What is ApoCas9 in the CRISPR-Cas9 system?

In general, "apo" is used to indicate an apoenzyme — that is the protein part of an enzyme without essential cofactor(s).

This is actually defined in the Experimental section of the paper:

  Cas9/Cpf1 without gRNA (ApoCas9/Cpf1)

So, in this case ApoCas9 is Cas9 endonuclease that is not bound to a guide RNA.


Can the spinal cord contain an "epileptic focus"?

Short answer
Epilepsy is a disorder confined to the brain.

Background
Terminology is crucial in this question. The International League Against Epilepsy (ILAE) defines epilepsy as a disorder of the brain characterized by an enduring predisposition to generate epileptic seizures and by the neurobiologic, cognitive, psychological, and social consequences of this condition. ILAE defines an epileptic seizure as a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain (Fisher et al., 2005).

Hence, by definition, epilepsy is a disorder of the brain. Note that the ILAE is an authorative organ and their definition overrides whatever your medical textbook on internal medicine says.

An epileptic focus is a commonly used term, but as far as I know not well-defined. It's often used in relation to EEG and other methods such as MRI and PET that attempt to define the hot spot of seizure activity. More strictly defined terms in this regard are eloquent cortex and epileptogenic zone. The eloquent cortex refers to any cortical area in which injury produces symptomatic cognitive or motor deficit. The epileptogenic zone refers to the region of cerebral cortex that is both necessary and sufficient to generate epileptic seizures. Its entire removal can be used as a treatment for intractable epilepsy (Richardson, 2003).

With regard to your question, I expect you are referring to the epileptogenic zone. By definition, this refers to a region in the brain.

References
- Fisher et al, Epilepsia (2005); 46(4): 470-2
- Richardson, Brit Med Bull (2003); 65: 179–92

Note
I expect this answer may not be entirely satisfactory. If you are looking to the  physiological basis of the occurrence of seizures and why they occur in the brain and not in the spinal cord, it may be wise to formulate a more specific separate question. Preferably do not grossly edit this question given it received three answers. vervet's answer on focal epilepsy clearly shows the confusing terminology in epilepsy world. Focal epilepsy is not the same as an epileptic focus. However, epileptic focus is a term often used for focal epilepsy. Long story short, specific answers need specific questions, preferably with the definitions embedded to prevent deleted answers and under-appreciated answers like vervet's.


where can I find a full list of examples of data types in biology?

I am also a little confused about what exactly do you mean by "data type". As far as I know in programming "data type" is something you use to obstruct 0s and 1s e.g string, int and array is the way you'd reference your own data and something that language interpreter/compiler can understand and allocate right memory for. Whereas type of data you can get in biology (bioinformatics), I think is what you are asking. The type of data you get is flat text file i.e ASCII or binary and there are few different binary formats in bioinformatics.

In genomics, which is DNA/RNA type of data you mainly dealing with ASCII files. These are the files that I know of:

FASTQ hold raw - sequenced data. The main two types of sequencing you can do is DNA sequencing (DNA-seq) and RNA sequencing (RNA-seq). Usually FASTQ files always gzip ed and file extension is fq.gz or fastq.gz I wrote this tutorial explaining FASTQ
FASTA can hold different type of sequence data, which is different to raw-sequence held in FASTQ. You can actually convert FASTQ to FASTA, but you'd loose quality information. The two broad classes of sequences you can have in FASTA file are nucleotides sequence i.e DNA/RNA sequence or  amino acid sequence i.e protein/peptides sequence. FASTA is also almost always gziped, file extension varies a bit, most common once are fa.gz or fasta.gz, but you will see fna.gz or fna or faa which tries to indicate FASTA with nucleotides or amino acids. FASTA usually used for reference files e.g reference genome. Here is a link to Ensembl repository for mouse genome
GFF and GTF files these are annotation files, used together with reference genome FASTA files. Here is another one of mine tutorials
SAM and BAM okay here is an example of binary type of data. Sequence Alignment Map, file extension .sam depending on the organism, can be very big. For mouse RNAseq data for example SAM file can be between 1 Gb - 40 Gb, makes sense to compress it. BAM is binary SAM. you need samtools to work with BAM files. Here is pure python BAM parser if you are interested.

This should cover first two of your points. Although proteomics has few more type of data, again mainly text. Mass Spectroscopy is the tool proteomics people use to get they "raw-data" and there is some finny file format(s) that I'm not aware of and there will be a few downstream file formats I'm sure.
As for gene expression, that's mainly tabular data, csv or tsv again flat text file.
One other format that I should mention that covers your point 7 is VCF which is variant calling format here is specifications for it again flat text format.

One thing that I should say; it is somewhat common and preferred, at least in the past to be able to parse biological files with Unix tools such as grep, awk and cut and therefore most of the files are tab separated text files.. I think now bioinformatician coming around and using more structured and compressed data formats.

This isn't exhaustive list of file format by any means, but I think this should give you enough to google for.

One last link to Kegg pathway which is your biochemical pathways, they might explain there the type of data they use


What is the mechanism by which myelination reduces the capacitance of the axon membrane?

Circuit analogies don't 100% apply to myelin because membranes have complex electrical properties, but both of those explanations work and they are in fact essentially interchangeable: Take a membrane with distance d across the membrane and capacitance c. Then we add some myelin to get a new capacitance C at a new distance D.

If you 4X the distance between plates (D = d * 4), C=c/4 (from the formula you posted as (2) ); if you add 3 extra plates (so now you have a total of 4 plates), C=1/(1/c + 1/c + 1/c + 1/c)=c/4.

Importantly, myelin also increases the membrane resistance, and because myelin is typically very thick compared to a normal membrane (~10nm for one layer vs. 500-2500nm for myelin), you can almost consider myelination to increase resistance to infinity (compared to the axial resistance of cytoplasm) and the capacitance to zero.

See this page for some more info.

Note that the reason these explanations are interchangeable is that there is effectively no distance between the added plates in series and no difference in capacitance for each individual capacitor/piece of membrane (for example, see this page).


Reason behind using inducible promoter for heterologous expression

Heterologous promoters often express genes that are toxic to the organism when expressed in too high quantities. When the genes are expressed constitutively, the organism will either grow slowly or die before they reach a high density suitable for production of the protein.

As such, it is not about expressing the genes all the time, but expressing the maximum amount of gene product over the shortest period of time. It doesn't make sense for the cells to express the gene product all the time, if they can't reach sufficient densities first. More product will be made if the cells are allowed to grow to a relatively high density, then inducing expression on all of them. This would allow relatively large production levels in a short period of time.


Heart Rate being normal when under treatment for the bends

You are wrong on several accounts:

Bends occur due to bubbles that form in muscles and joints and not lungs - They fall under Mild or Type 1 Decompression Sickness (Type 1 DCS).
Formation of bubbles in blood stream do occur in the Decompression process - Hyperbaric chamber is used to treat this condition.

What happens when diving:
During deep sea diving the pressure surrounding a person increases at the rate of 1 atm (atmospheric pressure) for every 10 m in sea water and 10.3 m in fresh water. This relation is linear.
The pressure inside the body equalises with the pressure outside to prevent any deformation. The solid and liquid components of the body can withstand pressures upto 151 atm (depth of 1.5 km underwater) without undergoing any noticeable compression. But air, being extremely compressible undergoes compression.
So at 2 atmospheric pressure the space occupied by the air in our body is halved. This would shrink the lungs to half the total volume. To circumvent this the divers breathe air compressed at the same pressure as the water pressure around them, so that the pressure gradient across the chest wall is normal.
Pressure Concentration relationship:

Dalton's Law:
This law states that the Barometric Pressure is the sum of the partial pressures of the individual gases in the air mixture.
Barometric Pressure - The total pressure measured

In air at 1 atmospheric pressure (760 mm Hg) the partial pressures of various gases are:

Nitrogen ~ 593 mm Hg
Oxygen   ~ 159 mm Hg
Co2 ~ 0.2 mm Hg
Others   ~ 7 mm Hg

According to this Law, as the pressure inside the Lungs increase, the partial pressures of each gas increases. At 2 atm, the partial pressures of every gas doubles.
The gas exchange in the lungs is based on partial pressure of the gases. Thus due to increased partial pressure, the amount of gases dissolved in blood increases (This increase is proportionate to the pressure levels).

During a extended dive (one lasting several hours) the body tissues gradually equilibriate with the high-pressure gases. At sea level our body contains 1 L of dissolved nitrogen, equally distributed between body's water and fat. As partial pressure of Nitrogen rises, the nitrogen equilibriates with the body's lipid stores because adipose tissue is relatively underperfused.

Once equilibrium is achieved the volume of nitrogen dissolved in tissues is proportional to the alveolar partial pressure of nitrogen. Thus at 4 atm the body will contain 4 L of nitrogen.
The same principle applies to oxygen as well, though the solubility of oxygen and the speed at which equilibrium is attained are different.
Decompression
During ascent from the depths, the Barometric Pressure (surrounding pressure Pb) falls. As the Pb falls the pressure inside the alveoli fall as well. This causes a fall in the partial pressures of all gases in the lungs creating a gradient of gases from the tissues to the alveoli.
So the diver has to ascend slowly to give enough time for the gases to move into blood from the tissues and then get washed out. If the ascent is too rapid, gases dissolved in the tissues - due to high pressure - attains the gaseous form (due to pressure drop) and become bubbles. This is similar to opening a pressurised coke can where one can observe gas bubbles forming.
The bubbles are the reason for the bends. Bubbles can also cause serious problems like arterial gas embolisation, CNS disorders (due to formation of bubbles in the myelin sheath of axons which compromise nerve conduction), pulmonary symptoms (due to pulmonary emboli), sometimes even Disseminated Intravascular Coagulation.
Solution
The decompression is done in stages - in which the divers spend various amount of time at various under water levels to allow complete diffusion of dissolved gases into blood and into the alveoli which is consequently breathed out.

Hyperbaric Chamber
The hyperbaric chamber is used when the above solution is not applied i.e. the diver has surfaced rapidly without spending sufficient time at various levels to allow proper decompression.
In a hyperbaric chamber the diver is recompressed to the pressures equal to the pressure experienced at the level to which the diver dived. Due to the increase in pressure, the bubbles get dissolved again. This instantly relieves many symptoms - like the nerve conduction delay, bends, niggles etc... Now the decompression is carried out by under controlled environment, simulating the various intervals the diver has to stay at various pressure levels under water.
Hope this explains your doubt.
So coming to myocardial infarction, the hyperbaric chamber redissolves the gas bubbles thus preventing myocardial infarction.

For more info read chapter 61 of Medical Physiology, 2nd edition, by Walter F. Boron and Emile L. Boulpaep.


Do Asian giant hornets (Vespa mandarinia) prey on other nests of Asian giant hornets?

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.


By what mechanism do our nerves lengthen as people get taller?

They grow

Nerve axons can grow rather quickly as long as the body of the cell is intact, quickly as in the mm/day range. This is also the basis of how nerves can regenerate.


DNA Topology. Question on twists and writhes

It is all explained here in Wikipedia. If you want to make a 3D model of your own, you can use two pieces of tygon tubing (like the rubber hose for a Bunsen burner), that are both circularized and attached with connectors that can be opened and closed--that lets you simulate nicking and re-sealing the strands.


There are a few plausible ways:
As someone mentioned in the comments; Alcohol works well for this. We have samples from a hundred years ago (e.g. Thylacine), which have been stored at room temperature in a museum for that period of time and have had DNA easily extracted from them.
Unfortunately for many species, alcohol preservation fell out of favour due to it shrinking (by dehydration) specimens, so that they no longer look "realistic" in terms of morphology (something that is very important for classical identification methods). In addition, ethanol and other alcohols tend to evaporate fairly fast if not sealed properly. For these reasons aldehyde based solutions came into favour about 100 years ago. The downside to this is that formaldehyde and other aldehydes cross-link the genetic material, making it more or less impossible to extract and use.
Another possible method is dehydration - mummification. Small samples like embryos or tissues can be dehydrated quite fast. In the absence of water, these samples should last more or less forever - we can extract DNA from mummies in many places around the world, but these ones might interest you in particular.
There are also specialist chemical solutions such as RNAlater that are routinely used in labs for preservation of precious genetic material.
Given that we knew these sorts of things in the 1980's and that the lab was staffed with competent scientists, and that they knew that the lab was going to shut down but would re-start at some time in the future, then it is entirely plausible that they would have used alcohol or something like RNAlater.
In the absence of this knowledge, but still competent scientists, it is much more likely that they would have used some sort of cold (frozen) storage method;  whether this was cryopreservation (liquid nitrogen), such as is used for storage of cells or a specialist -80 $^\circ$C freezer or a -20 $^\circ$C freezer like you might find at your house. Some samples may have been still stored in chemical preservation in the interests of space-saving in freezers though.


Help identify this small spiney praying mantis?

This appears to be a species of Sub-Saharan flower mantis in the genus Pseudocreobotra.

Specifically, it resembles the spiny flower mantis Pseudocreobotra wahlbergi.

 © 2013-2018 carlarush

The species gets its name from the spiny structures on its abdomen. According to Wikipedia, the color is variable:

  being typically greenish, but it can equally be yellowish, pinkish or reddish

According to here, you can determine the sex of your specimen by counting the "abdominal appendages" (i.e., spikes):

  females have just 5 abdominal-appendages on the underside, however males have 6

 © 2004 Steffi Schuttauf

This might also be P. ocellata, which would be able to be distinguished from P. wahlbergi based on its smaller adult size [source].


Why does the stomach ache if you take a brisk walk after lunch or dinner

The reasons for Exercise-related Transient Abdominal Pain are unknown. The current theories are:

Irritation of the parietal peritoneum, a structure lining the abdominal wall as it rubs against the visceral peritoneum, which lies against it and over the top of the abdominal organs
Strain on the ligaments that suspend the abdominal organs (however somewhat unlikely as it occurs during swimming

It used to be thought that blood was diverted away from the diaphragm during exercise causing pain however that has been found to be incorrect.

See this link: http://www.ausport.gov.au/ais/nutrition/factsheets/hydration/cramps_and_stitch


Why do genetic drift generates negative linkage disequilibrium?

Genetic drift is the change of allele frequencies in a population due to random sampling during reproduction. This can cause some allele combinations to become more or less common than would be expected without drift, thus creating a disequilibrium. However, it's the combination of genetic drift AND selection that generates negative (instead of positive) disequilibria. From the discussion of the article you linked to:

  Selection eliminates positive disequilibria more efficiently than it eliminates negative disequilibria, because negative disequilibrium reduces the genetic variance upon which selection acts. Consequently, the average disequilibrium over loci ... becomes negative over time.


Does freezing microorganisms such as probiotics kill them?

Yes, they do. For a look at survival of Lactobacillus and other bacterial species after multiple freeze/thaw cycles, check out Harrison 1955 (below).

The awesome hand-drawn graphs show that many bacteria survive after being frozen for 11 weeks. There's also a figure on the following page showing that many bacteria also survive after multiple freeze-thaw cycles, but I won't include that page here for brevity.

Prof. Don Schaffner of Rutgers also supports this conclusion:

  So it's possible, even likely, that frozen and thawed yogurt will contain
  living lactic acid bacteria, although it may only be 10% or 1% of the
  total number of bacteria that were there before the yogurt was frozen.

I couldn't find a great deal of official resources on the topic, hence the paper from 1955 and random quote from a food science professor. However, in a lab setting, scientists regularly freeze bacteria and even eukaryotic human cell lines. Usually scientists use a cryoprotectant like glycerol, but many foods (like yogurt and ice cream) may contain an FDA-approved cryoprotectant (Wikipedia):

  One recent, successful business endeavor has been the introduction of [anti-freeze proteins] AFPs into ice cream and yogurt products. This ingredient, labelled ice-structuring protein, has been approved by the Food and Drug Administration.

So, yes, at least some of the bacteria in your frozen yogurt are still alive, and will have whatever beneficial/harmful/lack of effect when you ingest them.

Judging from figures 1-3 above, bacterial survival depends on how long and how many times you freeze the bacteria. My rough estimates of the graph above say 40%-10% after a single freeze, and after multiple freeze-thaws getting into the 1% range. Also, it doesn't matter whether you thaw it first or eat it frozen as far as bacterial content is concerned, the bacteria will be unfrozen either way when they reach your digestive tract.


Do taller people have larger somatosensory cortices than short people?

I would say no.

Your question somehow implies that somatosensory cortex is equally distributed among the different sensory areas of the body, whereas in the reality this is the known "cortical homunculus" concept of how this distribution looks:

If you look at this representation you'll see that chest and legs take only about one third to one fourth of the cortex, thus the changes between short and tall people don't seem to have noticeable contribution to the overall cortex size.

If we just walk away from cortex size and discuss the amount of nerve cells in these areas I would say that these numbers should correlate with the number of peripherial receptor cells that provide input for them, and since there is no known changes in receptor density among different body sizes, even the amount of nerve cells seems to be more or less same.


How can I find some pieces of the genome of a microorganism?

You can use already available tools to extract information from available database. For finding specific genes, use this. For protein, use this. There are lot more tools. Just explore NCBI, EMBL or DDBJ sites. All information is self explanatory.
If you want specialized information for specific organism, you can use specialized database ( like Flybase for flies, SGD for common yeast, EnsemblBacteria for bacteria and archaea or HGMD for human mutations. Best way is to search in Google. You will get everything you want :D


Blood Pressure: Significance of difference between systolic and diastolic

The difference between systolic (the upper number) and diastolic (the lower number) pressures is known as the pulse pressure:

  Systemic pulse pressure = Psystolic - Pdiastolic

For a typical blood pressure reading of 120/80 mmHg the pulse pressure is therefore 40 mmHg.

It is proportional to stroke volume, the amount of blood pumped from the heart in one beat, and inversely proportional to the compliance or flexibility of the blood vessels, mainly the aorta.

A low (also called narrow) pulse pressure means that not much blood is being expelled from the heart, and can be caused by a number of factors, including severe blood loss due to trauma, congestive heart failure, shock, a narrowing of the valve leading from the heart to the aorta (stenosis), and fluid accumulating around the heart (tamponade).

High (or wide) pulse pressures occur during exercise, as stroke volume increases and the overall resistance to blood flow decreases. It can also occur for many reasons, such as hardening of the arteries (which can have numerous causes), various deficiencies in the aorta (mainly) or other arteries, including leaks, fistulas, and a usually-congenital condition known as AVM, pain/anxiety, fever, anemia, pregnancy, and more. Certain medications for high blood pressure can widen pulse pressure, while others narrow it. A chronic increase in pulse pressure is a risk factor for heart disease, and can lead to the type of arrhythmia called atrial fibrillation or A-Fib.


What controls Fructose regulation in plants?

Preamble

In short, fructose kinases (like Fru6P,2-kinase) and fructose phosphotases (such as Fru2,6bisP) regulate and are in turn regulated by fructose (specifically Fru6P)  levels in plants. There are also several metabolites that regulate the rate at which those fructose enzymes function creating quite a complex fructose regulatory network. This phosphorylation can make fructose unavailable or available to proteins as well as providing energy in the process (and aparently the rate of this can be controlled effectively in vivo (Stitt, 1990)).

I haven't come across any cell uptake regulation, but remember plants are physiologically very different to humans and there may not be a like for like system in this case. Although I suspect there will be since in plants fructose can be concencentrated in fruiting bodies. Perhaps another answer, or a major edit to this answer can explain that.

Fructose is often referred to as a regulatory metabolite in plants i.e levels of fructose affect other pathways due to its phosphorylated state. However, there are lots of sugar regulating systems in plants. Although this article focuses more on glucose and galactose, it emphasises the idea of a regulatory web rather than a cycle when it comes to plants and sugar regulation. Below the studies are based on plants such as spinach and other leafy vegetation, not fruiting plants I'm afraid!

Kinase Control

3PGA, 2PGA, PEP, dihydroxyacetone P, and the 2-carbon intermediate glycollate-2-P are all metabolites that control phosphorylation that inhibit the kinase, whilst Pi activates the kinase. Interestingly PPi also inhibits the kinase by competing with ATP. As one can imagine, this causes sigmoidal ATP saturation kinetics and is clearly indicative of regulation.

Phosphorylation

Fru6P and Pi both inhibit Fru2,6bisP hydrolysis by FRU2,6PASE.

This article from 1996 has a figure showing just how complex sugar pathways can be. To expand on your question, we can see how fructose phosphorylation plays a role in regulating in Sucrose and Starch glycolysis (Plaxton, 1996).

Disclaimer: I haven't studied this since undergraduate level, so constructive comments are welcome and I encourage people to edit this answer to improve it and help it more aptly answer the question!


Are the social-distancing measures implemented against SARS-CoV-2 also suppressing the spread of other viruses?

Yes, this helps as well with other infectious diseases. A good example is the flu, which season was measurably shorter this year than in other years on record. See the figure from the reference 1 for comparision:

Reference 2 shows that this is also true for other respiratory diseases (figure 2):

This shows very well that the isolation measures and the social distancing work very well to control such transmissable diseases.

References:

How coronavirus lockdowns stopped flu in its tracks
Monitoring respiratory infections in covid-19 epidemics


As @Chris commented, when assayed in vitro with a single substrate (which may not even be the physiological one) most enzymes can catalyse a reaction in either direction. And enzymes such as pyruvate kinase were discovered before the pathways they are constituents of were worked out in full. Furthermore, the ways of naming enzymes only became more sophisticated as more were discovered and characterized. (Try googling for ‘old yellow enzyme’.)

Let us take pyruvate kinase as an example. The name kinase is clearly not chemically descriptive but was applied to any reaction using ATP. But, never mind, go to the Wikipedia page for pyruvate kinase and click on the EC (Enzyme Commission) number — 2.7.1.40 — in the box on the right. You will come to a page where you will see that, like TS Eliot’s cat, the enzyme has three different names:

Accepted Name: pyruvate kinase
(because that’s what everyone uses and is in all the text books)

Other names: phosphoenolpyruvate kinase; phosphoenol transphosphorylase
pyruvate kinase (phosphorylating); fluorokinase; fluorokinase (phosphorylating); pyruvic kinase; pyruvate phosphotransferase
(note these include naming it for the reverse reaction)

Systematic name  ATP:pyruvate 2-O-phosphotransferase

So why is that the systematic name? If you click back from this page to the group EC 2.7.1 to which this belongs, you will find that this group is of ‘Phosphotransferases with an Alcohol Group as Acceptor’, itself a subgroup of phosphotransferases.

So, to summarize, there is a systematic name that have been arrived at after long and careful deliberation and appears in the introductory paragraphs of scientific publications. Thereafter the common name is used, which although sometimes now recognized as a misnomer, seemed most appropriate at the time.


OK, It does not look like a fungus. just going by the single close up photo - I'm pretty sure it is an abandoned bumblebee nest (or that of some similar social insect).  These bees often nest out of sight under logs or under the ground. Below is a link that may help you with a positive identification. I hope this provides at least a hint. Maybe you can fill in the blanks from your knowledge of your local fauna in Portugal.

http://www.bumblebee.org/lifeCcolDev.htm


Problems with SDS-PAGE, no separation - what could be the problem?

After readjusting the pH of everything and making new running buffer with new SDS solution the separation seems to be back.


(Rough) Model for DNA evolution in E. coli genes

Bacterial DNA evolution is like other evolution in the sense that the mutation rates are probably random and biased somewhat by the physical and chemical structure of DNA as well as the presence and activity of DNA repair enzymes.  The mutation protocols for preparing mutant libraries from UV or chemical mutagens are a good place to start I would think - like this reference. Most of this stuff is oriented towards protocols used in the lab, not in the wild.  Like how much UV does E coli get in your gut?  Not much.  Still it does happen and is a typical baseline factor in evolution.

Bacteria also mediate their own adaptation via phage transfer as well as direct lateral gene transfer, chromosomal rearrangement.  The dynamics of this evolution is just as interesting I think as site mutation as the bacteria can use its repair mechanisms and even actively upregulate some adaptation itself, responding to environmental changes.  The fundamental differences between bacterial evolution and say evolution of animals and plants come from the fact that life is relatively cheap - a single well adapted survivor can repopulate very quickly and so that even radical genetic diversity has a benefit even if some of the population dies off every generation from being a bad adaptive experiment.  (BTW animals do this too, but in the short lived haploid gamete phase, not so much as diploid animals).

Well anyway back to bacteria.  Eric Alm's lab at MIT started with his work with operon evolution.  Genes grouped together on a single mRNA leap from one cluster to another across evolution, allowing for coordination of biochemical processes in the cell.  Lately they have been looking more intensely at the evolution of bacterial species, and how the selective environment influences bacterial adaptation.

Its hard to be more specific since I'm not completely clear on your focus and needs here, but this is what I know.


During bridge amplification of DNA sequences, why aren't sequences amplified in both orientations?

See this document on how Illumina sequencing works.

When you are doing a single end sequencing, the reverse strands produced after the bridge amplification + denaturation (step-7) are specifically removed (clipped at the junction of primer and the "insert" region). Furthermore, the free 3' ends are blocked (by chemical modification) to ensure that there is no unwanted priming.

For paired end sequencing, both strands are sequenced; so in one flow cell the forward strand is cleaved while in the other the reverse strand is cleaved.


Is protein production doubled if you have homozygous dominant genes as opposed to heterozygous genes?

Dominance is defined based on the phenotype

Dominance is defined based on a phenotype of interest. Pick a phenotype, say coat color for example. If genotypes AA and Aa have the same coat color while aa has another coat color, then A is domiant over a.

The concept hold even for sequence that do not produce proteins

The concept of dominance can be applied to any locus which variance explains phenotypic variance, whether this locus codes for a protein or not.

Most sequences that affect the phenotype are regulatory sequences that do no produce any protein. In such case, your intuition that dominance is the allele that produce more proteins really does not make much sense.

Mechanism

A whole lot of mechanism can yield to such dominance relationship. It is not uncommon that the recessive allele comes from a loss-of-function mutation. In such case, yes it is likely that the AA genotype produce twice as many proteins as the Aa genotypes. But this is definitely not the only possible mechanism. Note that whether the number of proteins produced of the AA genotype is twice the number of protein produced of the Aa genotype, won't change anything to the phenotype of interest by definition of what dominant mean.

Dominance is actually pretty unusual

Most phenotypic traits actually result from the influence of several loci and allelic relationship at these loci are rarely perfectly dominant. Perfect dominance exist in reality but is definitely over represented in intro classes as they are simple to understand study cases.

Fitness

Note that there is a positive correlation between how recessive an allele is and how deleterious it is. It does not mean that the recessive allele is necessarily deleterious but there is a tendency.


Do species other than humans have distinct daily feeding patterns?

Preamble

This is a very interesting question one which I don't immediately know an answer to. I think this overly succinct answer and the fact nobody else has answered highlights the degree to which the age old darwinian assumptions play a role in the field.

Zoological POV

I'm not an expert in this area so I went to a zoology lab technician and this is what they had to say (I'm paraphrasing here):

  Most animals are opportunistic and can't afford the luxury of a late
  brunch... The only animals that spring to mind that appear to 'plan' for
  meals are the hoarders (squirrels for example). But they don't
  typically cache food in the same way we would for a weekly shop, but
  do so for fear of food scarcity (overwintering, rival competition);
  Not unlike the mad dash for bread and loo roll when it starts snowing
  slightly!

Maybe animals do have their diet set to a circadian rhythm, or maybe not. We can't say for sure. Darwin implied, even a peaceful meadow is full of starving ravenous animals clinging to survival. There is no real time for luxury. If food is there, they eat it. Many animals don't even get full the same way we do.

Scarcity of Literature

The problem lies in that there is no body of literature around animal eating times since animals seldom have enough food in their natural environment to monitor any regularity. If you want specific questions on a particular species for optimum feeding times, I would recommend opening another question as lab animals do have recommended diets. Many predators have optimum hunting times (for example nocturnal, or dusk). However one could argue this is to do with success rates/effective hunting strategy and not necessarily scheduled eating times.


The probability of indirect human fertilization?

I don't have answers to all of your questions, but here is one example of a highly unusual conception via the gastrointestinal tract: http://blogs.discovermagazine.com/discoblog/2010/02/01/ncbi-rofl-thats-one-miraculous-conception/.

To cut a long story short, a woman born with a congenital defect that caused her to have no vagina was stabbed in the abdomen when her boyfriend found her performing fellatio on another man. She was taken to the hospital and patched up but a few months later:

  Precisely 278 days later the patient was admitted again to hospital with acute, intermittent abdominal pain. Abdominal examination revealed a term pregnancy with a cephalic fetal presentation. The uterus was contracting regularly and the fetal heart was heard. Inspection of the vulva showed no vagina, only a shallow skin dimple was present below the external urethral meatus and between the labia minora. An emergency lower segment caesarean section was performed under spinal anaesthesia and a live male infant weighing 2800 g was born…

The article concludes that:

  A plausible explanation for this pregnancy is that spermatozoa gained access to the reproductive organs via the injured gastrointestinal tract. It is known that spermatozoa do not survive long in an environment with a low pH (Jeffcoate1975), but it is also known that saliva has a high pH and that a starved person does not produce acid under normal circumstances (Bernards & Bouman 1976). It is likely that the patient became pregnant with her first or nearly first ovulation otherwise one would expect that inspissated blood in the uterus and salpinges would have made fertilization difficult. The fact that the son resembled the father excludes an even more miraculous conception.”


Looks like this is a European wool carder bee (Anthidium manicatum)
More precisely a female, judging by the round end of the abdomen.

Information regarding the nest it was found in:

These bees construct their nests in preexisting cavities, using the trichomes of wooly plants.
Females use their mandibles, which are sharply toothed, to remove trichomes from the stems and leaves of various plants. They then roll up the trichomes into a ball and bring them to a preexisting cavity. Inside the cavity, the bees fashion the trichome ball into cells, where they deposit an egg as well as a provisioning mass consisting of nectar and pollen. Once finished, she seals the entrance to the cavity with a terminal plug, which consists of inorganic and organic materials that she brings to the nest. Source


phosphorylation of Glyceraldehyde 3-phosphate

Yes, the cytosol contains a high concentration of orthophosphate (in yeast, between 10--75 mM) so it is readily available for this reaction. The notation P$_i$ is commonly used because the orthophosphate ion can exist in multiple forms in water solution:

H$_3$PO$_4$ $\leftrightarrow$ H$_2$PO$_4^{-}$ + H$^+$ $\leftrightarrow$ HPO$_4^{2-}$ + 2H$^+$$\leftrightarrow$ PO$_4^{3-}$ + 3H$^+$

When we don't need to specify an exact form, P$_i$ is convenient as a shorthand for "some phosphate ion".

At the cytosolic pH (about 7.2), almost all orthophosphate is in the H$_2$PO$_4^{-}$ and HPO$_4^{2-}$ forms, which are roughly equally abundant. So yes, there is (at least) one hydrogen on orthophosphate available for the enzymatic reaction.

The term "orthophosphate" rather than just "phosphate" is common in biochemistry because phosphate also exists as polymers, including the di- and triphophates (in nucleotides, for example) as well as longer polyphosphate chains. These form are all referred to as "phosphates", while "orthophophate" specifically means the "monomer" P$_i$.


What are the ecological effects of moderately high and prolonged concentrations of nitrogen deposition on an ecosystem?

Too much nitrogen can run off during rain and collect in ponds, leading to eutriphication, find more here: https://en.wikipedia.org/wiki/Eutrophication

It's probably also responsible for dead zones: https://en.wikipedia.org/wiki/Dead_zone_%28ecology%29

This is an important question because we've more than doubled the amount of bioavailable nitrogen on Earth in the last 100 years simply because of the haber process and man made fertilizers. This amount of nitrogen has never been available before.


Definitions of hermaphroditism, dioecious and monoecious?

Below are definitions that I've seen; there may be less strict definitions under which monoecy (the noun form of 'monoecious'). and hermaphroditism would be the same thing.

Dioecious: Although rarely used for animals, one could say that human are dioecious because each individual produces only one type of gamete. In a dioecious species, some individuals are males and others are females.

Monoecious: In monoecious plants, individuals carry both males and female flowers but not flowers that can produce both female and male gametes.

Hermaphrodite: Hermaphroditic plants have flowers that can produce both male and female gametes.

Then, there are many other fancy terms such as dichogamous, gynomonoecious, subandroecious, heterostyly or androgynomonoecious! Plant mating systems are fantastically diverse and complex!

More information

Some of these terms are defined in The Evolution of Sex Determination, which is very pleasant to read. For shorter articles, consider Barrett 2002 or just Wikipedia > plant reproductive morphology or Wikipedia > dioecy (the noun form of 'dioecious').


Is this a valid definition of independent assortment?

That's a valid explanation, but not definition. Mendel's law of independent assortments states that during the formation of gametes, the alleles for one trait segregate independently of the alleles of another trait.


If a gene is missing from an operon that structures a protein, then would that protein not be made properly?

From my understanding, operon is a series of genes that are regulated by a single promotor. In many cases genes in an operon form subunits of a protein.

Genes in an operon can code for protein subunits, but they can also code for separate proteins. Often an operon will have a few genes responsible for one core function, with other accessory genes that may help regulate or enhance that function is some way. Sometime genes are fused, combining multiple subunits into a single gene. In other cases, subunits can have related functions in the absence of other units.
For example, The ArsAB complex uses ATP to pump arsenic from bacterial cells, conferring resistance. But many bacterial Ars operons lack the arsA gene. Minus this subunit, the ArsB transporter still functions to efflux arsenic from the cell, just less efficiently, harnessing the proton motive force instead of burning ATP.

... ended up finding that one of the genes in an operon was missing.
Does that imply the protein made from those genes in the operon will not be made properly or other genes will compensate for the loss?

If the gene is truly missing, it's can't be transcribed, and the subsequent protein can't be made, but the remaining genes will probably still work. I would start by asking what the operon's function is, and then consider whether the missing gene is essential for that function (hint: If it's missing and the rest of the operon is still there, it's probably not essential). If it is essential, then consider whether it's truly missing. Are there other open reading frames in the operon that could encode something with similar function? Could the organism have multiple copies of the same operon (possibly found on a plasmid)?


Do plants have preference for the form of nitrogen as nutrient?

Quoting verbatim from this site. The reference is not really a scientific article but you can check the references it cites. Some were not in English so I did not check. However these points are fairly logical

  Nitrates are the preferred nitrogen source:

  Non-volatile: unlike ammonium, nitrate is non-volatile, so there is    no need to incorporate it in the soil when applied by top- or side dressing, which makes it a convenient source for application.
  Mobile in the soil - direct uptake by the plant, highest efficiency.
  Nitrates synergistically promote the uptake of cations, such as K, Ca    and Mg, while ammonium competes for the uptake with these cations.
  Nitrates can be readily absorbed by the plant and do not need to    undergo any further conversion, as is the case with urea and ammonium, before plant uptake.
  No acidification of the soil if all the nitrogen is applied as    nitrate-nitrogen.
  Nitrates limit the uptake of harmful elements, such as chloride, into    large quantities.
  The conversion of nitrates to amino acids occurs in the leaf. This    process is fuelled by solar energy, which makes it an energy-efficient process. Ammonium has to be converted into organic N compounds in the roots. This process is fuelled by carbohydrates, which are at the expense of other plant life processes, such as plant
  growth and fruit fill.

Many plants can carry out nitrification but this is not universal. From this article:

  Nitrification is sometimes considered so universal and rapid that
  applications of NH4-N are considered equivalent to
  NO3-N. This is not true in many forest, orchard, and
  grassland soils.

However, nitrate being more soluble is susceptible to leaching and wash off, care has to be taken when using nitrate based fertilizers. From the previously mentioned paper:

  Unlike the positively charged ammonium ion, which is relatively
  stationary because of its adsorption to organic matter or clay
  particles, the negatively charged nitrate ion is freely mobile in the
  soil solution (166). Thus, leaching and denitrification primarily
  involve a loss of NO3-N (171). Inhibition or retardation of
  nitrification of applied NH4-N can reduce nitrogen losses,
  increase efficiency of applied N, and establish a predominantly
  ammoniacal form of nitrogen available for plant uptake (105, 171,222,
  232).


What specific membrane adaptations do cells have for saline-rich environs?

This 1969 Steensland paper seems to suggest that the membranes of halophiles are stabilized by sodium ions and they rapidly denature at lower-salt conditions (2.2 vs. 4.3 M).  The protein composition of the membrane was generally acidic, stabilized by all the Na+.

As far as what the role of the halophile membrane is in sheltering the cell from the high ionic strength solution seems left unsaid.


Passing virus/diseases immunity to newborn

Newborn mammals get something called "passive immunity", in which the mother's antibodies are passed across to the fetus or newborn. Depending on the species, this can happen by the antibodies crossing the placenta, or more commonly by being transferred in the first milk the mother forms, "colostrum", which is very rich in antibodies. (At the same time, the newborn has special adaptations to absorb antibodies from the colostrum into its body; this only works for a short period after birth.)

Passive immunity
IgG Placental Transfer in Healthy and Pathological Pregnancies
Colostrum

This allows the newborn to have a temporary resistance to whatever pathogens happen to be common in its immediate environment (because presumably the mother would have been exposed to them). It's very much temporary, lasting typically a few weeks or so before the transferred antibodies half-life away. During this time, the newborn has a chance to start developing its own active immunity, which is dynamic and lasts much longer.

Edit to add:

Are there other modes of heritable immunity? Sort of but probably not what you're thinking of. Innate immune responses are often triggered through recognition of molecular patterns that are common to many different pathogens ("Pathogen-associated molecular patterns" or PAMPS). The receptors that recognize these patterns are inherited, and they are essential for starting innate immune responses which are in turn very important for starting acquired immune responses. So yes, every newborn mammal, and reptile, fish, sea urchin, arthropod, nematode, etc. inherits mechanisms for recognizing pathogens.

However, it's important to understand that these don't change during the mother's lifetime. This system doesn't provide any inheritance of recognition of pathogens that are locally important, or that the mother has met during her lifetime. This is the basic toolkit that every individual of the species (often, that every individual in the genus, or kingdom) has, that's needed to answer the general question "Is this a dangerous situation? Should I activate the immune response?"

In other words, as far as the innate system is concerned, "the child has a completely fresh set of 'default' defenses"; the only non-default information that's passed from mother to newborn is via the passive immunity described above.


Why insects are so small compared to mammals?

The standard answer to this question is - it's down to the delivery of oxygen to respiring tissues. Insects depend upon a process that is essentially diffusion-driven (via spiracles and the tracheal system) whereas vertebrates have a circulatory system that allows oxygen absorbed in the lungs to be carried via the blood to peripheral tissues. And of course the blood contains specialised carrier cells (red cells) which in turn are packed with haemoglobin which acts as a molecular carrier for oxygen.

The giant dragonflies of the Carboniferous (Meganeura) existed at a time when oxygen levels in the atmosphere were much higher than now (32.5% vs 20.9%), so the diffusion-driven gas exchange system could support a larger body size.


Mosses are able to transport water and nutrients internally through intercellular voids and cell-to-cell connections involving exchanges of cytoplasm, as well as externally across their surface. Labeling mosses as nonvascular plants is misleading because mosses in the Polytrichales order have highly specialized water and nutrient conducting systems which are reminiscent of xylem and phloem. But in general, a moss's main vascular system can be said to be its outer surface which is carefully designed to store and conduct water across the plant.

External Conduction

Moss cells absorb water and nutrients directly from their environment, so many of their nutritional needs can be met simply by ensuring water and its dissolved nutrients can spread across the entire surface of the moss plant. The water is able to spread through capillary action, aided by a carefully designed surface. Moss leaves are frequently appressed to the stem and have sheathed bases which create small places for water to climb along a stem. The leaves may also be covered in small bumps (papillae) which create capillary spaces. Rhizoids, which are somewhat like roots except typically only 1 cell thick, can also make good paths for water to flow across. Some mosses have their stems covered in rhizoids or paraphyllia to help conduct water. Sphagnum mosses have large cells across their leaves which exist mainly to absorb water like a sponge, and Leucobryum mosses have a layer of water holding cells on both sides of their leaves. Colonies of mosses often form compact mounds that allow for water to flow across the entire mound.

As far as I know, moss cells do not deliberately dump nutrients into the film of water on their surface in the hopes that it will be absorbed by other cells of the plant that need it more. But, when dessicated moss is rehydrated, solutes in the protoplasm may leak into the external film of water. These contents might be able to be reabsorbed by other cells of the moss, forming an incidental external nutrient transport pathway.

Internal Conduction

Water and nutrients are also able to flow through cells or spaces between cells from inside the moss. Experiments have shown that nutrients are relocated from old growth to new growth using cytoplasm-linked pathways in Sphagnum and Polytrichaceae mosses. Many moss stems and almost all seta (the stalk connecting a spore capsule to the main body of the parent moss plant) have special nutrient conducting parenchyma cells surrounding water conducting cells called hydroids. The central ribs of moss leaves also often show a similar pattern. Sometimes these chains of nutrient conducting cells in the leaves connect to the main conducting strands in the stem, but usually the leaf conducting strands come to an end somewhere in the stem cortex without connecting.

Mosses in the Polytrichales order have the most specialized nutrient and water conducting cells of all mosses. The nutrient conducting cells for mosses in this order are different enough from other mosses to be given a special name--leptoids. The vascular system in these mosses are not evolutionarily homologous to xylem and phloem, but serve the same basic transport purpose. In Polytrichum moss, water has been measured to flow 200 cm/h through the stem and organic compounds at 32 cm/h. These specialized hydroids and leptoids are what enables the tallest moss, Dawsonia superba, to grow up to 70 cm.

The water and nutrient transport architecture for mosses outside the Polytrichales is more variable and less specialized. Andreaeopsida, Andreaeobryopsida, and Sphagnopsida completely lack hydroids. Takkakia's hydroids are unique in that they are short instead of tall and transfer water through pores formed from plasmodesmata at their ends. Sphagnum has nutrient conducting cells, but they are not homologous to the nutrient transferring parenchyma cells of other mosses. Some mosses in families which typically have central conducting strands have lost that feature over time, and mosses which would normally have hydroids may fail to develop them if grown underwater.

Outside of the usual stem, seta, and leaf midrib conducting cells, it has been suggested that rhizoids and caulonemal cells also conduct nutrients due to similarities in cell organization to the nutrient conducting parenchyma cells. The cells that form the interface between the parent gametophyte and the sporophyte foot also transfer nutrients.

Sources

Chopra, R. N. Biology of Bryophytes. 2005. Chapter 11 "Conduction in Bryophytes".

Goffinet, B., and A. J. Shaw. Bryophyte Biology. 2009. Pages 60-70, 83, 301.

Ligrone, Duckett, and Renzaglia. Conducting tissues and phyletic relationships of bryophytes. 2000.


Why are red blood cells not attacked by NK cells?

The question states, not quite correctly, that "if they stop presenting anything at all, they will be eliminated by the NKs".  In fact, simply not having MHC is not enough to trigger destruction by NK cells.

NKs have a two-part trigger. Part 1 is an activator; part 2 is a suppressor. When the activator is present, and the suppressor is not present, then NK cells will destroy the target.

The suppressor is typically MHC class I, which is present on almost all normal cells. That means that NK cells will not destroy normal cells. There are many different activators, but most normal cells have at least one of the activators also present. That means that NKs are normally primed to destroy, but refrain from destruction because they also sense the suppressor.

With that explanation, it should be clear why RBC are not destroyed by NK cells. Even though they lack the suppressor, they also lack any activators. Since there are no activating signals, the NKs don't need to be also suppressed, so the lack of MHC doesn't lead to an attack.

Sample references:

Two-signal requirement for activation and effector function of natural killer cell response to allogeneic tumor cells
Controlling NK Cell Responses: Integration of Signals for Activation and Inhibition

It's also possible that RBC further protect themselves by showing a "marker of self" on their surface (Role of CD47 as a Marker of
Self on Red Blood Cells) but that doesn't change the important point about NKs mode of activation.


Does exhalation help us speak, and if so, how?

Not including water vapor, argon and trace elements, inhaled air at sea level: ~79% nitrogen, ~21% O2, ~0.04% CO2. Exhaled air: ~79% nitrogen (the body doesn't "use" inhaled nitrogen), ~16% O2, ~4% CO2

It is this exhaled air we use to speak. However, there is a very minimal increase (and I do mean minimal) in the CO2 concentration and decrease in the O2 depending on how fast we speak, how often we stop to take breaths, etc. compared to plain, expired breath. This is because the inhaled air is being held back in the lungs and released more slowly as we speak, giving more time for O2/CO2 exchange to occur. However, it will mostly occur in what's called "dead space" and the %CO2 will be changed for a few breaths thereafter as well.

To demonstrate this, speaking until we're "out of air" should make us slightly dizzy because maximal exchange will have taken place at a certain point, after which our blood CO2% will rise, and our blood O2% will fall.

After that, the higher serum CO2 will cause us to take a deeper breath, a 'cleansing breath' if you will, to jump start the return to normalcy in blood gasses. It is very, very hard to resist this deep breath (which is why breathing has a voluntary and an involuntary component, i.e. you can't hold your breath until you die.)

Breathing


What's the difference between an embryo and a fetus?

Yes, you are correct. You can read the wikipedia article about an embryo:

  An embryo is a multicellular diploid eukaryote in its earliest stage of development, from the >time of first cell division until birth, hatching, or germination. In humans, it is called an >embryo until about eight weeks after fertilization (i.e. ten weeks after the last menstrual >period or LMP), and from then it is instead called a fetus.


Can the psychology of a person alter his immune system and health?

I'm not sure what you mean by psychology exactly, but assuming you are referring to a persons mental state there is a known link between stress and immunity. This link occurs through neuro-endocrine pathways. The central nervous system and endocrine (hormonal) systems are linked through the hypothalamus, a key controller of hormone release in the central nervous system. In a state of stress our central nervous system reacts by increasing the release of hormones such as the steroid cortisol and catacholamines such as adrenaline (a.k.a epinephrine in USA).

We know that steroids have an effect of dampening down the immune system (in fact steroids are often used for this intentionally in the case of autoimmune conditions for example). Thus based on this we have a scenario where stress can lead to increase in cortisol (and other hormones) which in turn can have an effect on your immunity. The effect to which this impacts on your life is then further dependent on your psychology and social support.

More generally, the links between illness and psychology are integrated together in what is called the biopsychosocial model of illness. I suggest you look this up to gain a more in depth understanding of this complicated issue.


If your restriction enzyme only targets a single site on the DNA sequence then it will split each DNA strand into two fragments. If the restriction enzyme cuts every strand then you will see those two fragments. Note that if the two fragments have the same length they could appear as a single band when separated using gel electrophoresis.

If the enzyme doesn't cut everything the uncut DNA will also be present. This is why you should always separate some uncut DNA in the gel electrophoresis.


Solubility of Amylopectin and Glycogen in water

The answer is relatively simple: Amylopectin is watersoluble, and this seems to be a classical textbook error, which has been propagated now for decades. As you say yourself, the only difference is the number of 1,6-glycosidic branches, which occur every 8-12 glucose monomers in glycogen and every 15-30 monomers in amylopectin.

There are even scientific articles which show that amylopectin is watersoluble, see the references below:

Green et al., Journal of Chemical Education vol 52, p.729 (1975) Which  Starch Fraction  is  Water-soluble,  Amylose  or
Amylopectin?
J. Robyt, Encyclopedia of Life Sciences (2001) “Polysaccharides: Energy Storage”


Can lysozyme also lyse gram-negative bacteria and if yes, how fast?

Gram-negative bacteria also have peptidoglycan which can be degraded by lysozyme. However they have an outer membrane lying outside the peptidoglycan layer and this will block lysozyme action.

Because of this if you intend to treat Gram-negative bacteria with lysozyme it is necessary to add something that will disrupt the outer membrane—the usual choice is EDTA since removal of magnesium ions by chelation will destabilise the outer membrane.


Primer design for introduction of restriction sites flanking a gene of interest

I think the best way is option #2:

Suppose that your gene of interest is AAAAAAAAAAAAAAAAAAAAAAAGGGGGGGGGGGGGGGGGGGGGGGG

and you want to insert EcoRI restriction site GAATCC

Then your Fwd primer will be  GAATCC AAAAAAAAAAAAAAAA

and your Rev primer will be GGATTC CCCCCCCCCCCCCCCC

But in general, it shouldn't matter which option you choose, as long as you calculate the Tm of only the part of the primer that hybridizes to your template.


What are these black masses floating on my pool?

I was looking in the wrong kingdom. After much searching I asked myself: are those eggs? Silly me, of course they are. I should have thought it from the start. Mosquitoes plant their eggs on water over night. I was confused because in the past I've never seen the eggs, only the larvae and the pupae in the water. So, that's what I have every morning floating in my pool, groups of mosquito eggs.
http://animalia-life.club/other/mosquito-eggs.html


Which functional annotations could be useful?

I'd add genetic effects of the gene and its orthologs in that own
host. Knockouts and overexpression are powerful in uncovering
function.
In terms of baseline or normal expression, I would add    tissue,
developmental or differentiation time points, and conditions which stimulate or repress expression.


Why do almost all SNPs have two alleles?

Well, though it is possible to have SNPs of more than two alleles, and some exist, due to the low probability of having a basepair change twice in the same base-pair (there are aproximately 3.000 Mb in the human genome) and have it in more than 1% of the population (remember we are talking about single nucleotide polymorphism) to classify as a polymorphism is a very rare phenomenon.

I can check the maths for it if you need it, but it's just matter of probability.


what is the name of this small plant with yellow flower?

This looks like Sphagneticola trilobata also known as Singapore daisy, creeping-oxeye, trailing daisy, and wedelia.  It is now found throughout the Neotropics but is native to Mexico, Central America, and the Carribean.  It is a weed that is classified in the top 100 worst invasive species in the world.

Source: Sphagneticola trilobata (ePlants)


Can I use a basic compound microscope to analyze the ploidy of plant chromosomes?

If you want mitotic chromosomes then you want to look at apical meristems — probably the primary root from germinating seedlings will be easiest.  Apical meristems are at the growing tips of roots (and shoots) and contain regions of rapidly dividing cells.  Since you can only see chromosomes as separate bodies when they are condensed for cell division this increases your chances of visualizing chromosomes.

However, you will need to stain the roots to visualize the chromatin (material that makes up chromosomes).

This paper has a protocol for staining dandelion root tips, but I don't know whether you can obtain all the necessary compounds.  However, colchicine and para-dichlorobenzene probably aren't really necessary (they will increase the number of cells in mitosis) and are toxic so best to avoid those steps anyway.

Note, it looks like you would also need a 100x oil immersion lens, which doesn't look like it comes with the microscope you listed.

You may also find this paper useful as a starting point for making "homemade" chromosome stains.

Good luck!


It could be difficult for RNApol to access genes inactivated because inactivated genes are often tightly packed by chromatin. Many genes have enhancer elements(specific DNA sequences) as well as TATA, and transcriptional enhancers, which are proteins, would recognize enhancer elements in a sequence dependent manner and loosen chromatin structure to make RNApol access TATA sequences easily. Transcriptional enhancers also bind to the General Transcriptional Factor complex (GTF), which contains RNApol, therefore enhancers could bring RNApol to TATA sequences.
Many tissue specific and/or developmentally-regulated transcriptional enhancers are identified. You could say transcriptional enhancers regulate RNApol which to bind.

You can check this link and this.


Why does the hydrolysis of ATP increasing entropy increase the Phosphoryl-‐transfer Potential?

The phosphoryl transfer potential is one way to think about the free energy available to do useful work when ATP is hydrolysed.
As you can see from the free energy equation below, a positive change in entropy will help to decrease (i.e. make more negative) the free energy change.
This is why an endothermic reaction can still occur spontaneously if the entropy change is big enough to create an entropy term that outweighs the enthalpy term in the Gibbs free energy equation.

ΔG=ΔH - TΔS
where:
T= temperature
G = Gibbs free energy
H = enthalpy
S = entropy


Is it safe to use an egg incubator to grow bacterial cultures?

A good practice to minimize the contamination of a Petri dish and of the external environment is by never completely removing the lid of the Petri dish: to access the content of the Petri dish with an inoculation loop, lift the lid on one side, slowly: just high enough for the inoculation loop to get in, get some of the content, and get out.


How do you dilute forward and reverse primers for a master mix?

Would I just add 500μL of my forward primer and 500μL of my reverse
  primer for a mix of 1000μL in which both concentrations are still
  10μM?

No.  Diluting your 10μM solution in half will half the concentration.  Mixing equal parts of 10μM primer will make a master mix where each primer is 5μM

But in general, primers are added to these reactions in great excess, so 5μM of primer might be okay.


You might want to start by browsing the research papers (think of them as "essays") at https://www.plos.org/ to find the areas you are most interested in.  They have thousands of peer-reviewed articles which you can read for ideas for your essay and research ideas.   You might then consider contacting the authors of those papers to inquire about education or work at their institutions.


How do we call a region of low carrying capacity?

If you ask about quantity/numbers only, I would suggest using "the zone of low population density" or "intermittent zone" which in turn borders the "buffer zone" and "the zone of intermediate/high population density".

The "buffer zone" is the zone between two different populations where the number of the animals in question is zero.

J.Potts, M.Lewis "How do animal territories form and change? Lessons from 20 years of mechanistic modelling"

There are other classifications based on the "main usage" of the territories.


Is it possible to contract the plague by kissing a wild chipmunk?"

The causative agent of the plague, Yersinia pestis, can be indirectly (via a flea vector) or directly (via exposure to infectious fluid or a bite) transmitted by rodents. In the western United States in particular, Y. pestis is endemic, and ground squirrels, prairie dogs, chipmunks, and woodrats are important reservoirs (see Cecil Medicine Ch. 320). US National parks have signs warning against feeding squirrels and chipmunks for this reason. You can read more about it in a national park brochure . Chipmunks and squirrels indirectly and directly transmit a variety of other diseases as well, including Tularemia (Cecil Ch 319) and various tick and flea borne encephalitides.


The NF-κB family of transcription factors is very modular, with different combinations having different effects. The active (nuclear, DNA-bound) TF is a dimer, composed variously of RelA/p65, RelB, c-rel, NFKB1/p50, and/or NFKB2/p52 subunits. For example, the "canonical" p65/p50 dimer is activated in response to stimulants like TNF-α (tumor necrosis factor alpha, released in response to inflammatory signals like the presence of pathogens) and LPS (lipopolysaccharide from the cell walls of Gram-negative bacteria), while the RelB/p52 dimer plays an important role in the development of B cells (the immune system component that produces antibodies). The AP-1 transcription factor is also heterodimeric, containing proteins from the Jun, Fos, JDP, and ATF families, and there are numerous other examples of multimeric transcription factor complexes. This recent article in Nature Immunology (disclaimer: I was not involved in that research, but my old lab did similar work) shows DNA sequence-specific binding by different NF-κB dimers.

Polymerism in general, and dimerism in particular, are quite common modes of transcriptional activation and regulation. The large number of ways in which a relatively small number of transcription factors can be combined allows for the exquisite control of genes, responding to a huge variety of cellular situations. Unfortunately, it also means that mutations in key, common components can result in transformation, unrestricted growth, and the generation of tumors.


Assuming the jar is airtight--

I think your oxygen consumption rate may be too high and that 40$\mu l$ per hour$^1$ might be closer but since it's a high figure anyway we can use it. 40 $\mu l$ per minute would be about 2400 $\mu l $/hr.

A 12-ounce jar is about 0.355 liters. At sea level, air contains about 20% oxygen so the volume of oxygen in the jar is about 0.0709 liters.

At altitudes which are considered high for humans (17000 feet or higher) the percentage of oxygen falls to about 15%. If a bee is able to get 2400 $ \mu l$ of oxygen per hour from a jar, the volume of oxygen will fall to about 13% after ten hours.$^2$

Based on oxygen consumption alone I think a bee would be stressed at this level, especially at temperatures exceeding 32C. I would guess the bee would be stressed well before this, maybe after 5 hours (16.6% oxygen). If we factor in the likelihood that the bee's respiration is up due to the agitation of confinement I think we can shave another hour off.

Depending on the age, size, species, variety, temperature, location, etc. I think an outside limit of 4 hours in an airtight jar is a good guess.

Toxicity from CO$_2$ may be a problem but bees have a much higher tolerance for CO$_2$ than humans, according to one set of entomology notes. At 0.04% the concentration will only increase marginally due to a drop in oxygen alone but the bee itself will produce CO$_2$ and in far greater quantities under stress. A chart here shows production of CO$_2$ in reaction to a light being turned on. 400 ppm is 0.04% but in this case it is due to the bee. If the bee during respiration returns CO$_2$ as quickly as it consumes oxygen the jar could reach 7% CO$_2$ in four hours, a level that may be toxic for humans. But we have already suggested the bee is under stress from oxygen depletion at that point.

There are many assumptions in this note. A conservative estimate might be an hour in an airtight jar. I would not bet on more. There are probably other issues I haven't thought of. Bees are very fragile and the chart linked above suggests they would not fare will in such an environment.

$^1$ Respiration of Worker Honeybees of Different Ages and at Different Temperatures, Allen, 1958, J. Experimental Biology 36, 92-101. At page 97 Allen gives a chart showing log $\mu l$ $O_2$/mg body weight/hr. For a 14-23 day old bee at 32C he appears to give about .5 which means 1.65/mg/hr or about 115 $\mu l$ per hour for a 70mg bee. It may be a typo or perhaps I am misreading the chart. Also the study uses an older method of measuring respiration.

$^2$ This is a simplification. The bee will start breathing a mixture containing falling oxygen levels and this may slow the oxygen depletion a little. But if we say the bee needs what it needs this saves us a differential equation.


Can all biological processes be understood as computations and studied as such?

If you abstract enough, anything cam be considered as a computational device. The issue with doing this with cells is the sheer number of variables.

For any given cell, the following internal variables exist:

Internal ion concentrations for dozens of ions of importance importance
Internal concentrations of hundreds or thousands of various simple organic molecules, including "raw" internalised molecules, various steps in dozens or even hundreds of metabolic processes, and metabolic end-products and by-products.
Internal concentrations of hundreds or thousands of different proteins and other complex biological "mechanical parts", as well as the states of these "parts".
The physical state of the cell - stretched, contracted, relaxed, hot, cold, etc.

This list is not exhaustive.

It's also worth noting that the above variables may also exist for multiple separate "compartments" within the cell; vesicles, the endoplasmic reticulum and the golgi apparatus being three which come to mind immediately.

The other issue is that cells do not exist in a vacuum; the external environment plays an important role in their functioning. The human body is at any one moment existing in direct contact and interaction with the following extracellular environments:

The atmosphere (Mainly, but not only, temperature exchange)
The air within the respiratory system, including nose and mouth
Stomach contents
Small intestine contents (which would need to be considered in several segements, since the nature of the interaction changes along the path of the small intestine.
Large intestine contents
Blood
Cerebrospinal fluid (Fluid found "inside" the brain)
Extracellular fluid, or "tissue fluid" (A separate compartment for each small swatch of tissue in the body)
Lymph
Pleural fluid (Fluid surrounding the lungs; a separate compartment for each lung)
Pericardial fluid (A small amount of fluid surrounding the heart)
Joint capsule contents (A separate compartment for each joint)

...and the list goes on. Each of these compartments requires tracking of the same variables as individual cells.

This is yet further complicated by the fact that some of these compartments can't easily be considered as one big compartment, because of the importance of spatial relations. For example, the oxygen and carbon dioxide concentrations of blood (as well as the concentrations of other substances like alcohol) change centimeter-to-centimeter. Yet another issue is the fact that cells are not static in terms of their relations to each other; red blood cells move with blood flow, and experience turbulence and other effects, and other cells (like macrophages) are capable of "deliberate" movement in the blood and in tissue.

You would also have to account for physical disturbances - things like a stab wound or even a pinprick are ludicrously complex at a cellular level.

Of course, human beings are very complex organisms, and there exist much simpler organisms. You might be interested in OpenWorm, which is an attempt to computationally simulate Caenorhabditis elegans, a species of roundworm, at a cellular level. Doing so even for an organism as simple as C. elegans is a massive undertaking, as evidenced by the fact that even with the contributions of dozens of experts in their fields the project has been ongoing for some time and is yet to reach stage one.

The short version: Is it possible? Perhaps. Is it easy? Definitely not.


Voluntary actions of Autonomic Nervous System

I have no idea what the author has in mind, but their statement is wrong from the beginning: somatic motor activity is not always voluntary. Reflexes are a good and obvious example.

"Fight or flight" response is basically half of the entire ANS (the sympathetic part), so that's incredibly broad. Parts of that response are definitely involuntary.

I think it's more likely that Wikipedia is thinking of things like breathing, which is normally under ANS but you can also manually control your breathing. They may also be thinking of things you can do to directly influence your autonomic responses, for example, if you start running, you are voluntarily moving your muscles, but the autonomic nervous system will also participate (for example, by increasing your heart and breathing rates).


Is there a reason for the lack of full RTK structures?

Large proteins are challenging for NMR: the more amino acids, the more peaks one has to assign. Peak overlap is also more likely the more amino acids you have, making assignment difficult. Some NMR strategies work well for studying dynamics of large proteins, but as far as structure determination is concerned, there definitely is a critical size past which NMR is simply not the tool for the job.

Flexible proteins are challenging for crystallography: too much flexibility can simply prevent crystallization, you can spend years only trying to get crystals, and once you do manage to grow crystals they might diffract poorly or not at all. But crystallography is often very useful to solve high-resolution structures of individual, isolated domains; this is of great help down the road to interpret a lower-resolution cryoEM map of the full-length protein.

Membrane proteins are challenging for biochemistry: purifying them and getting them to remain stable in solution is difficult.

Receptor Tyrosine Kinases (RTKs) are all of that at the same time! Large, flexible membrane proteins.

Now, with tremendous technological progress of cryo-electron microscopy (cryoEM) recently, such challenging structures become more tractable. Conformational flexibility is still an issue, but unlike with crystallography it can be dealt with to some extent (i.e. it won't prevent you from collecting initial data and getting preliminary results that can guide your next attempt).


Are there bacteria that respire anaerobically in aerobic conditions?

Are there any organisms that would still perform anaerobic respiration even when shifted to aerobic conditions?

Yes, there are. They are called aerotolerant anaerobes as shown in this figure on tube 5. In the thioglycollate broth, growth is seen throughout the length of the tube

Legend

Obligate aerobe
Obligate anaerobe
Facultative anaerobe
Microaerophilic
Aerotolerant anaerobes

  Are there any which can survive?

Obligate anaerobes wouldn't survive in aerobic conditions. Hence they are named so.

  Such a bacterium would be read false positive for oxidizers in such a case because it would ferment glucose even in aerobic conditions.

The thioglycollate broth shown here is used to differentiate bacteria into the above said criteria. The Hugh-Liefson test does'nt do that. You can not conclude that a bacteria is aerobic or anaerobic using that test. The H-L test, is interpreted in two ways.

Fermentative - When both the closed tube and open tube show a colour change
Oxidative - Colour change only in the open tube

In short, the words aerobic/anaerobic are not used to interpret the H-L test. But we can draw parallels.

Obligate aerobe - Open tube (+), Closed tube (-) - Oxidative
Obligate anaerobe- Open tube (+ at bottom), Closed tube (+) - Fermentative
Facultative anaerobe- Open tube (+), Closed tube (+) - Fermentative
Microaerophilic- Open tube (+), Closed tube (-) - Oxidative
Aerotolerant anaerobes- Open tube (+), Closed tube (+) - Fermentative


What causes the sound of climaxing bees?

Firstly, those aren't bumblebee faces ... those are big fly eyes. Those are Bumblebee Hover Flies (Volucella bombylans):

The noise in the first part of the video is identical to a fly flying around your head and the noise at the end sounds like what a fly would sound like when you press it against a surface like a wall or screen (or a newspaper, apparently)


A very long head start
To elaborate on Drake Johnson’s comment, CO2 used to be much higher in concentration. During the Great Oxygenation event, when cyanobacteria (ancestors) began photosynthesizing, they converted much of the CO2 into O2, driving CO2 concentrations down as they drove O2 up.


How do opportunistic infections affect an immunocompromised or AIDS patient?

Clinical diagnosis of AIDS in a person infected with HIV is based on the following criteria:

A CD4+ T-cell count below 200 cells/µl (or a CD4+ T-cell percentage of total lymphocytes of less than 14%)

OR

The patients has one of the few "indicatory" diseases that strongly suggest severe immunodeficiency. See the list of this diseases here. Usually they have fatal consequences.

As we can observe, there are mostly fungal and viral infections that live inside the host cells or (in case of tuberculosis) diseases caused by intracellular bacteria. They can be overcame only with working mechanisms of cellular immunity. Other mechanisms are simply too slow, not specific or not precise enough.

Another issue is an impairment of the immunological surveillance and much higher risk of cancer in individuals diagnosed with AIDS. Precise elimination of malignant cells is fully dependent on cellular immunity.

[EDITED]
For further reading, recent paper analysing the most common causes of death in patients with AIDS in the era of anti-retroviral therapy.


Does a mutation in the sense strand of a particular gene affect the polypeptide formed?

We’re doing it for the children!

The basic misconception in this question is that the important effects of mutations are seen in the cell that undergoes mutation. This is not the case. So focusing on the whether the strand that receives a mutation is the non-transcribed, sense, strand or the transcribed (anti-sense) strand is of little relevance.

  What is important is whether or not the mutation is passed on to the progeny.

Don’t we have a life too?

Why isn’t it important? Consider a mutation occurring in a single E. coli cell in a population of millions of E. coli, or a single muscle cell in a human muscle. Even if there is a mutation in the strand that is transcribed into mRNA and translated into protein, the change in that one cell will not have a significant effect on the overall population.

The birds and the bees

The way in which a mutation — on sense or anti-sense strand — can affect a population of bacterial cells or whole tissue in an organism is:

(For bacteria or in tumour cells) if the mutation is passed on to some of progeny, which then have a selective advantage so that they can outgrow the wild-type population
(For normal tissues in animals) if the mutation is passed on to the progeny through the germ line so that it is present in all (e.g. muscle) cells

Still harking on about sex (Yawn)

The key point is easier to explain with bacteria. Consider a simplistic situation in which a mutation occurs on one strand (and is not corrected by the DNA-repair mechanisms). Before the cells divide into two daughter cells the double-stranded DNA replicates — each strand is the template for a complementary strand in a daughter double-stranded DNA. One cell will have the daughter dsDNA (double-stranded DNA) copied from the unmutated strand and the other will have the daughter dsDNA copied from the mutated strand.

  In the case of the dsDNA copied from the mutated strand, both
  strands will clearly carry the mutation, so it is irrelevant whether
  the mutated strand in the parent was sense or anti-sense.

If the mutation is advantageous these cells will grow and divide and out-compete the other bacteria in the population.

A similar explanation holds for tumour cells in a differentiated animal tissue.

In the case of germ-line cells in animal tissues the situation is slightly different — the mutation either will be present or absent in both strands of the dsDNA in the fertilized egg, and so will affect all of the cells in the tissues of the progeny in which it is expressed.


In short, yes.

A good example of an orally-administered vaccine is this Polio vaccine.


Is the regulation of lactose operon different between Gram + and Gram -?

I know it's stupid but I answer my own question, for those who are interested.
It is different.  CAP protein regulates lactose operon only in Gram -. In Gram + the presence of glucose shuts down the operon with another mechanism: the TCRS that relies to concentration of fructose 1,6 phosphate.


Role of Calcium and Magnesium in capacitation/acrosome reaction

The process is not clearly understood. Calcium helps in capacitation: During capacitation calcium enters the spermatozoa through ion channels; blocking these channels inhibits the acrosome reaction but what calcium does inside the spermatozoa is not very clear. This paper says that calcium activates a certain tyrosine kinase in the spermatozoa which in turn activates a protein called p32. This they say occurs "concomitantly with capacitation". Other papers cited by this article talk about involvement of calcium dependent adenylate cyclase.

This article also says that protein tyrosine phosphorylations are important for capacitation but doesn't describe how.

I could not find a more precise information on this topic. I shall update the answer if I find one.


If gene differs between chromosome pair does individual get a mixture of protein shapes?

Yes, that mixture of shapes can happen.  Differences in the nucleotide base sequences between the two alleles of a gene can lead to differences in amino acid sequence, which in some cases large differences in protein shape.  One example would be if one allele changed a cystine codon to any other codon, leading to loss of a disulfide bond needed to stabilize the tertiary structure of a protein.  For an extreme example, consider a mutation causing sickle-cell anemia; in this case, the disease-causing allele leads to altered shape of the entire red blood cell.

If a heterozygote carries a healthy allele and a disease-causing recessive allele, the protein produced by the healthy allele provides enough activity to mask the lack of activity of the "broken" protein provided by the recessive allele.  If, instead of being a true recessive, the disease-causing allele is partially penetrant, then the heterozygote would suffer from the reduced level of the active protein (only one allele is providing the good stuff).


Can supplements affect DNA? (Could 10,000% Methylcobalamin affect MTHFR genotype)

What the DNAfit test does is analyse some of your genes for common variants (called SNPs - single nucleotide polymorphisms). These are hard-written in your genetic code, they won't ever change (you could in theory have mutations in some individual cells, but we can ignore that).

Taking supplements or any other environmental influences will therefore not affect these tests.

The environment can affect certain markers on the DNA, that control how active a given gene is (how strong its expressed) - this is called epigenetics. Since these markers are written on the DNA they are also potentially heritable and the two effects (the genetic code itself and the markers on it) are often thrown into one pot when some news report about 'changes to your DNA'.


How to determine the number of parameters in a phylogenetic model?

The number of parameters depends both on the number of taxa and model of sequence evolution. The topology is not typically considered a parameter in the usual sense of statistical inference (as it is the a priori specified topology the likelihood was calculated on).

So, for example, if you infer a tree from nucleotide data for 25 sequences under the General Time Reversible (GTR) model with gamma distributed among-site rate heterogeneity and empirical stationary frequencies (this is commonly called GTR+F+G), then you would have 56 parameters with the following breakdown: 2n - 3 = 47 branch lengths (where n = 25, the number of tips), 3 frequencies (because these sum to 1, once three are known the other is automatically known, so we only count 3 estimated parameters), 5 substitution rates (there are actually 6 substitution parameters in GTR, but it is typical to set one, usually G > C, to 1, and estimate the others relative to this, hence only 5 estimated) and 1 alpha parameter for the shape of the gamma distribution of rates (gamma distributions actually have two parameters, alpha and beta, but for phylogenetics we usually constrain them to be equal).

In total, this gives 47 branch lengths and 3 + 5 + 1 = 9 model parameters, and 47 + 9 = 56


How does this diagram illustrate carbon cycling in lakes?

This shows the major biological transformations of carbon in any system (not just lakes).

On the Left Side:

$GPP$ (Gross Primary Production) is the total amount of $C$ from atmospheric $CO_2$† that is reduced into organic molecules during the calvin cycle of photosynthesis.  This is the process performed by photosynthetic organisms like green plants and algae.

† atmospheric $CO_2$ diffuses into water and develops into several species of inorganic carbon molecules that plants and algae can use but in general you can think of this carbon as being very closely related to atmospheric $CO_2$

$OM$ is a pool of organic matter, which is a general term for reduced carbon molecules.  $OM$ can be living organism tissues (e.g., a fish), dead tissues (e.g., senescent leaves) or biologically generated organic molecules (e.g., sugar that leached from a plant).  $OM$ is the principle pool of energy and raw materials for all living things on Earth so this is a really important pool of stuff.

Since $GPP$ is taking $CO_2$ and converting it to $OM$ as the left side progresses, the amount of $CO_2$ in the atmosphere goes down and the amount of $OM$ in the biosphere goes up.

On the Right Side:

$R$ (respiration) is the oxidation of reduced carbon-containing molecules for the purpose of extracting usable energy.  This may be familiar as "cellular respiration" but there are other metabolic pathways that accomplish the same goal.  In the end when the $C$ in the $OM$ is oxidized and the energy released the $C$ that was in the $OM$ gets converted into $CO_2$.

Note that this is the opposite of the Left Side, so as this occurs, the amount of $OM$ in the biosphere goes down and the amount of $CO_2$ in the atmosphere goes up.

If the Left and Right sides are balanced, then there is no net change in the size of the $OM$ pool or the amount of $CO_2$ in the atmosphere.  However, note that over relatively short time scales these can be very out of balance.  Any time plants or algae are growing (i.e., gaining mass as $OM$) the Left Side > the Right Side or $GPP$ > $R$.  Once those plants die, they accumulate in the system as dead $OM$.  The decomposition of accumulated dead $OM$ by microbes will generally make the Right Side > Left Side or $R$ > $GPP$.

This picture from Wikicommons shows the same cycle in a more realistic setting.


First of all, you can look at the papers published in the Journal of the Avian Biology, the Journal of Ornithology and the Auk. There you can see how bright is the field. It is about conservation biology, distribution of species, ecology of species, behavior, migration etc.


If I remember correctly pymol can edit pdb structures (as well as visualize them).

I've used a student version though (which is a free full version) and I'm not quite sure if its possible to use pymol without buying a license nowadays (though the source code is still open source, so can in principle always install it from that)


Allopatric speciation

  Allopatric speciation [..], also referred to as geographic speciation, vicariant speciation, or its earlier name, the dumbbell model, is a mode of speciation that occurs when biological populations of the same species become isolated from each other to an extent that prevents or interferes with gene flow.

Sympatric speciation

  Sympatric speciation is the process through which new species evolve from a single ancestral species while inhabiting the same geographic region. In evolutionary biology and biogeography, sympatric and sympatry are terms referring to organisms whose ranges overlap or are even identical, so that they occur together at least in some places.

Yes, sympatric speciation appears to be a thing but estimates of how common that is avery hard to come by.

Now, what you describe is not so much sympatric speciation as you refer to a case of reproductive isolation between extant individuals and their ancestors. I am not sure that was really what you had in mind because otherwise you would have not put it in opposition to allopatric speciation but it is what you seem to phrase. Of course, such type of "temporal reproductive isolation" is obviously a thing.


From the derivation of Michaelis-Menten kinetics you can see that:

$$K_m=\frac{k_f + k_{cat}}{k_r}$$

Where $k_f$ and $k_r$ are binding and unbinding rate constants (for Enzyme-Substrate binding), respectively, and $k_{cat}$ is the turnover number. This is for the Quasi-Steady-State approximation (QSSA). For the equilibrium approximation:

$$K_m=\frac{k_f}{k_r}$$ which is same as the association constant.

In both the cases pH can affect the rate of binding and unbinding by affecting the affinity between the enzyme and the substrate. For example lets assume that the substrate binding site is negatively charged. Low pH would increase the electrostatic potential of the substrate binding site towards zero by affecting the ionization of the functional groups.

pH can also have indirect effects on the substrate binding site because it can modify the overall structure of the protein.

Many enzyme catalysed reactions involve acid-base catalysis i.e. there is a transfer of proton. In reactions like these, pH can affect $k_{cat}$.

  If pH does change Km, is this how I determine the Km value of a
  different pH value if the Km value at another pH is already known?

You can do that by making a Lineweaver-Burk plot for the changed pH.


Does Goryaev's chamber have the same grid layout as the conventional counting chamber used in the West?

From the description at http://cldtest.ru/hdbk/chamber

It appears to be functionally the same device, except the only the smallest square are marked (0.25 nL and 4 nL), and the total capacity is 90 nL instead of 100 nL. A hemocytometer could be used in place of a Goryaev's chamber (though not necessarily the reverse).


Reading an amino acid physicochemical properties diagram

Polarity and hydrophobicity are not discrete phenomena and, therefore, categorizing amino acids as such has some measure of arbitrariness, especially at edge cases. It all depends on one’s definition.

Other properties have similar problems. Charge depends on pH. And what is the cut-off between “large” and “medium” sides chains?

What is, in my opinion, more important than memorizing charts/diagrams/etc (unless you have an exam) is understanding why different amino acids have these properties. For example, why can threonine or tyrosine be classified as both hydrophobic and polar? Why can cysteine or serine, which are classified as uncharged, act as strong nucleophiles in enzymatic reactions?


Why would a venus fly traps mouth that's still "chewing" die?

There are many things that could affect the rotting of your venus fly trap while digesting including: size of the bug, age of the trap, and temperature.

Sometimes a venus fly trap will turn black and fall off while it's digesting a bug when the trap is very old. As the trap ages, the digestive juices are recycled and as a result form a weaker mixture which slows the digestion process.

The bug it was digesting was also probably very large or had a hard shell inhibiting the trap from properly closing. This allowed bacteria and mold into the trap to digest the insect also proliferating the rotting of the fly trap itself in the process.

Temperature also has an effect on the trap's digestion where higher temperatures speeds up the enzymatic process of digestion. However, this is probably not a factor in your case.

It's not so much that your venus fly trap decided to give up on the valuable resource, it was either too old to properly digest the bug or it couldn't close properly because the bug was too large that bacteria infested the bug and the trap speeding up the process of the trap falling off the plant.

For more detailed explanation see: http://science.howstuffworks.com/life/botany/venus-flytrap4.htm


what is linkage disequilibrium supposed to measure?

Linkage disequilibrium refers to a situation whereby two or more alleles, from different loci, segregate non-randomly. Therefore we have a statistical association between this two alleles.
The linkage disequilibrium can be used in gene mapping, because we assume that these loci are in the same region on the chromosome. The more often they appear together, the more they segregate non-randomly, the closer they should be on the chromosome.

http://www.researchgate.net/post/What_is_the_difference_between_Linkage_Equilibrium_and_Linkage_Disequilibrium


The other two phosphates come from inorganic phosphate* in solution (Pi — in my diagram below) at the glyceraldehyde phosphate dehydrogenase stage. (Two, of course, because there are two molecules of triose.)

This is covered in Berg et al. Section 16.1.5.

*The term inorganic phosphate is used because there are various different anions in solution derived from phosphoric acid, depending on the pH. At physiological pH the predominant species is the double-negativly charged, monohydrogen phosphate.


Why didn't Escobar's hippos introduced in a single event die out due to inbreeding

I think one of the important things to understand in thinking about this case is that it just hasn't been that long, generationally.
Escobar imported the hippos in the late 1980s. Hippos reach sexual maturity at an average of about 7.5 years old for males and 9.5 years for females, space births about 2 years apart, and live for 40-50 years.  Thirty years out, this means that only about 3 generations have passed for females. Moreover, the dominant males are highly territorial, which means that much of the breeding might even now be still coming from the initial male and not his descendants. Still, the initial male breeding with his own daughters would indeed produce a significant inbreeding coefficient.
The impact of inbreeding, however, is also affected by the density of deleterious alleles. In geographically restricted species, the higher natural level of inbreeding can result in purging selection that leads to a much lower frequency of accumulated deleterious alleles than in highly social and gregarious species like humans and dogs. Hippos appear likely to be such a species, as well as having overall lower genetic variation than other large African mammals, suggesting a fairly recent expansion.
In short: it hasn't been that many generations, and if the inbreeding sensitivity of hippos is indeed fairly low to begin with, it may indeed be that there simply isn't any significant impact from inbreeding at this point in time.