Could light/occasional smoking strengthen the lungs? Here's my thought process, correct me where I'm wrong.  It seems the human body has thresholds.

Examples: You lift too much weight, and the muscles and tendons risk serious injury, but otherwise they tend to rebuild stronger to handle more weight.  Too much sun can lead to sunburn or worse, but moderate UVB exposure can lead to melanogenesis and increase protection to UV damage.

Do the lungs behave in a similar manner where a small amount of smoking might actually strengthen your lungs before reaching the threshold where you're causing severe damage?  My guess is the answer is "probably/somewhat" but that there haven't been any studies since it'd be difficult to analyze and quantify, but maybe somebody has an answer based on theory.

From your examples only the first is really true. Exercise leads to better physical abilities (within some boundaries).

Sunlight on the other hand is always potentially dangerous, depending on the dose. But the damages accumulate over the years which finally lead to the so called senile lentigos (others call them aging spots) occuring in sun exposed skin from the age of 50.

And the same is true for cigarette smoke. Here you expose yourself to a nasty cocktail of potentially harmful to cancerogenous substances (tar, polycyclic aromatic hydrocarbons, benzene, nicotine and much more). These do potential harm to your lungs depending on the dose (meaning how many cigarettes you smoke a day), but there is nothing like a harmless amount. Your lungs will eventually recover from this (tar takes the longest to be removed), but it is definitely not good.


does phagocytosis dependent on opsonization? does phagocytotic activity of macrophages and neutrophils depends on opsonization by IGg (antibody) and C3 complex,if it does, so then why macrophages and neutrophils are categorized in Innate immune defense system (despite the interference of antibody).

and if it is not dependent so why macrophages act as antigen presenting cells to make antibodies, while they lysed it and fragmented it (the pathogen) on it's surface by it's own,so what is the need for it to make antibodies while the innate system can handle it alone?

Well, phagocytosis does not depend on opsonization, but it works better with it because the macrophages can detect the intruders more easily, but the secondary inmune response with IgG depends on the work of the APC cells, so let`s say a bacteria gets in your body for the first time, it can get phagocytated by a macrophage that will after present the parts on his MHC II to start the secondary inmune response.


How does a stonefish get oxygen out of water? It is said that the stonefish (Synanceia) is able to stay out of the water for up to 24 hours. I wonder how they get oxygen from the air. Could someone explain this?

I have been trying to find an answer to this question, but until now, no one seems to have really analyzed why this is possible. The only hint I found comes from this paper:

A study of the distribution, habitat, behaviour, venom apparatus and
venom of the stonefish.

They state:

  At periods of low water, stone-fish are often left partially exposed
  by the retreating tide. At such times they may be surrounded only by a
  small quantity of water which fills the depression in which each lies
  and the main mass of water may be a considerable distance away. They
  can survive long periods (at least 24 hours) out of water providing
  their surroundings are kept moist.

Obviously the fish only needs minimal moisture to get enough oxygen. I would further speculate that the fish turns down its metabolism during this time to minimize the need for oxygen. This paper is widely cited as a source for this survival time, but there seems to be no follow up on it. What is widely analyzed is the toxin of the stonefish.


Insect identification - Is this a bedbug? This bug was found on a couch in Cape Girardeau, Missouri. The couch, and the two beds in the room show no signs of other bugs. Is this a bed bug that I should worry about or something harmless? It was slightly larger than a common tick.

Unfortunately, you're the first I've seen on here actually to have a bed bug.
See  this picture  from University of Kentucky for comparison:

Here is one moving (more footage & info here):

Below is a picture from Bed-Bugs-Handbook.com demonstrating the relative size and appearance of 6 different life (molt) stages:

From Left to Right: Nymphs to adults both before (top row) and after (bottom row) feeding and becoming engorged with blood.

General Info:
Bed bugs are parasitic insects of the cimicid family that feed exclusively on blood. Cimex lectularius (or the common bed bug) is the most well known species as it is the one that feeds primarilly on human hosts and infests human dwellings. These insects often dwell in beds, couches or other upholstered furniture, and they are also known to live in cracks and crevices in walls, behind wallpaper and wood paneling, or under carpeting (Krueger 2000).
They usually feed nocturnally, and in the absence of allergic rashes from their bites, their presence can go unnoticed. The first signs of a bed bug infestation are often the bed bugs themselves or small dark stains bed bugs can leave behind.

See this EPA page for more information about locating bed bugs in a potential infestation.

Description
From University of Florida:

The adult bed bug is a broadly flattened, ovoid insect with greatly reduced wings (Schuh and Slater 1995). The leathery, reduced fore wings (hemelytra) are broader than they are long, with a somewhat rectangular appearance. The sides of the pronotum are covered with short, stiff hairs (Furman and Catts 1970). Before feeding, bed bugs are usually brown in color and range from 6 to 9.5 mm in length. After feeding, the body is swollen and red in color (USDA 1976).

Nymphs and larvae are smaller than adults, with late-stage nymphs being about 4.5mm long. (see here for size ranges). However, only adult females can lay eggs (see here and here for sexing tips). Their small (~1/10") white eggs are laid in clusters in mattresses, furniture, or in cracks in the wall, baseboard, or floorboards. (See here for more egg info).
Do you have a problem?
From Wikipedia:

Certain signs and symptoms suggest the presence of bed bugs; finding the adult insects confirms the diagnosis.

However, other than being a nuisance (e.g., having a "gross" factor + some skin conditions such as rashes), bed bugs have not been known to transmit dangerous human diseases (e.g., see Dolling 1991 and Kolb et al. 2009)
What to do:
Below, are a number of reputable and useful resources for handling and ridding yourself of bed bug infestations:

Bed Bugs: Get Them Out and Keep Them Out (U.S. EPA)

How to Treat Bed Bug Bites and Find the Pest (U.S. pest control company Terminix)

Bed Bugs: How to Get Rid of Bedbugs (pest-control company Orkin)

Finally, a quick search for "bed bug" on this site as well as visiting this reddit page can provide info for a myriad of species that are often mistaken to be bed bugs (e.g., carpet beetle larvae, psocids, fleas, ticks, etc.). Again, unfortunately, you're the (un)lucky winner and do in fact have a definitive specimen.

Citations:

Dolling W.R. 1991. The Hemiptera. Oxford University Press, New York, New York.

Kolb, Adam, Glen R. Needham, Kimberly M. Neyman, & Whitney A. High. (2009). "Bedbugs". Dermatologic Therapy. 22 (4): 347–52. doi:10.1111/j.1529-8019.2009.01246.x. PMID 19580578.

Krueger L. 2000. Don't get bitten by the resurgence of bed bugs. Pest Control 68: 58-64.


How would you use readthrough as part of a genetic circuit design? Traditionally, in synthetic biology, researchers tried to avoid some transcription phenomena (like roadblocking of tandem promoters or readthrough of weak terminators) since they are not in line with the discipline's strive to design modular, digital genetic circuits. However, some researchers have started using these "problems" as part of the intended design (see Bordoy et al., for example).
How do you think transcriptional readthrough could be used as part of a genetic circuit design? When would you want to have a readthrough? What kind of logic or function would this emulate?

Readthrough has already been used to implement transcriptional NOR gates, wherein tandem input promoters express a repressor that represses an output promoter. (First time I recall here: 21150903, used widely here: 27034378, roadblocking modeled here: 32141239.) An advantage of this design is that the repressor need only be encoded in DNA once, which can significantly reduce the DNA footprint of the design and the likelihood of recombination if the repressor's DNA sequence is long (e.g., protein-based repressors). OR gates have similarly been implemented as two tandem promoters expressing a common output gene. (An alternative NOR design—which is common with repressors with short DNA sequences (e.g., sgRNAs)—is to duplicate the repressor and express it separately from both input promoters. This approach circumvents the roadblocking and input asymmetry that can occur with tandem promoters.)
Readthrough has also been used with antisense promoters to tune gene expression (see 26769567). In these designs, an input promoter must read through a downstream antisense promoter, and the strength of the antisense promoter can be used to tune the response of the input promoter.
Another application that comes to mind is encoding the relative ratio of expression of multiple genes by separating them with weak terminators (e.g., to achieve X-fold expression of the first gene relative to the second). This begins to evoke an operon, as jakebeal notes. The closest example I can think of comes from this paper: 23727987, although they actually used readthrough to address the inverse problem of characterizing terminator strength.


Can mitochondria become cancerous? Given that mitochondria have their own DNA and can replicate independently, can they ever become cancerous? For example, could a mutation in their DNA cause them to rapidly replicate, ultimately killing the cell it's in?

Interesting question.

As a prelude, I should probably mention that single celled organisms cannot get cancer as we understand and define it. Mitochondria are not, of course, single celled organisms, they are organelles, but this interesting question involves treating them as if they were autonomous. We'll come back to that later. First, single-celled organisms and cancer...

Of all the hallmarks of cancer, unregulated replication is probably the most fundamental, but all the same, cancer is necessarily a disease of multicellular organisms with differentiated tissues. Bacteria do not get cancer. Protozoa do not get cancer. Yeast do not get cancer. I'm spending too much space on my prelude here, but let's pretend like this isn't an issue and just address unregulated replication. Incidentally, the review I linked is an updated version of the classic review of cancer biology. If you're interested in cancer biology, I highly recommend reading it, and perhaps the original 2000 review.

Ok, now to the question. Let's put aside the problem of a single organelle or single celled organism getting cancer, and consider whether mitochondria can develop mutations in their DNA that cause them to replicate in an unregulated fashion.

Yes, mitochondria do have their own DNA, but they are not fully autonomous.  They do "replicate independently", but what is meant by this is that mitochondria replication (via fission) is a process that occurs independent from the replication (via mitosis) of its enclosing cell. The process is regulated by proteins encoded in the nuclear genome (not the mitochondrial genome)

Both fission and fusion are regulated by dynamin related proteins, which you can read about in this, fairly dense review. The mitochondrial genome encodes very few genes, 14 at last count, and while problems with those genes and proteins are implicated in a few diseases, uncontrolled replication is not one of them.


What is this white fluff growing in my basement? I live in the countryside of Western Europe by the beach with a temperate climate. After a period of unusual humidity at 84%, I noted this white fluff in the basement floor:

The first picture is about 40 cm and the second 10 cm.

The basement is usually closed and keeps humidity. Temperatures average 18-20ºC, and humidity is now 77%. I assume it's a fungus since the floor was clear before and it seems to collapse when I rub my foot on it.

What is this species, and how can I prevent it?

Update: Following @anongoodnurse's suggestions, it's definitely a salt. I scraped the stuff, poured water, and it shriveled instantly. Here are photos before and after:

Here is a close-up of another piece, where the shards look like a crystal:

It did not smell indeed, and I did not taste it. I opened the basement door to ventilate the area, and I understand that it would accelerate the evaporation of the salty water.

I don't know if this growth has happened before, e.g. because of a leak in a pipe, or is a one-off occurrence, e.g. because of the unusual humidity in the last few weeks. I will check if the basement has any pipes.

Might as well make this an answer.

  ...it seems to collapse when I rub my foot on it.

As @tyersome stated, it appears to be salt, not mold. Salt crystals would definitely collapse easily underfoot, and should be mostly quite dry, whereas mold would be... maybe squishy (?) but likely unpleasant in some way. Mold also smells, which you haven't mentioned, whereas salt is odorless.

To test, scrape a bit up (salt crystals should feel a bit sandy, not mossy) and see what a drop or two of water does. Mold doesn't dissolve in water; it floats. If water seems to dissolve some of it, add more. If it all dissolves, it's probably a salt, and since you live near the beach, it might be mostly salt, i.e. NaCl, with trace minerals thrown in.

If it dissolves and you're brave, you can taste a tiny bit then spit and rinse. While salt isn't toxic, I can't vouch for what was in the grout.

My guess is that there may be a low spot or two in your basement where salt water is entering through the porous grout; as it evaporates, it leaves salt crystals behind. More water = saltier solution = bigger crystals as the water evaporates.

If you have a magnifying glass, you should see crystals in the undisturbed deposit. If instead it looks soft and hairy, it is mold. I can't think of a white mold off the top of my head (well, Candida albicans, but that smells yeasty and is definitely not crumbly). Mold/yeast needs a substrate (food) to grow on, and wet grout isn't very nutritious. Mildew, sure, but mot big fluffy mold.

 I don't like this reference because it's not scientific, but it explains efflorescence well.)


Is it possible to lose synapses over time? I mean, what if a person is for a long time submitted to conditions in which his mental capacities are not explored, are the synapses undone? I've heard that drugs may cause such an effect, but what if the person is not submitted to drugs or any severe accident, may the forgetfulness be related to the simple lack of usage of a certain knowledge?

Is the lack of brain usage the main cause for Alzheimer's?

Regarding your question about losing synapses; yes, synapses are regularly lost in a process called Synaptic Pruning. From the Wikipedia article:

  A decrease in synapses is seen after adolescence reflecting synaptic pruning, and approximately 50% of neurons during development do not survive until adulthood. Pruning is influenced by environmental factors and is widely thought to represent learning.

Synaptic pruning is most significant during development due to "excessive" Neurogenesis that creates a large number of neurons, many of which will later be pruned. It's not excessive in a bad way, it's simply the case that more neurons are generated than necessary and thus pruning is needed to keep the connections efficient. There's no "measure twice, cut once", instead pruning is used to refine connections.

Synaptic Pruning really doesn't have anything to do with forgetting; Forgetting is natural and simply happens because connections (via Recall/Rehersal) are not made strongly enough to fully encode memories into Long Term Memory.

Note that Synaptic Pruning is not the cause for Alzheimer's or other age related degenerative disorders. From Wikipedia again:

  Synaptic pruning is classified separately from the regressive events seen during older ages. While developmental pruning is experience dependent, the deteriorating connections that are synonymous with old age are not. The stereotyped pruning can be related to the chiseling and molding of stone into a statue. Once the statue is complete, the weather will begin to erode the statue and this represents the experience independent deletion of connections.

Synaptic Pruning is a normal process of development and occurs in all individuals. Alzheimer's is a very visible disorder due to media focus, but not part of normal developmental/aging effects.

Instead I suggest you read more specifically about Alzheimer's disease, there's quite a bit of information on it.


Antiparallel DNA Strands - Error Correcting Code? Let me quote Wikipedia.org:

"The two strands of DNA run in opposite directions to each other and are thus antiparallel."

There is a practice or method used for error correction with regard to parking tickets: First the number plate is written down from left to right, then again but in reverse (right to left) order.

So my question is: to what extent does the antiparallelity of both DNA stands constitute an error correcting code?

Double-stranded DNA does have redundancy giving a basis for error-correction, but it has nothing to do with the antiparallel nature of the DNA.

Each strand has an orientation, that is the pieces of the backbone are not symmetric and so chemical reactions have to happen in one of the two possible orientations along the strand.  One end of a strand is called the 5' end and the opposite end of the strand is the 3' end.  The two strands of a DNA molecule run in opposite directions (antiparallel), with the 5' end of one strand being adjacent to the 3' end of its partner strand.  The two strands do not contain the same codes in opposite order like your license-plate coding example.

The redundancy is only pair-by-pair.  A nucleotide in one strand is paired with a unique complement nucleotide on the other strand.  It is thus redundant like bit-for-bit odd parity is redundant.  This redundancy allows errors to be detected from a mismatch in what should be a pair, and a damaged nucleotide can be replaced with the correct nucleotide by using the complement of the nucleotide on the other strand.


When the sister chromatids are joined in the centromere, why is it stated that the number of chromosomes is 46 and not 72? Before the DNA is replicated in a human somatic cell, the cell has 46 chromosomes. Also, after the sister chromatids are separated during Anaphase, the chromosome number in the cell doubles to 72, so when the sister chromatids are joined, why isn't the chromosome number also 72? On the internet, some sources say that one chromosome in a cell that hasn't replicated its DNA is equal to one chromatid. Is this correct, or are chromosomes and chromatids structurally different?

When I was learning genetics for the first time I have also found naming the two chromatids joined at centromere as chromosome a little bit strange. The number of DNA molecules and their behaviour in cell cycle seemed to me more important for understanding of genetics.
What you need to understand.is the term chromosome predates knowledge of DNA structure. The name literally means colored (chromo) body (soma). It is an object visible under the microscope when using specific dye. In metaphase two chromatids joined at centromere look like a single object - a chromosome. Sometimes the two chromatids of one chromosome are so close together it is difficult to tell them apart. In anaphase the chromatids separate and one object (two-chromatid chromosome) visibly splits to two objects (single-chromatid chromosomes of daughter cells)


Do restriction enzymes on read 3' to 5'? Every chart of palindromic restriction enzymes I've seen lists their restriction sites from 5' to 3', something like this:

EcoR1 cuts GAATTC between the G and A:
          5' NNNGAATTCNNN 3' --> 5' NNNG____ AATTCNNN 3'
          3' NNNCTTAAGNNN 5' --> 3' NNNCTTAA____ GNNN 5'

Will restriction enzymes match and cut a site if it's running antiparallel? For example, will EcoR1 cut this sequence?

5' NNNCTTAAGNNN 3'
3' NNNGAATTCNNN 5'

Whatever sequence (plus direction) is target, so enzyme will cut. In your example "correct" and "antiparallel" sequences are two different sites.

Actually, your example of 5'-CTTAAG-3' is cut by AflII enzyme.


How can evolution make such complicated beings? So what I understand is, evolution is a mere mistake in the replication of DNA and this change is sometimes good and sometimes bad.

And the other day, in our biology class, we were told the functioning of the lungs and how the RBCs fetch the O2 from the alveoli and dump the CO2 out.

And I also know a little bit about some complicated processes in the body like, how the digestive system works, how the muscle cells switch to  anaerobic mode when we run out of O2 causing cramps, how the cells make ATPs in the mitochondrea.

And 1 more notable thing- the amount of complicatedness and all the neural networks in brain.

My question is- how can evolution(a mere mistake in copying a strand of DNA) make such a complicated machine, like our body. There are SO many organs, all working in collaboration to make the body work. And all of those organs are doing SO many things.

I know that this is a result of 3.8 billion years of evolution...but still... how can even a million "mistakes" make a body which is so well deisgned?

ALSO was the whitening of the polar bears a mistake too? Then what are the chances of such a mistake occuring in the replication of DNA? If it was evolution then why don't birds become the colour of the sky?

If this is a general question about how evolution works then Roland's comment is correct - you should start with one of the excellent resources available online, like http://evolution.berkeley.edu/evolibrary/home.php. However, this specific question sounds more like something we used to call the 'argument from personal incredulity' to me - you're willing to accept that evolution occurs, you're just not sure whether it is sufficient to create something as complex as the organisms you see around you. This is quite a common issue people have with evolution by natural selection, and it's a perfectly reasonable question to ask. Essentially, it originates in the difficulty of appreciating the sheer scale of the processes involved. To paraphrase Douglas Adams, "[life] is big. Really big. You just won't believe how vastly, hugely, mind-bogglingly big it is." But I'll do my best to try to help you understand this a bit better.

The number of single-celled organisms on the ocean floor is estimated at 2.9×10^29 - that's roughly three hundred billion billion billion. The current global human population is about seven billion - that's already effectively impossible to imagine. If every one of those people had seven billion tiny people living on them, and every one of those had seven billion people living on them, that's roughly the number of single-celled organisms on the ocean floor right now. Many of those appeared less than 24 hours ago and will be gone tomorrow. Natural selection is acting on every aspect of every one of those organisms simultaneously and has been doing for roughly 1.5 trillion generations. One-and-a-half thousand, thousand, thousand, thousand, thousand, thousand generations.

Natural selection is also a fantastic mechanism for homing in on solutions to complex problems - so good that we've started using it to solve mathematical and computational optimisation problems.

Essentially, it's one of the best approaches to solving complex problems we have been able to conceive of and it's had an insanely, mind-bogglingly long time to act on a planet-sized test tube. That's how we ended up with so much amazing stuff on our planet.


Why is Sanger sequencing inferior for detecting SNPs in cancer cells? I am familiar with Sanger sequencing, but at the level of an undergraduate. A lecturer of mine tried to describe Sanger sequencing as losing the sequence information in noise when used to detect cancer. This paper also says "lacks sufﬁcient sensitivity for detecting mutant alleles in tumor biopsies,"(Thomas et al., 2006). What is it about Sanger that makes it too insensitive for SNP analysis?

Thomas, R.,K., et al. (2006) Sensitive mutation detection in heterogeneous cancer specimens
by massively parallel picoliter reactor sequencing. Nat. Med. 12, 852–855

In the Sanger approach, DNA would be isolated from the biopsy and would contain both normal alleles and mutant alleles of genes associated with the development of the tumour. If, for example, PCR amplification was then used to derive a sample of a target template region, this material would end up being sequenced as a mixed population: the derived sequence would be an average of that population of sequences, and rare alleles would be masked.
The key difference in most next generation approaches is that the template DNA is "cloned" physically (e.g. by sequestering individual molecules into droplets, or by binding them to a surface) so that the sequences of these individual molecules can be determined in parallel. This approach would reveal tumour-associated polymorphisms when the sequences of the individual template molecules were compared.
Added later as supplementary information.
I have now looked at the paper cited in the question. This quotation from the Introduction bears out my main point about sequencing a mixture of templates differing at just a few key positions.

Although commonly used in many clinical settings, dideoxynucleotide chain termination (or ‘Sanger’) sequencing of PCR products often lacks sufficient sensitivity for detecting mutant alleles in tumor biopsies, where the failure rate has reached 75% in some cases. Gain-of-function oncogenic mutations are frequently heterozygous events or may represent a single allele of an amplified gene; thus, the signal for mutated residues is typically reduced relative to neighboring bases. Moreover, the ability to detect single base mutations or small insertions or deletions in biopsy material by Sanger sequencing depends heavily on sample purity (for example, the extent of contaminating stromal DNA) and genomic DNA integrity. Furthermore, resistance to kinase inhibitors may correlate with low-frequency second-site mutations. These observations underscore the challenges for accurate mutation detection in cancer specimens.
A massively parallel sequencing-by-synthesis approach, ‘picotiter plate pyrosequencing,’ provides a new alternative to Sanger sequencing. This approach relies on emulsion PCR-based clonal amplification of a DNA library adapted onto micron-sized beads and subsequent pyrosequencing-by-synthesis of each clonally amplified template in a picotiter plate, generating over 200,000 unique clonal sequencing reads per experiment. Sequence variants that represent a fraction of a complex sample can be vastly oversampled, thus enabling statistically meaningful quantification of low-abundance variants.


Under what conditions does the body burn fats, proteins and carbohydrates? Searching the internet, I have found lots of conflicting information from various fitness sites concerning when the human body burns fats, proteins and carbohydrates.

My basic understanding was that the body will first utilize glucose and glycogen stores, followed by fats and finally proteins once the fat and glycogen stores become depleted.  Also I believe there is some overlap in this process.

However many fitness websites claim that during high intensity physical activity, the body will prefer to burn protein over fat.

Scientifically speaking, when does the body ordinarily burn the following food groups (proteins, fats and carbohydrates) and how does exercise influence this process?

If you are able to provide graphs or data to back up your answer this will be extra helpful because I am bored of all the speculation I see on other sites.

Introduction

The system that regulates body energy store consumption is hugely complicated, but is mainly a cooperation between hormones released by the pancreas (insulin - lowers blood sugar and glucagon - raises blood sugar) and the liver (as the bodies main glycogen store and factory for various energy related tasks).

Fed State

In the fed state (high blood glucose e.g. after a meal), the body produces a large amount of insulin.  When the ratio of insulin:glucagon is high (≈0.5):

Dietary glucose is absorbed by the liver when glucose concentrations are over 8mM.  This glucose is then either

used in respiration by the liver
converted to glycogen to be stored in the liver
converted into fatty acids which are then transported out to the periphery in very-low-density lipoproteins (VLDLs)

Adipose tissue (fat tissue) takes up glucose in the blood.  This glucose is then:

used in respiration by the adipose tissue
converted into fatty acids then tri-acyl-glycerols (TAGs) - fat.  VLDLs from the liver can also be absorbed by adipose cells to be used for this.

Skeletal Muscle again directly absorbs glucose from the blood

During contraction glucose is used directly in respiration to fuel the activity
In preparation for future contraction it is converted into glycogen and stored in the cell
Amino acids are incorporated into cellular proteins though if they are superfluous then they can be used in respiration

The brain directly absorbs glucose and uses it in respiration

Early Fasting State

Where the insulin:glucagon ratio has dropped to around 0.15

In the liver

Glycogenolysis is activated to release glucose from stored glycogen to compensate for falling plasma glucose levels (signalled by elevated glucagon)
Triglycerides in the liver are preferentially broken down for hepatic respiration - fatty acids are transported in from the blood to meet the livers own energy demands
The liver begins the process of gluconeogenesis - making glucose from non-carbohydrate precursors

Adipose tissue

Rapidly starts lipolysis - stored fats are broken down into free fatty acids and glycerol.
Some of the free fatty acids are used for the adipose tissues own respiratory demands
The majority is released to the periphery to be utilised by other tissues
The glycerol released can't be used by most tissues, but is taken up by the liver where it can be used to make glucose by gluconeogenesis

Skeletal Muscle

Uptake of glucose from the periphery is reduced to preserve glucose for cells that can't easily use other fuels - e.g. the brain or red blood cells
Free fatty acids become the main fuel for skeletal muscles to conserve the glucose for elsewhere
Unlike in the liver, glycogenolysis is not activated as there are no glucagon receptors in muscle tissue.  This means glucose is only produced from glycogen when muscles are actively contracting, as before.
At this point proteins can start to be broken down,  their skeletons used as an immediate source of energy and amino acids released to be taken up by the liver and used in gluconeogenesis

The brain directly absorbs glucose and uses it in respiration.  Fatty acids can not be used as these do not cross the blood brain barrier

Late Fasting State

If there has still been no glucose intake, the insluin:glucagon ratio falls even further, to around 0.05.

Liver

No further glucose has entered the liver and within 24h all hepatic glycogen stores have been depleted
Gluconeogenesis becomes the principle source of all plasma glucose - the liver creates new glucose from:

Amino acids - muscle & liver protein breakdown
Glycerol - from adipose tissue
Lactate - from red blood cells and muscles

High amounts of fatty acids are converted into Acetyl CoA to be used in respiration by the liver, but too much Acetyl-CoA is produced.  The remainder is converted into ketone bodies that are useless to the liver, so jettisoned to be used by other tissues (esp. the brain)

Adipose tissue

As the fast continues into a few days, adipose tissue adapts to producing large amounts of free fatty acids.  This becomes sufficient for most body tissues
These fatty acids are used preferentially by all tissues that can use them, conserving glucose for the brain

Skeletal Muscle

Fuelled almost entirely by fatty acids and ketone bodies from the liver and adipose tissue
Protein breakdown continues to release carbon skeletons and amino acids for gluconeogenesis - but this is inhibited in the presence of high levels of ketone bodies to prevent unnecessary muscle wastage (still allowing the human to hunt)
Amino acids are incorporated into cellular proteins though if they are superfluous then they can be used in respiration

The brain

Once ketone levels reach a critical level, they can cross the blood brain barrier to be used as a supplementary energy source
However, it is not sufficient alone, so a net source of glucose is needed from somewhere in the body

Progressing to starvation

This process can continue for a number of weeks, with the body eventually exhausting fatty acids in adipose tissue and being unable to produce ketone bodies in the liver, losing the inhibition of proteolysis causing a last ditch response of muscle breakdown for energy.  Death is usually from heart failure resulting from cardiac muscle breakdown.

Summary

This chart might be useful in summary, it shows where the glucose levels in the blood are coming from at various stages, the gluconeogenesis line indicating protein and fatty acid breakdown:

Exercise

Exercise has to be very intense to have any effect on this system in normal situations.

Resting Muscle metabolises stored fatty acids for its own energy.  Glycogen stores are replenished from glucose ready for more vigorous contraction.
Brisk Walking fatty acid metabolism again provides almost all the energy
Sprinting Glycogen stores are used, respiration is almost entirely anaerobic as blood vessels are constricted by the muscle activity and ventilation has not had time to increase.  Lactic acid is produced, which can be used by the liver for gluconeogenesis
Middle distance running: aerobic metabolism takes over as the body adjusts to the higher oxygen demand.  Lactate is still the major end product

One example of where this may be more noticeable is during a marathon.

0 Mins - Muscle is resting at the start line, as above.
10 mins - Muscle and liver glycogen released to power muscle contraction
2 Hours - A marathon requires roughly 700g of glycogen to complete, however the liver can only store around 500g.  This is largely depleted after roughly 20 miles.  Blood glucose levels fall rapidly and the body switches to fatty acid metabolism.  This only provides around 60% of the power output and pace falls off (known as hitting the wall).  At this point, virtually every reserve power source is being used simultaneously to keep the body going.
Finish - Muscle and liver glycogen are entirely depleted. If glucose levels haven't been maintained by other means, hypoglycaemia results causing confusion, hallucinations and even coma and death.


Effect of pH on life? Use buffer or HCl? How about lactic acid? I'm trying to find the effect of pH on living things like E. coli and such. At first I thought of using a buffer solution which maintains its level of pH, but it's possible that the inactive ions of each buffer have their own effect on living things that I can't account for. On the other hand, I could use hydrochloric acid and sodium hydroxide at different concentrations by diluting it. This will be a little bit more effort (I'll be diluting the acid and base myself), but much cheaper than the buffers, and I'll know that the only other ions present beside H+ and OH- are just Na+ and Cl-, the ingredients of table salt. According to this paper, the effect of pH on the population also depended on the acid (HCl vs lactic acid).

I would like a second opinion on this:
If I'm investigating the effect of pH on growth of living things, do I use specially made buffers or just properly diluted HCl and NaOH?

That is a variable that you have the pleasure defining yourself. Just know that using a buffer will introduce other atoms that could affect the "living things". Conversely, if you don't use a buffer, it is likely that the pH of your "living things" will be easily altered by the metabolism of your living things (IMHO, this is worse).

I don't know the details of your project, but recommend:

-use a buffer like.. Tris, phosphate...
-use 10 mM Tris-Cl without any extra electrolyte (aside of the HCl or NaOH that you use to modulate the pH of your buffer to different pH's that you want to test)
-e.g. Tris-Cl pH 7, 8, 9.. or Phosphate pH 2,3,4,5,6,7,8,9..


How does the splicing enzyme recognize where to splice the introns? When the DNA from the nucleus is transcribed to an mRNA, the mRNA is spliced by an enzyme before it goes outside through the nuclear pore. What is the name of this enzyme and how does it recognize where to splice the DNA so only the introns remain inside? Would it not need an instruction set itself to recognize exactly where to cut so the sequence does not change?

There are two factors that involve the ability of enzymes to process RNA.
1) Structure see wikipedia
2) Binding affinitya

Let's take a look at the splicing process:

The active 'sites' (GU,A & AG) need to be in spatial proximity (point one), and the enzyme needs to be able to bind there, aka forming hydrogen bonds with the nucleotides, which is mostly the case if:
a) the nucleotides are 'free' as in they are not paired with other nucleotides
b) it is energetically favorable for the enzyme to bind and do its work, which factors like temperature, and of course on the correct nucleotides

If there were some mutations, the splicing might not work.


What species is this? Seashell from Indonesia Anyone know exactly what species this is?  I gather it may be an auger (family) or cerith (family) of some sort.

This particular one is native to Indonesia's black beaches.

I would like to know what is the genus and species of this specimen.

That is a piece broken off of a sea urchin shell.

Without it's spines, it's not possible for me to say which species it is.


Are the transitions between the different brain frequencies states easy to see on an EEG? Are the transitions between the different brain frequencies states: Gamma to Beta, Beta to Alpha, Theta to Delta, etc. easy to distinguish on an EEG? How quickly can the brain transition between any of these states?

Delta/theta/alpha/beta/gamma are not different states and so there are no changes "between" them. These are terms used to label different bands of the frequency spectrum. Every EEG has energy in all of these bands. Brain state can change/be measured by the relative changes in different bands (either relative to each other, or in absolute power change over time), but there is always some energy in every band.
Here are some example spectra from different brain states (stages of sleep and anesthesia states) across different brain regions:

(from Banks, M. I., Krause, B. M., Endemann, C. M., Campbell, D. I., Kovach, C. K., Dyken, M. E., ... & Nourski, K. V. (2020). Cortical functional connectivity indexes arousal state during sleep and anesthesia. NeuroImage, 211, 116627. Disclosure: I am an author on this paper)
WS and WA refer to "wake" in the sleep and anesthesia experiments respectively; N1, N2, and REM are stages of sleep. S refers to sedated under anesthesia - subjects can still respond to commands, and U refers to unresponsive under anesthesia. These are actually not from EEG but from electrocorticography where the electrodes are placed directly on the brain, sometimes called iEEG, but there are a lot of similarities with EEG.
You can see that in all brain states, there is energy across all the frequency bands (identified with Greek letters), but there are changes with state. For example, delta has more power during N2 sleep across the brain. A trained eye could also easily pick this up in the time-domain EEG signal, but it's much easier to convert to the frequency domain like in this figure.
You'll notice that the energy decreases with increasing frequency. This is normal, and is typical of natural frequency spectra with certain properties, see Pink Noise; it's rare to ever have less power in the delta band than any other band, for example. You will also see that for the most part the spectra are gradually changing: there are few peaks in the spectrum, and it can be a bit misleading to refer to energy in a specific band or to compare between bands when there is no peak there. Some exceptions are that there is typically a peak in the alpha band for humans, especially with eyes closed. Hippocampus tends to generate rhythms in the theta band, and rodents have very large hippocampus relative to the rest of cortex, so you'll often see a theta peak in rodents especially during locomotion.
Lastly, these EEG differences are probably not the best way to discriminate between different brain states. There are lots of other measures that seem to do better. In the rest of the paper that I've taken this figure from, my colleagues and I use a specific measure called the weighted phase lag index which does a much better job at discriminating between putative conscious and unconscious states.


Transformation of a multicellular organism I was reading about using RNA-interference as a method of introducing pest-resistance in plants. In tobacco plants, using Agrobacterium vectors, genes specific to the nematode Meloidegyne incognitia were introduced. This was done in such a way that it produced both sense and anti-sense RNA in the host cell, forming dsRNA and ultimately silencing specific mRNA of the nematodes.

My question is, how can every single cell, or a proportion of cells sufficiently large so as to confer pest-resistance, of an already mature plant be transformed? Are a large number of vectors introduced, and as the infection gradually progresses, the immunity spreads throughout? Sorry if it's a stupid question, I've been out of touch with biology for a while.

Your inference is basically correct. The Agrobacterium acts as a vector for a plasmid containing the genetic construct one wishes to introduce into the plant genome. A medium containing a large number of bacterial cells transformed with this plasmid is injected into plant tissue, and the plasmids enter plant cells where parts of their DNA are integrated into the host genome. The overall effect of this is that there is localized integration in the areas where the Agrobacterium was introduced. A nice visual illustration of this comes from a paper from our lab where my colleagues introduced the genes for betalain biosynthesis into the tissue of Nicotiana benthamiana: in Figure 3 you will see only a localized area of cells around the injection site gain the ability to produce betalains.
You can find a nice review of the whole process of transformation with Agrobacterium here.


How many neurons are stimulated by electrodes in memory engram experiments? Researchers have recently identified "engrams" in the mouse hippocampus, "sparse populations of neurons" or "small clusters of cells", stimulation of which elicits a specifically trained fear memory association. For example...

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4874022/

http://www.nature.com/nature/journal/v484/n7394/full/nature11028.html

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3331914/

http://www.smithsonianmag.com/innovation/meet-two-scientists-who-implanted-false-memory-mouse-180953045/

My question: Roughly how big -- how many neurons -- are the regions stimulated in these experiments? I looked through a number of papers and was unable to find this information.

10/18 -- Changing the title and wording to clarify that I am asking just about experimental procedures with electrode implants, not fMRI studies, and not about how engrams might actually work.

edit: More directly answering the initial question, thank you, I misread what you wondered and was mislead a bit by a previous comment and your response to that comment.

In these experiments, they are using optical, not electrical techniques. Therefore it is a bit difficult to estimate exactly the number of cells activated directly, because light will scatter in the tissue but also fall off with distance. Based on the density of labeled and affected cells (to be stimulated, the cell has to be both a) labeled by a virus injection, and b) active in the engram) pictured in the second link you included, it seems like no more than a few to a couple dozen cells would have been activated directly.

In your comment, you said "IOW, how finely can implanted electrodes read and stimulate neurons?" - this is a different question. Implanted electrodes can read from and stimulate single neurons, or populations, depending on the electrode and experiment. It is difficult to target particular neurons with electrodes without an additional optical technique.

In the experiments you reference, optogenetic tools are used to selectively label cells that were active earlier in an experiment, and then reactivate those same cells with light. These sorts of experiments have only become possible recently with the development of those tools.

(original answer below)

Standard answer of biology applies here: "it varies", probably by species, type of memory, brain structure, etc.

But, to give you some ideas, one area that has been studied a lot in this field is the dentate gyrus of the hippocampus (the second and third links you sent, for example). One paper showed that a given memory activated something like 2-4% of the cells in that structure in a mouse http://www.sciencedirect.com/science/article/pii/S0166432811006462 with something like 1,000,000 dentate gyrus cells total in a mouse. So, that's a lot of cells, but those cells might be doing something special (pattern separation), so maybe it isn't right to think of them as the "engram" itself, or maybe we should be counting them PLUS all the cells activated in CA1, PLUS all the cells activated in cortex, etc. Whatever the case, one thing that is clear is that cells are involved in many many different engrams - if you are familiar with pop neuroscience you might recall the excitement about "grandmother cells" and "Jennifer Aniston" cells from a few years back. That's almost certainly not how engrams work, but that out of the subset of neurons and stimuli they examined, there was only limited overlap in those cases.

For fMRI studies, it's pretty hard to get a handle on the number of cells involved, but it isn't really possible to measure from "small clusters of cells" in fMRI on the same scale as in other measurement techniques. What is going to be more important for the fMRI decoding studies is "variation within a brain region" where the total number of neurons is many many millions, but the exact number involved in any one engram can't be measured with current technology.


Why do humans retain two kidneys? If one kidney can function just as well as two, why do humans have two kidneys? The cost of growing two kidneys must surely be quite high, especially since one kidney is all that is really needed.

One of the easiest answers to the question; "Why do we have ____?" is "Because our ancestors did". This is not trivial or flippant, as it is a significantly important answer that is so often overlooked. Humans are members of Bilataria; a deep branch of the animal tree that is characterized by bilateral symmetry. Humans are typical of other vertebrates in having two kidneys. Selective pressure to reduce to one of two organs is typical in snakes, whose body form favors reduction. But even snakes have two kidneys. Natural selection does not reduce features we don't need unless such a reduction would increase fitness.


Does every gland type have stem cells for regeneration? Is there any gland in which there are no stem cells?

I know that:

sebaceous gland is maintained by unipotent stem cells
thyroid gland - some stem cells, apparently unipotent

Glands about which potency I am not sure

pancreas gland - contains probably many types stem cells, at least unipotent
pituitary gland - not sure if any exist

I cannot find any such gland that does not have stem cells.

Stem cells are not all 'unipotent' - they cannot necessarily differentiate into any type of cell. For instance, resident stem cells in tissues such as muscle - myo-satellite cells - are partially differentiated and during cell division one daughter differentiates further to become a myocyte (for example), and the other daughter the replacement myosatellite cell. As far as I'm aware, the majority of tissues have resident stem cells in varying degrees of differentiation (exceptions might include neurons and cardiac muscle, where cells are not replaced over the lifespan of the organism).

Here is some evidence for resident stem cells in glands;

The adult pituitary gland shows stem/progenitor cell activation in response to injury and is capable of regeneration (Fu et al, 2012),
The pancreas has been heavily studied from the perspective of diabetes research, with many studies looking to implant stem cells from elsewhere (Rezania et al, 2012). However there is some evidence for resident stem cells of the pancreas that may turn out to be more promising as treatment strategies in the future (Xu et al, 2004, Venkatesan et al, 2011),
Sebaceous glands are found throughout the skin, and secrete 'sebum' which keeps the skin waxy and waterproof. There is plenty of evidence for epidermal stem cells (Eckert et al, 2012),
There is also recent evidence for the existence of thyroid stem cells too (Fierabracci, 2012, Malaguarnera et al, 2012),
Saliva is mainly produced by the submandibular glands also contain resident stem cells, with this paper stating that stem cells have been isolted from salivary glands in humans (Okumura et al, 2012),

Given the limited (and very recent) evidence for the above (relatively well characterizd) glands, it seems likely that other glands will also have resident stem cells that remain to be identified.

Ageing: The so-called stem-cell pool gets depleted over a lifetime, so tissues lose the regenerative potential. However rejuvenation medicine is becoming a heavily invested in area of research (see www.SENS.org).


How long does it take for a cell to synthesize an enzyme? Where can I find data regarding the times distinct cells take to synthesize distinct enzymes?

In human cells it takes about 20 s to make a 20,000 dalton enzyme.

Assuming that the cells concerned are already making mRNA for the enzyme, there will be two main factors:

(1) The time taken to synthesize the polypeptide

(2) Any time taken to fold the protein

(If the enzyme is secreted from the cell there will also be the time taken for the protein to traverse the secretory pathway - perhaps you want to include this time - if so it could be 10's of minutes.)

Here I will focus on (1). What is the rate of polypeptide elongation?

For bacteria:

  Young & Bremer (1976) Polypeptide-chain-elongation rate in Escherichia coli B/r as a function of growth rate Biochem. J. 160: 185-194

They quote values of:
17 s-1 for fast-growing cells
and 12 s-1 for slower-growing cells.

For yeast:

  Bonven & Gullov (1979) Peptide chain elongation rate and ribosomal activity in Saccharomyces cerevisiae as a function of the growth rate. Mol. Gen. Genet. 170: 225-230

minimal glucose 9.3 s-1
minimal acetate 5.5 s-1

In human cells:

  Ramabhadran & Thach (1981) Translational elongation rate changes in encephalomyocarditis virus-infected and interferon-treated cells. J. Virol. 39: 573-583

They measure a control value of 9.4 s-1 and quote (with citations) values of 9-10 s-1 in reticulocytes and CHO cells.

Let's use 9 s-1, and assume 110 daltons per amino acid

Then e.g. a 20.000 dalton enzyme (= 182 amino acids) requires 20 seconds.


Cell type that expresses 90% of the genome Cells that are differentiated express the genes that are necessary for their own usage. I've heard that some cell type expresses about 90% of 30,000 proteins that are encoded in the genome. Can anybody tell me what this cell type is?

Well, I found this paper:
Danan-Gotthold M, Guyon C, Giraud M, Levanin EY, Abramson J. 2016. Extensive RNA editing and splicing increase immune self-representation diversity in medullary thymic epithelial cells. Genome Biol 17:219.

Medullary thymic epithelial cells [mTECs] express ~85 % of the entire coding genome
...to better determine the fraction of genes expressed in mTECs and other mouse tissues, we took advantage of RNA-seq technology... The analysis... revealed that most of the tissues [see below for those tested] express 12,000–14,000 genes (i.e. 60–65 % of the coding genome). The lung and two immunologically privileged sites, brain and testis, were the only tissues that expressed a larger fraction of the genome, in the range of 70–75 %... In line with other recently published studies, the mTEChi population expressed nearly 18,000 genes, which represents ~85 % of the coding genome, while Aire-deficient mTECs (AireKO) expressed approximately 15,000 genes, suggesting that Aire is responsible for the induction of ~3000 genes in mTECs. Interestingly, even in the absence of Aire, the mTECs expressed a relatively large fraction of the genome (~75 %), considerably exceeding the overall genome expression in other peripheral tissues. Interestingly, neither [cortical thymic epithelial cells] nor [skin epithelial cells] demonstrated higher overall genome expression than other tissues, suggesting that promiscuous gene expression is indeed unique to the mTECs population.

These cells express such a wide complement of proteins because they are involved in T-cell maturation, specifically negative selection.

List of tissues tested in the study:

brain, testes, liver, kidney, lung, colon, skeletal muscle, spleen, cortical thymic epithelial cells, skin epithelial cells


Genetic Diversity in Mitochondria As I was studying for my GRE exam, I was reading on Mitochondria. I then remembered that they undergo replication similar to bacteria. So I googled for info and found on Wikipedia that there is a " near-absence of genetic recombination in mitochondrial DNA"
https://en.wikipedia.org/wiki/Mitochondrion#Replication_and_inheritance

So then, if there is a lack of genetic diversity, how can these mitochondria still be functional? If we assume they are affected by random mutations as DNA can be. Is it the case that they replicate infrequently enough to not suffer ill-effects of low diversity?

Your claim that "there is a lack of genetic diversity" in mitochondria is not correct. There is no connection between recombination and mutation rates per se. In fact, mitochondria have much higher mutation rates than nucleus and different types of mitochondrial DNA can even co-exist in one organism, a phenomenon called heteroplasmy (which is found at a frequency of ~90% in human).

But: there is a connection between mutation fixation rate and effective population size. Because mitochondria are normally inherited through maternal line, effective population size for their genome is smaller than that of the nuclear genome, and thus any mutations in the mitochondrial DNA reach fixation faster, but again this is counteracted by high mutation rates.

There is no problem with functionality: as always if something gets broken (and it is easy to break something in the mitochondrial genome, since genes are normally tightly packed in it) respective genotype is eliminated or reduced in frequency by natural selection. In the case of mitochondria this selection acts both upon the level of individual organisms (intra-individual somatic pool of mitochondria: positive and negative selection) and the level of populations (mostly purifying selection in humans). It is nevertheless true, that given the virtual lack of recombination, selection becomes the only force of purging deleterious mutations.


How are the various classes of E coli genes determined? Looking at some more detailed codon usage tables, genes may be further clustered into three gene classes: Metabolic genes, highly expressed genes during exponential growth, and horizontal gene transfer. Looking at the original paper by Medique et al., they clustered the genes based on the CAI and then by a variant of k-means determined 3 classes. Note that this is different from a class II gene which is determined by the types of RNA polymerase used.

How did they end up determining what the three classes are? It seems as if they made this generalization without any proteome data. Would the same genes be classified using a protein expression data during exponential growth and stationary growth?

I read through the paper. The author starts by stating that as of the time of writing, two different classes of codon usage profiles were known (or at least putatively so). All 782 unique CDS sequences used were subjected to a two-step classification method. In step one, each CDSs was broken down into a 61-dimensional vector representing each of the 61 possible codons. A factorial cluster analysis (the categorical, multi-variate equivalent of principle component analysis) was run on these vectors, condensing 61 dimensions down to 2 dimensions. Now that the data complexity has been reduced to 2D, it is more manageable for a k-means algorithm to partition the data. In the end, the genes were clustered into 3 orthogonal groups (classes I, II and III, with 502, 191 and 89 CDS, respectively).

Only after the authors clustered the gene set were they able to go back and look at the canonical definitions of each gene. It so happened, fortuitously, that each class of the genes had a strong bias for subsets of cellular function (eg, metabolism, protein biosynthesis, transport). They did not use proteome data, but they were able to define the role for a large number of these genes based on the body of literature at the time.


How does an excessive amount of beta carotene affect skin colour? How much is the daily need of beta carotene and how many carrots have to be eaten in order for one's skin to turn "orange".

I found 2-4 mg/ day as basic need, 30 mg daily over three weeks turns white skin orange. Is this correct? And what is the reason behind this?

How much beta carotene does it take to change someones skin colour?

To turn the skin yellow, rather than orangish, a person would have to eat about 10 carrots a day for a period of at least two weeks, consuming at least 51 grams of beta-carotene each day. The average carrot contains about 5 to 6 milligrams of beta-carotene

What is the reason behind this?

A very high diet of food which contain carotenemia (such as carrots, squash, sweet potatoes and others) can cause skin discoloration. The skin, and especially the palms of the hands, turn yellow, rather than orange. This change in skin colour fades and eventually disappears when the individual's diet changes back to normal.

  Carotenoderma is deliberately caused by beta-carotenoid treatment of certain photosensitive dermatitis diseases such as erythropoietic protoporphyria, where beta carotene is prescribed in quantities which discolor the skin.

What does an excess of carotenoids do?

  An excess of carotenoids, being eliminated via sweat, may cause a marked orange discoloration of the outermost skin layer. This benign and reversible condition – which is most easily observed in light-skinned people and may be mistaken for jaundice – is known as carotenosis or carotenoderma.

sources:

https://en.wikipedia.org/wiki/Carotenosis
http://www.webmd.com/vitamins-supplements/ingredientmono-999-beta-carotene.aspx?activeingredientid=999&
http://umm.edu/health/medical/altmed/supplement/betacarotene
http://emedicine.medscape.com/article/1104368-overview


PSI-BLAST website algorithm parameters http://blast.ncbi.nlm.nih.gov/Blast.cgi

In this website, when I want to apply the psi-blast algorithm on a sequence, under the section of algorithm parameters , what does PSI-BLAST threshold mean? The question mark says it means that:

  Set the statistical significance threshold to include a sequence in the model used by PSI-BLAST to create the PSSM on the next iteration.

Another parameter is there called pseudocount. Did not understand that too. Could not understand what this means, someone please explain in simple language.

PSI-BLAST is an iterative algorithm. Each cycle it uses a model (the position-specific scoring matrix, or PSSM) to search for sequences matching the model, next updates the model with the sequences found, and then runs the search again with the updated model. That P-value controls which of the sequences found in each iteration should be included in the new model (i.e. only include those sequences satisfying the P-value).

Regarding the pseudocounts, this is a value to be added to each column in the PSSM. The reason is to avoid zero count entries, which may give problems later. But as the help suggests:

  Pseduocount parameter. If zero is specified, then the parameter is automatically determined through a minimum length description principle (PMID 19088134). A value of 30 is suggested in order to obtain the approximate behavior before the minimum length principle was implemented.

It is probably OK to leave the default option unless you have some reason to change it.


Can the spike protein created by the Covid mRNA vaccines be created independently of the human body, and is there a higher cost to that? How different in principle is using the bodies own mRNA to create the coronavirus spike protein differ from other methods of using genes to manufacture other drugs or proteins and is there a cost benefit to it?
Take the scheme for instance that uses genetically modified genes in goats to manufacture spider silk, as shown in this link - The goats with spider genes and silk in their milk or Yeast cells genetically modified to create morphine-like pain killer
I understand that in the case of the Covid vaccines the human body's genes themselves are not modified, but it is the principle of using the body's own cells as a manufacturer of some desired protein that I'm inquiring about.
Even without any cost-cutting benefit does the way Covid mRNA vaccines work differ in principle from other gene based compound manufacture?

It is quite costly and difficult to manufacture and store proteins. It's very likely more efficient to have the human cells create as much protein as they can, from a relatively small amount of mRNA. Remember than one mRNA molecule can be translated into protein many many many times, so the manufacturers need to only make one mRNA molecule to get many protein molecules, whereas it would be more expensive to manufacture many protein molecules.
It's kind of a "give a man a fish, he eats for a day, teach a man to fish, he eats forever" situation. Better to give the body the instructions (mRNA) than the product, for cost effectiveness.


What is this creature? Since it has six legs, I believe it's some sort of insect, but I could be wrong.

I spotted it in my Central Texas backyard (Austin area). It was very slow and not at all skittish.

For size reference, it's standing on a 2x4. It was a good 3-5 inches long, not counting antennae.

Walkingsticks, like that in your photo, belong to the insect order Phasmida (also sometimes called Phasmatodea). The species in your photo belongs to the family Pseudophasmatidae. Texas has two species documented for this family. One is Anisomorpha ferruginea, commonly called the dark walkingstick or northern two-striped walkingstick.  The other species is Anisomorpha buprestoides, commonly called Florida stick insect or two-striped walkingstick.

According to W.S. Blatchley's Orthoptera of Northeastern America (1920), pg. 145, A. ferruginea has narrow stripes and is a bit shorter than A. buprestoides, which has broad stripes. Based on the appearance of the stripes in your photo, I'd say you have A. buprestroides.


Is DNA sequencing coverage a function of sample purity? How is coverage affected by the purity of a sample? And can coverage for a sample be affected by other things, like the library preparation or manner in which the sample was stored?

So factors which go into coverage in short-read sequencing (and Sanger sequencing).

Depth is the obvious one. All else being equal you get a bang-on Poisson distribution of coverage over a genome, which is why more sequencing = more coverage.
The human genome and transcriptome is not all equal. Illumina sequencing is ultimately (most protocols) dependent on PCR amplification which means that any factors which influence PCR-amplification ability will also effect sequencing depth. The two obvious ones in this respect are: 1) Regions of extreme GC content and 2) Regions containing secondary structures (RNA mainly).
Alignment is the next major source of error for regions being 'dropped off' depending on how your aligner deals with multi-mapping reads. Some genomes have very young transposable elements which are highly similar to one another and very abundant. For most aligners that means that you can get either huge coverage or really small coverage depending on how the genome is assembled.
For low-input sequencing techniques you get major sources of DNA/RNA contamination from the enzymes, reagents and preparation of the samples. This can largely be minimized by having 'clean' samples and using large amounts of input DNA/RNA.

Depending on the sequences you're studying read-depth can be the only factor you consider or if you have difficult regions or specific questions you can deal with a whole swath of problems.

So in answer to your question: yes DNA quality will directly effect coverage. Sometimes you can 'just sequence more' to get over this problem, sometimes you need to go back to the drawing board.


Is reverse senescence/"anti-aging" actually scientifically possible among humans yet? I have been very interested in this since I myself am interested in reversing my skin's aging/genes/damage/etc. I also am interested in volunteering any future genetic altering of skin quality.

Basically I've heard of experimental drugs called senoyltics that are believed to (and have actually done so) have the ability to truly reverse aging at the cellular level and/or aging damage of skin and etc.

I am very intrigued and want to know if this is feasible for humans yet -- or any such breakthroughs. I really want my skin's genetic quality to be enhanced, but reversing aging damage by genes will suffice.

So skin aside, in general, is reverse senescence (with or without senolytics) anywhere near possible to reach human success? I've heard of labs and etc. working on this for testing, but nothing more.

My question is basically: is it possible? Are we really in the near future to reversing aging in humans?

As a note: I don't mean "anti-aging" as in preventing death -- more so as in making yourself younger in a myriad of ways, such as by appearance and physical ability (like heart; brain; skin texture/youth; etc.)

Short Answer

You might be interested in learning about telomeres, telomerase, and telomerase gene therapy.

For example, Boccardi & Herbig (2012): describe a mouse study in which they used telomerase gene therapy to improve the healthspan and lifespan of mice by up to 24%.

As far as I know, we have no successful human trials of similar therapies that have targeted and succeeded at "decreasing the age" of humans.

However, this source does claim that a woman attempted to do so. I cannot substantiate these claims in any way, so I'm skeptical at best...

 Long Answer:

Telomere 101:

Telomere: non-coding nucleotide sequences on the tips of chromosomal DNA strands.

Due to the inability for DNA polymerase to replace RNA primers on the end of linear strands of eukaryotic DNA during DNA replication, ~50-100 base pairs are removed from the daughter strand from each replication event.

The "junk" (i.e., non-coding) telomere sequences (which could repeat 1000s of times) provide buffers against losing more valuable DNA when this happens. Eventually though, the telomeres run out, and replication events could lead to loss of coding regions of DNA...

According to Boccardi & Herbig (2012):

  As we age, telomeres in most of our tissues progressively become shorter and therefore likely contribute to the failure of our organs and tissues observed in old age. Supporting this are data demonstrating that healthy lifespan is positively correlated with longer telomeres in humans, and patients suffering from age‐related diseases and premature aging syndromes display shorter telomeres compared to healthy individuals (Zhu et al, 2011).

The enzyme, telomerase can replace these telomeres, but telomerase is really only active in stem cells and white blood cells, so most adult cells lack this regeneration ability.

This is where telomerase gene therapy  comes into play.

In the simplest sense, this approach attempts to artificially add telomerase to adult cells to essentially add back telomeres and potentially slow or even reverse the aging process.*

 *Note: As far as I know, we don't actually know whether short telomeres are simply an effect of aging or if they are actually the cause of aging (and ultimately death), so this gene therapy is running on an relatively unsupported hypothesis.

For example: Boccardi & Herbig (2012) "Telomerase gene therapy: a novel approach to combat aging".

They found that adding telomerase to 1 year old mice increased their lifespan by 24%.

 Credit: Boccardi & Herbig (2012):

As Boccardi & Herbig (2012) note, however, applied human studies are still a thing of the future.

  While these studies provide a proof‐of‐principle that telomerase gene therapy is a feasible and generally safe approach to improve healthspan and treat disorders associated with short telomeres, a clinical application in humans is likely still some time away.

However, this source does claim that a woman (Elizabeth Parrish, CEO of Bioviva USA Inc. -- notice the website :p) attempted to do so -- I cannot substantiate these claims in any way, so I'm skeptical at best...

Citations and additional suggested reading:

Boccardi, V. and Herbig, U., 2012. Telomerase gene therapy: a novel approach to combat aging. EMBO molecular medicine, 4(8), pp.685-687. read here
Campisi, J., Kim, S.H., Lim, C.S. and Rubio, M., 2001. Cellular senescence, cancer and aging: the telomere connection. Experimental gerontology, 36(10), pp.1619-1637. read here
Zhu, H., Belcher, M. and Van Der Harst, P., 2011. Healthy aging and disease: role for telomere biology?. Clinical Science, 120(10), pp.427-440.


Is urban beekeeeping harmful or are there good practices to follow? I have found several newspaper articles on how good could be urban beekeeping both for the bees and for agriculture.
Today I read this one: Urban beekeeping is harming wild bees saying that urban beekeeping is harming wild pollinators. I did not find a direct link to the paper, but it is probably referring to Conserving honey bees does not help wildlife. Unfortunately I only have access to the summary of the paper.

Are there good practices that could be followed to practice urban beekeeping without harming wild life (for example avoid placing hives close to a forest...) or is it harmful in any case?

Beekeeping in urban areas often require that beekeepers supplement their colonies with feed since urban areas have, on average, very little forage available to sustain a colony year-round. There are usually very little in terms of wildlife (or wild pollinators) when it comes to urban settings. In contrast, suburban areas would have more to offer as there are often backyard gardens and unmanicured lawns that could provide food throughout the season.
The wild pollinators within suburban to rural areas are probably under the biggest threat from managed colonies, but the impact is also usually very difficult to assess. Even with the limited range of managed colonies forage (around 5km), there's usually not enough of the colonies stretched out across a wide area in such big numbers that it would out-compete with other wild pollinators. The wild pollinators are often solitary, with much greater foraging capacity. As such, they would just move away from any competing resource if they're unable to defend it themselves until the threat subsides.
Regardless of the location (urban, suburban or rural), best practices still include protecting your colonies against diseases and pests. If you don't you may end up losing your colony, or spreading diseases to other colonies or wild pollinators. Probably the most significant threat nowadays globally (except for Australia) would be Varroa Destructor. So, best practices here would include keeping on top of these mite loads to avoid it from spreading and/or overrunning your colony.
As reference, here is a visual capture of the article:


Is the bulbourethral (Cowper) gland turned on during puberty or is it on at birth? I am trying to find information about the bulbourethral (Cowper) gland and if it gets turned on during puberty or not. I tried asking several other online sites and they said they couldn't help. I don't know where to ask or where I could look up the answer.

Yeah, because the bulbourethral glands are from accessory glands of the male reproductive system as the seminal vesicles and prostate gland. The male reproductive system starts working at puberty.


Do Asian giant hornets (Vespa mandarinia) prey on other nests of Asian giant hornets? Asian giant hornets are known to attack nests of other bees and wasps, but should they encounter another nest of their own, would they attack it?

Yes. According to this clip uploaded to YouTube on the Smithsonian channel, Asian giant hornets will attack and pillage other nests (of Asian Giant Hornets) if no other food source is readily available.


Does denaturing proteins lead to loss of epitopes? I am doing an experiment where I have to do both Immunohistochemistry and SDS-PAGE. I am assuming that the native conformation of the protein is maintained in the IHC. But during the blot, we heat the protein (at least in our lab) at 95oC in mercaptoethanol to denature the protein by breaking the disulphide bonds thereby destroying the tertiary structure.

My question is when we are using the same antibody against the protein in the tissue (intact for IHC) and isolated (denatured for SDS-PAGE) protein, how can it bind both? So, the antibodies bind to the epitope based on the AA sequence or the 3D conformation? Wouldn't there be a lot if cross reactivity if it binds just based on sequence (since you could have the same sequence in many proteins, having the same conformation is much less likely)?

Many but not all B cell epitopes will be destroyed by denaturing.  Those that are conformational will be destroyed, but there are also many B cell epitopes that are linear, based on amino acid sequence only without strong conformation dependence.

Also, depending on your IHC protocol, there's often a fixation step that involves a certain amount of denaturation, though rarely as drastic as in immunoblotting.  Conversely, some proteins are capable of at least some restoration of native conformation after they bind to your blotting substrate.

Bottom line, it's unpredictable, but it works often enough to make it worth trying.


Do octopuses have better eyes than humans? I've read that unlike humans, octopuses have eyes "designed" the "right way", i.e. with the nerve fibers behind the retina, thus getting rid of the blind spot we humans have as well as theoretically improving eyesight.

Have there been tests to compare octopus sight with that of humans, and do they indeed have better vision than us?

There are a couple of advantages and disadvantages of possessing the eyes of octopuses.

The first advantage of the octopus eye is that it has no blind spot. This means that octopuses can see everything that is going on in their environment, and are more aware of predators and prey than some vertebrates. Also, they have many more photoreceptors than vertebrates, at roughly 20,000-50,000/mm2 which means that their vision is much better than that of any human.
The disadvantage of the octopus eye is that it can not see in colour. The eyes possess no cones, only the invertebrate equivalent of rods. This means that  octopuses can only distinguish between light and dark.


Can a single strand of mRNA form different polypeptide chains? My book has a statement:

A single strand of mRNA is capable of forming a number of different polypeptide chains.

In my opinion this statement is wrong because a single strand of mRNA will have same sequence of codons. So, every time it gets translated, it produces same polypeptide chain. But, according to my book this statement is correct.

Am I wrong or is my book wrong?

I believe, your book refers to  polycistronic mRNA. This is mRNA where multiple genes are encoded together in one mRNA and are often (but not necessarily) translated one after another. This is mainly found in prokaryotes where the proteins encoded on the same mRNA often form a metabolic pathway together.


Can salt-water frogs survive in normal water (A well)? I don't know much about frogs, but there seem to be salt water frogs.

1) Are there such things as salt water frogs?

2) Are there frogs that live in the sea? (in reference to Vivekananda's quote)

3) Can salt water frogs survive in well water or fresh water?

  Well, one day another frog that lived in the sea came and fell into the well. - Vivekananda

According to Wikipedia the Crab-eating frog is the only amphibian that can survive in sea water. However Wikipedia also suggests that it can only survive brief excursions into the sea.
There are no such things as sea frogs.
Even the Crab-eating frog doesn't live in the sea though. Its natural habitat is mangrove swamps.

The crab-eating frog (Fejervarya cancrivora), is a frog native to south-eastern Asia including Taiwan, China, the Philippines and more rarely as far west as Orissa in India. It inhabits mangrove swamps and marshes and is the only known modern amphibian which can tolerate brief excursions into sea water.
This frog can tolerate marine environments (immersion in sea water for brief periods or brackish water for extended periods) by increasing urea production and retention, and by remaining slightly hyperosmotic within urea and sodium flux. Adults can survive in salt water with salinity as high as 2.8%, and tadpoles can survive salinities as high as 3.9%.

https://en.wikipedia.org/wiki/Crab-eating_frog


What is the benefit of oxygen tanks to persons trappped in an enclosed space? When people are enclosed in an air-tight space, the levels of carbon dioxide will rise to lethal levels (hypercapnia) long before the oxygen is exhausted (hypoxia).  For example, the astronauts of Apollo 13 were in danger because the carbon dioxide scrubbers in the lunar module were inadequate.  They never "ran out of oxygen", even though the oxygen tank of their service module exploded.

What would be the benefit to supplying such persons with tanks of additional oxygen?  It seems to be a futile gesture to me.

The reason I ask is a news story ongoing for several weeks.  Twelve children and one adult have been trapped by water in a cave for several weeks.  At the time this question was written, four boys were already rescued.  Officials have repeatedly expressed concerns that the "oxygen is running out" and are placing oxygen tanks in the cave.  Is there any benefit to this, or are officials simply ignorant of human physiology?

There are a couple of ways to answer your question. If we assume the cave is an air-tight chamber, we've entered the domain of a very specialized field in medicine, so I can't speak as authoritatively as I'd like there, but lets start, with the fact that the cave is not air tight.
It's a cave
A cave is not a submarine or a lunar module. It is not air-tight, but in a large environment with various types of gas exchange. The cave may already have it's own $CO_2$ scrubber of a sort, since common minerals reversibly bind $CO_2$. I expect there is a whole science around $CO_2$ cycles in, e.g., limestone caves, but the point here is there is likely a sink of some sort for the $CO_2$ produced by the boys. For example, I think we could reasonably speculate that the following equilibrium in a limestone cave would be driven to the right with additional $CO_2$:
$CaCO_3 + H_2O + CO_2 \rightleftharpoons Ca(HCO_3)_2$
Why would you give oxygen?
Here I can speak authoritatively. I'd refer you to both of West's excellent texts (Respiratory Physiology and Pulmonary Pathophysiology) for further reference.
Lets clear up a misconception in the comments. It is correct that we're concerned about the concentration (typically expressed as partial pressure) of gas, not the amount. It is not correct that $O_2$ eliminates $CO_2$ from the body. This can be confusing, but it is a misapplication of Dalton's law to human physiology, based on a misunderstanding about where and how the gas is exchanged. By Dalton's law, you can reduce the concentration of $CO_2$ in a container by increasing the concentration of some other gas (e.g., $O_2$). If $CO_2$ is accumulating in the cave (rather than being taken up by the environment), then delivering compressed gas with no $CO_2$ would decrease the concentration of $CO_2$ in inspired air. Inspired air, however, is not the same as alveolar air or arterial or venous gas, and the human body is not well modeled as a container full of various gases.
While it is true that when $CO_2$ is retained in respiratory acidosis, arterial $P_{O2}$ must go down by whatever amount arterial $P_{CO2}$ goes up, it doesn't work the other way around. Delivering a higher $F_{iO2}$, or fraction of inspired $O_2$ does not cause an inverse change in arterial $CO_2$. This ends up being fairly complicated, and a full discussion is beyond the scope of this question. Let me just emphasize that supplemental $O_2$ specifically treats low $O_2$ (or, in a very specific case, $CO$, carbonmonoxide, poisoning). High $CO_2$ is treated by increasing ventilation. In fact, there are a few special cases where supplemental $O_2$ actually increases a patient's $CO_2$ levels, two of which involve hypercapnic respiratory failure. We do give $O_2$ for hypercapnic respiratory failure, but it is given to treat the associated hypoxia, not the hypercapnea. The only way to decrease $CO_2$ is to increase ventilation. This is a very important concept in critical care and respiratory medicine. I'd refer you to West Pulmonary Pathophysiology, Chapter 10, or any critical care textbook.
So, back to the reason you might want to give oxygen...
CNN reports that oxygen levels in the cave have reached 15%. If the atmospheric pressure of the cave is 760mm Hg, then the $P_{O2}$ in inspired air is about 107mm Hg, ((760 - 47 for water vapor) * 0.15, see West Respiratory Physiology, or any physiology text). At 600mm Hg (equivalent to an elevation of ~2000 meters) $P_{O2}$ in inspired air is 83mm Hg. This is low, and could start to be a problem (leading to hypoxemia and hypoxia), depending on the ability of the boys to compensate (again, see West, either respiratory physiology or pulmonary pathophysiology). If the $O_2$ levels in the cave continued to drop, or if the boys weren't compensating well, then it would be reasonable to give supplemental oxygen to treat their hypoxia, regardless of what the $CO_2$ levels were.
But if $O_2$ was low, wouldn't they also have to have high $CO_2$?
I'm not an expert in cave ecology, but it doesn't seem that strange to me that the rate of $O_2$ consumption by the boys could exceed the environment's capacity to produce or release $O_2$ from organic sources, dissolved sources, or ventilation, without their rate of $CO_2$ production overwhelming the environment's $CO_2$ sink. I have no good evidence one way or the other for this speculation.
What if it is an air-tight container?
Atmospheric $CO_2$ is on the order of 400ppm, or 0.04%. Normal levels in the body are 5% (40mm Hg / 760). We rely on this gradient to dump the $CO_2$ produced by cellular respiration using ventilation, but can still operate, with difficulty, with 5% $F_{iCO2}$. Serious problems (same reference) occur at higher levels. Again, in this particular case we're beyond my personal expertise (Dammit, Jim, I'm a doctor, not an aerospace or submarine doctor!), but in an air-tight container without a $CO_2$ sink, if $CO_2$ levels were higher than 5% and rising, I'd expect you would need to directly address $CO_2$. If it's a small container, adding other gases from pressurized canisters, or pumping gases in would decrease the $F_{iCO2}$ by Dalton's law, provided you could overcome the rate of $CO_2$ production by the boys. If $CO_2$ had accumulated in the boys blood (hypercapnea), they would (need to) increase their ventilation as well, adding more $CO_2$ to the chamber.


What does "Activation" refer to in the context of the symptoms of Schizophrenia and Schizoaffective Disorder? In this journal article certain symptoms are called "activation" in nature. I have never come across this term prior to coming across this article, so I would like to know quite simply what does it mean.

The authors use the Positive and Negative Syndrome Scale (PANSS) to assess symptoms.  One of its cluster scores is activation factor.

Summary:
http://en.wikipedia.org/wiki/Positive_and_Negative_Syndrome_Scale

Original publication of the article, which doesn't list activation factors:
http://schizophreniabulletin.oxfordjournals.org/content/13/2/261.long

Marketed currently here:
http://www.mhs.com/product.aspx?gr=cli&id=overview&prod=panss

None of the sources I saw specified what is meant by activation factor, and many didn't even mention it. It's possible that it's the hyperactivity mentioned in the original publication.  Also, it's possible that it's a modified category in the version sold at the last link. Hopefully this is enough information to get you started, if you want to hunt down the details.


Body size, what are the evolutionary trade-offs? Background

Considering just the "Kingdom Animalia" branch of organisms. It is clear that bigger does not necessarily mean better - there is large variation in body size...

From the 94 µm long Tantulocarid arthropod (Stygotantulus stocki)

To the 25.5 m long Blue Whale (Balaenoptera musculus)

Questions

What trade-offs exist between having a particular body size (very large, very small) to other traits and factors?
Alternatively, what evolutionary/ecological advantages/disadvantages are there to having a large or small body size?

Thank you!

I don't think one can fully answer to such a broad question. It depends on the population, the environment (presence of predators for example), the genetic background (having a big stomach is good but only if the intestin is big too), the population's social relations, .. Many traits are correlated and one might want to say that a given trait is beneficial but it is not because this trait is correlated (because of genetic, physical or social constraints).
Trade-offs
Here is a list of possible advantages/disadvantages.

visibility to predators
ability to hunt bigger preys or to manipulate smaller preys
running faster
be more impressive
fighting ability
energy consumption for maintaining a body
Quantity/quality of food to be found
homothermy (heat loss)
sustaining its own weight
Rooms for the organs
Attractiveness to the other sex
being more able to move freely (in viscous environment (water))
mechansisms for bringing nutrients and air to the tissues
density of the body (water)
excretion of wastes
moving in small habitats
Hiding in small areas
bearing big and complex structures
Parental care
flying better
acceleration in each movement
etc...

Allometric relations
You might be interested in life-history traits, and in allometric relations. You might be interested by this article as well. The reason for allometric relations can be found here:

If an animal were isometrically scaled up by a considerable amount, its relative muscular strength would be severely reduced, since the cross section of its muscles would increase by the square of the scaling factor while its mass would increase by the cube of the scaling factor. As a result of this, cardiovascular and respiratory functions would be severely burdened.
In the case of flying animals, the wing loading would be increased if they were isometrically scaled up, and they would therefore have to fly faster to gain the same amount of lift. Air resistance per unit mass is also higher for smaller animals, which is why a small animal like an ant cannot be seriously injured from impact with the ground after being dropped from any height.
As was elucidated by J. B. S. Haldane, large animals do not look like small animals: an elephant cannot be mistaken for a mouse scaled up in size. This is due to allometric scaling: the bones of an elephant are necessarily proportionately much larger than the bones of a mouse, because they must carry proportionately higher weight. To quote from Haldane's seminal essay On Being the Right Size, "...consider a man 60 feet high...Giant Pope and Giant Pagan in the illustrated Pilgrim's Progress.... These monsters...weighed 1000 times as much as Christian. Every square inch of a giant bone had to support 10 times the weight borne by a square inch of human bone. As the human thigh-bone breaks under about 10 times the human weight, Pope and Pagan would have broken their thighs every time they took a step." Consequently, most animals show allometric scaling with increased size, both among species and within a species.
The giant monsters seen in horror movies (e.g., Godzilla or King Kong) are also unrealistic, as their sheer size would force them to collapse. However, the buoyancy of water negates to some extent the effects of gravity. Therefore, sea creatures can grow to very large sizes without the same musculoskeletal structures that would be required of similarly sized land creatures, and it is no coincidence that the largest animals to ever exist on earth are aquatic animals.

This post talks about the reasons for the allometric relations between animal size and speed of movements.
Concerning the relation between heat loss and size, you might be willing to have a look to the Kleiber's law. This law has been extensively debated and is today thought (or known) to be wrong.

Just a philosophical note
You might also be interested in the philosophical discussion of adaptation, optimality, cost and benefit like this book (which I haven't read!) for example.


Need for two oxygen sensors in E. coli E. coli has two oxygen sensors: FNR (fumarate-nitrate reductase) and ArcBA (Anoxic Redox Control, two component control systems). FNR directly senses the oxygen, while the interaction of ArcB with oxygen is indirect one via quinone pool. Out of theree quionones in E. coli, which one (oxidized and reduced forms of all three types)  play roles to what extent in what direction (inhibiting/activating) is much debatable. I would like to see some intuitive level arguments for why a cell, even in principle, need to have two sensors for oxygen?

It is not uncommon for cells to have parallel pathways for same outcome. This ensures foolproof response and makes the system robust. E.coli also has another sensor for aerotaxis (Aer and Tsr proteins). See my answer on your previous post and the linked paper.

Also look for coherent feed forward network motifs.


How does the mechanism which controls blood pressure in the brain work? I know that pressure is sensed in the skin by mechanoreception mediated by skin receptors. Static pressure stimuli are mainly sensed by slow-adapting fibers connected to receptors like the Merkel discs. Vibratory stimuli are sensed by rapidly adapting receptors like the Pacinian corpuscle.

Blood pressure is also sensed by the body and the brain regulates blood pressure by influencing the peripheral nervous system that can increase or decrease the blood output of the heart.

How are blood pressure differences in the brain sensed and how do these receptors mediate cardiac activity? Are blood pressure differences in the brain sensed by rapidly adapting receptors akin to Pacinian corpuscles?

Blood pressure is sensed in blood vessels by baroreceptors. Baroreceptors are stretch-sensitive nerve fibers located primarily in the aortic arch and carotid sinuses. The baroreceptors send afferent fibers via the glossopharyngeal nerve to the nucleus tractus solitarii in the dorsal medulla in the brainstem. From there, efferent cardiovascular neurons send projections to the medulla and spinal cord. There are also stretch-sensitive receptors in the heart and pulmonary vessels, called cardiopulmonary receptors that use the same nerural connections as the baroreceptors.

The baroreflex loop results in activation of sympathetic or parasympathetic fibers to the heart, the smooth muscle of the peripheral blood vessels, and other organs such as the kidney to maintain arterial pressure at normal levels.

In a simplified scheme, increased pressure stimulates baroreceptors, which attenuates the sympathetic outflow to the peripheral vessels and the heart, restoring pressure to normal levels. The parasympathetic influence will dominate which is mediated by acetylcholine. Conversely, a decrease in pressure relieves the baroreceptors and increases sympathetic outflow. Sympathetic activation causes a release of noradrenaline that leads to vasoconstriction and increased cardiac output and hence an increased blood pressure (see Fig. 1).

Fig. 1. Control of blood pressure. Source: Human Physiology (2011).

Reference
- Cougias et al., Med Sci Monit (2010); 16(1): RA1–RA8


What does "generalisation" mean? I am trying to understand a paper about ethanol: "Generalisation of ethanol with drug mixtures containing a positive modulator of the GABAA receptor and an NMDA antagonist" (Stolerman & Olufsen, 2000)

In the abstract it says,

  "After drug-appropriate responding with the training mixtures reached 85%, generalisation to ethanol was examined in extinction tests."

I can't find a definition for "generalisation" in Google searches. What does it mean? I don't have a background in biology, so simple answers are preferable. Thank you.

Generalisation

  Generalisation is the phenomenon of an organism responding to all situations similar to one in which it has been conditioned.

or

  Not biologically differentiated or adapted to a specific function or environment

This means that  the the rats responded to ethanol the same way that they responded to the training mixtures.

Sources:

Mangan, G. L. The Biology of Human Conduct: East-West Models of Temperament and Personality. Oxford: Pergamon, 1982. Print.
"Generalized." - Memidex Dictionary/thesaurus. Web. 04 Mar. 2016.
"Generalisation." - Biology-Online Dictionary. Web. 04 Mar. 2016.


What is it called when there is natural truncation selection? Truncation selection is when a breeder selects for animals that exhibit a value for a trait that is above a certain threshold.  What is it called when nature selects for a value of a trait that is above a certain threshold?  I want to say natural truncation selection, but I don't see any mention of that.  To clarify, what I mean is, what is it called when, as a result of natural selection, all perish but those with a value for a particular trait that exceeds a particular threshold.

Truncation selection

The term  truncation selection has been used a lot in theory papers because it is a simple model and because it is of interest to breeders. Truncation selection is most likely more common in a breeding setting than in nature and from wikipedia,  truncation selection is defined as specific to breeding

  In animal and plant breeding, truncation selection is a standard method in selective breeding in selecting animals to be bred for the next generation

However, as much as the definition fail to repeat animal or plant instead of just animal, IMO it fails to recognize that such notion could as well exist in nature. I would personally not be shock to read a paper talking about  truncation selection in wild populations.

Threshold model

If you really want to avoid talking about truncation selection, then you can eventually picture the phenotypic trait as a liability factor (as it is done in sex determination literature, see Perrin and Beukeboom's book) and selection acting as a threshold on this factor. Note that the concept of threshold and threshold model is very common and everyone will understand what you mean.


Proteins with alpha helices alone and beta sheets alone? I would like to see some examples of proteins with PDB ID so that I can download and see them in VMD software. I need some proteins with alpha helix only and proteins with beta sheets alone.

You may consider taking a look at the SCOP structural classification of proteins to check all beta proteins and all alpha proteins. As per specific examples and though not belonging to the SCOP classes mentioned above, Porin for a beta protein (PDB:1A0S), and Rhodopsin for an alpha protein (PDB:1F88) are two nice structures to look at.


What do memory cells actually do? So I know that memory cells "remember" the most efficient way to kill a pathogen should it show up again... but what is the mechanism by which memory cells become activated by the second contact with a pathogen? How do they interact with the other immune cells to enhance immunity?

For example: phagocytes engulf pathogens and plasma cells release antibodies, but what do the memory cells actively do?

I think memory cells will efficiently do clonal expansion so that it can produce immune cells which can actually remove the pathogens quickly compared to the first time as it now remembers the method it used before.