Transcript(omics) terminology: cDNAs, ESTs, RNA-seq, etc I've worked pretty frequently with genome and transcriptome data for several years now, but I'm still not 100% sure I understand the proper usage for certain terminology related to transcripts and transcriptomics. Let me give it my best shot.

cDNA: in general, this term corresponds to any DNA that is derived from an RNA template via reverse transcription (complementary DNA); however, it is often used to refer to full length cDNAs, DNA sequences that correspond to complete mRNA molecules
EST: expressed sequence tags correspond to cDNA (sub)sequences obtained from a single read of a cDNA sequencing experiment
RNA-seq: this refers to the use of high-throughput sequencing technologies to characterize entire transcriptomes, such as by transcript assembly or expression analysis

Here's my concern: I've seen ESTs described as "one-shot" or "single-pass" sequences, which I interpret to mean a single sequence read. However, they are also typically described as being hundreds of base pairs in length (Wikipedia claims about 500-800bp in length max), which (currently) limits this definition to reads derived from Sanger-style sequencing.

Does this mean that a short read derived from a high-throughput sequencing platform is not an EST? Is this distinction based on read length? platform? throughput?

Due to technical limitations, short reads are often assembled before they are used for other downstream analysis. I have sometimes heard the contigs belonging to these assemblies as ESTs, but this doesn't seem to be consistent with the previous definitions.

Is our terminology becoming inconsistent due to the rapid improvements in sequencing technology, or am I missing or misinterpreting something?

The quick answer is that you are misinterpreting ESTs. EST stands for Expressed Sequence Tag. They are obtained by collecting and sequencing any mature (i.e. poly-A) mRNAs found in a living cell. Well, it was living until the experiment was performed at any rate :).

The term EST is not applicable to sequences derived from genomic data. It only applies to expressed sequences. You do have ESTs that are derived from cDNA libraries but these are expressed cDNAs. Short reads are not ESTs because we have no information on whether that sequence is actually expressed in a living cell.

You could apply the term to RNAseq reads (depending on the experimental procedure involved) but that is not what most people would understand by the term.

In summary, the operative term of EST is "expressed". You cannot call anything an EST if you do not have evidence that it is actively expressed in a living cell.


How frequent are selective sweeps? Introduction

Selective sweep is the most famous genetic signature of selection. We know of a number of classical examples of selective sweeps, some of them in humans. See the classical example of the sweep on a sequence relgulating the lactase gene in the post Are humans the only species who drink milk as adults?.

Question

I do not have a good intuition about how common such sweeps are. Are there constantly 5 to 10 sweeps happening in a species genome or is there a sweep every 1000 generations only?

How frequent are selective sweeps?

Clarification

Of course, the answer will vary (and will probably vary greatly) among species. I would welcome empirical estimates and/or theoretical expectations coming from any species (I would prefer an estimate coming from a eukaryote species though).

I know this question is a bit old, but I read a paper recently which (claimed) to answer this question.
I think the answer to this question is suprisingly controversial. I don't really have a formed opinion yet of which answer is correct, but I will try to discuss the different viewpoints here.
Argument 1: Sweeps are rare
On one hand, we have the people who are sceptical of how common sweeps are. This, in my understanding is most researchers. Many people believe that polygenic is the predominant form of selection in humans.
There is the paper by Hernandez et al (2011), who find scant evidence of selective sweeps in recent human history. Essentially, they looked at the reduction in diversity (something which is associated with sweeps) around amino acid substitutions and synonymous substitutions and found that the two were statistically the same. They say it's probably more likely that this is caused by strong purifying selection at linked sites rather than sweeps.
Szpak et al (2019) suggested that most of the time, the criteria for designating something a sweep in human populations was probably too lax, and many of the previouly claimed sweeps were probably artefacts of some kind. In fact, they only find compelling evidence for 2 sweeps in recent human history.
Argument 2: Sweeps are more common
Alternatively, there are some studies which have apparently discovered a relative abundance of sweeps in human history. Some might make the argument that sweeps are likely to be common, since humans have a relatively small effective population size (~20,000) and low mutation rate.
Souilmi et al (2020) claimed to have discovered 57 (fpr<10%) sweeps using genomes from ancient Eurasian individuals. 35 of these 57 were inferred to have occured before 35kya. The reason they claim to have found many more sweeps than previous studies is because they used ancient DNA. It is well established (Hellenthal et al 2014) that admixture is virtually ubiquitous within modern and ancient human populations. Admixture likely obscures the signal of sweeps by introducing non-selected haplotypes from the admixing population, making hard sweeps look like soft sweeps, or perhaps not even sweeps at all. They confirm this using simulations and show the power to detect sweeps is massively reduced when you are looking at admixed populations.
However, their method uses ancient DNA, which is highly prone to various artefacts, which they didn't appropriately test with simulations. It also hasn't been peer reviewed, so there may well be other potential issues.
References
Hernandez et al 2011
Szpak et al 2019
Hellenthal et al 2015
Souilmi et al 2020


Alpha wave frequency variance in EEG of single subject over period of a few hours? I have an Emotiv EPOC (EEG headset: 128 SPS, notch filter @60 Hz, felt saline contacts) I've been playing around with. Over the course of two or three hours using CCA to plot an SNR contour against frequency and time over O1, O2, P7, and P8, I noticed that a strong background signal in the alpha-wave range was existent at ~10 Hz, but then after a while of doing other things and coming back to it the strong background signal at 10 Hz disappeared but a strong background signal at a smidgen over 8 Hz was present instead.

Naturally, this leads me to ask the question: what the heck is going on? Unfortunately, that doesn't make for a good stackexchange question title, so the replacement question:

Can alpha wave frequencies vary within a single subject over the course of a single day? If they can, by how much, and under what conditions?

(if they can't, I have to start figuring out what the heck caused those artifacts...)

I noticed that a strong background signal in the alpha-wave range was existent at ~10 Hz, but then after a while of doing other things and coming back to it the strong background signal at 10 Hz disappeared but a strong background signal at a smidgen over 8 Hz was present instead.

Alpha-waves (7-13 Hz) are related to a dozen of things. Here is an easy first experiment for you:

Sit still, stare at a wall, eyes open. Remove sources of noise such as TV, radio, etc.
Repeat the same, but now hold your eyes closed.
Record the signals in both conditions for about one minute.
Compare the power spectrums between the two conditions: you will see a big difference in the alpha power, especially at the occipital electrodes.
This is actually a standard test for resting-state analysis.

Back to the actual question: What you noticed is probably about drowsiness. When one gets sleepy, the alpha power starts to increase. You can try this by watching a boring movie.

  Can alpha wave frequencies vary within a single subject over the course of a single day? If they can, by how much, and under what conditions?

Yes, because of the varying cognitive load, thoughts, sleepiness, emotions, etc. The brain signals vary a lot.

Also notice that all sorts of artefacts (e.g. movement, cardiac, eye-blinks, biting of teeth) have a dramatic effect on the measured signal. If you blink your eyes it produces a signal that has 100x higher amplitude compared to the signal that comes from your brain. You cannot really say much what causes any differences in the EEG unless you would do research-level recordings with research-level equipment.


API for gene names by location Is there any API where I can input chromosome location and it will provide us gene names, for example input chr: 1 location 154714693:154754070 and it will return a list of gene names or ID within this region?

With R biomaRt you can retrieve them.

  library(biomaRt)

  ensembl = useMart("ensembl",dataset="hsapiens_gene_ensembl")

  filterlist <- list("1:154714693:154754070","protein_coding")

  genes <- getBM(attributes=c('hgnc_symbol', 'chromosome_name',
  'start_position', 'end_position'),
                     filters = c("chromosomal_region","biotype"),values = filterlist, mart = ensembl)

  genes
  hgnc_symbol chromosome_name start_position end_position 1
  KCNN3               1      154697455    154870280


What is the healing process of mouth wounds? When we have an external wound, blood generally tends to clot there, forming a layer of solid scab.

Yesterday, while brushing my teeth, I somehow hurt my gums and it got all bloody. However, it did not clot, neither did it hurt just after the incident.

After maybe like 12 or 15 hrs I had trouble opening my lips and when I looked at the spot in the mirror the gum tissue around and on the wound had colored white/yellowish.

Our mouths are supposed to be the among the most contaminated parts of the human body, so why do mouth wounds heal in just about a week and don't get infected?

What is the healing mechanism found in the mouth tissue, because I figure it is completely different from the processes in wounds occurring in the external skin.

To build on the answers from @Armatus and @S-Sunil

The healing mechanism involves the inflammatory process, which is the same in almost the entire body. In particular in both skin and mucosa (both referred to as "epithelial" tissues), when there is a break, platelets and clotting factors clot off any bleeding vessels, white blood cells (neutrophils and macrophages in particular) collect and destroy any bacteria, dead cells and muck, and then the process of regeneration occurs (with ongoing inflammation), where stem cells in the surrounding tissue regrow cells, new blood vessels may be formed and scar tissue is laid down to give extra strength. Eventually after these stages of healing, there is "remodelling" where the structure basically gets better.

As to why oral wounds heal quickly and don't get infected that much? There are a bunch of reasons. One is that the head and neck has an excellent blood supply- just think of scalp wounds where you bleed like crazy but then they heal very well. Another is that mucous membranes have immune functions that stop invading microbes. Generally speaking we divide this into "innate" immunity which is a general response, and "adaptive" immunity which is tailored towards specific bugs. The mucosa has both. There are neutrophils and macrophages (innate) which live in that area, there are lymphoid patches (like lymph nodes, and adaptive), there are immunoglobulins specific to mucosa (IgA) which is adaptive in nature, and the epithelial lining cells themselves will signal to the rest of the immune system if there is damage or an infection. Plus, saliva itself has chemicals and enzymes which break down oral bugs.

Most of the oral bacteria themselves are not particularly invasive. Just think, every time you brush your teeth, you cause multiple abrasions in your mouth. In fact, measurable amounts of bacteria from the mouth end up in your bloodstream every time  you brush your teeth! And yet, we don't end up with bloodstream infections as a result. This is partially because the rest of our immune system (and the structure of our heart and vessels) is intact, and partially because oral bacteria are not very invasive or pathogenic. They kind of have a sweet deal living in your mouth minding their own business and not killing their host, and even causing infection in an oral wound would make their continued survival less likely.

In addition I should probably point out that skin has a great deal of bacteria on it as well, and yet we rarely get infections from them (unless colonised by an invasive species), for the same reasons.


What is the smallest difference in light wavelength that the human eye can detect? Is there a lower limit to the difference in wavelength (colour) our eyes can detect? If so, is this consistent between individuals? Are there any other traits correlated with precise colour vision?

The eye really on can sense 3 colors, or to be more precise it only has three types color sensitive each of which detects a large range of wavelengths with no way to distinguish between them within the same cone. We only determine color by the different levels of activation between the different cone cells. This means we need a lot of light to see color and our ability to detect differences in color really depend greatly on where on the visible spectrum that color falls.

As for more precise color vision. The greater the number of types of cones cells the more color sensitive the eye ,birds and reptiles can see far more colors than use becasue they have 4 types of color sensitive cells as opposed to the human 3. More widely spaces base colors will give greater sensitivity. This is why even among trichromats human color vision is poor becasue two of our base colors are close together and overlap greatly.  That is because humans (and primates) are secondarily trichromats, gaining a third base color from a recent mutation. wiki on the subject


What would happen if you "rewired" your eyes with your nose? The nose sends sensory input through transduction of chemicals in the air via the olfactory nerves/tracts to the primary olfactory cortex.
The eyes send sensory input through transduction of light via the optic nerve/tract to the visual cortex of the occipital lobe of the brain.
Although both senses receive different stimuli, they (like all of our senses) convert external stimuli to a nerve signal. Given that, it seems possible that one could "rewire" the brain so that sensory organs sent sensory signals to different parts of the brain.

For example, it seems possible that we could splice olfactory tracts to the optic chiasm to send signals to the visual cortex.

My question: If we rewired the cranial nerves so that our nose was connected to our visual cortex, what would we see??

(or what would happen if we rewired any of our major senses with a different processing center of the brain?)

"Rewiring" the brain isn't quite that simple: simply splicing a nerve to another doesn't necessarily mean the axons of that nerve will then grow into area. I am unaware of any studies that cross these specific pathways but as I am writing this answer I see you have already updated your question to ask about other modalities! So, with that in mind...

Crossing Auditory and Visual Pathways

Some related experiments have been done with other modalities: the ones I am aware of involve the auditory and visual systems. Both auditory and visual information traveling to cortex mostly comes through two nuclei in the thalamus: the medial geniculate nucleus, MGN, for auditory information, and the lateral geniculate nucleus, LGN, for visual information.

These thalamic nuclei are adjacent to each other. In Angelucci et al 1998 and Sharma et al 2000, lesions were made to cause retinal projections to innervate the part of thalamus that usually processes auditory information (medial geniculate nucleus, MGN). (note: there are also a bunch of older experiments in rodents and ferrets besides these, I'm not going to do a comprehensive review of the literature here but you can find many relevant citations within those other papers).

Briefly, the technique is to damage both the LGN and the pathways that normally project to MGN. The result is that the retinal axons, which normally synapse in the LGN, will instead path to the MGN. Note that it is important to do this very early in development, such experiments would not work in an adult brain.

The result, in the papers I cited earlier, is that the part of cortex that normally responds to auditory information begins to respond to visual information, and develops a hallmark of visual cortical response properties: selectivity to the orientation of presented stimuli. Therefore, it seems like if you give an auditory cortical area visual information, it doesn't "try to process it as sound" but rather processes it just like the visual cortex would.

Effects on perception

It is hard to ask the ferrets what their actual perceptions are, but the best guess is that perceptions are built by what we put into the system: there is no way for an area that receives anything but visual input to interpret that information as anything other than visual input. There is no context to interpret it any other way. Cortex develops and responds based on the information it is given. In the animals in these experiments, their auditory systems have been lesioned so there is really no way they could interpret the stimuli they "see" as "sounding like" something.

Similarly, if you send olfactory information to visual cortex, you will process smells in visual cortex. Olfactory processing is a bit different than the other modalities, so depending on where you took this information from things may not develop properly, but that gets into a lot of speculation that is beyond this .SE site.

Crossmodal plasticity in blind individuals

There are some experiments in humans that also look at this type of cortical plasticity. Probably the best ones are those in blind individuals. Again, I won't review the entire literature, but can give some examples: Cohen et al showed tactile representations in the visual cortex of blind individuals, such as when they are reading Braille. Bedny et al, 2015 show that, especially in children who are blind, the visual areas of the brain respond strongly to information from other modalities, especially spoken language. Again, these individuals are not "seeing" these stimuli, beyond the type of "seeing" that you can do when you reconstruct a scene with your eyes closed (if they were at one point sighted). Rather, part of their brain that would normally be used for vision is now being used for other tasks.

Effects on olfaction haven't been studied as often, but in Kupers et al, blind individuals were shown to have olfactory responses in brain areas that don't show olfactory responses in sighted individuals, including areas that usually process vision.

References:

Angelucci, A., Clascá, F., & Sur, M. (1998). Brainstem inputs to the ferret medial geniculate nucleus and the effect of early deafferentation on novel retinal projections to the auditory thalamus. The Journal of comparative neurology, 400(3), 417-439.

Bedny, M., Richardson, H., & Saxe, R. (2015). “Visual” cortex responds to spoken language in blind children. Journal of Neuroscience, 35(33), 11674-11681.

Cohen, L. G., Celnik, P., Pascual-Leone, A., Corwell, B., Faiz, L., Dambrosia, J., ... & Hallett, M. (1997). Functional relevance of cross-modal plasticity in blind humans. Nature, 389(6647), 180-183.

Kupers, R., Beaulieu-Lefebvre, M., Schneider, F. C., Kassuba, T., Paulson, O. B., Siebner, H. R., & Ptito, M. (2011). Neural correlates of olfactory processing in congenital blindness. Neuropsychologia, 49(7), 2037-2044.

Sharma, J., Angelucci, A., & Sur, M. (2000). Induction of visual orientation modules in auditory cortex. Nature, 404(6780), 841-847.


Is "Monophyly" context dependent? I am thinking about this thought experiment: Suppose we have three taxa which are grouped into the following tree: {{A,B},C}, clearly {B,C} is a paraphyletic group. But if A go extinct in the near future, we are left with {B,C} only, then can the group be called monophyletic?

To expand on Remi.b's answer, groups are defined based on all the species we know about. This includes extinct species. So in your example, the group {B,C} is paraphyletic regardless of whether A goes extinct or not.

But what if A went extinct ages ago and we don't know about it at all? In that case we would only have B and C to base a group on, and they are the only descendants of their common ancestor that we know about, so we would indeed define {B,C} as monophyletic.

The question comes when we discover A's existence, and that it is more closely related to B than to C. At that point we have a choice: expand the definition of group {B,C} to include A, in which case the group becomes {{A,B},C} and is monophyletic, or keep the group {B,C} and accept that we were wrong about it being monophyletic, it was really paraphyletic all along.

You can see these processes happen as paleontology and cladistics advance. Birds used to be classified differently from dinosaurs, but as our knowledge of how birds are descended from dinosaurs increased paleontologists chose to classify them as a subset of dinosaurs, keeping the group "dinosaurs" monophyletic.

On the other hand as our understanding of how mammals/birds are descended from reptiles and tetrapods are descended from fish increased, making both of those groups paraphyletic, the attempts to redefine them as clades have largely failed, so they are now considered paraphyletic groups. "Amniotes" has replaced "reptiles" as the name of the clade containing reptiles, mammals and birds, and "Craniata" is the monophyletic group containing various fish and tetrapods.


Immediate stroke/seizure Therapy Can an oncoming stroke/seizure, be stopped by a setup consisting of a brain-computer-interface (BCI) that immediately detects the variation in wave-form, and then another machine that neutralizes the anomaly by sending a measured voltage to select areas of the brain OR by Transcranial Magnetic Stimulation?

Yes, these devices and treatment programs are being actively developed. General idea is that epileptic episode follows certain path within the brain. It can start in thalamus, after which sporadic activity spreads into cortical areas, for example motor cortex. There is a number of papers on prediction of epileptic seizure, e.g. Seizure Prediction and its Applications.

The device then will detect initiation of seizure before evident symptoms and provide inhibition via cortical electrodes, microelectrode array (MEA). It seems that currently MEAs are used more for research (recording from tens of neurons), but single electrodes are useful for actual control of epilepsy. Also one can control vagus nerve, which causes parasympathetic response (general inhibition, aka "rest-and-digest"). More you can read here.

Transcranial magnetic stimulation, as I understand, is not portable enough to be useful.


What are known methods of non-surgically disabling neural tracts/pathways (esp. Corpus Callosum)? I think I've read something about usage of TTX and optogenetics, but I cannot find the papers for either anymore. Any reference would be much appreciated, especially those concerning mice and the Corpus Callosum.

Edit: By surgical, I mean to say methods that are based on actually cutting through the tract using a surgical knife (or lasers etcetera), as is commonly found in literature.

I was able to find one non-invasive method to sever the corpus callosum (callosotomy). This method is referred to as gamma knife radiosurgery (Mathew et al., 2007). Basically, 201 beams of gamma beams are focused on the corpus callosum and where the beams intersect, the energy is high enough to permanently damage the tissue. I doubt this technique is available for routine use in animals, though.

Another interesting technique is photothrombosis. This method is based on the systemic injection of a photosensitive dye named Rose bengal. Subsequent focal illumination of the brain with a cold light source through the intact skull leads to focal cortical infarcts of reproducible size, location and geometry (Schroeter et al., 2002) . Brain damage is induced due to photo-activation of the dye and subsequent endothelial damage with platelet activation and thrombosis, resulting in local blood flow interruption. The light source can be applied on the intact skull with no need of craniotomy, which allows targeting of any cortical area of interest in a reproducible and non-invasive way (Labat-Gest & Tomasi, 2013). However, although the light source penetrates the skull, I don't think the method is useful for the induction of deep-brain lesions, as I was able to locate only studies using it to model cortical lesions.

Having not answered the question, I'd like to say that either surgical sectioning, or chemical ablation using micro-injection of neurotoxins are the most commonly encountered methods to perform a callosotomy.

References
- Labat-Gest & Tomasi, J Vis Exp (2013); 76: 50370
- Schroeter et al., J Neurosci Methods (2002); 117(1): 43–9
- Mathew et al., J Neurosurgery: Pediatrics (2007); 106(4): 312-5


Resource plant anatomy/lifecycle vocabulary I've been curious about a lot of vocabulary words in the world of botany. I've had quite a bit  of trouble finding somewhere online to help me out, but I'm having some trouble finding a resource like that.

Optimally, I'm looking for something with diagrams of anatomy, over the course of time, maybe some photo examples, and some sort of dictionary to accompany. Is there anything like this, online or offline that anyone knows about?

specifically development-focused

An Introduction to Plant Structure and Development by Beck looks comprehensive and has been well-reviewed. It has both photos and diagrams, and sections certainly deal specifically with growth/lifecycle. It's available to preview or purchase as an ebook on Google Play.

more general plant anatomy vocabulary resources

In print, Plant Identification Terminology: an illustrated glossary by Harris and Harris is a fairly standard reference, and I've found it very useful both for looking up terms and for just flipping through.

Online, but with fewer diagrams, you could try the Glossary page on the Angiosperm Phylogeny Website.

This might sound silly, but if you're looking for more of a course on the fundamentals rather than a dictionary of the specifics, the Botany Coloring Book is actually a great, seriously useful work.


Sickle cell life span How long do sickle red blood cells "live" before being broken down in phagocytosis?

I had trouble doing a normal search as it brings up life span of those inflicted with the disease. Also, I have been doing a semester long assignment, where we are delving into all aspects of this disease, and I have 20 sources so far and still haven't come across the answer.

Sickle cells usually die after about 10 to 20 days, compared to normal red blood cells, which live an average of 120 days. The bone marrow can't make new red blood cells fast enough to replace all the dying ones which causes anemia,low blood count that results in fatigue,shortness of breath and related symptoms.As the cells are made normally but die too rapidly,this is termed as haemolytic.


What happens to the molecules of the pathogens after phagocytosis? For example, what happens when a bacterium gets digested by a macrophage? I suppose that the macrophage produces the presented antigen from leftovers from the digested bacterial particles. What happens to the rest of the bacterium? Can the molecules from bacteria be used as a source of nutrients for the body? Or will they accumulate/get transported as waste products?

The ingestion of a bacterium by a macrophage involves phagosome lysosome fusion, which you can read about in Abbas Basic Immunology, Ch 2. As you suspected, in addition to bacterial killing and antigen processing, the phagolysosome breaks down bacterial macromolecules, as any lysosome does, using a variety of lysosomal hydrolases. There are export pathways for the end products, including lipids, carbohydrates, and amino acids, as discussed in this review, which does allow for re-use by anabolic pathways. As discussed in the linked review, the process of digestion and catabolite export is regulated, as should be expected. In culture models, nutrient availability appears to be important.


What is the correct medical procedure(s) for taking a resting heart rate? Note: I thought the Biology stack exchange would suit this question better than the Fitness stack exchange. Please let me know in the comments if this is not suitable here.

I am interested in tracking my resting heart rate as it decreases with aerobic training.

At the moment I take it immediately after I have woken up before I get up out of bed.

What is the correct medical procedure(s) for taking a resting heart rate?

I'm aware a standardized procedure is important but what about:

Body position: Should I be sitting or lying down?
Heart rate: Should I take the lowest value or an average HR?
What duration should I take it for?
How relaxed should I be?

In an academic situation how would one reliably take resting a heart rate?

Please include answers that can be referenced to scientific or medical literature.

1) According to this article you should be taking it in the most preferred position you want. It would change according to the position you are in so make yourself comfortable sitting or lying down (reference).

2) You take the number of beats of your heart in a minute. If you take the number of beats for 2 minutes, then average your count by 2.

3) One minute (reference).

4) Completely relaxed, most articles recommend taking it in the morning while waking up so you are doing the right thing (reference).

I don't understand what you mean by an academic situation so I could try and answer it if you clarified it.


Does minimizing hunger maximize weight gain? Due to the "obesity epidemic," there is a lot of focus on the causes of weight gain. We typically talk about strategies to cause weight loss, but what about strategies to minimize/maximize hunger?

Is there a way that hunger can be cured by eating a certain distribution of calories as a function of time? For example, if I have 2000 calories of food and I can eat it at any time, how should I spread out eating it over a day to maximize/minimize weight gain?  What would be the physical differences for me if I ate a small snack every minute of the day versus eating all 2000 calories at once?

Likewise what about weight gain? Would it be easier to gain weight if someone waits until they are very hungry and overeats during that hunger window, or if they eat over a wider window?

Regarding the question in your title: minimizing hunger could be synonymous with leptin responsiveness. For example, leptin deficient or leptin resistant mice are known to become extremely obese - this is because leptin, the 'satiety' hormone, not only signals for you to stop eating, it also elevates the body's energy expenditure and stimulates thermogenesis.

An interesting strategy I've heard, though I don't know how effective it is, is increasing leptin sensitivity through the composition of your diet.

Another interesting element is that hunger, which is mediated by hormones such as ghrelin, decrease energy expenditure by multiple metabolic methods. So being hungry isn't always conducive to losing weight.

I believe most of the answer to your questions relies in these concepts. If you're talking about food distribution throughout your day, schedule it so that you're not very hungry for prolonged periods. Same with food type, eat foods that satiate for longer periods of time, unlike foods such as white rice.

If you want to read up a bit more, I suggest looking into AMPK, and the role these hormones and food composition has on it. AMPK reading


What are pit fields? I found this statement from my biology text book,

  "The sieve tube elements and the companion cells are connected by pit fields present between the common longitudinal walls".

Is the pit field same as Plasmodesmata ?

Pit vs plasmodesmata

From wikipedia > pit

  Pits are thin portions of the cell wall that adjacent cells can communicate or exchange fluid through, utilizing plasmodesmata.

The definition of "pit" is therefore very related to the one of "plasmodesmata". From wikipedia > plasmodesmata

  Plasmodesmata (singular: plasmodesma) are microscopic channels which traverse the cell walls of plant cells and some algal cells, enabling transport and communication between them.

I think the following quote (from wikipedia > plasmodesmata again) will help you to distinguish pits from plasmodesma

  Primary plasmodesmata are formed when portions of the endoplasmic reticulum are trapped across the middle lamella as new cell wall is laid down between two newly divided plant cells and these eventually become the cytoplasmic connections between cells. Here the wall is not thickened further, and depressions or thin areas known as pits are formed in the walls. Pits normally pair up between adjacent cells. Plasmodesmata can also be inserted into existing cell walls between non-dividing cells (secondary plasmodesmata)

Pit field

A pit field however is just an area where there are plenty of pits! From Merria-Webster

  [A pit field is] an area in the wall of a plant cell in which one or more pits develop


Programmatic way to differentiate homodimers from heterodimers? For pdb files is there a simple programmatic way to determine if the file is made up of homodimers or heterodimers.

I have many files so an online tool or some psuedocode/scripts would help more than manually assessing each one.

I'd just compare the amino acid sequences of the individual protein chains. With some leeway for residues not observed in the density, ie only require 90 or 95% sequence identity, or ignore gaps.

This will not tell you anything about whether the dimer (if you observe several molecules in the asymmetric unit) is actually real. For that, you'd need to do an experiment, literature research or see whether software like the PISA-server could give you a clue.


Are HeLa cells edible? I'm curious if HeLa cells are intrinsically poisonous or dangerous to ingest.

My understanding is that some of the contamination in HeLa cells such as HPVs are not readily expressed.

I have no plans to do so, but I'm trying to understand why they might or might not be.

I think HELA cells are edible, although from moral point of view this would be cannibalism.

Despite they are cancer cells, they are safe for foreign organism, because any ate matter is destroyed. Even if these cells were implanted into another being by surgery, they will be safe since immunity will recognize them as foreign and kill. They are much less cancerous for recipient than just foreign.

Remember, then when we are eating meat, we don't care if cow or pig had cancer. Even if we avoid eating explicit tumors, we can still eat metastatic cells from sick animals. I think this happening all the time and has no consequences.

Simultaneously HELA cells are dangerous for other cell cultures in laboratory. There were several cases, when other cultures were infected by HELA cells and crowd out. HELA cells were traveled by air and on objects unexpectedly. Scientists were not ready for this phenomenon.


What is the evidence that plants and animals had a common ancestor? According to the theory of evolution (which I don't dispute), plants and animals evolved from a common ancestor, probably a eukaryote. I'd like to know how we know that to be true.

Specifically how did scientists come to that conclusion, and what verifiable facts did they rely on? It would also be interesting to know who (and when) was the first to propose that plants and animals had a common ancestor. Was it Darwin himself?

Note that I'm not asking for the details of when and how that happened (the diversification/evolution of eukaryotes into plants, animals and other types), but rather the evidence we have to support it.

Darwin did propose that all extant organisms have a common ancestor:

  Therefore, on the principle of natural selection with divergence of character, it does not seem incredible that, from some such low and intermediate form, both animals and plants may have been developed; and, if we admit this, we must likewise admit that all the organic beings which have ever lived on this earth may be descended from some one primordial form. But this inference is chiefly grounded on analogy, and it is immaterial whether or not it be accepted. No doubt it is possible, as Mr. G.H. Lewes has urged, that at the first commencement of life many different forms were evolved; but if so, we may conclude that only a very few have left modified descendants. For, as I have recently remarked in regard to the members of each great kingdom, such as the Vertebrata, Articulata, etc., we have distinct evidence in their embryological, homologous, and rudimentary structures, that within each kingdom all the members are descended from a single progenitor.

--Darwin, Origin of Species

He probably wasn't the first one; Darwin cites a previous suggestion:

  From a circular lately issued it appears that Dr. Freke, in 1851 ("Dublin Medical Press", page 322), propounded the doctrine that all organic beings have descended from one primordial form. His grounds of belief and treatment of the subject are wholly different from mine; but as Dr. Freke has now (1861) published his Essay on the "Origin of Species by means of Organic Affinity", the difficult attempt to give any idea of his views would be superfluous on my part.

--Darwin, Origin of Species

As you can see, he offers no real evidence for this; he explicitly says it's speculation. Of course, nothing from Darwin is necessary for modern evolutionary theory, and other groups have tried to make this more concrete. Several lines of evidence provided increasing evidence for a universal common ancestor (UCA):

  For a century after the publication of Darwin's bold proposition, before the advent of molecular biology, the UCA hypothesis remained an untested and hardly testable speculation. However, first the universality of the genetic code and later the demonstration of the (near) universal conservation of approximately 100 RNA and protein-coding genes among cellular life forms provided ample evidence in support of the UCA. Although generally considered compelling, this evidence fell short of a rigorous, formal test of the UCA hypothesis.

--The common ancestry of life

A relatively recent approach has tried using information theory to formally test a UCA:

  Here I provide the first, to my knowledge, formal, fundamental test of UCA, without assuming that sequence similarity implies genetic kinship. I test UCA by applying model selection theory to molecular phylogenies, focusing on a set of ubiquitously conserved proteins that are proposed to be orthologous. Among a wide range of biological models involving the independent ancestry of major taxonomic groups, the model selection tests are found to overwhelmingly support UCA irrespective of the presence of horizontal gene transfer and symbiotic fusion events. These results provide powerful statistical evidence corroborating the monophyly of all known life.

--A formal test of the theory of universal common ancestry

Formal positive proof of theories in science, outside of math, are rare to non-existent (what actually happens is that competing theories are disproved) and I don't think that this approach is different. It's not a formal proof, it's yet more powerful evidence that theories not involving a UCA suck.

  A formal demonstration of the Universal Common Ancestry hypothesis has not been achieved and is unlikely to be feasible in principle. Nevertheless, the evidence in support of this hypothesis provided by comparative genomics is overwhelming.

--The common ancestry of life


Estimates of historical human population size What are the estimates of minimum historical human population size, and how are they obtained from the current human genetic diversity?
I seem to recall a Scientific American article from over 30 years ago claiming a figure of 500-1000, but I can’t find any estimate now.

Although I cannot find the Scientific American article to which the poster refers, I assume that the “historic human population size” is the size of the human population in Africa before it underwent the expansion that accompanied the emergence from the African continent. Some important papers on this subject were published in the late 1990s (somewhat later than 30 years ago) and there is a suggestion in one of earlier estimates that I have not yet found a reference for.

There is an implication in the Harpending et al. paper (below) of earlier estimates of the order of 1,000. I will try to find the source (help on this welcomed).

Harpending et al. published a paper in PNAS of February 1998 in which they conclude an effective population size of the order of 10,000 individuals for most of the Pleistocene.

Reich and Goldstein published a paper in PNAS of July 1998 in which they conclude a maximum pre-expansion population size of 5,900.

A more recent study by Huff et al. published in PNAS in February 2010in which they estimated that the effective population size of human ancestors living before 1.2 million years ago was 18,500, and in which they rejected all models where the ancient effective population size was larger than 26,000

Why should the later estimate be more likely than the earlier ones?
Although the details of the calculations are complex (or at least too complex for me), it appears that the genetic markers that are used are crucial, and that it is important to have markers that represent rare mutational events. The earliest studies apparently used mitochondrial genes and the non-combining parts of the Y chromosome as markers. (These are used and are valid for studies of more recent time.) The limitations in these resulted in a shift to Alu repeats and microsatellites in the two 1998 papers, respectively. The 2010 paper used the insertion of the longer LINE repeats, which occur about one tenth as often as Alu insertions.
There is a Wikipedia article on this topic that may be also be of interest.


Cardiac Excitation Threshold - in C++ modelling So I am trying to write a code in C++ about the cardiac excitation threshold.

I know that this excitation threshold is the shortest stimulus2 value at which it can conduct an action potential (known as the effective refractory period) at that stimulus1 value.

So my question is: In my code should I have: apply_stimulus1 for basic_cycle_length = 1000 and while you are applying this stimulus1 apply and a stimulus2 and print out the shortest value of s2 where I can have a potential? -> the way I am thinking this is apllying both stimulus simultaneously. If we say .... this is stimulus 1 and this is ,,,, stimulus2 at the end I will have ;;;;.

Or should I say when you finish applying that stimulus1 apply a stimulu2 and give me the shortest time where I get action potential? But here I will have stimulu1 .... || (meaning ends applying stimulus1) ,,,, apply stimulus2.

Is this how I am thinking it correct or I just got lost in my own thoughts and it is easier than I make it look?

My question is:

How do I get the cardiac excitation threshold using stimulus1 and stimulus2 and how can I incorporate the theory in my C++ code.

You wouldn't normally apply the stimuli simultaneously. The idea is to apply stimulus1, which has a given amplitude and duration, and follow that with stimulus2, which also has a given amplitude and duration, after a variable lag. You'll then see that the effective refractory period is dependent on the amplitude of stimulus2 (at least until you hit the absolute refractory period).


How are DNA segments selected in PCR? I understand that in PCR we're able to amplify only selected portions of the DNA... however despite reading it from multiple sources, I cannot figure out how this selection actually takes place.

I know that by using proper primers, one each for coding and template strands, we can direct the DNA polymerases to specific sites to start with. I also understand that these primers make the replication proceed in opposite directions, towards each other. Like follows:

However, I wonder what makes the replication terminate when the polymerase reaches the primer at the other end? Because as far as I understand, replication should continue indefinitely until the physical end of the sample strand is reached... such that we may decide the starting points but never the ending points.

Note: In your PCR program you always set extension time.

Case:

Product length = 500bp
PCR extension time = 50sec
Assuming that polymerase adds 1000 nt/min

Cycle 1:

Strand that binds FP: extends ~800nt to the right (as per the polymerization rate): 300 bp ahead of RP complementary site. This product is lets say P1
Strand that binds RP: extends ~800nt to the left: 300bp ahead of FP complementary site. This is P2

Cycle 2:

The products of cycle-1 become templates for next round.
FP binds to P2 -300nt from its 3' end. Similarly RP binds to P1 -300nt from its 3' end.
The resultant products will be 500nt which give rise to a 500bp perfect dsDNA.

Some P1 and P2 will keep forming at a linear rate; since your template is low in amount compared to the amplified cycle1 and cycle-2 products, your expected PCR product will be much higher (which gets produced at an exponential rate).


Relative rates of migration of circular, linear and supercoiled DNA in agarous gel electrophoresis I have read the supercoiled plasmid DNA migrates fastest when subjected to agarose gel electrophoresis and this makes sense to me because it is small and experiences the least friction because of its supercoiled structure.

Linear DNA migrates faster than the circular form. I didn't understand why exactly. Shouldn't the circular one be considered to be smaller than the linear, and thus quicker?

First let me supply an illustration of the situation described in the question, together with a reference.

Although you can see this sort of thing, just by searching for “plasmid migration on agarose gel”, this is one of my own from the last millennium (plasmid pBR322), appearing in a text from the last millennium, Adams et al. The Biochemistry of the Nucleic Acids (11th ed).

The poster’s attempt to rationalize the results, though expressing the quandary, is marred by the loose use of the word small, and the absence of any statement as to why ‘small’ pieces of DNA should migrate more rapidly.

The different forms of the plasmid have exactly the same molecular mass, so what is meant by small? My own initial way of looking at this is to consider the agarose gel as a mesh or sieve through which the molecules must pass, so that the larger the volume they occupy in space, the less likely they are to pass through the ‘holes’ in the mesh. The volume that they occupy in space might be regarded as that generated by rotating them from their midpoint in three dimensions. On this basis the supercoils, in which the DNA is collapsed into a short fat pseudo-linear shape should occupy the least volume in space, and the long thin linear the greatest. The diameter of the circle should place it somewhere between the other two.

So, we reach the same conclusion as the poster: the faster migration of the ‘linears’ than the nicked circles does not fit this simple model. In the text accompanying the figure I wrote “…a result that is a little unexpected” without attempting to explain it.

Am I able to explain this somewhat unexpected result now? An internet search produces either hand-waving or evasion (I stand to be corrected on this), so that I can only imagine that the result has something to do with the linear molecules having a greater chance of their ends being directed to the holes in the ‘mesh’ than the nicked circles, because of the open nature of the latter. One can perhaps imagine an hour-glass shaped portion of the sphere for the rotation of the linears that allows the ends to be directed at the holes.

More waving of hands? Perhaps. But the main point is that the physical explanation for the migration of molecules of different shapes during electrophoresis is more complex than a mere biologist might have hoped.


RNA polymerase question In this question we are examining a bacterial RNA polymerase that elongates at 20 codons per second.
Question 1: How long will this RNA polymerase take to transcribe the Lac Z gene at 3510 base pairs?

My answer: A codon is 3 base pairs so I start by dividing 3510 by 3 and then by 20 to get 58,5 seconds.

Question 2: Your bacteria can produce a Lac Z mRNA about every other second. How can you explain this?

My answer: I am very lost on this one. I thought that the mRNA would be as long as the gene so wouldn't this be 58,5 seconds not roughly 2 seconds??

Multiple RNA Polymerase transcription complexes engaged on the lacZ gene at the same time, staggered along the gene.


Heterocyst function in cyanobacteria and its localization 1.What is the function of heterocyst?

2.Where it is present?

A heterocyst I think may be a protecting organ in cells!

According to wikipedia :

  Heterocysts are specialized, pale-yellow,thick-walled cells with disputed function nitrogen-fixing formed during nitrogen starvation by some filamentous cyanobacteria, such as Nostoc punctiforme...

Thus by definition these are not within the cells, but differentiated cells themselves.

This is a good paper that can give you details on nitrogen fixation in the cyanobacterium Anabaena variabilis.

In general: cyanobacteria are photosynthetic prokaryotes, and many of them are capable of fixing nitrogen (that is the ability to use and incorporate nitrogen from the air as N2 gas). The enzyme called nitrogenase is oxygen sensitive thus either temporal or spatial separation of nitrogen fixing must be done to avoid damage to the enzmye from oxygen produced by photosynthesis.

  In Anabaena spp., aerobic nitrogen fixation is confined to differentiated cells called heterocysts that form in a semiregular pattern in a filament in response to nitrogen starvation. Fixed nitrogen in the heterocysts is transported to vegetative cells in the filament, while vegetative cells supply carbon and reductant to heterocysts

So as you can see spearate cells work together to supply each other with necessary nutrients. It is important to note that when sufficient fixed nitrogen source is available the number of such specialized formations is low due there is no need for extra nitrogen to be fixed

There are plenty of details on heterocysts and nitrogen fixation in the linked article. Also this paper hold details of regulation of nitrogen fixation and also has a thorough image of the process:


do game animals have poor eyesight? I have been watching some bow hunting videos on youtube. When hunting with a bow, the hunter needs to get really close to the animal, sometimes less than 10 meters.

It seems to me implicitly, and some hunters even say explicitly, that the animals (deer/elk/moose/buffalo) only see the hunters when they move. As long as the hunter has reasonably camouflaged clothes and is not smelled by the animal, they can stand in plain sight and the animal does notice them.

Do these game animals (deer/elk/moose/buffalo) really have such poor eyesight?

here are some videos as examples:

https://youtu.be/OqGSaGXHXgY?t=654

https://youtu.be/9tx_l9Jco_M?t=213

https://youtu.be/bP38tYhyhW0?t=303

https://youtu.be/xP9L885noEI?t=58

These species likely don't see you as a predator, or if they do they don't know if you've seen them yet.

A study indicated that the vision of the White-tailed deer was good;

  As expected for a crepuscularly active prey species, the visual system of white-tailed deer is specialized for sensitivity in low-light conditions and detection of predators.

The observation that many prey species only notice movement may relate to behavioural adaptations that increase their chances against natural predator species. Staying still while monitoring your surrounds decreases the chance of the predator seeing you.
I'll quote D'Angelo et al again;

  The visual streak of deer in combination with
  their wide-set eyes likely provides them with enhanced ability
  to monitor the horizon and to detect movement with a
  wide field of view while keeping their head stationary.

Visual specialization of an herbivore prey species, the white-tailed deer.
G. J. D’Angelo, A. Glasser, M. Wendt, G. A. Williams, D. A. Osborn, G. R. Gallagher, R. J. Warren, K. V. Miller, M. T. Pardue
Canadian Journal of Zoology, 2008, 86:735-743, 10.1139/Z08-050


What is the fastest but not venomous snake? Is it known which non-venomous snake can attack most quickly? I guess it is a snake that attacks its opponent by bites, and not some kind of constrictor.

The fastest non venomous snake is arguably the Eastern Coachwhip with a top speed of upto 10 mph (reference). If it feels cornered, it will attack with bites but otherwise, it prefers to flee.


Which ionic channels of Pacemakers can work in very low frequencies in extrasystole? At frequency 0-3 Hz.
Like computer processors which can work at low frequencies and controlling under- and overvoltage.

Normal most significant channels are Ca2+ and K+ that are changing.
However, I am not convinced that they can work with such a low frequencies.
There must be some other channels that are triggering the extrasystole on.

Which ionic channels of Pacemakers can work in 2-3 Hz triggering extrasystole?

I think none.
It is so specific frequency range that the possible sources are

autonomic nervous system and
some reflex arch.

Also, the frequency is logically low with autonomic triggering.
My conjecture is that sympaticus starts up extrasystoles.
I think it must go through some reflex arch to be so specific.


What happens if an IV drip with a saline solution slips out of the vein, but keeps dripping into the body? A patient has a saline solution IV drip into the vein. They have somehow moved around and the needle has fallen out of the vein, but remained in the body. Nobody has noticed and for a few hours water has accumulated like a balloon in the arm.

What happens? Is it dangerous? If untreated, would the body absorb the water, or would it remain as a balloon / pocket? If a pocket of water forms, what is the treatment?

The most common IV drip that would be sent home with a pet owner is Ringer's solution. This fluid is also commonly injected as a subcutaneous (between muscle and skin) bolus into both cats and dogs. Although IV administration is more efficient, this fluid is completely harmless if an IV catheter were dislodged allowing it to accumulate in the surrounding tissue.


Confusion about a gene's description I have a very basic biology question. I am reading the description of gene FAM166A here, and I have no idea what "sequence similarity 166" means. What does 166 stand for, what is this gene's sequence "similar to"? And what does member A mean?

The FAM symbols are defined in the HUGO Gene Nomenclature Committee guidelines.

The FAM symbol is an anonymous and temporary identifier that is given to groups of poorly characterised genes which share more than 40% amino acid sequence identity (see Section 4.1).

There are two human genes/proteins in the sequence similarity 166 group; FAM166A and FAM166B. These have some sequence similarity (more than 40%) but  function of this similar sequence is currently unknown. Once further characterisation has been performed for any FAM group they will likely receive more meaningful names.


How can a haploid plant be bisexual? According to Wikipedia:

  Meiosis is a specialized type of cell division that reduces the chromosome number by half. This process occurs in all sexually reproducing single-celled and multicellular eukaryotes, including animals, plants, and fungi Because the number of chromosomes is halved during meiosis, gametes can fuse (i.e. fertilization) to form a diploid zygote that contains two copies of each chromosome, one from each parent.

So it means that a haploid plant body will give rise to either a male sex organ or female sex organ that produces gametes to form zygote thus completing the alternation of generation.
We also know that chara a monoecious plant can be dioecious, which means that haploid plant body is producing both antheridia and archegonia which produce gametes by mitosis.
Coming to my question, "HOW CAN A PRODUCT OF MEIOSIS BEFORE FERTILISATION BE BISEXUAL?"
Does this implies that reduction division is not responsible of sex differentiation? If yes then what is responsible for sex differentiation in plants like chara where a haploid produces both gametes ?
Explanation will be appreciated

Meiosis does not determine sexual form. Eukaryotes use meiosis and fertilization to recombine genes to form new combinations.  Meiosis does produce haploid cells from diploid cells, but that has nothing much to do with the sexual forms involved.

In the case of the algal genus Chara, the organism's life cycle is entirely haploid except for the single-celled zygote formed during fertilization; this is called a haplontic life cycle.  Being haploid does not require an organism to be of one sex (or any sex), so there is no difficulty to being monoecious and having both male and female structures on a single organism.  The reason for having two kinds of gametes, sperm and ova, is simply practical: the specialized job of sperm is to move to another gamete, adn the job of the ova is to provide a maximum amount of nutrition for the future zygote (which means larger size and hence limited mobility).


Homologies to insect wings All winged vertebrates have wings which are homologous to each other and to the forelimbs of the non-winged vertebrates. But what about insect wings? Are all insect wings homologous, and are there any homologies between insect wings and any vertebrate limbs?

Insects and vertebrates are extremely distantly related: they're on opposite sides of the oldest split among bilaterally symmetric animals.  Their most recent common ancestor lived in the pre-cambrian and was almost certainly worm-shaped with no limbs at all.  There's no way that insect wings are homologous to any body parts of vertebrates.

The evolution of insect wings is a somewhat difficult topic, because it happened 350 million years ago in animals that do not fossilize well.  Wikipedia discusses several possible theories for what parts of non-winged insects are homologs of insect wings.  Currently the situation does not seem to be resolved.


Use lab agar for cooking Our lab manager suspect that something wrong with our lab Bacto agar (Difco). So she decide to throw it to the garbage. I think that it's just a waste to throw that thing.
Can someone think of reason why don't use that agar for molecular cooking in my kitchen?
(My lab manager think that i am totally crazy without give any reason)

Technically agar has first been used (and still is) in the kitchen and then adopted to the lab.
In the 19th century, gelatin was used in the microbial laboratory. The problem is that gelatin is much less thermostable than agar and at higher cultivation temperatures plates will melt and get liquid again.
In 1882 the german microbiologistt Walther Hesse (at that time an assistant in Robert Kochs laboratory) followed the suggestion of his wife Fannie Hesse to use Agar instead of gelatin. See the two references for some interesting details.

I personally would never use anything which comes from the lab in my kitchen since you never know if there are any contaminants in there. This is also probably the reason, why your lab manager doesn't want you to have it.

References:

Walther   and   Angelina  Hesse-Early Contributors  to  Bacteriology
History of the agar plate


Single channel micro arrays What does single channel microarray mean?
When is it used?
 Thank you for your case in advance.

Single channel refers to the system used to detect the labelled probes.  A single channel array, as shown in this slidedeck (slides 6-8) uses one type of molecule for detection.  In the example, (slide 8) the optical label is phycoerythrin.   Contrast that to a double channel array (e.g slide 7) that uses a "green" or "red" molecule used to label probes.  Detecting two different labels requires two channels, one to detect red and one the the green.   The key to using two (or more) labeling molecules is to ensure that your detection system can discriminate between the light spectrum emitted by each of the labels.   Many modern microarray readers have designs that handle multiple labels.
When you see single channel results, they often have colors.  The color is a pseudo color representation of the intensity of the emission of single-color label, which is due to how much probe has bound to the array at that spot.


The human has 46 double chromosomes or simple chromosomes? What I mean: does the human cell have 46 of these:

or 46 of these:

Thank you in advance.

Your first picture shows a chromosome that has been (1) condensed and (2) undergone DNA replication. During G1 interphase (normal cell activity; not dividing), your chromosomes actually do not look like either of the pictures. They look more like a mass of noodles (called chromatin; look at the image provided below); it is only during prophase (step 1 of mitosis, where the cell undergoes division) that the chromosomes condense into the form you have depicted in picture 1. Now, in G1 interphase, you only have single chromosomes. You have 46 of these, which can be grouped into 23 pairs—23 from your father, and 23 from your mother. Remember they aren’t condensed during this stage.

I have also included a diagram of the cell cycle:

In S interphase, DNA undergoes replication, and each of the 46 chromosomes create a double. This double sticks to the original chromosome at a point called the centromere. So long as the two “chromosomes” are conjoined at the centromere, the two “chromosomes” are considered as one chromosome, consisting of two sister chromatids (each like the “single chromosomes” you had previously). Again, in S interphase, chromosomes are not condensed, and look more like noodles than either one of your pictures.

During prophase, the chromosomes look like picture 1. Picture 2 depicts a sister chromatid during prophase (and metaphase), which is considered a chromosome after anaphase (when the two sister chromatids are separated from their centromere). Remember that when the chromatids are not conjoined at the centromere, they are considered each as their own chromosome.

Thus, the human body always has 46 chromosomes. They are “double chromosomes,” as you call them, during S phase of interphase to the beginning of anaphase of mitosis. They are “single chromosomes” from anaphase of mitosis to the beginning of S phase of interphase. As most cells spend the most time in G1 interphase (normal activity), you can say that most of the time their chromosomes exist as single chromosomes. Again, note that most of the time they don’t look like your pictures, except for the times that I mentioned above.

EDIT: To answer the question in your comment:

  If during interphase the DNA is not yet condensed and looks like a mass of noodles, then how can we know that there are 46 chromosomes (single ones in this case)?

During interphase, it is indeed difficult to tell how many chromosomes there are. It is only when they condense that they become visible to the eye and can be observed through a microscope. Chromatin, in its noncondensed form, is considered as euchromatin—that is, true (noodly) chromatin. When it is condensed, it can be referred to as heterochromatin. We can only count the number of chromosomes when they are in heterochromatin form; euchromatin is invisible to us. If we align all the chromosomes present, we will get something called a karyotype. Look below.

(You can see each chromosome in each of the 23 pairs are “double chromosomes.” These chromosomes were likely documented during prophase. Some karyotypes show "single chromosomes," most likely taken during anaphase or early telophase.)

In any case, double or single, we can observe that there are 46 chromosomes at all times. If we see "double chromosomes," we would find 46 chromosomes. If we see “single chromosomes,” we would still find 46 chromosomes. In both cases, we would find 46 centromeres, and ergo, 46 chromosomes.

References

Reece, Jane A., Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, and Robert B. Jackson. "The Cell Cycle." Campbell Biology. 10th ed. Glenview: Pearson, 2014. 232-50. Print.
https://micro.magnet.fsu.edu/cells/nucleus/images/chromatinstructurefigure1.jpg
http://www.everythingmaths.co.za/science/lifesciences/grade-10/03-cell-division/images/d62a6708a4a3942f21e003500ddf9664.png
https://study.com/cimages/multimages/16/karyotype_karyogram.png


Where does DNA fit on the Chomsky hierarchy? Since adenine pairs with thymine and guanine pairs with cytosine, this seems to imply that there's a trivial Regular Expression for DNA (i.e. it's trivially a Regular Language, which is Type 3 on the Chomsky hierarchy). With that said, is there a "less trivial" Regular Expression for DNA? Or, even better, is there a "deeper" grammatical structure for DNA, such as a Context-Free Grammar?

In truth DNA doesn't fit in the Chomsky hierarchy at all. DNA isn't a language, it is a complex molecule in a complex chemical environment. The fact that in many situations we can usefully abstract the structure of DNA as a string of four symbols should not obscure the underlying complexity. There is a simple code that describes the aminos acids encoded by triples of nucleotides, and some elements of a "grammar" in the structure of genes if you squint (start codons, stop codons, introns, and exons). But much of the function of DNA is stochastic and driven by the biophysics of the binding of RNA and protein molecules to DNA.


Taking care of Birds: Unwanted species scaring away a less common one from a birdhouse Near my house, I have set up a birdhouse, which has become home to a pair of Oriental Magpie Robins. They are not a common species in Delhi, India, and are generally shy of human interaction and avian conflict (territory disputes with other species):

However, the birdhouse is constantly visited by a pair of Common Myna. This bird is notorious for being an invasive species and had chased away a pair of Oriental Magpie Robins in the past.

Is there some way for me to get rid of the Mynas without scaring away the Oriental Magpie Robins? The bird is a real menace and I'm afraid it'll push away the Oriental Magpie Robin and other species of smaller birds that visit my locality. It is already considered an invasive species in Australia and South Africa. I don't want to kill the Myna, and trapping is out of the question as well. I just want to scare it off or restrict access to the birdhouse. Is there some way to make the birdhouse and surrounding area more appealing to the Oriental Magpie Robins?

^Oriental Magpie Robin. The darker one is male, the lighter one is female.

^Myna.

Update: The Mynas seem to be guarding the bird house from a distance, since I have been shooing them away. The Oriental Magpie Robin hasn't showed up since.

The best way to foil Mynas is to use an Anti Myna baffle over the nest box. Since Myna always fly directly into the nest box hole, this baffle prevents that while allowing other species to enter the box.


Can a brain dead person recover? Many times I have heard someone having to pull the plug because the patient was declared brain dead before the body healed fully? Why do they pull the plug without first waiting till the body/brain has a full recovery? What situations if not recoverable would they allow the body to fully heal before pulling the plug?

No.

Brain death is permanent damage to the brain. Depending on the specific definition, it may refer to either cerebral death or to failure of the brainstem to maintain functions like respiration.

It could be possible for mistakes to be made and for brain death to be declared in a patient who has not actually experienced brain death. However, this is incredibly incredibly rare: zero cases have been reported when appropriate guidelines are followed (Wijdicks et al. 2010). If someone is diagnosed as brain dead after a trauma, the medical staff involved in making that decision are stating that there is effectively no chance for recovery. Brain death is not diagnosed lightly.

Wijdicks, E. F., Varelas, P. N., Gronseth, G. S., & Greer, D. M. (2010). Evidence-based guideline update: determining brain death in adults: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology, 74(23), 1911-1918.


Effect of spaying on the female cat organism and health Veterinarians often recommend spaying a female cat if the owner does not want her to have kittens. What does biology know about the effect of spaying on female cats' organism and health (apart from lack of fertility, of course)?

From the standpoint of the skeletal system, spaying is definitely not good for her health. Removal of the ovaries mimics what happens at menopause, when circulating estrogen levels fall. Estrogen is necessary for maintenance of bone mineralization. Without estrogen, bones start to demineralize (the same process that happens in human females after menopause, leading to osteoporosis).

Then again, some animals, if they do not get pregnant, will cycle indefinitely until they get anemic and die. Ferrets are an example. So it's better to have these spayed.


Which statement is incorrect for Rubisco? My question is this:
Which of the following is NOT correct for rubisco?

a. It is the most abundant enzyme
b. It catalyzes two different reactions
c. It is involved in photorespiration
d. It is not used by CAM plants
e. It is not efficient in fixing CO2

My issues with picking one are because:

a. It is the most abundant enzyme due to its inefficiency
b. It catalyzes both oxygenase and carboxylase
c. It binds O2 meaning its responsible for photorespiration
d. Malate eventually provides a molecule of CO2 to the calvin cycle where it is bound to rubisco, meaning it is used by CAM plants.
e. It only fixes 3 molecules of CO2 per second, making it inefficient. The only reason why this doesn't matter is because of the abundance of rubisco.

Short answer
D

Background
A. Is correct, as it is the most abundant enzyme on land, and probably also in marine environments (Raven, 2013).

B. Is correct, as Rubisco catalyzes the carboxylation, or oxygenation reaction depending upon the molecular concentration of CO2 or O2 (Sudhakar et al., 2016).

C. Is correct, as it reveals the inefficiency of Rubisco, as CO2 and O2 compete for the active site. Fixation of O2 during photosynthesis oxidizes ribulose‐1,5‐bisphosphate into 3‐phosphoglycerate and phosphoglycolate - which is basically a waste of energy.

D. Is incorrect and hence the answer to your question: Rubsico is present in CAM plants.

E. Because of the photorespiration described under B & C, Rubisco is indeed regarded to be inefficient.

References
- Raven, New Phytologist (2013); 198(1): 1–3
- Sudhakar et al., Phenotyping Crop Plants for Physiological and Biochemical Traits, 2016


Why is Sleep apnea only risk to males? I was reading this article. In Risk Factors, it clearly mention "Being a male".

Why is Sleep apnea only risk to males?

Wikipedia actually means that being male is a risk factor for sleep apnea, which is a jargony way of saying that males have been observed to develop sleep apnea more often than females.

The article pointed out by com.prehensible suggests that this difference in the prevalence of sleep apnea between genders is due (in part) to a difference pharyngeal airway length (illustrated below), which is longer in men than in women even when corrected for (body) height.

Since the pharyngeal airway lacks any bones or cartilages for structural support, the theory goes that a longer pharyngeal airway is more likely to collapse during sleep, when breathing is reduced via mild to moderate hypoventilation (in everyone). Here's an illustration (3rd one in the set below) what that collapse looks like (source):

Another theory of this structural kind is that the pharyngeal cross-sectional area is smaller in women relative to men, but studies measuring this cross-section didn't all come to the same conclusion.

Finally, an experimentally observed difference between males and females during sleep is the so called "hypocapnic apneic threshold", which means that relative to men, women require a more substantial reduction in PETCO2 (a measurement of carbon dioxide partial pressure during expiration) before they show signs of apnea. A more prosaic way of saying this is that men's bodies are more prone to go into a state where a reduction CO2 in the expiration causes the brain to decide to stop breathing for a bit because it seems it has enough oxygen (based on the lack of CO2). This mechanism is substantially inhibited during wakefulness and least inhibited during NREM sleep (and in REM sleep it's somewhere in between).

Why there's a difference in this threshold between men and women is not known precisely, but another experiment established that giving testosterone to women increased their breathing instability during sleep. And conversely, blocking some of the effects of testosterone by administration of finasteride increased breathing stability in healthy men during sleep. Note that this is a pretty new (2013) study. Neither finasteride nor any other medication is currently FDA-approved for treating sleep apnea.

And one more thing to point out is that there are different types of sleep apnea, so the two mechanisms discussed above are not necessarily contradictory or competing; the first one (airway length and its collapse) is mostly relevant to obstructive sleep apnea, while the second one is more often discussed in the context of the so-called central sleep apnea.


Term for a prey animal's recognition that something potentially threatening is looking at it? On my daily walks I frequently see individual or small groups of cattle egrets. At first I would try to photograph them but they would fly away. This vexed me because they ignored everyone else walking by as well as bicycles or loud vehicles in areas where there were roads.
I took it personally until I realized it wasn't me or my clothes, but the act of looking at them and taking an interest in them that spooked them.
This even happened at distances approaching 100 meters in open spaces, so I am not sure they could resolve my eyes and determine if my gaze was fixed on them. However, a few non-scientific tests suggested that they seemed to get nervous when I turned my head and looked at them, even though I kept moving. But even if I didn't look at them but instead continued to look forward, simply stopping and standing in place to take out my phone to snap a photo was enough to trigger them to fly away.
Question: Is there a term for this phenomenon in birds or other animals, not the flying away or fleeing part, but the recognition that something or someone potentially threatening is looking at them and/or may have taken an interest in them? Are there separate terms for responses to motion and responses to a gaze based on eyes or perceived face orientation?
Note: I have noticed a similar phenomenon with Malayan Night Herons as shown in What kind of big bird is this seen walking around Taipei? The individuals I see are more acclimated to people, but I still have to act at least disinterested when photographing them.

"Gaze" is the typical term for the direction something is looking, including head/neck and eye position. Gaze detection, gaze following, and gaze perception are used in the literature; there might be other combinations with the term "gaze", as well, I see lots of results with a more general gaze+predator search.
These are all more general terms than the specific use by prey animals, particularly in social gaze: being able to figure out what others around you are looking at, but they are to some extent the same sort of ability.


How do our eyes see an inverted image? How exactly do our eyes see an inverted image of what we are looking at?
Does it have something to do with the shape of our lens (i.e. convex)?

This isn't particular to eyes. Anything without mirrors would show the same behavior.


Is there a biological mechanism for evolution encoded into our DNA? Throughout high school, I remember learning about Darwin's theory of evolution as if it were near-fact. But something always seemed wrong about the ideas presented.

Survival of the fittest
Random mutation
Natural Selection

All of these things seem to account for some margin of evolutionary progress, but I always remained skeptical that the extremely complex features of life could have formed from these methods alone, even after hundreds of millions of years.

Here's what I notice:

Any time a species has needed the development of a specific feature to survive, it has developed that feature, and that feature precisely.

I'm going to use this example:

Turtles on an island where shrubbery grew higher up developed longer necks, to reach the leaves.

I imagine that turtle looking up at that food, and sub-consciously wishing to get to it, constantly straining, for its entire lifetime.

It seems plausible to me that we (advanced life) could have a biological mechanism to "write" needed alterations into either our own DNA or our reproductive DNA over time, triggering the very specific evolutionary developments necessary to our survival without relying on random mutation.

My question:

Is this possible? Does any similar mechanism exist that we know of? If not, how can so many specific (advanced) evolutionary leaps be otherwise explained?

This entire answer will be long, so read the short part first, then read the rest if you (or anyone else) is curious. Citations are included in the long section. I can include additional citations in the short section if needed.

Long Story Short

Your question touches on some common misconceptions about how the evolutionary process. Organisms don't "want" to evolve traits. Traits evolve through the biological processes of random mutation and natural selection.

Organisms do not "want" to evolve traits.  (Well, OK, I'd love to evolve an extra pair of hands but that is not possible.) Natural selection works by modifying existing traits. Your turtle can stare all she wants at food out of reach but she will not evolve a longer neck. Instead, natural variation exists among neck lengths of the turtles because of variation of the genes that determine features related to overall boxy size. Those individuals with longer necks may be able to get a bit more food, live a little longer, and reproduce a little more. They will pass along their genes to their offspring, so perhaps more of their offspring will also have longer necks. Over many generations, the turtles may have somewhat longer necks.

A common misconception is that the traits of organisms are precisely adapted for a specific need. They are not, for a few reasons. First, natural selection occurs relative to the current environment. Adaptations that work well in one environment may not be so useful in another environment. Environments are rarely stable over evolutionary time so traits are subject to constant change.

Next, as mentioned above, natural selection can only work on what traits are present. While an extra set of arms would be handy, I am a tetrapod. My four appendages, along with the appendages of all other tetrapods, trace back to our common ancestor. The appendages of all tetrapods are modifications of that ancestral trait.

Finally, organisms haven't "sampled" the entire realm of possible mutations and combinations of mutations. In other words, a certain mutation or set of mutations might actually be able to adaptively improve a particular trait in the current environment but, if the mutations never occur, then the improvement can never happen.

We only need to look at ourselves to realize how imperfectly adapted we are. We get bad backs and knees because our bodies weren't designed to walk upright. We evolved from quadrupedal organisms. This has happened so recently that changes in the structure of our knees and backs haven't yet evolved (and may never).  Search the internet for the "blind spot" eye test. We have a mass of blood vessels in front of the retina of our eyes, which reduces our visual accuity. We often have to have teeth pulled from our jaws because the flattening of our face (relative to our australopithicine ancestors) has shorted our jaws. We don't have as much room for our teeth but we have not evolved a reduced number of teeth.

As for human technology being able to make direct changes to our DNA to improve our adaptability, I would say no. While I do not have the ability to see into the future, the complexity of our genome, and more specifically how genes are regulated, suggests to me this would be a very daunting if not impossible task.  See the long answer below for more on regulatory genes but the gist is that a small set of regulatory genes control most of the other genes (including other regulatory genes). The interactions are extremely complex and we have a detailed understanding of very few of these interactions.  I speculate that affecting one such gene in a "positive" way is very likely to have many unintended negative consequences.

Below are some simple math and other ideas to show you how mutations can lead to the many adaptive traits that you see among the diversity of life on earth.

Long Story

  how can so many specific (advanced) evolutionary leaps be otherwise explained?

Mutations occur at random throughout the genome. Most mutations will be neutral. That is, they are neither bad or good from an evolutionary viewpoint. The mutations are neutral because the genome for most organisms is non-functional. Mutations that occur in the functional regions of DNA (i.e., protein-encoding and related regions) are more likely to be detrimental (bad) because the mutation may negatively affect the function of the protein or even the ability to produce the protein.  However, some mutations are beneficial. The mutation may actually enhance the functionality of the protein or even produce new proteins.

A couple of factors have to be considered regarding mutations.  The mutation rate is very low.  For example, Kumar and Subramanian (2002) compared the DNA sequences of 5669 protein-encoding genes from 326 species of mammals.  Their results suggested that the average mutation rate among mammals is 2.2 x 10$^{-9}$ per base pair (bp) per year.  This means that, on average, a point mutation has changed each DNA nucleotide position in the mammalian genome slightly more than twice (2.2 times) every billion (10$^9$) years. That's a lot of time!

However, this same rate occurs in every individual in the population, so you have to consider the population sizes of the organisms. So, let's do a simple exercise. Consider a species like the rock pocket mouse or another small mammal that has a very short generation time. For this simple example, let's assume the generation time is one year. That means that the mutation rate of 2.2 x 10$^{-9}$ per bp per year would then correspond to 2.2 x 10$^{-9}$ mutations per bp per generation. Generation time is important because new mutations are inherited only through reproduction.

Assume the average mammalian diploid genome is about 6 billion (6 x 10$^9$) nucleotides in size. The number of heritable mutations that occur in a single offspring is

$$(6 \times 10^9) \times (2.2 \times 10^{-9}) = 13.2.$$

Next, assume that about 2.5% of the mammalian genome is composed of functional, transcribed sequences that may affect the phenotype (the traits of the organism). That means that, of all the mutations that occur in every offspring every generation, about 2.5% could potentially affect the phenotype.  That is,

$$13.2 \times 0.025 = 0.33.$$

Still a small number.  But, now we have to account for population size. Small mammals, like mice and voles, generally have large population sizes.  Assume that the population of rock pocket mice contains 100,000 reproducing individuals. If so, then

$$0.33 \times 100,000 = 33,000,$$

which is the number of new heritable mutations that could occur in the population. Most of these mutations will be detrimental and removed from the population by natural selection but, if even a small fraction of these new mutations are beneficial, then natural selection can cause these beneficial mutations to increase rapidly in frequency in the population during future generations.

In humans, Nachman and Crowell (2000) estimated that the average mutation rate was 2.5 x 10$^{-8}$ mutations per bp per generation (not year), by comparing the genomes of humans and chimps. If we assume the same genome size and effective human population size of 500,000 individuals, then applying the same math suggests that 1,875,000 new mutations that potentially affect phenotype occur in the human population every generation. Again, only some of these will be beneficial but that is still the possibility of a number of new beneficial mutations. In evolutionary terms, a mouse or human generation is the blink of an eye.

How long would it take for a beneficial mutation to spread through a population? That depends on two things. How beneficial is the mutation (called the strength of selection, s) and the population size? To estimate how long it would take for a beneficial mutation to spread through a population, we can use the formula,

$$t = \frac{2}{s}\mathrm{ln}(2N_e),$$

where $t$ is time in generations, $s$ is the strength of selection, and $N_e$ is the effective population size (number of reproducing individuals). For the strength of selection, let's assume $s=0.01$, which is weak but positive natural selection. Going back to our rock pocket mice with $N_e = 100,000$, then the beneficial mutation would be spread throughout the population in only 2441 generations (remember, we're talking evolutionary time so 2000 years is nothing). If $N_e = 10,000$, the mutation spreads in only 1981 generations.  If we increase the strength of selection t 0.2, then the times are 122 and 99 years for population sizes of 100,000 and 10,000 years, respectively.

These "back of the napkin" calculations show just how quickly even weakly beneficial mutations can appear and spread throughout a population. Yet, this doesn't include other types of mutations like gene duplications that can also allow new proteins to evolve. For example, human ability to see red colors is due to a simple gene duplication (Nathans et al. 1996 and references therein). This duplication also explains the common form of red-green colorblindness.

Whew!

There's yet more to our mutational story. Consider humans and chimps, which are nearly identical from a genetic standpoint (between 96-99% depending on how you calculate it) yet they appear very different.  If humans and chimps diverged from their common ancestor within the past five million years, how could they differ so much? This question was initially posted by [King and Wilson (1975)]. They argued that mutations to structural proteins (like those that compose bones and muscles) would not be enough to explain the phenotype differences between humans and chimps. The proposed that regulatory genes are the key to understanding the big differences. Regulatory genes are those that control other genes, by turning them on or off and other important functions. Changes to the regulatory genes can cause fairly rapid changes to the phenotype.

This understanding has led to the broad (and fascinating) field of evolutionary developmental biology. This field focuses on how mutations in regulatory genes associated with development (from embryo to adult) have had a long-term evolutionary impact. The field is rich with examples, but one cool one is associated with duck feet and bat wings. Let's begin with the embryo. Most vertebrate embryos have membranes between the digits (fingers and toes) during an early stage of development. For most vertebrates, the membranes are lost later in development. The small flaps of skin you have between your fingers are the remnants of your embryonic membranes.

A set of regulatory genes called BMPs (and a couple of others) are responsible for causing the loss of the membrane in vertebrates. However, through different sets of mutations, the BMPs are not able to function in duck feet and bat hands. Thus, they both end up with membranes between their digits (Weatherbee et al. 2006).  Thus, two different mutations block the same set of developmental genes, leading to novel adaptations in two very different types of vertebrates. One final example is the evolution of bird feathers from scales. As you may know, birds are evolved from dinosaurs. It turns out that bird feathers and alligator scales (alligators are birds closest living relative) use the same regulatory genes to develop. The genes are BMP2 and SHH (sonic hedgehog for fans of the old computer game) (Harris et al. 2002). Other regulatory genes underlie the different types of feathers, like downy feathers and flight feathers (Harris et al. 2002).

Literature Cited

Harris, M.P. et al. 2002. Shh-Bmp2 Signaling module and the evolutionary origin and diversification of feathers. Journal of Experimental Biology 294: 160-178.

King, M.-C. and A.C. Wilson. 1975. Evolution at two levels in humans and chimpanzees. Science 188: 107-116.

Kumar, S. and S. Subramanian. 2002. Mutation rates in mammalian genomes. Proceedings of the National Academy of Sciences USA 99: 803-808.

Nachman, M.W. and S.L. Crowell. 2000. Estimate fo the mutation rate per nucleotide in humans. Genetics 156: 297-304.

Weatherbee, S.D. et al. 2006. Interdigital webbing retention in bat wings illustrates genetic changes underlying amniote limb diversification. Proceedings of the National Academy of Sciences USA 103: 15103-15107,


Why do cucurbits produce so much fluid when their stems are cut? When carrying out some germination tests on species in the Cucurbitaceae, I notice that young plants of this family produce a lot of clear fluid when they are dissected. Most plants I dissect do not produce any fluid, even ones which appear to be turgid and have large cells. Why do cucurbits do this, and what's the fluid?

Looking through some papers it is not clear to me that botanists actually know why this should be the case, and I am sure that you are more qualified than me to comment on this Richard! However, there's some discussion of this in Zhang et al. (2012).

These authors argue that the "exudate from curcubits is copious" because of physiological adaptations due to their growth habit - i.e. they are vines and as such often require the structural support of other plants. Vines compensate for a lack of a supporting stem structure by having xylem vessels that are wider than comparable freestanding species  and "high hydraulic conductivity" (which is a measure of how readily water will flow through pores - in the case of curcubits - very readily). Similarly, sieve tubes and sieve pores are very wide compared to species in other families. Since these sieve tubes have such a large cross-section, they do not readily self-seal.

The Origin and Composition of Cucurbit Phloem Exudate
C Zhang, X Yu, BG Ayre, R. Turgeon - Plant Physiology, 2012 - Am Soc Plant Biol. 158, 3

See also:

Why vines have narrow stems: Histological trends in Bauhinia (Fabaceae), Ewers, F., Fisher, J, Oecologia, 1991, 88, 2


Fasting gastric pH versus normal gastric pH I want to know if someone is fasting (no food or drink for a whole day) will they have a higher or lower pH than a person who is eating regularly? If so what is an estimate of both of those pH's in the stomach?

The stomach linings generally secrete gastric acid (HCl, KCl and NaCl) and the native pH of the stomach is around 2. The longer you fast, gastric acid levels keep increasing until it reaches around 1-1.5. The food that you eat increases the pH levels of your stomach because the acid reacts with the food while digestion. Depending upon the type of food you eat, the pH levels of your stomach vary, but it is generally around 4-5 (again it varies depending upon the type and amount of food there is in the stomach).


How many palindromic sequences in human genome? I'm writing an article on palindromes (the words) and I wanted to mention the existence of palindromic gene sequences. Roughly how many palindromes exist in the human genome? I understand the number will vary from person to person. All I want to know is the order of magnitude. Is it 10^2, 10^3, 10^6?

The human genome contains approximately 1.25*10^7 palindromes longer than 6 bp (that is 8 bp or longer). Some interesting facts are also known about their distribution.

  We found that 24 palindrome-abundant intervals are mostly located on G-bands, which condense early, replicate late, and are relatively A+T rich. In general, palindromes are overrepresented in introns but underrepresented in exons. Upstream region has enriched palindrome distribution, where palindromes can serve as transcription factor binding sites. We created a Human DNA Palindrome Database (HPALDB) which is accessible at http://vhp.ntu.edu.sg/hpaldb . It contains 12,556,994 entries covering all palindromes in the human genome longer than 6 bp.

And no, the number of shorter ones (shorter than 8 bp) isn't mentioned in the paper because they are considered unimportant, biologically.


What is the reason behind more severe proteinuria in nephrotic syndrome than in nephritic syndrome? Why is there less protein loss via urine in case of nephritic syndrome than in case of nephrotic syndrome?

It is to do with the extend of the damage to the glomerulus. In nephrotic syndromes the glomerulus is damaged so that there is death of the podocytes. This happens to sufficiently high number of podocytes so that large proteins such as albumin and clotting factors can leak out causing large proteinuria. Damage to the basement membrane may also occur, such as in minimal change, where there is a loss of charge on the basement membrane.

In nephritic syndrome the damage is as a result of inflammation which does not lead to the same structural damage as in nephrotic syndrome, therefore there is not leakage of protein to the same degree.


Will a Codon result in same amino acid across organisms Will all organisms with the same 3 nucleotide sequence in the codon produce the same exact same amino acid. I read that the three nucleotide sequence will code for a particular amino acid. I did not understand if that is the case across organisms. Can someone explain this in simple terms.

Although the answer to this question may be found in Mitochondrial Genetic code, because that answer is primarily about mitochondrial genetic codes, I shall give a more directed answer here.

Because the same genetic code that was elucidated in bacteria was found to apply to higher eukaryotes, it was initially assumed that the genetic code was universal, and was referred to as such. Subsequently it was discovered that mitochondria did not generally employ this ‘universal’ code, which is now usually referred to as the ‘standard’ code — indeed different mitochondrial codes were found in different organisms.

However the question seems to be more concerned with the genetic codes of  bacteria and the nuclear genetic codes of eukaryotes. Here also there are deviations from the standard genetic code, which can be found listed either on this Wikipedia page or at NCBI.

Below are some examples from the NCBI list (where references may be found) with the standard coding in parentheses:

 Mycoplasma
 UGA      Trp          (Ter)

 Ciliates, Dasycladacean and Hexamita
 UAA      Gln          (Ter)
 UAG      Gln          (Ter)

 Euplotidae
 UGA      Cys          (Ter)

 Candidate Division SR1, Gracilibacteria
 UGA      Gly          (Ter)

 Pachysolen tannophilus
 CUG      Ala          (Leu)

Finally, tRNAs for the ‘additional’ amino acids, selenocysteine and pyrrolysine recognize, respectively, the UGA and UAG stop codons in specific contexts.