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How does Humira work when injected into patients with rheumatoid arthritis?
OK, I have rheumatoid arthritis and I've been injecting Humira 2 times a month for the last 8 months.
As far as I know rheumatoid arthritis is simply an immune system disorder which makes the immune system produce more proteins called Tumor Necrosis Factor alpha which regulate body disorders.
When I inject Humira I actually import a protein called Adalimumab which is a TNFα inhibitor.
So far so good but my question is
Does my body throw this protein away after some time? How is this protein removed from my body?
What about the way Adalimumab inhibits TNF, does it bind to TNF?
Also the details of how rheumatoid arthritis appears are not well known but the main reason is because of the patients DNA isn't it?

Adalimumab is an antibody that binds to tumor necrosis factor alpha (TNF-alpha). Antibodies have high-affinity binding sites for their antigens, and for a small antigen such as TNF-alpha, would bind to it and prevent it from binding to its target receptors. Antibodies, like all proteins, degrade over time and are then removed from circulation, and since the body does not produce more of this antibody, it must be re-administered every few weeks.
The mechanism is somewhat ironic in that the chief role of antibodies is binding to (and thus neutralization of) foreign antigens, but this antibody binds and neutralizes a part of the immune system itself. This part is TNF-alpha (a cytokine) whose function is to promote inflammation at a site, which draws white blood cells to it and activates them. TNF-alpha also induces fever, and suppresses tumor formation and viral replication by activating programmed cell death pathways.
Aggressive immune responses always cause collateral damage to surrounding tissue, but in autoimmune diseases such as rheumatoid arthritis the damage is compounded by the fact that the target of the immune response is an element of the body itself. The immune system should be tolerant to self; sometimes tolerance fails and while it is known that genetics is part of it, the process is not yet well-understood.

Prufrock +1 for the answer ! It would be helpful if you could include a source for this.

i still dont know how exactly this antibodies degrade after a certain period of time . As far as i know things in our world dont just disapear they just transform to other things.

Recall that antibodies are proteins, and proteins are composed of smaller molecules known as amino acids. Proteins are extraordinarily elaborate entities, but as all things become damaged over time and no longer function. The antibodies eventually break in a literal sense, and the cells of the blood decompose them back into amino acids to be made into new proteins. The matter in the body is not static but is constantly being reorganized.

@biogirl - Although not a great general source, Wikipedia gives most of this information regarding Adalimumab. One of the original pharmacokenetic studies of this drug is described by Weisman et al. in the journal Clin Ther. 2003 Jun;25(6):1700-21. In PubMed there is also a review by Bang and Keating in BioDrugs. 2004;18(2):121-39, but I do not believe it is freely available. It is likely there are other reviews of Adalimumab that are freely available.

Here's a nice image that can help visualize how Humira and other similar drugs bind TNF-alpha and prevent it from participating in the signal cascade that causes abnormal immunologic activity.

@Don_S Your "image" link seems not to work.

Afaik. RA and psoriasis are probably caused by a malfunction of genes which regulate IL-23 production. IL-23 is required for Th17 cells to survive. Th17 cells produce a lot of things which result in inflammation and since TNF-α is a key mediator in inflammation and break down of joints, reducing the amount of available TNF-α reduces the inflammation.
(Th17 cells produce IL-17, IL-21, IL-22, IL-6 and TNF-α. Th17 cells are playing against Treg cells, which try to protect self cells. IL-17 promote osteoclastogenesis, and osteoclasts break down bone. According to several Wikipedia articles IL-17 induces the production of other cytokines such as IL-6, IL-1β, TNF-α. IL-21 is required for sustained CD8+ T cell effector activity. IL-22 is a mediator of cellular inflammatory responses. IL-6 modulates the resistance of T cells against apoptosis, induces activation of T helper cells and promotes osteoclastogenesis. TNF-α is an endogenous pyrogen which is able to induce fever, apoptotic cell death, cachexia, inflammation and inhibits tumorigenesis and viral replication. IL-1β is a mediator of the inflammatory response, and it is involved in the regulation of apoptosis as well.)
Adalimumab is an immunoglobulin, which binds to TNF-α, and so it prevents it from binding to TNF-α receptors and causing inflammation. After it is bound to its target you cannot reuse it, that's why you need daily doses of it. It is degraded by liver and kidney cells, and probably by phagocytes.
There are other TNF-α blocking pharmaceuticals. There are IL-23 inhibitors, one of which is ustekinumab. It is an immunoglobulin too and it is used for treating psoriasis. For, RA it is currently under clinical trial, but I guess it will work for RA as well. There is an IL-23 inhibitor which is not an immunoglobulin and can be taken orally, called apilimod. Sadly it failed the clinical trials; it had only a mild effect. It probably does not reach the inflammation in sufficient amounts. Maybe one day there will be an effective delivery method and thus a drug which can be taken orally.
There are alternative natural therapies: TNF-α inhibitors which you can take orally, for example γ-linolenic acid, ω−3 fatty acids, chondroitin sulfate, etc... These can be useful for mild cases of RA. Probably fever therapy works for mild cases as well. Afaik. cryotherapy has nice results in treating RA and its positive effect lasts much longer than the effects of any drugs, so if you aren't afraid of cold, that is a nice alternative therapy as well.

2013 - The interleukin-23/interleukin-17 axis and the role of Treg/Th17 cells in rheumatoid arthritis and joint destruction
2010 - IL-23 in the pathogenesis of rheumatoid arthritis.
2003 - Dihomo-γ-linolenic acid inhibits tumour necrosis factor-α production by human leucocytes independently of cyclooxygenase activity
2011 - Omega-3 supplementation lowers inflammation and anxiety in medical students: A randomized controlled trial
2006 - Discovery of a TNF-α Antagonist Using Chondroitin Sulfate Microarrays
A Study of the Effectiveness and Safety of Ustekinumab (STELARA) and CNTO 1959 Administered Under the Skin of Patients With Active Rheumatoid Arthritis, Despite Existing Methotrexate Therapy
2014 - Cryotherapy in inflammatory rheumatic diseases: a systematic review
2012 - A Phase IIa, Randomized, Double-Blind, Placebo-Controlled Trial of
Apilimod Mesylate, an Interleukin-12/Interleukin-23 Inhibitor, in Patients With
Rheumatoid Arthritis

Fever therapy for rheumatoid arthritis is not written about much, it seems. The little I could find seems to deprecate it, except for infectious arthritis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2242205/pdf/tacca00014-0256.pdf .As for cryotherapy there's a lot about it on the internet but Wikipedia mildly deprecates cryotherapy, it seems. As for whole body cryotherapy : ttps://www.fda.gov/consumers/consumer-updates/whole-body-cryotherapy-wbc-cool-trend-lacks-evidence-poses-risks

@MatthewChristopherBartsh I would try them out if I had RA. You lose only a little money with them. If it is urgent, then Humira works pretty well.


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Do people of the same height walk at the same speed?
I'm working on a project that concerns movement and the human body. Before I begin to experiment, I need an answer to a question I'm sure has an answer, but doesn't Google well.
What I need to know is firstly whether I can assume that if people have the same height, they will also have the same leg length?
Secondly, if two different people have an identical height, will they take the same amount of time to cover the same distance when running at the same speed, regardless of their unique technique for running?
An Example:
Say I'm with a friend, we're both 6 feet tall exactly, we both get on to treadmills side-by-side and set it to a speed of 7.5km/hour.
Will we be moving exactly the same body parts at the same time - will our feet land on the treadmill at the same time?
Is there a possibility that people of the same height do not have the same leg length? If so, how likely is it on average?

People of the same height can easily have different leg lengths. Think western women models - currently they are typically women with relatively long legs while ordinary people can easily have shorter legs for the same total height. There's even leg-to-body ration section in Body proportions Wikipedia article.
This is why pedometers always require calibration - the procedure in which you have to walk a known distance and count steps and then know how much steps you need per mile. There're no tables that would assist by assuming certain steps-per-mile ration for known height.

Of course, yes you're correct. Thanks for the link. Do you know of any other variable I could use to determine leg lengths? So far I've got trouser length (not a strong option) or establish a baseline via other methods.

@Dominic: When clothes are crafted the typical measure is "inner leg length" measure which more or less maps to how long a leg is. This typically has one inch increment though and so I guess isn't very reliable.

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Does the Petri dish lid orientation on workbench affect aseptic technique?
When examining an incubated plate, it is rather clear that holding the plate in one hand and the lid in another is best for aseptic technique, or simply resting the lid on the plate as shown below.

However, I can't seem to find an answer for what to do with your Petri dish lid when doing manipulations like plating. It's pretty obvious that the above practice is, well, practically impossible.
Thus, I always went under the assumption that when placing the Petri dish lid on the workspace, the orientation of the lid did not particularly affect risk of contamination, assuming that you're technique is indeed aseptic (ethanoled workbench, Bunsen burner, etc). However, discussing with collegues has resulted in mixed answers. Some say it doesn't matter, some say the lid should be facing up, some say down.
When doing manipulations like plating, is there a common practice for exactly how to place your Petri dish lid?

What do you mean by plating here ?

Plating = Spreading.

If you are spreading then there isn't any need to put the lid down. One hand simultaneously opens the lid and holds the dish, the other does the spreading. That's what I used to do. However the best solution is to use glass beads - see http://www.youtube.com/watch?v=TACbj-ixW-U although ironically I don't think much of his lid technique!

@AlanBoyd why are those beads a good idea? I understand that they can spread liquid around very nicely but you then need to pick the things out one by one (there were 9 in that video) which means extra work, I would guess it takes more time to pick them out than to manually spread in the first place. It also means more time with the dish uncovered which increases the chances of contamination. Is the uniformity of the spread so much better as to justify their use?

I agree with the "plate lid facing down" comments below. Contamination falls, so keeping the inside surface of the lid away from the air column is always a good idea. I work with mammalian cell/tissue culture most of the time, and so always do all of my work inside a laminar flow biosafety cabinet, but when I'm doing cloning and whatnot with bacteria the lid is always off for as little time as possible, always faces down, and I always try to work in an area with as little air flow as possible.

@terdon You don't have to pick out the beads. Once you have "spread" you invert the plate as usual and they fall into the lid. After incubation,as you check the plates you can tip the beads out for reuse. I put beads onto plates before adding the liquid - the lid is opened slightly for a second or two. (I autoclave beads in glass tubes and tip a few on to each plate). The main advantage of the method (apart from no alcohol, no disposable plastic) is in plating a whole stack of plates: add beads, pipette samples and then swirl the stack all at once. Really, I recommend that you try it out.

@AlanBoyd Ah, that makes perfect sense, thanks. The video you had linked to showed the beads being removed one by one which seemed tedious. What you describe sounds much easier.

@terdon I admit, I didn't watch it till the end   - I just wanted a quick link to illustrate the idea.

DISCLAIMER: I am a computational biologist and haven't touched a Petri dish since I was an undergraduate biology student.
I would expect that the best thing to do would be to place the lid face down.
When placed so on the bench, it is only the tip of the lid that comes into contact with your (presumably sterile-ish) bench. If you place it face up, the interior of the lid will come into contact with the air of the lab. Despite the presence of the bunsen, I would expect that to gather more contamination.
Since the lid is larger than the dish itself, the lip of the lid never touches the dish. Therefore, if the lip of the lid touches the bench and becomes contaminated that is not a big problem since that contamination should be blocked from spreading to the actual culture. If, on the other hand, the lid were placed face up, the interior of the lid (which hangs just above your culture when closed) will have come into contact with possibly contaminated air and could then cause contaminants to drop onto your culture.

@LanceLafontaine I asked a grad student I know in the microbio department and she says the same thing as terdon.

Working with petri plates both microbially and in tissue culture, there is one rule of thumb to follow. Contamination falls. Your main enemy is time, how long the medium is exposed (bar actually touching the surfaces). Ethanol DOES NOT sterilize the working surface. Think of it as a convenient scrubbant which evaporates quickly. The flame DOES NOT work to sterilize the air (except in the heated column above it, where you can't work). The flame creates an updraft near your workspace (see the rule of thumb), reducing falling contamination.
Placing the lid on a "clean" working surface is a common and reasonable practice. If you are coordinated, holding the lid in the non-dominant hand can also be done. If you are using a 'hockey stick' spreader (dip in alcohol, then flame, then spread a dispensed drop after cooling), there may be a better way.
Get a good petri plate turntable (might have to lubricate it with dry graphite).
Dry your petri plates for a while until no free moisture is visible in the dish.
Obtain some small volume glass pipettes (say 1 ml), with smooth tips, and sterilize them.
When you are ready to plate your suspension, place your petri dish on the turntable, remove the lid and give a good spin.  Dispense 0.2-1 ml of your suspension onto the medium directly, working the tip on the medium surface from the center to the edge, keeping a wet edge (surface tension). If you press too hard or hold the pipette too vertical, it digs in. Quick to learn this though. Replace the lid, and rest the plate a little while on the bench. A perfect spread (slight spiral) every time. Okay, a little practice helps. No flame, no alcohol, more free time for beer. Moisture content in the media is the only issue, but drying the plates inverted in a standard microbial incubator is easy enough.
I've used this method for years, with no major contamination issues.

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How can Pyridostigmine have the indication of Myasthenia?
I am thinking how pyridostigmine can be used in the treatment of myasthenia gravis.
Its similar compound (neostigmine) is also anticholine esterase.
This compound has the indication of myasthenia gravis but with the stimulation of the nicotinic receptor.
I cannot understand how pyridostigmine is causing the effect.
Probably, pyridostigmine is similar to neostigmine in structure, which can be why more pieces of information is about neostigmine than pyridostigmine.
How can pyridostigmine have the indication of myasthenia gravis?

Pyridostigmine is an analog of neostigmine, so has the same basic mechanism of action. Please forgive me for repeating information you may already know.
There are two main families of acetylcholine receptors: muscarinic and nicotinic. Acetylcholine receptors at the neuromuscular junction (NMJ) are exclusively nicotinic (N1 or NM), so that's the only receptor I'll address.
Myasthenia Gravis is caused by an immune response to nicotinic postsynaptic receptors on skeletal muscle. An antibody can either destroy or block the receptor site. The antibodies destroy the receptor sites more rapidly than the body can replace them. In MG, there can be as much as an 80% reduction in the number of these receptor sites.
Acetylcholinesterase (AChE) is an enzyme that breaks down acetylcholine (ACh) at the synaptic cleft. AChE has a remarkably high specific catalytic activity: each molecule of AChE degrades about 25000 molecules of ACh per second. Any drug which serves to inhibit AChE will increase ACh concentration at the N1 receptor. AChE inhibitors can be irreversible or reversible. Reversible inhibitors, (competitive or noncompetitive) have therapeutic applications; irreversible AChE  modulators are toxic.
Carbamates are organic compounds derived from carbamic acid (NH2COOH). They are reversible AChE inhibitors. This group includes neostigmine, pyridostigmine and physostigmine. Pyridostigmine is an analog of neostigmine, so has the same basic mechanism of action. Because they are not lipid soluble, they are selective for the NMJ; both also have direct action on Nm Receptors. The major difference between them is that pyridostigmine has a slight but significantly longer duration of action.
Drug Bank: Pyridostigmine
NeuroLex.org (get's it's info from PubChem)

Thank you for your excellent answer with great details! It is never wrong to repeat. Pyridostigmine is parasympathomimetic  and reversible cholinesterase inhibitor. These two features seem to work in different directions, but the latter is the main one. It leads to the property of reversing muscle relaxants and its indication of myasthenia gravis. The former effect does not seem to be a major one. -- Let's consider Pilocarpine which is cholinomimetic and exclusively muscarinic (nothing about nicotinic?). It seems that only acetylcholine inhibitors are exclusively nicotinic with (N1 or Nm).

If I'm understanding you correctly (and I'm not sure that I am) pilocarpine is a muscarinic agonist with no nicotinic effects. But there are AChE that are both Nm and muscarinic.

You are understanding me correctly. It seems that also the other short-acting and long-acting AChE are Nm and nicotinic besides neostigmine and pyridostigmine such as ipidacrine, donepezil and rivastigmine.


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Ephedrine or pseudoephedrine indirectly central alpha2 mimetic?
I started to think this problem by first thinking if the alpha2 mimetism is possible in either case.
It seems to be indirectly in either one.
Ephedrine seems to have more prominent effect in CNS.
So I propose that Ephedrine has indirect central alpha2 mimetic effect.
Is ephedrine central alpha2 mimetic?
I think one evidence about that would be if there is a alpha2 receptor which is activated by ephedrine somehow indirectly.

Anongoodnurse provide an excellent comment in other discussion about how to search PubChem.
Ephedrine is not alpha2 mimetic.
Pseudoephedrine is alpha2 mimetic, source:


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Effect of Western chicken and GH
I heard this clause from my teacher one week ago:

Chicken are grown in half a year until eaten in Baltic countries - Estonia, Latvia and Lithuania, for instance, [probably in other parts of Europe, too]. How do you imagine this to happen so fast? - - Growth hormones are used to grow them fast. This affects your endocrine system and can replace its natural function. We cannot even know the withdrawal symptoms when you stop eating food of growth hormones. - - Eat pork instead. No growth hormones used in their life cycle because not needed and not so useful in practice.

I started to think what. Can this really be true that the effect of growth hormones is big economically on poultry but not on pork so it is not used.
The size of chicken is small compared to pork so they have different muscular structure.
So probably more musculature in chicken and bigger effect therefore.
Why does growth hormones have bigger growth effect on chicken?
Is it true that growth hormones are used more in the growth of chicken than pork in Western countries?
I do not understand the critique presented against poultry industry here, in favour of pork industry.
Probably, there is some truth too.

Their conclusion relies on 1) chickens being fed more growth hormones, 2) that growth hormone leaves some sort of chemical trace in the meat we eat, 3) we absorb those trace chemicals, 4) those chemicals are bad for us - this is of course irrelevant to the question but if I were you I'd be asking the teacher for some evidence, there's too much of this sort of thing based on myths and hearsay.

@GriffinEvo Yes, I know that there is much myths and hearsay about this. I want evidence based thinking. The main argument is that chicken meat growth needs GH, but pork not, therefore GH is used in chicken.

Poultry raised for meat in the US (called broilers) reach butchering size in 5 to 8 weeks (compared to 10 weeks for half the size 40 years ago. It's not a GH miracle; it's a result of generations of selective breeding (as cows have undergone for unhealthy udder size).
GH use is illegal in the US and many other countries. Honestly, it's an unnecessary additive/expense.
I raised poultry for more than a decade, mostly chickens and ducks (but almost everything else as well). Once I bought 25  1-day-old broiler chicks (early broilers were a Plymouth Rock X Cornish) alongside my usual mix.  Within 2 weeks the broilers were at least 3 or 4 times the size of the other chicks, and more than a couple of them died (under ideal conditions - all free-range outside, cooped only at night). By 10 weeks, they were enormous.
They were also dumber than a bag of hammers, unfortunately. I felt so sorry for them that I let them live out their natural lives, which wasn't terribly long, partly because of their docile stupidity.
Growth hormone is unnecessary in the poultry industry.
Murray McMurray Hatchery: Jumbo Cornish X Rocks
Modern Meat Chicken Industry

Thank you for your excellent answer with indepth knowledge in the area! I will discuss this issue with my teacher more detail what he meant. Is there anything else used in the growth which may be more harmful for people, in contrast to pork -industry? I cannot think anything.


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To get Standard ECG from PhysioNet?
I am trying to get standard ECG by using PhysioNet's ATM with parameters

but I get

It should be something like

How can you get complete standard 12-lead ECG out of Physionet database?

Programmatically attempt here http://biology.stackexchange.com/q/52955/86

PTB Diagnostic ECG database here.
Review here.

I don't think that all leads are available.
I looked at the Signals combobox for different databases. This combobox seems to be the list of all available leads.
For example, take a look at iafdb (Intracardiac Atrial Fibrillation Database). It will plot you an ECG containing leads II, V1 and aVF and some other leads.
Another example is the EEG database eegmmidb (EEG Motor Movement/Image Dataset) which contains many leads.
Look also at the mimic2wdb/39 (MIMIC II waveform database, version 3 part 9) which contains 4 ECG leads and some other parameters like breath rate.

I do not understand how this work has managed to use Physionet's data and got such a 12-lead solution: http://web.utk.edu/~xzhao9/research/Physionet2011/ECGQuality.html Do you?

Is any of these databases AAMI standarded? There is no 12 lead AAMI databases available online. I verified the St. Petersburg database and it is not AAMI - big entanglement of energy. They have problems with some analog components and other things - too many unknown variables.

How can you get programmatically data with rdsamp? I extended the thread here http://biology.stackexchange.com/q/52955/86

As another answer suggested, it's a matter of choosing a database that has all of the leads. The St Petersburg INCART 12-lead Arrhythmia Database (incartdb) contains all 12 signals. Here is the directory. The tracings are available by selecting it from the drop-down menu on the page you linked.

Is this AAMI standard data?

@Masi I don't know. There are several email contacts listed on the page I linked. You may want to write to them to obtain more info about the data.

I contacted them. I will write here when I get the answer. In ambulatory ECGs, there is the situation that MIT-BIH is the only available AAMI standard data when also requirement that two datasets of one patient (particularly patient #201).

@Masi does it need to be ambulatory?  Was the UT example from a database?  I didn't think they had one.  Anyway looking at St Petersburg it appears to be AAMI

@AtlLED It does not need to be ambulatory. What is UT? Do you have reasons why ST Petersburg is AAMI?

@AtlLED St Petersburg database is not AAMI. I verified this through a long process made by me and my friends. They have problems in many components of their system. So there is no AAMI standarded 12-lead databases online.


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Typical cellular respiration lab with a respirometer -- why is potassium hydroxide (KOH) necessary?
For context, if you are unsure what this question is in reference to, feel free to take a look at this video by Bozeman science and go forward to about the 2:00 mark. In a typical cellular respiration lab, in particular the one outlined by the College Board, a respirometer and some peas are used to measure the rate of respiration. What confuses me is why KOH (potassium hydroxide) is necessary so that the interior volume of the respirometer won't change. Why wouldn't the solid formed by 2KOH combining with CO2 (K2CO3) cause a change in volume, since it occupies space in the respirometer just like the gasses? Sorry if this seems like a silly question, I have very poor background knowledge of chemistry.
For an animation, feel free to view this link from Pearson.
Thanks!

The solid precipitate does not contribute as much to the pressure inside the vial as the gas does. Intuitively, the gaseous molecule contributes to the pressure by collisions that exert force on the vessel (which would push the water out). By contrast, the solid precipitate only contributes to the pressure insofar as it decreases the volume of the vessel, which is negligible in comparison to the loss of kinetic energy per gas molecule.
Basically, just because they both occupy space, doesn't mean they occupy the same amount of space (or rather, they don't contribute equally to the pressure in the vial). Gases tend to occupy more space than liquid or solid phase molecules of identical size, due to their kinetic energy of motion and the force of their collisions on their surroundings. The KOH reacts with the CO2 to remove it from the pool of high energy gas molecules, converting them to low energy molecules in the solid. With the lower number of molecules contributing to the pressure (ideal gas law), the pressure is lowered and the force of the water becomes greater than the force of the gas, and the water enters the respirometer.

Cool. Is there anything I can add to improve the answer, like including a more quantitative explanation using the ideal gas law?

No, I think I understand it. Thanks again! And sorry for forgetting to award you the bounty yesterday.


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What is the Genetic Cause of Homosexuality?
So, I'm just wondering about this because I read the following in my Biology textbook about fruit fly genes:

"Normal male and female flies express distinct forms of the fru gene. When females are genetically manipulated to express the male form of fru, they court other females, performing the role normally played by the male..."

Out of curiosity, have any studies been conducted to see what causes homosexuality? Is there a similar gene in humans that, if randomly altered, causes attraction to same-sex individuals?
EDIT: a similar post exists, but nobody provided an answer related to the poster's question.

The phrasing suggest some misunderstanding of what genetic cause could mean. On this answer I linked a number of posts where I explain the concepts of heritability (which is related to this misunderstanding even if it is not necessarily obvious to you right now).


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identify this tree
location: trabzon(turkey) planted for recreational purpose

dont forget to accept good answer


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Introducing evolution into the Hodgkin-Huxley equation
How would the Hodgkin-Huxley equation change when the geometry of dendrites and axons are introduced?
Also can we model a situation of membrane activity during the corse of evolution, hence the equation would be subject to a periodic function ad it varies with time?
Taking the example of membrane transmission of electronic signals(in humans), can we model the change in conduction of the e-signal through the axon as its speed and geometry changes with evolution?

The two processes occur at drastically different time scale. One could clearly model that by assuming the evolutionary state (whichever way you track it) is a constant while the other process reaches its equilibrium conditions.

Although you mention evolution, I think what your question is really asking is in your last paragraph: what happens to conduction within dendrites and axons when geometry changes. There might be some evolutionary implications of this question, but you will also find vast variations in geometry among neurons in any one organism, as well.
You might want to look into expansions of Hodgkin-Huxley into compartment models that allow you to test the influences of geometry, see wikipedia for a list of different models at different scales of complexity.
There is a tool available called NEURON that is good for student or curious non-student experimentation, though you will have to read the documentation and hopefully find some examples that are close to what you want and then tweak them.


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On Deformation of the body due to dipole orientation in the cells
Our bodies are made up of billions of atoms and molecules, and each cell has many molecules with dipoles that are initially random and orient themselves in one specific direction when an electric field is applied.
So with the static fair-weather electric field in the atmosphere being ~150 volts per meter (V/m) near the Earth's surface,the dipoles in molecules of our body would orient themselves and provide charge to the cell thus changing its geometry, then why isn't all of our bodies deformed?

@AlwaysConfused sorry that was a typo, I meant "why isn't ". Thanks for pointing that. As for the electric field of earth-The static fair-weather electric field in the atmosphere is ~150 volts per meter (V/m) near the Earth's surface, but it drops exponentially with height to under 1 V/m at 30 km altitude, as the conductivity of the atmosphere increases.

@AlwaysConfused please refer here: https://en.m.wikiversity.org/wiki/Natural_electric_field_of_the_Earth.


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Why do hand/fore-arm muscles "lock up" after very high-powered effort?
Inspired from Why does it hurt the next day after doing significant exercise? with its excellent answer:
In climbing, you can put tremendous load on the hand/fore-arm muscles (specifically, flexor pollicus longus and flexor digitorum profundus). What happens is often that you are not just fatigued, but that the muscles seem to "lock up" - they subjectively feel "hard", it seems impossible to relax and the problem does not go away after a few minutes, by stretching (which will actually become quite painful) or by self-massage.
The muscles are not necessarily showing the burning sensation that indicates lactate buildup according to the answer for the linked question. This effect seems to be a main cause for athletes to prematurely end a training session because there's little hope to solve it except for a long (hours...) rest. People have trouble opening doors etc. because the muscles seem to be completely wasted. Onset is immediate during or after a straining exercise, not later, like DOMS would be. After a good nights sleep, the problem usually seems to go away, it is not a day-long soreness.
Is that effect rather related to damage (micro tears etc.) or some chemical process? Is there a good way to prevent it, either in the short or long term, i.e. by training specifically for/against it? Are you aware of other muscles that show the same behaviour? I have only experienced it in those.


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How to turn teosinte into corn?
If I want to turn teosinte into corn, using ancient methods like the Native Americans did, then how much time it takes, and what do I have to do?
For the sake of the question, let's assume that time is not a problem for me. Say I live 10,000 years. But of course, I prefer to have maximum efficiency. If I can get the result in 3,000 years, that's better than 5,000 years.

Breed together the plants that have any properties that seem more like modern corn, like bigger or more accessible kernels, stir gently, find a cure for aging, repeat over a few thousand generations.

@GerardoFurtado Even modern corn (not counting GMO) is quite a bit different from corn 200 years ago. I guess I agree that it doesn't take as many generations before you would classify the plant 'corn' rather than 'teosinte' but it seems like it took at least 1000 years to get to that point, with thousands of years further selection since then to get closer to what we are familiar with today.

@GerardoFurtado FYI someone at my institution is trying to do this see here but expects only fairly minor changes over 30 generations. But your broader point is well-taken. I believe some Russian scientists domesticated a fox within just a few generations, for example. I would say there is a difference between initial domestication and the extreme changes we have built into plants over thousands of years of agriculture.

From the link I gave: "Teosinte from this area is the least maize-like of the Mexican annual teosintes and it only rarely hybridizes with maize (Wilkes 1967, 1977). Being free of maize "contamination" is important for my selection experiment because I don't want to merely filter out maize genes that were introgressed into teosinte, but to select natural teosinte variants and thereby move the phenotype in the direction of maize." I don't know if its possible to know how similar this strain is to the original, just that it isn't contaminated with modern corn.

It's of course possible that, being a strain that doesn't hybridize well with maize, it might actually more teosinte-like than the original strains that were eventually bred to corn. Not my area of expertise I'm afraid.

Initially I didn't like this question very much, but I changed my mind when I realized that there is actually ongoing research to do exactly what you propose in order to study just how long it takes to get maize from teosinte.
John Doebley at the University of Wisconsin-Madison has a project ongoing to breed 30 generations of teosinte to be more "corn-like" on a single parameter, the length of the lateral branches.
The first challenge is to find a strain that isn't already contaminated by modern maize - that isn't completely possible, but he selected a strain that has minimal hybridization. You would have to do the same.
Second, you have to plant someplace isolated to further prevent hybridization. Dr. Doebley has a plot in Hawaii for this purpose.
Note that even though this scientist is only selecting over 30 generations, he doesn't anticipate that much of a change (i.e., he doesn't expect to have anything like corn when he is finished), and he is only selecting on a single parameter and furthermore, this parameter was chosen specifically for being easy to score, showing a lot of variation in the existing population, and influenced by a known single gene. Many more generations would be expected to get a product like modern corn. And even domesticated corn has changed significantly over thousands of years of agriculture.
For this answer, I simply reference the project site that I linked above, but in case that link goes dead, here is some literature that the project cited directly:

Beadle, G. W., 1977  The origin of Zea mays, pp. 615-635 in Origins of Agriculture, edited by C. E. Reed. Mouton, The Hague.
Beadle, G. W., 1978  Teosinte and the origin of maize, pp. 113-128 in Maize Breeding and Genetics, edited by D. B. Walden. John Wiley & Sons, New York, NY.
Doebley, J., A. Stec and C. Gustus, 1995  teosinte branched1 and the origin of maize: evidence for epistasis and the evolution of dominance. Genetics 141: 333-346.
Doebley, J., A. Stec and L. Hubbard, 1997  The evolution of apical dominance in maize. Nature 386: 485-488.
Doebley, J. F., A. Stec, J. Wendel and M. Edwards, 1990  Genetic and morphological analysis of a maize-teosinte F2 population: implications for the origin of maize. Proc. Natl. Acad. Sci. 87: 9888-9892.
Iltis, H., 1987  Maize evolution and agricultural origins, pp. 195-213 in Grass systematics and evolution, edited by T. Soderstrom, K. Hilu, C. Campbell, and M. Barkworth. Smithsonian Inst. Press, Washington, D. C.
Wang, R.-L., A. Stec, J. Hey, L. Lukens and J. Doebley, 1999  The limits of selection during maize domestication. Nature 398: 236-239.
Wilkes, H. G., 1967  Teosinte: the closest relative of maize. The Bussey Institute, Harvard University, Cambridge.
Wilkes, H. G., 1977  Hybridization of maize and teosinte in Mexico and Guatemala and the improvement of maize. Econ. Bot. 31: 254-293.

Thanks a lot. While your answer is very informative and useful, I'm still confused about how much time it takes to convert teosinte into corn. What I need is an order of magnitude: 500 years, 1000 years, 3000 years..

@BearBear Well, all of those time frames you give are roughly the same order of magnitude :) I think it's partly a semantic issue of when you declare the crop to be "corn": the archaeological evidence suggests that corn has changed a lot over the last 3000 years, but even before that was already distinct from teosinte.


text:
Why is the heart adversely impacted by chronic psychological stress, yet it benefits from routine physical exercise?
Chronic psychological stress is commonly said to be deleterious to the heart, and predispose one to cardiovascular disease. Yet the opposite is said about regular aerobic exercise. Physiologically, What is the difference between psychological stress and physical exercise, with respect to their impacts on heart function/health? Both involve an increase in sympathetic cardiac input, and thus more vigorously contracting cardiac muscle; but how is one damaging and the other beneficial?

That's a interesting question. If in a few days, you still haven't got an answer here, you might to give it a try on Health.SE.

they involve different hormones, I would start there, I know stress hormone damage a lot of things, not sure about exercise ones.

From the perspective of sympathetic nervous system

Exercise induced adaptations of heart

A common phenomenon in endurance athletes is the athlete's heart /athletic heart syndrome

Once athletes stop training, the heart returns to its normal size.

You must understand why this type of adaptation is happening in them:
Firstly the athletes train to produce work output at near maximal levels/ sub maximal levels of work done which cannot be physiologically achieved in a day.So the increased heart rate generated by the sympathetic stimulation is sufficient to fulfill oxygen demand of the body only at certain levels of work done by raising the heart rate
As the grade of work done nears submaximal level the oxygen demand increases in the body and the increased sympathetic stimulation (which also restricts the cardiac muscle efficiency by decreasing diastolic time,coronary blood flow) is no longer able to suffice it.Such high oxygen demand is responsible for the useful adaptations of the heart in the form of athlete's heart.Athlete's heart reduces the need for sympathetic stimulation to increase cardiac output .

During intensive prolonged endurance or strength training, the body signals the heart to pump more blood through the body to counteract the oxygen deficit building in the skeletal muscles. Enlargement of the heart is a natural physical adaptation of the body to deal with the high pressures and large amounts of blood that can affect the heart during these periods of time.

Comparison with chronic psychological stress

During stress the body may or may not have high oxygen demand (the principal stimulus for adaptation) because the sympathetic stimulation is psychological and not in response to physiological work.So the heart instead of adaptating gets afflicted with detrimental pathophysiological effects of prolonged sympathetic stimulation.

stressors’ contributions to diverse pathophysiological changes including sudden death, myocardial infarction, myocardial ischemia, and wall motion abnormalities, as well as to alterations in cardiac regulation as indexed by changes in sympathetic nervous system activity and hemostasis.

From the perspective of cortisol (stress hormone)

Effect of psychological stress on athletes

When we are talking about the detrimental effects of psychic stress it is important to note that it may override the cardiac adaptations and severely affect performance like,for example high cortisol levels in blood released in response to stress (physical/ psychological).Although cortisol levels in the blood observe a circadian rhythm in normal healthy indivituals, some reports claim that exercise reduces detrimental effects of high cortisol levels on the heart.However,stress may override exercise induced effects in athletes but this is a prospective study, subject to greater research

A prospective study found a clinically significant increase in overnight urinary cortisol:cortisone ratio during a high training load period in triathletes, who subsequently underperformed and reported fatigue

REFERENCE TEXTBOOKS:

Exercise Physiology And Ergonomics (An Introduction) Asis Goswami Academic Publishers.Pg-39 to 57

Essentials Of Exercise Physiology (4th Ed.) Victor L.Katch,William D.McArdle,Frank I.Katch pg-302-333

I have an answer, but it is not ideal because science's current understanding of the answer to your question is somewhat limited.
The detrimental influence of physiological stress upon the heart is thought to occur because the physiological stress causes the cardiovascular system to prepare to meet anticipated energy needs by 1) increasing pulse and blood pressure, which can cause a heart attack that immediately follows the stress and and 2) increasing the production of glucocorticoids, which are thought to cause atherosclerosis, thereby increasing the likelihood of future cardiac maladies. Why do glucocorticoid levels increase in response to stress?  That is somewhat controversial.  See this article:  https://www.ncbi.nlm.nih.gov/pubmed/10696570.
What about physical exercise?  To some degree, whether the exercise is favorable or not is dose-specific.  Comparatively moderate exercise (relative to what the body is capable of) will have a favorable effect, while exercise that is too strenuous will not.  Physical exercise also increases pulse and blood pressure, which can also cause a heart attack that immediately follows the stress.  But if the exercise is of moderate severity, there will be two sources of beneficial effect upon the heart:
1)  There is the general phenomenon by which muscle fibers become stronger in response to the imposition of stress upon those muscles, whether those muscles are skeletal or cardiac muscles.
2)  There is the phenomenon of hormesis which is characterized by a general improvement process to all cells (including cardiac cells) at the cellular level in response to many different kinds of stress, including physical exercise and caloric restriction, both of which are sources of stress that have a hormetic effect at the right doses.  Edward Calabrese has been the most prolific researcher in demonstrating the hormesis effect, but its mechanism is not well-understood.
(A difference between psychological stress and physical exercise is that I do not think even moderate doses of psychological stress offer these two benefits.)

I believe the best answer to your question is that psychological stress increases the levels of a chemical compound called cortisol in the body (a glucocorticoid stress hormone) while physical exercise tends to decrease the levels of this "stress hormone".  Of course, physical exercise also positively affects muscles and the heart in other ways, so this is another factor. The benefits of low levels of cortisol vs. the deleterious effects of high levels of it are explained and outlined at length in links below.
https://en.wikipedia.org/wiki/Cortisol#Regulation
https://en.wikipedia.org/wiki/Exercise
https://www.mayoclinic.org/healthy-lifestyle/stress-management/in-depth/stress/art-20046037


text:
What type of point mutation and chromosomal mutation cause Albinism in humans?
First of all, I know that OCA1 (Oculocutaneous Albinism Type 1) is autosomal recessive which means that both parents-who are unaffected-have to pass down one copy of a mutated gene in order to activate the mutation (in this case it is Albinism). Based on the following link, "TYR (The TYR gene provides instructions for making an enzyme called tyrosinase. This enzyme is located in melanocytes, which are specialized cells that produce a pigment called melanin) is the only gene in which mutations are known to cause oculocutaneous albinism type 1." Also, there is a table on the website but it does not justify the exact point mutation that causes OCA1...unless I'm wrong.
----> http://www.ncbi.nlm.nih.gov/books/NBK1166/
What type of point mutation and chromosomal mutation?
Point Mutations:
http://www.britannica.com/science/point-mutation
Chromosomal Mutations:
There is good insight on Chromosomal mutations at http://biology.about.com/od/genetics/ss/chromosome-mutation.htm
I would really like help, this information is for my biology project!

I suspect albinism in general due to pigment deficiency is due to polygenic(quantitative) inheritance, that is to say, recessive for all three (?) pigmentation determining genes. Not really a point mutation. However, PKU, as it is due to tyrosinase deficiency, also causes albinism.


text:
Green feather-like formations in tap water - what is it? (with pictures)
These things recently appeared in my tap water Copenhagen Denmark, this summer 2013. They are very small, and have a feather like structure. I've called the water supply, and they thought that it was some tracer put in there by humans to trace if the warm water supply leaks into the tap water. But I could not show them the pictures.

What are they? Are they dangerous?
For size comparison: the green stuff is located on the top right of a piece of A4 paper.

Some sort of algae? You might need (somehow) an even closer picture to get a good identification.

I'm also thinking algae or moss (overall apperance could match species in Dicranaceae?). Better picture probably needed though. Would be strange for something like a moss to find its way through your tap water supply though.

I have had a biologist out taking some samples of the water. She examined them in a microscope, and identified the algae as blue-green algae/cyanobacteria. She could not identify the species further.
She said the reason probably was that my pipes where exposed to sunlight, and also that the pibes with hot and cold water ran too close to each other, creating a nice lukewarm temperature for the algae to thrive in.
I'm of course going to change the pipes :)


text:
How does the modern theory of evolution solve these apparent problems?
I hold to the truth of Evolution, but I've encountered several problems with it, that I can't answer, and I can't find an answer for, despite much research. If would be great if anyone can answer these supposedly fatal problems for Biological Evolution, since I find it troubling that there appears to be no answer for these.
Problem/Question #1:
The first one is called the mutation protection paradox. Simply put, Evolution has evolved mechanisms to protect itself from mutations, that if left unchecked, would build up and wreck the biological system, yet the mutation repair and protection mechanisms guard and stop the very changes that allow Evolution to occur, which is mutation.
Is there an answer to this paradox?
Problem/Question #2:
The problem of genetic entropy. John Sanford has supposedly shown in his book Genetic Entropy and the mystery of the genome, that the human genome is degrading so quickly, that we could not have evolved from ape like creatures over millions of years.
The problem is supposedly that we have 100-300 more mutations than either of our parents. This is supposed to mean that 100-300 new mutations accumulate in every person, in every single generation. Then it's said that these mutations are so small they cannot be gotten rid of by natural selection, and that the vast majority are harmful to the human genotype.
Because the mutations are unselectable, they are left to build up in all people until the entire human race becomes extinct, and it is estimated that this should have occurred in less than 80,000 years. So if Evolution were true, we wouldn't be here to talk about it.
The person presenting this problem gave answers to two responses. He gave a response to the Evolutionist retort that most mutations are not harmful but neutral by saying "most mutations are neutral from the perspective of the organism’s physical fitness (phenotype), but all mutations must have effect on the genetic content (genotype). In no way are mutations truly neutral – they all must have effect on the genotype, even if they only affect the efficiency of transferRNA production. And as pointed out above, most are harmful."
Then he gave a response to the Evolutionist retort that -almost all of the unselectable mutations will occur in non-coding regions of the DNA (the so-called, Junk DNA), and therefore have no effect. Thus, the individual will not die and the population will not become extinct- by saying quote:
"Non-coding DNA does not code for proteins and scientists have previously thought it is largely useless. But mutations in the non-coding DNA won’t make them without effect since non-coding DNA helps during embryonic development and can be a part of many diseases. The idea that non-coding DNA absorbs mutations, thereby making them neutral, is false and is merely an argument from ignorance."
Is there an answer to this?
Problem/Question #3:
This can be called the meta-informaton paradox. How it goes is that you have two types of dynamics. Primary DNA which tells what proteins to make, and meta-information which tells the cell how to maintain the primary DNA. So it is said that primary DNA and meta-information are completely dependent on one another. If they become unrelated to each other, both become unusable and the animal would die.
The problem is that mutations are random, and thus completely independent events, and this means primary DNA and meta-information would evolve by completely random and independent events and thus would not be able to stay relevant and related to one another, which then creates a barrier stopping microbes to man evolution from taking place.
Problem/Question #4:
The person claims his calculations show that there is 1 chance in 10 to the 150 billion, that all species have evolved, each from a previous species. Here's how his calculation works.
He says he is being as generous as possible with Evolution, and has five assumptions:
Assumption 1: Evolution must occur by a net gain in new information. However, this is completely disregarded. We will simply assume that all beneficial mutations produce evolutionary change (including so called 'neutral mutations' which become beneficial later on).
Assumption 2: The rate of beneficial mutations is widely thought to be 1 for every million mutations. Indeed, scientists have observed millions more harmful or 'neutral' mutations than beneficial mutations. But we will assume that the frequency of occurrence is 1 beneficial mutation per 1,000 mutations.
Assumption 3: It will be assumed that 5,000 mutations are needed to make a species 'evolve' into another species (where the two species cannot interbreed). Although the number needed for new single-celled species to arise is probably less, other higher animals require millions more beneficial mutations than accounted for here (40 million mutational differences exist between chimpanzees and humans[1], though different genus).
Assumption 4: We will assume that the total amount of species that have lived in the past is 10 million. In fact, this is the upper end of the estimate for species living today. If 99% of all species have become extinct as many Darwinists claim, then our assumption is extremely generous.
Assumption 5: It will be assumed that every single beneficial mutation is fixed in the population after occurrence. This is very unrealistic (in favour of evolution, of course). Beneficial mutations can be lost from a population in a variety of ways; sexual reproduction and death being just a few causes.
Calculating the chance that 50 million species have evolved from a common ancestor:
Chance of 1 beneficial occurring: 1 in 1,000.
Chance of 2 beneficials occurring: 1 in 1,0002.
Chance of 5,000 beneficials occurring (needed to make one species evolve into another): 1 in 1015,000 (i.e. 1 in 1,0005,000).
Chance that 10 million species evolved: 1 in 1015,00010 million.
Therefore: 1 in 10150 billion.

Welcome to Biology.SE! Each one of these points really should be a separate question. Please read through the Help Center, particularly the "How to ask a good question" section. It should help you focus your question down to something that can theoretically be answered in several paragraphs. If you can imagine an entire book being written about your topic, then it's probably too broad.

Do John Sanford and the person who has done the calculation described in problem 4, have proposed any other mechanism  to explain how organisms arise ?

@biogirl of course they have. It is a very elegant and parsimonious theory that posits the existence of a beneficial old potter in a beard who spends his time creating animals from clay.

I don't think this should be closed. Yes it is broad since it is many questions rolled into one but it is the kind of question that often turns up when people have been confused by pseudo-science and we may as well have a good answer to it. I would actually recommend reopening, and even turning this into a community faq post. There are a couple of quite detailed answers both of which answer the question quite well (if I do say so myself).

Responding to questions about how biology and evolution works is probably one of the more useful things this site does.

Wow, someone changed my title, but spelled the word problems wrong. What in the world.

I truly think this question should not be closed, it would help people like me with similar questions about Dr. Sanford work

OK, I'll have a go although you really shouldn't combine so many questions into one.
1 The mutation protection "paradox"
As already mentioned while many mutations are caught and corrected, not all of them are. You have to consider that a body (the human one, for example) contains several trillion cells, each of which contains 3 billion nucleotides each of which can be mutated. So, if the human body has, say, 50 trillion cells (a relatively conservative estimate), that means that a mutation could occur at any of
                              $3e10^9 * 5e10^{13} = 15e10^{22}$ = 150000000000000000000000
different sites. So even though the cell is pretty good at catching and correcting errors, some are bound to get through from pure statistical chance. In any case, you know that not all errors are corrected, diseases such as cancer are often the direct result of such mutations and errors.
I should also point out that in sexually reproducing species (such as humans) mutations are passed on to offspring only if they occur in one of the cells that become gametes (sperm or eggs) so this does not accurately represent the number of available sites that can give rise to mutations that can directly affect evolution for sexual species. Other species however, do not reproduce sexually. For example, cutting a worm like C. elegans in half will result in two worms so a mutation in any of its cells could be passed on to its offspring.
Anyway, point mutations are not the only way that diversity is generated. Even in the absence of mutations, processes such as chromosomal cross-over during gamete cell division (this is what makes you into a mixture of your Mom and Dad) would still produce differences that selection can act upon.
2 Genetic entropy
This one is a bit harder to answer, largely because it is complete poppycock. I'll try though. Let's see, we do not have "more mutations than our parents", what an absurd idea! The silent assumption here is that there was a "perfect" genome and each mutation is carrying us further from it. Therefore, since my parents were closer to this platonic ideal of the perfect DNA, each mutation that occurs in my cells takes their genomes a further step from that perfection.
This is very simply wrong. There was never a perfect genome, each cell in each individual of each species in the world is constantly undergoing mutations and has always done so. The genome is dynamic, not static and it has never been static, it can't be. DNA is a chemical substance and undergoes chemical reactions (such as mutations) all the time. Like all other chemicals it exists in a thermodynamic equilibrium, but not a static one. The only way that I have "more mutations" than my parents is if you accept as a premise that humanity comes from the perfect genomes of Adam and Eve. Since this is what Mr. Sanford is, presumably, attempting to demonstrate, using it as a premise is, at best, a circular argument.
Unless you assume the existence of a platonic ideal of a genome you cannot say whether I have more or fewer mutations than my parents because how can you compare them? In order to say that I have more mutations than my parents, you would need to quantify the number of mutations that each of us has and that cannot be done. How do you count mutations? You would need a reference genome of the ancestral human and we don't have that.
The rest of the argument is even more nonsensical. Mutations can either be completely neutral and therefore "unselectable" or they can have an effect. By definition, if a mutation has an effect, it can be selected for or against. That's how selection works. So, stating that these tiny mutations (which do exist) cannot be selected for/against and yet are harmful is a direct contradiction. You can only have one or the other. If they are harmful, there will be a selective pressure to change/correct/lose these mutations.
In any case, if these things "are left to build up in all people until the entire human race becomes extinct" all that means is that these things build up in individuals of a species and the species changes. Ummm, well, yes, we have a name for that, it's called evolution.
Just a final point, tRNAs have their own specific genes, a random mutation in an intergenic region will have no effect on them, why should it? This just shows the fundamental ignorance of the author in question.
Oh, and the whole "Junk DNA" is a very complex question. Yes, we now know that a lot of what was termed "Junk DNA" has a function (this was no surprise by the way, "Junk" was never intended to be taken literally). All this means is that mutations in non-coding DNA can also be harmful. OK, fine, then they will be selected against because that is how evolution works.
3 "meta-informaton paradox" (whatever that is)
This idea is often bandied by creationists but is a basic misunderstanding. Mutations are random(ish), evolution is not remotely random. Advantageous mutations that make an individual more likely to reproduce will tend to be selected for and spread across a population while deleterious mutations will tend to be selected against and be removed from the gene pool. This is not a random process at all.
As for the "meta-information", nothing is "independent". The cell is a complex system with extremely complicated interactions and a lot of cross-talk between the different processes. The DNA is not separate from the cell, it is an integral part of it. The Aristotelian idea of reductionist logic where you study complex systems by cutting them into little bits and understanding those bits is all very well as an intellectual tool but that is all it is, a tool. In reality, complex systems should be studied in their entirety, you cannot disassociate DNA from DNA regulation.
4 The pseudo math hypothesis
Let's have a look at these assumptions.

Assumption 1: "Evolution must occur by a net gain in new information. "
Of course not. Evolution can create a net loss in complexity (information) just as often (indeed, probably more so) as a net gain. The classic example of this are viruses. They have evolved into lean, mean, minimalist killing machines. They have nothing that is not absolutely essential. Hardly a net gain in information.

Assumption 2: I don't know where these numbers are coming from, whenever you read a phrase that starts with "scientists have observed", run away. What scientists? How have they observed this? How do they define beneficial? Anyway, let's say these numbers are right (I really really doubt it, but let's say they are for the sake of argument).

Assumption 3: Huh? Let's just throw some random numbers and see if they stick. There is no magical number of changes that results in speciation. In mutations as in real estate, it's "location, location, location". The question is not how many mutations but where they have occurred and what effect they have had.

Assumption 4: Wow, this one is just completely wrong. To pick just one problem here, if 10 million species is the upper limit of species living today, and 99% of all species have become extinct, how does it follow that 10 million can also be a good estimate of all the species that have come before? If the 10 million of today are only 1% of all the species that have ever lived (99% are extinct right?) then it follows that the number of species that have existed is around one billion.

Assumption 5: It is most certainly not true that every beneficial mutation is fixed. Many are, others aren't. Also, bear in mind that the same mutation can be both beneficial and harmful in different contexts. For example, a mutation that makes me more resistant to cold would be very useful during an ice age but less so (and could be harmful) during a period of high temperatures. To take a classic example, there is a known mutation in some humans that makes them susceptible to sickle-cell anaemia. However, the same mutation also protects from malaria. So, is this one harmful or beneficial? That depends on whether you are living somewhere where malaria is prevalent or not.

OK, so now the numbers. These wonderful probabilities all assume that evolution happens through "beneficial" mutations. First of all, that is not the only way that genomes change. I mentioned chromosomal crossing over earlier and you also have things like genetic drift (you also have all sorts of other weird things such as horizontal transfer).
In any case, it does not take X beneficial mutations to make a new species. As I said, there is no magic number and evolution is not restricted to beneficial mutations. Just mutations.
However, the most serious problem in this reasoning is that you are not calculating probabilities, you are calculating frequencies. What the argument you are presenting says is that it will take $10^{150billion}$ events for 10 million species to evolve from a common ancestor. It says absolutely nothing about the probability of such events because you are not taking into account the size of the event pool.
Let me explain. If you toss a coin, you have a 50-50 chance of getting either heads or tails. Therefore, getting 5 heads in a row is not very likely if you throw five times. If, however, you throw a few billion coins a few trillion times, you are very very likely to at some point get 5 heads in a row. In order to calculate the probability of something you need to take into account the number of tests performed.
If we keep the arbitrary numbers you have quoted, we have 10 million species, let's say each of them has a genome of 1 million base pairs and each has just 10 cells whose genome is passed on to their offspring (non-sexually reproducing species are actually the vast majority but most of them are unicellular so let's just take 10 as an average). Let us also assume that the creationists are right, the world is about ten thousand years old and let's say that species live for an average of two years (absolutely wrong of course but let's just pick small numbers). Finally, let's say that each species has only 1 million living individuals (again wildly conservative, just think of the number of ants in the world). This means that we are talking about

10 million species * 10 cells each * 1 million individuals * 1 million bases per cell = 100000000000000000000

If the rate of mutations is a tiny (much much smaller than the real value) 1 mutation every 24 hours, this means that there are $10^{20} * 365$ potential mutations a year. And, therefore, there have been $10^{20} * 3650000 = 365*10^{23}$ opportunities for mutation in the last 10000 years, that's 365 followed by 23 zeroes, that's a hell of a lot of chances. So, yes, if one in a thousand of them were beneficial that still makes it really quite likely that such mutations have occurred and have caused speciation events. This becomes even more likely if we take a realistic estimate of the time elapsed (10000 years is extreme for all but the most bullheaded of creationists).

Excellent answer +1. As an extra for point 3, it may be worth adding support for some mutations being neutral that often a nucleotide in a triplet can be changed with no effect on the protein it codes for (ie synonymous substitution)

Thanks to everyone who answered, but a special thanks to Terdon. Your answer was excellent, and I appreciate the amount of feedback you gave. These problems were very troubling to my belief in Evolution. Shook it pretty good cause there was no answer for them despite me trying to research it deeply.

Nice answer. However, I do not like how you highlight the large number of cells in an organism in parts 1 and 4. Yes, mutations do occur in somatic cells (and could lead to cancer as you mention), however this is irrelevant to discussions of evolutionary biology. Only mutations present in the gametes have the potential to be passed to the next generation.

@JohnBlischak fair enough, I have edited my answer to make that clear. The point still stands for non-sexual species but they do tend to have fewer cells. In any case, I have factored in the number of individuals so we a re still in the same ball park.

@terdon: Trying to help out here with the statistics. I think you need to adjust for the fact that you were considering sexually reproductive organisms and you assumed random mutations to get genomes.  What you actually need to assume is random mutations that produce two viable partners (unique species) of both male and female within the same generation.  Unfortunately, that might add orders of magnitude to the statistical unlikeliness of getting a proper match.  Maybe I missed something in your example?

@Jim I already have, that's why I said "10 cells whose genome is passed on". Also, new species are not created within the same generation, that was Lamarck's idea and has been discredited for 200 years. You might be interested in the answers here. Also note that I am not giving any measure of likelihood, I gave an (extremely conservative) estimate of "opportunities for mutation". Finally, as I say in my answer, mutations are random(ish), evolution is not.

For an idea that has been discredited for over 200 years, it sure seems to have a strong hold in some parts of academic discussion. I wasn't familiar with this and appreciate the link. But now I'm really puzzled, because the Lamarck idea seems to be best suited to the fossil record. How do we evaluate the fossil record in light of the idea of "fuzzy" development of species.  We would be highly likely to find much more subtle variation within the record than we actually have.  Or are we to ascertain that the fossil record is just way too spotty to make good educated guesses? Help?

@Jim 1) there is variation even in the fossil record 2) the fossil record is incredibly spotty as you called it. Consider that we have, say, a few tens (in the best cases) of fossils that are supposed to represent the various millions of individuals of a given species that existed over a period of, at the very least, thousands of years. For example, how much of the variety existing in today's dogs would you be able to infer from 5 random fossils? These are great topics for questions by the way, hint, hint :).

My apologies. I came over here from the older stack exchanges I frequent and I'm accustomed to issues that normally have very succinct and concisely defineable answers with related questions that sometimes make you want to avoid spamming new questions. LOL  Not trying to troll up posts!

@Jim no worries, you're not, I'm just saying that it would make a good question and could be answered better that way. It was not an attempt to shut you up but to get you to speak up :).

@terdon Apparently this post is the basis for a current discussion on MetaBiology. Just wanted to ping you in case you want to participate.

Thought I'd try this one too...
1) The DNA repair mechanisms in an organism can be fairly minimal ( bacteria with smaller genomes such as M genetalium do not seem to have DNA repair enzymes at all) or there can be many redundant backup genes for DNA repair (I'm thinking of D radiodurans, a bacterium found growing in the Chernobyl reactor after the disaster).  In each of these cases the DNA repair genes do not stop mutations, they only reduce the number of mutations that occur.  Its well known that all sorts of living things can die of radiation poisoning and new mutations that have occurred recently are observed in all living things.
2) The argument has been given some detail in Wikipedia.  I would just say here that if some mutations has little selective power, but when there are enough of them to show a real disadvantage, then they will be eliminated from the gene pool.  They don't just all of a sudden get together and say 'here we are - you are dead!'  Selection is pretty good at finding pretty small disadvantages and kicking out the responsible variants. I guess the answer is the system is more robust than is assumed in this statement.
That's not to say that low profile mutations can't combine and kill a living thing - they do.  Every generation of people genetic diseases kill thousands of people.  There are also lots of others who do not experience such diseases.  No family will be exempt from such defects over time, but nearly all families will continue as well.  The proportion being predicted here is not realistic.
There are species that go extinct too.  So all this does happen, but not in the proportions or degree being speculated. Really mountains are being made of molehills here.
3) There may be some cases where 5000 mutations (or even fewer) might prevent interbreeding between subpopulations to create species of a sort.  But in most cases it takes a lot more mutations than that to create a new species.
Bacterial species are entirely different from animals and plants.  They don't need to breed to make offspring in the sense eukaryotes do.  Often they can't.  Bacterial species usually reproduce by single celled fission - they cells just split.  occasionally they transfer DNA, but they can do so between species by more than one means.  In the link its noted that bacterial speciation has been observed in the lab.  Just among the 30 or so E coli strains that are sequenced the number of genes can vary by 50%.
So though there are very few species of bacteria named, its also possible to say that there are many trillions of bacterial species, because they work in such a different way than we are used to seeing among animals and plants.
4) While I can't really verify the numbers here, the idea that we could estimate all the possible species seems difficult.  There are definitely more species possible then there are atoms in the universe.
There are many more powerful arguments that there is one common ancestor to all living thing on earth.  Each living thing shares exactly the same mechanisms for preserving information - DNA, copying the DNA into RNA and then translating this into protein.  The idea that this would evolve in the same way twice seems completely unlikely.  Moreover there are genes in bacteria that have the same shape and work in the same way as in human beings and every other animal.  In fact the phylogenetic 'tree of life' shows that the more similar two living things are, the closer they resemble each other in terms of their sequence.  This is the primary argument for the last universal ancestor (LUA).  Most folks would have to have a counterargument that against this evidence.  The generation of a ribosome in the laboratory from primordial chemicals might be such an argument, since we think it took nearly a trillion years for it to happen the first time, I would be genuinely astonished to see it happen again.

1: Not a paradox.  Mutations are generally protected against, especially in more complex organisms.  Protection mechanisms are not perfect, hence mutations still arise.  Plus, diversity can arise through other mechanisms.
2: "...these mutations are so small they cannot be gotten rid of by natural selection, and that the vast majority are harmful..." is a very dumb and self-contradictory statement.  If there is an effect it can be selected for or against.  Also, 100 mutations compared to 3 billion bases...
3: This is nonsensical.
4: Very confused assumptions and statistics.  You previously pointed out that many mutations happen in an individual.  Individuals do not evolve, populations do.  You don't need a single individual to mutate a lot, you need changes in genotype to accumulate, and millions of years is a very, very long time.

So the absurdly low probability that was calculated was like calculating the chance that a gorilla in the zoo through random mutation turns into a human and gets released. Very unlikely indeed. Evolution is about the chance that humans can over millions of years evolve from apes or from a common predecessor.

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Is there any evidence of increased life expectancy for animal species?
Life expectancy for human has significantly increased during the last century or so. We all know that there are many reasons that are not linked with "evolution", but I am wondering if such change in life expectancy has been observed "naturally" (not counting animals in zoos or domestic ones). Does evolution favor long lasting individuals?

The prolonged life expectancy over the last century can be explained by better medicine, hygiene, food and better working conditions. It is not connected to evolution (which generally takes place over long time periods, not just over the course of only three generations). The same is observed for zoo animals.

There is life extension work with animals, but just as Chris says its more about changing conditions or finding mutations that change life expectancy.

@Chris thanks for your comment. I've tried to edit my question to make it more clear. I know that it is not due to evolution for humans and zoo animals, but I was wondering if it had been observed for some species as a consequence of the "survival of the fittest". A millenimum was maybe to short (though it is more than 3 generations), but I guess that it is difficult to observe, so maybe it can only be shown for species with small longevity.

@shigeta thank you for your comment. Are the mutations that change life expectancy beneficial to the population ? I mean, long life expectancy can reduce the possibility to adapt quickly, so this can make the species more vulnerable to, e.g. habitat change, but does it provide any advantage.

The answer kinda depend on what you'll accept to be an observation. It seems that you want an observation where we measured the mean life expectancy of a species over a (very) long term and find out that it is increasing. Such study very probably does not exist for obvious reasons. But you might be interested in some key mutations that changed life expectancy and on proof that this mutation rises through time (selective sweep) or you might be interested to know more generally about life history traits or to seek for correlations between life expectancy and some ecological traits.

As far evolution is concerned, there is no benefit whatsoever in having long lived individuals. Evolution only "cares" about individuals while they are capable of reproducing. Survival past the maximum age of reproduction is irrelevant from the evolutionary point of view since it does not make you any better at reproducing, and therefore your genes will not be selected for.
This is highlighted by the various species that die to give birth to or feed their young. One of my favorite examples is the giant pacific octopus (Enteroctopus dofleini) whose females lay their eggs and then die, leaving their body to feed the emerging young.
Now, a mutation that makes an individual both longer lived and capable of reproducing at a greater age could well be selected for. It just always needs to be combined with the ability to reproduce. By itself, dying older will confer no selective advantage unless it is combined with producing more offspring.

The life expectancy of an animal (or anything) is just one aspect of how 'fit' they are to survive.  having them live too long can be a detriment to the species.
There is no simple 'better/worse' relationship of fitness to life expectancy.  In simple population models predators which reproduce to much or live too long will tend to eat all the prey and starve to death for instance.
The most famous example of life extension molecular biology is the discovery of a 'Methuselah worm' by Cynthia Kenyon about 10 years ago.  With a single mutation these C. elegans worms can live about 50% longer, and seem to be pretty energetic while doing it.
It would be interesting to put some of these Methuselah worms into a wild population and see what happens to their life span as they interbreed.  C elegans is a highly programmed organism - each cell has a predetermined plan for development and lifespan, which made this worm relatively easy to find.
For human beings (the best studied animal on Earth) there is no simple genetic relationship to longevity for most of us, but there appear to be some simple combinations that are responsible for the oldest living humans:

a genetic model comprising 150 SNPs in order to compute the predisposition of an individual toward EL. Their model successfully predicted exceptional longevity in a different sample of centenarians (individuals that live to age 100) with 77 percent accuracy. This demonstrates that EL is strongly associated with complex combinations of genetic variants.

So for humans this experiment has sort of been done.  Longevity phenotypes are possible but don't overall convey a reproductive advantage and so while they hang out in the gene pool,  they aren't enough of an advantage to reproduction to be spread about widely...


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most different human tissues with respect to gene expression profiling
Is there a PCA showing the relative distance in terms of gene expression / functional genomics among the different human tissue types?
So far I have found:
(1) A paper based on gene expression with some tissues/tissue groups, not many:
https://genomebiology.biomedcentral.com/articles/10.1186/gb-2010-11-12-r124
(2) A paper based on gene expression signatures and aging:
https://www.nature.com/articles/npjamd201614/figures/1
(3) A paper on Gene and Protein Expression in Normal and Cancer Tissues:
https://www.nature.com/articles/srep24799/figures/3

Assuming you know what distance measure you want to use, I think the best approch is download a tissue data set such as GTEX yourself and compute the pairwise distance matrix. If you're a bioinformatics person this is should be straightforward. PCA projection to 2D (or even 3D) is only an approximation of the actual pairwise distances, and for tissue gene expression that approximation tends to be poor, in my experience.

You can navigate the GTEX project. PCA section.
https://www.gtexportal.org/home/histologyPage?tab=PCA
You have different samples for many tissues. Currently you can navigate it tissue by tissue but perhaps there's a way of visualizing the whole dataset (or you can ask for it).

The website looks very promising, but it seems, as you say, that you can only PCA tissue by tissue.


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What is the another use of de Bruijn graphs in bioinformatics except DNA assembly?
I implemented own generic de Bruijn graph, which I use for DNA assembly (alphabet: A, C, G, T). I try to find purpose of de Bruijn graph for another bioinformatics problems, if some exists. I want use/modify my implementation to solve this.
Are there another problems in bioinformatics which we can solve with de Bruijn graphs?
I found only RNA assembly, which is similar to DNA assembly.


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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]


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What biological functions does crying serve?
Tears suddenly start flowing out of our eyes when we find our long lost friend or when someone unexpectedly decides to break up with us. Do tears really save us from harm? Or are they just the reflex shown?
What biological purpose do tears serve for the body?
As I understand it, crying causes endorphin release, specifically leucine-enkephalin. This serves as a painkiller for us. Are tears the only way to accomplish this? It seems I am missing something because oozing out of our eyes is an inferior pain distribution system to say; the circulatory system.

Homeostasis is the property of a system in which variables are regulated so that internal conditions remain stable and relatively constant. Your concluding sentence makes sense (what is the function of tears), but linking it to homeostasis per se draws the question specifically to the realm of fluid balance and ion balance. You should clarify this question I think.

I've edited it. If they don't account for homeostasis then why we consider them as reflex?

I would read the wiki page on Tears first

@علیآفاق I've made some big edits to the question to move it away from homeostasis. Feel free to roll back.

Lets break this question into parts and answer them one by one.

Do tears really save us from harm?

Well, yes. Tears, mucus and saliva contain an enzyme lysozyme that breaks down the cell wall of many bacteria. Those that are not killed immediately are trapped in mucus and swallowed.1
You can, obviously, search on google for another reference if you do not believe this one.

Or are they just the reflex shown?

It depends on what type of tears you are talking about. Tears are divided into 3 categories:

Basal tears
Reflex tears
Psychic tears

In "reflex action" part, the cause is reflex tears. Reflex tears result from irritation of the eye by foreign particles, or from the presence of irritant substances in the eye's environment, which trigger TRP (Transient Receptor Potential) channels in the ophthalmic nerve. It can also occur with bright light and hot or peppery stimuli to the tongue and mouth... These reflex tears attempt to wash out irritants that may have come into contact with the eye.
These are, of course, different from those tears which "suddenly start flowing out of our eyes when we find our long lost friend or when someone unexpectedly decides to break up with us". These are psychic tears i.e. increased tearing due to strong emotional stress, pleasure, anger, suffering, mourning, or physical pain. This practice is not restricted to negative emotions; many people cry when extremely happy such as during times of intense humour and laughter.2
But the actual relation of tears with emotions can be summarized as:

There is an area of your brain specifically to deal with your emotions, called the limbic system (specifically the part of it called the hypothalamus), which is hard-wired into your autonomic nervous system (that’s the part you don’t have any control over).
This system, via a neurotransmitter called acetylcholine, has a degree of control over the lacrimal ‘tear’ system; and it is this tiny molecule which then stimulates tear production.
So in short, your emotional reaction to the break-up triggers your nervous system, which in turn, orders your tear-producing system to activate.3

Moving on to next part:

crying causes endorphin release...Are tears the only way to accomplish this?

Certainly not. Even when you exercise, your body releases endorphins. These endorphins interact with the receptors in your brain that reduce your perception of pain. So, tears are not the only way to accomplish this.4
At last, I would answer this part

What biological purpose do tears serve for the body?

as tears are necessary for the continued health of the ocular surface. Normal constituents include water, mucin, and lipids, electrolytes, non-electrolytes, and proteins. Retinoids are also important for ocular health and prealbumin may be a carrier for vitamin A in the tears to supply corneal epithelium with its requirements. Changes in tear constituents may cause certain ocular disorders.5
It is important to know here that by the above part, I meant basal tears and not psychic ones. Basal tears lubricate the eye, and help to keep it clear of dust. Tear fluid contains water, mucin, lipids, lysozyme, lactoferrin, lipocalin, lacritin, immunoglobulins, glucose, urea, sodium, and potassium. Some of the substances in lacrimal fluid (such as lysozyme) fight against bacterial infection as a part of the immune system. Lysozyme does this by dissolving a layer in the outer coating, called peptidoglycan, of certain bacteria. It is a typical body fluid with a salt content similar to blood plasma.
EDIT 1: Now, as you asked in the comments

what if we don't maintain our ocular surface?

I can tell you a very common example of dry eye syndrome. Dry eye syndrome is a common tears and ocular surface multifactorial disease, described by changes in the ocular surface epithelia related to reduced tears quantity and ocular surface sensitivity, leading to inflammatory reaction. It is believed that decrease in the tear volume on the corneal and conjunctival surface caused by either a decreased tear secretion or accelerated evaporation plays the main role. The clinical features of dry eyes include ocular discomfort, feeling of dryness, feeling of eye fatigue, hyperemia, kerato-conjunctival epithelial disorders and abnormalities of vision.6
EDIT 2: When it comes to function of psychic tears, then how could one leave talking about why we feel better after crying (except headache). It is now proven that psychic tears contain a higher amount of hormones than basal or reflex tears. See this article7:

Emotional tears are composed of more protein-based hormones, such as prolactin, adrenocorticotropic, and leucine enkephalin (a natural pain killer), which is suggested to be the mechanism behind the experience of crying from emotion making an individual feel better.

Though these hormones do not have any direct relation with emotions (excluding prolactin which counteracts the effects of dopamine), they can be related to emotions as long as another biological reason for their secretion through tears is discovered.
Bonus: From the same article 7, here is a very unusual function of tears i.e. controlling arousal! See this paragraph:

On a study conducted by the Weizmann Institute of Science in Rehovot, Israel, emotional tears from women have been found to reduce sexual arousal in men. Also, emotional tears are made up of a different chemical component than those evoked by eye irritants and can relay chemical messages to others. The change in sex drive could be attributed to a drop in testosterone provoked by the tear chemicals, reducing aggression. In the animal world, it has been found that some blind mole rats rub tears all over their bodies as a strategy to keep aggressive mole rats away.

This way, we can soon have a long list of functions. I hope these many functions are enough to answer your question.
References:
1: The body’s first line of defence
2: Tears - Wikipedia
3: Why do we cry? The science of tears
4: Exercise and Depression
5: Eyelid secretions and the prevention and production of disease
6: Recent developments on dry eye disease treatment compounds
7: Chemicals in tears - Wikipedia

In the last part you've talked about"Tears are necessary for the continued health of the ocular surface" but we do cry hardly a year ( males) what if we don't maintain our ocular surface?
can you elaborate it little more ( last part) ?

This does not seem to actually answer the question: you didn't explain what is the biological reason of what you called "psychic tears". It is not obvious why emotional stress should trigger a response which basically serves to "wash" the eyes.

@علی آفاق as I have told in the answer, crying is actually psychic tears, which is only one type of tear. Ocular health is maintained by basal tears. I will describe them too in the answer.

@gIS I have added that part too in the answer, hope this helps :)


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Do animal cells have vacuoles?
I overheard a rather heated argument about whether or not animal cells have vacuoles.
One person said that they do, but they're much smaller than vacuoles in plant cells.
The other person said they don't. While there is something there that acts similar to a vacuole, it's slightly different. The person also noted that the only websites that say that something as a vacuole aren't credible sites (ie. not University sites, etc...)
I'm really curious as to which it is: Do animal cells have vacuoles or not?

They are both right.
Animal cells do have vacuoles, but they are smaller, larger in number (plant cells usually have just one or a few large vacuoles) AND serve a somewhat different purpose than those of plants.
A vacuole is basically a membrane-covered compartment (vesicle) filled with molecules, that shouldn't, right now, be in the cytoplasm. For plants, this means long-term storage of water and waste products, which cannot be removed from the cell due to the cell wall. For animals it means mostly taking part in exocytosis and endocytosis - they are much more dynamic structures.
And about some half-professional sources, here is a bit from Molecular Biology of the cell which in fact calls plant vacuoles "a kind of specialized lysosome".

If their function and purpose are different, so we could not call them vacuoles.

Yes, animal cells do have vacuoles. They just have a larger number of them and some sites call them with different names. In a plant cell there is just one vacuole. Pictures of cells in textbooks,online,etc should show you that they have vacuoles, despite contrary beliefs elsewhere.

Provide a reference for ur answer.

Yes! As a matter of fact Animal Cells do have vacuoles.  Even though they are much smaller than the Large Central Vacuole of Plant Cells, they still do exist in Animal Cells.  Unlike the Large Central Vacuole of the Plant Cells, they do not take up 90% of the cells and instead there are multiple slightly smaller vacuoles.  Also in a Plant Cell, there is usually only one vacuole: the Large Central Vacuole.

can you provide some citations to reliable sources?


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How would a medication cause a one to maintain a different weight?
This isn’t really a medical question, I’m just really curious about this.
I was maintaining weight A and then started taking a medication that brought me to weight B. While on the medication, I maintain weight B. When I stop taking it, my weight goes down presumably to weight A.
The increase or decrease of weight in changing medications doesn’t puzzle me. It’s the maintaining of the weight.
Would the medication be affecting metabolism or what?

Based on my reading, weight gain, as in resetting your maintenance set-point, which is what it sounds like you are describing, is a very well-known side-effect of the serotonin selective reuptake inhibitors (SSRI).  In some cases, patients may even discontinue the medication.  As far as I know, the underlying physiology behind this specific example is not well-understood.
In recent years, the use of next-generation sequencing (NGS) of DNA has been used to characterize the so-called microbiome in the gut of individual humans (sequencing faeces).  Some studies have reported that thin, or skinny people have somewhat different microbiomes than fat, or obese people, leading to the hypothesis that some overweight people might have bacteria that are more efficient at breaking down their food such that more of the calories are available for absorption.  Some evidence supporting this interpretation comes from experiments with fecal transplants.
If a medication also affects a patient’s microbiome (in addition to the drug’s intended therapeutic effects) then that could be another, less obvious(?) mechanism for weight changes.

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