Is there an evolutionary advantage for coconut oils to be rich in saturated fats? I know that coconut oil is composed of multiple saturated fatty acids, but is there a reason why this would have increased the fitness of the coconut plant?

This is entirely speculation, but the part of seeds that is pressed for oil(the endocarp) is enriched in saturated fats and long fats in ocean-going fruits. The coconut is 91% saturated fats, the oil palm is about 50%, etc. The tamanu or 'ballfruit' produces monounsaturated long-chain fatty acids in the endocarp, about 75% C18 oils, mono- or di-unsaturated.The calabash is astonishingly 20% saturated and 78% C18 oils, and is also sea-distributed(these seeds are called disseminules).

It's not a totally straightforward correlation. Peanut oil is 75% C18+ and 15% saturated and the oil palm mesocarp is only 50% saturated, but the endocarp is 81% saturated fats.

There's an additional consideration here: longer chain fatty acids are slightly more energy efficient per unit mass than shorter chain ones.

Without better data on energy density or spoilage rates on different blends of long-chain fats I can't conclude conclusively that spoilage and energy density are why disseminules tend to have longer-chain oils and more heavily saturated fats, or even that they definitely do. But it looks like they do, and that would make sense.


Nucleoside analogs that cause mutation I'm confused with this explanation in my book:
2-aminopurine is incorporated into DNA in place of adenine but can pair with cytosine, so an AT pair becomes a CG pair.

This sentence seems odd to me. It says that adenine is replaced with 2-aminopurine, but can pair with cytosine. And the AT pair turns to CG pair. Does it mean that 2-aminopurine substitute adenine, and then it works like cytosine to bind with guanine?? Because 'AT pair becomes CG'. But it says 'but can pair with cytosine', which one is going to bind with cytosine??

I've Googled on this but couldn't reach to a clear explanation about this. Can someone please explain to me how this analog works or rephrase the sentence in my book? Thank you.

The book that I'm referring is Microbiology: an introduction 10th ed. By tortora, funke and case. Page 229.

If you feed bacteria 2-aminopurine then at some low rate it gets incorporated into into the DNA instead of adenine during DNA replication. In other words there will be a base pair between thymidine and 2-aminopurine.

Two things could happen:

DNA repair could detect the unusual base and attempt to correct. If the 2-aminopurine is excised then adenine will be inserted--no mutation. If, however the thymidine is excised then sometimes a cytidine will be inserted. This gets resolved below.
During the next cell division the replication machinery will sometimes incorporate a dC across from the 2-aminopurine. Then in the following cell-division a dG will be incorporated across from the C, so what used to be an A-T base pair has become a G-C base pair (eventually).


Accurate surveys of urban pigeon and bird populations I've been working on an assignment to develop mathematical models of urban pigeon populations. (As a disclaimer, this is part of a math course, not a biology course). I already understand the mathematics behind this and have developed several plausible models, but I'm at the stage where I need more detailed data in order to validate my models.

It's surprisingly difficult to find accurate population dynamics data for urban pigeons (especially given my inexperience with this kind of a literature search and general "unsophisticated" understanding of biology).

I do have access to some journals (e.g., via my university library, Google Scholar and Amazon.com), but the best resource I've been able to come up with so far is Illinois Birds: A Century of Change (published by the University of Illinois). The books on urban bird populations I've found so far all seem to be targeted to bird watchers (which I'm not).

Is anyone aware of a detailed/accurate data set on population dynamics (either of urban pigeon populations in particular or of urban bird populations in general)?

You can find population data for lots of species at The Global Population Dynamics Database, which can be used to test and fit population models. When searching for Columbidae (the dove family) I find 16 datasets of different lengths, but none for Columba livia though.

To search and download data you first need to register for a user account.


RNA seq and using of Poly(A) or non-Poly(A) based amplification of RNA I'm studying "Deep sequencing the circadian and diurnal transcriptome of Drosophila brain" Hughes et al., 2012. I've got some problems with the materials and methods.
Before RNAseq, the authors amplify RNA. They use two kits: Poly(A) based and non-poly(A) based. For the samples Poly(A) based amplified they do a sequencing to generate 100 bp paired-end and for the samples Non poly(A) based they do a sequencing to generate 75 bp single-ends.
I read in the strategy:

Total RNA was amplified, and ribosomal RNA was depleted, using a non-poly(A)-based amplification kit, which significantly diminishes the 3' bias in downstream libraries used for RNA-seq (see Methods).

I don't understand why they use both kits. Actually, they say that they want to asses the bias introduced by an alternative amplification methods BUT the following sequencing is not the same in both cases so there is more than one parameter which change between the two protocols so I don't understand how they can compare.

For the poly(A) based I understand that the rRNA are not polyadenylated so they remove rRNA from the amplified sample. However, don't they remove non-coding RNA too (long or short)?

For the non poly(A) based, I don't understand how they remove the rRNA but I understand that since they don't select the RNA according to their poly(A) tails they keep the rest of the RNAs which are not kept in the poly(A) based amplification.

When I look to the RUM statistics, I see that there are fewer total aligned reads in non-poly(A) based: 70-80% (non polyA) and 80-90% (polyA). So it seems like we lose some information with non-poly(A) based.

To sum up, why the authors use Poly(A) and non-poly(A)? Why do they show all the rest of the results from the non-poly(A) amplification since they have less aligned read? How do they compare since the following sequencing is not the same? How the rRNA are removed in both techniques and especially in non-poly(A)?
I didn't find the protocols kit with exactly the same name but here are the links to the protocols which are closer (I think).
http://www.mscience.com.au/upload/pages/nugen/nugen_ov_rna_seq-brochure.pdf
http://excilone.com/client/document/ug-arcturusE%E2%80%9E%C2%A2-riboamp%C3%82-hs-plus-amplification-kit-user-guide_38.pdf

Yes, it was odd that they said that. The second protocol with the polyA based method had another purpose though, which was "examine the reproducibility of period-regulated genes in an independent genetic background". I would suspect this was its main purpose, and not so much to look at fragment bias, which has already been done in other papers. They didnt even publish this data in the main paper, they put it in the supplement.
Yes, this would remove any transcript without a polyA tail.
One way of purifying is by using oligos that are antisense specifically to rRNA. The oligos will be attached to some solid phase, on a column or a bead or something, and the rRNA will stick to it and everything that doesnt is what will remain in your sample
It is not safe to say that you lose information with polyA based kits. The polyA based technique had reads that were single end and only 75bp long. This is compared to the other protocol which was 100bp paired. Reads that are 75bp will align much more easily than 200 bp (100 x 2 since its paired). However, there will not be as much certainty in the alignments, as there is a greater chance it will align to multiple locations in the genome, or align to the wrong location. So yes they have more reads aligned but I would be hesitant to make any conclusions from this. And if you look at total numbers of reads, the non-polyA method aligned more. Again, I dont think the main purpose was to show that one method is better than another.

Basically the method you choose depends on your experiment and your samples. Random hexamers will give you non-coding RNA which is important in some experiments, and that is its main advantage. It will also give more uniform coverage across the gene (no 3' bias). Poly(A) selection will give you only mRNA, however you will miss any transcripts that are degraded or partially degraded. If you have a high quality sample or a large amount of starting material this is less of a concern. As mentioned before you end up missing parts of the 5' end on some transcripts with this method. If you have a low abundance transcript that you are trying to find, polyA selection is probably best, as it is more likely to be captured and you will capture the whole thing, rather than just getting bits and pieces of it with random hexamers. They both have advantages and disadvantages. Hopefully this helps you or someone make a decision.


Like size and colour constancy, why does the brain not maintain focus constancy? I have progressive myopia. I grew up with perfectly normal eyes but slowly started getting myopic.

The thing is, my brain knows (or should know) what the world looks like -- it knows that far away objects do not suddenly blur. So when the input from the retina changes, why doesn't the brain correct it in perception?

I'm assuming here that this should work by the same principles as size and colour constancy. In both cases the input from the retina is different but the brain doesn't perceive it as an actual change in size or colour.

Interesting question. I concur with @Chris. Color constancy and size constancy are neural mechanisms and can therefore be imposed on visual input from the retina. In contrast, a blurry input cannot be neurally improved. As an analogy: Visual perceptions are processed and rendered by the brain and therefore represent "photoshopped" perceptions. In other words, perceptions are subjective representations manufactured by higher-level visual processing. However, focus is determined by optics. An out-of-focus picture, to push the analogy, cannot be fixed by fotoshop, nor the brain.


How long does it take to stain cells? I'm never going to run these type of experiments but I do need to have a good idea of their timescale. After I fix my cells, if I stained my cells with histology stains like DAPI, Fluorescein, and various labeled antibodies, how long do I have to wait before I can examine my cells with microscopy?

For fluorescence immunocytochemistry, there are 3 main incubations that determine duration of the procedure. Generally it takes 2 days to stain your cells before you can visualize them. Once cells or tissue are fixed onto glass, you first incubate with a primary antibody to directly target a specific antigen(s), usually overnight. After primary labelling, a secondary antibody is applied to target the primary antibody, which usually takes a few hours. These secondary antibodies come conjugated to some fluorescent dye (Cy5, TRITC, FITC, AlexaFluors, etc). A nuclear counterstain is really quick, only 5 minutes. After all the labelling and nuclear stain, you can mount the coverslip with mounting media and once it cures you can visualize them.

Abcam has one of many quick reference guides.


Distribution of fitness in wild populations If I get out in the wild observe wild populations and measure the distribution of fitness $f(w)$ in a given population. What will I find out? Will I observe a Gaussian distribution, a Poisson distribution, an exponential distribution, ….?

It probably depends on the species under consideration, typically it may depend on whether there is an sexual selection in this species. I welcome any insights!

Long for a comment but consider this to be an extended comment and not an exact answer:

At least for Poisson I can say that the random variable should fit the three Poisson postulates. Poisson RV generally describe discrete events in continuous intervals. A fitness function doesn't seem to be such a type of RV; it is a property of a population rather than an event.

I would also not expect it to be exponentially distributed which would mean that probability is highest for the most fit (or most unfit) individual i.e the more fit are more frequent. I assume that it cannot be decided who is the most fit until selection happens. This may still be the case just after a selection event but not otherwise.

It seems that this function should be Gaussian: assuming that there is little variability between individuals and what exists is because of independent events of mutation, these should converge to Gaussian as per the central limit theorem.

But generally the term that best describes this RV is a performance function. Fitness would always be a conditional RV.

For e.g. I would very roughly define fitness like this:

$f(X) = P(m(X)\ |\ p(X),S)$

where $f(x)$ is the fitness of $X$, $m(X)$ is the survival probability of $X$, $p(X)$ is performance in different tasks and $S$ is selection event.


Computing Percent Identity between DNA / Amino Acid Sequence What are some tools where I can input a pair of DNA sequences (or alternatively a pair of Amino Acid Sequences) and compute a percent similarity identity metric between them?

Is BLAST the right algorithm for this or something else?

The context is that a certain patent protects all sequences at least 90% or more identity to a given sequence. I wanted to test some candidate sequences and verify the percent identity metric.

Below I post a patent-snippet where they actually define their identity metric.

tBLASTn, BLASTx and tBLASTx can be used.

It is clearly illustrated here.

If you have just two sequences you need not do a search against the database. You can simply align them using Smith-Waterman or Needleman-Wunsch algorithms, as David mentioned. However, you still need to translate your DNA to protein before doing the alignment. Again, as pointed out by David, with protein alignments you do usually not use identity. Scoring matrices like PAM or BLOSUM are used to calculate similarity.


Popliteal artery for a heart bypass My father undergone surgery 10 years ago to get 3 bypasses close to the heart. Surgeons did a very long cut on his leg to get the material to make the bypasses they would later put on his chest.
What I understood at that time, is that they took three sections of the popliteal artery to obtain the material to make those bypasses, and that they fixed the cuts again to restore such artery. The reason why that artery was chosen is because it is very elastic and surgeons can extract a section and stick it together again.
My father is convinced they removed the whole popliteal artery from that leg and chopped it down to make the material they would use for the bypasses.
I am trying to find information about this procedure to find out who is wrong. The problem is that we both are completely illiterate in medical stuff, so we are lost in the mist. What I found is that the popliteal artery is important and blockage could be problematic.

I'm not a physician, but I suspect the popliteal artery may not have been the vessel used.  The popliteal artery has a very important role in supplying the leg with blood, and maintaining the blood supply from it to the lower (distal) leg is sometimes reason for harvesting other vessels.
You described a very long cut, which sounds like what you would see for harvesting the great saphenous vein.  The great saphenous vein is the longest vein in the body, and dominates recent scientific publications in response to a query of ''coronary bypass harvesting''.  (There are publications in that batch evaluating newer endoscopic techniques in which the long cut can be avoided)  Wikipedia reviews the use of this vein reasonably well.


Can ACE2 receptors be syntesized? I read that there are labs that can produces the spikes of the coronavirus. I wonder can they also synthesize ACE2 receptors or parts of them? If yes, can they be used as drugs?

The drugs you are referring to are called receptor mimics or peptide inhibitors.  Yes, molecular mimics for human ACE2 can and have been synthesized.  Binding of these mimics to coronavirus spike proteins leads to sequestration or inactivation of viral particles.

Relevant literature:
Romano M, Ruggiero A, Squeglia F, Berisio R. An engineered stable mini-protein to plug SARS-Cov-2 Spikes. bioRxiv. 2020.
Han Y and Král P. Computational Design of ACE2-Based Peptide Inhibitors of SARS-CoV-2. ACS Nano. 2020;14(4): 5143-5147.
Walls AC, Xiong X, Park YJ, et al. Unexpected Receptor Functional Mimicry Elucidates Activation of Coronavirus Fusion. Cell. 2019;176(5):1026-1039.e15.


What is this bizarre in-growth in this red bell pepper? I just chanced upon a rather strange red bell pepper (or capsicum?):

The green formation is bulbous to touch, just the like the outside of the bellpepper, and it has the same smell as one. I'm no biology expert, but I have a feeling that's a tiny ingrown bellpepper in there. My mom thinks it's a strange genetic experiment and wants me to throw it away!

What is that strange growth, and what might have caused it? Is this safe to consume?

This is very likely to be parthenocarpy, which is an “internal proliferation” and varies from an irregular fruit to an almost carbon copy of the larger pepper. What is known is that it shows up in seed lines through natural selection and is unaffected by weather, pests, or other external conditions. Please see page 27 of this document.


Does DNA analysis allow determining amount of chromosomes? Nowadays it is possible to sequence the DNA of extinct species, such as the Neanderthals, the Denisovans, and others.

Is it possible to determine, solely from the sequenced DNA or from known bone fragments, how many chromosomes the individual (or the species represented by the individual) had?

This depends completely on the quality of the DNA. Since each chromosome is essentially a very long strand of DNA, breakages and missing sections are very common in extinct species due to degradation over time.

If a full DNA read is absent, no determination of chromosomal number can be performed.

Assuming a full read (covering all breakages) of the DNA is present, the telomeres of each chromosome can be found, and since chromosomes usually only have one set of telomeres each, this may be useful for chromosomal number determination.

Caveat 1: Chromosome 2 (human) is an example of how this method may fail, since a recently fused chromosome will still possess the tandem repeats characteristic of telomeres.

Caveat 2: Telomeres may vary in length due to the age of the cell, as well as be broken in multiple regions. Due to the tandem repeat nature of telomeres, it is nearly impossible to tell these different states apart experimentally.


Ramifications and possibility of a diet consuming exclusively of human semen Semen is a thick, nutritious liquid, rich in vitamins (such as C, B12), amino acids, lipids, monosaccharides (fructose), et cetera. Can semen's ability to fulfill the needs of human organism provide enough essential nutrients to keep the body alive and functional? And if so, would it be a healthy life?

Can a glass of ejaculate a day keep The Reaper/doctor away? If not, how long could a person survive on a "diet" like this?

No, you cannot live off of semen.

A source from Columbia.edu:

  A typical ejaculation fills up about one teaspoon; the actual amount is determined by a man's age (younger men usually make more semen), when he last ejaculated, and how long he's aroused before ejaculating, among other factors. Contrary to what you've heard, semen is not loaded with calories. Each teaspoon of ejaculate has about 5 - 7 calories and some 200 - 500 million sperm. Since sperm make up only about 1 percent of semen, what accounts for the other 99 percent? Well, its other ingredients include:

  Fructose sugar
  Water
  Ascorbic acid (a.k.a., vitamin C)
  Citric acid
  Enzymes
  Protein
  Phosphate and bicarbonate buffers (bases)
  Zinc

  Can swallowing semen enrich a protein poor diet? Unless you're gulping gallons of it each day, it's no substitute for real nutritious cuisine!

From a non-academic, but apparently well-informed source, semen contains:

  Semen contains only 15 calories and boy does it have a lot of stuff in it. So let's have a look. Ejaculate contains ascorbic acid, blood-group antigens, calcium, chlorine, cholesterol, choline, citric acid, creatine, deoxyribonucleic acid (DNA), fructose, glutathione, hyaluronidase, inositol, lactic acid, magnesium, nitrogen, phosphorous, potassium, purine, pyrimidine, pyruvic acid, sodium, sorbitol, spermidine, spermine, urea, uric acid, vitamin B12, and zinc.

I've highlighted the nutritionally-relevant ingredients. You'll notice that there is some overlap - with the Columbia source. What you won't notice, though, are the rest of the Essential Vitamins and Minerals:

Vitamin A (retinol)
Vitamin B1 (thiamin)
Vitamin B2 (riboflavin, vitamin G)
Vitamin B3 (niacin, vitamin P, vitamin PP)
Vitamin B5 (pantothenic acid)
Vitamin B6 (pyridoxine, pyridoxamine, or pyridoxal)
Vitamin B7 (biotin, vitamin H)
Vitamin B9 (folic acid, folate, vitamin M)
Vitamin D (ergocalciferol, or cholecalciferol)
Vitamin E (tocopherol)
Vitamin K (naphthoquinoids)
Chloride (Cl−)
Chromium (Cr)[4]
Cobalt (Co) (as part of Vitamin B12)
Copper (Cu)
Iodine (I)
Iron (Fe)
Manganese (Mn)
Molybdenum (Mo)
Nickel (Ni)
Selenium (Se)
Sulfur (S) numerous roles[5]

I should also mention that the specific amounts of each ingredient will vary from person to person, as diet can play a major role in flavor resulting from the changed nutritional content (i.e. - higher fructose levels).

As perhaps the most reliable source I could find, there is a Wikipedia article with references concerning the makeup of human seminal fluid and has this information:

  amino acids, citrate, enzymes, flavins, fructose (2–5 mg per mL semen,3 the main energy source of sperm cells, which rely entirely on sugars from the seminal plasma for energy), phosphorylcholine, prostaglandins (involved in suppressing an immune response by the female against the foreign semen), proteins, vitamin C

  acid phosphatase, citric acid, fibrinolysin, prostate specific antigen, proteolytic enzymes, zinc

It echoes the other sources closely, and still yields insufficient evidence that a person could live off of semen exclusively.

As for how long you can live? From a Scientific American article concerning starvation there have been confirmed instances of hungers strikes lasting up to 40 days. Assuming you could consume enough semen to sustain your body's daily Caloric requirements, you would die of malnutrition eventually. Scurvy - the inadequate intake of Vitamin C (Ascorbic Acid) - would probably be the culprit, as deficiency becomes clinical in 1 to 3 months with the later stages of Scurvy being: "...more severe and life threatening; common manifestations include generalized edema, severe jaundice, hemolysis, acute spontaneous bleeding, neuropathy, fever, convulsions, and death."

Assuming that there is enough Vitamin C in semen, you would die of other deficiencies. Since Vitamin B1 (Thiamine) is water-soluble (is not stored in your fatty tissues), not found in semen at all, and the body only reserves about a month's worth, after 30 days you would start to experience Beriberi - which is only slightly less fun than Scurvy.


What's a protein pulldown assay? I'm reading a paper and the authors mention a "protein pulldown" assay.

I've never done this before, and googling doesn't bring up much. Could I get a rundown of the basic theory behind it?

Also does % coverage have anything to do with this assay?

Pull down mostly refers to immunoprecipitation, however pulling down can be done using other interactions such as streptavidin-biotin or His-tag-Nickel.

In a protein pull-down a protein is enriched along with the molecules bound to it. When the DNA that is bound to a protein is studied, the experiment is called ChIP (Chromatin ImmunoPrecipitation). When other proteins that are bound to a given protein are studied then the experiment is called Co-IP.
Similarly RNA bound to protein can also be studied.

It is also possible to pull-down an RNA or a DNA fragment using complementary oligonucleotide, streptavidin, antibodies etc and study their interacting partners.

In the linked paper, they have immunoprecipitated a HA (haemagglutinin) tagged protein using an anti-HA-tag antibody (Note that this is just a small tag of 9-10 amino acids and not the entire HA protein. Such tags are useful when you don't have the antibody for a given protein).

They have done both co-IP and ChIP:

  HA-tagged, full-length PfSET10 protein and interacting proteins from
  3D7/PfSET10HA and control line 3D7 were purified using anti-HA beads

  Chromatin Immunoprecipitation (ChIP) and Transcriptional Profiling

  ChIP analysis was performed as described (Flueck et al., 2009).

Coverage is a term used in sequencing experiments which usually refers to average number of reads that map to any locus; this is also called depth. This is commonly used in RNA/DNA sequencing studies (See this post too). In this paper, as mentioned in the other answer, the term coverage is used for peptide reads (analyzed by mass spectrometry) and it is the horizontal coverage not a vertical coverage. Horizontal coverage refers to the fraction of actual molecule (DNA/RNA/protein) covered by the assembly of reads.

Coverage has got nothing to do with the pull-down assay; it is used in the context of the downstream experiment.


Plant identification in UK I need some help identifying this plant please. It is summer flowering in the UK. Its height is approximately 30cm, flowers approximately 2cm across.

This plant has been identified as Viscaria oculata.


During acid reflux and vomiting, is the burning sensation from pepsin or acid? When one's stomach contents enter one's esophagus, a burning sensation usually ensues. Is this from the enzyme pepsin breaking apart your cells or just from the acid?

It is the acid that causes the burn

Medicines like proton pump inhibitors (e.g. Prilosec), or H2 receptor antagonists (like Zantac) that reduce acid secretion reduce the burning sensation.  Medicines that neutralize the acid like calcium carbonate (e.g. Tums) also reduce the burn.  These medicines do nothing to the secretion of enzymes.

ADDENDUM. @anongoodnurse wants references.  Maybe in exchange she will remove that pesky down vote.

Cimetidine won the team that developed it the Nobel prize - the first rationally (as opposed to empirically) designed drug.  It was designed to very specifically reduce stomach acid.

https://www.acs.org/content/acs/en/education/whatischemistry/landmarks/cimetidinetagamet.html

  Smith Kline & French's multidisciplinary research team first looked at
  the physiological cause of acid secretion. They confirmed that a
  molecule found in the body called histamine triggers the release of
  acid when it binds to a specific receptor (now called the H2-receptor)
  in the stomach lining. Their aim was to find a molecule that
  successfully competed with histamine in combining with the receptor,
  but then blocked, rather than stimulated, acid release. Such a
  molecule was called a histamine H2-receptor antagonist and represented
  a new class of drugs.

This and the successor class of drugs (proton pump inhibitors) are very specifically designed to decrease acid secretion and do little else.

The fact that billions of dollars worth of these drugs are sold means that persons suffering from reflux pain / stomach ulcer perceive that their pain is reduced by a decrease in acid secretion, and so are willing to pay.

  Tagamet® was greeted with great enthusiasm by doctors and patients
  alike. Ten years after its introduction, it had achieved sales of one
  billion dollars and had become the world's number one prescription
  drug.


Does the pyloric sphincter contract after ingesting only liquid? At university, I was told by one of my fellow students that the reason why eating before going on an alcohol laden night out was a good idea, was because the pyloric sphincter contracted once food was in your stomach, and only let it into your lower intestines gradually. Their theory was that if you then drank alcohol, it would also sit in your stomach (with your food) and would only be let into your intestines gradually as the food was allowed through, thus slowing your rate of inebriation. Drinking on an empty stomach would conversely not cause the pyloric sphincter to contract, thus allowing the alcohol to enter your intestines at a much faster pace. However, I've been trying to find some online sources to corroborate / disprove this, and I'm having problems finding any information on it at all.

So my question is: does the pyloric sphincter stay relaxed if only liquid is consumed on an empty stomach?

NO IT DOESNT CONTRACT AFTER INGESTING LIQUID

1)The pyloric sphincter always remain  tonically contracted even in an empty stomach.However this tone of the pyloric sphincter is insufficient to prevent the passage of liquids to the duodenum.Thus almost all the liquid intaken in an empty stomach passes immediately to the small intestine.

2)Filling of the stomach triggers an enteric reflex that increases the tonical contraction of the pyloric sphincter.When fluids are taken then,their rate of passage to the duodenum is considerably reduced.(Although little is slowly absorbed into blood from the stomach).

REFERENCE:TEXTBOOK OF MEDICAL PHYSIOLOGY(GUYTON AND HALL)

3)As the small intestine is the seat of absorption,delaying passage to it delays large amount of alcohol absorption into blood.This not only delays its effect in the body but also fascilitates the persons capability to intake more alcohol.(This varies considerably in different persons but the central physiology is this)

REFERENCE:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1705129/


Nature of sight/ color perception? I am wondering how we perceive color and whether that is dependent on the wavelength of the light, or on something manufactured in the brain.

For instance, if we evolved on a planet orbiting a red dwarf star, would we see colors differently than we do now, given that our sunlight has another wavelength composition?

I know that there have been experiments where volunteers have worn glasses that make them see the world upside-down and eventually the brain corrects this and they see right-side-up again (and have to re-adapt when removing the glasses). I wonder if something similar would happen with color perception.

Does anyone know of any studies done that have tested this?

The color you perceive is ultimately dependent on the relative contributions of the color photoreceptors in the retina, namely the red, green and blue cones. The sensation of color, therefore, is physically determined by the wavelengths in the light source and the absorbance spectra of the cones. Thereafter, the neurophysiological wirings of the retina and the brain take over and these paths are pretty well defined too. However, one cannot say anything about the qualitative perception of someone observing a light source. This is the big difference between sensation (peripheral processes including the retina) and perception (central processes).

To quote the late Bach-y-Rita: 'You see with your brain, not with your eyes.'

Everything we perceive ('see') is a subjective construct devised by our brains. No red dwarf star is necessary to pose the possibility that you perceive my perceived red as green, or vice versa. No experiments can be conducted to prove or disprove a hypothesis like this.

In terms of experiments: we can test stuff like 'up' versus 'down', as with the prisms mentioned in the question. This, because a subject can qualitatively point out where an object is perceived relative to others, and that can be objectively measured. However, we cannot test the subjective quality of color. We can test relative color contributions through color matching experiments (Kalloniatis & Luu, 2012). These experiments will tell you which contributions the red, green and blue cones have in a certain color mixture, but they will not tell the researcher anything about the subjectively perceived color by the test subject in a qualitative way.

Reference
- Kalloniatis & Luu. Color Perception. In: Webvision. The Organization of the Retina and Visual System, Moran Eye Center (2012)


Biological contamination from ground I took samples of tapwater in order to examine concentrations of escherichia coli and enterococcus, in a rural area. I was told, by the analytical lab, to take samples in four sterilized vessels bought from pharmacy. The problem is that at the completion of the last vessel, its cap fell frοm my hand down to the soil and some grains of sand stack on the inner surface of the cap. As fast as I could, I picked it up and washed it off totally with the water of the sampling tap. After that I closed my last sampling vessel with it and this was the completion of the sampling. How great is the possibility my sample has a serious contamination of these twο biological pollutants after this incident?

Thanks and sorry for the long story and bad english

Document the incident and notify your supervisor. For environmental testing where SOP is involved, this would count as an incident, i.e. anything that falls outside SOP. Whether the incident is a non-conformance, deviation or nothing at all is up to your quality team. You can always take another sample, supplies withstanding, too.


Blood clumping in mosquitos Will a mosquito die due to blood clumping if it sucks blood from two people who have different blood groups? What will happen in its gut? Is there any mechanism to avoid clumping? Or do mosquitoes know what group it should suck?

Female mosquitoes need blood for laying their eggs. This actually means that they need a source of rich protein and iron for their kids and hence, prey on us.
It is worthwhile for us to pause here and ponder over the difference between clumping and clotting before proceeding to the actual answer.

Agglutination tests as you may have come across are essentially antigen antibody reactions visible to the naked eye. Antibodies and antigens (on the RBCs) bind leading to the clumping that you talk of.
Clotting on the other hand is a complex set of reactions involving the thrombins and the platelets.

When a person is transfused of a wrong blood type, as in blood of another group is injected into his blood, something very bad is ought to happen. The clumping is extensive (an immune reaction) which leads to a clotting reaction, leading to a condition called DIC (Disseminated Intravascular Coagulation). This is an emergency situation since there can even be Acute Kidney failure.

Coming to the mosquito,

In the human case, we injected into the blood. Here it gets into the gut. The gut has enzymes which breaks down the proteins. Theres no antibody no antigen left out there!! Proteolytic enzymes start right from the very beginning.
Even if some clumping occurs, it doesn't actually matter. It mattered in the human case since it was a transfusion and the sequelae mattered.
Another important thing to keep in mind is we are talking only of clumping and not clotting. The mosquito takes care of clotting by secreting anticoagulants into the blood stream right when it is ready to have it meal. Clumping on the other hand, per se, doesn't turn the blood into a clot. If you have seen blood clumping in agglutination test, its not such a dramatic thing to occur. The blood still stays in liquidy. So clumping wouldn't pose much of a problem.

Hope this helps! Sorry but the climax wasn't that dramatic :)


what is the difference between pituitary dwarfism and thyroid dwarfism? My book (Comprehensive Biology class XI, by J P Sharma ) mentions of two kinds of dwarfism- "Pituitary Dwarfism" and "Thyroid Dwarfism" but does not provide any details about the matter. so please help me.

Pituitary Dwarfism is a condition where less amount of growth hormone results in abnormally slow growth and short stature. Growth hormone is released under the influence of hypothalamic growth hormone-releasing hormone(GHRH), and is inhibited by hypothalamic somatostatin. Growth hormone deficiency has different negative effects if happens according to age it manifests;  in newborn, the primary manifestations may be hypoglycemia, while in later infancy and childhood, growth failure is more likely. Growth hormone deficiency can be congenital or acquired. It is usually permanent, sometimes transient.

Thyroid dwarfism is a condition arising from the deficiency of a thyroid hormone. It happens when there is lesser thyroid hormone secretion (defect of manufacturing or lesser supply of Iodine) before attaining the full development congenitally. It causes retarded growth and development of bones with disproportionate body proportions (that's dwarfism ).


Some question about materials for PCR I'm planning to order oligo, polymerase, nucleotide, buffer for my first diy PCR experiment (now I have nothing), so I have some questions.

How and how long I can storage them?  I have only a fridge that can freeze to -10 -> -20C.
I see the size/concentration of polymerase is 400 units and 25 nmole of oligo. So what can I do with 25 nmole oligo and 400 units of polymerase? How many PCR experiment I can do with 400 units of polymerase, and how many PCR experiment I can do with 25 nmole of oligo?
If I have a HPLC machine, can I reuse the polymerase by purify it after reaction?

The manufacturers of each component should have information available on their website regarding storage temperatures, along with recommended protocols on how much of each component to add to the PCR reaction. I would not try to reuse the polymerase, as depending on the kind you buy it may be a complex of proteins, and it may not be functional after purification. However, you're welcome to experiment all you want, it's your stuff!


Why can we eat salty food, but can't stomach salty water? I know that too much sodium is bad for our health. However, it struck me as odd that we like to add salt to pasta sauce or other foods we eat, yet trying to drink salt water can bring on the gag reflex.
Is this because sea water is many times more salty than the salt we would add to our food? Or is there another reason?

Seawater is many times more salty than the "pinch" of salt that is often recommended to add to cooked dishes.
According to the USGS

the concentration of salt in seawater (salinity) is about 35 parts per thousand. In other words, about 35 of 1,000 (3.5%) of the weight of seawater comes from the dissolved salts

To translate that to a typical glass of water: seawater is equivalent to adding a bit more than an entire tablespoon (17.5 mL) of salt to a 16oz (~500 mL) glass!
By the way, 1 tablespoon of salt is about 7100 mg. To put that into perspective, you'd have to consume almost two entire 8-cut pizzas (using Domino's as a reference) or more than 7 McDonald BigMac cheeseburgers to consume that same amount of salt.
In fact, consuming 7,100 mg of salt would more than triple the recommended amount for daily intake. According to the FDA:

Americans eat on average about 3,400 mg of sodium per day. However, the Dietary Guidelines for Americans recommends limiting sodium intake to less than 2,300 mg per day—that’s equal to about 1 teaspoon of salt!


Which organism is this? Place: Bangalore, India

Month: September, 2015

Current weather: Cloudy and rainy

Google images search was just giving me dragonfly photos. That organism is on grass blade.

Image is captured by me.

This is an insect in the order Neuroptera, definitely neither a dragonfly (order Odonata) nor a grasshopper (Order Orthoptera).  The name of that order means "nerve-wing", which referes to the intricate network of veins throughout the wings, which have a very different appearance and pattern than the wings of either dragonflies or grasshoppers.  I'm not familiar with Indian fauna per se, but the long antennae with slightly curved/hooked tips make it look more like an antlion (family Myrmeleontidae within the Neuroptera) than an owlfly (family Ascalaphidae within the Neuroptera; their antennae have small clubs at the ends), though it's a bit hard to tell from the photo.


How does CO₂ concentration affect photosynthesis? I have heard the theory that with the increase of CO2 in the air, the speed of the photosynthesis would increase, thereby limiting the increase of CO2 levels.

What is currently the rate limiting factor of photosynthetic reactions in plants? Is it really CO2, or rather the limited energy that a plant can absorb from sunlight?

The rate-limiting step of photosynthesis is the CO2 assimilating enzyme Rubisco (short for ribulose-1,5-bisphosphate carboxylase/oxygenase) (Jensen, 2000). It uses ribulose-1,5-bisphosphate and CO2 as substrates to generate glucose.

Given that Rubisco is the rate limiting step in photosynthesis, an increase in its substrate CO2 would expectedly lead to an increase in photosynthesis. However, the regulation of Rubisco is complex and is influenced not only by CO2, but also by O2 (which competes with CO2 for the active site), Mg2+ and a regulating enzyme called Rubisco activase (Jensen, 2000). Hence, the effects of an increase in atmospheric CO2 may be more complex than simply enhancing photosynthesis by increasing Rubisco activity.

Indeed, a review by Poorter (1993) showed that a doubling of CO2 lead to an average increase in photosynthesis of only 37% across more than 150 plant species. He describes various factors that determine photosynthesis rates other than CO2:

One factor that limited photosynthesis under high CO2 was nitrogen (N). Since Rubisco is an enzyme, it has to be synthesized from amino acids. As Rubisco constitutes about 30% of the total protein in a plant leaf, Rubisco is probably the most abundant protein on earth and a major sink for plant nitrogen (Jensen, 2000). For example, C3 species capable of symbiosis with N2-fixing organisms had higher growth increases compared to other C3 species under high CO2;
Certain plants utilize CO2 better than others. CAM species were the least responsive, followed by C4 plants, while C3 plants increased their photosynthesis rates the most under high CO2. Examples of C3 plants are herbaceous crop plants (Poorter, 1993);
Plants with a large intrinsic growth rate may benefit more from high CO2. These plants are said to have a high sink strength, as they rapidly convert additional photosynthesis products into outgrowth.

References
- Jensen, PNAS (2000); 97(24): 12937–38
- Poorter, Veg (1993);104/105: 77-97


Does low gravity exposure to early stages of human fetus have potential to unloc unused genetic information from earlier stages of evolution? The title seems quite self explanatory but let me elaborate.

New mutations do take a very long time and many generations to occure in the genetic code. But our genetic code already holds all the information gathered trough evolution process...even information that are older than mammals.

In case of start of pregnency in zero g or gravity of Mars (0,38 g)... there are many replications from the single cell egg to fetus couple month old...

Can gravity in this case has potentional to "open new variant" of genetic information gathered in our cells? Does diferent gravity has impact on metabolic processes on cellual level?

No
The question itself does not even make sense, we do not hold onto much unused information, there is nothing to unlock. Unused genes mutate and get co opted for other purposes. We have about a hundred new mutation per generation. Much of so called junk DNA is actually just used for other purposes besides coding for proteins.

Will a colony evolve differently sure, any isolated population evolves along its own lines but it will happen at evolutionary speeds.


Can exhaustive algorithms produce MSAs that are suitable for 3D structure modelling? While predicting 3D structure of a protein through homology modelling, the most important step is Multiple Sequence Alignment of template sequences with the target protein whose 3D model is to be predicted. At this step according to my book for Multiple Sequence Alignment, the either T-coffee or Praline software is used; these programs are heuristic in nature and based on a progressive alignment method. There are always concerns regarding the sensitivity and specificity of heuristic  algorithms.

To avoid that problem I imagine one option is to use exhaustive algorithms. During this alignment step, which is very critical in 3D modelling, can we use exhaustive algorithms to yield good models?

No.

Methods for multiple sequence alignment (MSA) like T-coffee, which you mention, and Clustal (http://www.clustal.org), which is also widely used, employ heuristics for the alignment for the very good reason that exhaustive algorithms to do this are NP-complete.

You mention the dynamic programing algorithm as exhaustive in your comment. Alignment of two sequences by dynamic programming has an order of time complexity (big O) of $n^2$ and may take a few minutes depending on sequence length etc. Alignment of three has a big O of $n^3$ and can be done if you have lots of time on your hands, but it should be obvious that that's the limit to the number of sequences that can be aligned using dynamic programming.

There's no shame in heuristics. Perhaps the most widely used bioinformatics program in the world, BLAST, employs a heuristic. (And your brain makes decisions that your life depends on every day using heuristics.)

The methods that use heuristics for MSA have been successively modified to deal with known factors that can cause problems, so often they perform very well. How can you tell? What you need to do in using MSA programs is to perform a "sanity check" on any alignment that the programs produce — does it look reasonable, has it matched up similar regions well or are there vast gaps introduced or obvious regions of homology missed. And if you are doing 3D modeling and you don't get an alignment that looks good, then your modelling isn't likely to work.

Finally you always have to consider the possibility that there aren't any proteins of known structure that are similar to the one you want to model so you'll never get a good MSA.


Evolution and Phenotypes. This may be better suited for the English language SE, but When discussing evolutionary changes in species is it proper to refer to their phenotypes?

In this context:

  "Imagine if a cow did not have to cart around however many gallons of
  culture nor expend personal time and effort into chewing its cud. It
  could lose all that anatomy and energy expenditure from its phenotype."

it could just be me, but it sounds strange using it in that context.

Yes, absolutely. That's what a phenotype is (definition from the biology online dictionary):

  noun, plural: phenotypes

  (1) The physical appearance or biochemical characteristic of an
  organism as a result of the interaction of its genotype and the
  environment.

  (2) The expression of a particular trait, for example, skin color,
  height, behavior, etc., according to the individual’s genetic makeup
  and environment.

I don't see anything strange in the sentence you quoted. It is phenotypes that are selected for. Genotype differences that don't affect phenotype will have no selective advantage (or disadvantage) and cannot be acted upon by evolutionary forces. What else would you use when discussing evolutionary changes? That's what the word phenotype is for.


Species Identification - small insect I found a few of these walking in the middle of the night (about 3 AM) on a wall in my room near the floor. They are at most a few millimetres long (no more than 2 I would say). I am living in Poland, in a block of flats.

EDIT:  Since I first wrote, I have seen few more - very small - less then 1 millimetre long. They seemed to be coming from behind the baseboard. This time I've seen them during daytime.

I think @fileunderwater is definitely right, these are psocids (of the family Psocoptera, AKA booklice).

Specifically, the body shape looks very similar to that of Dorypteryx domestica or some closely related species.

See here for an additional photo.

According to this site, the species is present in many countries including Poland.

The source cited at this site (Kučerová 1998) mentions that this species can be brachypterous (i.e., having very reduced wings. I can't tell from the quality of the photo whether your specimens has tiny wings or not. Your top picture looks like it might.

Citations:

Kučerová, Z. (1998). Wing polymorphism in Dorypteryx domestica (Smithers) (Psocoptera: syllipsocidae). Insect Systematics & Evolution, 29(4): 451-57.


Does a non-extinct gliding species of bird exist? According to wikipedia was Archaeopteryx rather glider than capable of active flight. As a hunting strategy it crawl up to a tree (or other high positioned place) and glide from it to a prey.

Most of the modern birds are capable of active flight. Does anybody know if a (purely) gliding species of bird exist in present?

There is a classification of birds called Soaring birds.
Soaring Birds

In definition, some land birds, such as vultures and certain hawks,
sustain flight for long periods without flapping their wings. They
take advantage of updrafts produced when the wind blows over hills and
mountain ridges or make use of rising columns of warm air called
"thermals."
Vultures stay within thermals by flying slowly in tight circles. They
have short, broad wings and a low wing loading (ratio of bird weight
to wing area) that allows them to remain aloft and to be highly
maneuverable at slow speeds. [1]

List of soaring birds

Birds of Prey

Buzzards
Condors
Eagles
Falcons
Harriers
Hawks
Kites
Osprey
Secretary Bird
Vultures

Passerine

Chough

Cranes

Sandhill

Sea birds

Albatrosses
Frigatebirds
Gulls
Herons
Pelicans
Petrels
Shearwaters
Storks
Terns

Extinct

Argentavis

Buzzard

Chough

Sandhill

Albatrosses

(source: scienceviews.com)
Argentavis[Extinct]

(source: mnn.com)
Update:
Most similar morphology to Archaeopteryx is found in Hoatzin (Opisthocomus hoazin) like claws as hands as they hold the branch when they are small.

(source: pbworks.com)
Source:
[1] Soaring Birds by Paul R. Ehrlich, David S. Dobkin, and Darryl Wheye.


What controls specific gene silencing during cell differentiation? I am intrigued by the fact that all cells of our body use the same DNA. How do the cells differentiate during the post fertilisation divisions?

I read about gene silencing, which can be an answer to this. But still I do not understand how the cells decide which gene it is supposed to silence, by making the micro RNA.

Consider a zygote that is beginning to divide. I would assume that the chemical and physical context of each daughter cells would be more or less similar in beginning. Then how can there be a differentiation? Is there some supervising authority present in the zygote that decides what to make out of each daughter cell?

The cells differentiation during post fertilization period is govern by a set of regulatory genes called Homeotic genes.These are genes that "select" the identity of entire segments or structures in the bodies of developing organisms.
These gene encodes a transcription factor that is expressed in a specific region of the organism starting in its early development i.e. embryo stage. The transcription factors change the expression of target genes to enact the genetic “program” that's right for each segment.

The homeotic transcription factors shown in the diagram above[homology between Hox genes in mice and humans] contain a DNA-binding protein region called the homeodomain, which is encoded by a segment of DNA, called the homeobox.The animal genes containing homeobox sequences are specifically referred to as Hox genes. This family of genes is responsible for determining the general body plan, such as the number of body segments of an animal, the number and placement of appendages, and animal head-tail directionality.

In addition to this genes, the early developmental cascade include the following genes:

Maternal effects genes:These are genes whose mRNAs are placed in the egg cell by the mother before fertilization. Some of the mRNAs are “tied” to the head or tail end of the embryo and are responsible for setting up the head-tail polarity. The maternal effects genes encode regulators of transcription or translation that control each other as well as other genes.
Gap genes: They are activated through interactions between the protein products of the maternal effects genes, and they also regulate each other. They're responsible for defining large, multi-segment regions in many organisms.
Pair-rule genes: These are turned on by interactions between gap genes, and their expression patterns are refined by interactions with one another. They appear in multiple “stripes” along the embryo, similar in pattern to the segments of the adult organism.When a pair-rule gene is missing due to mutation, there is a loss of structures in the segment regions where the gene is normally expressed.

For further information you can refer this link:
-  Click here 1
- Click here 2
-  Click here 3


Help me identify these creatures found in sink The conical flask was kept in a sink for about 3 or 4 week, was waterfilled, and I have no idea if they grown after the flask was waterfilled or before the flask was waterfilled. We do not work with animals so these arenot any experimental material, but maybe they are soil borne if the conical flask contained soil sample (I do not have any idea what was kept in that flask before it was left in that sink)

They were not moving and they were sticked firmly on the glass wall. They had some constriction marks. Length apporox 0.2 to 0.5 cm, Width approx 0.1 to 0.3 cm. colour pale white to brown.

I think this will be a larva. Check this video. If it was in a sink, is very probably than will be a fly. But the specie only will be identified with a genome assay, or taxonomically once they out the pupa.


Nomenclature of enzymes involved in synthesis of glutamine I am considering nitrogen fixation and in my lecture notes, there is the statement

  The glutamine synthetase- glutamate synthase system requires use of an ATP molecule as well as reducing power. Although it is energy intensive compared with glutamine synthase, the Km of glutamine synthetase is much lower than that of glutamate dehydrogenase. When NH3 is scarce, the additional ATP investment is worthwhile.

Try as I might, I can't find anything about glutamine synthase. Searches online seem to only return results for glutamine synthetase. I was wondering if this is a mistake in my notes? If so, I can only think that this should be 'glutamate dehydrogenase', in which case the statement is about comparing the method used by animals and fungi (which use glutamate dehydrogenase to fix nitrogen via a Schiff base) compared with plants and other microorganisms  (which use the glutamine synthetase glutamate synthase method).

This is my first exposure to learning about nitrogen fixation, so I would very much are coated any clarification.

Also, I was wondering what the general difference is between a 'synthase' enzyme and 'synthetase', if there is one.

Probably a mistake in your notes, or in the lecture notes for the class, but not a very important error in either case aside from the confusion it has caused you.

See the wikipedia article on Synthase and on wikipedia article on Ligase for a note on the terminology: historically synthetases use ATP, synthases do not, but this terminology is not adhered to strictly, and the current standard is that the terms are essentially synonymous; in my experience, however, a particular nomenclature dominates the literature even if the synonym is technically correct.


Definitions of common and rare disease Is there an epidimiological way to define rare and common diseases ?

While "common disease" has obscure incidence and prevalence definitions, "Rare" or "orphan disease" is more defined.

In the US, the rare disease defined as a condition which affect one (or less) of 200,000 people in population. However, this definition can be different in other countries, p.e. in Japan 1:50,000 or less.

We can assume that "common" disease is much frequent than "rare" one, thus the incidence and prevalence are much greater than per "rare disease" definition. However, again, there is no agreement of clear cut of "common disease" incidence and prevalence.


Do all fungi dislike acidic environments? I know that some fungi prefer mildly alkaline environments and dislike acidic environments. Is that true of all fungi, or do some fungi prefer acidic environments? If so, are such acidic fungi rare exceptions or is it common for there to be acid-loving fungi?

Fungi that grow in acidic media are well known, here just one reference: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC518635/pdf/jbacter00651-0183.pdf

About their spread, they are less common in mild environments (like you hands, or your garden soil) but of course in acidic environments, they will be predominant.


Single hormone opposite effects Often, a smooth response to a hormone means that some processes must be sped up and others must be slowed down.

How can a single hormone have opposite effects like this?

An hormone is not different from most other molecules. To have an effect on a cell it binds to a (more or less specific) receptor, located either on the plasma membrane or inside the cell, and it initiates an intracellular cascade of events1.

There are several ways an hormone can have different effects:

there can be multiple receptors for the same hormone. For instance, prolactin can bind to two receptors, called prolactin receptor (PRL-R) short and long form. The short form of the receptor has been shown to lack the ability to promote milk protein genes transcription (See Lesueur et al., PNAS - 1991).
the same receptor can be coupled to different intracellular pathways in different cell types / physiological conditions, thus resulting in different effects.
each cell type/tissue expresses a set of protein that will interact in a different manner with the intracellular cascade promoted by the hormone.
an hormone can interact with receptors for other molecules. For instance allopregnanolone, a metabolite of progesterone, is a potent agonist of the GABA-A receptor, giving it anxiolitic properties.

An interesting example is that of estrogenic compound. Several receptors exist for estradiol (E2). The "classical" receptors are called ER-alpha and ER-beta, and they are located in the cytoplasm. The binding of E2 to the ER promotes their dimerization and entrance into the nucleus where they can promote the transcription of various genes. ERs can also bind to other transcription factors and modulate their activity. So, depending on which transcription factors are present different genes will be transcribed in response to E2. Moreover, ER-beta can have opposite effects then ER-alpha (see for instance Weihua et al., PNAS - 2000). In addition, receptors like ERs can be activated also in absence of the endogenous hormone: for instance, dietary amino acids activate ER-alpha in liver by a mTOR-dependent phosphorylation (Della Torre et al., Cell Metabolism 2011)

To make things more complicated, membrane receptor for estrogen have been described, such as GPR30 (Revankar et al., Science - 2005), membrane "versions" of the classical ERs, plus various splicing variants of the ERs (mostly expressed in tumoral tissue).

GPR30 in breasts has been shown to activate certain molecular pathways (notably Erk1/2) that contribute to cellular growth (Filardo et al., Mol Endocrinol. - 2000), possibly linking it to proliferation of ER-negative breast tumours. Other tissues that do not express GPR30 will lack this E2-induced proliferative stimulus.

So, tissue- or time- dependent modulation of the receptors and of the intracellular pathways associated with it can allow the body to respond to the same hormone (or, more in general, to the same molecule) in opposite ways.

1 This is a simplification, not every substance (and not every hormone) acts by binding to receptors, but let's keep things simple.


How to interpret Glimmer scores? I am trying to find orfs with Glimmer. At the end, Glimmer gives me a .predict file with the orfs and a corresponding raw score.

When I look at the documentation, it says about the score, "This is 100 times the per-base log-odds ratio of the in-frame coding ICM score to the independent (i.e., non-coding) model score. It gives a rough quantification to how well an orf scores that can be compared between any two orfs." You can look here for the documentation-

https://ccb.jhu.edu/software/glimmer/glim302notes.pdf

But what does the score really mean in an absolute manner? How do I realize for an orf, if the score is significant or not?

The score is the log odds ratio, times 100, that the ORF that you input is a coding region. For example, if Glimmer thinks the log odds are 10 to 1 that your region is coding, then your score will be 10x100 = 10000. Log odds of 10:1 imply more than a million to one certainty.


Please identify this tree in the Netherlands Please identify this tree for me. It was found in a park in Eindhoven, Netherlands.

I suspect this is a hazel (Corylus avellana) based on:

the leaves
the male flowers (not mature in your photo)
the fact that it is a common tree in Europe)

This one has twisty branches, so it could well be of a particular variety called "contorta".

According to
https://en.wikipedia.org/wiki/Corylus_avellana#Cultivation_and_uses

  A selection with twisted branches has been propagated horticulturally as Corylus avellana 'Contorta'.


How do detergents get in hydrophobic membrane interior? According to Molecular And Cellular Biology (Stephen L. Wolfe),

  Membranes disperse almost instantaneously if exposed to a nonpolar environment or to detergents, which are amphipathic molecules that can form a hydrophilic coat around the hydrophobic portions of membrane lipids and proteins in water solutions.

This might be a stupid question but... if detergents can 'form coats around hydrophobic portions' of membrane-suspended molecules, they must, somehow get in the hydrophobic membrane interior... right?

How do they get in the membrane interior? Do they form clusters like endocytic vesicles? What happens after they form hydrophilic coats around hydrophobic molecule regions?

It depends on the concentration, but at higher concentration the detergent molecules build so called micelles, where the hydrophobic "tail" is orientation into the inner part and the hydrophilic "head" is orientated to the outside. This allows the micelle also to fuse with the membrane and then to desintegrate it.
This illustration from the Wikipedia shows the schematically:

Its from the surfactant article, which has more details.


Is there any size limit to the amount of information a human (or other) brain can hold Im not sure how this would ever be tested but is there a limit to how much the brain can 'hold' before it reaches capacity ?

I guess this could also be interpreted in terms of memory, as how well some one remember something before reaching capacity / forgetting 'old' memories to make way / space for new ones.

Yes, there is a limit:

  Despite the impressive complexity and processing power of the human brain, it is severely capacity limited [1].

Human brain has 78.82– 95.40 billion neurons [2] and about $3.6 \cdot 10^{14}$ synapses in the cortex [3]. We shouldn't worry about running out of space, because neurons connect with each other to exponentially increase brain capacity to about 2.5 million gigabytes as Paul Reber, professor of psychology at Northwestern University claims for Scientific American [4]:

  Each neuron forms about 1,000 connections to other neurons, amounting to more than a trillion connections. If each neuron could only help store a single memory, running out of space would be a problem. You might have only a few gigabytes of storage space, similar to the space in an iPod or a USB flash drive. Yet neurons combine so that each one helps with many memories at a time, exponentially increasing the brain’s memory storage capacity to something closer to around 2.5 petabytes (or a million gigabytes).

References:

Marois R, Ivanoff J. Capacity limits of information processing in the brain. Trends Cogn. Sci. (Regul. Ed.). 2005 Jun;9(6):296-305. doi: 10.1016/j.tics.2005.04.010. PubMed PMID: 15925809. Full text available on http://www.psy.vanderbilt.edu/faculty/marois/Publications/Marois_Ivanoff-2005.pdf
Azevedo FA, Carvalho LR, Grinberg LT, Farfel JM, Ferretti RE, Leite RE, Jacob Filho W, Lent R, Herculano-Houzel S. Equal numbers of neuronal and nonneuronal cells make the human brain an isometrically scaled-up primate brain. J Comp Neurol. 2009 Apr 10 513(5):532-41. p.535 right column top sentence. Via Bionumbers http://bionumbers.hms.harvard.edu//bionumber.aspx?id=106322&ver=4
Roth G, Dicke U. Evolution of the brain and intelligence. Trends Cogn Sci. 2005 May9(5):250-7. p.253 right column 1st paragraph. Via Bionumbers http://bionumbers.hms.harvard.edu//bionumber.aspx?id=106138&ver=2
Paul Reber. What Is the Memory Capacity of the Human Brain? Scientific American. Apr 2010. Available from http://www.scientificamerican.com/article/what-is-the-memory-capacity/. Accessed 12.07.2014


Chromosomal pair possible in metaphase - I There is this question which was asked in my exam.

A diploid cell contain 6 chromosomes. How many possible random arrangement of homologous chromosomes could occur during metaphase-I?
 (consider that allele for only one character present on chromosome and they are in heterozygous condition.)

Options are :

i)4

ii)8

iii)16

iv)64

Answer given is : ii)8

But my answer is : i)4

My solution :

Aa       | Aa     | Aa     |  Aa

Bb       | Bb     | bB     |  bB

Cc       | cC     | Cc     | cC

Here,  1 column represents 1 possiblity.

These are the possible combinations according to me in metaphase-I.

Am i missing something?

Please tell me where am i wrong.

PS : i would have loaded the picture of my solution but it ain't getting loaded.
Sorry for any inconvenience.

Thank you. =)

The correct answer is 8 as given by the formula 2n , where n is the number of chromosome in haploid cell.

Explanation:

During prophase 1, synapsis take place as a result of which bivalents are formed. Now each bivalent can arrange itself in two possible manner ( known as independent orientation). Since in this question there are 6 chromosomes which means 3 bivalents, the possible number of arrangement is 2 × 2 × 2 = 8

The photo here explain independent orientation in a cell having two chromosome pair. You can work this out for 3 chromosomal pair as well.

Your doubt:

As far as I can understand your doubt is that arrangement one is actually same as arrangement third ( with reference to the photo). Well, it might seem like this but if you look carefully the two non homologous chromosomes are arranged in different manner in them .. relative to each other and the homologous partner. And hence the whole arrangement is considered as different arrangements and not the same.

Thus, for 3 chromosomal pair, there are 8 possible arrangement of homologous chromosomes which could occur during metaphase-I.


Why does max heart rate decrease with age? I have heard that max heart rate declines steadily with age, and can be approximated by the equation Max Rate = 220 - Age.

What is the physiological reason for this decline, and how is it consistent with the fact that most endurance athletes reach their peak cardiovascular performance at around age 30?

There are many reasons why the maximal heart rate decreases with age.
The most prevalent is the heterogenous thickening of the walls of the heart.
Cardiac output is stroke volume times heart rate.

When the wall thickens, the heart needs more energy to achieve the same pumping (bigger stroke volume) or it needs to increase heart rate at rest.
Because of physical limitation, the stroke volume cannot be increased.
Heart needs to also rest which it does before the action potential reaches the AV conduction system.
Note the long time just after the action potential reaches AV node.

However, the heart cannot increase its maximal heart rate if the elasticity of the walls have decreased in ageing.
Ageing often leads to heterogenous thickening of walls of the heart.
If this is the case, then T wave gets high fast; which causes the risk of bleeding when exercising.
Doing sport or just feeling tired can cause a long-standing pain in the heart area in the chest.

Sport then again leads to dynamic hypertrophy of the heart tissue, which increases the maximal heart rate.
Ageing then again does not have such a dynamic changes.

There are secondary reasons caused by ageing

hormonal changes
decreased metabolism
decreased physical activity
...

which are associated with decreased maximal heart rate.

Why most endurance athletes reach their peak cardiovascular performance at around age 30?

Human's best age is at about 25 years old physiologically.
Muscles grow in rest.
When practicing at that age, recovery time of muscles is short.
It takes long time to improve cardiovascular performance (1-5 years), since heart muscle improves slowly.
I think the slow hypertrophy of heart musculature and the best physiological age of human are the reasons why the most successful endurance athletes are about 28-30 years old.


Mitosis in human body I've heard that stomach lining has the fastest reproducing cells and the brain has the slowest.

Where in the human body does mitosis occur and at what rates do these cell reproduce? Is there a chart for the whole body available?

In many cases cell division depends on the stage of development an organism is in. The rate of cell division is obviously much faster in a developing organism and from what I understand fully differentiated cells such as neuron and those in skeletal muscles don't divide (correct me if I'm wrong here).

In early development totipotent cells (stem cells that can become anything) begin to differentiate dependent on environmental factors, turning into multipotent (partially differentiated) cells that can only lead to certain cell types. For example: mesodermal precursors can differentiate to myoblasts, which can go on to differentiate into myotubes, later forming muscles.

Epithelial and and blood cells are the two of the main types of cells that need to be constantly replaced in developed organisms. As far as I know cells lining the gut epithelium are fastest to divide. They are created from stem cells in 'crypts' (pockets) in the lining and are pushed outwards, where they are later broken down (by what I would assume would be abrasion and intestinal juices). My book gives them a lifespan of 3-5 days. External skin cells are much slower to divide (though I'n not sure by exactly how much).

Red blood cells have have a lifespan of approximately 120 days. They are replenished by stem cells in the marrow of certain bones (e.g. a femur). Neutrophils are the next most common blood cell, with a circulating life of 8 hours (but lifespan may be a few days). Per day, roughly equal numbers of RBCs and neutrophils are created and are most numerous new cells created per day. Lymphocytes, another white blood cell, are responsible for immune 'memory' can persist for years. The fastest recorded mitotic cycle for a mammalian cell (in culture) is ~8-10hrs.


How was the cama's life expectancy computed? A cama is a hybrid between a male dromedary camel and a female llama. The first cama was born on January 14, 1998, yet on the Wikipedia page it is said that a cama's life span is 30–40 years. How was that number determined? Is it simply the average between a camel's and a llama's life spans?

Since no source is given for the 30 - 40 years estimate in Wikipedia, we can't find out how the authors of the Wiki page reached that estimate, but 'someone made an educated guess' seems likely. There are a few reasonable ways that one might educatedly guess the longevity of the cama, but there are good reasons to treat those educated guesses with caution.

First, as you suggested, you could just estimate the cama's longevity from the life expectancy of camels and llamas. This is likely to fall in the right ball-park, but should be interpreted with caution: ligers (lion - tiger hybrids) are reputed to have high rates of premature death, and the same may well apply to camas.

Second, you could plug the animal's body measurements, metabolic-rate measurements, or similar measurements into a model which relates species' attributes to a measure of their longevity. Many different models of lifespan have been built (e.g. here), and if your goal is to get a rough estimate of how long a member of a particular species will live, those models are not a bad way of making a first guess. The 'this is a weird hybrid and might have issues with premature death' caveat still applies, though.


Is vitamin D a vitamin or a hormone? Some people like to say that vitamin D is a hormone.
A simple set of differences between hormones and vitamins is described here.

Vitamin D is not (for the most part) absorbed through food but created by our body when our skin is exposed to the sun, so it does look more like a hormone than a vitamin.

Another difference listed is whether it has catalytic action or not (that I don't know what it means - answers with an explanation would be nice).

So, is vitamin D a hormone? And if so, why is it called vitamin D?

There's an open access article "From vitamin D to hormone D", which explains the difference(s). Vitamin D is a family of substances, but for humans the most important one from this family is vitamin D3 aka cholecalciferol. "Hormone D" (1α,25(OH)2D3, the substance that normally regulates calcium etc.) aka calcitriol is closest to vitamin D3. So if one wants to be technical about it, the vitamin(s) and the hormone are slightly different substances. Vitamin D itself is more aptly called a prohormone (i.e. a hormone precursor):

Vitamin D[3] is not technically a vitamin, ie, it is not an essential dietary factor; rather, it is a prohormone produced photochemically in the skin from 7-dehydrocholesterol. The molecular structure of vitamin D is closely allied to that of classic steroid hormones (eg, estradiol, cortisol, and aldosterone) in that they have the same root cyclopentanoperhydrophenanthrene ring structure. Technically, vitamin D is a secosteroid because one of the rings of its cyclopentanoperhydrophenanthrene structure has a broken carbon-carbon bond.

The above view is also endorsed by Horst et al., but they have a much more detailed discussion, including the fact that in vitamin D poisoning, calcifediol (25(OH)D3)--an intermediate compound in the pathway between the vitamin and the hormone--can itself act as a hormone, i.e. it has some binding affinity to the calcitriol receptor, but only at at very high doses.
As for how the vitamin label came about, "historical accident" is one way to put it...

Considering the fact that now we accept that the biologically active form of vitamin D [what the other paper calls "hormone D"], namely 1a,25(OH)2-vitamin D3, is a steroid hormone, it is somewhat ironic that vitamin D, through a historical accident, became classified as a vitamin. It was in 1919/20 that Sir Edward Mellanby, working with dogs raised exclusively indoors (in the absence of sunlight or ultraviolet light), devised a diet that allowed him to unequivocally establish that the bone disease, rickets was caused by a deficiency of a trace component present in the diet. In 1921 he wrote, "The action of fats in rickets is due to a vitamin or accessory food factor which they contain, probably identical with the fat-soluble vitamin." Furthermore, he established that cod liver oil was an excellent antirachitic agent.
Shortly thereafter E.V. McCollum and associates observed that by bubbling oxygen through a preparation of the "fat-soluble vitamin" they were able to distinguish between vitamin A (which was inactivated) and vitamin D (which retained activity). In 1923 Goldblatt and Soames clearly identified that when a precursor of vitamin D in the skin (7-dehydrocholesterol) was irradiated with sunlight or ultraviolet light, a substance equivalent to the fat-soluble vitamin was produced. Hess and Weinstock confirmed the dictum that "light equals vitamin D". They excised a small portion of skin, irradiated it with ultraviolet light, and then fed it to groups of rachitic rats. The skin that had been irradiated provided an absolute protection against rickets, whereas the unirradiated skin provided no protection whatsoever; clearly, these animals were able to produce by uv irradiation adequate quantities of "the fat-soluble vitamin", suggesting that it was not an essential dietary trace constituent. In parallel studies, Steenbock and Black at the Biochemistry Department of the University of Wisconsin found that rat food which was irradiated with ultra violet light also acquired the property of being antirachitic. However, because of the rapid rise of the science of nutrition -- and the discovery of the families of water-soluble and fat-soluble vitamins -- it rapidly became firmly established that the antirachitic factor was to be classified as a vitamin.

As an amusing parallel to this, calcifediol was identified in 1968 as an active metabolite of the vitamin, but it wasn't until 1971 that calcitriol was properly identified as the metabolite that exercises the hormonal action under normal circumstances. (cf. DeLuca)


Why do adult insects have 6 legs? Apparently, there is an advantage to having 6 legs in the insect world. What is that advantage, if anything? Why would such an advantage exist for insects, but not for other, larger land animals?

What do those middle legs do that the front and hind legs cannot, if anything? Are they really essential, or do they just generate more muscle power?

Short answer
Six legs allow for locomotion, while maintaining a supportive tripod at all times.

Background
There are several million species of insects, all on 6 legs. This implies that any change in this number is promptly selected against. It is generally agreed that insects were derived from many-legged ancestors, e.g. centipedes.

One explanation is the tripod gait that results from having six appendages. This hypothesis, formulated more than 6 decades ago (Lanham, 1951), reasons that a reduction of the number of legs during evolution did not go further than 6, because locomotion of a small animal encased in a rigid exoskeleton is not effective with less than 3 pairs of legs. Insects generally walk by lifting the two outer legs on one side and the middle on the other side, sweeping them forward and placing them down together. Hence, insects support their rigid structures with a tripod at all times. Tripods are among the most stable configurations, and they never wobble (why on earth do tables have 4 legs?). Figure 1 shows an illustration of insect locomotion (Lanham, 1951).

Fig. 1. Insects' locomotion resembles a double tripod. Insects have a cyclic gait which consists of two phases, the stance phase and the swing phase. The stance phase is the power stroke, it pushes the body forwards in the direction of travel while the leg remains on the ground. Three legs are used is this phase by forming a tripod with the front leg and the hind leg on one side of the body and the middle leg on the other side. This formation is why this gait is known as the tripod gait. Source: Insect robotics.

Larger animals can afford to have less legs, because their vestibular systems have more time to maintain balance and adjust gait during locomotion. Because insects are so small, their strides are so quick that the nervous system may not be fast enough to deal with gait control. Instead, insects rely on the tripod gait to prevent any imbalance, rather than adjusting it. In addition, the exoskeleton effectively restricts small bodily movements to control balance. Larger animals such as mammals make small adjustments in their gait constantly to maintain balance. An insect has less opportunities to do so, because of their rigid exoskeleton (Lanham, 1951).

Reference
- Lanham, Science (1951); 113(2946): 663


What is the name of this insect? Is it venomous or possess any threat to human life if someone gets stung? I found it in Northern part of India, on a mango tree. When I intended to move it away from home, it seems to bite like a snake with front part lifting like a king cobra.

This insect is 6-7 inches long, 1-2 inches wide, and appeared during summers.

That looks like some kind of lappet moth caterpillar. Although I am no expert in them, especially not species that would appear in India. But hopefully my answer gives you the right direction of research.

You can see some visually similar observations on iNaturalist:

https://www.inaturalist.org/observations/42382365
https://www.inaturalist.org/observations/40958993
https://www.inaturalist.org/observations/40137289


What is the "male gender rudiment" that women allegedly have? In The Man without Qualities Robert Musil wrote (my emphasis):

  "But the nature," he thought, "gives the man nipples and the woman
  a male gender rudiment. We cannot conclude from this, however,
  that our ancestors were hermaphrodites."

What male gender rudiment does he mean? It must be some "useless" body part in female body (like man's nipples).

Original German text:

  "Aber die Natur" dachte er "gibt dem Mann Saugwarzen und der Frau
  ein männliches Geschlectsrudiment, ohne dass daraus zu
  schliessen wäre, unsere Vorfahren seien Hermaphroditen gewesen.

First, let's briefly discuss the development of the the male and female internal genitalia and sex glands:

These include the ejaculatory duct, prostate and seminal vesicles for males, and uterus, uterine tubes and the proximal part of the vagina for females.

They all develop from two tube-like structures called mesonephric and paramsonephric ducts.

These ducts initially exist in both males and females, but normally, only one develops while the other degenerates, depending on the presence of sex-determining factors and hormonal activity.

The mesonephric ducts will develop to the male internal genitalia (the organs are mentioned above), while the paramesonephric duct will develop to the female internal genitalia (also mentioned above).

Now, to your question:

A male rudiment that exists in females is the non-fully degenerated mesonephric duct, named the Epoophoron and Paroophoron in adults, which later in life may form the Gartner’s cyst.


Unknown Lamiaceae plant identification A while ago I received a pack of seeds described as Pycnanthemum Pilosum / Mountain mint. The seeds are small (below 1 millimeter) and brown:

Plants grown out of these seeds are around 40 centimeters high and spread widely. Leaves are bright green and smooth, around 3 - 4 centimeters long:

with strong minty smell (though quite distinct from let's say Mentha × rotundifolia or Mentha spicata).

Stems are square, with very short hairs.

Recently plants started to flower:

producing clusters (around 1.5 cm in diameter) of small (3 - 4mm long), slightly  flowers along the stem. Flowers are white, with light shade of purple. with no spots or other marks.

The plant started to flower in the first year after sowing (the plant is around 4 months old, planted outside, in Central Europe).

The plant doesn't really resemble Pycnanthemum pilosum descriptions I found online (for example this or this), which, among other differences, describe long and narrow leaves.

I wonder if someone can help me identify it. Thanks in advance.

I'm going to take a stab at this. If your plant is not particularly aromatic, I feel pretty confident it is Lycopus uniflorus.  There are good descriptions here and here.  In particular, the description of the flowers at the Minnesota site, as having 2 purple-stemmed exserted stamens seems to match your flowers.  Apparently this species should have a tuber (should you end up digging yours up), while Lycopus virginicus which is probably a good second guess does not have tubers (see the differential description at the bottom of the Minnesota page).

Updated and Revised Answer

With additional pictures of now more mature flowers, which are clearly lilac in color, and the info that the leaves are strongly minty smelling, we'll revise the answer to Mentha arvensis, which fits all the available info. More here.


Why does decreasing ion channel density result in an action potential not firing? I'm pretty confused, when i run a simulation of an action potential reducing the sodium and potassium channel densities gradually over time results in an action potential not being fired, and when i only reduce sodium channel density it stops the action potential from firing even faster. My question is why? what role does density have in firing an action potential?

It is very straightforward. More the density of sodium channels, more the influx of sodium ions. More the influx of sodium ions, more the depolarization. If there are sufficient sodium channels, then the large influx of sodium ions will cause membrane depolarization above the threshold value, thus resulting in firing. If the density of channel is reduced, the depolarization value will not cross the threshold. Thus causing a net change in membrane potential, but not firing.

Potassium channel acts in coordination with sodium channel. Only if there is an influx of positive sodium ions into the cell, potassium channel will act and release potassium ions outside the cell in order to maintain the membrane potential. If sodium channel is reduced, no further processes happen, thus no firing.


What is the scientific name of this plant? I found this one on a hill here in Palestine. It's about 20 cm in height. Note that it does exist in this regions, but scantily.

The plant is of Lamiaceae family and its common name is Shell Flower or Bells of Ireland.

Its "scientific" aka latin name is Moluccella laevis.


Are there people blind to touch? There are people who completely blind or deaf. Are there people who are completely blind to touch in a particular area or in the entirety of their body? If not, are there people in whom the temperature modality of touch or the pressure modality of touch is completely absent? It seems that this might be related to congenital insensitivity to pain, but it is not quite the same thing.

Short answer
In a way, yes.

Background
One prime example where the sense of touch is diminished is when peripheral sensory neurons degenerate, which is called sensory neuropathy. Diabetes is currently a common cause of this disorder, resulting from the high blood glucose levels that damages the small blood vessels which supply the nerves. This prevents nutrients reaching the nerves, eventually damaging nerve fibres, which may end up in a disappearance of the nerve altogether (source: diabetes.org).

Sensory neuroptahy can lead to a multitude of complaints, including weakness, numbness and pain, usually in the hands and feet (source: Mayo clinic).It can also lead to the loss of ability to feel pain, changes in temperature and coordination when you lose proprioception is affected. The loss of the sense of pain is dangerous. An often heard complaint is that wounds to the feet are not noticed. If ignored, even minor injuries can develop into infections or ulcers (source: diabetes.org). I fact, my grandmother-in-law recently underwent an amputation of the lower leg, because of a diabetes-related, neglected injury to her toe. It lead to an ulcerating wound and eventually necrosis. At a certain point it caused terrible pain, but the initial wound had gone unnoticed.

A related condition is Carpal Tunnel Syndrome, also called median nerve compression. It is a condition that causes numbness, tingling, or weakness in your hand. It is caused by pressure on the median nerve that traverses a passage in the wrist called the carpal tunnel.

This may not be exactly the answer you are after, as sensory neuropathy mainy causes numbness of the extremities, rather than a complete loss of sense of touch. Remember, however, that blindness rarely results in a complete blackness. Beside the fact that the great majority of blind people are 'only' functionally blind, as they still have rudimentary visual function left, perceptions of phosphenes are in fact really common, and some people even start seeing complete visual scenes with people and objects included (Charles Bonnet syndrome). This is not unlike deafness, where many people still have residual hearing, yet too little to be of any functional use. For instance, people that are eligible for a cochlear implant often still have substantial residual hearing left. Like phosphenes in the blind, tinnitus in the 'deaf' emerges akin to 'phantom' sounds. These 'hallucinatory' sounds are actually generated more centrally by the brain after prolonged deafness. In short, blindness and deafness are relative, the great majority of folks don't lose their senses, they have reduced functionality of them.


Is there a command line molecular cloning tool? There are many softwares such as SnapGene, Geneious, Vector NTI, ApE, Gentle and others for assistance with cloning. Their key functions are:

Making maps of plasmids
Annotating plasmids with common features
Finding restriction sites
Mapping Sanger sequencing reads
Showing sequence, reverse complement of the sequence, translations in different frames
Designing primers for specific applications (such as Gibson cloning)

Is there a tool that does functions such as these, but runs from a command line?

Note: My intent is not so much to get recommendations for what to use, but to get an idea of what software is currently available. Obviously there exist many CLI tools which can be made to serve also these purposes, up to and including general purpose text editors like vi.

I'm interested in what effort has already been made to produce CLI software specifically intended for cloning (by which I mean the functions described above).

Making maps of plasmids Annotating plasmids with common features

Plasmapper works through commandline

  Finding restriction sites

Simple regex searches can do that

  Mapping Sanger sequencing reads

BLAST will do it.

  Showing sequence, reverse complement of the sequence, translations in
  different frames

EMBOSS has a collection of tools for these things. (getorf is a tool for finding ORFs)

  Designing primers for specific applications (such as
  Gibson cloning)

Primer3 works through commandline

You can just download the entire EMBOSS collection. It has many useful tools.


Does a plant have to be alive for its roots to prevent erosion? One argument often given in favour of saving current and planting additional plants/saplings is the roots hold soil together and prevent soil erosion.

Unlike plants that may be uprooted, a large tree may only be chopped down; its roots continue to remain buried. Do these, now dead, roots continue to prevent soil erosion, or does the plant have to be alive and kicking?

My guess is the latter, perhaps because absorption of water possibly 'compresses' the soil over the root.

The roots do actually continue to hold soil without being alie.  The stabilizing properties are structural in nature.  You begin to lose those though as the roots decompose, and the important roots against erosion, millions of fine root hairs, will go first. But leaving the roots in on a dead tree will help for a bit, but isn't a long term solution.


Why does high blood pressure not damage the body during exercise? Exercise is commonly understood to lower blood pressure by making the heart stronger. Mayo Clinic says,

Regular physical activity makes your heart stronger. A stronger heart can pump more blood with less effort. If your heart can work less to pump, the force on your arteries decreases, lowering your blood pressure.

While exercising, though, systolic blood pressure will often go up significantly.
Why does this dramatic increase in blood pressure not damage the cardiovascular system? Stress, for example, can damage the blood vessels,

Increases in blood pressure related to stress can be dramatic. But when your stress goes away, your blood pressure returns to normal. However, even frequent, temporary spikes in blood pressure can damage your blood vessels, heart and kidneys in a way similar to long-term high blood pressure. (Mayo Clinic)

Does daily exercise, for example, not cause "frequent, temporary spikes in blood pressure"?
Why does a blood pressure increase from exercise not damage the cardiovascular system as a similar blood pressure increase from stress (or other sources)?

Actually it can. See https://clinicalhypertension.biomedcentral.com/articles/10.1186/s40885-016-0052-y for instance:

Deleterious effects of HRE [hypertensive response to exercise] on structure and function of left ventricle (LV) has been reported consistently. Theoretically, individuals with HRE would be exposed to abnormally high pressure loads to left ventricle (LV), which may result in global subendocardial ischemia due to mismatch between demand and supply from excessive rate-pressure stress. Indeed, a previous study demonstrated a greater likelihood of new or worsening abnormalities of wall motions from echocardiography in individuals with HRE, even in the absence of angiographically significant coronary artery stenosis.

The issue is that you're confusing somewhat high blood pressure with abnormally high blood pressure during/after exercise, i.e.


Do plants produce any heat? Many plants (e.g. roses, palms) can be protected from frost during the winter if shielded with an appropriate coat that can be bought in garden shops. Do plants produce any heat that can be kept inside with these "clothes"?

Cellular respiration in plants is slightly different than in other eukaryotes because the electron transport chain contains an additional enzyme called Alternative Oxidase (AOX). AOX takes some electrons out of the pathway prematurely - basically the energy is used to generate heat instead of ATP.

The exact purpose of AOX in plants is still unclear. Plants will make more AOX in response to cold, wounding, and oxidative stress. We know of at least one plant (skunk cabbage) that exploits this pathway to generate enough heat to melt snow. This link gives a pretty good overview.

(AOX is dear to my heart, since my first 3 years working in a laboratory were spent studying this gene <3)


Pretty Flower Fungus in Oak Tree Found this on a nature walk in the town of Lincoln, MA, USA. Is this edible? I believe it is a type of fungus.

I believe it is a type of fungus.

Yes, this is a kind of fungus. Specifically, I believe it's of the genus Laetiporus sp., and is commonly known as "chicken of the woods" and "sulfur shelf". Notice that in both images the mushroom is growing on an oak tree.

  Is this edible?

I strongly recommend that you watch this and this video. Collectively, they provide more than enough information on how to properly ID the fungus, how to harvest & cook, any potential look-alikes, and even possible medical applications.

IF my suggested identification of your posted organism is correct, then yes, it's edible.


Why do smaller mammals move intermittently? I was watching a nice little video on youtube but couldn't help but notice how snappy smaller animals such as rats and chipmunks move. By snappy I mean how the animal moves in almost discrete states pausing between each movement.

Is this a trivial observation or something inherent in the neuro-synapse or muscular make-up of these animals?

Short answer
Intermittent locomotion can increase the detection of prey by predators (e.g.  rats), while it may lead to reduced attack rates in prey animals (e.g., rats and chipmunks). It may also increase physical endurance.

Background
Rather than moving continuously through the environment, many animals interrupt their locomotion with frequent brief pauses. Pauses increase the time required to travel a given distance and add costs of acceleration and deceleration to the
energetic cost of locomotion. From an adaptation perspective, pausing should provide benefits that outweigh these costs (Adam & kramer, 1998).

One potential benefit of pausing is increased detection of prey by predators. Slower movement speeds likely improve prey detection by providing more time to
scan a given visual field.

A second plausible benefit is reduced attack rate by predators. Many predators are more likely to attack moving prey, perhaps because such prey is more easily detected or recognized. Indeed, motionlessness (‘freezing’) is a widespread
response by prey that detect a predator.

A third benefit may be increased endurance. For animals moving faster than their aerobically sustainable speeds, the maximum distance run can be increased by taking pauses. These pauses allow the clearance of lactate from the muscles through aerobic mechanisms.

PS: If you mean with 'snappy' not only that small animals move intermittently, but also 'fast', then Remi.b's answers nicely covers the story why small critters are quick. Basically, it comes down to Newton's second law, namely acceleration is inversely proportional to mass (a = F/m), but the size of muscle power is not. Hence, bigger animals have more mass and need a lot more force to build up to accelerate at the same speed. That build up of force needs time (ever witnessed the vertical lift-off of a space shuttle?) Hence, small critters accelerate quicker and allow them to move 'snappy'.

Reference
- Adam & kramer, Anim Behav (1998); 55: 109–117


Why marker and control are loaded in the beginning or ending lane of the gel? I have seen gel images in several literature. Almost in all, markers and controls are loaded in the  extreme lanes (before 1st sample or after last sample) of the gel. I am just curious, is there any reason or logic to do so? Is there any problem if I load it in the middle lanes, in between my samples

No important reason. It is for esthetics, and also for ease of description in figure legends. One could argue that it might be confusing to have the markers or the control in the middle, but since the relative locations of these wells would be recorded, it does not matter where you put them. In publication, it would be easier to say, for example, "The control is in the far right lane, and the ladder is in the far left lane" Rather than saying, for example "Third from the left".