Why is cannibalism not an evolutionary stable situation?

Cannibalism is incredibly common in nature. There are more species that eat their own kind than do not. Chimps eat other chimps. Lions eat other lions. Wolves eat other wolves. Prairie dogs go into the burrows of other prairie dogs and eat their babies to get the protein-rich meals needed to produce milk for their own litter. The only animals that don't regularly engage in cannibalism are some birds, and that is more because they physically cannot fit other members of their species down their throat than any moral qualms.
However, cannibalism is typically a bad evolutionary strategy, long term. For several reasons...

in a dioecious species (i.e., one with two sexes), cannibalism means a 50% chance of eating a potential mate and losing the opportunity to pass on your genes
diseases are more likely to transfer between species the more closely related they are. If you are a cannibal you are eating a species with a 99% similarity to you and are more likely to get diseases or parasites. Like kuru/mad cow/chronic wasting disease.
it precludes social behavior and all its benefits. Why engage in mutually profitable behavior when you can just eat those around you? This is thought to be one reason why pack-hunting is rare in some groups of vertebrates like monitor lizards.
on a broad-scale evolutionary perspective, cannibalism means removing members of your own population from the gene pool. It may be good for the individual but it's bad for the species as whole
cannibalism means you are feeding on an animal that is potentially your own size. That's a bad strategy in general. Most cannibalism in nature tends to be adults eating infants or adults scavenging carrion of their own species. By contrast predators are normally larger than their prey, with a few exceptions like pack-hunting wolves and lions.


Is there a comprehensive life science techniques/methods database?

There's Benchfly, which is a video-based protocol library:

http://www.benchfly.com/video-protocols.php

There's also JOVE, which is a peer-reviewed video journal that sometimes covers protocols:

http://www.jove.com/


How good are the hematologic parameters (e,g, IL6 or others) in predicting which patients will develop a severe COVID-19 disease?

A recent pre-print has studied this by measuring 86 accredited diagnostic parameters and plasma proteomes at 687 sampling points, in a cohort of 139 patients during hospitalisation.

We identified 26 protein biomarkers and 14 routine diagnostic markers
(Fig. 4a, Supp. Fig. SF20) that correlate with the time between the
first sampling point and release from inpatient care. The proteomic
signature associated with longer duration of inpatient treatment and
hence more severe COVID-19 progression includes upregulated components
of the complement system (C1QA, C1QB, C1QC) and reflects altered
coagulation (KLKB1, PLG, SERPIND1) and inflammation (CD14, B2M,
SERPINA3, CRP, GPLD1, PGLYRP2, AHSG).

They used a learning classifier to then predict survival in critically ill patients:

In a last step, we established a machine learning model based on
parenclitic networks52,53 (Methods) to predict survival in critically
ill patients (WHO grade 7, n=49) from the proteome of the earliest
single time point sample at WHO grade 7 for a particular patient. On
the test subjects (the data of whom were excluded when training the
machine learning model), high prediction accuracy was achieved, with
AUC = 0.81 for the receiver-operating characteristic (ROC) curve. Of
note, the model correctly predicted survival or adverse outcome weeks
in advance (median time from prediction to outcome 39 days,
interquartile range 16 - 64 days).

The 'predictive power' can be captured (not in a perfect way) by the AUC value - a value of 0 has the worst power to separate patients and 1 has perfect power, so 0.81 is pretty good overall. I haven't read the paper fully, but from a brief scan it looks as though their methodology is at least reasonably sound.


Good question--I think the first point to address is "a means to an end" seems to imply willful action. That is, evolution (according to Ridley) would be a conscious effort by a species to optimize the gene pool for survival of future generations; a rationalization for each species to mutate and diverge.

This is not the case, for a couple of reasons. First, evolution is largely due to environmental factors that exert much more control over the genetic drift of a species than any internal (i.e. willful) factors, such as sexual selection. Additionally, optimal performance is often sacrificed for the sake of reproduction (peacocks, now functionally flightless). All sexual selection happens in the context of the organism's environment--phentoypes can change, but if there's only one food source on your island, it's the limiting factor and will exert strong evolutionary pressure to maintain certain traits.

Second, no evolutionary trait is guaranteed to push the species towards a so-called optima. The influence of sexual selection on populations has left many species (again I lean on peacocks as an example) expending energy on developing traits that do not make them more viable or "optimized" as an organism, but instead make them more desirable mates and thus more likely to reproduce and pass on their genetic material. Peacocks could be much more resilient to predators without all that extra plumage, but they've traded off flight for mating success.

Finally, as an aside, evolution happens on such a large timescale that individual populations would barely be able to change their genetic makeup in the course of a single lifetime. This point is not as robust, but if general societal consensus was driving evolution, there would be extinct species littering the corners of the planet. Ridley seems to have missed the mark a little--nobody is doing anything to cause evolution; evolution happens to you over many years of mutations and environmental pressures.


Original Answer

It looks to me like a species of sculpin, for example, the "short-horned sculpin" Myoxocephalus scorpius.

http://www.luontoportti.com/suomi/en/kalat/short-horn-sculpin

Best answer

After some deliberation, and it appears the other very good answer was for some reason removed: the OP fish appears to be a northern sea robin Prionotus carolinus.

This conclusion comes from the aid of user chauxvive, so much thanks for the identification, though his answer is oddly gone. The conclusion is based off of (1) the morphology of the head and face plate, (2) the longer and tapered pectoral fins, (3) the distinguishing long feelers at the sides anterior to the pectoral fin, and (4) the more probable distribution.


What determines the reversibility of cell of G0 phase in cell cycle?

The answer is quite complicated. One of the major issues in understanding what factors drive senescence vs quiescence has been the absence of a clear, uniform molecular definition of senescence. That said, multiple tumour suppressors, including p16 (and the other genes that occupy the INK/ARF locus) , as well as TP53, can modulate the expression of senescence associated transcriptional programmes.

Additionally, epigenetic remodelling, including heterochromatinisation at E2F target genes (which are a major driver of cell cycle progression through the S phas) , is also known to be a feature of senescence.

A very good starting point to survey the literature surrounding the topic is https://www.nature.com/articles/nrc3960?message-global=remove


primary structure
focus = peptide bonds (because these link the amino acids
The sequence of amino acids, for example AGGVHIL..

secondary structure
focus = H-bonds between the parts of the backbone
 There are several different types of secondary structure (α-helices, β-sheets, etc.). However the most import thing to remember is that the secondary structure refers to the the patterns of hydrogen bonds formed between amine hydrogen and carbonyl oxygen atoms contained in the backbone peptide bonds of the protein

your confusion
You are partly correct from a very simple perspective you can see the secondary structure of β-Sheets just as connected primary structures. However when talking about a piece of secondary structure you have to take the hydrogen bonding into consideration as this is what connects your primary structure parts (β-strands) to form a β-sheet.


It depends.

It's likely that another point starts setting the pace instead of the SA node. More infos about cardiac pacing on Wikipedia

Or maybe different points try to set the pace contemporary, without generating a valid contraction but only electrical activity (such as in atrial fibrillation/AF, a very common disease mostly in elders).

An electrocardiogram could answer the question for the specific patient. If there is completely no atrial activity you'll find no P waves (no atrial activity) or baseline continuous little waves (in case of AF because of the irregular atrial activity) and probably bradycardia (because the pacer in the AV node is slower than the SA node).


How does mass spectrometry detect histone methylation?

It is not simple MS, it is tandem MS. They send the sample through multiple MS and they fragment it between them. So they can get info about the molecular structure as well, not just the mass/charge of the molecule.

A quote from your article:

  MS/MS spectra of the methylated H3 protein (top down) and fragments
  upon electron transfer dissociation fragmentation. Fragments of the
  methylated H3 have a mass shift of 42 starting at C14, indicating a
  modification site at the K14 at the N terminus of the peptide.
  Normalized collision energy = 35%, activation Q = 0.250, activation
  time = 100 ms, accumulation time = 5 min.

A reference from your article:

  Frese et al., 2011 C.K. Frese, A.F. Altelaar, M.L. Hennrich, D.
  Nolting, M. Zeller, J. Griep-Raming, A.J. Heck, S. Mohammed

  Improved peptide identification by targeted fragmentation using CID,
  HCD and ETD on an LTQ-Orbitrap Velos

  J. Proteome Res., 10 (2011), pp. 2377–2388


Can the innate immune system defeat a pathogen by itself? Fast enough that we don't develop antibodies, etc.?

Generally antibodies are formed, but it is possible that innate immune system has cleared out the pathogen. But antibodies will be formed even after that, as adaptive immune system has received  the stimulating signals from helper T cells, which are matured during the innate immune responses triggered by an infection.
This signal triggers B cells to produce antibodies. Antibody production is activated because of signals from innate immune system.

So, even if infection is cleared by innate immune system, still antibodies will be synthesized.

Reference:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3399021/

https://medicalxpress.com/news/2020-05-dont-antibodies-immunity.html


Why do physicians try to match HLA complexes for organ transplant?

Cells with low MHC1 or non-recognizable MHC1 are destroyed by NK cells, so e.g. viral infections, intracellular bacterial infections and cancer cells cannot hide with their "abnormal" proteins...


Selection on linked loci in a diploid population

These equations describe how the haplotype frequencies will change over time due to a combination of recombination and natural selection.

Before I proceed, I need to change your four $\delta X_i$ formulas above. Lewontin and Kojima (1960) writes the equations as:

$$\Delta X_i = \frac{X_i(w_i - \bar w) \pm Drw_{14}}{\bar w}$$

where the minus sign is used for $i = 1,4$ and the plus sign is used for $i=2,3$. (See also this chapter by Sergey Gavrilets.) Decreasing the frequency of a haplotype through recombination will necessarily increase the frequency of a different haplotype (adjusted by selection).

$D$ is the measure of linkage disequilibrium. It ranges from $-0.25$ to $0.25$ and indicates how much the haplotype frequencies deviate from an expectation of no linkage ($D=0$, the loci are independent).

First, assume no natural selection. That is, $w_i = 1$ and therefore ${\bar w} = 1$. When fitness is equal, the equations reduce down to

$$\Delta X_i = \pm Dr$$

Some recombination will occur between the linked loci proportional to the distance between them. In a large randomly mating population with no selection, $D$ will eventually decay to zero.  The larger the value of $r$, the quicker that decay will occur. Eventually, the haplotype frequencies will appear as if they are not linked. (See this figure.).

For example, assume that $A$ and $B$ are linked, with these four haplotype frequencies:

$$A_1B_1 = 0.5$$
$$A_1B_2 = 0.38$$
$$A_2B_1 = 0.05$$
$$A_2B_2 = 0.07$$

In the absence of natural selection and assuming that $r=0.1$, then $\Delta X_i = \pm 0.0016$, again with plus or minus depending on the value of $i$. This is the rate the frequencies will change each generation.  As $r$ decreases, the rate of decay decreases.

Differential fitness among the haplotypes will also affect the rate of decay. The fitness interactions among loci on the same chromosomes and between homologs can get rather complex depending heterozygote advantage, epistasis, etc. (see Lewontin 1964 for several fitness models).

The equation $w_i = X_1w_{i1} + X_2w_{i2} + X_3w_{i3} + X_4w_{i4}$ is the average fitness of the each haplotype in combination with all the other possible haplotypes. For example, for $w_1$, you're calculating the average fitness of four genotypes: $A_1B_1/A_1B_1$, $A_1B_1/A_1B_2$, $A_1B_1/A_2B_1$, and $A_1B_1/A_12B_2$.

I am uncertain why $w_{14}$ is used in the second term of the numerator. I thought it might be because that combination is heterozygous at both loci so recombination generates all four possible haplotypes. However, both Lewontin and Kojima (1960) and Lewontin (1964) use $w_{11}$. It may also be that a relative fitness component is necessary for comparison so the fitness of any one of the genotypes could be used there. I don't know.

Regrdless, as a simple example to illustrate the effects of selection, assume $r=0.1$, $\bar w = 0.5$, and $w_{14} = 1$ (heterozygote advantage, given maximum relative fitness). For $w_1 = 0.9$ then $\Delta X_1 = 0.397$. Selection strongly favors this haplotype in all genotypic combinations so it will increase in frequency.  For $w_1 = 0.3$ then $\Delta X_1 = -0.203$. The haplotype is selected against and decreases much more rapidly, relative to no selection at all.  The same idea would apply for the other haplotypes.

References

Lewontin, R.C. 1964. The interaction of selection and linkage. I. General considerations; heterotic models. Genetics 49: 49-67.

Lewontin, R.C. and K.-I. Kojima. 1960. The evolutionary dynamics of complex polymorphisms. Evolution 14: 458-472.


How does a cell distinguish left from right?

Developing symmetry is is just a matter of Homeotic genes creating axial patterning, genes that produce a chemical gradient across a cell or group of cells. This is how developing organisms orient individual cells, up, down, left, right, anterior, posterior, medial, lateral, are all just gradients of different chemicals, the cells can detect the difference in concentration one one side or the other to orient itself. Most of these start getting produced when the embryo is only around a few cells so there is not much room for ambiguity.  Later more homeotic genes are added to create gradients for things like segments and limbs. Note polarity is often exhibited in a single cell, even in single celled organisms, this is a chemical gradient that orients the inside of the cell, this can easily be turned into orientation of dividing cells.

As for why things move away form this symmetry that's easy, evolution can mostly only work with what it has, evolution is about good enough not perfection.  Often good enough creates a kluge, a rube goldberg type solution then descendants then get stuck with. The earliest vertebrate ancestor pikaia is completely symmetrical even down to the gut,  A fish is nearly perfectly symmetrical, with the only deviation being to increase the length of the gut without increasing the length of the fish, which would waste a lot of material The solution is to coil and pack the intestines instead of having a straight line. This does not just happen in vertebrates you can see these solutions again and again in mollusk, insects, and even echinoderms, keeping the body compact while making the gut longer means asymmetry. As Some organisms progressed further and further away form the "fish" body plan alteration would result in asymmetry. Lungs for instance force a big asymmetry because you are taking what was a simple one way path into two divided systems, blood now has to return to the heart twice before making a complete circuit. More energetic animals specialize even further abandoning or partitioning part of the circulatory system to close off these two parts entirely so they can have high pressure blood flow without exploding their lungs. Now asymmetry is not a bad thing limbs and sense organs stay symmetrical because there is a stronger evolutionary pressure to keep them symmetric, moving with asymmetric limbs wastes a lot of energy (try running with only one shoe on).

Image sources.


Finding Rna-Seq dataset for C. Elegans (Caenorhabditis elegans)

Go to NCBI-SRA or GEO and search for RNAseq data. Set organism as C. elegans and optionally any other keywords that you are interested in. This search term will give you all RNAseq data in SRA from C. elegans: ("caenorhabditis elegans"[Organism]) AND "strategy rna seq"[Properties]

You will generally find files in fastq format which you can easily convert to fasta. There are many tools that do that; you can also do it with your own script. Following awk command will do the job:

awk 'NR%4==1{print ">"substr($0,2)} NR%4==2{print}' data.fastq > data.fasta

Apart from SRA you can also look at ENA (European Nucleotide Archive) and DDBJ


Are viruses more common due to modernity?

Short answer: there are a lot of viruses, and they're all different. The answer to your question is going to be "it varies by virus". Some of the ways population density and urbanisation affect virus transmission are summarised very briefly below.

Population density

Any pathogen's ability to sustain itself relies on every infection causing, on average, at least one other infection. This is called the basic reproduction number or R0. The transmission rate of a pathogen depends on its transmission mode, but with some modes of transmission (like droplet transmission, a major route of transmission of viruses that cause the common cold) population density is important. There's an excellent explanation of density- versus frequency-dependent transmission here. This means that as people live at higher densities, the potential for transmission of some viruses increases purely because of that difference in density, while it has little effect on other viruses.

Critical community size

However, transmission rate is only part of the story. Assuming infected people eventually become immune, a pathogen can burn itself out before new hosts are born or immunity is lost. Stochastic effects become more important in small communities, and there is a critical community size below which pathogens tend to go extinct. Small or isolated communities cannot sustain the virus causing measles, for example.

Urban environments and transmission (and vector-borne diseases)

Urban environments aren't just higher density, they are different in potentially important ways. For example, some viruses need to be transmitted between vertebrate hosts by arthropod vectors like mosquitoes. If you don't have the mosquito, you can't get the virus. Viruses like yellow fever virus, dengue virus and Zika virus are primarily transmitted by Aedes aegypti, which nowadays breeds preferentially in urban environments, so as urbanisation increases the potential for transmission of these diseases also increases. Without adequate sanitation, the potential for faeco-oral transmission also increases at high population densities, for example. Things like sewage treatment, air conditioning and exposure to wildlife all affect transmission in important ways.

So, basically, it's complicated.


I am not sure if such a complete list exists. There are some lists available, which look pretty complete. Have a look at Labrat and Microbexpert. There is also a book available, which contains an approved list of bacterial names, see here. Otherwise you can of course search your way through PubMed and see, what comes out.


Is there any math formula that can be used to describe shape of leaves?

There are algorithms which can be used to describe leaves, if that is what you mean.

The following description takes into account that leaf shape is not solely a function of genetics, but is also effected by environment. It also models how different growth rates within the cells have consequences. Mutant, cloning cells are also factored into the description.

The mathematical model has interesting allometric implications.

Here is a very readable paper (PDF),which endeavours to describe differences using mathematics and for which for which we can thank Cornell University Library for hosting the paper and Lawrence Livermore National Laboratory.


This is basically the same solution as @AlanBoyd's answer, but since he asked me to, I will post my solution as well (also a reason to try out $\mathcal{MathJax}$ a bit more).

Assuming:

$f(A)=p=0.3, \\f(a)=q=0.7$

and the standard formulas:

$f(AA)=p^2\\
f(Aa)=2pq\\
f(aa)=q^2$

gives these genotypes in the parental generation (G1), before and after selection (using the fitness vector $w$):

$$
\begin{array}{c|cccc}
\text{genotype} & \text{freq G1} & w & \text{freq breed.pop} & \text{freq breed. rescaled}\\
\hline
AA & 0.09 & 1 & f(AA)\cdot w_{AA}=0.09 & 0.119\\
Aa & 0.42 & 1 & f(Aa)\cdot w_{Aa}=0.42 & 0.556 \\
aa & 0.49 & 0.5 & f(aa)\cdot w_{aa}=0.245 & 0.325\\
\text{sum} & 1 & & 0.755 & 1
\end{array}
$$

The genotype frequencies in the breeding population (rescaled so that they sum to one) are then used to calculate allele frequencies as:

$$f(A)=f(AA)+\frac{f(Aa)}{2} = 0.397\\
f(a)=f(aa)+\frac{f(Aa)}{2} = 0.603$$

These are then used to calculate the genotype frequencies in the next generation (G2), using the same HW-equations as in the beginning:

$$\begin{align}
f(AA)&=0.397^2=0.158 \\
f(Aa)&=2\cdot0.397\cdot0.603=0.479 \\
f(aa)&=0.603^2=0.363 \\
\end{align}
$$

I do not understand where the given answer $f(Aa)=0.435$ is coming from.


If I understand you correctly what you are saying is

  There is envrionmental variance and epigenetic variance underlying the phenotypic variance. There can even be a covariance between the envrionment and epigenetics.

Yes, this is true. You might want to have a look at this intro post to quantitative genetics.

Note, there are several definitions of epigenetics. Epigenetic effects are some kind of factors that affect phenotypic variance and that are external to the DNA sequence. Often we think of modification directly on the nucleotides on on the histones (such as a methylation on the histon tail) but we sometimes also extend this context to include all the stuff that is the in the zygote or sometimes even further. In its broadest sense, the term "epigenetics" would be a synonym of "environment".


The variance of a trait's allele frequency can follow different trends over time depending on several factors such as whether one or several of the alleles are consistently selected for or the population dynamics. For example Disruptive Selection will tend to increase the allele variance. On the other hand Directional selection, or Stabilizing selection will tend to decrease variance by driving the allele frequency to one side of the distribution (in the first case) or by "cutting down" its sides in the second case. It is true that stabilizing and directional selection processes are more common especially under relatively stable environments. Therefore for the majority of cases, during the first phase of selection for a trait variance will most commonly decrease . This, however, is not a rule.
There are additional, rare, but from an evolutionary point of view extremely important cases where allele frequency variance can see a sudden "ballooning". Consider for example the case of selection processes after mass extinction events. Then, because of the sudden availability of previously occupied niches, genetic drift due to small population sizes as well as changed conditions the previously stabilized traits will start...well...drifting. The same is true for almost any circumstances that will destabilize equilibrium and lead to speciation.


Scaling is not the same as normalization.  You have empirically discovered how scaling affects PCA, and it's purpose is to control whether large peaks dominate the analysis or not.

Normalization on the other hand is typically done when samples were in a solvent and the concentration could vary due to the extraction method, the hydration of the tissues etc.  So normalization tries to compensate for these varying concentrations.

Normalization would normally be applied across the peak intensity vs time dimension.  Two typical normalization schemes are 1) normalization to constant sum (usually 1) and 2) Probabalistic Quotient Normalization which uses a slightly more complex approach (and is frequently preferred).  I don't work with LC-MS data, there may be other methods that are preferred with this type of data.  Whatever software you are using probably has several options built-in.

Probabalistic Quotient Normalization is reported in F. Dieterle et. al. Analytical Chemistry vol. 78 pages 4281-4290 (2006). The exact same mathematics are called "median fold change normalization" by Nicholson's group, reported in K. A. Veselkov et. al. Analytical Chemistry vol. 83 pages 5864-5872 (2011).


When are neuropeptides loaded into vesicles?

Neuropeptides are packaged in the soma via the Golgi into dense core vesicles, similar to how other types of secreted proteins are packaged.

These vesicles are transported to axon terminals where they await release signals.

Sossin, W. S., Fisher, J. M., & Scheller, R. H. (1989). Cellular and molecular biology of neuropeptide processing and packaging. Neuron, 2(5), 1407-1417.

Wong, M. Y., Zhou, C., Shakiryanova, D., Lloyd, T. E., Deitcher, D. L., & Levitan, E. S. (2012). Neuropeptide delivery to synapses by long-range vesicle circulation and sporadic capture. Cell, 148(5), 1029-1038.


How accurate does the alignment of molecules in DNA have to be?

In the case of replication the parent strands do not pair up back into the original helix. Instead, as your picture and the one below show, the complementary bases are paired up on one of the parent strands, resulting in two copies, each with one parent strand and one new one.

Source: Kathy's webpage on DNA


Why do germs live longer on surfaces than on skin?

because some skin cells which are alive , secret fat and other materials , these materials make the skin acidic , and acidic environment is not good for many germs , on the other hand , there is an enzyme in  sweat (lysozyme)which destroy the wall of bacteria


(Non-expert-question) What exactly do chloroplasts do when they "convert light into chemical energy"?

I see you've given this a try, so here's a synopsis hopefully appropriate to both your current knowledge level and curiosity.

Light excites electrons in chlorophyll to a higher energy. Higher energy means less stable, those electrons want to return to a state of lower energy. The chloroplast is structured in such a way that the electrons, instead of just plopping back to the lower energy state in the chlorophyll to liberate the light they just absorbed, are handed off to another molecule. As the electrons get passed off to other molecules, they lose energy. All of this is taking place on a membrane within the chloroplast. The energy being "lost" by the electrons is harnesed to pump hydrogen ions across that "thylakoid" membrane in the cholorplast. The increased concentration of H+ within the thylakoid space is another form of energy that can do work. The work done is the creation of ATP.

We're not done with those electrons yet. They get passed off to yet more molecules, losing energy again in each hand-off. This energy is used to create additional energy-rich substances that will power the creation of energy-rich organic molecules in a process termed the Calvin Cycle. The Calvin Cycle, which creates the sugar G3P from inorganic CO2 from the atmosphere, also takes place within the chloroplast.

So, the chloroplast is a multi-talented factory for the conversion of CO2 into sugars. These sugars provide both energy and carbon, in a useable organic form, for other processes in the plant. Chloroplasts also contain DNA. This, and other evidence, suggests that chloroplasts, like mitochcondria, were once free living organisms that got co-opted by other organisms and now exist within cells in a mutualistic association (the Endosymbiont Theory).


Why is cancer more lethal than (hypothetical)infections?

Cancer is not inherently more lethal than bacterial infections. That's simply an artifact of the time we live in. Broad spectrum anti-bacterial drugs we invented in the 1st half of the twentieth century. Before that, most folks died of infections. Cancer was relatively rare because most folks didn't live long enough for cancers to become apparent.

Why do we have generic drugs for bacteria and not for cancer?  Largely because bacteria are not eukaryotes and we are. The biology of bacteria and human cells are so different that it's relatively easy to find drugs that dramatically affect bacteria, but not people. I say relatively easy, but still took several thousand years of human history to figure it out.

Because cancer cells are just variations on our normal cells, it's very hard to find something that kills the cancer cells, but not the rest of us. That's why chemotherapy makes folks so sick: the chemotherapy agent is killing, or significantly impairing, fast growing healthy cells along with the cancer cells. The most successful cancer drugs have identified rare metabolic pathways that are important to specific types of cancer, but not so important to healthy cells.


Short answer: You need to buy some more, but you need the sequence also for ordering.

Long answer: The Taq polymerase needs a piece of DNA (or RNA) to prime the reaction and be able to enlarge the DNA chain, this is why we use primers in the first place (also to ensure reaction specificity to the region we want to amplify). To enable the reaction you would need a primer complimentary to the one you used of about the same length (or at least not much shorter), so this actually doesn't really make sense, because you would have to have a primer to make your primer. Since primers are cheap today, order some more.


Yes, you have to count every individual colony.

However, in practice the question is more, what is deemed a countable plate and how important is it. In many laboratories you will find that technicians and scientists won't bother to count each and every colony on the plate if you have a visibly high number of colonies. They will for example simply say (with a bit of experience), the count for this plate is greater than 300 (write >300).

Nevertheless, you will of course still need a count, so it is common practice to do one of the following:

Split your plate into sectors of equal size (you can draw lines on the bottom of the plate), count all colonies in one sector and then multiply this number by the number of sectors you have divided in. So, say, you have split your plate into 4 sectors (quadrants) by drawing a big cross on it, you would count the colonies in one quadrant and then multiply by 4. This is obviously an extrapolation.
The other option, is to dilute your sample until you get it within countable range. So you could do a serial dilution, put it onto plates and then once your organisms have grown you can count the entire plate and then multiply by the dilution factor. So, say, for example you have your sample in an enrichment broth and do two 1/10 dilutions (1/100) and then plate out 0.1mL (counts as 1/10), you have a final dilution factor of 1000. So you would need to multiply the count that you get on this imaginary plate by 1000.

In your sample you obviously have a variety of different organisms. It is probably advisable to check official methods for what they recommend. Here is an excerpt from the official BAM method for Yeasts, Molds and Mycotoxins:

  Count plates after 5 days of incubation. If there is no growth at 5 days, re-incubate for another 48 h. Do not count colonies before the end of the incubation period because handling of plates could result in secondary growth from dislodged spores, making final counts invalid. Count plates containing 10-150 colonies. If mainly yeasts are present, plates with 150 colonies are usually countable. However, if substantial amounts of mold are present, depending on the type of mold, the upper countable limit may have to be lowered at the discretion of the analyst. Report results in colony forming units (CFU)/g or CFU/ml based on average count of triplicate set. Round off counts to two significant figures. If third digit is 6 or above, round off to digit above (e.g., 456 = 460); if 4 or below, round off to digit below (e.g., 454 = 450). If third digit is 5, round off to digit below if first 2 digits are an even number (e.g., 445 = 440); round off to digit above if first 2 digits are an odd number (e.g., 455 = 460). When plates from all dilutions have no colonies, report mold and yeast counts (MYC) as less than 1 times the lowest dilution used. Isolate individual colonies on PDA or MA, if further analysis and species identification is necessary.

Please see link here.


Aren't current explanations for the evolution of human cooperation a little too reductionist?

Interesting question!

I think that in terms of 'tribal' fitness, altruism would be strongly selected for, as communities would tend to be quite small (relative to, say, a town today). In modern civilization cultures have developed differing levels of altruism, but I imagine this is a result of upbringing rather than inherent differences in tendency toward altruistic actions.

So in my opinion you cannot rule out altruism being selected for because it is clearly an advantage (in terms of survival / fitness) in smaller communities - we just don't live in that kind of society any more; people don't have to be altruistic to get by, and this kind of mind-set can 'evolve' culturally, outside genetics. But on the whole I would still argue that most people are inclined toward altruism - ether because they feel naturally inclined to help others, or feel that by helping others some benefit (such a reputation) would be bestowed upon them (the former may be the same as the latter, but at an unconscious level).


What are the differences between the margins of the lateral and medial condyles of the tibia?

The proximal end of the tibia is broad and flat known as tibial plateau. The intercondylar region crosses through the midline of this plateau, separating the medial and lateral condyles of the tibia.

The two condyles are in form of flat and broad surface for articulation with the medial and lateral condyles. The medial surface  is convex and subcutaneous. The lateral surface, also known as articular surface is smooth surface and somewhat concave, and articulates with the talus.

[Sources:
https://www.physio-pedia.com/Tibia
http://en.wikipedia.org/w/index.php?title=Medial_malleolus&oldid=240146811
http://www.bartleby.com/107/61.html ]


Machine learning for light microscopy -- problems to solve?

I know this question is going to close. But, if you want to work something you can work on:

Cryo super-resolution fluorescence imaging

  Highlights

  CryoFM allows imaging of vitrified biological samples with fluorescence microscopy.
  There are significant challenges to achieve high-resolution cryoFM imaging.
  Fluorophore characteristics at low temperature offer additional advantages.
  Cryo super-resolution fluorescence imaging will give dramatic resolution improvement.

Source: Fluorescence cryo-microscopy: current challenges and prospects.


I don't know the exact half-life of this special Pfu polymerase, but generally Pfu polymerases are pretty stable. This source gives a half life of 18-25 hours at 95°C, meaning you keep the enzyme at 95°C for the whole time a you still have 50% activity after that time. Since you don't do that, I wouldn't worry too much about the activity. To be safe, you can add an extra long (probably 10-15 minutes) single amplification step before cooling down.


First,do you have any probe that your type is AB chimera transferase? I discovered it because my mother is type AB and my brother type O. I have 2 sisters and my self cis-AB (my younger sister and me rh-). If you carried a cis-AB allele and another allele was  B1, surely you got A and B type compatible, but if you carried an A1 or O1 allele, surely you got O type compatible or worse luck. For example, I have a very rare multi-blood genotypes (rh D- C-G-, K1-, M+N-S+s+ and another unknown antigen). Actually, it doesn't matter if you are cis or trans AB phenotype, the most important thing is to know if another 34 blood groups and 200 minor groups and 600 blood antigenes have a rare combination that makes blood incompatibily or autologous like Bombay phenotype or autotransfusion like me.
If you want to be sure about your genotype, you must make dna test with SNPs of 10 cis-AB alleles


According to Wikipedia in 1998 a vaccine was approved by the FDA. It was directed against the outer surface protein A (OspA) of B. burgdorferi, but was taken from the market in 2002 after a large number of recipients reported the development of autoimmune diseases. An investigation of the FDA and the CDC found no connection to these claims, but afterwards the sales went to the bottom until the vaccine was withdrawn from the market. An interesting article on this story (with a number of references) can be found here.

There are two new approaches to develop vaccine candidates. One is directed against the outer surface protein C ("An octavalent lyme disease vaccine induces antibodies that recognize all incorporated OspC type-specific sequences.", another against glycolipoproteins on the bacterias surface ("Synthesis of an experimental glycolipoprotein vaccine against Lyme disease."). As far as I see, none of these vaccine candidates is already licensed.

Another approach is to vaccinate the animal reservoir hosts, as this has been done successfully for rabies. Here either vaccinated baits ("Reservoir Targeted Vaccine for Lyme Borreliosis Induces a Yearlong, Neutralizing Antibody Response to OspA in White-Footed Mice") or recombinant vaccines ("An ecological approach to preventing human infection: Vaccinating wild mouse reservoirs intervenes in the Lyme disease cycle") were used with good results. Neither of these methods is already been used, as far as I see.


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

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

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

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

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

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

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


What is the lower temperature limit for ion channels function?

The lower temperature limit of ion channels likely is dependent on various factors, including the type of channel and the recording conditions (tissue type, medium etc.). Reports on the suppression of voltage spikes (i.e., the inhibition of action potential firing) range from 1 to -20oC in squid axons, dependent on the species (Leuchtag, 2008). I couldn't find information on specific channels.

Reference
- Leuchtag, Voltage-Sensitive Ion Channels: Biophysics of Molecular Excitability (2008)


Why does the cloned cat, CC, exhibit mosaic fur color?

There are mechanisms through which the X-chromosome that has been turned into a Barr-body can be re-activated. This happens during cloning, but is also seen in some cells that turn into cancer cells. This paper discusses a lot of intriguing lessons we've learned from transplanting nuclei from one cell to another in frogs and mice.

Interestingly, though the succes rate of cloning is surprisingly low (see this paper), but it is equal for male and female clones. This implies that the failure to turn a Barr-body into an active X-chromosome does not contribute significantly to cloning failure.

Of course, if the Barr-body gets re-activated again and turns into a normal X-chromosome, that means that later in embryonic development it can get de-activated again (at random, as is normal in cats), leading to mosaic phenotypes such as the calico. The inherent randomness in this process (at least in some animals, such as cats) means that the calico pattern of the clone is highly unlikely to resemble the calico pattern of the original.


What are some difficulties animals had to overcome to reproduce on land?

The disadvantages you mention have not much to do with reproduction, but with locomotion and oxygen absorption.

Difficulties to reproduce on land are the fact that aquatic egg-producing creatures typically lay soft eggs with porous shells to promote exchange of water and waste products with the surrounding water. Water is essential for growth as a typical creature consists for some 70% of water. Soft-shelled porous eggs when laid on on land dry out very quickly and are prone to predation.

The main adaptation to reproduce on land instead of water has been the development of the amnion. The amnion is basically a membrane filled with water (the amniotic sac) in which the embryo is immersed during development. Hence, you could argue that the transition to land in terms of embryonic development has never taken place, as the embryos develop in a protected aqueous environment contained within the amnion! The early amniotes laid eggs on land where the embryos develop, while the later ones such as humans carry their embryos/fetuses around. But early as well as late amniotes are characterized by a developing embryo immersed in a watery environment contained in the amnion. Other structures that aided the transition to land were eggs with hard shells, and the allantois. A hard outer shell in amniotes that lay their eggs on land  helps to protect them against drying out, the harsh terrestrial environment and predators. The allantois helps to exchange and store waste products produced by the embryo, a structure not needed when eggs are immersed in water and waste products can diffuse freely through a weak and porous shell.


Behavioral change in dolphins during different hemispheres activity periods?

Sleeping is a biological stage which we presume as a relaxation period but its really a highly functional stage for brain. Most of the memory related processing such as management of working memory and cognitive functions such as decision making, reasoning, and episodic memory are closely related with sleep.

Dolphins never sleep in the sense that we do, CORRECT, because we close our both eyes and enter into a stage of decreased ability to react to a stimuli. But in the case of dolphins they need to breath, so by fully entering into a sleep stage like us is suicidal in their case.
Dolphins have a specialised way of dealing with this problem, they do a "unihemispheric slow-wave sleep". They only sleep with one hemisphere of the brain while the other being active, when the right hemisphere is sleeping the left eye is closed and vice-verse, as the right hemisphere controls the left part of the body. The observable change in their behavior is visible from the closed single eye.

Humans and dolphins had a common ancestor that lived 95 million years ago. During the last 50 million years dolphins have been evolving in water and their brain evolution had taken a different route. The neocortex, the outer most layer of brain which is considered as the recent evolved part of brain. The neocortex is actively developing in both humans and dolphins, one of the most striking features among them is that human neocortex is having large thickness and dolphins are having thin one with more folds than ours. The folding in neocortex is a technique to increase its surface area. This substantial difference is due to the evolutionary divergent way both the species took.

Dolphins have a complex echolocation system and binocular eyes, they need to create the visual and sonar image of their surroundings and studies shown that their increased brain size is due to the tremendous volume of data they need to process for these purposes. Also being a social animal their neocortex consists of connections like us but as we both are evolutionary separated for about 95 million years ago most of the brain areas are diversified and evolved.

  Dolphins showed that they can understand a symbolic, human-based
  language, where the words are either whistles or hand gestures. And
  the dolphins could easily understand that we use different word orders
  to mean different things. So they understand syntax. The dolphin brain
  is arranged in a completely different way from ours, and yet they can
  still understand what we are trying to teach them. Lou Herman also
  showed that dolphins are right up there with humans and chimpanzees in
  being able to understand that when we point at something or look at
  something, we’re meaning “Don’t look at me; look at what I’m looking
  at.” He’s done all kinds of really fascinating things, and his work
  has contributed the most to our understanding of what these animals
  can do.Reference


Why were dinosaurs not as smart as humans are?

We are all equally evolved

All life that exist on earth today had the exact same amount of time to evolve (3.5 billion years). Therefore, one cannot say that one species is more evolved than another one. It just makes no sense (at least if "more evolved" means "have evolved for more time").

Being a dominant species/clade for some time (whatever dominant may mean to you) doesn't make this species/clade more evolved than any other one.

Your question need not be specific to intelligence

You can think of any other phenotypic trait (wings, toxins in the skin, good eyes, good smell, strong leaves, etc...) and ask this same question. You seem to assume that being smart should be some kind of goal or necessary direction toward which species should evolve. Following your reasoning I would rather ask why the hagfishes, the oyster, the lampreys or the turtles are so dumb although they exist for so long (once again remember that this notion that some lineages have existed longer than others is flawed).

You might also want to have a look at: Why evolution should not be equated with progress?

Being clever is not a goal of evolution

Most of these trait have associated cost to the benefice they might bring. For example having a big brain asks for much energy (20% of ATP in humans) and it also has a cost due to its weight. The sperm whale for example has a brain that weights 7.8 kg. Obviously it is not a big cost for such a big animal to carry heavy organs while it would be impossible for a migratory bird to carry such a brain.

taking different evolutionary path This part is not complete!

Now the question of why Homo sapiens are smart while Tyranosaurus rex are not or why wings evolved in bat and not in mice is rather interesting and hard to answer. I can think of 2 main causes:

1) The newly arising trait (which is usually not the trait you can observe today. Big brain did not appear suddenly, first there were individuals they had slightly bigger brains than the other individuals in the population) is not beneficial over the wildtype trait. There are so many parameters that will affect if a trait is beneficial or not. You can think of the predators, the humidity in the environnement, the social structure, the population size, the type of reproduction, the genetic background etc...

For example, think of a species that is fixed, has no social contact, has nothing it can really predict in the environnement. What would an individual from this species do with a brain? Think of a bird that needs to make food stock for the winter. This bird needs to remember where it hide something. It has been found by the way that some birds have an awesome spatial memory, way better than humans.

2) The trait never happen to occur (or never in a strong enough individual, or never in a population big enough to not suffer from to much drift while the trait is at low frequency) just because the necessary mutation never happen. Mutation is just a random process.

For example. It seems rather hard for a tree to have the necessary mutations to have develop a brain! But we don't need to go to such a extreme example. If you split a population of clone mice in two, the two subpopulation will evolve differently (even in absence of genetic drift (infinite population size)) just because  some mutations occur on one side while some others occur on the other side. Or maybe the same mutation might occur but once in an individual that has low fitness and once in a very fit individual.

Evolution of human cognition abilities

So what are the factors that drive humans to evolve big brains? This question is not solved yet. We have many models to explain this but I don't we have much solutions to test these models. The 2 most common models explain big brains

for social purposes (understanding relationship between other individuals, being able to coordinate the movement for a hunt, etc...)
due to sexual selection. Being intelligent would be a proxy for having good genes.

For more information concerning the evolution of human cognition, this wikipedia article might be a good start.

UPDATE

  Why do you think mutation is a random process?

Our genetic data are encoded into a succession of 4 types of nucleotide bases (A,T,C and G). A mutation results from a modification of this sequence such as a replacement of a T by a C. These mutations are due to mistakes usually while duplicating the DNA. Most of these mistakes do not affect the fitness (survival + reproduction ability) of the individual, very often these mutation are deleterious and rarely these mutations are beneficial. Some mutations are more probable than others but nevertheless some individuals have a higher mutation rate than others. In order to make things slightly more complicated, some sequences have a higher mutation rate than others. For example, the sequence AAAAAAAAAAAA is more likely to mutate than the sequence ATGTGCATCTA. But even if some mutations are more likely to occur it is still a random process (we couldn't talk about likelihood otherwise!). Two clones living in the exact same environment that both have a baby at the exact same time wil not create babies with the exact same genome given the randomness of mutations. One baby might have a very bad mutation that will make him die, while the other baby might synthesize (=construct) a new enzyme that increases its digestive capacity.


Yes; she wouldn't necessarily have to be of the same species, but "mitochondrial Eve" must exist. The proof is pretty simple if you assume no one has more than one mother and that some mothers share a mother (and some other reasonable biological assumptions like the finite number of offspring).
Consider all living maternal lineages at any slice of time. This would effectively be a slice of all mothers, let's call it Generation N. In turn, these mothers all have mothers. We can call this Generation N-1. Not all women who have children in this generation are included: N-1 only contains mothers of the Generation N mothers. Generation N-1 must then be smaller than Generation N, because no mother has more than one mother. In practice, it's likely much smaller, since any mother who has more than one daughter who herself becomes a mother reduces the total possible by 1 more. You can recursively go through maternal generations N-2, N-3, etc this way and will find that every successive generation gets smaller. Eventually it will converge to 1 person, and that's your "Eve".
You can think about it similarly in the opposite direction, and find that as you go forward, extant maternal lineages can disappear but once a lineage disappears it cannot come back.
See also the Galton-Watson process.
A lot of "mothers" the same age as mitochondrial Eve have descendants today (in fact, they are likely to be either ancestors of everyone or ancestors of no one), but those lineages did not pass maternally. See also https://en.wikipedia.org/wiki/Pedigree_collapse


Flies can and do evolve quickly thanks to a short generational time. However, your question seems to stem from a misunderstanding of what evolution entails.

Evolution occurs when the genome mutates. Why it mutates isn't particularly relevant, but a gene (or genes) mutates and as a result of that mutation a characteristic of the organism changes. It doesn't have to be a big change. Maybe a single protein somewhere operates 2% less efficiently, giving practically no outward signs of evolution. Sometimes it can be big - changes in coloration, changes in sensory perception, lifespan, etc.

In order for mutations (beneficial or detrimental) to have a significant effect across an entire population, the population itself has to be fairly small or the mutation has to give a large advantage over the old version.

Flies are not avoiding motorways because a mutation that specifically codes "AVOID CARS" is going to be very unlikely given that it would you would first have to encode what a "CAR" is in order to avoid it. That probably won't happen because on the time scale that evolution usually acts over very large populations (which flies have) we won't be driving cars by the time necessary for deaths due to cars has a serious effect.

Flies have huge populations and breed extremely quickly, so even if a few million are killed by cars, it doesn't put a dent in their population numbers. There's no reason for the change to occur. Combined with the extreme difficulty of actually encoding a gene specific to cars, the odds are it just won't happen in any realistic time-frame.


Salvaging a plasmid from a cell culture stored at the incorrect temperature

I would rinse the cells off the agar using a small volume of LB or similar rich medium. Then use a small aliquot (10 μl) to inoculate a 5 ml culture under selection to see if anything will grow. Meanwhile the remainder of the cell suspension from the vial can be used as input for your favourite miniprep procedure.

If necessary, the DNA that you recover should then be used to transform a suitable E. coli strain. Don't bother trying to analyse the rescued DNA first since polysaccharide contaminants from the agar will probably inhibit any restriction enzyme that you might use.

Good luck!


Relation between biomass and radius of roots system

Your question specifically asks for an equation which gives root radius and your sample equation is for typical root length, neither of which I'm aware of. However, there is a known relation between the above-ground biomass and the below-ground biomass of a plant, which varies with species and environmental factors. This is the root:shoot ratio.

This is a linear model where the constants represent differences in starting conditions (the intercept) and biomass partitioning (slope).

  Roots and shoots are functionally interdependent and these two systems
  maintain a dynamic balance in biomass which reflects relative
  abundance of above-ground resources (light and CO2) compared with
  root-zone resources (water and nutrients). Whole-plant growth rate and
  root : shoot ratio are thus an outcome of genotype × environment
  interaction, but source of control is ambiguous.

The actual size of the roots - as in their extent - will depend on the soil characteristics, water table, the plant species, etc.

Source: http://plantsinaction.science.uq.edu.au/edition1/?q=content/6-3-1-biomass-distribution


Why does wood become darker when it ages?

While most wood we see comes from stain or oils, wood left on its own will darken.  As far as this article suggests, this is caused by the polymerization of polyphenols from lignin into tannins which are dark red or brown in color when they are highly polymerized.

The specific content of the lignin in different woods will affect the density, strength and color of the wood.

This woodworking reference shows that intense UV exposure to wood will darken it to give it an aged look.


pBR322 is a distant ancestor of pET28a. If you compare the two maps below you will see that they have the same replicon labelled as ori or pBR322_origin.

The map of pBR322 is shown in the conventional orientation: the single EcoRI site is at coordinate 0/4359 and numbering proceeds in a clockwise direction through the BamHI site. The map of pET28a is presented with the pBR322-derived ori element in the same orientation (note the labelling of a pBRrevBam_primer also). Because of the way that the pET vectors were built, this means that in the conventional depiction the expression region runs counter-clockwise.


It is a matter of deduction. We know that:

Viruses entering a cell are capable of making more copies of themselves.
The only part of a virus that actually enters the cell is its DNA (or RNA, depending on the virus in question).

Based on these two facts, we can conclude that the DNA ̣--since it is the only part of the virus to enter the cell-- somehow contains the information necessary to make new copies of the virus and is, therefore, the genetic material of the virus.


You are mixing things. First: Codons have nothing to do with the synthesis of amino acids.

A codon is the sequence of nucleotides on the DNA (or RNA) which code for a certain amino acid. For example UGU and UGC code for the amino acid Cysteine and given these codons it will appear in the protein being synthesized. The codons are basically a way to code the sequence of a protein with the smallest amount of information (simply by the sequence of the four nucleotides in DNA/RNA). For further information have a look at the Wikipedia page on Codons.

This look like this (image from the Wikipedia):


Araucaria araucana is an evergreen. The pictured "fruit" is actually more of a cone (which I don't think you'd want to eat). However, the seeds are edible, and look like this:

Let the cone dry and it should open up.


Exact average molecular weight of a dsDNA basepair

The different protonations forms are considered in the averaged Mw.
Removing two H2O is the step that makes your average different than the traditional 650Da per base pair. But you must remember that the last base pair in the sequence will have it's OH group so you need to add 17.008 gr/mol * 2 = 34.016 gr/mol.
The effect of this changes with the length of your sequence, here is a graph showing it.

Blue line is your calculation and red line is the one from literature.
Literature one is achieved around 60bp (I calculated Mw(63bps) = 617.93) and yours at 10^6.6 (Mw(10^6.6) = 617.3892085)
Why you need this calculation to be so exact? Knowing the length of you sequence and region can help. Remember that some regions are richer in one type of nucleotides (CpG islands, hairpin coding sites)


How long can a human neuron live outside the body in a controlled environment?

According to this paper from 2001, they've got the survival time up to about a year on average. The trick is sealing the neuron inside a permeable membrane so you don't actually risk contamination when feeding. This paper lays out experiments that take many weeks to perform, so as far as I can tell the science of keeping neurons alive has advanced to 'as long as I keep feeding them and nothing bad happens'.


The development of cancer has various reasons. For example in more than 50% of tumors, p53 is mutated. p53 among other things regulates mitosis and forces the cell to arrest in a specific growth state if other systems detected a mutation in the DNA.

But in your special case we have to look at major histocompatibility complexes (MHCs) and NLRC5. There are two types of MHC, namely MHC class I and class II. MHC II presents mostly bacterial peptides to CD4+ T cells causing a immune response. However, MHC I presents viral peptides and peptides from your own body. These peptides are detected by CD8+ T cells which are cytotoxic T cells initializing apoptosis. Without these own peptides natural killer (NK) cells are activated because of a missing-self signal causing apoptosis, too.

Watson et al. (figure 1, Watson et al., Int.J.Cancer, 2006) showed that patients with high MHC I expression or an absent MHC I expression have a higher survival than patients with low MHC I expression. If patients express high levels of MHC I, the chance that these proteins present cancer peptides is higher than patients expressing low levels of MHC I and therefore cancerous cells get killed by cytotoxic T cells probably more often. Without MHC class I, NK cells will initiate apoptosis and cancerous cells will die, too. Patients with low MHC class I expression won´t present so much peptides to cytotoxic T cells and therefore less cancer peptides are presented. But as they have MHC I, NK cells keep inactive. So the cancer finds an escape mechanism in tricking the immune system.

NLRC5 is the biggest member of the NOD-like receptors (NLRs). Expression of NLRC5 can be enhanced by IFN-gamma which activates the JAK/STAT signaling pathway. STAT 1 enhances the expression of NLRC5 and NLRC5 itself can build an enhanceosome with RFX. This enhanceosome raises the expression of MHC class I! NLRC5 is often mutated for example in colorectal cancer. Research now has to focus on how to enhance NLRC5 and therefore MHC class I expression in different cancer types and out of these results to develop an efficient cancer treatment.

I hope that I could help you. Further literature especially on NLRC5 you can find in following paper.

Kobayashi et al., Nat. Rev. Immunology, 2012

Meissner et al., PNAS, 2010

Neerincx et al. (different paper, just google it ;) )

Staehli et al., J. of Immunology, 2015

Yao et al., Protein&Cell, 2012

Of course there are even more, but I think, these paper show a nice overview about this field.


The large lozenge-shaped scales suggest me it could be some sturgeon species. The location is compatible with what Wikipedia says:

  In North America, they range along the Atlantic Coast from the Gulf of Mexico to Newfoundland [...]

Specialists may be able to refine a little more the identification, based on location and visible features.


Why do glial cells of the retina become more abundant the closer they are to the optic nerve?

Any particular glial cell you're noticing this with?

I know that Astrocytes modify Calcium concentrations in the synaptic cleft. Perhaps at places where there are more synapses, more Astrocytes must exist to regulate such thing? Here's an interesting paper on a possible role of Astrocytes on associative networks:

http://www.antanitus.com/


I think it is Chord Diagram. you can see this for more information.

  "A chord diagram is a graphical method of displaying the inter-relationships between data in a matrix. The data are arranged radially around a circle with the relationships between the data points typically drawn as arcs connecting the data." based on the Wikipedia


What is the Importance of Acid Alcohol and Sodium Bicarbonate during staining?

This is described with better detail (and better prose) in John Baker's classic description at StainsFile, but to summarize:  The procedure you're describing is a regressive hematoxylin stain with Harris hematoxylin.  To start off with, let's bear in mind that hematoxylin, a compound from the wood of the logwood tree, is actually used as hematein, by oxidizing it with sodium iodate.  (The colorless hematoxylin would naturally "ripen", oxidize over 4-10 weeks in the presence of air, even without that step, but this is more controllable)  Additionally, aluminum ions are added as a mordant, creating hemalum by binding =O and -OH on the hematein.  The Al atom is what actually binds to something in the nucleus (I found reference to lysine side chains of histone proteins and the phosphate of the DNA - I haven't sorted this part out yet).
When acid is added, it competes with aluminum, which can be thought of as Al3+.  The real bonding may be more covalent than that, but that point is considered controversial.  For whatever reasons, the H+ interferes with the Al3+ mediated attachment of stain to tissue, especially at sites of background attachment (differentiation).  The hematoxylin washes away somewhat, leaving lighter, more specific staining.  (this tactic is called a regressive stain, and is certainly not needed to do the procedure.  This is very much more art than science at this point...)
But ... the acidic hematoxylin has a reddish color, and it isn't as blue as it can be unless it is neutralized to around pH 8 - hence the second step with bicarbonate, though often plain tap water can be used.  That is an ordinary instance of a dye changing color with pH, and can be called "bluing the hematoxylin".


Smallest unit on which selection can act

The smallest unit that can be selected is, of course, the single nucleotide. The most striking examples of this are Single Nucleotide Polymorphisms (SNPs), many of which confer selective (dis)advantages.

To take a simple example, imagine a SNP that introduces a frameshift mutation, rendering a gene incapable of producing its protein. If that protein is something relatively important like p53, the SNP in question will be lethal and will be selected against. So, to take your questions one by one:

What factors influence the minimal size of a sequence to be considered as a unit on which NS acts? Mutation rate, generation time, selection differential for this sequence, recombination rate, ...?

any sequence unit whose alteration can affect fitness is a candidate for NS.

Could we consider a nucleotide as a unit of NS? Why?

Yes, if it can affect fitness (which it can, see above) it can be selected for or against.

How does the quasispecies model fit into the question of what is the smallest unit of NS?

As far as I can tell, it is irrelevant. NS can act on any self-replicating entity as long as the process of replication can produce variation that can affect fitness. If I understand correctly, the quasispecies model simply posits a group of entities with a very very high mutational rate. However, the rate of mutation does not affect the smallest unit that NS can act on, as I said above, anything that can affect fitness will be subject to NS.

Is it worth talking about that? Is this question biologically relevant? Or is it rather a question based on a choice of definition such as "Is a virus alive?"

Yes, it is worth talking about it if you have the misconception that the smallest unit is a gene :). No, but seriously, it is an interesting concept and a very useful tool. The selfish gene hypothesis for example, helped us see the world of evolution in terms of sequences rather than species or individuals. NS did not change, our conception of it did.

These are all useful conceptual tools that allow us as scientists to understand complex questions. However, NS is not a directed or conscious process so it does not care or know what it acts on.

PS. Please do not confuse protein-coding sequences with genes. As I said in my comment, there are many genes that do not produce proteins (tRNA genes for example) and that was even before the waters were muddied in the past few years. The current definition of gene is something like:

  any nucleotide sequence with a job to do

Read the ENCODE papers for a more technical definition or take this one from wikipedia:

  A gene is a molecular unit of heredity of a living organism.

UPDATE: First of all, you have to remember that Dawkins wrote The Extended Phenotype more than 30 years ago, in a time when the only complete genomes available were those of a few viruses. The first bacterial genome was sequenced in the mid nineties and the first human genome draft human in 2000. It was a time when selection was seen as acting at the level of the individual, and the importance of genes was underestimated. Dawkins books were instrumental in bringing genes into the spotlight.

However, if he did argue that a nucleotide cannot be selected (I have not read this particular book) he was simply wrong. A nucleotide can indeed affect its chances of being replicated. Think about it, if you have a G at a given position in the genome, and that G is mutated to an A, then the chances of the original G being replicated are obviously very low. Therefore, the nucleotide 'affected' its chances of replication. Alternatively, a mutation of a single nucleotide in the promoter of a gene can also cause the entire gene not to be transcribed and, as I mentioned before, frameshift mutations can wreak havoc as well. All of these are down to single nucleotides.

In any case, our vision of what a gene is has changed enormously since Dawkins wrote his book, we understand the genome much better now, and we have realized that it is far more complex than originally believed. 30-year old literature about genes, even if written by such luminaries as Rihard Dawkins, should be taken with a pinch of salt today.


How do I know which molecular structure is glycine's "base state"?

Short Answer: You need to define base state.

Background: The point to keep in mind here is that the base state (as you call it) is not constant. As @jeppenielsen points out in the comments, amino acids are zwitterions. According to Wikipedia:

  In chemistry, a zwitterion, formerly called a dipolar ion, is a neutral molecule with both positive and negative electrical charges. (In some cases multiple positive and negative charges may be present.) Zwitterions are sometimes called inner salts. Unlike simple amphoteric compounds that may only form either a cationic or anionic species, a zwitterion simultaneously has both ionic states.

In glycine, the center of positive charge is the -NH2 group while the center of negative charge is the -COOH group. At different pH (acidic, neutral or basic), the structure of the molecule keeps on changing as shown in the image below:

source

Structure of other amino acids also changes similarly. To know why this change occurs, just keep in mind that (in very simple terms) pH is inversely proportional to the concentration of H+ ions in a solution (higher the pH, lower the concentration of H+). The exact formula is $\ce{pH = - log[H_3O^+]}$ (yes, it means that a pH of 4 is 10 times more acidic than pH 5 and so on). Also, as pH changes, so does the formula for the amino group (see the diagram again).


Is there an "Adam and Eve" for each new trait during (not just human) evolution?

For most traits, there is no clear line where the trait is present or not. Exceptions are traits that occur with a single mutation, like lactose tolerance. So to pick one example, you had a population of fish that had a lung-like organ, and that by genetic drift that organ got more lung-like in a sub-population. So for most traits, you have a combination of mutations that lead to the traits, and these mutations need not occur in a direct line of ancestors. (I.e., a descendant will combine independent mutations from its parents.)

So there is no "Adam and Eve" in the sense that these are the only ancestors of all living individuals of a species. This would be a terrible genetic bottleneck! See this illustration, which comes with the estimate that the population size of the chimp-human ancestor was around 100,000.

You ask for "a first dinosaur with feathers who is the father or mother of all birds". It's possible that feathers arose multiple times from the same feather-like structures, or only once. But it is clear that this first dinosaur is only one of many dinosaurs that lived at the same time, and who are also ancestors of all birds.

Further reading: Lactose tolerance evolved several times independently (see "Convergent adaptation of human lactase persistence in Africa and Europe.").


I think that the potential survival of your seedlings could more likely be credited to your care and management than random genetic mutations. While, of course, DNA mutations happen during cell replication, evolution at the whole-plant scale primarily occurs over the course of generations, not the lifespan of a single plant. You may well be able to get these trees to thrive in your environment with some care and love, although they may not grow as vigorously. Here is a link to a gardening website with tips on growing ceaders in a home garden, although I agree with the commenter that you'll get much better help at the Gardening and Landscaping Exchange!

Best of luck with your horticultural endeavors!


For lambda:

  If the distance between the two cos sites is less than ~37 kb, the resulting phage particle will be unstable. When the DNA is inside the capsid, it exerts pressure on the capsid. Likewise the capsid exerts an inward force on the DNA. If there is not enough DNA inside the capsid, it will implode from the inward force of the capsid. If the distance between the two cos sites is too far (~52 kb), then the capsid will be filled before the second cos is reached. The tail cannot be added because the DNA hanging out of the capsid is in the way and no infectious phage particle is produced.

http://www.microinmuno.qb.fcen.uba.ar/03-Bacteriophage.pdf

In contrast filamentous phage like M13 have no upper size limit, but since they get longer with more DNA they become physically fragile.


Both your linked fact from the University of Arkansas

  When you sneeze, the intrathoracic pressure in your body momentarily increases. This will decrease the blood flow back to the heart. The heart compensates for this by changing its regular heart beat momentarily to adjust. However, the electrical activity of the heart does not stop during the sneeze.

...as well as your 'myth' from webMD

  For instance, it's not true that your heart stops when you sneeze. When your chest contracts because of a sneeze, your blood flow is momentarily constricted as well. As a result, the rhythm of your heart may change, but it definitely doesn't stop.

...come to the same conclusion, namely the heart does not stop during a sneeze.


Molecular/cellular biology textbook to consolidate what I know about molecular/cell biology

Campbell's Biology is, I quote my biology teacher, "the Bible of AP Biology". I know you're a medical student and therefore far past that introductory college level, but Campbell's does quite a good and thorough job of explaining a plethora of biology topics. It's a fairly reliable textbook, I think you might like it. It also gives a good deal of examples for the various concepts and avoids such abstract statements as those you quoted from your textbook. I would suggest skimming through the book at a local bookstore if you can and seeing if it fits your criteria.


Yes. I think it would certainly be possible for raw sawdust to be made digestible by humans through some sort of fermentation process with some kind of microbe or another.

Pickling (as is done with kimchee and cucumbers and lots of other fruits) uses naturally occurring bacteria that are artificially selected for by using a strong brine solution so that most microbes die but the ones that naturally survive in strong brine also convert the organic materials they find (raw cucumber or cabbage) into different organic materials (pickled cucumber or pickled cabbage in the case of kimchee).

If you could find a microbe that could digest wood (there are many I'm sure; the gut bacteria in termites provide evidence of at least one or some), and if you could find a way to select for that particular microbe, then fermenting sawdust for nutritious human consumption becomes feasible. The only remaining problem is finding that particular microbe whose excretions were digestible to humans.


What indices can we use to describe fitness landscapes?

This paper uses 4 metrics for discreet landscapes.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240586/

Deviation from additivity: How much your genes interact (normalized). Fitness in a purely additive landscape with three genes, for example, is F=f(x)+g(y)+h(z) where f,g, and h are each functions of one variable (the x,y, and z "genes"/coordinates). Deviation measures how far from additivity the fitness is. Higher is not always rougher but it is "trickier" since the effects of changing a gene depend on other genes.

Peak fraction: The % of points that are local peaks (discreet landscapes only), higher is rougher.

Tree component: The % of points that have at most one neighbor of higher fitness. Lower is rougher and indicates that there is a choice as to which direction to travel.

% monotonic paths: The fraction of paths (of all possible shortest paths from a given point to the peak) that don't go downhill. This calculation is averaged over all starting points in the landscape (excluding the peak). Lower is rougher.


Glycogen vs cellulose-curvature of glycogen molecule?

Interesting question. Here, the question actually comes down to how the bond actually looks vs how we depict the bond. In detail, see this image of maltose from here:

Pay attention to the geometry of the glycosidic bond. From how it is depicted, one would conclude that it is straight in geometry. But how it actually looks is like this:

Now, the obvious conclusion is that the glycosidic bond does have an angle.
Now, with introduction over, lets come to the main point. After searching a lot, I found the value of this angle. It is 109°, much closer to the general tetrahedral angle (109.5°) of sp3 hybridized oxygen atom (deviation could be due to steric hindrance). See this article:

300 alpha-glucose units, bonded by $\alpha$-1,4 glycosidic linkages, making a 109 degree angle between 2 C-O bonds
causing the polymer to twist into a helix. -OH group of C2 projects out into the middle and form H bonds with each other, stabilising the shape.

Yes, the glucose molecules in amylose form intermolecular hydrogen bonds which stabilize the molecule. See this article and in the diagram, notice that the hydrogen bond is formed between adjacent glucose units (to the left and right of the glycosidic oxygen atom):

Although the $\alpha$-(1$\rightarrow$4) links are capable of relatively free rotation around the ($\Phi$) phi and ($\Psi$) psi torsions, hydrogen bonding between the O3' and O2 oxygen atoms of sequential residues tends to encourage a helical conformation. These helical structures are relatively stiff and may present contiguous hydrophobic surfaces.


Found this:

http://www.mybacharach.com/fyrite-gas-analyzers.htm

Probably what I need


Was iron important for the first life on Earth?

Cyanobacteria require iron for photosynthesis and can be found as fossil stromatolites dating back to 3.5 billion years ago.  Stromatolites are layered structures made up of cyanobacteria and sediment.

Source: https://en.wikipedia.org/wiki/Stromatolite

Modern stromatolites can be found at Shark Bay in Australia, Chetumal Bay in Belize, and Laguna Bacalar in the Yucatan Peninsula.

Cyanobacteria are also believed to have evolved into the first microbes to produce oxygen by photosynthesis, which was a catalyst for the Great Oxygenation Event which occurred around 2.45 billion years ago.


There is absolutely no problem here. Primers will degrade only very slowly at 4 degrees and even at room temperature leaving them out overnight would not degrade them enough to be of practical consequence. In fact, if you're using them today it's probably better to have stored them at 4 degrees than -20 because repeated freeze/thaw cycles will also degrade primers.


Any soil microbiology textbook will tell you that there are a great number of fungi in most soils. I believe there are 12 or 13 species of non-legumes capable of fixing atmospheric nitrogen. Podocarpus is one of them. Look at the roots of podocarpus and you will see nodules all along the roots.


What is meant by translational repression by an upstream open reading frame?

Summary

The statement refers to the small but significant translation of short open reading frames (ORFs) of huntingtin mRNA, 5′ to the main open reading frame that encodes the large (3144 amino acid) functional product of the mRNA (and gene). It has been reported that the translation of these short ORFs decreases (i.e. inhibits) the translation from the main ORF. It is implied that this is a mechanism for regulating the expression of the gene, and, as it occurs on the mRNA in the cytoplasm, it is an example of ‘translational regulation’ — specifically inhibition. The precise mechanism of this regulation — although not unique to this mRNA — is apparently unknown.

Translation of ORFs in eukaryotic mRNA

Most eukaryotic mRNAs are functionally monocistronic — i.e. they encode only a single protein — unlike bacterial mRNAs. Initiation of protein synthesis involves selection of an initiation codon (usually AUG) by a complex of initiator-tRNA and the small ribosome subunit, but, in contrast to prokaryotes, the mechanism in eukaryotes involves scanning along the mRNA from the 5′ end. In the majority of cases the initiation codon of the protein product is the first AUG, but the significant number of exceptions suggest an effect of sequence context or mRNA secondary structure.

In recent years evidence has accumulated that in cases where the first AUG is not that of the main protein product, a small amount of translation from such 5′ upstream ORFs does often occur.

Diagrammatical representation of mRNA with upstream ORF (blue with initiation codon represented as an open triangle) and main ORF (black with initiation codon as closed triangle.)

Regulatory role of upstream ORFs

Johnstone et al. (2016) have reviewed a large body of evidence that indicates that upstream ORFs are translational repressors in eukaryotes. This has generally been established by measuring the extent of translation of the main ORF after manipulation or removal of the upstream ORFs. Much less is known about the actually mechanism of such regulation, which may vary from case to case, and certainly the paper on huntingtin only offered speculative possibilities. These include:

Binding of small peptide products of the upstream ORFs to the AUG of the main ORF
Pausing of ribosomal initiation complex at upstream ORFs impeding the progress of other to the AUG of the main ORF
Change of mRNA secondary structure by the binding of the ribosomal initiation complex at upstream ORFs increasing the difficulty of the initiation step in which the 5′ end is ’melted‘.

It also appears that the extent of the translation of upstream ORFs — and hence the extent of the repression — can itself be regulated by mechanisms such as the phosphorylation of initiation factor eIF2.


Why can't a corn cob have 13 rows of seeds?

Most varieties of corn bred for modern use have between 8-20 rows of kernels (Bommert et al. 2013.. Nearly all varieties have an even number of kernel rows.  This is due to the early development of the ear.  Ears of corn are developed from pistillate flowers on the ear (Bortiri and Hake 2007). Pistillate flowers are the female flowers, so they will bear seeds. The seeds are the individual kernals.
Long before the ear of corn has the kernels, it has several rows of flowers. The flowers develop on the ear in long rows. Early in development of the ear, the individual rows of flowers double, forming rows of double flowers, as shown in the simple diagram from Bortiri and Hake (2007). Both male flowers (left) and female flowers (right) have this two-row structure.

You can see the doubled pattern forming in this scanning electron micrograph of the very early development of the ears, also from Bortiri and Hake (2007). Notice the tip of the ear still has the single rows but the rows begin to double a little farther away from the tip. You can usually see this even on mature ears of corn.

You can see remnants of this arrangement if you look carefully at a cross section of an ear of corn. I've drawn arrows to show the connections where the flowers once connected together. If you look carefully at the ear of corn, you can identify the rows. The doubled rows have the kernels exactly opposite of each other. Each doubled row is staggered slightly from the neighboring rows. I've drawn lines to highlight each doubled row.  These two photos are from the agriculture extension office at Purdue University.

The development of corn flowers and all other flowers follows what is called the ABC model of floral development (Krizek and Fletcher 2005). The model has been greatly expanded since molecular genetics has increased our understanding of flower development. Many genes are involved, and the genes are used in different ways by different species of plants. The pattern of gene usage is similar in most grasses, which explains the double-flower arrangement of corn. Most grasses have the double-flower arrangement, and corn is a type of grass.
Some highly inbred variety of corn can produce odd numbers of kernel rows, as shown in figure below, taken from Bommert et al. (2013). KRN is kernel row number.  RIL is recombinant inbred lines, which means different varieties that have been inbred for particular traits. Thirteen is possible, as are other odd row numbers. An odd number of rows is unusual, however.

Citations
Bomblies, K. et al. 2003. Duplicate FLORICAULA/LEAFY homologs zfl1 and zfl2 control inflorescence architecture and flower patterning in maize. Development 130: 2385-2395.
Bommert, P. et al. 2013. Quantitative variation in maize kernel row number is controlled by the FASCIATED EAR2 locus. Nature Genetics 45: 334-337.
Bortiri, E. and S. Hake. 2007. Flowering and determinacy in maize. Journal of Experimental Botany 58: 909-916.
Krizek, B.A. and J.C. Fletcher. 2005. Molecular mechanisms of flower development: An armchair guide. Nature Reviews Genetics 6: 688-698.


What are the longterm effects of pancreatitis?

Pancreatitis may cause a condition called ''systemic inflammatory response syndrome'', a immune system reaction affecting the whole body.

Also, more frequently, pancreatitis is linked with steatorrhea, which means oily fat, and it may cause malnutrition and weight loss, due to restriction of secretions containing digestive enzymes. Longer term inflammations of pancreas may cause fibrosis (scar tissue) in the organ, therefore restricting the endocrine functions including insulin secretion, so acquired diabetes is another risk.

Obstruction of the bile duct and jaundice, leading to possible liver damage is another complication of pancreatitis.


Saliva buffer usualy provides stability at RT for month or even years. Genotyping companies like 23&me use collection kits like Norgen's (https://norgenbiotek.com/product/saliva-dna-collection-preservation-and-isolation-kit) which allows to store the sample up to 5 years.

So my advice would be: get the spitting vial at your place, send it as regular mail to your brother, and then ask him to send it back to you once filled with saliva. By doing so you won't have to worry about temperature.

Sending fresh saliva should be ok if your brother sends it refrigerated (4°C). I keep fresh cells up to at least one week in the fridge in proper medium, and saliva is a pretty decent buffer and has some antimicrobial properties.


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

  noun, plural: phenotypes

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

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

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


Recommend good conversational books to learn about cell and developmental biology or biochemisty?

Endless Form Most Beautiful: The New Science of Evo Devo introduces the reader to several classic embryology experiments and some key principles too.

I'll edit this answer when I find more books or reading material of this nature.


Does Human being have potential to perform parthenogenesis?

'Possible' is a tricky word here. There are a lot of things that are possible that just don't happen, because they are so exceedingly rare; or that happen but are unknown because they are hard to spot.

As it happens, we know that parthenogenesis-like effects can be induced in humans, because we've done it. If you remember the cloning debacle around Hwang Woo-suk, it turns out that while he didn't clone anything, he did manage to induce parthenogenesis, so … good for him, I guess?

Whether or not it happens in the wild… we just don't know. It's possible that it does, but it's really difficult to look for, since women have sex and then subsequently have babies, and a vanishingly small proportion of them are ever DNA tested; so even if one in every one million live births (which is a lot) were the result of parthenogenesis, we might never, ever know.

Basically, it's definitively possible with external meddling; it may or may not be possible without, and it may or may not actually ever happen.


How can one accurately diagnose the cause of human hearing loss without surgery?

I am not an ENT doctor, but I think the following diagnoses would suffice to determine each of the conditions:

Blocked Eustachian tube: Complaints would be of sudden onset and likely associated with a common cold, or ear infection. Providing the patient with standard decongestant should provide quick relief.
Ruptured eardrum: Patient should have subtle hearing loss apparent on audiogram and it would be relatively easily identified by routine otoscopic examination.
Perilymph fistula: This condition is hard to diagnose and I quote from Vestibular Disorders Association:

  A physician can arrive at a presumptive diagnosis [of a perilymph fistula] through a thorough probing for events close in time to the onset of symptoms, along with a variety of tests. These tests can include hearing tests (audiogram, ECOG), balance tests (VNG, VEMP) and some form of a “fistula test.”

The periplymph fistula is by far the most severe condition and the one with the most prominent effects on the vestibular system (balance). Multiple tests and rigorous medical exam is necessary.

With regard to your presented case study: Again, I am not an ENT doctor but a ruptured ear drum can result in dizziness due to the fact that one inner ear is exposed to cold air due to a rupture and the other ear is not. Unilateral inner ear cooling can result in dizziness. However, blowing your nose is unlikely to cause a ruptured eardrum as it is generally caused by more serious barotrauma (diving accidents and in-air plane cabin pressure malfunctions) (Web MD).

Similarly, the fistula is most often caused by more serious traumatic injuries (Vestibular Disorders Association).

A blocked Eustachian tube sounds the most plausible, as it is associated with the common cold (Web MD). Violently blowing your nose can cause fluid to travel up the middle ear, and possibly cause subsequent infections.


Are bacteria necessary for an individual's life, or, how long could a person live without bacteria?

You might need to demote your single-celled 'lords' to 'squires'. They're not essential to an individual's life. You wouldn't die (dispensing with the "how" right off the bat.) You'd be just fine if no bacteria reentered your body. Your fecal output would be greater; you would derive somewhat less nutrition from your food, you would need to take vitamin K, and there would be an adjustment period, but theoretically, you'd be just fine. You might even be healthier.

Your hypothetical is impossible, of course, because experimentation on humans is unethical. However, it might surprise you to learn that there are colonies of germ-free animals (also called gnotobiotic) used to study the effect of certain bacteria on animals.

The derivation of such subjects was initially fairly gruesome.

  The process of engineering biology and machine began by removing intact uteruses from near- to full-term pregnant animals within a purpose-built germ-free "surgical isolator." The uterus was subsequently passed through various disinfection procedures, involving total immersion in germicide-filled "dunk tanks," before the progeny were surgically released and hand reared within a second microbially sterile isolator.

These animals are costly to keep, as you can imagine. The originals must be delivered by Cesarean section, and housed and raised in sterile conditions. But once you can do that, they can multiply.

  To start a germ-free colony, one must remove a young animal from its mother’s womb through a careful surgical procedure to avoid exposing it to the microorganisms in the mother’s vagina and skin. Then, the animal is raised in a sterile cage and only exposed to food, water, and other equipment that has also been sterilized. On a weekly basis—or more often—a technician swabs cages and animal feces to ensure that no bacteria have contaminated the sterile housing. Once the colony has been created, it becomes easier to rear new germ-free animals; a germ-free mother can give birth naturally without exposing her newborns to any bacteria.

By the 1950s, researchers were rearing germ-free mice, rats, guinea pigs, and chicks inside sterile stainless steel (and later, plastic) housings. Germ-free animals are especially useful in researching, among other things, diabetes, auto-immune diseases, obesity, genetic engineering, cancer, immunology, nutrition, and the effects of normal intestinal flora on health.

Vitamin K must be added to their diets, and it is important to sterilize their food without destroying nutrients, but otherwise they do well in their environments. Their feces, of course, are sterile. Everything is microbe-free. They also have no "normal" antibodies.

Since generations of germ-free animals can exist and multiply, it is not only possible but quite likely that germ-free humans can exist as well.

Which is not to say that gut (and skin, etc.) microbiomes are unimportant. If you release a germ-free animal into a normal environment, it can die if it picks up pathogenic bacteria before more normal gut flora. To do this safely, a germ-free animal is first given a cocktail of bacteria to colonize the gut. After a while, they can be in a normal environment without problems. But your hypothetical human wouldn't even have this problem.

Germ-Free Mice
Gnotobiotics
Technology Highlights：ESTABLISHMENT OF THE FIRST GERMFREE MOUSE AND RAT COLONIES IN TAIWAN
"Life in a Germ-Free World":
Isolating Life from the Laboratory Animal to the Bubble Boy


Collective name for the X- and Z-chromosomes

I think you can safely use the terms heterogametic (Y/W) and homogametic (X/Z) chromosomes, meaning that a heterogametic chromosome is the chromosome which makes one of the sexes heterogametic (i.e. defines the difference between the two types of gametes of the respective sex).

These terms applied to chomosomes do have some usage in the literature, e.g. in this article.


What about 23andMe's SNP test gives it such bad efficacy as a diagnostic tool?

The long and short of it is that genetic variation is actually not very predictive in comparison to "environmental" effects such as lifestyle.

Only a quarter of the variation in lifespan between twins is attributable to inherited factors (including genetics and epigenetics) [1] - the rest is environmental, from lifestyle to air quality.

Most genetic variants (such as those measured on the chip used by 23andMe) have a very small impact on outcomes such as "Risk of disease X, Y or Z". Many risk loci have been identified, but without a full understand of what this risk means, the results of the 23andMe analysis can be misleading.

Some few rare genetic variants have a larger impact on diseases (such as early onset diabetes), but this comes under the "monogenic" category of genetic variation, rather than the common variants typically observed in large populations.

Basically, genetic risk scores are, at the moment, only indicative of an individuals risk, and to get the real picture a lot more information is required - for instance smoking is a better predictor of early mortality than any "common" (>=5% frequency in a population) genetic variants, likewise a high fat diet is more indicative of cardiovascular disease.

Skytthe A, Pedersen NL, Kaprio J, et al. Longevity studies in
GenomEUtwin. Twin Res. 2003;6(5):448–454. [PubMed link]