what I describe in my answer. That is, over-expressing a gene from a plasmid and driving that expression with a strong promoter. I think you'll see that a lot in studies like this one.

So how does one go about finding the actual DNA sequence for what they call PGAL1 / PGAL10. A search for these on Genebank / Yeast databases produced no hits.

Ok, maybe I did find the sequence! Would it be this one, you think? http://www.ncbi.nlm.nih.gov/nuccore/218616465


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What were the Neanderthal innovations?
At some point the neanderthal and modern human lineages diverged. I'm not sure what exactly their most common recent ancestor was (I see some sources suggesting homo heidelbergensis), but in any case I'm interested in the innovative/apomorphic features of neanderthals relative to that MRCA. What new features did they have, and what existing features changed most?
In particular I am not asking how neanderthals differ from modern humans.
This question is partially inspired by popular science pieces (e.g., Human Hands More Primitive than Chimp Hands) discussing human hands, which are essentially basal, vs. chimpanzee hands which are less similar to the common ancestor.

Two issues here: 1) What features are you talking about? Morphological trait or Ecological niche? 2) You are asking for a species comparison but you don't want the comparison to be done with modern humans. You who should the neanderthals be compared to? To the MRCA? If this the case you are just asking how the neanderthals evolved since they split with modern humans, right?

@Remi.b: 1) Morphological traits and 2) comparison with the MRCA, and yes -- just asking how they changed since they split. I suppose for #1 the traits will relate to their ecological niche and so that information might also be useful.


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Big Bug from Peru
I'd like to have a name for this guy.  There were 5 or 6 of them zipping around the flower bed on the coast of Peru about 120 kms south of Lima.

Nice photo! :) :)

That is a hawkmoth, probably Hyles annei (Guerin-Meneville, 1839). It is one of a number of moth species commonly called "hummingbird," "sphinx," or "hawk" moths in the family Sphingidae.
Beautiful, isn't it? :)
edit - sorry, I originally misidentified this as Hyles lineata - the pattern is slightly different.

Image search on "hawkmoth" turns up some stellar photos. Here is a close-up of an eye.

@DavidS That is amazing.


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Goodwin oscillator explained
Hello I have been reading papers about the Goodwin oscillator and I found that the equations are kind of tricky. Specially the part of the hill coefficient. In his paper "An entrainment model for timed enzyme synthesis in bacteria" from 1966, in the part of the differential equation of the mRNA concentration Xi, there is the term Zi and this term also exists in other books that talk about this oscillator. However, I don't know what it means. Goodwin never mentioned what this term means. I'm guessing it is about the hill coefficient, but still I do not quite understand well.
I share the link of a chapter book that explains the equations of this oscillator (page 244):
Biochemical Oscillations
Thanks for your help.

Adding a link to the paper and including the section in question would improve this question a lot.

I can´t put the link of the paper because you need a subscription to download it. But i can share the link of the chapter of a book that explains this oscillator.

A link to pubmed is fine. Many folks here have Uni library access.

The ODEs for the Goodwin oscillator are:
$$\begin{align}
\frac{dX}{dt}=&\ k_1\frac{K_i^n}{K_i^n+Z^n} -k_2X\\[1em]
\frac{dY}{dt}=&\ k_3X-k_4Y\\[1em]
\frac{dZ}{dt}=&\ k_5Y-k_6Z\end{align}$$
If you assume $X$ to be mRNA and $Y$to be protein then $Z$ can be thought of as an activated form of the protein (lets for instance assume a phosphorylated form).
The Hill coefficient, $n$ roughly tells you how many monomers of the activated protein co-operatively bind to the promoter or the number of protein monomers that form a multimeric repressor complex which inhibits the production of $X$. $K_i$ is a measure of how strongly would $X$ be inhibited by $Z$. To be precise it is equal to the concentration of $Z$ at which the production of $X$ is half its maximum rate. (Similar to Michaelis constant)
What the model says is that at higher values of $n$ (>8) there are sustained oscillations (which are called limit cycles). At lower values the oscillations damp. Note that even for low values of $n$ sustained oscillations (but not limit cycle types) can arise if there is substantial delay in the loop. However these oscillations are not as stable as limit cycles to perturbations.
Have a look at this post.
These are some advanced concepts and you may start by reading this book by Steven Strogatz called Non-linear Dynamics and Chaos*.

*Strogatz, Steven H. Nonlinear dynamics and chaos: with applications to physics, biology, chemistry, and engineering. Westview press, 2014. (latest edition);  ISBN-13: 978-0813349107; ISBN-10: 0813349109


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How to compare Smith–Waterman algorithm implementations?
Assume that you have two implementations of the Smith–Waterman algorithm (with what ever heuristic they apply to speed up) for local sequence alignment of genomic sequences.
I would like to know if one can be certain that these implementations do a good job of aligning (i.e the program has been correctly written). How do I benchmark this?

Is this a question on DNA? Could you give some more context to the question? Better tagging may help too.

They don't apply any heuristic to speed it up. The essential feature of the Dynamic programming algorithm is it gives you one of the  correct answers. You don't have to speed it up because it runs in real time. This is an important point and I suggest you modify your question.

I am not sure that 'i.e.' is a right word. Alignment quality is a matter of substitution matrices and gap penalties and it has nothing to deal with correctness.

You need to clarify the question. Smith-Watermann is a specific algorithm. There are no other implementations of it. There can be additional steps that are used in conjunction with SW and unless you atleast tell the names of these packages, we cannot comment on how one of them may be better than the other. As far as comparison goes, the one that does your job reasonable well in less time is the better implementation. To check if the program has been correctly written you should look at its source code. That is essentially bug finding.

There are only two possibilities for Smith-Waterman alignment with a given cost matrix. It's either right or it's not.
Honestly, whatever you're using, it's really really unlikely that a pure Smith-Waterman implementation is wrong. It's not that complicated, really. There are a lot of heuristic improvements on Smith-Waterman, but if you're both a) sure you don't want to test them b) sure they're not being used, you can always generate lots of random sequences and align them in pairs. If any pair doesn't align with the same score in the same way, something is wrong and you should investigate further.

I imagine that technically your question can only be answered on a computing science Stack Exchange. The pragmatic biology answer is there is no problem. This is such a well established algorithm that the implementation on any reputable site or from any reputable provider is likely to be OK. No heuristic is involved so if you compare different implementations you should get similar answers. I say similar rather than identical because there may be more than one alignment with the same score but only one is selected. Generally it makes no difference.
I suppose there is one aspect of the Smith–Waterman algorithm that could differ between implementations, but it is one for which you, the user, will have the ultimate responsibility — the scoring system. Your basic assumption is that two sequences are related, and you are asking the program to give you the pairwise alignment that  ‘best’ expresses that relatedness. ‘Best’ in the program translates into the highest score on a system that assigns a different value to the alignment of different pairs of all 20 amino acids (a comparison matrix for proteins) and specific penalties for the introduction of a gap (to allow for an insertion or deletion) and the extension of a gap once introduced. The implementations offer default values (I imagine these are similar in most programs) but its up to you to decide whether they are appropriate for the sequences that you are comparing, and to change them if necessary.
What are your options and when might it be necessary to exercise them? You can choose from different comparison matrices derived from aligning blocks of sequences for the same protein in organisms of different evolutionary separation. These matrices differ because some amino acid changes require only a single base change in the codon, whereas others require changes at all three positions of a codon,. The latter are less likely to occur over short evolutionary time spans (e.g. between mouse and rat) than at longer ones (e.g. between mouse and bacterium). So ideally you should employ the comparison matrix most appropriate to the sequences you are comparing.
Circumstances where you might wish to change the gap penalties or even customize the comparison tables are, admittedly, esoteric, but I would advise that it is better to think about the applicability of the scoring system to your biological problem than to worry that someone might have made a hash of implementing the computer algorithm.


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Questions on adding a protein to a DNA library
Two questions regarding finding the DNA sequence of a amino acid sequence (AA):
1) If you are able to find out the mRNA sequence of an AA, then don't you automatically know the DNA sequence?
2) When determining the mRNA sequence of an AA, how do you account for the various permutations in the genetic code for a given AA. Ex. Leucine is CUU and CUC. Or does it not matter?

Homework questions and trivial questions about basic biological concepts are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

@MattDMo This is not a homework question. I am just curious about the answer based on a lecture I attended and couldn't grasp. Thanks for the help

For 1, that is how retroviruses such as HIV work, and of which scientists have utilised to use in gene therapy. It requires a process called reverse transcription.
However, this would only show you the gene the mRNA was from, but no information about its location, or if it is repeated elsewhere.
As for 2, this is to do with the fact that one base cannot code for one amino acid; as there are 20 common amino acids used to make proteins. With 2 bases, you are only getting 16 possible codes from the various base pairs you can create. However, with 3 bases, 64 possible combinations are possible, more than enough to suffice for the 20 needed. This is called the triplet code;
and therefore, there are more possible combinations of the base pairs in DNA than there are amino acids to be made from them. The 'left over' combinations can code for the same amino acids as other combinations, making it the code degenerate. Therefore, it doesn't matter, as the combination is always read in 3s (non-overlapping), and if it codes for a particular amino acid, then that amino acid will be produced at the ribosomes when its corresponding code is read.
I hope this increases your understanding of the topic.
http://www.genetherapynet.com/viral-vector/retroviruses.html (Question 1)
http://www.chemguide.co.uk/organicprops/aminoacids/dna4.html (Question 2)

Excellent! It definitely helps @Butallati
For 1, is it every important to know where in the human DNA the gene if you have the mRNA sequence to make synthetic DNA?

Well, if we're talking about 'synthetic DNA', it's gonna be pretty difficult to create millions of pairs - so often scientists only create synthetic DNA in the form of genes, which are more...measurable. By taking the mRNA that you know will be used to produce a particular protein, and using a retrovirus, you will just be inserting that gene back into the DNA (just like how HIV will insert its own gene into your DNA, after all, it too is a retrovirus). Therefore the location of gene on the DNA is not particularly important for that instance.

If you wish to know more on the uses of retroviruses in gene therapy, feel free to google about "SCID" and gene therapy. There may well be some processes, or maybe just general knowledge of how DNA works, which requires knowing the location of genes on DNA, however I personally don't know any.

thanks so much for the exciting information! I'm a medical student whose eyes are just opening to the world of therapeutics and biotech start ups. Most of my experience has been in retrospective clinical research but I'll be taking a research year soon to expose myself to clinical trials and basic science work

Awesome, glad I could help. I'm just an A2 student (1 year prior to University), so it's nice to see possible applications of what I've learnt to this website. In addition to what I mentioned earlier, some other interesting things under the topic of DNA technology are the use of gene markers, in vivo gene cloning (using vectors such as retroviruses, as explained above) and in vitro gene cloning (using the polymerase chain recaction). Those should help further your understanding of DNA technology (which is closely related to your question)


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Henry Fingerprint Classification System Disrepency Among Articles
I know that the formula for fingerprint primary classifications is [1+(even finger value sum)]/[1+(odd finger value sum)]. So according to this formula and the Henry Classification System finger values, if a person has whorls on all ten fingers, then the classification ratio would be (1+31)/(1+31), which is 32/32. But some of the articles I have read say that it is actually 31/31 for a person with whorls on all ten fingers. Here are two articles that say that: article 1 and article 2 while other articles such as article 3 say 32/32. To me, the first two articles did not add the +1 to the numerator and denominator. Which is correct?


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Controlling the pursuit path of the human eye
The human eye scans images by panning focus along a certain path. Stork et al. (2002) revealed that there is a feedback process involved in moving ocular focus along a path that produces minimum muscular stress.
This got me thinking that, possibly, I could augment a video such that I slightly blur most of the image in each frame leaving a path (with some significant width) of the unblurred image or a path of clarity, if you will, to "control" a third party's ocular pursuit path. I hypothesize that this control would be won from imposing a path of clarity , because the eye adjusts it's pursuit path to reduce stress.
Could you help me to decide if this is even remotely possible?
Thanks in advance! :)

Welcome to Biology.SE. You said I've read that [..]. Can you please to link to your source as it could be helpful.

That comment pulls from a few places, but search this: "Intentionally-evoked modulations
of smooth pursuit eye movements".  It might help.

Assuming the the article for which you give the title reported the claim you're doing, I edited the post to include this reference. Thanks +1


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Are there animals that can deliberately manipulate their metabolism, apart from hibernation?
Are there animals that can slow down their metabolism deliberately? I know that hibernation would be one mechanism, and maybe being cold-blooded, but I was wondering if there was maybe an animal that could crank up or slow down metabolism based on food resources?
Are there chemical compounds that could have this effect?

By deliberately do you mean voluntarily? Pythons are known to modulate their metabolism. Are you looking for examples like this?

Yes, sorry, voluntarily would be a better word!

Humans.


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Toxicity of Zinc to fungi
I would like to know what are the mechanisms and overall effects of Zinc on fungi.
I know that Candida albicans is susceptible to Zinc deprivation and Zinc-infused paint is also used to repel mold.

http://goo.gl/sPhcyn and http://goo.gl/wrIX58 might be of interest to you

You might be interested in this (PDF) too. I couldn't find definitive reports on mechanisms of Zn toxicity on fungi, so it doesn't seem that the exact cause is known yet.


text:
Do hydrogen ions contribute to water potential?
I was thinking about lysosomes and how they maintain an acidic pH inside themselves by pumping H+ ions from the cytosol. Do hydrogen ions set up a concentration gradient that causes water to move by osmosis? If so, why doesn’t water rush in to the lysosomes to raise their internal pH?

Osmosis is prevented by cell membrane.

Why would that be the case? If osmosis couldn’t occur across phospholipid bilayers, we would be dead.

We have special pores like aquapores which enable osmosis only when required. Did not you read it in class 11?


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Is the zygote the only totipotent cell?
I’ve been told that the unfertilized egg contains cytoplasmic determinants (e.g. proteins, transcription factors, mRNAs) that are divided unevenly during the early stages of cell division in an embryo. Thus, each embryonic cell has a different cytoplasmic composition with a different set of transcription activators, allowing the expression of only certain genes.
By this token, it seems to me that this uneven partitioning of cytoplasmic determinants occurs in the very first division of the zygote. Thus, the first blastomeres are already no longer totipotent. Is that correct?

Search on fraternal/ maternal twins

Initial 3 divisions are equal.

Can you explain why my reasoning is incorrect? What really happens to maintain the totipotency of the first few cells?

Did you search on fraternal twins? Well I know this much only.

As I also said , first few are equal and unequal partition does not lead permanent differentiation and it matters only at later stages.

If this were actually the case, identical twins would be impossible (yet they are far from rare.) There may be a bit of confusion regarding the identicality of two blastomeres (they are not always - maybe even never - completely identical), but totipotentiality means they have everything needed to develop into complete beings. Also, the zona pellucida plays a role in survival of divided blastomeres (e.g. 8 cell stage cells have been seperated, and have developed into normal mammals (horses, cows) if supplied with a zona pellucida.


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UV light-induced mutagenesis during gel extraction
this is a very short question I did not find the answer for online, neither on this nor other fora. At the beginning of my cloning protocol, I extracted the band with the sequence of interest directly from the gel upon electrophoresis, and failed to minimise the exposure time of my sample to UV (did not switch off the lamp between cutting of different bands). Now, the gel was sitting in the cast tray the whole while (altogether maybe 30 to 50 seconds), and I wanted to know whether this eliminates the risk of mutagenesis, or at least minimises it, due to the absorption of UV light by the cast tray. Thank you.

I've imaged gels for a few minutes on UV, then went to cut out bands. I managed to get successful plasmids from them after miniprep. Always check your minipreps for proper gel digestion and confirm by sequencing.

Thanks for your answer. Do you remember the size of your inserts? Mine are about 2.5 kb. I will have them sequenced next week, but was just curious as to whether the cast tray is made of plastic that absorbs UV light.

The gel tray does not absorb UV, otherwise you wouldn't be able to see the bands in the gel.

@MattDMo They often absorb a little, when I slide the gel off the tray and put it directly on the transluminator, the bands get brighter. I wouldn't bet on the tray making the difference between damaged and undamaged DNA though.


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Does a zygote express all genes?
If a zygote has all the cytoplasmic determinants and all the specific transcription factors, does that mean that all genes in the genome are expressed?

There are some obvious counter examples: myelin, immunoglobins, keratin, crystallin, haemoglobin.. you could just go on....

The short answer is that no, a zygote doesn't express all genes simultaneously.
A zygote is like any other cell, in that it represents a distinct phenotype. And like any other cell, this phenotype is maintained by tight regulation of gene expression patterns. Check out this paper, for a nice description of the process of embryonic gene activation.
An important way in which the zygote differs from other cells, and which might be what drives your question, is that the zygote has the potential to differentiate into all the other cell types found in the body. This process of differentiation is also very tightly controlled in terms of gene expression.


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In percentage, how much is the human genome (DNA) similar to the mouse genome?
Some guy argued with me against evolution theory, and he claimed that human and mice share 98% just like human and chimpanzee.
I've tried to search online for a simple and accurate answer, but I couldn't yet.
In simple words, how much is the human genome (DNA) similar to the mouse genome?
Please use numbers as much as you can and provide references.

This question cannot be answered as simply as you put it, but it's not too much to elaborate on.
The order of the base pairs will be drastically different, but the same proteins and amino acids will be coded for in genes, just at different points along the DNA. For example, you may find the same sequence to code for a protein in a mouse as in a human, but they will not be found in the same place along the DNA code (although they will still be read and eventually produce the same protein).
http://www.nature.com/nature/journal/v420/n6915/full/nature01262.html
Additionally, this article shows that, if we take your question literally, "at the nucleotide level, approximately 40% of the human genome can be aligned to the mouse genome", that is, if human and mouse DNA was lined up side-by-side, and a percentage of identical match-ups was calculated.
However, taking a 'looser' approach, it is worth noting that about 5 percent of both of genomes consist of protein-coding genes (https://www.genome.gov/10001345), and the remaining 90%+ is non-coding. If we only count the protein-coding genes, the average similarity of genes between humans and mice in only protein-coding genes is 85%. The link above says that some are 99%, and some are 60% - there is a clear similarity here between humans and mice, albeit not 100% identical.
If you wish to know the explanation, simply it is because mice and humans both have a common ancestor (the last link also explains this) about 80 million years ago. Due to these similarities, and the striking similarities, scientists simulate genetic changes in mice that can occur to humans, and have used computers to analyse the similarities in mouse genome.
I hope this is understandable, if you need any clarification on terms, please ask :)

But what objective or rational reason does one have to only count the protein-coding genes? The other genes, as I understand it, are responsible for gene expression--in essence, the "program" running on top of the protein "building blocks". By that reasoning, Windows 3.11 is 90% the same as Windows 8, because they use almost the same underlying set of instructional building blocks in the processor, yes? Gene expression is an absolutely fundamental part of what makes up an organism, and it's absurd to just throw away some set of genes without a good reason to–I'm eager to hear such a reason!

Fair point, it's just that OP's said that he wanted to know "in simple words". I did add about how 40%~ similarity can be aligned, but considering when you align only protein-coding parts of the genome, the percentage shoots up to an average of 85%.Considering these are found within all animals of nature, just like how Windows is all built upon the same, original code, then it can be seen as subjectively more important to focus on those ones, rather than including "junk DNA". I'm sorry for not fulfilling everything in my answer, but OP did want it to be 'simple'. I am only a student, after all

The idea that "junk" DNA is actually junk is greatly disputed. Also, your answer lacks any references. Without that, it's just a random opinion.

Well it was my first answer of this website, so I was limited to two links. I only use the term 'junk' DNA since it is widely used, and is only 'junk' from the perspective of "non-protein coding" and "protein-coding" DNA. I absolutely agree that 'junk' DNA is not 'junk' by definition, but in accordance to OP's question, I thought it was worth referring to it as such to further understanding of the difference in percentages being so drastic as a result of whether they code for proteins or not. I'm sorry if the answer was inadequate to you, but please add your own if you feel you can do better.

I don't have time to post an answer, but I have already balanced comment.

Fair enough, thank you for your criticism of my answer. I will try to improve upon it the next time I decide to post one :)


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What is rotational diffusion and lateral diffusion in plasma membrane?
There are no good reads on internet. The idea that I have formed so far of these topics, is that lateral diffusion is translational movement of protein in a leaflet.

From this paper, rotational diffusion describes the movement of a membrane lipid around its axis that is perpendicular to the plane of the bilayer, analogous to a person spinning around while standing up.
Lateral diffusion describes the movement of membrane lipids exchanging places with each other across a face of the bilayer, rather like two dancers spinning about their mutual center of gravity.


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What are these curious cetaceans?
At the beginning of the superb documentary film “Un jardin d’Eden sous les mers” (“A garden of Eden under the seas”) [1], we see a group of curious cetaceans. At about 1 min.
What are these cetaceans?
I think that they are odontocetes. But what species are they? This is a mystery.
[1] Documentary film “Un jardin d’Eden sous les mers” (“A garden of Eden under the seas”). It will be rebroadcasted on Arte on 2016‑04‑01 at 7:45 Paris time. You can watch it on-line here.
Thank you.

Adding a screenshot would enhance the change of getting an answer, not many people will go and watch a movie.

I am completely shooting in the dark here, but do you mean the ones between 1:06 - 1:13 minutes in the video? (After Hammerhead and before Baby and Mama white Shark :) )

SPECIES IDENTIFIED: Pseudorca crassidens (False Killer Whale)

Matching image from the internet (used for identification):

Courtsey: UAE Dolphin Project
PS: Images are screenshot from the video Documentary film “Un Jardin d’Eden sous les mers” (“A garden of Eden under the seas”) are completly owned by the owner of the video and "arte HD" channel.
PPS: Anyone reading this, if you haven't already, then please watch the video. Though it is completely in french, the videography is amazing.
References:

Pacific Islands Cetaceans
Other Whales

Yes, I mean these nice cetaceans. I have thought about pseudorcas too, in the meantime. Indeed, these cetaceans are pseudorcas! Thank you for this great answer!


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How much of the Neanderthal genome is living on in humans?
I've understand that outside of African, most ethnic groups carry some (4% or less) Neanderthal DNA.  So en masse, across all living humans, what percentage of the original Neanderthal genome is still alive in human decedents today?

I think this question is meaningless. What is the point of calculating an average? It's as useful as calculating that on average people have one testicle.

Isn't it more than 90% same. All mammals have a lot of same genes. Neanderthal belongs to same genus even. So, answer needs to be more than 90%. There  can be just 1% difference in any homosapien gene population.

Even though individual humans only have around 2-5% Neanderthal genome, it's not the same 2-5% across people. In total, at least 20%, and perhaps as much as 40% of the Neanderthal genome could be recovered from modern human populations:

We identified Neandertal lineages that persist in the DNA of modern humans, in whole-genome sequences from 379 European and 286 East Asian individuals, recovering more than 15 gigabases of introgressed sequence that spans ~20% of the Neandertal genome

--Resurrecting Surviving Neandertal Lineages from Modern Human Genomes
However, there are stretches of the human genome that are almost completely devoid of Neanderthal genes. These include male-fertility associated regions (leading to the suggestion that male sapiens/neandertalis hybrids may be been subfertile or sterile):

Genes that are more highly expressed in testes than in any other tissue are especially reduced in Neanderthal ancestry, and there is an approximately fivefold reduction of Neanderthal ancestry on the X chromosome, which is known from studies of diverse species to be especially dense in male hybrid sterility genes. These results suggest that part of the explanation for genomic regions of reduced Neanderthal ancestry is Neanderthal alleles that caused decreased fertility in males when moved to a modern human genetic background.

--The genomic landscape of Neanderthal ancestry in present-day humans
And some brain-specific regions (suggesting that those are uniquely human):

Regions depleted of archaic lineages are significantly enriched for genes expressed in specific brain regions ... A large region depleted of archaic sequence spans 11 Mb on chromosome 7 and contains the FOXP2 gene (Fig. 4B), which has been associated with speech and language

--Excavating Neandertal and Denisovan DNA from the genomes of Melanesian individuals

I see the "~20%" in the quote, but where does the "as much as 40%" come from? Was that related to "Coalescent simulations for a broad range of admixture models suggest that 35 to 70% of the Neandertal genome persists in the DNA of present-day humans (figs. S1 and S2)" from that paper?

The comment from Anubhav Goel below the question is a good one, presumably that 20% is the proportion of the Neanderthal exclusive DNA in their genome that isn't shared by practically all humans .. so 20% of something like 1%, would that be right?


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Why does evolution only involve heritable traits?
If natural selection favors a certain behavior that is learnt, then wouldn’t that behavior be found more often among a population (as more offspring will learn that behavior from their parents or their peers)? Since the behavior is not encoded in the genes, it is not heritable, but it is transmitted through other means and will thus accumulate in the population. This, to me, seems a lot like the effects of evolution, yet this is not a heritable trait. So my question is why does evolution concern only heritable traits and not those that can be reproduced by learning?

If offspring learn it from their parents, isn't it heritable by definition? Apparently, not in genetics. It seems to me that this question is mainly about definitions. If you're studying genetics, you want to define "heritable"  so as to apply to genetic inheritance only, and other features passed from parents to offspring may be considered environmental. These other traits would have to be analyzed in a different way.

I assume the definition of ‘heritability’ in genetics is the one used in evolution, unless I am mistaken. My question is why this definition is used rather than one that encompasses environmental factors as well.

There is a lot to say to address this question fully. I will be brief and a little messy to try to introduce you to some concepts and that will hopefully push you to learn more by yourself.
Heritability in genetics
In genetics, heritability is a statistic that describe the fraction of the phenotypic variation that which is caused by underlying genetic variation. Please have a look at this post to understand the concept of heritability as used in genetics. Note that there are two such statistics, named heritability in the broad sense $h_B^2$ and heritability in the narrow sense $h_N^2$.
Basics of non-genetic inheritance
Here, I will refer to "heritability in the broad" as the passation of trait value (such as behaviour for example) and environment characteristic to another organism. One must not confound what I call here "heritability in the broad" and heritability in the broad sense as defined in genetics ($h_B^2$).
Sure, a lot of things can be inherited from one organism to another. Any such heritable (in the broad sense) trait is susceptible to show interesting variation in the frequency at which trait values are found in a population. If, in addition to that, this trait is susceptible to spontaneous changes (the equivalent of mutations in genetics), then this trait can show interesting evolutionary patterns. If in addition to that, different trait values have different aptitude to replicate (the equivalent of natural selection in genetics), then such trait can evolve in an "even more interesting way".
What can be non-genetically inherited?
Two things can be inherited without the use of any sort of genetic information (I also exclude epigenetic information incl. DNA methylation or protein concentration in the yolk).

Environment (Ecological inheritance)
Meme

See more on Ecological inheritance and memes below.
Ecological inheritance
This is probably the first type of inheritance one would think of when not thinking about biology. In humans, it is not uncommon for offspring to inherit "stuff" from their parents when they die. Similarly, beavers can inherit a dam that has been built by their parents. This type of inheritance in generally called Ecological inheritance.
This type of inheritance might eventually be important to evolutionary processes (see literature on niche construction).
Inheritance of a meme
Definition
A meme has been named by the analogy to a gene. A meme is any idea, behaviour, thought or tradition (piece of culture) that can be inherited. The concept of an internet meme is now quite popular, but a meme is more than just an internet meme. While genetics is the study of genes (and much more actually), memetics is the study of memes. Memetics is a very interdisciplinary field of study that attract biologists, philosophers, mathematicians, linguists and archeologists among others. The hypotheses built in the field of memetics rarely offer predictions that can be easily tested, and therefore a good part of the work in this field remains very uncertain.
Analogy to genes
A meme could be a joke for example. If the joke is funny it will replicate easily and enter in new brains. This meme could be said to have high fitness. The joke may come into spontaneous changes (mutations). Be careful with analogies and they may show nothing but similarity. For example the nature of memetic mutation seem to be quite different than from the nature of genetic mutation.
Example
In humans, the examples are very easy to find. As I am writing this answer, I am currently trying to pass on a meme which has been given to me by some other authors. Hopefully I won't mutate this meme too harshly.
Lots of monkeys and apes are transmitting traditions, foraging methods and other memes to their offspring, sometimes through active teaching but often through imitation (or emulation). A classic example is the one reported in Rhythms of Vision in 1975 (I could not find the original peer-reviewed paper). A female monkey, one day had the good idea of washing a sweet potato. This behaviour has since increased in frequency throughout the population so that most monkeys now wash their sweet potatoes.
Pitman and Durban (2011) (and others before them) report that some population of orcas use cooperative hunting while some other population does not. Variation for this trait seems not to be caused by genetic variation.
How does inheritance work?
Inheritance can be "vertical" (parent to offspring) or "horizontal" (between individuals of the same or different species). This holds true for both genetic (consider transduction) and non-genetic inheritance (teaching to offspring or to the neighbors).
In addition to that the passation of a meme can be active (teaching) or passive.


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How does AIDS affect the immune system vs. SCID?
AIDS

acquired immune deficiency syndrome

According to wikipedia,
Caused by infection with the human immunodeficiency virus (HIV).Following initial infection, a person may not notice any symptoms or may experience a brief period of influenza-like illness.  As the infection progresses, it interferes more with the immune system, increasing the risk of common infections like tuberculosis, as well as other opportunistic infections, and tumors that rarely affect people who have working immune systems.
SCID

Severe combined immunodeficiency

According to wikipedia,
.....is a genetic disorder characterized by the disturbed development of functional T cells and B cells caused by numerous genetic mutations that result in heterogeneous clinical presentations. SCID involves defective antibody response due to either direct involvement with B lymphocytes or through improper B lymphocyte activation due to non-functional T-helper cells. Consequently, both "arms" (B cells and T cells) of the adaptive immune system are impaired due to a defect in one of several possible genes. SCID is the most severe form of primary immunodeficiencies, and there are now at least nine different known genes in which mutations lead to a form of SCID.
Both the diseases affect the immune system of the human body. So, why they are classified as different disease? What is the property that differentiates the diseases?

The flu and common cold both affect the respiratory system, yet we have separate words for them. Osteoarthritis and rheumatoid arthritis both affect the joints. Why do you think diseases are solely distinguished by what part or the body they affect?

Homework questions and trivial questions about basic biological concepts are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. "Homework" is interpreted to mean any academic or other assignment, test preparation, or task given in relation to a class, educational setting, or self-learning.

AIDS -

It is caused by Human Immunodeficiency Virus (HIV).
HIV attacks helper T cells and, therefore, helper T cells reduce in number, i.e. individual can produce T cells, but they are destroyed by the virus.

3.HIV can be transmitted at any stage.
SCID -

It is a genetic disorder.
The individuals are born without T-cells and B-cells and are incompetent to produce them.
This disorder is found in new born children.

A disease is characterised not by its target organ/tissue, but how it infects that organ.

HIV (Human immunodeficiency virus)
Cause:

HIV is a retrovirus that infects helper T-lymphocytes
Reverse transcriptase allows viral DNA to be produced from its RNA code
After years of inactivity (Th cells continued reproducing), the virus becomes active and starts to destroy T-lymphocytes
This results in lower immunity, as antibody production is compromised
HIV is the lowering of the immunity of a certain individual, over a number of years
AIDS is the final stage where observable symptoms develop

Transmission:

Exchange of body fluids (sexual intercourse, breastfeeding, childbirth, needles, etc.)
There is a very small fraction of people who are immune to HIV (no CD4+T receptor)

SCID (Severe combined immune deficiency)
A severe combined immune deficiency, a rare genetic disorder in which affected children have no resistance to disease and must be kept isolated from infection from birth.

Genetic disorder characterized by the disturbed development of functional T cells and B cells caused by numerous genetic mutations that result in heterogeneous clinical presentations
SCID involves defective antibody response due to either direct involvement with B lymphocytes or through improper B lymphocyte activation due to non-functional T-helper cells
Consequently, both "arms" (B cells and T cells) of the adaptive immune system are impaired due to a defect in one of several possible genes

Sources:

https://en.wikipedia.org/wiki/Severe_combined_immunodeficiency#Classification
https://de.wikipedia.org/wiki/AIDS
http://www.avert.org/about-hiv-aids/what-hiv-aids
http://www.ncbi.nlm.nih.gov/books/NBK22254/
https://en.wikipedia.org/wiki/Severe_combined_immunodeficiency
https://www.genome.gov/13014325
https://www.scid.net/


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What is the best test for SNV clustering?
I am looking for a method to cluster single nucleotide polymorphisms based on clinicopathologic data (mainly receptor immunoistochemistry). So far, I've came up with only two that handle dummy variables as long as I want to examine minor allele presence or absence;

Principal Component Analysis
A priori (association rules)

Do you know of any papers supporting the abovementioned methods, or maybe suggest an alternative one?


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Starch vs Cellulose. What are the differences between Alpha and Beta glucose ring structure in them?
I'm studying "Campbell Biology, 10th Edition" and in chapter 5 page 71 there's a statement I can't understand. according to book:

In starch, all the glucose monomers are in the α configuration.

and then says:

In contrast, the glucose monomers of cellulose are all in the β
  configuration, making every glucose monomer “upside down” with respect
  to its neighbors.

My question is if all glucose monomers of cellulose are all in the β
configuration (according to figures) why each monomer in cellulose is “upside down” with respect to its neighbors and is not just all the same as in glucose monomers.

The reason the monomer units are shown as alternating orientation in the cellulose case and not for starch is due to the angles required for the bonds between the atoms involved.
Note that in α-glucose the OH groups of the #1 and #4 carbons are shown on the same side of the ring.  When these two groups are changed into a single O joining two α monomers into starch, they have to remain in the same position.  When a single O joins them together, that oxygen requires the angle between the bond be less than 180 degrees, so the two glucoses have to be on one side of the oxygen.  That's fine in the drawing because in α glucose both OH groups are pointing down.
On the other hand, in β-glucose the OH groups of carbons 1 and 4 are on opposite sides of the glucose ring. Joining two β monomers to make cellulose requires that these two OH groups point in the same direction so that when changed into bonds to the single O, the angle which the oxygen requires can be provided.  To get the two OH groups pointing the same way requires one of the two β-glucoses to flip relative to the other.  Hence you get the monomers of cellulose alternating in orientation.
Part of the problem may be trying to visualize these 3-D relationships from the 2-D diagrams.  On this α-/β- glucose webpage there are some rotatable images of the molecules which may help visualize the relationships.

I'm having trouble understanding the last part of your question: "why each monomer in cellulose is “upside down” with respect to its neighbors and is not just all the same as in glucose monomers."
I assume you want to know more about the beta configuration of cellulose. Cellulose is made of monomers of glucose linked together via B 1-4 glycosidic linkages. In contrast, "starch" more specifically amylose is made of monomers of glucose linked together via A 1-4 glycosidic linkages. Our bodies have glycosidases that can break down the alpha linkage but not the beta linkage.
This is the first time that I have seen cellulose polymers drawn that way. I am more accustomed to them being drawn like this: http://chemwiki.ucdavis.edu/Core/Biological_Chemistry/Carbohydrates/Polysaccharides/Cellulose