Are neurons capable of buffering a signal to sync up with other data? The brain is the most complex thing that mankind discovered thus far in the universe. Super computers aren't able yet to outperform the human brain (running only on ~25 watt or so) on the domain of general intelligence.
With a computer it is fairly straightforward to capture an image stream and split it into 2 streams. So in a videoclip depth data could be contained by alternating the images from 2 streams from two different angles.
What if an organism would loose sight in 1 eye. And the other eye would be fed with data that contains actually 2 image streams, with these alternating angled images, at an always exact framerate. Would the organism (the brain basically) be able to comprehend the data and experience depth? For that it would kind of need to buffer every other image and put them through simultaneously, mimicking the feed from two eyes basically.
Would this be possible? Is there any research done on a topic similar to the example above? Where data is buffered by a neural network to be send in combination with other data?

For this answer, I'll use a very broad definition of "buffer" as a mechanism to integrate information at different delays. I have no interest in getting into specific computer science definitions of what a buffer is and I don't think it makes any sense to use them in biology.

Parallel processing and predictive coding
The brain is a massively parallel system, so of course there are different "streams" of information flowing at all times. Certainly the brain as a whole does some level of buffering, though the mechanisms available to individual neurons are unlikely to do what you suggest. The "buffering" in individual neurons has a lot more to do with learning and memory, for example in spike-timing-dependent plasticity which incorporates a physical record of past inputs in a learning rule.
One model of cognitive function is predictive coding, in which the brain holds a model of the world at different hierarchical scales and updates this model with new information. This model is effectively a buffer against which new incoming information is compared to draw attention to discrepancies that require further attention (such as the sudden appearance of a predator).
Audiovisual integration
One simple example of buffering is in audiovisual integration: the brain's processing of visual information is much slower than auditory information, and yet the perception of, say, a human speaker's voice vs. lips or the sound and sight of a bouncing ball are perceived in synchrony (see for example Recanzone 2009; note this has absolutely nothing to do with speed of sound vs speed of light).
It's important to understand that the visual system doesn't process visual information anything like a computer. There are no frames in biological vision. That said, humans can deal with a lot of unnatural sensory input, and they also use a lot of other visual cues besides stereo vision, the so-called "monocular cues".
Motion parallax and wiggle stereoscopy
One of these monocular cues is motion parallax (binocular vision can also utilize parallax without motion). Wiggle stereoscopy simulates motion parallax, as if your head were oscillating back and forth, to create an illusion of 3D, and seems much like what you are proposing. It doesn't matter whether you view the image with one eye or two.

Recanzone, G. H. (2009). Interactions of auditory and visual stimuli in space and time. Hearing research, 258(1-2), 89-99.


Effects of exercise on the brain I am well aware of the phenomenon of neurogenesis induced by exercise, as well as the dopamine release that results from exercise. I am really interested in neuropsychology and the effects of exercise on personality. What are some other biological processes that are stimulated by exercise, does it activate our parasympathetic nervous system? Is there any cool research out there for me to read? I am grateful for any input. Any information about exercise and its effects on human biology is appreciated.

UPDATE
While this answer was appreciated, i'm interested in other biological processes... What happens to stress and anxiety? Do our adrenal glands stop secreting as much corticosteroids? What effect does exercise have on circadian rhythms? With exercise, can you circumvent the problem of not getting enough light in the winter? What effect does exercise have on memory? It should probably help, since it would lead to decreased damage to the hippocampus. How does exercise effect sleep, learning, memory, metabolic processes??? I'm searching for the comprehensive list of different primary and secondary effects of exercise from a biological standpoint. I'm really interested in what the short term and long term effects of exercise are on the brain.

Although current research has little to say about the effects of exercise on personality, there has been recent correlations demonstrated between personality and the "drive" to exercise--specifically, aggression as a personality trait has been linked to higher metabolic rate. See http://phys.org/news206006380.html for more information about this.

The causation in exercise-induced neurogenesis is not well understood. A correlation that has been found (in mice) is the presence of a hormone called beta-endorphin, which is attributed to positive affect (a boost in mood). Exercising mice that demonstrated the presence of beta-endorphin in their hippocampal region did experience exercise-induced neurogenesis, while those that naturally lacked beta-endorphin did not experience neurogenesis.

The basic worth of circulation should not be overlooked, either. Anything that gets your blood pumping more efficiently means that the more distal parts of the body will appreciate an influx of nutrients. A smoker with poor circulation (as a result of lowered oxygen in the blood -- carbon monoxide competes for hemoglobin-binding) will have cold hands and brittle fingernails, and this is just a simple example of this phenomenon. The value of increased circulation to the brain shouldn't be overlooked -- the blood is our main transportation system, and the brain gets nothing that is not delivered via circulation. It's akin to watering a plant -- sure, it may grow it you give it 30 minutes of sunlight and 1/4 cup of water a day, but it will certainly grow to its full potential if it is fed as much as it needs.

Exercise is important, but it's easier to think about the questions you pose if you consider exercise more as a physiological stressor on the body. Muscle tissues are torn and damaged by exercise, but the body recognizes that it must need these resources (because of some present danger in the environment that caused you to run/strain yourself) so you begin to see the typical skeletal muscle hypertrophy. The heart is also made stronger through this strain, which is why regular exercisers have a lower resting heart rate -- it takes their heart less effort to pump the same amount of blood.


Are there animal species that sense infrared light with their eyes? I asked a question earlier today about birds with infrared vision but this time I am asking about animals in general. I know that many snakes have receptors between their eyes and their snout that allows them to sense infrared radiation but I am looking for an animal that actually uses its eyes.

Googling and searching around found me this statement:

  It's worth noting that, though there are numerous animals that sense
  infrared light, relatively few of them sense it with their eyes

The article didn't list any specific animal that used its eyes to sense infrared light, it just says 'very few'. However, I haven't been able to find any species that can sense infrared light with their eyes.

Short answer
As far as I can see, there are no animalia with high-sensitivity infrared photoreceptors in their retinae. Instead, infrared is detected at low thresholds with a dedicated sensory system in some species - the pit organ. This organ is separate from the retinae and its output does not merge with the retinal image. However, red cones, and even green cones for that matter, have low sensitivity to infrared light and when intense enough, infrared stimuli may be detected by the eye, as was shown in a small study in ferrets.

Background
Infrared (IR) light is classified as light at wavelengths of 700 nm and up. In Fig.1 is depicted the light sensitivity of man under scotopic (dark-adapted) and photopic (light-adapted) conditions. It is readily apparent why we cannot perceive IR.

Species that can detect IR use it in general to detect heat. Notable examples are the blood sucking species, including mosquitoes, bed bugs and vampire bats as well as nocturnal predators including species of snake (source: National Geographic). Although this heat detection can be classified as IR vision, IR is not detected by their eyes. Instead, all of these species use specialized IR-sensing organs called pit organs to detect IR. Basically, these are heat detectors (source: NSF). While snakes are able to construct heat-maps, the IR image and visual images as detected by the retinae are not combined into a single image. As far as I understand, the visual image and IR images co-exist in snakes and are not fused (or 'overlaid') (Campbell, 2002).

So the most notable of IR detecting species have IR vision, but these heat maps are sensed by dedicated pit organs separate from the retinae and as far as I can see the images are not combined.

However, last but not least - IR cameras are often used to study nocturnal critters as it is assumed they cannot detect the IR. Interestingly, a study on a small population of 5 ferrets showed that 3 of them responded at above-chance level to light stimuli well into the IR (870 nm) (Newbold, 2007). It should be noted that sensing of stimuli is all about thresholds. The Fig. 1 shows a nearly zero-response in humans at 700 nm, but when we would make the stimuli strong enough, we may elicit a small response nonetheless. Fig. 2 shows the absorption spectra of red and green cones. As becomes apparent here, red cones and even green cones have spectral sensitivity in the IR domain. Then it might become a question not whether we can sense IR, but at what level we can detect it. Under normal everyday lighting conditions, we obviously can't, but that does not exclude the possibility we may perceive it at extreme light intensities.

Fig. 1. Human spectral sensitivity. source: Webvision

Fig. 2. Spectral sensitivities of red and green cones. source: Dowling, 1987)

References
- Newbold, Master's thesis. University of Waikato, NZ
- Kalloniates & Luu. In: Kolb et al (eds). Webvision. The Organization of the Retina and Visual System
- Schnapf et al, Nature (1987); 325: 439-41


Are chromosomes from each parent split between gametes with equal probability (esp. in humans)? I've recently read a little on Wikipedia about genetics, but I can't find a direct answer to this question.

My rough understanding is this:

Both males and females have pairs of chromosomes, one copy from each parent
Both produce gametes (eggs in females, sperm in males)
The gamete is produced during something called 'meiosis' to take only one set of genes

What I can't find an answer to though is whether that selection is completely random, such that every chromosome in a gamete has an equally likely chance of being taken from the male parent set and the female parent set.

Another way of putting it, perhaps: Would the range of 100% male parent to 100% female parent chromosome selection in the gamete be a binomial distribution?

My background is computing, so please assume very little knowledge of biology.

Other answers are correct in their own terms, but because of homologous recombination during meiosis, the idea of maternal and paternal chromosomes becomes meaningless. Any chromosome in a gamete will be a mosaic of the maternal and paternal versions. In this sense the chromosome is not the unit of inheritance.


What is the meaning of "gap" in G1 phase? The full form of G1 phase is Gap one phase. G1 os also called first gap phase. Is there any specific meaning of " gap" here ?

The $G_1$ gap is the period between the last cell division and that start of DNA replication (synthesis). That's what "gap" means here. A period of time between two events. It's often described as time spent synthesizing proteins, but I prefer to think about it as the period before the signal to start synthesis lands. A cell can do any number of things in the meantime: synthesize proteins, grow, interact with other cells, move, differentiate, enter and exit $G_0$...

Albert's has a good chapter on the overview of the cell cycle and on the control system


How are proteins formed? Somewhere, I have read that we need to consume proteins to make amino acids to make new proteins. What does it suggest? How do we make proteins from proteins?

Essentially, yes, "proteins that we consume form new proteins that are different".

The processes are each of them topics for themselves. In short, consumed proteins are digested by peptidases (enzymes) in the stomach, breaking them down into their consituent amino acids. These are absorbed in the gut and transported in the blood to all cells. These take up amino acids and attach them to tRNA molecules which are used in translation to form new body proteins.


Where can I find DNA Sequence data for colon cancer I am a computer scientist studying pattern recognition, and I am hoping to do some supervised learning on colon cancer.  Unfortunately, I'm having a heck of a time finding DNA data in the following format.

Benign DNA (Adenoma?)     Malignant DNA (Carcinoma?)
A                         A
A                         A
T                         G
G                         G
C                         C

So I just need two columns (don't care if it goes down for 3 billion records/ amino acids): one with the good DNA and one with the bad.

Is there anywhere I can find data in that specific format?

You may try the data for "Colon Adenocarcinoma" made by the TCGA project:
http://gdac.broadinstitute.org/runs/analyses__2015_04_02/reports/cancer/COAD/

The file with mutations called by the tumor against a matched normal,
http://gdac.broadinstitute.org/runs/analyses__2015_04_02/reports/cancer/COAD/MutSigNozzleReport2.0/COAD-TP.final_analysis_set.maf

What you need are column 11, 12 and 13. Column 11 is the reference allele (your so-call good DNA). For each row, the alternative allele (bad DNA) is column 12 if column 12 does not equal column 11, otherwise it is column 13. -- It would be a piece of cake to make by coding :)

In case you are interested, column 16 and 17 are the tumor and normal sample IDs.


Density of cells in human tissues? Where can I find values, or estimates, of the density of cells in human tissues? Maybe an overall estimate, or distinct values for distinct tissues? Or maybe not human, but mammal tissues (which should be similar)?

Well, Sender, Fuchs, and Milo wrote a paper to discuss the total number of cells in the body and compare it to the number of bacteria in the body (http://dx.doi.org/10.1101/036103). Their discussion is quite in-depth.

There are a number of ways to calculate it, but an interesting one involved calculating mammalian cell density by a study measuring the DNA obtained from a 25 g mouse. Researchers were able to determine there were 3*109 cells in the mouse (Baserga, 1985). From this study we can simply divide to find a value for "typical" mammalian cell density--1.2*108 cells/g.

If you want to know the number of cells per mL, you'll need the density (g/mL) of the tissue you are measuring. As the comments have mentioned, this is typically around 1 g/mL and varies from person to person. There is a web page that has some tissue densities for various tissues.

Baserga, R. (1985). The Biology of Cell Reproduction (Harvard University Press).


What is refractory proteinuria? I've stumbled upon the article "Telmisartan Treatment of Refractory Proteinuria in a Dog."* What is refractory proteinuria?

*Bugbee AC1, Coleman AE, Wang A, Woolcock AD, Brown SA. J Vet Intern Med. 2014 Sep 30. doi: 10.1111/jvim.12471. [Epub ahead of print]

Proteinuria is the presence of proteins in urine. Refractory means "persistent" or "stubborn", but in medical terms it means resistant to treatment or cure.


What is difference between several mRNA RefSeq for one gene? I'm looking for mRNA RefSeq sequences for a given gene in the UCSC genome browser by searching gene name "HLA-F" in human (scroll to Refseq genes section). There are several RefSeq mRNA for the gene, what is difference between these RefSeq sequences and which one of them is what I want?

I'll walk you through the process of determining this:

Note that there are two gene names presented: HLA-F and HLA-F-AS1. The "AS" part means, "anti-sense", so it's on the opposite strand...so ignore all of the HLA-F-AS1s.
Note the associated chromosomes. chr6 is a normal chromosome, but things like chr6_cox_hap2 aren't. Instead, these are haplotype patches/chromosomes. The HLA regions are highly variable, so having only a single reference sequence ends up being problematic in many analyses, such as finding sequence variants. For your purposes you may or may not want to ignore these, it depends on what your goal is.
If you ignore the haplotype patches then you're left with 3 listings on chr6. These are the 3 isoforms of HLA-F. You end up needing to use the refseq IDs for each of these.

BTW, Gencode/Ensembl list 4 isoforms for HLA-F, rather than 3. Whenever UCSC disagrees with Gencode or Ensembl, go with Gencode or Ensembl.


If body temperature is 37°C (98.6°F), why are most people more comfortable at around 21°C (70°F)? It may be different for other people, but for me, anything above 32°C (90°F) is very uncomfortable, and my body is inclined to seek cooler temperatures.  But I would think that at 32°C, the body would have less work to do to get itself to 37°C.  So why is it not comfortable in those temperatures?

My theory is this, but I don't know if it's right:

The body's abilities for warming itself are much more sophisticated than its abilities for cooling itself (which are non-existent, possibly?). So it likes to be in an environment 20-30 degrees below optimal because it can easily handle that.  But up in the 32's and we're dangerously close to going over the optimal, and the body doesn't know how to get it back down after that, so we are inclined to seek safer temperatures.

Is it something like that?

This is due to the fact that skin is the interface where heat is lost.

Our body due to constant functioning, produces heat constantly as a by-product (due to exothermic reaction of ATP break mainly). The excess heat needs to be conducted away from the body, or it will cause a decrease in the body metabolism to prevent temperature rise.

Heat is lost mainly through the skin by:

Sweating - Through evaporation
Radiation - As heat waves (IR rays - That's why IR camera captures people at night)
Conduction - Directly through objects that touch skin
Convection - Through air circulation

When the ambient temperature rises, the heat lost through radiation, conduction, and convection drastically decreases. And often when the temperature is high, there is a accompanying rise in the relative humidity which decreases the heat loss through sweating (as the amount of water vapor is high in the atmosphere, the sweat does not evaporate, so no heat is lost).

So the heat which is not lost is felt as the "hot sensation". It relieves by stopping any activity, seeking shade or a cool place, etc... all of which increases the heat lost or decreases the heat produced.

You have to note that the temperature of skin is lower than the body temperature.

The Skin temperature is lower than the core body temperature for two reasons:

The skin acts as a medium through which the external temperature is measured - as such the skin temperature is at equilibrium with the external temperature. The brain regulates the core-body temperature in response to temperature measured through skin. If a person is exposed suddenly to cold environment, skin looses much of its heat in the form of radiation (radiation is direclty proportional to the temperature difference) this will cause perception of cold and the body starts shivering even though no actual heat loss has occured from the core body thermal load (only skin looses heat, not the body core). The brain anticipates that the core will loose its heat when exposed to such low temperature for prolonged periods and starts the warming mechanism before the actual cooling occurs such that the cooling is either prevented or minimized. This is called Anticipatory control and the temperature of skin being close to the ambient temperature within physiological limits is needed for this.
Skin is the medium (almost the only medium) through which the excessive heat produced by the body core during activity is expelled. The skin temperature is lower so that a constant gradient can be created between the body core and body surface to maintain the flow of heat. (Heat losses through urine and feces is minimal)

For more details see this question. All the answers in this question are good and will increase your understanding of what actually happens.


What don't we know about cancer? I was wondering, after decades of research what we do not know about Cancer yet as in what unanswered questions are still puzzling biologists about cancer?

I have read that cancer research, in its modern form, is a quest for biological immortality. Does this hold any truth?

I think this thread will become a jungle very fast and very soon, so I suggest you to have a look at the cancer research reviews of the last 2 years to get a grasp. Have a look at cancer hallmarks and at other important key concepts, you will most certainly answer your question yourself :) I am not a cancer researcher so I cannot comment on the topic in a detailed fashion (I work on plants), but that's what's going to happen.

In general, I'd say that what we don't know about cancer is a "common ancestor" of all types of it that will enable us to tailor a one-sized cure.


Can anyone help identify which insect is this? I know this may not be the right forum for insect identification, but I couldn't find any reliable source of information. Please bear with me

The insect was found on my front door, total length may be about 2 rice grains

You can see wings and slender legs behind the body

I live in India, if it matters.

I think this is some species of mayfly (order Ephemeroptera). There are some 3000 species in the world so I can't be more precise than that. It looks very pale and it's got a bit of a strange posture, so I'm guessing it just emerged from it's larval skin (in that case the skin should be left behind close by).


Why do chromosomes uncoil back to chromatin after cell divisions? At the telophase of meiotic and mitotic cell divisions, the chromosomes of daughter cells uncoil back to chromatin, but after interphase, it coils up again to form visible chromosomes. Why do this happen? Isn't it simpler and more convenient for the chromosomes of the cells coil up in 1 cell cycle?

It’s happening because genetic information from DNA can be read only if it’s in the chromatin form, it can’t be read from chromosomes and so the cell can’t fulfill its functions. But if it’s need to take apart cell’s genetic material, the form of chromosomes makes it easier


How does tree resin capture arthropods? In regards to a published paper of a spider about to make a meal out of a parasitic wasp (http://www.tandfonline.com/doi/abs/10.1080/08912963.2011.640399#.U1kSV14gVBU), it reminded me of a issue I've often contemplating for some time:

Isn't tree resin very slow moving, for instance maple sap has an extremely high viscosity and therefore how does the resin engulf both an arthropod, such as a spider, quick enough for it to not move away from the slowly moving amber?

I believe it is more of the fact that the organism gets stuck to the residual resin on the plant itself, and becomes encased and later fossilised in the amber.

From LiveScience.Com:

  A host of bugs, fungus and other life forms have been found trapped in amber from the time of the dinosaurs.  Bugs can become encased in amber if, while alive, they get stuck in the resin.

Although plant resin is slow-moving, the bug stands to be encased in it if it is already stuck to the tree itself, as there is a large amount of resin on the surface of the plant.  If they are crawling over the plant, or land on the surface, they would become stuck and later encased. It would be similar with other organisms as well, as plants and other organisms have been discovered preserved in this way.

  These fossils represent some of the earliest African fossil records for a variety of arthropods, including wasps, barklice, moths, beetles, a primitive ant, a rare insect called a zorapteran, and a sheet-web weaving spider. Parasitic fungi that lived on the resin-bearing trees were also found, as well as filaments of bacteria and the remains of flowering plants and ferns.


Why is propanoic acid often added to the diet of C. elegans? And what are its effects on C. elegans?

The paper is  Burnett C, Valentini S, Cabreiro F, Goss M, Somogyvári M, Piper MD, Hoddinott M, Sutphin GL, Leko V, McElwee JJ, et al.. 2011. Absence of effects of Sir2 overexpression on lifespan in C. elegans and Drosophila. Nature 477: 482–5.

Propanoic acid is toxic against many types of mold, fungi and bacteria (wiki), but same time has almost no effect to C. elegans ("fivefold less", reference). This is why propanoic acids and (more commmon) its salts are used as conservants for C.elegans cultures (as well as for other animals, like Drosophila).


Does the brain have a clock and can it be sped up? Before i start, I'm an engineer and have very limited knowledge on biology and neuroscience. My question is, does the brain have a clock like a computer where it has a set processing speed?

Clocks in CPUs can be overclocked to increase processing speed and I am wondering if the brain has something similar. The average human reaction time is around 0.25ms, Is it possible to react faster to stimuli and not only react but perceive surroundings faster than others. What I mean is while everyone perceives 1 second to be 1 second long, Is it possible to focus and stretch 1 second out mentally to 3-5 seconds and move/think/react faster as a result?

How could this theoretically be achieved too? BCI headset, Chip implant in the brain, serum or chemically?

While the brain is often compared to a computer (sometimes even rightfully), one key aspect people often overlook is that the brain is inherently analog, whereas computers are inherently digital:

All a computer really does in any single operation is to combine 0's and 1's really really fast - and the faster it's able to do that, the faster it will generally be.

A brain however, fundamentally works by combining a multitude of signal inputs with varying strength's and each single operation (encoded by a single neuron) will give output depending on the weighted sum of all inputs.
Such a 'single operation' in itself is reasonably fast, whats make a brain 'slow' is the propagation of the signal to next neuron/operation: Brains are orders of magnitudes bigger than computer chips and instead of metal/wires they use concentration gradients to propagate the electrical signals. Of course it's possible to increase the speed on individual connections between neurons by insulating them, which nature already does.

However, you can't just 'overclock' the whole brain, because there's simply not enough space to add 'full insulation' to every single connection between two neurons (of which there a lot: ~100 billion neurons, with a couple thousand connections each) and because electrical signal propagation by concentration gradients will always be slower than by wires.

I guess if would replace all neuronal connections with metal wires and some concentration gradient to power/voltage/frequency converter using nanobots, you could potentially speed up the brain - or just built cyborgs instead.

Also, not really what you asked  -  but there IS a clock in the (mammalian) brain and changing it speed, will seriously mess with your day/night or sleep rhythm.


Spermatozoa and sperms Does  spermatozoa and sperm have different meaning?If they are same why do wikipedia have 2webpages ? But most websites mention them as the same thing.I am confused .Thank you in advance

In broad way we call it sperm but the motile sperm is precisely called spermatozoon and plural form of spermatozoon is spermatozoa. A non motile male gamete is sperm but not spermatozoon but there is a term for that too its spermatium.


What is the advantage to neurons being asymmetrical? Does having a central axon and dendrites result in any advantage compared to if the neuron was symmetrical?

Asymmetry to essential to neuronal function, particularly in the peripheral nervous system. This is because the dendrites of a neuron receive synaptic potentials, which are graded and decay with distance. Dendrites are typically short such that a synaptic potential is still above threshold by the time it reaches the axon hillock (sometimes called trigger zone), so that a subsequent action potential can fire. Axons need to be long (some are up to a meter long, in the leg) to transmit signals long distances in the body. To make a neuron symmetrical, one of these qualities would have to be compromised and neuronal function would suffer as a result.

Source: Principles of Neural Science, 5th ed (2012), Kandel et al. Chapters 1-6.


Is water released when a phosphodiester bond is made between two nucleotides during DNA replication? I know that when two sugar molecules (like glucose) connect to each other, H2O is released because of the -OH and -H groups in both of the molecules. I want to know if the same thing happens when two nucleotides connect to each other during DNA replication.

No, nucleophillic attack by the activated 3'-hydroxyl on the α-phosphate of the incoming nucleoside triphosphate results in the formation of a new phosphodiester bond and release of pyrophosphate (PPi), which is subsequently hydrolyzed.

[image source]


Is hydrochloric acid suitable for pickling food? I was wondering whether it is possible to pickle food using hydrochloric acid (HCl), rather than acetic acid. I am not very familiar with the biology of the fermentation process involved in pickling and I do not know if HCl would give rise to a suitable environment. Is HCl-based pickling possible? What percentage of HCl should be used?

Short answer
Weak organic acids are more effective for food preservation then strong mineral acids, mainly because undissociated weak acids can cross the cell membrane and disrupt cell physiology from within.

Background
Natural fermented, or pickled materials are traditionally cured in a brine solution (salt, water, sometimes spices and sugar). Desirable anaerobic bacteria convert carbohydrates to acetic acid that “pickle” and preserve the food. The brine protects the vegetables from aerobic organisms. However, most contemporary pickles are not fermented at all; instead they rely upon the direct addition of acetic acid (vinegar, a product of fermentation), and usually heating for additional preservation. This way the acetic acid production through the fermentation process is simply bypassed.

So the basis of the traditional and contemporary pickling is the addition of organic acids like lactic and acetic acids. These small organic acids are known to be more effective against bacteria than inorganic mineral acids like HCl (Rode et al., 2010)

Acetic acid is a weak acid. In undissociated form, it is lipid soluble and able to rapidly diffuse through the plasma membrane (source: World Nutrition Science blog). It is thought that diffusion of acetic acid and other organic acids into the bacterial cell is the main mechanism of action behind its preservative effects. Preservation by acidification is especially effective in certain species of pH-sensitive bacteria such as E. coli and Salmonella. In contrast, strong mineral acids are nearly completely ionized in solution and ions do not pass the cell membrane's hydrophobic lipid bilayer.

The mechanism of action of small organic acids in food preservation are thought to be at least threefold:

Once diffused in the cell, organic acids will dissociate because the internal pH is near or above neutrality and thereby lower the bacteria's internal pH and disrupt cell physiology;
The anionic part of the organic acids, which cannot escape the bacteria in its dissociated form, will accumulate within the bacteria and disrupt many metabolic functions. This is one advantage of using organic weak acids like acetic acid, because they are normal constituents of the cells. Acetic acid and lactic acid for example are both intermediates in glucose metabolism. Accumulation of these metabolites will disrupt the glucose metabolism essential to the cell's survival.
Eventually, upon progressing accumulation, osmotic pressure increases become mechanically incompatible with bacterial life.

Another advantage of acetic acid is that it is a natural metabolite in human metabolism, and because it has been used in food preservation for thousands of years it is not classified as a food preservative, at least in the EU, and can be freely added to foods. Last but not least, acetic acid has a certain taste to it that may be preferable over inorganic acids.

Reference
- Rode et al., Can J Microbiol (2010); 56(9): 777-92


Histidine protonation In histidine structure , full protonation gives a structure with only the double bonded nitrogen having been protonated in the ring and not the single bonded nitrogen. Why is that?

Textbooks tend to report structures as relatively static, whereas advanced biochemistry texts explore structural tautomerism. In essence, the histidine imidazole sidecvhain may move around it's protons and electrons when pH is roughly equal to pKa. Thus, the sidechain exists as two tautomers where the two nitrogens sort of "share" the double-bond character and the proton, like so:

And it's even more accurate to depict that the double-bond character is like so:


How is achieved the loss of heat through vasodilation? I know it is the widening of blood vessels, loosing heat in this way. But is it achieved through: sweat evaporation, the increase of cardiac rhythm, the increase of respiratory/ breathing rhythm or frequent urination?

Sweat evaporation is the most correct answer you have mentioned.  Vasodilation increases blood flow, allowing for more blood to be cooled be vessels closer to the surface of the skin.  It's increasing the surface area the blood interacts with, which always allows for faster heat transfer.


Influenza infections and drug design Why is the neuraminidase used as a target for drugs against influenza virus instead of haemagglutinin? Is there some basic reason that this will make a more effective drug?

It's not that people didn't want to use hemagglutinin as a target for antivirals, it's that they haven't been able to get the antivirals through the approval process yet. There are a number of experimental inhibitors (see for example Progress of small molecular inhibitors in the development of anti-influenza virus agents) but the approval and licensing process is slow and difficult.


The use of proteins in memory creation I have very limited knowledge of how the human memory works as I think, at this time, most people do. However, I have been reading and some articles which say, and I quote the article just linked

  Memories are made by messenger RNA (mRNA) that encode β-actin protein.

Now, correct me if I'm wrong but proteins of any sort have mass. So, why following this rule of proteins being used to create the memory does our brain not grow in mass with each memory we create/ encode. And also, if our memories are encoded using proteins, why can neurodegenerative  (E.g. Alzheimer's) cannot be cured by artificial proteins in the same way we use insulin. I quote again,

  memories were merely out of reach

full article
Surely this means that, it is possible to, by using artificial proteins or possibly electrical stimuli we could recover memories. Or have I wandered off on a wrong track here? Am I correct? Or are my concepts of memory slightly wrong?

I think its important to mention that the particulars of memory storage in the brain are still being worked out.  I think what we do know about it is that memory storage depends a lot on the physical configuration of the neurons in the brain.  They move about and make new connections as they process information (and probably also when they are not processing information!).  Different regions of the brain store short vs long term memory and different sorts of memories.  They neurons themselves have a lot of internal cell physiology that can change as well - there are many different neuroreceptors that constitute the synaptic junctions.

All these things may not be a comprehensive list.  But at the basis of all these processes, the cell expresses new proteins in mRNA and these proteins are doing all this work.  beta-actin and histone de-acetylase, as mentioned in your link, are responsible for the cell rearranging itself in the cell shape and in terms of its internal transport processes and in the nucleus respectively.

I'm pretty sure that exactly what is happening here is not really well understood.  monitoring the interior of the cell is difficult.  The work where histone deacetylase is inhibited is a fresh new thought, showing that the arrangement of the chromosomes in the nucleus is involved in hiding memories.  Its still the equivalent to getting a stopped watch to start again by shaking it - there are parts there that fell into place and started ticking again, but we don't really know what the parts are doing in any detail yet.

This hints that if you were to disrupt the cells in some ways you might be able to free up memory, but its a long way from guaranteeing that any given approach will work.  I'd be surprised even if Dr Tsai's cell treatment worked even 70% of the time in her experiment.  Hypnosis or a focused meditation session might still be just as effective.  I think that its a bit too much to expect that Alzheimer's memories are completely preserved and recoverable.  In some cases probably, but categorical statements rarely hold in bioscience.

Like a lot of neuroscience, this work is suggestive, but still just progress towards a clearer understanding of these processes.


Dealing with Repetitive Bases in DNA? I have been given a project involving a plasmid that contains long stretches of Adenine (60 or 120 bases each). These PolyA stretches are interrupted by the occasional G or C.

I understand that performing PCR, cloning, DNA synthesis, mutagenesis, and sequencing on repetitive sequences is difficult. What techniques and practices should I follow to improve the accuracy when dealing with these PolyA sequences?

You can use much longer primers (up to 70bp or so), such that they span the repetitive region you want to change and some more specific sequence to anchor the primer (assuming your vector allows). If the multiple sites you want to change are within range of one another, you can order primers with 2 or more mutagenised sites - though expect your efficiency to drop. Your other option would be to do multiple rounds of mutagenesis, altering one position at a time.

I would then simply try these primers on a gradient PCR using a good enzyme like NEB's Q5. Trying to find a temperature for the correct size band will likely be key.

The real problem you're going to have though probably isn't the cloning, it'll be proving it. Homopolymer stretches are a real problem for sequencing, and the longer they get the worse it is. Automated sequencers find it difficult to tell between, for instance, 29 Adenines, and 30 adenines in a row. When your sequencing results are returned, if your sequencing is off by a base or two, it will be pretty much impossible to tell if your sequencing was wrong, or your construct was.


How much smaller is the diffusivity of a molecule in the retina as opposed to the vitreous of the eye? I'm interested in the diffusivity of macromolecules inside the mammalian retina, relative to the vitreous.

For example is the diffusion coefficient for a macromolecule (protein, 50-150 kDa for example) 10 or 100 times smaller in the retina than the vitreous?

The diffusion coefficient for such a macromolecule is about 10^(-6) cm^2/sec in the vitreous - roughly that of a protein in water. I can't seem to find any information on how much smaller it would be in the retina, a tightly packed tissue.

Unfortunately, I don't have a good, simple answer for you. The reason is that the answer may depend significantly on details of the macromolecule more than its size - like how strongly it binds to the environment.

In addition, within an environment that is more elastic than viscous, and with a very complex shape, you might expect to get various sorts of anomalous diffusion, rather than a single diffusion coefficient.

Transport in tightly confined biological spaces is complex, and still pretty controversial. A paper I found useful as a simple introduction to some of this:
Morphogen Transport - http://dev.biologists.org/content/140/8/1621


How does the microbial environment in your gut initiate? Clearly, a zygote does not harbor any microbes. As it develops, and the alimentary canal tissue is differentiated, I logically assume that there is still no microbial activity in the fetus's gut. I'm thus also assuming that the commencement of microbial activity in the intestines occurs after birth, but when, and how?

Do newborn babies just happen to ingest only certain e.g., E.coli strains? Is the gut a selective environment in which only certain E.coli strains develop?

Are there any mechanisms to ensure that harmful bacteria do not initially reside in the gut? Is a newborn's digestive tract particularly unstable and ineffective until the proper microbes are established?

The initiation of gut flora come from maternal cervical and vaginal flora (Bezirtzoglou, 1997)1. These predominantly include facultative anaerobes (e.g., Staphylococcus, Enterobacteriaceae and Streptococcus). Birth by caesarean section can cause problems because these bacteria are not passed on in the  usual manner.

Vael et al. (2011)2 found an association between early gut flora and obesity later in life

  High intestinal Bacteroides fragilis and low Staphylococcus
  concentrations in infants between the age of 3 weeks and 1 year were
  associated with a higher risk of obesity later in life.

suggesting that monitoring or alterations of gut flora might be effective in reducing rates of obesity.

Bezirtzoglou E. 1997. The intestinal microflora during the first weeks of life. Anaerobe 3:173-177.

Vael, C., Verhulst, S.L., Nelen, V., Goossens, H., Desager, K.N. 2011. Intestinal microflora and body mass index during the first three years of life: an observational study. Gut Pathog 3: 8.


Why do ion leak channels exist? I've recently learned about ion leak channels in the context of membrane potential and action potentials. Neurons have ion pumps that require energy in order to maintain the resting membrane potential and concentrations of K+ and Na+, yet the K+ and Na+ leak channels seem to directly oppose this purpose. It seems like, if left unopposed, the ions would eventually diffuse across the membrane such that there would be equal concentrations on both sides and a membrane potential of 0.
If the ion pumps spend energy and store it in an electrochemical gradient, don't leak channels let that potential energy dissipate back across the membrane? Wouldn't it be more efficient to tightly seal ions into their respective sides until the energy is released during action potential?
Am I missing:

An important function of leak channels directly involved in maintaining membrane potential or causing action potentials?
Some broader evolutionary purpose of leak channels that help ensure a cell's health in other ways?

Additional clarification requested: Would it be correct to say that leak channels function in facilitating changes in membrane potential (and return to "baseline") until the threshold, at which point the voltage-gated ion channels allow for a much larger influx/efflux?

Check the parameters that go into the Goldman equation... it shows that permeability of ions is as important as their concentrations. If the permeability is zero, there is no potential. Because other conductances are mostly closed at rest, the leak channels are almost entirely responsible for the resting membrane potential (there is a minor component, a couple mV, supplied by the sodium-potassium pump itself, that is missed by the Goldman equation). If there were no leak channels, there would be effectively no resting potential, and certainly no useful one.
Additionally, there would be no return to "baseline" after a signalling event.
Leak channels are entirely integral to nervous system functioning (and the function of other excitable cells, including muscles and immune cells) - a system without them would be nothing at all like what we actually observe in any biological nervous system. The membrane potential massively amplifies the concentration differences into an electrical signal, such that large changes in voltage occur merely by opening and closing channels: very few ions need to move for this to happen, making a very efficient signalling system, requiring only the maintenance of ion concentration gradients (which change very slowly).
I would say it's correct to say that the role of leak channels is quite diminished during an action potential, since voltage-gated conductances ultimately overwhelm the leak conductance. You can see this from the Goldman equation, too. But they are quite important in setting threshold itself, and in returning to rest after an action potential. However, even during an action potential there is very little actual ion flux. Electrical forces are very strong, so not many ions need to move (see again the answer I linked above).


Phenotypes caused by mutations in mitochondrial DNA? Will mutations in mitochondrial DNA necessarily affect phenotypes?

I have some cursory knowledge of serial endosymbiotic cell theory, and find it difficult to consider that the DNA of the former cell — now organelle — would affect anything outside of the mitochondrion itself, although I can imagine the alteration of mitochondrial processes having an indirect effect on non-mitochondrial processes associated with certain phenotypes.

Assuming that I have understood (and reworded) the question correctly, I find the logic strange. It is the disruption of or change in process that produces phenotypic changes following a mutation in the gene, so if the process is critical for life — like those occurring in the mitochondrion are — what difference does it make where it is encoded?

Perhaps the problem is the endosymbiotic theory of mitochondrial origin. Yes, most of us believe that, but, whatever it was millions of years ago, the mitochondrion is an integral part of modern eukaryotes. Extensive changes have occurred, the most relevant to clearing up this way of thinking is the fact that most human mitochondrial genes are now encoded in the nucleus. Would you these genes would be any more or less likely to produce phenotypes on mutation? Hardly.

Now to the facts. There are certainly mutations in mitochondrial genes that are associated with disease in man and hence produce phenotypes. Some are listed in the table below, taken from a review by Taylor and Turnbull in 2004.

An account of Mitochondrial DNA and Mitochondrial Diseases written for less advanced audiences is this Scitable article.


What type of insect in this? Can anyone tell what of kind of insect is in this image ? They have been showing up in my room for the past month; never happened before that. The room is generally hot during daytime.

Thanks

Brown marmorated stink bug (Halyomorpha halys):

Source: Brown marmorated stink bug (wikipedia)


Getting goosebumps at will I can get goosebumps at will, regardless of the environment. Its mostly visible on my arms, and I can feel it on my head. It requires some level of concentration to achieve this.

My questions are : what biological mechanisms are involved in doing this ? Is it common ? Is it useful ?

Interesting!  I haven't seen anyone able to do this deliberately.

Goose bumps are caused by the tiny muscles at the base of hair follicles contracting, and the hair stands up.  The skin around it puckers.  It's mediated by the sympathetic nervous system (the "fight-or-flight" aspect of the system).  This is how animals' fur stands up when afraid or upset (think of a scared cat).

It's called the pilomotor reflex.  It also helps them keep warm (fur insulates) - so it happens when we're cold too.  But since we have so few hairs, it's not very useful to us. It's more of a vestigial reflex than anything.

It happens for other reasons too.  See the wikipedia article, it's a good place to start.  For more info, look at this article or a medical textbook.

If you can do it at will, you likely are in tune fairly well with your sympathetic nervous system.  That's excellent.  You may be able to make minor alterations in your pulse and blood pressure through breathing regulation - check out the concept of biofeedback.  It is a way to help manage stress, keep yourself calm in terrible situations, manage anxiety or panic disorders, anger management.....

Being able to use physical self-awareness to affect physiological changes takes practice to develop as a skill.  You've got a great start!


Are there any generic (not dependent on symptoms) ways to find parasite infections? Are there any generic ways to determine if a person is infected with a parasite?

With "generic ways" I mean ways that do not rely on symptoms caused by a particular parasite. Also I am mainly concerned by parasites that are too large for the immune system to completely handle on its own (such as worms).

For example, can parasites be seen in x-rays, MRI scans, or through some body fluid samples?

The first thing that comes to mind would be eosinophils numeration. It is a specific type of white blood cell that handles parasitic infections. So in most cases, a blood sample would show an increase in this type of cell.


What is a protective epitope? What is a protective epitope? An epitope is basically a part of antigen. So does it mean that when the epitope combines with an antibody, it helps in the functioning of the antibody instead of going against it?

Lets define the nomenclature first: An antigen is a large structure (protein, virus, bacteria and so an) which is recognized by the immune system as foreign. The word antigen derives from the abbreviation ANTIbody GENerator. Exposure of our immune system to an antigen results in an immune response and the generation of many antibodies.

An epitope is a small part of an antigen - typically these are small structural elements or small peptides (8-11 amino acids in length) which are recognized by the binding site of an antibody. See the picture below (from here):

Here the antigen is the albumin protein. On the surface you can see 8 different epitopes which lead to the generation of 8 highly specific antibodies against the epitopes (antikörper is the german word for antibody). Every antibodies is highly specific for its epitope and will recognize no other epitope and helps raising an immune response against it. What happens after an antibody bound to its epitope can be read here.

Antibodies directed against a protective epitope are directed against (highly) conserved structures of the antigen. For example the recognize a highly conserved structure of a virus which means that even when this virus mutates (like influenza does) it will still recognize the conserved epitope and give protection against this virus (or better: antigen).


Are prions an important driver in evolution? I understand that prions have been implicated in the passing on of epigentic information[1]. Are prions thought to play a significant role in the evolution of organisms?

 Alberti S, Halfmann R, King O, Kapila A, Lindquist S. 2009. A systematic survey identifies prions and illuminates sequence features of prionogenic proteins. Cell 137: 146–58.

It is proposed that prions are a good mechanism for "testing" phenotypic variation.

There are many identified proteins with prion-determining domains (PrD) in the yeast genome that can spontaneously switch between conformations with some low probability (eg: check SUP35 for one example, and [1] for a good overview of more). The theory is that:

the low probability of switching from non-prion to prion state allows for many more mutations and variations to accumulate -- generating greater genetic diversity than in standard expressed gene variability where most mutations are silent or detrimental
the prions provide a ready form of non-permanent inheritability that can be "trialed" by offspring and others in a colony of organisms -- this can be especially beneficial during say temporary changes in environment
if the prion phenotype is widely successful, selective pressure can easily mutate it into a more permanent fixture in the genome.

Check out the excellent paper published just last week in Nature exploring this this topic [2]. To give a sense of just how evolutionarily-advantageous prions can be, in the author's experiments and analysis they note that 40% of the prion traits they analyzed were beneficial to growth (eg:  in the paper strain UCD939 gains additional resistance to acidic conditions from the prion [PSI+]).

Assuming these hypothesis, prions would thus play a significant role in the evolution and variability of organisms.

[1] Crow, et. al. 2011. doi:10.1016/j.semcdb.2011.03.003

[2] Halfmann, et. al. 2012. doi:10.1038/nature10875


Why is the Red Fox colored bright orange? They're not poisonous or anything, so it can't be aposematism.  As far as I know it doesn't come from diet like the flamingo.  They're not apex predators, so they can't get away with it (like tigers), and honestly it seems like a big risk factor given how many species prey upon them.  As well as something that would make hunting more difficult for them.  I understand they prefer dense brush, and I think hunting during low light hours, but orange against green is about as starkly contrasting as it gets.  So does that just leave sexual selection?  One of their sexes thinks it's pretty, basically?  Or is there some other reason for it, one that might have something to do with the rest of the odd coloring?

Their fur colour is actually a pretty good camouflage


Gene APOA2 SNP rs5082 alleles are A or G, but papers describe it with CC and TT? rs5082 is a SNP in the APOA2 gene. It is associated with obesity and heart disease risk.

According to this article the alleles can be A or G
https://www.ncbi.nlm.nih.gov/snp/rs5082#frequency_tab

Why does this article only discuss CC or TT?  Where is the A or G?
https://academic.oup.com/ajcn/article/108/1/188/5036568

The rsID letters are assigned based on the genome being the default "forward" direction while the researchers on that gene think of the nucleotides of the context of the transcript, (or in this case the promotor sequence) which runs backwards.


Is there evolution in humans since the first homo sapiens sapiens Has the human species changed since first defined as homo sapiens sapiens?

I'm asking this question partly because I'm wondering how we might evolve next.

We continue to evolve all the time: http://www.npr.org/2013/09/27/226837803/modern-humans-still-evolving-and-faster-than-ever

  For those who think the forces of natural selection no longer apply to modern humans, paleoanthropologist John Hawks would urge you to reconsider. In recent times — that's 10 to 20 thousand years, for a paleoanthropologist — Hawks says we've picked up genetic variations in skin color, and other traits that allow us to break down starch and digest cheese.

Homo sapiens sapiens is over 100,000 years old and we have changed in many ways since then, as noted in the above NPR article!

I'm not sure we can say there is a "first" homo sapiens sapiens -- the change from one species to another is gradual.  You may know that mixing red and blue gives purple, but at what points do we officially have red, purple, or blue when mixing different levels of red and blue?


Why are low throughput methods more trustable for protein interaction? I read that protein interactions found using high throughput methods are less trustable than those found using low throughput methods.

For example, searching for interaction of BRCA2 on BioGRID, I got this result.

So, we won't be sure about the interaction of BRCA2 with SIRT1 as it has been found with a high throughput method.

My question: Could you give me a very simple explanation of what is the meaning of high and low throughput techniques ? (I have a vague idea reading it on web but I am not satisfied with my understanding.) Why is high throughput not reliable in this case?

One reason I can think is that they involve mostly in vitro studies.

This article is a bad example, it has been retracted. See here.
But this doesn't matter for the methods.
This is usually done by so called "genome wide association studies". There you compare the regulation of your group of interest with a "normal" group to find genes which are differently expressed. This is something we did: We overexpressed a transcription factor in a cell line and compared it to the untransfected cell line, which doesn't have this factor. The comparision brings up differently expressed genes. This is either done with microarrays or today more like by ChIP-sequencing (let me know, if you want to know more, I can go into the details).

When you analyze such data, you first cut-off all data, which is below a certain threshold to be sure, that you reduce the number of false positives. A low threshold for the recognition of changes means that you are more likely to have false positive genes in your final list. This might happen due to changes in the cell or the conditions, secondary effects and so on. And you will also have signals, which appear statistically and which are false positive.

If you choose your threshold too high, you will reduce the number of false positives, but on the downside you will also generate false negatives, since you refuse genes which only have a relatively low change but are real. The balance between this is not always easy. As a rule of thumb usually everything which changes at least twofold in expression is used (unless you control better).

Even when filtered, the output of the experiment will still contain some false positives. Then you will also record some secondary effects, meaning that you gene of interest regulates a second, which regulates a third. Since both will come up in the analysis, it will look like that the third gene is regulated by the first (and not the second, as it would be correct). And these are the reasons why usually every intereaction between two genes (or better: Between a protein and a gene when talking about a transcription factor or two proteins) needs to be verified in the wet lab. And this is work, which can be pretty hard.


Why do eyes feel overwhelmed by light when we wake up? Many people (I saw a 9gag post 3 days ago and couldn't find it, I'll edit later if I do find it)experience dry/hurting/overwhelmed eyes when they wake up because the light feels too bright. I happen to "suffer" the same. Why this occurs? Is it because the eyes are dry, or because the pupils are contracted, or why else?

The reflex responsible for the phenomenon you described is called the Pupillary Light Reflex. According to the Textbook of Medical Physiology, Guyton & Hall, Elsevier, 11th edition, 2005, p. 649 (reworded by me in order to avoid direct copying):

When light reaches the retina of the eye, the optic nerves are stimulated. Most of the generated nerve impulses participate in the creation of an image in the brain etc., but a few reach an area in the brain called the pretectal nuclei. These nuclei then generate secondary impulses to another nucleus called Edinger-Westphal nucleus, which sends a signal through parasympathetic nerves to constrict the sphincter of the iris.
Conversely, in darkness, the reflex is inhibited, which results in dilation of the pupil.

To summarize, in darkness (either when you are in a dark room with your eyes open, or when you are anywhere with your eyes closed) the pupil will be dilated since stimulation by light does not occur. When stepping into the light or when opening your eyes, light immediately stimulates the optic nerve, which causes a signaling cascade that results in constriction of the pupil to a certain size, depending on the amount of light present (primarily to protect it from exposure to too much light).

Naturally, you can see this constriction happening every time you open your eyes in front of the mirror (focus on the pupil). It was also depicted rather accurately in the end of Disney's excellent rendition of the Hunchback of Notre Dame (skip to 1:22).


Spinal cord injury bypass When the spinal cord is damaged, the connection between the brain and some part of the body may be lost.

To restore this connection, researches are considering either:

Repairing the damaged area so that the spinal cord works again.
Bypassing the spinal cord by connecting the brain directly to the affected part of the body.  This is done by implants in the brain connected directly to electrodes in the muscles creating a new circuit in parallel.

My question is has there been any attempt to bypass only the damaged part of the spinal cord?  To create a bridge over the damaged tissue?

Interesting question!

There has been at least one study that bypassed a spinal lesion site with autografted neuronal tissue (Tadie et al., 2004 - doi:10.1089/089771502320317069). The study participant regained voluntary motor skills 8 months after bypass surgery. The surgery involved the implantation of nerve autografts between the rostral spinal ventral horn and the caudal ventral roots. Regain of motor function was observed after the patient had been paralyzed for 3 years.


Viruses. Alive or Not? I saw this fascinating article today about how HIV moves through a mouse host in real time.

http://www.engadget.com/2015/10/02/watch-hiv-spread-through-mouse-in-real-time/#continued

It's common to hear a virus' activity described in the way the article does: with intent.

I have a hard time understanding this. Something is considered alive when it has a metabolism, takes in nutrients and expels waist.  It has to have some kind of respiratory system and it's own reproductive mechanism. Although locomotion is optional, most forms of life have some form of getting around.  Some plants are able to move somehow...

Viruses have no sensing organs and no method of locomotion.  They cannot smell or see or move on their own.  This means they have to be carried inside a cell or if free floating in a host's fluids, rely on random motions to get about.

In order to invade, as far as I understand this; they must essentially wait until they come into physical contact with a compatible target.  At this point, their protrusions (I call them "keys") attach to a host cells "door" and they then inject their DNA.

Most (or all?) cells use Mitochondria for "power" so they can do things - like metabolize and reproduce.  I've never seen a diagram of a virus that shows where it get's it's energy to power the 'injection' part of it's 'life cycle'.

How is this done?

In the mouse video, the HIV virus looks like it has a "plan" and that it knows how to select which initial cells to invade and then how to pick a good method of remaining hidden.  How can this be when they have no sense organs?  How can they "know" of other virus particles are being successfully attacked by the host?

This is incredible and incredibly complex.

I'm not a medical professional. I'm just a fascinated by-stander.

When we're thinking about cells that get infected with viruses, we have a two of subgroups to consider, often denoted susceptible or permissive. In essence, a cell which a virus is meant to successfully infect must not only possess a receptor to that virus for adhesion, but also the ability to replicate the virus (so it needs the machinery!). So these cells must be susceptible and permissive!

After adhesion you end up with an entry phase, this differs by virus, but you can essentially break it down into endocytosis, membrane fusion, or injection. You can get an idea of injection from something like lambda phage, outlined here. Enveloped viruses can fuse with the host membranes because these envelopes are often derived from ER, golgi network, or another plasma membrane. (Remember, viruses are essentially coding 3 basic sets of genes: for structure, replication and binding. It can't just code for everything it needs, either, so viruses hijack the host cell machinery to replicate.) Naked viruses, those that are just a protein coat and nucleic acid in essence, enter the cell through endocytosis and end up uncoating in a vesicle. And to stress it again, if the cell didn't have a receptor for the virus, it probably didn't get it. Portal of entry does make a difference, but I'm trying to keep it simple for our purposes!

Being said, when we're considering most viruses, membrane fusion and endocytosis aren't really using any energy but the host cell's, right? And then when the virus gets in there, they continue to use the host's resources becauase they really didn't bring a lot of baggage, either!

On the matter of "knowing" what they're doing, viral particles really don't do anything themselves. What I'd argue is that they've evolved methods of becoming particularly good at being viruses, many of which make it seem like they're making conscious choices, but suppose the following: Most of the time, viruses are probably just reproducing in such great numbers that it's just faster to get lucky and produce a strain with a better overall fitness.

Mind you, this whole time your body is attempting to fight off the virus, as in HIV, for example, eukaryotic cells have methods at each stage of attempting to protect themselves,

Source: Cellular Self-Defense: How Cell-Autonomous Immunity Protects Against Pathogens

You also have NK cells and macrophages responding to IFN produced by cells distressed by viruses, and eventually the presentation of viral antigens which result in effector T cells and antibodies unique to the virus in question. Another article here shows some methods by which some inhibitors of HIV infection can be evaded by the virus, as well, and just as likely, you also see that HIV has mechanisms of evading innate/active immunity as well! For example, if your antibodies recognize a viral capsid protein, what do they have to bind to if there's a lipid membrane in the way, as in HIV? What if the receptor composition changes?

In closing, viruses are obligate intracellular parasites. They need you to survive, but their objective is to replicate, so sometimes they do end up killing their host, but they aren't really communicating with each other in a fashion like: "I wonder how those other viruses are doing?" They really don't have a means of responding like that, so the end goal? Just keep moving from host to host and keep replicating, in the most basic sense.


Does one neurotransmitter travel all the way through the nervous system? Nerve impulses of course go really fast, but the neurotransmitters have to travel through millions of nerves, so how can it go that fast?

Is it a sort of relay with lots of neurotransmitters taking over at each nerve cell, or do the neurotransmitters go all the way from A to B?

You've got a few things mixed up here:

A signal may travel down a pathway, passing through several neurons (e.g. around 4-8). However, this signal is not always in the same form: From one end of a neuron to the other, it is merely an electric potential which travels down the neuron's cell membrane (from the dendrite to the axon hillock, where the cell decides whether to carry the signal on; if yes, a new potential is sparked to travel down the axon).

When the potential reaches the end of a neuron, i.e. an axon terminal, it causes exocytosis of neurotransmitter. The signal has become chemical now. This diffuses through the synaptic cleft to the next neuron, where it acts on ion channels in the membrane to cause a new electric potential.

So the actual distance a neurotransmitter travels is only the distance between the two membranes at the synapse, i.e. the synaptic cleft. This is only about 20-40 nm wide, so it's fairly rapid :)


Part of a fish outside the intestinal sac on the back? I saw an expert Japanese chef fillet a mackerel (Scomber scombrus). He cut off the head and the whole intestinal sac came out with it as a single unit. Then he took the knife and scraped something from inside on the back. The object(s) were dark and bloody. Would those have been the kidneys?

You can see the video here: https://www.youtube.com/watch?v=udTHiRg34KI. The moment is at 2:20.

Yes, those are the kidneys. They're quite different from mammalian kidneys.
This is a picture highlighting the kidneys in a salmon dissection from the Pacific Streamkeepers Federation (http://www.pskf.ca/sd/). A very different fish, but similar enough to show the kidneys.

You can also see a dissection of the fish urogenital system here: http://necropsymanual.net/en/teleosts-anatomy/excretory-and-osmo-regulatory-system/, though I can't tell what fish species they're dissecting.


Can prawns be classified as fish, or is their position ambiguous? Today a zoologist told me that prawns and fish are very similar, but zoologists/taxonomists have put them in different categories because their distinction is unclear (like hydrogen in the periodic table). This completely bewildered me, as I know prawn and fish are in different classes because there is no similarity between them. I have no connection with biology now but studied it in high school — but even then, I could not believe it. Can someone please elaborate on this?

Introduction to phylogeny

What makes that two species being closely related or not has nothing to do with whether they look a like or whether they live in similar environment. It has to do with their evolutionary history. Evolutionary history used to be inferred from phenotypic traits ('phenotype'≈'how an individual looks like') but today it is most often inferred from genetic data.

First you should have a look at this recent answer to get a short introduction to phylogeny.

Phylogeny of animals

Here is a basic tree of all animals

From wikipedia

  A fish is any member of a group of organisms that consist of all gill-bearing aquatic craniate animals.

Craniates are Chordates, therefore fishes are chordates. You can have a look at the position of chordates on the above graph. Note that all mammals, birds, reptiles and others are also chordates. Note that fishes do not represent a monophyletic group (if you don't understand the term 'monophyletic', then you need to read the linked post above).

A prawn is a crustacean. Crustacean (incl. prawns, shrimp, crabs, ...) and Hexapoda together form a monophyletic group. Crustaceans are arthropods and are therefore much more closely related to insects, molluscs and spiders than to any lineage that we would call fish. Here is a tree of arthropods (and related clades). See the position of arthropods in the above tree. You can also have a look at the position of crustaceans within arthropods below. Please note that the tree is a bit outdated a present crustaceans as being monophyletic which is wrong (according @har-wradim, see comment below).

Your discussion with your friend

There is no doubt about the phylogenetic position of crustaceans as being part of arthropods and therefore not being very closely related to fishes. I think you misunderstood what your friend tried to tell you.

A note on developmental biology

All multicellular animals, undergo a grastrulation during development during whihc a hole is formed called the blastopore. In all deuterostomia (incl. fishes) the blastopore becomes the anus, while in prostomia (sister clade to deuterosomia which includes arthropods), the blastopore becomes the mouth. This a very major difference in how these different clades develop from a single cell (after fertilization) to a multicellular adult.

Online ressources

If you want to have a look at the tree of life, you can find great ressources on this post.


Understanding Enzyme saturation curve From the above picture it can be seen that, in the region "B" the activity of enzyme is not proportional to the substrate concentration.

Why don't we achieve enzyme saturation linearly? Why do we go through that curved phase( region B )?

Why don't all enzyme gets saturated at a point?

Your image is not correct.

According to Lehninger (2000):

  At relatively low concentrations of substrate, V0 increases almost linearly with an increase in [S]. At higher substrate concentrations, V0 increases by smaller and smaller amounts in response to increases in [S]. Finally, a point is reached beyond which increases in V0 are vanishingly small as [S] increases. This plateau-like V0 region is close to the maximum velocity, Vmax. (emphasis mine)

This is the image that comes after that paragraph:

FIGURE 6–11 Effect of substrate concentration on the initial velocity of an enzyme-catalyzed reaction. Vmax is extrapolated from the plot, because V0 approaches but never quite reaches Vmax. The substrate concentration at which V0 is half maximal is Km, the Michaelis constant.

Thus, regarding your questions ("Why don't we achieve enzyme saturation linearly? Why do we go through that curved phase( region B )?"), the answer is: there is no line, it's all curved.

Source:

Lehninger, A., Nelson, D. and Cox, M. (2000). Principles of biochemistry. New York: Worth Publishers.


What kind of tree could this be? This may be a strange question, but does anyone know what kind of tree this could be?

I know, it's just a comic, but these trees, at “walking distance” within that comic are easily identifiable as Grandidier's Baobabs:

(That might indicate, of course, that the above tree also occurs on Madagascar, but it's a comic, so all bets are off.  And yes, we know, there are no squirrels on Madagascar.)

It reminds me of the smooth-barked Australian gum trees / eucalyptus, like a salmon gum, ghost gum, etc.

Although there are no squirrels in Australia :)

This photo of a Salmon Gum is from http://www.fpc.wa.gov.au/content_migration/plantations/species/arid/salmon_gum.aspx


Resources for interesting facts about biology Are there resources for interesting or fun facts about biology, for example:

fastest animal/bird/insect
largest organ in human body
largest virus
largest genome
largest de novo synthesized genome
largest protein
longest experiment done so far
most expensive experiment done so far
biggest discovery by luck
...

You get the idea. It would be nice if these is a curated "database" for all these interesting facts that might be fascinating to lay people as well.

Whether you find the content interesting or not I can't say, but you might want to check out the BioNumbers database. It has a category for "Amazing bionumbers" and a "BioNumber of the Month" section.


How do ants know where they are going without eyes? I know that ants have some sense of direction, but what is the physiology behind this sense?

Well, first off, they have eyes, so there's that.

However, a lot of what ants wish to achieve can be done through a combination of a random walk and chemical trails.

When ants are exploring their surroundings, they are essentially wandering about without much in terms of a sense of purpose; laying down a chemical signature as they go.

When they find something interesting, like food, they use their own chemical trail to backtrack, laying down a new chemical trail indicating the nature of what they have discovered, making a kind of smell-road from the hill to the point of interest.

Any ants that subsequently come across this trail follow it, and subsequently join in transporting the food back to the hill.

An interesting implication of this behaviour is the antmill, wherein an ant will lose their trail, and revert to following a nearby ant. If the ant they follow are following them to begin with, this can lead to a spiral of ants that can reach miles in diameter, consisting of confused ants walking until they die from exhaustion.


What is the reason behind high resting membrane potential of pacemaker cells? Pacemaker cells have high resting membrane potentials of -50 to -40 mV, whereas normal cells have their resting membrane potential around -70 mV. Which ions, and what kind of channels are responsible for the high resting potential of pacemaker cells?

The pacemaker potential is interesting (to a biologist) as it involves your typical Na/K channels, Ca channel, as well as a funny current (If) or alternatively called hyperpolarization-activated current.

  The funny current is a mixed sodium-potassium current that activates
  upon hyperpolarization at voltages in the diastolic range (normally
  from -60/-70 mV to -40 mV). When at the end of a SA potential the
  membrane repolarizes below the If threshold (about -40/-50 mV), the
  funny current is activated and supplies inward current, which is
  responsible for starting the diastolic depolarization phase (DD); by
  this mechanism, the funny current controls the rate of spontaneous
  activity of sinoatrial myocytes, hence the cardiac rate.

  Pacemaker activity (or spontaneous electrical activity) of the
  sino-atrial node is based on the presence of a special phase called
  the diastolic depolarization during the action potential, in which
  cells depolarize spontaneously towards the AP threshold. Animal
  studies (mostly conducted on rabbit heart) have identified that this
  net inward current during the diastolic depolarization phase is the
  result of a complex interaction of multiple inwardly and outwardly
  directed ion currents....

Verkerk, Arie O., Antoni CG van Ginneken, and Ronald Wilders. "Pacemaker activity of the human sinoatrial node: role of the hyperpolarization-activated current, I f." International journal of cardiology 132.3 (2009): 318-336.

Also this

  The SAN is a complex tissue with regional differences in morphological
  and electrical properties.Animal studies have revealed that
  pacemaking in SAN cells follows from diastolic depolarization driven
  by a net inward current, which results from an interaction of multiple
  ion currents. Inward currents are activated during diastole:
  hyperpolarization-activated pacemaker current (If), background Na+
  current (Ib,Na), sustained inward current (Ist), T- and L-type Ca2+
  currents (ICa,T and ICa,L, respectively), and Ca2+-release activated
  Na+–Ca2+ exchange current (INCX). Conversely, outward currents are
  deactivated: rapid delayed rectifier K+ current (IKr) and slow delayed
  rectifier K+ current (IKs). The relative contributions of these
  currents to diastolic depolarization are a matter of debate.

Verkerk, Arie O., et al. "Pacemaker current (If) in the human sinoatrial node." European heart journal 28.20 (2007): 2472-2478.

Might I suggest you read up on the papers mentioned above?

You might also be interested in this:

Noma, Akinori. "Ionic mechanisms of the cardiac pacemaker potential." Japanese heart journal 37.5 (1996): 673-682.


Which diagram correctly describe an effect of tar entering lungs? Which flow diagram correctly describes the effect of tar entering lungs?

Tar is a cause of Chronic obstructive pulmonary disease (COPD) which includes both chronic bronchitis and emphysema and it is also a carcinogen, too. So, I think that A, B, and C would be correct answers, but the solution is A. Why B and C are incorrect?

Thank you very much!

COPD is not caused by an infection (which would require a pathogen) but by the inflammation reaction the body triggers because of the tar particles. Thus the statement "mucus accumulated causing infection" does not correctly describe the effect of tar on the lung. Consequently, B and C are incorrect.


Ancestral Allele explanation I'm having some trouble understanding the concept of ancestral allele. What exactly does it mean? What does it have to do with Identity by descent/state? What does it have to do(if anything) with SNP's? Also, how is the concept useful in genetics/evolution? I've tried reading these up on various websites, but I'm not satisfied with my understanding yet.

SNP

Let's start with the definition that has nothing to do with the rest of the question :). A Single-Nucleotide-Polymorphism (SNP) is a kind of genetic variation that you find in population. This genetic variation is defined as a variation caused by only one single nucleotide (as its name indicates it). For example if you have in the populations the two following variants at the same locus: AGCCGT and AGCTGT, then you have a SNP at the position of the C and T. This type of variation is very common. We estimate that there are about 10 millions SNPs in the human genome. We often use these SNPs as genetic markers.

Ancestral vs derived alleles

An ancestral allele or an ancestral trait (depending on whether you look at the phenotype or a t the genotype) is the trait/allele that was carried by the common ancestor of the taxon you consider. For example: as you may know the taxon Reptilia includes lizards, snakes, turtles, birds, mammals and some other lineages. In the taxon Reptilia, the scales is the ancestral state (still exist in lizards for example) and the hairs and feathers are derived states. Usually, the ancestral state is the one that carried by the most basal lineages.

Identity by state (IBS) and Identity by descent (IBD)

If two sequences are exactly identical, then we say that they are identical by state (IBS). Such identity can occur either through convergent evolution or through common ancestry.

To understand the concept of "identical by descent" (IBD) it is important to understand the concept of coalescence. A coalescent event is, when looking backward in time, an event where two sequences were actually the same sequence. Often IBD is defined relatively to a given threshold in time. If the coalescent event occurs after this event then the two sequences are not IBD. If the two sequences coalesce before this time threshold and that the two sequences are still IBS, then the two sequences are IBD

Bridging everything together

So, if you look at sequences in a given group of lineages and see that they are all exactly the same then they are identical by state. If you know that all these sequences come from a common ancestor and even they all coalesce to a single individual in the common ancestor, then all sequences are identical by descent. But some mutations may have occurred since the last common ancestor resulting in some SNPs, then all the sequences are not IBS anymore and therefore not IBD either. You can use such sequence variance in order to create a phylogeny for example.

Hope that helps.


Plant cell question in age 12 science test Part II I'm a parent and I think the teacher had been a bit harsh with marking most of these questions but can someone help me answer the very last question on the paper please (where someone has written SP against it). Is the answer mitochondria?

So, to go through the question in total:

(a) Part A nucleus is correct, but Part B ist the cytosol/cytoplasm, as the line does not stop at the border, but goes through it and ends in the gray part of the cell.

(b) For part C, it is the same problem as in your first question. Yes, the picture may be a plant cell, however, upon this drawing one cannot differentiate a mitochondrium from a chloroplast. In my opinion, a good teacher should have marked this answer as correct, even if he/she wanted to hear the other possibility. Part D is correct.

(c) 'Photosynthesis takes place here': Photosynthesis takes place in the chloroplasts. Mitochondria would have been correct, if the teacher would have asked for the respiratory chain or for the often in school simplified powerhouses of the cell.
'Many of the cell's chemical reactions take place here': I think, the teacher wanted to hear the cytosol as answer.


Absorption of Topical Magnesium Can Magnesium be absorbed through the skin? Some athletes believe that Homeopathic magnesium lotions can reduce muscle pain. I've tried this and it doesn't work nor can I see how it can.

Homeopathic magnesium lotions don't* contain magnesium, so it seems a little irrelevant whether or not magnesium can be absorbed through the skin. However, magnesium ions can definitely be absorbed through the skin. There's no reason why that should reduce muscle pain(especially because ions would disperse throughout the bloodstream etc etc), but magnesium can be absorbed through the skin fairly efficiently.

*Footnote: they do, but not on purpose. If correctly prepared they would contain zero atoms of magnesium(depending on what 'strength' they are), but that kind of purity is impossible.


What is the prehistory of amino acids in cells? As a followup to Why 20 amino acids instead of 64? and What is the smallest number of amino acids required for life?, I am trying to understand the prehistory of amino acids in cells.

All living cells now use 20 (or 22 if you include selenocysteine and pyrrolysine) amino acids. Perhaps in the past there were fewer amino acids used in cells, especially if the theory of a 2-nucleotide codon is to be believed.

Is there any theory as to the order in which these amino acids were incorporated into cells?

This paper (by Akanuma, Kigawi, Yokoyama, "Combinatorial mutagenesis to restrict amino acid usage in an enzyme to a reduced set", http://www.pnas.org/content/99/21/13549.full) suggest that the full complement of 20 amino acids are not strictly necessary by reducing the number of amino acids in a certain enzyme to 13, yet still retain functionality.

Edward N. Trifonov is a professor at the Institute of evolution at University of Haifa, Israel. One of the main research topics in his group is the reconstruction of the origins of life. In one of his papers, The triplet Code From First Principles, he proposes the the chronological appearance of the 20 amino acids. There are a lot of hypothesis and testable predictions, among which is the theory of S. Miller that some biological compounds have been abiotically produced in the atmosphere. This prediction has been confirmed by imitation experiments, yielding ten different amino acids, as glycine and alanine being the prevalent ones.

The author tries to predict the chronological order in which the 20 amino acids appeared by taking into account various criteria (studies, hypothesis and viewpoints) that propose some order, as each one of them contributes to the consensus order to a certain extent. This contribution is described in the form of rank. He compiles a list of 60 rankings of 60 different criteria to derive the consensus order. Some of the criteria are:

  N1’. Criteria based on various evaluations of complexity of amino-acids. N1, N34, N35,
  N37 – as in (5), and N44 (6). G, A, S, P, V, C, D, T, N, L, K, I, E, (MQ), H, R, F, Y, W

  N2’. Criteria based on evolution of amino-acyl-tRNA synthetases. N2, N7 (5).
  (AG), (DFHKNPST), (CEILMQRV), (WY)

  N4’. Criteria based on amino-acid compositions of various sets of presumably ancient
  proteins. N4, N26 (5), N41 (7), N45 (8), N47 (9), N48 (10), and N58 (11).

The first ten (earliest) consensus amino acids are the same as in Millers’s experiments. The amino acids appeared last have their respective codons borrowed from already existing ones. The derived consensus order is G, A, D, V, P, S, E, (L, T), R, (I, Q, N), H, K, C, F, Y, M, W.

The author also proposes a reconstruction of the chronological order in which the 64 codons had appeared.


Statistics on energy consumption breakdown per biological functions across organisms? Are there any statistics available on how much energy organisms use for each biological functions (i.e. something similar to the line of "Bacteria spend X% of energy on information processing, Y% for tissue maintenance and Z% for locomotion. Mammals spend..."). I'm particularly interested on how much energy is spent on information processing.

I vaguely remember seeing such stats somewhere, but for the love of god I can't remember where...

This is not a proper answer. Bear with me. I'm in a hurry; will edit the answer to a decent form when I find time.

From the abstract of this paper:

  Of the 80% of oxygen consumption coupled to ATP synthesis,
  approximately 25-30% is used by protein synthesis, 19-28% by the
  Na+-K+-ATPase, 4-8% by the Ca2+-ATPase, 2-8% by the actinomyosin
  ATPase, 7-10% by gluconeogenesis, and 3% by ureagenesis, with mRNA
  synthesis and substrate cycling also making significant contributions.

Also check this out.


Regarding kidney transplant One of the options is correct

Kidney can be taken from a dying person who has the
a) cessation of neurological function only
b) cessation of cardiac function only
c) cessation of respiratory function only
d) cessation of kidney function only

I think that answer should be b. as if heart stops working then the person is definitely dead. but m not sure if on the cessation of neurological/respiratory function, one still has chance of revivial. Moreover answer is given as A. I don't know how. Could it be that on cessation of cardiac/respiratory function, kidney gets damaged while not so in case of neurological dysfunction?

There are actually very few situations where organs can be harvested from donors. For all deceased donor transplants, the donor must be confirmed as being brain dead (both brain stem and higher cortical functions).  However, in order for the organs to remain viable they must not become ischaemic - which is obviously a huge problem when the patients heart has stopped beating.  For this reason most patients who die and go on to become organ donors were already on a ventilator in intensive care in order to keep their blood oxygenated and circulating to perfuse their organs.

Kidneys are listed by NHSBT as a special case where a ventillator may not be required in advance to maintain viability - offhand I'm not sure why this would be - however to answer your question:

A. Neurological death - correct answer - the patient must be deceased without chance of recovery (hence brainstem and cortical death)

B. Cardiac function - were this to stop unilaterally then the patient may still be recoverable whilst the organs may be damaged due to lack of perfusion and thus not be viable for transplant

C. Respiratory function - almost identical to the cessation of cardiac function (and indeed will lead onto it very quickly)

D. Renal function - there's no point transplanting useless kidneys!

Have a look through the NHS Blood and Transplant Organ Donation site linked above, it's a great and trustworthy resource.


Where does vasoconstriction occur in limbs? When cold or in shock a person's blood vessels constrict in order to preserve heat or to move blood flow to protect vital organs.  I am interested in the mechanism by which this is achieved.  Does this occur along the entire length of the limb or are there 'pinch points' (for example is it possible to simply have a point of vasoconstriction just below the shoulder which would reduce blood flow to the entire arm)?  Am I correct in thinking that the response is neurological rather than endocrinological ?

Vasoconstriction is a phenomenon that can be caused by many factors, from mechanical events (such as stretching) to hormones (epinephrin, neurepinephrin, angiotensin ...). But no matter what is the cause, the end-result is an increase in intracellular calcium concentration in smooth muscle cells (which compose the arteries and veins). So it seems that constriction does not happen in specific points but rather all along the limb. Furthermore angiotensin receptors are found in high concentration in smooth muscle cells [1], suggesting that every such cell has the ability to change it's morphology in order to induce vasoconstriction.

As for your second point, I think the response is as much endocrinological as neurological, since it involves both peripheral and central regulations. (Well, as a side note, endocrine systems rarely have no interaction with central ones).

Angiotensin receptors : distribution,
signalling and function


Are there any alternatives to DNA as the hereditary material on Earth? I wonder are there hereditary materials other than DNA  deoxyribonucleic acid (may be on different planets).

In addition, I learned in my high school that carbon and silicon are similar. Is it possible to have hereditary materials with silicon replacing carbon.

Why and why not?

First of, depending on your definition of life (which is a matter of philosophy, not science) you may even accept as living something that has not heritable information passed onto 'offspring'. But let's consider only those hypothetical life forms who would have heritable information.

Of course, it is possible for different life forms to use some other mean of transferring heritable information. In fact, there are life forms based on RNA instead of DNA on earth (see RNA virus) and it is even thought by many that life first evolved using RNA and not DNA (see RNA world hypothesis).

To go further in this discussion you should have a look at wikipedia > Hypothetical types of biochemistry (I got the link from @RoniSaiba 's answer).


Providing small molecules to cells on a filter plate Lets imagine that I have mammalian cells that I've immobilized on a filter. Now I want to keep providing small molecules to these immobilized cells without resolubilizing the cells.

The caveat is that I would like to do so without fixing the cells or waiting for them to adhere to the filter. The small molecules are small enough to diffuse through the filter.

Perhaps you're looking for these hanging inserts, for example: "Millicells"


How do TLR1/TLR2 activate the MyD88 dependent pathway Recently, I've been reading about the MyD88 dependent signalling pathway, with particular reference to its activation in Macrophages and other cells of the immune system on recognition of a pathogen. I understand that when a PAMP (Pathogen Associated Molecular Pattern) binds with a PRR (Pattern Recognition Receptor), the receptor undergoes a conformational change, which precipitates a cascade of chemical reactions between various proteins, which eventually leads (inter alia) to the translocation of NF-κB to the nucleus, which leads to the production of cytokines. My question is about the finer points, particularly with respect to TLR1 and TLR2.

My reading suggests that these generally form a heterodimer - is this always true? Are both required for a pathogen to be recognised and an immune response produced?

Upon the pathogen binding with TLR1 (whether in a complex with TLR2 or not) what precisely happens to the receptor. I understand that MyD88 is, ultimately, recruited, but by what means?

I believe I understand everything that happens after the recruitment of MyD88, but I am less clear on everything before that. I had initially understood that the recruitment of MyD88 was the immediate next step, but other sources make reference to two proteins which I was initially unaware of: TOLLIP and TIRAP. What, if anything, is their role?

I'm still a little new to stackexchange so I apologise if this question is not up to standard, in which case, let the question simply be: 'How do TLR1/TLR2 activate the MyD88 dependent pathway?'

The TLR are usually working as homodimers (Toll-like receptors), although TLR2 can cooperate with TLR1 or 6.
Upon binding of its ligand (this is called pathogen associated molecular pattern) the receptors change their conformation and allow binding of TIRAP (TIR adapter protein) to their Toll-interleukin 1 receptor (TIR) domain. TIRAP then recruits MYD88, which then recruits IRAK1 or 4. The signal is then passed down the pathway as shown in the figure below (taken from the Wikipedia article on TLR).


Can we use the HIV antibody test to detect HIV in newborns? Adults and elder children can use HIV rapid test to test HIV infection. Can we use the HIV antibody test to detect HIV in newborns too?

The rapid screen usually tests the oral mucosa by swabing the inside of the cheek and checking for the presence of anti-HIV envelope antibodies. Although the precise target of these antibodies seems to be kept propriatary, my guess would be the detection of either p24 antibodies or envelope antibodies that bind the V3 region.

Regardless, the point is they test for the presence of antibodies, which a child does not start making until they are born. See this post for a great explanation

Since a child has mostly maternal antibodies, the presence of anti-HIV antibodies would only mean that the mother has started producing antibodies to HIV (Seroconversion). This means that although the child has been exposed, they may themselves not be infected.

The mucosa, particularly in the oral region has a very low titer of anti-HIV antibodies, so I think this test would probably be best to direct the physician to conduct additional tests that are more indicative of HIV infection like p24 western blot.


Madrid, Noise by the river: Bird or cricket? I currently live in Madrid, Spain. In July there was a loud animal near the river, in an out of town area surrounded by grassland, with trees along the river.

It's continued into August, though it has reduced.

It sounds like a cricket in general tone and rhythm, but it is always high in the trees, and sounds too deep to be an insect. It's in the frequency range of a squawking bird, so if it's a cricket it must be huge.

On the other hand, if it was a bird, I should have been able to spot one.

Does anyone have any idea what it is?

The sound is rhythmic, rasping note, with two beats of equal duration but slighly different tone, repeated over and over again without any pause.  The animal that makes it calls continuously for long periods.

EDIT: thanks to AliceD for the comment, I didn't realise we had cicadas in Europe. It could be a cicada, but it's deeper and more consistent / regular in its song than this one:

https://www.youtube.com/watch?v=DSdxm52VwOg

In this case i am going to agree with AliceD, because I live in Greece and here we hear cicadas everywhere. But in Madrid, there is a other kind of cicada that its "song" is more noisy and more deep.In this video you can hear how your cicada sings.https://youtu.be/mah26og11ms