text:
What physical or mental actions can be picked up by EEGs?
There certainly seem to be a lot of gadgets and gizmos leveraging EEG technologies to the control of devices.
This makes me wonder: what intentions/thoughts can be captured by EEG technology, and which ones can't?
For example: how about motor movements? If I am wearing one of these EEG devices, and I shake one of my fingers back and forth, is my brain generating waves that the EEG device will detect? Why/why not?

Many EEG responses are swamped in random brain activity, artifacts and background noise. A single movement typically doesn't evoke measurable activity, because its amplitude is so small with respect to background noise.
I think the potentials you are looking for are event-related potentials or ERPs (Fig. 1). During ERP recording, basically a regular EEG is registered, but certain events (presentation of stimuli or actions by the subject) are time locked with the EEG recordings. By repeatedly measuring (e.g., 25 times) the time-locked response to the event, an average EEG can be obtained. Assuming remaining EEG activity, noise and artifacts are random, the averaging process will decrease noise, but will not affect the ERP. The averaging hence leaves you with a clean ERP response (Yordanova et al., 2003).

Fig. 1. ERPs. Left are stimulus-evoked ERPs (auditory, visual) and right are ERPs associated with the motor response by the subject (button-press upon stimulus presentation). Source: Yordanova et al., 2003.
In Fig. 1, the reaction times indicated correspond to the subject's button press, so the intention to press the button in fact precedes the actual motor response. In fact, the covert (imagined) ERP response can be nearly identical to the overt ERP (the motor action), see Fig. 2 (Kranczioch et al., 2009).

Fig. 2. Overt motor-evoked ERPs (top three panels) and equivalent covert (imagined) ERPs (lower three panels). The three panels cover different electrodes. Source: Kranczioch et al. (2009).
By characterizing the exact shape and other characteristics of the ERP, computer software can be deployed to recognize this ERP wave within a normal EEG. This is done in computer-brain interfaces. By filtering the ERG outside the frequency range associated with the ERP a lot of the cleaning can be done on the fly in near-real time.
A list of various stimuli in ERPs can be found in Table 1 in (Goodman, 2010).
References
- Goodman, Atten Percept Psychophys (2010); 72(8): 10.3758
- Kranczioch et al., Human Brain Mapping (2009); 30(10): 3275–86
- Yordanova et al., Brain (2003); 127(2): 351 - 62

Thanks @Christiaan (+1) - one quick followup. A human can think about moving a particular muscle group (say, an arm or a leg), and then there is the process of actually moving it (not just thinking it). Can I assume that thinking about moving a muscle and actually moving it produce two distinct EEG/ERP signals?

@smeeb - see the added Fig.2 for your reference

Thanks again @Christiaan (+1) - last followup, I promise (!): so are you saying that it is possible (using software) to distinguish between overt/actual and covert/imagined signals, or is this evidence suggesting the signals are too similar to differentiate them?

@smeeb - that would warrant an extensive literature search. If there is a specific event you are interested in you could tease out the differences and similarities. It will also be dependent on location of the electrodes; e.g. electrodes on top of the motor cortex may favor motor over imagined ERPs, while electrodes over frontal cortex may favor the reverse. My answer is more of a general answer to a quite general question :-)


text:
Is the efferent arteriole a pathway for filtrate through the nephron ?
I am studying the urinary system. I have to identify what part of the nephron is not a pathway for filtrate. I believed the collecting duct is not a pathway for filtrate because once the filtrate enters this destination it is now referred to as urine, and no longer filtrate. I thought that inferred that it was not a pathway. However, the efferent may also be a strong answer because after glomerular filtration that small molecules that get filtered into the glomerular capsule are identified as filtrate. But the cell and proteins that do not get filtered are not, so not what are they referred to as non-filtered. However, later in the process of urine formation they become secreted back into the bloodstream through the peritubular network into the nephron at the distal convoluted tubule.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
What is it that specifically kills ALS patients?
ALS is a fatal motor neuron disease, and even though there are many different articles out there on the topic "How does ALS actually kill you?", none of them really delve deep enough into biology to adequately answer the question.
For instance, many articles cite "respiratory failure", or "CO2 poisoning". But the last time I checked, ALS doesn't make your lungs explode or cause your body to start producing toxic levels of CO2. So obviously, we need another level of detail here to support these claims. I'd be willing to be that with "respiratory failure", either the neurons innervating the diaphragm break down (hence you become physically unable to draw air in and push CO2 out), or perhaps the tiny/micronic structures inside your alveoli become impaired for some reason. If the former, then why wouldn't a ventilator/respirator help the patient?
Either way, I'm interested in a biological/neurological explanation for why ALS is considered to be (ultimately) fatal.

TL;DR Ventilation assistance does help but there are other factors.
ALS is a degeneration of the motor neurons, replacing them with hard material (i.e. sclerosis). The neurons innervating the muscles involved in respiration deteriorate and so it becomes difficult to breath, swallow, cough, etc. There's a compounding effect: we know that blood O2 and CO2 levels are balanced by respiration, O2 in/CO2 out, and we know that swallowing/coughing clear secretions from the respiratory tract. Basically you end up with trouble oxygenating your blood and riding it of CO2, hence CO2 poisoning. This can result in what is known as type 2 respiratory failure, characterized by low oxygen and high carbon dioxide levels (hypoxemia and hypercapnia). Low secretion clearance in the lungs can also result in aspiration pneumonia in addition to poor gas exchange.
Ventilation methods such as BCV are capable of mechanically assisting breathing, and maintaining ventilation-perfusion state in a way that prevents respiratory failure, but unfortunately doesn't slow the progression of the disease. The problem then is that in, for example, particularly severe cases, the quality of life has to be taken into account because tongue movement, gross movement in general due to motor neuron degeneration just fails. This can lead to what is essentially locked-in syndrome (LIS), and clinical outcomes can widely vary, though in this article they report the more pleasant outcomes of patients experiencing LIS. I think that for these cases due to poor communicaton patient-reported outcomes are fairly underreported, but family and caregivers at this point have to take into serious consideration options such as euthanasia. Cutting off ventilation can result in type 1 or 2 respiratory failure.
Now, I lack actual data for this statement but I should also point out that not all patients receive the same care or opt for assisted ventilation, in which case late-stage ALS would invariably lead to total neurodegeneration to breathing muscle innervation, where assisted ventilation becomes a requirement for survival.

Thanks @Kendall (+1) - however I'm missing a big part of your explanation!! In your 2nd paragraph you state "Basically you end up with trouble oxygenating your blood and riding it of CO2, hence CO2 poisoning."... but why?!? Is it because you can't swallow/cough/etc. to clear your respiratory track of secretions (meaning, if there's mucuous in your throat, you won't be able to suck air in or let CO2 escape)? Or is some other mechanism at play that actually prevents proper O2/CO2 exchange? Thanks again!

Secretions that block the alveolar gas exchange is one reason, not just in the throat but also down in the lung, and shallow/strained breathing is another.

Thanks again @Kendall (+1) - last followup question here, I promise (!): can I assume that eventually all motor neurons will be affected, including those controlling heartbeat and digestive motility (that is, moving food from end to end, so to speak)? Thanks again!

ALS does not affect the innervation of the heart, digestive organs or urinary organs.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
How does the mechanism which controls blood pressure in the brain work?
I know that pressure is sensed in the skin by mechanoreception mediated by skin receptors. Static pressure stimuli are mainly sensed by slow-adapting fibers connected to receptors like the Merkel discs. Vibratory stimuli are sensed by rapidly adapting receptors like the Pacinian corpuscle.
Blood pressure is also sensed by the body and the brain regulates blood pressure by influencing the peripheral nervous system that can increase or decrease the blood output of the heart.
How are blood pressure differences in the brain sensed and how do these receptors mediate cardiac activity? Are blood pressure differences in the brain sensed by rapidly adapting receptors akin to Pacinian corpuscles?

I've added background to the question and I vote to re-open.

Blood pressure is sensed in blood vessels by baroreceptors. Baroreceptors are stretch-sensitive nerve fibers located primarily in the aortic arch and carotid sinuses. The baroreceptors send afferent fibers via the glossopharyngeal nerve to the nucleus tractus solitarii in the dorsal medulla in the brainstem. From there, efferent cardiovascular neurons send projections to the medulla and spinal cord. There are also stretch-sensitive receptors in the heart and pulmonary vessels, called cardiopulmonary receptors that use the same nerural connections as the baroreceptors.
The baroreflex loop results in activation of sympathetic or parasympathetic fibers to the heart, the smooth muscle of the peripheral blood vessels, and other organs such as the kidney to maintain arterial pressure at normal levels.
In a simplified scheme, increased pressure stimulates baroreceptors, which attenuates the sympathetic outflow to the peripheral vessels and the heart, restoring pressure to normal levels. The parasympathetic influence will dominate which is mediated by acetylcholine. Conversely, a decrease in pressure relieves the baroreceptors and increases sympathetic outflow. Sympathetic activation causes a release of noradrenaline that leads to vasoconstriction and increased cardiac output and hence an increased blood pressure (see Fig. 1).

Fig. 1. Control of blood pressure. Source: Human Physiology (2011).
Reference
- Cougias et al., Med Sci Monit (2010); 16(1): RA1–RA8

With regard to blood pressure in the brain, note that besides the general baroreceptor in the aorta at the output of the heart, there are two at the carotid sinuses.  The latter are in the neck just under the head and sense the pressure of the blood flowing into the head, providing close control of the blood pressure in the brain.

The control mechanism in the brain for blood pressure is a endocrine hormone named ADH.  This stands for AntiDiuretic Hormone.  This hormone is produced by special nerves in the hypothalamus and stored in the posterior pituitary gland.  ADH is stimulated by increased blood solute (particles like ions and other molecules) present or decreased blood volume level.  When you have adequate hydration, this hormone is actually inhibited.  On a very elementary level, it works by stimulating kidney tubule cells to reabsorb water rather than eliminate it.  Some drugs also interfere with ADH, most commonly ethanol (drinking alcohol).
Edit: Forgot to add that ADH is also known as Vasopressin, and is also responsible for constricting the blood vessels.

Although AVP may affect blood pressure (does it?), its primary role is in fluid balance by affecting kidney function. And if EtOH affects AVP, it should also affect blood pressure according to your reasoning? Could you add some references to back your answer up? I don't buy it :-)

Fluid balance is the primary regulator of blood pressure.  EtOH most definitely affects blood pressure, as it is a CNS depressant.  ADH is also known as vasopressin, and is the main control for blood fluid, and solute levels which in turn is responsible for the mineralcorticoids (renin-angiotensin) synthesized in the Adrenal Cortex.  The method I've explained is how the brain regulates blood pressure.  What Christaan posted is how blood pressure is locally mediated. -- Edit: Maybe balance is the wrong word - but rather Fluid Volume regulation. --Edit2: ADH inhibitors exist to modulate bp.


text:
Concentration of a specific promoter in a cell?
I want to simulate transcription activation by a given transcription factor (TF) with known kinetics. The binding rate $k_{on}$ is given in $\mu M^{-1} s^{-1} $, describing a bimolecular reaction mechanism (second order reaction kinetics). However, what is the concentration of a specific promoter in a cell?

In a diploid organism there are two copies of DNA which means two copies or "molecules" of promoter in the entire cell. The volume of a typical eukaryotic cell (HeLa) would be 2.25×10-12 litres (Zhao et al. 2007, BioNumbers).
$$\text{Concentration }(M)=\frac{\text{Molecules per cell}}{\text{Avogadro No.} \times \text{Volume of the cell }(l)}$$
This comes to around 1.4758×10-12 M for 2 molecules of promoter. Accordingly, you can calculate for a haploid cell, multiple alleles or prokaryotic cell.
You can also assume a 2-compartment model with nucleus and cytoplasm as two different compartments. In this case, the DNA would be localized in the nucleus and therefore its effective concentration would be higher in the nucleus. You can look up nuclear volume in BioNumbers and plug that in the above formula to obtain the effective concentration.

Zhao, L., et al. "Intracellular water‐specific MR of microbead‐adherent cells: the HeLa cell intracellular water exchange lifetime." NMR in Biomedicine 21.2 (2008): 159-164.


text:
Does the source of caffeine affect the biological impact?
I've recently decided to give up my morning coffee in lieu of a caffeine pill. Both are around 200mg (my Tim Horton's XL 4x4 was 240 mg of caffeine) of caffeine. We were talking about the various impacts this has on my body (for example, I now need a different source of the whopping 680 calories the beverage used to give me) and one thing that came up was that the caffeine pill would be more damaging to my liver.
I was resistant to their claims, since they were simply basing it off what they heard in college from various health advisers, but three people from different backgrounds all concurred that the pills would be more harmful to my liver in spite of the the fact that there's a decreased quantity.
The points to their argument were:

The concentration of caffeine pills is greater than that of the coffee.
The caffeine in the pill is synthetic, and thus harder for the liver to process.

My counter to those points were that the tablet takes longer to dissolve than the coffee which I'd expect go straight into my bloodstream. (And in fact, I notice it takes longer to get the kick from the pill, and it lasts longer, which would be consistent with my counterpoint). As far as synthetic, I was under the impression a chemical is a chemical, that's what's so great about chemicals.
I understand that changing from coffee to pills will have some sideeffects (less antioxidants, a need to replace the sugars I had before, etc). But my question isn't around those - it's specifically around whether the effects on the organs (emphasis on the liver) are different when caffeine in similar dosages is delivered via a pill as opposed to a brewed liquid. Other comments (as opposed to answers) are welcome, as I would not blindly ignore wise consul, but I would appreciate if answers focused on the question.

For your body it makes no difference where the caffeine comes from. It works in the usual way.

The caffeine in the pill is synthetic, and thus harder for the liver to process: caffeine is caffeine, so that myth can be dropped from the question. The thing here is pharmacokinetics. Perhaps the pill takes longer, or shorter to be absorbed, that may, or may not affect liver function.


text:
What are most common natural causes of death?
What are most frequently occurring natural causes of death?

Without defining 'natural death' this question is opinion-based. I vote to close until clarified.

@Christiaan moreover, I see no point or purpose behind this question. This is not strictly in the realm of the biology that we consider here. This is more of a census report.

@WYSIWYG, agreed, and perhaps even more a definition question than anything else.

Beside the other comments, this also differes between countries, which makes the question a bit unclear and also very broad. And I assume you are talking about human causes of death?

If you survive everything else, you will die of cancer, specific to your own genetics (as the more "popular" types of cancer will be treatable, given some time for research).

The WHO has data from 2002 where they have classified and counted causes of death. I have treated the following as natural causes:

Cardiovascular disease (29.34%)
Infectious & Parasitic disease (23.04%)
Cancers (12.49%)
Respiratory disease (6.49%)
Perinatal conditions (4.32%)
Digestive disease (3.45%)
Neuropsychiatric disorders (1.95%)
Diabetes (1.73%)
Genitourinary disease (1.49%)
Maternal conditions (<1%)
Congenital abnormalities (<1%)
Nutritional deficiencies (<1%)
Endocrine disorders (<1%)
Neoplasms (<1%)
Musculoskeletal disease (<1%)
Skin disease (<1%)

I treated the following as non-natural causes:

Intentional injuries
Non-intentional injuries

The sum of the groups explains 96.7% of deaths. I think the remaining 3.3% would be other or undetermined causes, and rounding errors in the data. The natural causes accounted for 87.9%, and non-natural causes were 9.1%. The most common causes were cardiovascular diseases, infectious/parasitic diseases, and cancers.
It is difficult to assess how natural the cause of deaths are. For example, many cancers, cardiovascular, and respiratory diseases are more common in obese people and smokers (often self-inflicted damage), nutritional deficiencies are often caused by failing welfare and social systems.
Additionally, among the recorded causes of death in England and Wales in 2011, of the total 484,367 deaths recorded, 17,590* deaths were from extrinsic sources (accidents, homicides etc.). This is around 3.6% of deaths. In this data, the most common causes were cancers (29.6%), circulatory diseases 28.8%, and respiratory diseases (14.0%).
According to the CDC, in 2013 there were 2,596,993 deaths in the US, and 92.5% were of natural causes. Of those, the principle causes were heart disease (24%) and cancer (23%). There's a good table at the bottom of this site.
Rates of natural and non-natural causes of death will likely vary greatly by country given different health risks (e.g. malaria in Africa vs Europe), health care services, extrinsic risks (e.g. traffic accidents in Sweden vs India).
$*$ The table in the article features a potential mistake, it seems the columns are incorrectly labelled

I wonder if suicide due to depression should be considered natural.

I'd say depression is a natural disease, the whole division in to natural and non-natural causes is weird, too difficult to determine in many cases.

What is a natural death? All the lung cancers due to smoking? Cardiovascular disease due to overweight? The question, imo, is primarily what the definition of a 'natural' death is, more so than what the various examples are from a medical or pathological standpoint.

The question is, among deaths by natural causes, what are the most common? There is a general consensus, at least, as to what constitutes natural causes.

And which is...?


text:
What, if any, experimental evidence is there that flies rub their legs together in order to clean them?
Everybody's seen a fly rubbing its hands together like Mr Burns. And almost everybody's heard the standard explanation - that it's cleaning itself. Now, this is certainly a very plausible explanation, but has it been demonstrated? I can't find any references to experiments seeking to prove this hypothesis. I'm asking because, not being very familiar with these matters, I'd love to know what methods were used to demonstrate something like this.

A pre-existing answer is linked in the above comment. I admit it doesn't cover the methods used to determine it's really cleansing. However, you cannot ask a fly why its doing something. One can just infer. As a consequence, there's no scientific literature on this afaik.

@Christiaan Well, you could imagine an experiment attempting to prove that the legs are indeed cleaner right after the rubbing ritual. Or you could see if flies rub their legs more frequently in dirty environments than in clean environments.

Oh yes, I can imagine a dozen of experiments, but I can't imagine any funding body to support it

@Christiaan Hey, if there's people irradiating spider webs to track their path through the spider's digestive system, I'm sure someone's doing behavioral experiments on flies.

Haha nice one. In an attempt to answer the linked question I couldn't find anything.


text:
why does brain produces noise?
when i look at a white wall i see little colored dots moving in circles filling my whole visual view, just like the static on a tv but then in color.
I thought everybody had this but recently i discovered it is not normal ?
furthermore i see something which looks like tiny cells, just like you look under a microscope and bright white dots which are moving from the top of my view to the bottom. it is always present but some days more than others.
when it i see it more it is sometime together with a high pitched noise for a few seconds or a weird in my head like you have a beer or 2.
I cannot remember a time in which I did not have this (now 24 years).
I would like to know why the brain produces this noise ? it is not helping me to "survive" so why does it do this ? and what parts of he brain are involved in this ?

@rg255 nope thats totally not it, thats why i asked it seperately

I think you mean muscae volitantes Unfortunately, I couldn't find anything for your first ("i see little colored dots moving in circles filling my whole visual view") and third ("it is sometime together with a high pitched noise for a few seconds") questions.

it explains what the "tiny cells" and "bright white dots" are. Note: "it is not helping me to "survive" so why does it do this" - not everything is adaptive.


text:
How to incorporate intraspecific variation in discrete characters in comparative analyzes?
I'd like to run a multivariate analysis (Pavoine et al. 2011) that aims to disentagle the effect of environmental gradients on traits, considering its autocorrelation with phylogeny and space. It uses the RLQ approach and works with both discrete and continuous traits. However, I don't know how to incorporate intraspecific variation in discrete traits.
For example, I recorded categories of pigmentation on organs of several amphibians, but for some species, these categories vary among individuals. One way would be including individuals as polytomies at the species level, but this would make the test quite hard to interpret.
Thank you in advance,
Diogo

Kostikova et al. 2016. Syst. Biol. developed an algorithm to model trait evolution with inter- and intraspecific variation. The authors use it to show

whether a life-history trait (i.e. annual versus perennial) influences the evolution of intraspecific variation in the climatic niches of species

While they do not directly incorporate the space component as in the RLQ analysis, the approach might be informative in your case. The functions are available through dryad.

Thank for pointing that paper out to me Martinkova. I happen to see that paper when it was in 'accepted version', but didn't realized it was linked to my problem.


text:
What is the function of the polar bodies produced during oogenesis?
Why are polar bodies produced during oogenesis in human females?
I read that polar bodies are produced during meiosis so that the oogonium (or gamete mother cell) can be converted into a haploid female gamete or ovum by getting rid of the extra genetic material.
So, it is pretty clear that one follicle (containing one gamete mother cell) produces only one ovum.
So what is the point of producing polar bodies? Isn't it just a better mechanism over all for the meiotic devision of the oogonium to result in equal distribution of the cytoplasmic content to both daughter cells? That way, one oogonium can produce four ova, not just one. Th entire process of DNA replication during the synthesis phase (S phase) of the meiotic cell cycle seems like such a waste if 75% of the total genetic material produced is going to be expelled as polar bodies.
There is also the argument that since the ovum is non-motile and always within the female body, it need not be produced in large numbers as it is in a safe and protected environment. But, in that case, would it not be a better system is fewer follicles were produced, but each follicle divided to give four ova? This mechanism would end up producing the same amount of ova, but with lesser labour (such as DNA replication) going waste.
So, taking these arguments into consideration, what exactly is the function of the polar bodies produced?

You're saying about multiple eggs. I've a similar feeling too. You should've studied that: initially there are many follicle ( primary follicles) which are selected for oogenesis. Only one of them develops into mature graffian follicle. Can you tell how and why other follicles are kicked out from the race?
All of them were in same ovary, close to each other; what caused them to regressed except the one?
Should it be better for body to develop all those into mature follicle, each containing a separate egg?  If you can answer this, you probably will get your own.

"In other animals and some plants, polar bodies give rise to vital tissues that protect and nourish the embryo " ( http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164815/). This could be the same fucntion to humans since we are all eukaryote.
Polar bodies are not waste. They sacrifice themselves after giving their energy to the embryo, completing development and differentiation into a baby.

Polar bodies are not just mere discarded material in oogenesis as recent experiments have determined its key role in leading to stable embryo development.
Reference:
http://www.ncbi.nlm.nih.gov/pubmed/16102284/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164815/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3663962/

I appreciate your quick response. It would be nice if you can actually add what exactly polar body does. You can state and then quote (Ctrl+Q the selected text) from the article. I'll be glad to upvote then.

Please explain more fully. It would be helpful if you could briefly write the crux of the answer.

First of all, let me say that you have asked a really nice question!!
Now, if(according to your argument), each oogonium were to produce 4 ova each, then the cytoplasmic content of each ova would remain less. However, the ova has to be rich in cytoplasmic contents in order to compensate for the lesser amount of cytoplasm in the sperm, so that the zygote has enough of cytoplasm. Therefore, there is an unequal division of the oogonium, so that the ovum is larger.
Coming to your second argument, well, the oogonia are produced in large numbers as a preventive measure. What happens is that around 2 million oogonia are produced while the female is still in the fetal stage. No more oogonia can be produced after birth because of the formation of tunica albuginea between germinal epithelium and stroma of ovary. These oogonia develop into primary follicles containing primary oocytes. However, they undergo follicular atresia, resulting in a reduction of the number of follicles. As a result only 60000 to 80000 follicles are found at puberty. There is no guarantee that all of these will develop into graafian follicles, hence the large number.
Also, during ovulation, it is the secondary oocyte which is released into the fallopian tube, and not the ovum. Only when the sperm penetrates the zona pellucida of secondary oocyte, does it complete its meiosis to form an ovum and another polar body. So, if each oogonium were to produce 4 ova, then each secondary oocyte would produce two ova, and that would mean 2 ova present simultaneously in the fallopian tube, both of which would be fertilised. This would mean that humans would always bear 2 children at a time!!
I hope the above counter arguments will have satisfied you...
Cheers!!


text:
mRNA extraction from mice ears.
I am trying to extract RNA from mice ears and for some reason I don't have RNA when I perform the electrophoresis. I directly cut the ears and I put it in a tube with a bead and trizol. then I place it on ice and I use a mash machine for tissue lysis for 8 minutes and 4 ºC. After that, I perform RNA isolation according with a protocol using chloroform, isopropanol and ethanol.
I think the problem could be the extraction. Do you have any suggestions?
Thanks.

Do you see a pellet when you precipitate the RNA?

yes I saw a quite big pellet, but when I do the electrophoresis using a positive control, I suposse to see either two bands or a smears if it is degraded and it doesn't appear anything like that.

Let us know the composition, buffers, running conditions (voltage etc.) of your gel.

that's not the problem, since I use the samples to do a qPCR, I have used taqman, SYBRgreen, two different machines and I dont get amplification, but I do get in a previous sample used as positive control.  So the problem is I don't have RNA in my samples. (the gel it was just to check if I have RNA and it also works with a positive control but not with my samples)

@Bio What were the A₂₆₀/A₂₈₀ and A₂₆₀/A₂₃₀ ratios? The problem could be the beads as well. Were the beads sterilized properly and kept in RNAse free conditions (in DEPC water)?

The RNA may have denatured during extraction if there is no absorbance reading after PCR. Did you produce the control sample or is it supplied?


text:
Is there an acceptable term for 'male fox' other than 'dog'?
I'm writing a lab on sexual dimorphism in Arctic foxes. As such, I use the words 'dog' and 'vixen' fairly often. In the discussion section, I compare the results from the lab with the results from research on other animals. The most relevant research I consider pertains to dimorphism among dogs (Canis lupus: the kind we keep as pets and their immediate relatives).
The term 'dog' denotes a subspecies of Canis lupus, males of that subspecies, and male foxes.
There are ways to disambiguate what I'm writing, but none of them are elegant.
I'm considering using 'tod' or 'reynard' instead. Are either preferred in biological writing? If not, is there an alternative?

could just say males and females... this is how I write when referring to flies in my writing. e.g. "...body size for males and females was measured
from..."

Female foxes are called vixen. But there is no specific term for a male fox. In fact, it would be much better to say "male" or "female" fox in a scientific context in which "fox" would mean the species, as rg255 suggested.

@rg255 WYSIWYG I was doing that initially. The problem was that males and females is ambiguous when comparing two or more sets of sexes (e.g. Arctic fox males and Arctic fox females with dog males and dog females). Specifying the species disambiguates things at the cost of brevity and doesn't solve the problem of repetitiveness (i.e. after some number of occurrences of 'males' by itself and in 'females', its repetitiveness becomes obnoxious.). I might just have to make do, but it would be better if there were an acceptable substitute.

Another thing you could try is using abbreviations like mF, fD, etc. These need to be defined of course...

It seems that we agree that there are no other terms within the realm ob biology. Would Academia.SE or English.SE be a better for this question then?

Just use "C. lupus" instead of "dog" when referring to that species.


text:
What happens if both forward and reverse primers have same Tm?
One of the key rules in primer designing is that Tm (melting temperature) of forward and reverse primers should be in the range of ±5°C. For example, if Tm of forward primer is 62°C, then reverse primer should be either 67°C or 57°C.
What happens if both the primers are having same Tm?
Is this to be considered as perfect score of finding correct primers set?
Thanks

It is actually good if both the primers have the same Tm (Melting Temperature) because you would basically want both primers to anneal at your Ta (Annealing Temperature) which is generally set as Tm-5. If the Tm(s) don't match, then your Ta should be set according to the lower Tm.


text:
Structure of Cell
Are cells spheres or ovals/circles bound by phospholipidbilayer?
If they are spherical how are we able to see the nucleus through the phospholipid bilayer under a microscope?

It will largely depend on the type of cell!

Are guard cells spherical (completely bound by phospholipidbilayer)?

Many cells are spherical, but there is some variation.  Curiously, bright light often travels through all the structures of a cell.  In order to see things, the easiest way is to add some stain, which binds up to specific parts of the cell.  That way you can see the nucleus.  If you use dimmer light, or some other technique (eg cross polarization), you can sometimes see some structure as darker patches, but cells are translucent.

Not exactly.  That is a stereotype of cells.  Muscle cells are not round nor oval, but rather elongated rods.  If you were to look up epithelia cells, you can quickly see that cells are grouped based on their physical characteristics; simple (round/oval & single layer), columnar, and cuboidal to name a few.  Cells come in many shapes and sizes.  As Hans stated, stains are vital in viewing cellular components.  There is a diverse amount of stains used - which all carry a purpose and benefit in a specific application.

As MG_MD already pointed out, cells come in all shapes and sizes.
Take for example this image of a neuron. The central cell body contains the nucleus and is surrounded by a network of extensions called neurites which form neural networks. The extensions and the cell body have been stained fluorescently to make the cytoskeleton visible:

photo credit: ZEISS Microscopy/flickr (CC by SA 2.0)
The reason why we are able to see inside them is because the plasma membrane (a phospholipid bilayer) is transparent. Check out this website for some nice movies of cells moving under the microscope. In the left of these movie (keratocytes) you can clearly see that the cells have a bulge where the nucleus is which is surrounded by a flat so called lamellipodium giving the cell and overall "fried-egg"-like shape.
The only time when most cell types are rounded is during cell division. This is to make sure that the cells divide evenly and each daughter cell gets an exact copy of the DNA.


text:
How is CO2 related to acidity in plant cells?
Why does increase in concentration of CO2 in a plant cell increase the acidity of the cell sap?
Thank you

CO2 dissolves and forms a weak acid; carbonic acid (H2CO3 <-> H+ + HCO3- <-> H+ + CO32-)

CO2 is a Lewis Acid.  CO2 is a double carbonyl carbon which is electron deficient, and we know that Lewis Acids readily accept electrons, so when present in H20 it forms carbonic acid (H2CO3).  Christiaan posted the balanced equation of the formation of the acid.

Just a comment to say the OP is talking about a plant cell; the human body's acid-base coping mechanisms don't particularly apply.

I'd say there are other just as important factors also.

@anongoodnurse thank you for pointing that out, I edited my response.  Whether in blood or xylem, CO2 will form carbonic acid in solution with water.


text:
When you take a very cold or hot bath how is that influencing your breath?
It looks like when you take a cold shower or bath your veins get smaller and when you take hot shower your veins get wider. But is that right and do you need to breath more in both cases because you got less oxygen? If so how does it work in both cases?

There is an adaptation to being submerged in cold water in mammals called the Mammalian diving reflex.  Have you ever noticed when you jump into cold water, or enter a really cold shower you take a big breath?  While not exactly correlated with the dive reflex, it shows that there is a neurological reflex of entering cold water.  Here is a brief overview of what can happen when you submerge yourself in cold water:

Lower heart rate - aka Bradycardia, slowing down the rate of blood pumped will decrease the oxygen requirement of red blood cells, which in turn allow organs like the brain to use oxygen.
Smaller veins - aka Vasoconstriction, the blood flow in your fingers and toes is reduced, allowing more blood to be used in the more important organs.  Eventually the vasoconstriction will apply to hands and feet.
Blood shift - this adaptation allows the submerged animal to dive without having their thorax to collapse due to increased pressure.  Not necessarily attributing to breathing patterns though, so I left the boring stuff out and paraphrased.

In hot water, the opposite happens with respect to #'s 1 and 2.  Increased heart rate, like when you go running, tends to increase breathing frequency.  Vasodilation allows blood to flow more easily and is primarily for heat exchange.  Have the warmer blood in your fingers exchange heat to the environment will cool it for the return to systemic circulation.  Surface area is a large factor with heat exchange.  Hope this provided some insight.

Do you perhaps know what chemical proces causes the drop of heart rate in cold water. And is it true that when you take of hot shower you veins are getting bigger and because of that the bloodpressure drops so you get less oxygen and need to breath more?

The chemical process is just nerve signals that lower the heart rate.  I'm fairly certain it is parasympathetic regulation including the vagus nerve.  When your "veins" get bigger, and blood pressure drops, the heart compensates by increasing the pumping.  So technically you may need to breath more due to the increased heart rate.  You do not get less oxygen though.


text:
Looking for hard cell segmentation problem
I am a physicist working on a new image segmentation technique, and I would like to test it by segmenting some images with low-refined cells on a noisy background... Do you know where I could find such images? Thanks!

What type of microscopy? We have tons of phase contrast images of adherent human cells in our lab, and I have always wanted to try segmentation for automatic cell counting ... If interested, email me at roland.nilsson@ki.se !

Hi Roland, thanks for the reply! I'm gonna send you an email ;-)


text:
Obtaining a mapping of RefSeq ACs to Uniprot ACs
I am trying to obtain a mapping for RefSeq Accession Numbers to Uniprot Accession Numbers.
I can write a script to do this for a list of RefSeq ACs like this:
#!/usr/bin/python

"""
Derived from:
  http://www.uniprot.org/help/programmatic_access#id_mapping_python_example
"""

import urllib
import urllib2

url = 'http://www.uniprot.org/mapping/'

params = {
    'from':'P_REFSEQ_AC',
    'to':'ACC',
    'format':'tab',
    'query':'NP_511114.2 NP_004295.2 NP_031465.2 XP_004934106.1',
}

data = urllib.urlencode(params)
request = urllib2.Request(url, data)

# Please set your email address here to help us debug in case of problems.
contact = "email@example.com"
request.add_header('User-Agent', 'Python %s' % contact)
response = urllib2.urlopen(request)
page = response.read(200000)
print page

I am curious if there is a way to request the entire mapping of human genes to proteins.
I have tried to configure a query from the Uniprot resources, but I can't see how to get RefSeq data from this tool.
http://www.uniprot.org/uniprot/?query=reviewed:yes+AND+organism:9606#customize-columns
I am happy to use a resource other than Uniprot.

You can use BioMart. Have a look at this answer.

You have a bunch of options:

You can use Biomart.
Biomart is a standalone tool, but also have a pyton and R libraries. So it gives you more options depending on your preferred programming language. This is a widely used tool and in general works well.

biomart http://www.biomart.org/
biomart python library
biomart R library (from bioconductor)
Biomart is widely used and have extensive documentation.

Use a python library called pyEntrezID
https://pypi.python.org/pypi/pyEntrezId/1.4.7
You can do all sort of conversions of ids, however I've never tried it.
You can try NCBI eutils or one of the Ensembl REST API endpoints


text:
Why do carnivores evolve?
If humans can live without consuming other animals, then why do we do it? From a biological point of view, why do we eat meat? I would also extend the question to other animals because many animals are carnivorous: why did carnivory evolve and why do animals eat meat?

Answers to this question MUST cite a reference which should be either a peer-reviewed scientific article or a book. Unreferenced answers would be removed within 6h without notification. This rule is mandated because this is question, though quite interesting (and on-topic), is a popular topic that would attract a lot of opinion-based answers.

Because animal flesh provides a dense source of nutrients.  Evolution is amoral: anything that can be eaten, probably will be eaten by something.  Consider Darwin and the Ichneumonidae: https://en.wikipedia.org/wiki/Ichneumonidae#Darwin_and_the_Ichneumonidae  PS: And if you need a reference, start with "The Origin of Species" :-)

Besides that: Human cannot permanently develop and survive on a strictly vegan diet, since there are some important Vitamins which cannot be supplemented from vegetarian origin. Vitamin B12 would be a very important example, see this source.

@Chris That is incorrect, vitamin B12 is produced by bacteria, and in fact cannot be produced by any animal. You can get vitamin B12 supplements from a strictly vegetarian origin (https://en.wikipedia.org/wiki/Cyanocobalamin#Production).

@CactusWoman If you see biotechnical production as strictly vegetarian, ok. Still, vegetables (and fruit) still contain negligible amounts of B12 or B12 precursors and are not enough to maintain our needs.

@Chris I don't see why biotechnical production would not be considered vegetarian; the only requirement for a product to be vegetarian is that it does not contain meat. The vegan diet does need to supplement B12, but the supplementations are vegan, so it's incorrect to say "there are important vitamins which cannot be supplemented from vegetarian origin".

@CactusWoman: Are bacteria plants?  They don't meet the dictionary definition of plants, and many are capable of independent movement, like animals.

@jamesqf Vegetarianism and veganism is concerned with not consuming ANIMAL products. Bacteria are not animals. Fungi, plants, and bacteria are all considered vegetarian/vegan.

@WYSIWYG What is there to cite about "sometimes you live in a place where you can't find many plants to eat"?

@Superbest that is a layman's answer. You, as a biologist, can definitely say more than that.

Ana, evolution creates diversity (remember the diversification of Galapagos' finches). So, every available niche tends to be occupied, which includes carnivory.

A better question would be why wouldn't we eat meat, almost any animal will if given the opportunity, all but the most specialized herbivore can digest meat. Humans are good at acquiring food so why would we not eat something that is high nutrient density and easy to digest.

I'm going to focus on the why do carnivores exist part of this question, which should be extendible to answer why humans eat meat.
Let's start a thought experiment in which we only allow the consumption of vegetation (plants). In the simple system, we have our plants (lettuce) and our herbivores (rabbits). The lettuces have a constant population size and can support a limited population of rabbits. The rabbits satisfy their energetic and nutritional requirements by eating lettuces.
We then introduce a new species (humans) which are capable of eating both lettuce and rabbits (omnivores). If the humans limited themselves to only the lettuces as a food source they would have to compete with the rabbits in order to survive. Alternatively, the humans could hunt rabbits, as rabbits are also a potential source of energy and nutrition. The point being that, if a strategy has the potential to satisfy the energetic and nutritional requirements of a species, then that strategy has the potential to evolve. Because both plants and animals carry energetic and nutritional value, herbivory and carnivory/omnivory can evolve.

"All behaviour takes time. All behaviour consumes energy." [1]

Now consider the nutritional and energetic value of two the two food sources, plants and meat. Meat is typically richer in calories than vegetation, particularly those coming from fat and protein. 100 grams of lettuce contains around 14 calories, while 100 grams of beef contains about 200 calories. Protein is used by the body for growth, to repair tissues, produce hormones and enzymes and much more. Fat has a high energy content per gram (roughly twice as many calories per gram than protein or carbohydrate), is essential for the digestion of some vitamins,  and is an effective insulator. Given that behaviour takes time and energy, it is perhaps not hard to see that consuming meat can help to satisfy the energy requirements more quickly than consuming plants, allowing meat eaters more time for other essential activity like sleep and reproduction. Consider the activity of two large mammals, elephants and lions. Elephants spend a lot of time eating, some 12-18 hours per day (fortunately for them are quite able to eat on the move). Lions on the other hand typically hunt for short periods of the day (dawn and dusk), allowing them to avoid the heat (reducing water requirements), to rest, and reproduce.
Consider also that vegetation is often hard to digest — it is often is rich in cellulose. Many herbivorous species have complex adaptations to help digestion. Therefore, it's not necessarily easy, or easier, to evolve to eat only vegetation. Improved energy acquisition can evolve by both eating more energy rich foods and by more efficiently extracting energy.
Carnivory is also present in plants. According to this paper [2], such plants may be an adaptation to nutrient-poor conditions, where the ability to digest insects (and other small animals) would be a massive benefit, allowing carnivory to evolve rapidly.

Botanical carnivory is thought to have evolved in nutrient-poor and
  well-lit habitats such as bogs because the marginal benefits accruing
  from carnivory exceed the marginal photosynthetic costs associated
  with the maintenance of carnivorous organs.

The Egyptian mongoose is an omnivore. This species varies its diet across the year, according to what is available. For example, insects are the major component of its diet in spring, while no fish are eaten during summer (because of dry canals in the summer) and fish are a major component in the winter. This illustrates that allowing omnivory/carnivory can increase the resources available, potentially allowing better survival and reproduction relative to a herbivorous/narrow foraging strategy in the same species. Consider this problem in, for example, boreal or temperate climates, where winter can cover ground vegetation in snow and tree's will reduce foliage. Consuming animals would allow the acquisition of energy and nutrients through the winter.
In summary, carnivory can evolve because animals are a good and plentiful source of energy and nutrition, and may allow diversification of strategies, improving survival and reproduction. If animals were bad food sources then carnivory would be less common as it would be a more difficult/problematic behaviour to evolve.

While many people & organisations (including PETA) try to claim that we are not well adapted to being carnivores, many of the claimed adaptations to herbivory/lack of adaptations to omnivory are overstated, misleadingly presented, and even false, and are used in order to promote their own agenda. It's also worth noting that we are not well adapted to being herbivores (e.g. gut flora) and chimpanzees, one of our closest ancestors, are also omnivores.

[1] Krebs & Davies Behavioural Ecology, An evolutionary approach.* ISBN-10: 0865427313.
[2] Ellison, Aaron M., and Nicholas J. Gotelli. "Nitrogen availability alters the expression of carnivory in the northern pitcher plant, Sarracenia purpurea." Proc Natl Acad Sci, USA 99.7 (2002): 4409-4412.

+1, It would be great if you add the ISBN or citation for the book as a footnote instead of just providing the Amazon link. Also, please replace the journal link with pubmed/doi link as they are stable. It would be really good if you can add information from research studies on dietary/food-web models (to substantiate the lettuce-rabbit-human example). A note on evolutionary strategies would also be nice.

To illustrate the ease of digesting animals white tailed deer often eat nesting birds. http://www.bioone.org/doi/abs/10.1674/0003-0031(2000)144[0419:WTDOVP]2.0.CO;2 It is relatively easy for an herbivore to become on omivore.


text:
What are the highest and lowest amplitude values in ECG for humans?
I'm currently trying to parse the records captured from an ECG device and display them on a mobile application. I am wondering what the highest and lowest possible amplitude values for ECGs are in humans? What may happen if they exceed those values?

Amplitudes are notoriously unreliable measures for biological potentials in general. They can vary widely from person to person and from test-to-test. What are you after? The uttermost limits possible? Note that recording artifacts may exceed the actual ECG. And what do you mean with they exceed those values? What is they? Which values?

@Christiaan, sorry, I'm referring to the amplitudes. English is not my primary language. So what are the possible limits of these amplitudes? We're developing a software that will display these amplitudes and knowing the possible limits will greatly help us in displaying them.

The QRS complex is the part of the ECG with the largest amplitude.

I scanned a dozen ECG traces across the web, and as far as I can see, the QRS complex has amplitudes of up to 4 mV in a normal ECG:

ECG trace. 1 mm corresponds to 0.1 mV on the y-axis
Amplitudes are relative peak-to-peak measures. If you are asking about absolute values then the minimal voltage versus maximal absolute voltages depend on your baseline value, i.e., the offset in your voltage potential measurement system. Further, artifacts and background noise may add signal amplitudes on top of the ECG proper.
As an absolute minimum estimate, the graphs here posted show that -1 mV would be a safe minimal voltage.

As you mentioned this is the case for healthy ECGs, old infarcted areas (e.g. post MI) regularly cause these values to be exceeded - often with very prominent Q waves which I think would go beyond your suggested minimum voltage.


text:
Why does snow not stick to the fur of wolves and some breeds of dogs?
This question made me wonder, why for example wolves don't suffer from these "paw snowballs"?

(...) but after a few miles on the trails in soft snow, he often develops snowballs between his paw pads - usually one big one right in the middle. (...) I have heard really bad snow buildup can lead to raw/bleeding paw pads.

This might get a better answer on biology or maybe even pets? But it's probably due to the type of fur, huskies don't seem to get this either. Most dog breeds are bred now for look. They retain the high fat concentration in their paws to prevent their pads freezing though.

@Aravona Yeah, migration to biology might be a good idea...

they have very large paws so that prevents them going so deep, that would help.

I couldn't find scientific references, but regular web searches basically indicate that long fur as well as webbed toes promote formation of ice and snowballs in certain breeds.
From Hubpages:

The snow attaches to the dog's long hair, melts from the body heat, and forms ice balls that grow larger, stretching your dog's toes apart and causing cracking, bleeding, and hair pulling.  This is painful and distressing for the dog, who may then try to remove them by licking them, which then causes even more ice to build up.

And among the solutions:

Clip the fur between your dog's toes. [J]ust trim off the excess fluff.

A typical breed thriving in icy conditions is the Siberian husky. A comparison to to an airedale terrier breed shows the difference in fur length quite clearly, especially around the areas most suceptible to come in contact with snow (legs & chest areas):

And both breeds in the snow:


text:
What happens to the mold spores we inhale?
What happens to the mold spores we inhale?
I'm guessing when we exhale, many of them are expelled back out to the environment.
But given that disease can be caused by mold exposure, I'm also guessing that we do not immediately expel a percentage of them.
Molds can colonize in the lungs, causing detrimental effects.  Can they colonize elsewhere in the body?
For mold spores that do not colonize inside the body, what happens to them?  Are they expelled?  If so, by what mechanisms?  Are they alive or dead when they are expelled?

I think spores can cause problems only in immunodeficienc individuals.

@OleksandrPapchenko You may think it, but if you research it, you will quickly learn that is not true!

Maybe I'm reading too much into this post, but I think there may be too many questions here. Like asking about other parts of the body? I also don't know why you ask, "are they dead or alive when expelled?" It's not like our lungs autoclave the air we exhale or bombard the spores with UV light or anything. How would simple inhalation/exhalation kill mold spores?

@anongoodnurse You're jumping to conclusions. We likely only expel some of the spores immediately via the air we exhale.  The question specifically asks by what mechanisms we expel the rest of the spores and if they are alive or dead at that point.  So to answer the question, you need to look at all mechanisms, not just the exhalation of air.

Mold spores are capable of landing and becoming dormant. Unless conditions are severe enough, mold spores will not just simply die off; they will essentially wait for conditions to improve and once those conditions do improve, they will take root and grow. When it comes to the human body, it all depends on the type of mold and the overall health of the host. The body is designed with natural defense mechanisms - mucous, enzymes, beneficial bacteria, filaments, etc. - against airborne particles and microorganisms. Basically, you'll never know if a sneeze or cough - other forms of defense - saved you from a miserable existence as a mold host.
As for whether or not mold spores are expelled from the body, that is not so easily answered. Mold spores can sometimes teem in the millions, especially around a dense infestation (such as grain silos or a house that has structural mold rot). Research has concluded that farmers (who make up 30% of victims who suffer respiratory illness in the U.S. alone), for example, inhale up to 750,000 mold spores per minute. The odds aren't exactly in their favor when it comes to expelling mold spores simply by exhaling.
(I write for MoldBlogger, by the way. If you have anymore questions or are curious about other mold-related scenarios, feel free to check it out.)
Edit:
Here are some of the sources where a lot of this information can be read about.
National Institute for Occupational Safety and Health. Agricultural Safety. Centers for Disease Control and Prevention website. https://www.cdc.gov/niosh/topics/aginjury/. Published June 19, 2014. Updated December 15, 2014. Accessed February 1, 2017.
Glen H. Hetzel, et al. Farmer’s Lung: Causes and Symptoms  of Mold and Dust Induced  Respiratory Illness. National Agriculture Safety Database website. http://nasdonline.org/1853/d001796/farmer-039-s-lung-causes-and-symptoms-of.html. Published 2005. Accessed February 1, 2017.
Dennis J. Murphy. Agricultural Safety and Health: Farm Respiratory Hazards. PennState Extension website. http://extension.psu.edu/business/ag-safety/health/e26. Published 2017. Accessed February 1, 2017
Also, please feel free to check out a simple post that summarizes this type  of information: Occupational Respiratory Diseases: The Farmer, His Lungs, and Mold

Great that you took the time to answer an old question +1. Could you add your sources to this answer to allow other users to background-read on your topics covered?

Thank you. Sources have been added. I will keep an eye out for more sources that I've used in my own research and return to edit again at some point.


text:
Why do I see the world in blue when I open my eyes?
So I was standing outside, waiting for the train. I was tired so I closed my eyes for a while. Then when I opened them, the world was a lot more blue than it normally is - why is this? I tried it a couple more times to be sure that it wasn't just a mistake, which confirmed it, as the world kept being blue (of course, not permanent, it slowly gets back to the "normal" colors).
I'd appreciate a simple explanation, as I'm not a biology or physics student. I only have a very basic understanding of both subjects. Thanks in advance!

When your eyes are closed in bright light, you see red because the light shines through the blood vessels inside your eyelids. Eventually this will "wear out" your red cone cells so that they stop sending signals to the brain (a form of sensory adaptation). This results in you only seeing blue and green for a few minutes after opening your eyes until your red cone cells are able to recover and begin firing again. I am not sure why this question is on hold, it seems like a good question to me. Maybe I missed something...

I also don't really know why it's being closed. It says opinion-based, but I don't really find where I put in my opinion. However, this is my first question on this forum, so I guess I'm not familiar with your customs. Thanks for the reply though, you answered my question!

My pleasure. :)

Initially I also not clearly thought-out what could had happened. But after reading the clear-cut answer by user @CDB,  I couldn't think the answer  as 'opinion-based' from any viewpoint. It was an 'objective' answer.

@CDB your answer's flavor was like a detective story, than many-other types of scientific q/a.

@CDB too many times I also seen the "dark-adaptation" or "brightness-adaptation" also take place in colors also... especially when I look at intense coloured (bright as well as saturated) figures or images, like traffic lights or slide-shows or certain computer-games; it really happens.


text:
Escaping resource limitations during tumor evolution
In their discussion of the importance of r- and K-selection on tumors, Aktipis et al. (2013; figure 3) provide the following illustration of a hypothetical cancer growth curve:

In it, you can see alternations between selection for proliferation and selection for survival as the populations breaks through one carrying capacity after another. Of interest to me, is the overall shape of the growth curve as several sigmoids -- with each corresponding to a different serial resource limitation. However, this growth curve is a cartoon and not a measurement of some empirical system. Are there examples of such growth curves in the empirical literature on cancer?
An ideal case would be in a well studied animal model (or humans), with a corresponding analysis of which resource limitation was overcome at each step. With at least two, but preferably more, resource limitations in series. However, I will also be satisfied with answers from cell lines grown in vitro, since growth curves are usually easier to measure there.
Aktipis, C. A., Boddy, A. M., Gatenby, R. A., Brown, J. S., & Maley, C. C. (2013). Life history trade-offs in cancer evolution. Nature Reviews Cancer, 13(12): 883-892.

Time is the limiting factor here for in vivo studies. Normally the growth curves you can actually find span about 1-2 months tops, many between 7 and 30 days (mouse model). At the very least this webpage offers some models incl. growth curves for a number of cancers.


text:
Earliest to use media after autoclaving?
I am autoclaving media to use later to inoculate yeast. How much time do I have to wait before using the media and adding the culture? Can I use it a few hours after autoclaving?

There is a relatively simple (and yet logical) answer: You can use the media as soon as they are cold enough for your desired culture temperature. So if you want to use the media at 30°C, there is no need to wait longer. The media will only warm up again in the incubator until this temperature is reached.
The addition of antibiotics is also uncritical, since the media is ways to hot to be directly used when they still inactivate antibiotics. Your cells wouldn't survive this either.
There is also no waiting period necessary to use fresh media after autoclaving, since there are no processes going on when the autoclaving was done properly. If not, you will see contaminations pretty fast.

If not using antibiotics or other additives, it's just a matter of medium being cold enough. If it's too hot, the yeast (or whatever you are inoculating) might get killed or heat-shocked, which you maybe don't want.
Since the incubator will bring the culture to 30C anyway, there's no point cooling it past that point. Yeast are probably fine at 37C, maybe even 42C depending on what experiment you are running.
If you put the hot medium into your culture vessel first then wait, it will cool faster, since the glass won't be as hot. When I feel impatient I like to run cold water down the outside of the flask while swirling, cools it off very fast.


text:
Follow-up to The Red Queen by Matt Ridley?
I just finished reading The Red Queen: Sex and the evolution of human nature by Matt Ridley. Since this book is over 20 years old, I was wondering if more recent research made part of the book obsolete or inaccurate in some way. If so, would you have a recommendation for a recent book that would be a good complement to it?

Which part of the book? Which theory? I upvoted, but also vote to close because your question is unclear

Any part of the book, really. I was just wondering if any part of the book needed to be updated, I guess that would have been a clearer question.

This question is unfortunately too broad. Nobody is going to read the whole and search every single subject to see if there is need for updates.

My question was aimed at people who already know the book and the field. Maybe that's too narrow a target.

I haven't read the book, but in the context of parasite-host co-evolution, RQH-style thinking is very common.


text:
What is the number of influenza strains occurring at a given time?
My question was initiated by reading on mock-up influenza vaccines. I understand that the manufacturer pre-prepares a certain vaccine and tries to get it tested and ready before it is actually needed, by taking a novel virus strain that has infected a few people, and could potentially cause a pandemic.
My questions:

How many different influenza strains are there at any given time at one geographical spot (say, one US state? - narrow down at will). I always thought there would be just one novel strain appearing each year, explaining why people get sick time and again of the 'same' virus. However, the mock-up virus vaccine production seems to imply there are various strains occurring at once?
Do influenza strains vary on an annual basis, or is it a continuous process (like evolution), and is a new strain re-named after it becomes potentially dangerous (like speciation?) - i.e., what is an influenza strain? It seems, given the vaccine preps, that various strains occur at once, and strains survive for extended periods? Any hard evidence for these indirect assumptions?

And as a side -

Do vaccine manufacturers prepare a whole bunch of mock-up influenza vaccines on a yearly basis just awaiting to identify a dangerous strain and start manufacturing it once people get sick? Or are mock-up vaccines combined into a cocktail mix containing many strains and are these cocktails re-vamped annually? Or is a yearly shot necessary because immunity only lasts a year?
I might have to re-post this last question at Health.SE as a dedicated question, but since related to above I prefer to leave it here for now. Grab me in chat if need be!

Antigenic drift in the coding portions of the genes that involve antibody binding sites accounts for the seasonal variability of flu strains, i.e. they mutated enough that the antigens require new antibodies, hence a new strain. The process is as you said constant, like evolution, and in an analysis of pandemic H1N1 the authors are able to note 1 - 18.1 mutations per genome per replication cycle (ref). Because of this, flu vaccines tend to have more A strains than B strains due to the greater mutability of influenza A, at approx. 30% more mutations per site per infectious cycle (ref). At current It will take me time to research the remaining questions.
Interestingly enough, however, and I've never looked at this but CDC offers weekly influenza reports that detail by region what they're finding (CDC):

Source: CDC's so-called FluView
Beyond that, I'm pretty sure they take this weekly data, see what strain is on the rise in hospitals, and manufacture the vaccine to mirror the "popular" cocktail of strains.


text:
Converting miRNA names
I need to convert all of my microRNA names e.g. hsa-miR-30e-5p to e.g. entrez gene IDs, ensemble IDs or another ID. Does anyone know a good ID conversion tool for microRNAs?
(I managed to convert it to miRBase ID e.g. MIMAT0000692, but David does not recognise them apparently)

Does this help? https://www.biostars.org/p/85571/

miRbase is kind of an official database for miRNAs. So it is better to have miRbase ids for miRNAs rather than other (ensembl, entrez etc) ids.

It seems there're no ids for a mature sequence. You better search for a parent sequence ids. You could check, but it also seems that HGNC ids are -miR-30E- part.
So you could try Ensemble search (you should input names in 'Filter'-'GENE' section) or use Genenames. As you see, it has API, and you could use it programmatically with HGNC ids.


text:
Why lactate inhibits growth (or enhances death rate)?
Extracellular lactate tends to inhibit cellular growth or enhance cell death. This happens in the vicinity of tumors and in cell cultures.
See for example this reference: Ozturk, Sadettin S., Mark R. Riley, and Bernhard O. Palsson. "Effects of ammonia and lactate on hybridoma growth, metabolism, and antibody production." Biotechnology and bioengineering 39.4 (1992): 418-431 (available here: https://www.researchgate.net/profile/Mark_Riley5/publication/227705703_Effects_of_ammonia_and_lactate_on_growth_metabolism_and_antibody_production/links/540e0bcb0cf2f2b29a3a765a.pdf)
What is the mechanism behind this effect of lactate? Why lactate has these negative effects?

Are you thinking of effects of lactic acidosis rather than lactate? Note that lactate itself is a base, not an acid. The effects of lactate on cancer cells and tumors is still heavily discussed, can you give some references for your claim? Can you specify what types of tumors or cancer cells you are thinking of?

@Roland Almost all tumor types exhibit lactate secretion (this is called the Warburg effect). I think the cell secretes lactic acid, which once outside the cell, equilibrates with lactate, as any acid/base pair.

Most tumors do secrete lactate, but I'm not aware of any evidence that lactate itself inhibits cellular growth, as you stated in your question. So please provide references for this; or, if you actually mean effects of acidosis (low pH), then please revise and clarify. Glycolytic cells do not actually produce lactic acid; anaerobic metabolism is acidifying because of proton imbalance due to inadequate respiration. See https://en.wikipedia.org/wiki/Lactic_acidosis

@Roland Take this example: Ozturk, Sadettin S., Mark R. Riley, and Bernhard O. Palsson. "Effects of ammonia and lactate on hybridoma growth, metabolism, and antibody production." Biotechnology and bioengineering 39.4 (1992): 418-431. Available here: https://www.researchgate.net/profile/Mark_Riley5/publication/227705703_Effects_of_ammonia_and_lactate_on_growth_metabolism_and_antibody_production/links/540e0bcb0cf2f2b29a3a765a.pdf

They report growth inhibition as well as death rate enhancement when extracellular lactate concentrations go up. There many papers with similar statements. My question is what is the mechanism behind this. I've heard that lactate secretion ends up lowering pH, which seems related to what you're saying, and maybe this is a mechanism, but I can't confirm this.

Hm, that paper concerns bioproduction settings rather than tumors. They state in the introduction that lactate has variably been found to either increase proliferation or have no effect below ~40mM. They themselves use 55mM, on hybridoma cells. Not sure this is physiologically relevant for tumors. 55mM lactate would increase pH somewhat, since lactate is a base. At so high concentrations, lactate dehydrogenase might be also be disturbed ... But okay, now the question is clear I think. Please add the reference.

The cells deaths they observed in the reference paper were due to nutrient depletion and high medium osmolality, both of which delay growth and cause cell death, with glutamine being a key limiting factor.


text:
Would urination continue after death?
If someone was urinating, and they were to hypothetically suddenly "fall dead" (the brain is unconscious and all muscles / organs are unfunctional), would they continue urinating or would it stop?

Death of who? The person? The brain? Or the kidney?

@Superbest well the person of course. In 99.99% of cases I've read, "suddenly fall dead", refers to a person. It seems odd saying "if the kidney were to suddenly fall dead"

Many organs remain intact (and "alive" in that they can be transplanted) for minutes after brain death.

Yes. Moreover, even if they were not urinating at the time of death, they likely would at death, assuming adequate filling of the urinary bladder. There are two sphincters that close off the urethra. One is under control of the autonomic nervous system and the other is voluntarily controlled (somatic). At death, both sphincters will relax, releasing the bladders contents.

Related TVTropes. TVTropes warning.


text:
Efficacy of the 10-20 montage for EEG
I am trying to better understand the relationship between the placement of EEG electrodes and the quality of the "brainwave" signals they produce.
There is the standard 10-20 system which has me wondering a few things:

Is the 10-20 system just a standard based on uniform distribution of the electrodes (so as to maximize brain signal collection)? Is it safe to assume one could increase the "density" of electrodes (again, in uniform distribution) and receive better quality signals? In other words, how does the placement & quantity of electrodes affect the quality of the information that can be obtain via EEG?
Is electrode gel strictly necessary? Is the gel used for adhesion, conductivity or both? I can't imagine it helps much with conductivity seeing the most of the scalp is (typically) covered with hair?

The placement in terms of location on the scalp determines what region of the brain is sampled. The electrode density determines how many locations are sampled. The spatial resolution of an EEG has been reported to be 7 mm (Im et al., 2006), meaning the variability in determined source and verified source (via fMRI in the study cited) is approximately 7 mm. Hence, increasing the density below 7 mm may not be too helpful. The 10-20 system utilizes an inter-electrode distance of 60 - 65 mm (American Clinical Neurophysiology, 2006), indicating it may make sense to use more electrodes when high resolution is needed. Note, however, that MRI and MEG have better spatial resolution than EEG and are methods of choice when you wish to do accurate source localization. EEG has excellent properties in the temporal domain, and a combination of MEG/EEG has great characteristics in both spatial and temporal domains.
Standardized EEG montages indeed promote uniformity so that different studies can be compared more efficiently.
Scrubbing with electrode paste primarily reduces impedance (increases conductivity). Hair and the skin don't conduct well and by applying a conductive paste impedances are substantially reduced. Mostly the technicians also scrape a little bit to ensure even better conductance by removing the fatty top layer of the skin. Also important is that differences in electrode impedances negatively impact recordings (American Clinical Neurophysiology, 2006). Impedance matching is hence necessary and using paste aids this purpose. So yes, conductive paste is essential.

Reference
- Im et al., J Neurosci Methods (2007); 161(1): 142–54

Thanks for the awesome answer @Christiaan (+1) - the only part of your answer that I'm not quite following is the part surrounding spatial resolution. (a) When you state "The spatial resolution of an EEG is quite poor and has been reported to be 7mm..." what exactly do you mean (what exactly is "spatial resolution", and why is 7mm a poor value for it)? (b) It sounds like increasing density (e.g. 10-5 system) would help with this poor spatial resolution? Thanks again!

@smeeb - I adapted the answer.

I don't see how it follows from the resolution of EEG being X that there is no benefit to more narrow electrode spacing than X. For example, it is possible (and likely) that electrode spacing X is not sufficient to recover sources with accuracy X. After all, resolution refers to brain sources, spacing refers to sensor density.

If the error margin is 7 mm narrowing density down below that doesn't make much sense imo.


text:
Ions in Stomatal Opening Mechanism
When a stoma’s guard cells try to swell and open the stomata, they actively pump out protons outside of the cell. This causes a membrane potential, where the inside of the cell is negative with respect to the outside. This then causes potassium ions, which are positive, to rush into the cell, mitigating that potential. However, my texts say that anions such as chloride and malate ions follow potassium into the cell as well; their rationale is that positive ions must be balanced by the presence of negative ions. I do not understand why this is the case. If you extruded positive ions (protons) out of the cell and allowed positive ions (potassium) back in, there would be no ionic imbalance to draw the anions from where they’re idling. Could someone clear this up for me?

The ion concentrations are different inside and outside of the cell, allowing a potential.  The cell becomes even more polarized by the pumping out of H+ ions, making the cell even more negative (potential difference). Then this negative potential happens to cause voltage-gated channels to open and the uptake of potassium occurs. This will depolarize the cell (return it to the base potential difference).  It is usually very important for the cell to maintain the negative potential after it recovers. To combat the uptake of potassium, negative charges can be used to balance the increased positive ion influx so the resting potential is stabilized.
These mechanisms are usually mediated by special proteins that are regulated by actual electrical changes in the membrane.

You may find it an interesting sidelight that in many plants with potassium deficiency, we see necrotic leaf spots or leaf tip or marginal burn. The plant can't adequately close the stomates, so you get localized dessication in the leaf and therefore necrotic leaf spots. In this way, drought stress and potassium deficiency are somewhat related.

do you have any references that one can read for more information on your answer?


text:
Are human beings evolved to eat meat?
I know humans can cook and prepare almost anything, but are humans specifically adapted to eat meat?
One of my doubts humans are not particularly well adapted to eat meat because they lack canine teeth. I read more reasons for this here.
What does an evolutionary biologist have to say on this matter? Perhaps evolutionary biology is the field related to this?
Some links supporting my doubt:

http://www.peta2.com/blog/humans-supposed-eat-meat/
http://mindfullybliss.com/humans-are-designed-to-eat-meat/

Please correct my question edit it for something wrong and put related tags

Human beings, or any living creatures, are not designed to do anything. There is no "design" in evolution, merely the accumulation of changes in gene frequencies.

And of course humans have canines - just look in a mirror. I'm not likely to trust anything published on "celestialhealing.net"...

what about the lost tail bone that we have, i think i used the design as the wrong word . but if you say the accumulation of changes in gene frequencies what accumulation of changes in gene frequencies so far we have been got up to from thousand of years back to us humans.are we vegetarins or carnivores or both.I know we can cook and eat anything

have you googled any of that questions?

yes i did, http://www.rense.com/general20/meant.htm and http://www.celestialhealing.net/physicalveg3.htm

@MattDMo we have canines but why they are so under developed and not like a tiger

that is another secondary benifit from large canines i guess but primarily i think it is for ripping out flesh, holding a prey with claws and large  canines, and puttting those canines on the neck of the prey kiiling them perhaps by stopping airflow

If you really think humans were "designed", you should move this question to your religion-of-choice site.

@jamesqf design was a wrong word i should have used evolved instead i guess.I think comment from kelt here is good explanation for this.It seems like an answer that should be here in biology.stackexchange.com for my question.OK, I changed it to evolved

@Munish: I will rebut that page, even if Mr. Blomstrom has begun to do so.

Carnivores don't swallow food whole.  That's why they have other teeth rather than just four large fangs.
Birds have no teeth.  There are many birds of prey that eat other animals, and there are birds that are nut/seed/fruit eaters.
Stomach acid: we have an extremely strong acid in our stomach, that if it weren't for a mucous layer protecting us, we would have a dissolved stomach.  Average pH of stomach acid is about 1 to 3.5 - that's very acidic.
Our intestinal tract is intermediate.  Well suited for both, not just one.  More importantly we lack the enzymes that can break down cellulose in plants.  If we were strict herbivores, wouldn't it make sense to have the enzymes necessary?
We are probably the best hunters on earth.  We have been able to hunt and kill almost any animal wanted and allowed.  We have highly developed brains that allowed us to invent firearms and send men to the moon.  People around the world rely on fishing for their dinner, and hunt deer legally for food.  Hunting is just not that economical for most people.
To say that were weren't designed to process flesh is absurd.  I ate beef the last two evenings.  Safe food handling is the contributing factor in "meat illness", unless the person eating has a GI disorder.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1262767/ : This is one journal that concluded there was no evident relationship between excess protein intake and renal function.

That is a vegan website, and should stimulate skepticism considering they have a bias.  The point I'm trying to show isn't that we are made to eat meat, but rather choose for yourself.  Gain the information you need and make the choice based on the lifestyle you would enjoy more.

we can't eat raw meat like other animals do.i don't if our stomach will favour that , it won't taste good either but we can eat raw veggies and it tastes good. though there are some people who eat raw meat on live TV shows it seems favourable to their stomach

@munish: Humans certainly can eat raw meat, as attested by e.g. innumerable sushi bars.  Likewise, there are a good number of vegetables that can't be eaten unless cooked or otherwise processed, and others, like potatos, that are much better cooked.  There are also far more plants than animals that are actively poisonous when eaten.  It is also quite possible to get food poisoning from improperly-processed plant foods.  Indeed, from news accounts this seems more common than meat-related food poisoning.

Humans(aghoris) will do anything even eat discarded dead human bodies raw.Thats survival to save money, or may be religion

@jamesqf Great response, well said.  munish there is also a dish called steak tartare which is raw meat.  We can eat raw meat, but with all of the possible pathogens, it is advised to properly cook it first.  Many wild animals who eat raw flesh also can have a higher chance of parasitism, so it does come with negatives.

@MG_MD you are right that is a vegan website so they are vouching for that,  but i am not sure about this, do you have to say anything or those guys are wrong/manipulative.is this some sort of consipracy theory?the video and arguments seems legitimate.

@munish: If you want an answer, or even a comment, please post a link to readable text.  I do not wish to waste my time trying to extract information from videos.

@jamesqf though its not related to my question heres the link, just scroll down if you dont want to see the video

@munish I know that farming animals is not as ideal environmentally as hunting.  The sheer demand and amount of animals raised for consumption is beyond staggering.

@munish: Thanks for the text link.  However, it seems obvious that they are not addressing whether humans evolved to eat meat (the answer to that seems trivially yes, since basically all human societies do eat meat, when they can get it), but how & whether modern industrial agricultural methods can sustain massive human populations without causing environmental damage.  So one might, with equal justification, ask whether humans evolved to live in large cities, getting their food from supermarkets, instead of hunting & gathering.


text:
Why eyes don't get heated while converging sunlight into retina?
It is a common observation that a magnifying glass when used to converge rays of sun to a fine point in paper, the paper burns due to intense heat.
Why doesn't this happen in our eyes? Our eyes are also doing the same, they are converging the sunlight into our retina but our eyes don't get burned, or to say get heated.
Is viterous or aqueous humor absorbing heat? If so, then the tiny amount of fluid present in the eye shouldn't be enough to cool the eye for a longer period of time, but we can spend the entire day at sunlight without any eye stress or pain.
Size of eye lens small compared to magnifying glass? However a magnifying glass of the size of eye lens should also be able to produce significant heating by converging sunlight.
As far as I know, the heating effect is due to Infrared rays not because of UV rays so we can safely ignore them in this case, right?

If you look straight at the sun, you do burn your retina, in the same sense as you get burnt by contact to a hot surface: living tissue is full of water, so the burning process does not look the same as for dry paper e.g., and the harm will be done long before combustion.
To go a  little further, the first layer of retina in vertebrates is made of so-called Muller cells, which conduct the light as optical fibres do to the photoreceptor cells, but it has also been argued that they can in some measure filter too strong light in order to protect photoreceptors. See http://www.pnas.org/content/104/20/8287.full
These cells are also strongly vascularised, which allows to regulate its temperature. You can read http://creation.com/mueller-cells-backwardly-wired-retina-v-dawkins

Converging sun rays at my hand (tissue, as you said) produces enough heat to draw back my hand spontaneously. But with our eyes, we can look at sun for a slightly longer period of time without noticing any change except extreme brightness.
Even when we aren't looking directly at the sun, the sunlight is still entering our eyes. Why this indirect sunlight (For a long period of time) doesn't produce any heat (Which should, as we are exposed to a longer period of time)?

Light converges on your retina only when looking at an object at an infinite distance. The ambient light is not converged to a single focal point on the retina, so the heating is not more than on your skin. I advise strongly against performing this experiment of comparing for how long you can hold your hand in focalised sun light and look at the sun. See also my edit.

I didn't read those articles you linked to as they are too scientific for me to understand but your ambient light description seems to solve my question to the finest. Thanks.
Btw, I didn't performed any such experiments for the sake of this question because I know it's harmful, I was just narrating my previous experience, we all've done these, once at least.


text:
What’s wrong with a shriveled cell?
When you place a cell into a hypotonic solution, water rushes into it and it bursts/lyses. Thus, the cell dies.
However, when you place a cell into a hypertonic solution, water rushes out of it and it shrivels. The membrane is still in tact and all the organelles are still held inside. Why is having a shriveled cell a problem then?

Just as a comment at the moment: Water is the most important substance for the function of a cell. Without it, no reactions will take place etc.

@Chris Is that the only reason, though?

@lightweaver An interesting read if you're really interested.

Just to elaborate a bit on @Chris's answer - the protons and electrons that come from the disassociation of H2O are very important for reactions.  Also the hydroxide ion has some important applications as well in organic reactions.

You should google the effects of osmosis on living cells. It really is gonna give some good results

Adding on to @MG_MD's answer: a lot of metabolic reactions and cellular processes require water as a solvent and medium. Transport of electrolytes and dissociation of compounds into ions also requires water

Plant Cell
In the case of plants, shriveled cells are a huge problem. When plant cells are put in a hypertonic solution, the cell wall remains turgid and stays that way but the plasma membrane doesn't, it shrinks as you already know with the other organelles as well. This is known as plasmolysis. If this situation continues it causes death.

Shrivelling  causes the plant to wilt too.

Animal Cells
Well it does have affects overall and at cellular level

It changes the RMP(resting membrane potential) across the cell because of change of sodium ions outside the cell
-It decreases rate of metabolism

Perhaps you may want to elaborate here. For all cells, exosmosis will increase the concentrations of solutes inside the cell. This would affect all cells not just electrically active cells. You may also want to explain how metabolism is affected. Moreover, this question is general (not pertaining just to humans); so you can remove the perspiration and fatigue part and explain what happens at the cellular level (as you started your answer).


text:
Why plants and animals are so different even though they come from the same ancestors?
All the documentaries I have watched, books I have read so far on the starting of life on earth only talk about animals. The very first life form on earth was bacteria. Then evolution took us this far. But what about the trees? They must also come from that single cellular bacteria. Since when they got separated from animals? What made them to be so much different than animals? Besides, apparently their evolution is very slow, isn't it? Why are they lagging behind in the race of living organism?

because the last common ancestor was a long long looooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooooong time ago. (a quick google search shows estimates are around 1,600,000,000 years ago).

I strongly suggest reading through Understanding Evolution from the University of California, Berkeley. It will correct a lot of the misconceptions you have.

This question shows so much misunderstanding in evolutionary biology (no offense) that it is hard to fully answer. As @MattDMo suggested, you will benefit from having a look to an introductory course to evolutionary biology such as Understanding Evolution.

But what about the trees? They must also come from that single cellular bacteria

The Most Recent Common Ancestor (MRCA) of animals and plants was not a bacteria but single-celled eukaryote.
Once you'd have a look at the course Understanding Evolution, you might want to have a look at the tree of life on tolweb.org for example

Since when they got separated from animals?

The MRCA of animals and plants lived about 1.6 billion years ago.

What made them to be so much different than animals?

Time has passed and with time different lineages diverse through a number of different processes. By increasing your understanding of evolutionary biology (Understanding Evolution again), you will be able to understand these processes much better.
Note that while with time (1.6 billion years) genetic differences have accumulated between animals and plants, there are still a large number of similitudes. Some of these similitudes are also shared with other organisms such as bacteria for example and some are not shared with bacteria. Here is a short, non-exhaustive list of similitudes:

Both use DNA to store genetic information
Both use Adenosine Triphosphate (ATP) for transferring energy within cells
Both use lots of water.
Both have a cell membrane
Both undergo cellular respiration
Both undergo mitosis
Both undergo meiosis
Both have their DNA contained in a nucleus
Both have endoplasmic reticulum
Both have DNA organized in chromosomes
Both contain mitochondria
Both have histones

Note by the way, that I focused exclusively on similitudes that are caused by shared ancestry and not by convergent evolution.

Besides, apparently their evolution is very slow, isn't it?

The terms slow and fast are obviously relative. To discuss really how fast is evolution, you would need to know what evolution is and you would need to know a little more about the processes that drive evolution.
In very short and largely simplified: Evolution is a change in allele frequency (at a given locus) trough time. Such change occurs every second in a big population. However, the evolution of a large phenotypic trait that was previously completely inexistant may take much more time depending on how much genetic variance, you have to start with, depending on the mutation rate, depending on the number of mutations required, depending on the selection coefficient for each of these steps and depending on a number of different things.
So the answer to "How much time does it takes for evolution to occur" varies between a fraction of a second and infinity depending on what you mean exactly.

Why are they lagging behind in the race of living organism?

I don't understand this question. I don't know who is "they", I don't know what you mean by "behind" and I don't know what you mean by "the race of living organism".


text:
Why it seems that principles of chemistry are not being applied in this biochemical process?
According to an answer in this question, my concept used below does not apply:
In the non-cyclic photophosphorylation, consider splitting of two water molecules, then 4 e- (electrons) and 4 H+ (protons) are generated in the lumen of the thylakoid. Due to quinone cycle 8 H+ are transferred from stroma to lumen. 4 e- will reduce 2 NADP+ to 2 NADPH, these H+ are taken from stroma so there is a net decrease of 8 + 2 = 10 H+ and a net increase of 4 + 8 = 12 H+ in the lumen. So if we apply principles of chemistry then to attain equilibrium there should be equal number of H+ on both side. Therefore 11 H+ must be transferred from lumen of thylakoid to stroma. Now there is 1 H+ on each side at equilibrium. We know that F0-F1 ATPase will produce 1 ATP for 3 H+ being transferred so in this process 11/3 ATP should produce but in books it is given that all 12 H+ are transported which is violating the principle of chemical equilibrium and produces 12/3=4 ATP.
So I basically want to ask: Why does it seem that in this process the principles of chemistry are violated?

About which principles of chemistry are you talking?

@chris According to books all 12p will get transferred but we know from chemistry point of view that only 11p could get transferred as per the gradient created

@Chris the principle is that at equilibrium there must equal number of protons on both sides

A schematic of the reactions involved would help. It's kind of a narrative.

You should just write down the equation. Here is an explanation on how to write chemistry expression. Then, you'll probably want to use the term stoichiometry somewhere in your post. Finally, note that your question would be a better fit for Chemistry.SE than for Biology.SE but I would predict that the level of knowledge in chemistry needed to answer the question will be simple enough for us, biologists.

http://www.ncbi.nlm.nih.gov/books/NBK22519/ I think this answers the question, but let me know.

From the link given by @Kendall

Such a gradient can be maintained because the thylakoid membrane is essentially impermeable to protons.

I think this solves your dilemma of 'why not maintaining equilibrium' totally.

The reason for this difference is that the thylakoid membrane is quite permeable to Cl- and Mg2+. The light-induced transfer of H+ into the thylakoid space is accompanied by the transfer of either Cl- in the same direction or Mg2+ (1 Mg2+ per 2 H+) in the opposite direction. Consequently, electrical neutrality is maintained and no membrane potential is generated.

It precisely shows why electrical equilibrium is not disturbed due to pH disturbance.
Finally:

2 H2O + 2 NADP+ + 10 H+stroma => O2 + 2NADPH + 12 H+lumen
12 H+lumen + 4 ADP + 4 Pi => 4 ATP + 12 H+stroma