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

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

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

Coming to the mosquito,

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

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


importance of cDNA sequencing of a specific gene in different plants

No, cDNAs are copies of spliced mRNAs, and typically contain a 5'-UTR (untranslated region), an open reading frame, or ORF, and a 3'-UTR.
The cis-regulatory information might be revealed by sequencing the genomic DNA upstream of the gene(s).  That is where one usually finds the promoter (although there are some rare exceptions, particularly for genes transcribed by RNA polymerase III).


Does one need to perform two Chi-square tests?

You should just have 1 chi-square test to test the hypothesis.

Note that the problem is asking about F2 generation, not F1.

H0 in a chi-square test is your prediction based on a model; H1 is that the real outcome differs from what is expected, so you have that a little backwards. H0 should be the expected counts knowing the initial proportions and expecting autosomal dominant inheritance.

Start with your prediction:

F1 generation will be half heterozygous males/females, half WT males/females, so F2 generation has 3 types of mating events:

Cc x Cc occurs 25% of the time, and 75% of offspring are affected

Cc x cc occurs 50% of the time, and 50% of offspring are affected

cc x cc occurs 25% of the time, and 0% of offspring are affected

Multiply these probabilities and you should have 43.75% expressing the phenotype; your prediction for the chi-square test is that you will see this same percentage regardless of sex.

From there, doing a chi-square test is simple and there are many many resources online for this (here is just one).


The biotin-streptavidin interaction is extremely strong, one of the strongest (if not the strongest) non-covalent interaction between biomolecules. So you'll need pretty harsh conditions in any case.

Extreme pH values are generally a very bad idea for RNA. I'm pretty sure that the conditions you mentioned are not meant for elution of nucleic acids. Such low pH values (and high pH values as well) lead to a quick hydrolysis of the phosphoester bond of RNA, you can read more about the mechanism of that in this review.

A quick Google search lead me to the following protocol:

  To dissociate biotinylated nucleic acids from Streptavidin-Coupled
  Dynabeads®, incubate the beads in 95% formamide + 10mM EDTA, pH 8.2
  for 5 minutes at 65°C or for 2 minutes at 90°C.

This sounds reasonable to me, as formamide is also commonly used in sample buffer for denaturing gel electrophoresis of RNA. I haven't done anything like that myself, so I can't guarantee that this would work in your case.


Based on the image and on the description, it could be a woolly aphid, a kind of insect that produces filaments of a waxy, cotton-like substance that gives them a fluffy appearance.

The images on Wikipedia aren't convincingly similar, but I found a better reference on abundantnature.com:


According to the International Committee on Taxonomy of Viruses, it has had several official variations of that name over the years:

Minute mouse virus
Minute of mice virus
MVM Virus
Minute virus of mice
Mice minute virus

The current (2014) accepted name is: Rodent protoparvovirus 1

"Does it really matter?" As long as you write in full the name you're using the first time you use it, people will know what you're talking about. However, for consistency amongst current literature, perhaps we should all strive to keep up with current taxonomy.


What light intensity determines the start/end of a photoperiod in humans?

It isn't really a specific light intensity that an organism will interpret as the start of a photoperiod. Maynard Johnson reported in 1939 that intensity of light used had an effect on the rate at which mice would shift their circadian rhythms. So, brighter light has a stronger effect, but there isn't a cutoff point that I'm aware of. Johnson was using illumination as low as 2.5 foot candles, which is pretty dim. Aschoff and Pittendrigh did some more work on light intensity in the 50s and 60s, but I don't think anyone ever found anything resembling a cutoff point, only the degree to which intensity had an effect.

Computer monitors are pretty bright. Luminance rating is typically 250-350 cd/m2, which, for comparison with Maynard's experiment, is eqivalent to 23-32 foot-candles. http://computer.howstuffworks.com/monitor6.htm

Johnson, Maynard S. "Effect of continuous light on periodic spontaneous activity of white‐footed mice (Peromyscus)." Journal of Experimental Zoology 82.2 (1939): 315-328.


Enzyme inhibitors against common cold viruses

A human enzyme involved in the production of rhinovirus capsids has been successfully inhibited.

  Fragment-derived inhibitors of human N-myristoyltransferase block capsid assembly and replication of the common cold virus https://www.nature.com/articles/s41557-018-0039-2

The article also says that targeting a human enzyme could be more efficient since the risk of mutation is lower compared to a virus enzyme.


Identify this wild plant with brilliant scarlet red flowers

It looks like some kind of Lobelia. A close up of the flower itself would be very helpful.

I believe it is a Cardinal Flower:

  This 1-6 ft. perennial has showy, red flowers in 8 in., terminal spikes. Each flower has three spreading lower petals and two upper petals, all united into a tube at the base. Erect leafy stems, often in clusters, with racemes of flowers resembling flaming red spires. The lower portion of the erect stem is lined with lance-shaped leaves.


How much generation of hamster's family it takes to get first bad mutations

Everybody carry deleterious mutations anyway

Your two hamsters most definitely already carry a number of deleterious alleles at segregating sites (segregating sites = polymorphic sites). Also, I will not talk about inbreeding depression in your population coming from only two individuals which will be very important but I will only answer your specific question. In short, I will assume your are not interested in segregating sites...

Probability of an offspring to carry a new deleterious mutation

The vast majority of new mutations are deleterious (Shaw et al. 2003). I don't know of estimates of mutation rate in hamsters but in mammals (and in all eukaryote species anyway generally speaking; e.g. see this post and this post or directly bionumbers#mutationrate), the genome-wide mutation rate is of the order of 1 to 100 mutations per offsprings.

If the couple of hamsters have $x$ offsprings, then the probability to have at least one new mutation in at least one offspring is given by the cumulative exponential distribution

$$P = 1-e^{-U x}$$

, where $U$ is the genome-wide mutation rate. With $U=50$ and $x=1$ (one offspring), this probability is $P = 1-e^{-50} = 1 - 1.9 \cdot 10^{-22} ≈ 1$.

In short

In short, to a fair level of approximation, every new offspring carry at least one deleterious mutation that was not present in either parent.


Why are pharmacology studies so experimental?

The First thing is that that you can't study any process until it happens. So even if you know the structure of receptor molecule, you can't always be sure that it is completely safe.

It does seem a bit random in beginning but this is how it works. You can't just derive a medicine or drug and send it for mass production. You never know what are the side effects of the drug. For this reason, the drugs are tested on other animals (usually rats because they are quite in number, having short lifespan and not many oppose experiments on rats ethically.)

If the side effects are severe, then the drug is banned from mass production.
But if such drug is produced,more harm will be done than good. Also you can't give it to humans first. If all tests are successful, then only the drug is tested on humans.

So Screening and Testing are indirect but essential steps for studying the effects of it.


I photographed a couple of butterflies and birds in Argentina but can't identify them. What are my options?

First, I think it is more useful to post separate questions, at least for each taxonomic group (birds, butterflies etc). To make a question a dumping ground for all sorts of species determination pictures is a bad idea.

That said, the butterflies seem to belong to the families Nymphalidae,  (nr 5) and Papilionidae (Swallowtails) (nr 7), judged by overall apperance. I'm not directly familiar with South American butterflies, but two likely species are:

Doxocopa agathina (Nr 5), or related species in the Doxocopa genus.

(from wikipedia commons)

Papilio thoas (Nr 7)
This is the King Swallowtail, your specimen probably of the subspecies P. t. brasiliensis which is found in Argentina. Sometimes the name Heraclides thoas is used. Pictures of subspecies can be found here: Butterflycorner.net. Your speciemen have lost the tail appendages (could be due to wear-and-tear or bird attacks). A related similar species is Papilio astyalus, which is also found in Argentina (pictures), but it usually has a broader yellow band.

(from wikipedia commons)

The bird in nr. 6 looks like a Black vulture (Coragyps atratus).


How to use a published phylogenetic tree?

I don't know how generalized this is, but some journals require the authors to deposit the trees in a database, like treebase. In this case, papers should indicate the accession numbers of their trees.

You then need the appropriate software to load the tree, manipulate it and print it, for instance ete.


Has it been enough time for evolution through simple natural selection?

The evolution to the current state of life on earth has occurred through some 3.8 billion years. During this time it has gone from the most basic forms of life, simple self-replicating units, to the complex beings we see today. Evolution, the process of change within a collection of units, is caused by 4 factors, mutation, selection, drift, and gene flow. So firstly, the current state is not thought to just be the result of natural selection but instead a result of all the mechanisms of evolution.

Selection can itself be subdivided in to two types, natural and sexual selection. Therefore "natural selection" does not even contain all types of selection. Selection is not a simple process, but occurs in a very complex manner, simultaneously affecting the many levels upon which selection can act (nucleotide, gene, organelle, cell, organs, organism, population, species, ecosystem etc.).

There are a number of things to consider when discussing whether enough time has elapsed for the mechanisms of evolution to produce the variation we see today, a primary concern is quantifying how much variation there is in the world that has evolved. Here are some other factors which would determine the likelihood at arriving at that level of genetic variation:

Mutation rates (per generation)
Generation times
Offspring per generation (affects the number of potentially new lineages per generation)
Genome size (number of potential sites)
Complexity and strength of selection
Population size (affecting drift and the efficacy of selection)
Genetic admixture/inbreeding/potential gene flow
Recombination rates
Social structure
Environmental variation

These all vary wildly in contemporary populations and would also have varied in ancestral lineages too, this makes it, in my opinion, near impossible to even get a rough estimate of how likely our current state of variation evolved via the known mechanisms of evolution. But there is a simple answer, all variation you see today arose from simple life and evolved in the last 4 billion years via the four known mechanisms of evolution - which, in part, includes natural selection. The proof is in its existence and the absence of other possible (plausible) mechanisms.

To illustrate the complexity of the problem and the high likelihood of these mechanisms leading to substantial genetic variation (this is highly unscientific):

I'd suggest a very conservative estimate of just mutation rates and time since life began (3.8 billion years, Last universal common ancestor [LUCA]), using approximate human mutation rates (175 per generation and 25 years per generation = 7 bp mutations per year), would suggest a single lineage from LUCA to now could have had some 26 billion mutations, an average of 8 mutations per site in the human genome (this would assume constant mutation and generation rates, and starting genome size of 3 billion BP in LUCA - obviously completely ridiculous, but it's just an illustration and assumes evolution purely by drift and mutation).


Venous return from the limbs is largely facilitated by the action of neighbouring skeletal muscles compressing the veins and forcing the blood proximally past the valves which prevent back flow.  If you are inactive for a long time by sitting, or are sitting in such a way as to impede blood returning from your calves (i.e. with the back of your knees pressing into the edge of the chair) blood movement in this manner is greatly slowed.

Blood that is moving more slowly or turbulently has a greater propensity to coagulate and form a thrombus.  This is similar to the rationale for prescribing anti coagulants to patients with atrial fibrillation - the turbulent and slow movement of blood through their atria leaves them at greater risk of throwing a clot to the brain causing a cerebrovascular accident.

Hypoxia isn't really that relevant in the case you describe as arterial supply is unaffected (much higher pressure) meaning tissues do not become ischaemic. There is also collateral venous drainage from the limb although this can subsequently cause problems in the form of post thrombotic syndrome.  The most significant risk would be that of the thrombus breaking off and lodging in the lungs - a pulmonary embolism.


Is AT or GC content important in electrophoresis?

It does make a difference on polyacrylamide. A and C are faster while G and T are slower.

Image from publication:

The "standards" are AAA/TTT/GGG/CCC molecules.


Let's consider some situations real quick:

(1) A bacterial microbe enters through a fissure in the skin. What does an innate, systemic immune response look like? In short: it's lengthy, uncoordinated and has a lot of potential to damage tissue in the area of infection.

(2) A bacterial microbe enters the blood. The bacterium produces an AB toxin that enters cells and kill them.

(3) The host is infected by a helminth.

In situation 1: Innate immune responses are associated with the secretion of many cytokines and chemokines. Cytokines are associated with the inflammatory response, and chemokines are associated with lymphocyte trafficking. Inflammation and recruitment of lymphocytes, macrophages and the like are good for clearing the infection, but there's a lot of potential to damage the surrounding tissue. Effector cells from the adaptive response incl. humoral immunity don't elicit the same level of damage, and we can illustrate this in mucosal immunity. Since commensal (and some pathogenic) organisms are constantly stimulating mucosal immunity, there are (1) epithelial effector T cells, (2) plasma cells and (3) dendritic cells that make the response to these pathogens fast, efficient and little damage occurs to the tissue involved.

In situation 2: So let's say the pathogen has escaped the immune response, maybe it's encapsulated. There are AB toxins being produced that kill cells endocytosing them. What good will it do for a phagocyte to eat something that ends up killing it? Antibodies are particularly efficient for this extent because they can neutralize toxins they've encountered with the same fast, efficient response as we described above. This is achieved through antigen presentation. The host will then need to find other ways to clear the infection, however.

So: In situation 1 we illustrated that an innate, systemic response isn't always desirable due to tissue damage, and through the presentation to T cells by APCs, a later adaptive immune response mitigates this effect through formation of effector cells. In situation 2, we then illustrated that the first-line defenses can't always respond to the imminent threat for various reasons, which are overcome by the presence of effector cells.

Situation 3: This is the more complex concept. You have different subsets of CD4+ T cells that can be formed in response to the type of interleukin or cytokine that is present when the CD4+ T cells are being activated. This differentiation is driven largely by secretions of activated APCs! The APC performs this critical step based on what kind of receptors the specific types of pathogen are detected by. The differentiated CD4+ T cells, or T-helper cells of class: Th1, Th2, Th17, Treg, etc. each perform different roles which are effective in different situations. For example, you wouldn't see any benefit in throwing Th1 cells at a helminth infection, Th2 is the best effector for this. Treg cells are capable of abrogating autoreactivity, and Th17 cells are needed to assist B cell differentiation in response to antigen detection (which in the case of helminths, the B cell must class switch to IgE and this is stimulated by Th2 cells via IL-4).

Now, in situation 3, we've illustrated that CD4+ T cell intermediates are providing your overall immune response: flexibility, specificity, and checks/balances which are all-at-once critical to healthy functioning. I disregarded MHC-I responses and CD8+ CTL's because this is about APC-driven responses.


What is the purpose of the viscous gel in the Pacinian corpuscle?

Short answer
The adaptation process in Pacianian corpuscles (PCs) is mediated via the outer capsule. This capsule is an onion-like structure that quickly molds itself to pressure stimuli, thereby rapidly desensitizing the receptor.

Background
The Pacinian corpuscles are rapidly adapting (RA) skin receptors, as opposed to the slowly adapting (SA) ones, such as the Merkel cells. RA cells become swiftly unresponsive (i.e., they adapt) when a pressure stimulus is applied, but faithfully transmit rapidly changing stimuli (such as vibrations).

Pacinian corpuscles are specialized vibration receptors. Their dendritic region is shaped as an onion-like structure with layers of stacked lamellae:

Specialized dendritic capsule of the Pacinian corpuscle. Source: Biologymad

These lamellae act as high-pass filters that result in a sharp drop in sensitivity below 150 Hz (Johnson, 2001). If this capsule is dissected from the receptor and a pressure stimulus is directly applied to the sensor element underneath the capsule, the receptor response to a sustained stimulus substantially increases (Mendelson & Loewenstein, 1964). Basically, these elastic lamellae slowly mold their shape to the stimulus and pressure stimuli are only transmitted for a few milliseconds, after which the lamellae absorb the pressure. So only a one or a few spikes are generated at the start of a pressure stimulus.

You can imagine it this way, suppose you have a gel-like substance (say Play-Do) on a weight scale. Now suppose you press the Play-Do quickly and hold your finger steady at a certain point above the scale, within the Play-Do. The weight scale will shortly display a certain weight (equal to the pressure applied in Newtons), after which the Play-Do folds itself around your fingertip, and the pressure is released from the scale.

Upon release of the pressure stimulus another spike or two are generated in the PC. Hence, a continued pressure stimulus is not faithfully reproduced. However, vibratory stimuli generate spikes on the pressure onset as well as offset as well, and this happens on every phase of the vibration. Hence, vibratory stimuli are faithfully transmitted.

Response of Pacinian corpuscle to a sustained pressure stimulus (indentation of the skin) and superimposed vibratory stimuli. Note the vigorous response to vibrations, but the rapid adaptation to the static pressure stimulus. Source: Zavantag

References
- Johnson, Curr Opin Neuobiol 2001;11:455–461
- Mendelson & Loewenstein, Science 1964;3618:554-5


What should be evaluated in food decomposition experiment?

You could weigh the cookies in a time course to see how quickly the cookies are degraded. Also, you could take some samples and make cultures in Petri dishes to see if there are differences in the microbiota associated with each one. In this line, maybe you'd want to sterilize the samples by some means, just to ensure they have the same microbial conditions. You could also measure the porosity of the samples by pacing them in water and measure how much water it can absorb, or something like that. I assume you do not have an HPLC engine, but you could also make extracts and see how the spectra varies over time.


Ok, I'll bite. Now, I'm going to assume that in this scenario, Alice and Bob are stuck underwater. Alice has a SCUBA tank filled with compressed air (not pure O2) and though she won't share it with Bob, she magnanimously agrees to share her exhaled breaths with him.

Exhaled air contains 13.6–16.0% oxygen and 4.0–5.3% carbon dioxide in addition to other gasses which we'll ignore here. The real question here is: can you survive on that?

13.6–16.0% oxygen is 66%-80% of the amount of oxygen in normal air (which is ~20.1% O2). If we assume that the air pressure of the exhalation is the same as the air pressure at sea level, then the amount of oxygen available to Bob is roughly equivalent to being at an altitude of 2000 - 3500 meters above sea level, which is certainly survivable.

The CO2 is likely to be a bigger problem. CO2 is toxic and, in sufficient quantities, can case asphyxiation even in the presence of sufficient O2. Amounts above 1% can cause drowsiness, headaches, and mild narcosis while higher levels lead to dizziness, confusion, and unconsciousness.

It looks like you need amounts around 7%-10% for death, so Bob will probably survive in the short term, he definitely won't be happy and he won't be doing much. According to wikipedia's page on Hypercapnia, the time one can expect to perform useful activity varies greatly based on the exact amount of CO2:

1 week at 4%,
8 hours at 4.5%,
4 hours at 5%, and
1 hour at 5.5%

If Alice and Bob are just relaxing and waiting for rescue, it's likely that the CO2 in her exhalations will be on the low end of that range and Bob will likely be able to survive (albeit in great distress) for a significant period. If they were exerting themselves, however, Bob wouldn't do well at all.


Though Escherichia coli has only one origin of replication (oriC), replication proceeds in both directions from it. Thus, based on your calculations, DNA replication takes 40 minutes (which is still too long if the doubling time is 30 minutes). The solution is to start replication again before the previous round has completed, and here's some research which shows just that:

Yoshikawa H, O'Sulliven A, Sueoka N. 1964. Sequential replication of the Bacillus subtilis chromosome. Prod Nat Acad Sci 52:973-980

  Obviously, dichotomous replication is advantageous for bacterial growth because the bacteria can replicate chromosomes faster than by having one replication point. With one replication point, the replication time, and consequently the cell generation time, would be limited by the maximal rate of DNA polymerase.

Cooper S, Helmstetter CE. 1968. Chromosome replication and the division cycle of Escherichia coli B/r. J Mol Bio 31(3):519-540

  …cells growing faster than 40 minutes per doubling must initiate new replication points prior to the completion of DNA synthesis at the previous points; in other words, there should be multiple forks.

Skarstad K, Boye E, Steen HB. 1986. Timing of initiation of chromosome replication in individual Escherichia coli cells. EMBO J 5(7):1711-1717

  In rapidly growing cultures, with parallel replication of several chromosomes, cells will end up with 2n (n = 1, 2, 3) chromosomes if initiation occurs simultaneously at all origins. A culture with asynchronous initiation may in addition contain cells with irregular numbers (not equal to 2n) of chromosomes. The frequency of cells with irregular numbers of chromosomes is a measure of the degree of asynchrony of initiation.

Fossum S, Crooke E, Skarstad K. 2007. Organization of sister origins and replisomes during multifork DNA replication in Escherichia coli. EMBO J 26(21):4514-4522

  …initiation occurs at two origins in the ‘mother' cell. It can even occur in the ‘grandmother' cell at four origins if the time it takes to replicate and segregate the chromosome exceeds two generations.

This last image is interesting because you actually see the multiple replication origins in single cells by fluorescence microscopy.


Can virus resistance be acquired through generational exposure?

Perhaps the answer is in natural selection. Over many generations, if these plants are constantly exposed to the same virus, one of them may obtain a mutation or something similar that allows it to be resistant, thus that plant will have higher survival and growth rate and thus more seeds.

The current plant itself may also adapt to the presence of this virus (perhaps in growth patterns, etc.) over a long period of time.

As for the time for the genetic resistance to take place, it is almost impossible to say as it is almost completely random (and would also depend on what other plants you may pollinate it with as an already resistant plant would, of course, cancel the need for a mutation).

I hope this helps.


How do mutations and protein synthesis link to cancer?

Mutation in DNA can be beneficial, harmful, or may have no effect. This is dependent on the gene location where this mutation has occurred.

Various genes linked to cancer are:

Tumor suppressor genes: These genes regulate cell growth by keeping check on cell division, repairing mismatched DNA  and regulating cell death.  Mutation in this type of gene leads to unregulated cell growth and lead to formation of tumor.

Examples:

TP53 is most commonly mutated tumor suppresor gene. More than 50% of
cancers are caused due to mutation in this gene.
Mutation  in BRCA1 or BRCA2 genes is responsible for breast and
ovarian cancers. It  may also increase the risk of pancreatic cancer
and melanoma.

Proto-oncogenes: These genes help cells to grow normally. Mutation in this gene cause its permanent activation and unregulated cell growth takes place and lead to cancer. This abnormal gene is called oncogene.

Examples:

HER2 is responsible for breast and ovarian cancer.
RAS family of genes, responsible for cell communication, cell growth,
and cell death.

DNA repair genes:  These genes play role in repair of DNA, which is mismatched during replication.   Defect in DNA repair gene, leads to synthesis of incorrectly formed DNA and eventually incorrect protein synthesis.


Problems in optimisation with applications to biology?

Maximum likelihood phylogenetic trees. The trees are easily scored but the tree space is so large that finding optimal phylogenetic trees is extremely difficult. There's some research but there haven't been very many actual breakthroughs, so it's probably a pretty rich field.


Why do we use DNA sequencing methods such as shotgun?

This is a technique from the "old time" of genome sequencing. The underlying method for sequencing is the Sanger chain termination method which can have read lenghts between 100 and 1000 basepairs (depending on the instruments used). This means you have to break down longer DNA molecules, clone and subsequently sequence them. There are two methods possible.

The first is called chromosome (or primer) walking and starts with sequencing the first piece. The next piece of DNA (which is  and then uses a specific primer from the end of the sequence. The next (contigous) piece of the sequence is then sequenced using a primer which is complementary to the end of the first sequence read and so on. This technique doesn't require much assembling, but you need a lot of primers and it is relatively slow.

To overcome this problem the shotgun sequencing method was developed. Here the DNA is broken into different pieces (not all broken at the same place), cloned and sequenced with primers specific for the vector used for cloning. The leads to overlapping sequences which then have to be assembled into one sequence on the computer. This method allows the parallelization of the sequencing (you can prepare a lot of sequencing reactions at the same time and run them) which makes the process much faster and also avoids the need for sequence specific primers. The problems are to sequence repetitive sequences, as overlaps are not as clear here. To resolve this problems a first draft is made and then critical regions are resequenced using other techniques as primer walking. Have a look at the Wikipedia page about shotgun sequencing if you want to read more details.


What is the effect of a pure-oxygen environment on a plant?

As hinted in other answers, the key problem with a pure oxygen environment would be the inability to photosynthesise caused by the absence of carbon dioxide.
The overall equation for photosynthesis (the process in which energy from the sun is harnessed to fix inorganic carbon dioxide into organic molecules that  are of use to the plant) is:
6CO2 + 6H2O → 6O2 + C6H12O6
The carbon dioxide required for photosynthesis is obtained from the atmosphere by diffusion through stomata on the leaves.  Therefore if the atmosphere contains no carbon dioxide (i.e. in the scenario you suggest) photosynthesis would not progress, meaning glucose used by the plant in respiration would not be replaced.
This would eventually lead to the cessation of cellular respiration due to a lack of reactant.  This would cause the plant to die.


Ok. So, first of all, it depends on the power of the shock.

This relates to volts (electrical pressure) and amps (amount of electricity)

I strongly suggest you read
this article

That article explains what happens in great detail, but if you're still curious, here are some other things that would obviously happen:

If it is a constant DC Current, negative ions will rush to the anode, and positive ones will rush to the cathode. The negative ions (including oxygen and chlorine) will bleach the cells in the area and kill them.

The positive ones in the cathode area will raise the ph drastically and liquefy the adjacent cells.

If the current is high enough, the cells will heat, which will denature the proteins and enzymes within and kill them.


Effect of extremely hard water on marine life?

Hard water helps in direct and indirect ways.

Indirectly, hard water plays an important role in regulation of pH. Respiration and other physiological activities release substances into water that change the water pH and the ions that cause hardness act as buffers and help maintain pH.

Directly, they determine the ease with which osmoregulation occurs. The harder the water, the lesser the influx of water. So the fishes act like an open system and are influenced by the surrounding water.

There are very few fish who absolutely need soft water to survive.
Since your pH and hardness are pretty low, it allows you to raise multiple fish from South America. You could do tetras, dwarf cichlids and New World cichlids, Plecos as well.

Potentially discus and altum angelfish as well if you're up to the huge challenge.

However, livebearers will not tolerate this type of water. That goes the same for African cichlids.

Otherwise hard water is completely fine for marine life and other aquatic species.

Link

Link

Hope this information helped!

-Sartoaster


what is the princlple of using DMS (Dimethylsulphate) for structural analysis of rRNA?

Here is a good explanation of the theory and chemistry behind DMS footprinting, from chapter 11 of Probing RNA structure within living cells :

  In vivo chemical probing assay using dimethyl sulfate (DMS). (A) DMS methylates the N1 atom of adenosines and the N3 atom of cytosines. Both of these positions are located on the Watson–Crick face of the respective nucleotides. (B) Scheme of a structured RNA interacting with a protein ligand to exemplify residues accessible to DMS modification. (C) Mapping the modified positions by reverse transcription. The enzyme terminates the extension due to steric hindrance by the bulky methyl group at the Watson–Crick face of A and Cs. (D) The pool of cDNAs is separated on a standard denaturing gel. A and C denote the sequencing lanes, which are essential to map the modified positions. In addition, an RT control, which is prepared from RNA extracted from untreated cells, is essential to determine any natural stops of the RT (lane -). Comparison of the RT control lane with the cDNA pool created from DMS-modified RNA (lane +) reveals sites of modification. Note that the band resulting from a DMS modification migrates one nucleotide faster than the corresponding band in the sequencing lane, because the ddNTP is incorporated into the nascent cDNA, while the methyl group results in a stop one residue prior to the modification.

My take -- DMS adds a methyl group at the hydrogen-bonding face of exposed A and C bases. As and Cs protected by either proteins or base-pairing interactions are not methylated.  Methylated bases inhibit reverse transcriptase, resulting in a truncated DNA product that can be visualized on a gel.  Comparison to an untreated control allows for inference of which As and Cs of the RNA sequence are exposed and which are protected, from which the native RNA conformation can be inferred (or the possibilities greatly constrained).


Why do telomere lengths not predict differences in life spans among species?

The answer should be obvious: Telomeres do not determine an organism's longevity.

There's only a vague correlation between telomere length and a species' lifespan.  See Comparative biology of mammalian telomeres: hypotheses on ancestral states and the roles of telomeres in longevity determination for a starting point.  Telomeres are a part of the longevity story, but probably a fairly small part.

The Hayflick limit is generally associated with telomere length. Human telomeres are a little on the long side as species go, but are not extraordinary. Many species of mice, and other rodents, have far longer telomeres than humans, for example, and obviously have much shorter lifespans. There's also such a thing as a "mega-telomere", found in a number of bird species, which can hundreds of times longer than human telomeres.


Aspirin - does it inhibit enzyme of thromboxane?

Aspirin and some other NSAIDs inhibit cyclooxygenase which is the first enzyme in the prostaglandin/thromboxane biosynthesis pathway if you consider first substance is arachidonic acid (a fatty acid). Generally, arachidonic acid is present in the form of a phospholipid, and if you consider that in the pathway, substance-Y is arachidonic acid and enzyme-A is cyclooxygenase.

  From: Heckmann, Lars-Henrik, et al. "Outlining eicosanoid biosynthesis in the crustacean Daphnia." Front. Zool 5.11 (2008).


As a couple of counterexamples, species in the classes Symphyla (Pseudocentipedes) and Pauropoda within Myriapoda have 8-11 and 12 leg pairs respectively, so between 16 to 24 legs (sometimes with one or two leg pair stronlgy reduced in size).

(species in Symphyla, from wikipedia)

Another common and species-rich group with 14 walking legs (7 leg pairs) is Isopoda.

(Isopod, picture from wikipedia)

You also need to define 'legs' for the discussion to be meaningful. As you say, decapods have 10 legs on their thoracic segments (thoracic appendages), but they can also have appendages on their abdomens (Pleopods/swimming legs), which will place many decapods in the 10-20 leg range.

(Decapod abdominal appendages/legs in yellow, from wikipedia)

So overall, in Arthropoda, having 12-28 legs doesn't seem all that uncommon. There are probably other Arthropod groups besides those mentioned here that also have leg counts in this range.

However, for a general account, the most likely answer (if there is indeed a relative lack of 12-28 legged animals) is probably evolutionary contingencies and strongly conservative body plans within organism groups.


How does human body deal with inert solid material in the bloodstream?

Non-opsonized particles (Particles that can't be coated with opsonins like antibodies or complement proteins) can be engulfed by macrophages which could end up, for example, in the lung secretions and be coughed up one day. Note that a cell can only engulf a particle so large, so you'll not feel yourself coughing up anything out of the ordinary. Only tiny particles can be dealt with like this. Bigger particles can become trapped in fine vasculature (small veins; venules, and small arteries;arterioles). This can lead to abscess formation necessitating amputation of the affected limb.


If a trait does not appear to be advantageous to organism, why does the organism have it?

There are many reasons why an organism might have a trait that does not appear to be beneficial.

The trait is actually advantageous even if it does not appear to be.
The trait is a byproduct of another trait, which is beneficial. Not all traits are the product of direct selection; traits that are byproducts of other traits are known as "spandrels", a trait coined by Stephen J. Gould and Richard Lewontin
The trait was fixed by some process other than natural selection, such as genetic drift. Genetic drift can fix traits that are neutral or even evolutionarily disadvantageous.


Why is Carbon Dioxide a Greenhouse Gas whereas Ammonia is not?

This is better suited for the Chemistry site, but there are two reasons.  1) The gas allows visible light to pass, but blocks infrared.  (Which has to do with the nature of the bonds between atoms &c.) 2) It exists in the atmosphere in sufficient quantity to have an effect, which ammonia doesn't: https://www.livescience.com/57305-ammonia-detected-in-atmosphere.html  It's quite reactive, so ammonia that's released from e.g. fertilizers or urine doesn't stay around long.


This refers to base pairs.

File size has no particular meaning beyond practical considerations, given that it depends on the format. (For example, 2bit files use 2 bits per base, as the name indicates, compared to the 8 bits necessary for each letter in a plain text format like FASTA & derivatives.)

For your additional question, (number of reads * length of each read) gives the total length of sequence contained in the file. It is not really a property of the file format, but a parameter of the sequencing run.


The simple answer is that which X chromosome is inactivated varies in different cell lineages, so typically a female will have cells exhibiting either wild-type or mutant phenotypes. It was Mary Lyon's observation of mosaicism in heterozygous mouse coat colour that gave the phenomenon its name. So in the case of a recessive disease there will be a phenotype, but in many cases the 50% of cells expressing the normal gene will provide sufficient functional cells to get by. From the Wikipedia article about Mary Lyon:

  Her research has allowed us to understand the genetic control mechanisms of chromosome X, which explains the absence of symptoms in numerous healthy women that are carriers of diseases associated with this chromosome.

Edit - response to comments:

Plug, I et al. (2006) Bleeding in carriers of hemophilia. Blood 108: 52-56

Abstract:

  A wide range of factor VIII and IX levels is observed in heterozygous carriers of hemophilia as well as in noncarriers. In female carriers, extreme lyonization may lead to low clotting factor levels. We studied the effect of heterozygous hemophilia carriership on the occurrence of bleeding symptoms. A postal survey was performed among most of the women who were tested for carriership of hemophilia in the Netherlands before 2001. The questionnaire included items on personal characteristics, characteristics of hemophilia in the affected family members, and carrier testing and history of bleeding problems such as bleeding after tooth extraction, bleeding after tonsillectomy, and other operations. Information on clotting factor levels was obtained from the hospital charts. Logistic regression was used to assess the relation of carrier status and clotting factor levels with the occurrence of hemorrhagic events. In 2004, 766 questionnaires were sent, and 546 women responded (80%). Of these, 274 were carriers of hemophilia A or B. The median clotting factor level of carriers was 0.60 IU/mL (range, 0.05-2.19 IU/mL) compared with 1.02 IU/mL (range, 0.45-3.28 IU/mL) in noncarriers. Clotting factor levels from 0.60 to 0.05 IU/mL were increasingly associated with prolonged bleeding from small wounds and prolonged bleeding after tooth extraction, tonsillectomy, and operations. Carriers of hemophilia bleed more than other women, especially after medical interventions. Our findings suggest that not only clotting factor levels at the extreme of the distribution, resembling mild hemophilia, but also mildly reduced clotting factor levels between 0.41 and 0.60 IU/mL are associated with bleeding.

Bimler, D & Kirkland, J (2009) Colour-space distortion in women who are heterozygous for colour deficiency. Vision Research 49: 536-543

from the Introduction:

  About 15% of women are heterozygous for some form of colour vision deficiency (CVD). That is, they possess a genetic abnormality on one of their two X chromosomes, affecting the photopigments (opsins) which subserve colour vision. The retina of a heterozygous woman is a mosaic in which some cone cells express the aberrant gene while others express the normal copy, depending on which X chromosome is active (inactivation of one X chromosome occurs randomly in retinal stem-cells at some stage of fetal development). The normal cells are sufficient to provide full trichromatic vision.


Did Darwin ever reach the conclusion that selection will remove variation?

After reading your question, I had a vague memory that this subject was indirectly touched upon in "On the Origin of Species", so I did some text searches (in this pdf version I found online). From what I can see, Darwin never used the technical term 'variance' (I don't know how old this use of the word is), but 'variability' is often used, both with regard to accumulated variation but also meaning variation between individuals within a population.

All-in-all, I could not find clear support for the idea that selection will decrease the amount of variation. However, there are number of passages where the subject of variation vs selection comes up (often indirectly), but, to me, these just as often (most often?) indicate that Darwin saw no risk that selection would reduce variation as the opposite. Here are the most interesting passages I could find (searching for combinations of 'variab*', 'selection', 'decrease' etc), with page references referring to the pdf version and a short comment below each quote:

  A large number of individuals,
  by giving a better chance for the appearance within
  any given period of profitable variations, will compensate
  for a lesser amount of variability in each individual,
  and is, I believe, an extremely important
  element of success.
  (p. 44)

This is clearly discussing amounts of variation within species, where large numbers can compensate for a smaller amounts of standing variability, by increasing the chance of advantageous mutations.

  Nothing can be effected, unless favourable variations
  occur, and variation itself is apparently always a very
  slow process. The process will often be greatly retarded
  by free intercrossing. Many will exclaim that
  these several causes are amply sufficient wholly to
  stop the action of natural selection. I do not believe
  so. On the other hand, I do believe that natural selection
  will always act very slowly, often only at long
  intervals of time, and generally on only a very few
  of the inhabitants of the same region at the same time.
  (p. 103)

Not directly related to selection vs variation, but deals with the rate of evolution vs amount of variation.

  But what here more
  especially concerns us is, that in our domestic animals
  those points, which at the present time are undergoing
  rapid change by continued selection, are
  also eminently liable to variation. Look at the breeds
  of the pigeon; see what a prodigious amount of difference
  there is in the beak of the different tumblers,
  in the beak and wattle of the different carriers, in the
  carriage and tail of our fantails, &c., these being the
  points now mainly attended to by English fanciers.
  Even in the sub-breeds, as in the short-faced tumbler,
  it is notoriously difficult to breed them nearly
  to perfection, and frequently individuals are born
  which depart widely from the standard. There may
  be truly said to be a constant struggle going on between,
  on the one hand, the tendency to reversion to
  a less modified state, as well as an innate tendency
  to further variability of all kinds, and, on the other
  hand, the power of steady selection to keep the breed
  true. In the long run selection gains the day, and we
  do not expect to fail so far as to breed a bird as coarse
  as a common tumbler from a good short-faced strain.
  But as long as selection is rapidly going on, there
  may always be expected to be much variability in
  the structure undergoing modification.
  (p. 141)

This is maybe the most interesting passage, which to me indicates that he saw little risk that selection could/would limit variability (see especially beginning and end).

  For forms existing in larger
  numbers will always have a better chance, within
  any given period, of presenting further favourable
  variations for natural selection to seize on, than will
  the rarer forms which exist in lesser numbers. Hence,
  the more common forms, in the race for life, will tend
  to beat and supplant the less common forms, for
  these will be more slowly modified and improved.
  (P. 162)

Also on limitations for variation that selection can act on, and the value of large populations.

  ... firstly, because new varieties are
  very slowly formed, for variation is a very slow process,
  and natural selection can do nothing until
  favourable variations chance to occur, and until a
  place in the natural polity of the country can be better
  filled by some modification of some one or more
  of its inhabitants. And such new places will depend
  on slow changes of climate, or on the occasional immigration
  of new inhabitants, and, probably, in a still
  more important degree, on some of the old inhabitants
  becoming slowly modified, with the new forms
  thus produced and the old ones acting and reacting
  on each other.
  (p. 163)

On the limiting nature of variation, but does not connect selection to decreased variation.

  It cannot be asserted that organic beings
  in a state of nature are subject to no variation; it cannot
  be proved that the amount of variation in the
  course of long ages is a limited quantity; no clear
  distinction has been, or can be, drawn between spe-
  cies and well-marked varieties.
  (p. 425)

On variation over the long run.

These are the most interesting sections I found on the subject from my (quick and limited) searches. I hope you find them useful. However, this is only based on the first edition of "On the Origin of Species", and it is possible that it is is modified in later editions or that he touches upon this in his other writings. However, when looking at these particular passages in the sixth edition, I cannot see a major change in his thinking.


This is very likely a species in the Amaurobiidae superfamily, and I agree appears to be Callobius severus (the hackled-band weaver or the hackledmesh weaver).

 Source: Bugguide.net

 Source: Kyron Basu 2012
Moldenke et al. 1987 provide a key to spiders of the Pacific Northwest. Importantly, they note:

adult genitalia are necessary for identifying species and separating
Callobius from Amaurobius.

For example, here is a picture of Amaurobius ferox (Hackledmesh Weaver)

 © Danny Steaven 2008

I've seen numerous sites conflate this species with C severus and actually I've seen sources that identify them both as the "Hackledmesh Weaver".

So although the OP's specimen strongly resembles Callobius severus, a scope is necessary to truly identify to species. This Penn State page provides good information regarding these similar looking species in the superfamily.

Callobius and Amaurobius species have similar life histories and behaviors. They are most often found in damp locations under bark, leaf litter, and stones, as well as in woodpiles and other protected areas.

Stephen Ellis Lew (2011)  produced an atlas to the genitalic morphology of the Callobius genus, and he proposed a morphological diagnosis that is more consistent with principles of homology than those previously in use. [See the link for his dissertation on the subject].
Callobius severus
Description:

Cephalothorax and legs = reddish to dark brown [Source].
Abdomen = dark to light grey with fine hairs; often with large, bilaterally mirrored paler spots.

Ecology:

Nesting woodland species commonly seen in the Pacific Northwest

McIver et al. (1990) suggests that this species of spider is one of many that is characteristic of young forests.

Is it Dangerous?:

Not according to this Penn state website:

The one verified record of a bite by an immature Callobius species resulted in pain, itching, swelling, redness, and nausea.

Vetter & Antonelli provide evidence for how to differentiate this species from the "more dangerous" hobo spider.

in the side view, the palp of Callobius males has large, conspicuous, pointed projections (Fig. 7).


Using DTNP to find free thiol groups on a protein

This is a perfectly reasonable result. Remember that you are measuring an average value for a very large population of BSA molecules. Essentially what the 0.4 means is that at any one time, about 40% of the BSA molecules have a free thiol, while the rest of the cysteine residues are disulfide-bonded.


Is taking a shower unnecessary if good bacteria surround our skin?

the Phrase "good bacteria" doesn't mean it's not gonna be harmful to you . actually they called : normal flora . they are refer not just to bacteria they include all types of microorganisms .
http://www.ncbi.nlm.nih.gov/books/NBK7617/
I give you an example : there is some bacteria in our bowel they help our digestive system to work better . but these bacteria in case of some infectious disease or in the people with Immunodeficiency disease like AIDS turn to be pathogens .
the vision of David Whitlock is not irrelevant in fact in the field of industrial biotechnology we use micro organism to clean and digest environmental pollution like oil spills & ... just like him use bacteria too clean out his body but in fact the thing is he put non pathogens bacteria on his skin so there is no place for other bacteria .
but as a professional view  there amount of normal flora on our skin is 10 times more than our cells so you can not think our skin is a surface and you can just wipe every thing on it just by showering and ... I'm telling you these thing are odd and there is no scientific evidence that support this odd things . maybe in 100 years when we ran out of drinking water we force to make cleaning sprays base on this view . but you know such a crazy but possible thing in theory .


Are tumor-associated antigens unique to cancerous cells?

Carcinogenic tumor associated antigens correspond to any peptide chain (antigen) which triggers an immune response from the host. This means that they can be found anywhere inside, at the membrane, and outside of the cell: inside the cell (intracellular), at the cellular membrane and exposed to the extracellular environment, or even secreted.

Depending on the oncogene, they can be also eventually be over-expressed (anywhere there are supposed to be, including the membrane of cells).


Difference between prions and amyloid proteins?

Amyloids are protease resistant insoluble fibrils formed because of (mis)folding and aggregation of soluble proteins (Rambaran and Serpell, 2008, Sabate et al., 2015). The first definition of prion was given by Prusiner (1982):

  Because the novel properties of the scrapie agent distinguish it from
  viruses, plasmids, and viroids, a new term "prion" is proposed to
  denote a small proteinaceous infectious particle which is resistant to
  inactivation by most procedures that modify nucleic acids.

Many prionic diseases are characterized by amyloid fibril formation and therefore some (if not many) researchers consider prions to be a subset of amyloids.

  Prions are considered a subclass of amyloids in which protein
  aggregation becomes self-perpetuating and infectious.
  (Sabate et al., 2015)

However, the amyloid structure formation is not essential either for the autopropagation or disease progression (Moore et al., 2014).

  When wild-type C57BL/10 mice are infected intracranially with the RML
  mouse prion strain, PrPSc accumulates in diffuse nonamyloid deposits
  and brain pathology is distinguished by the hallmark gray matter
  spongiosis for which TSEs are named. Conversely, when transgenic mice
  homozygous for PrPC lacking the GPI anchor (Tg44 or “anchorless” mice)
  are infected with the same RML strain, the incubation time is longer
  and PrPSc accumulates in dense perivascular amyloid plaques with
  little or no gray matter spongiosis.9−11 Similar amyloid PrPSc
  deposition and disease resulting in death has been observed in humans
  with an aberrant stop codon in the C-terminal portion of the PrP
  sequence, resulting in the generation of PrP lacking the GPI anchoring
  group as well as some amino acid residues.13−16 Thus, GPI-anchoring of
  PrPC to the plasma membrane appears to be a primary factor determining
  the type of PrPSc deposition and the development of brain pathology.

You can say that the prion protein PrPC is amyloidogenic but it is not an amyloid.

There are non-pathogenic (and in fact useful prions) found in fungi. Many of these beneficial prions also form the amyloid (like) structure but they can be disaggregated by chaperones (Wickner et al., 2018). Now again, it is not essential for these beneficial prions to form an amyloid structure.

  Prions (defined as “infectious proteins”) need not be amyloids. The
  vacuolar protease B (Prb1p) of Saccharomyces cerevisiae is made as an
  inactive precursor that is normally cleaved and so activated by the
  action of protease A (Pep4p) [32]. However, in the absence of Pep4p,
  mature active Prb1p can activate its own precursor [33]. This
  self-activation can propagate and pass from cell to cell in an
  infectious manner, acting like a prion, and named [BETA] [34]. In the
  absence of Pep4p, [BETA] is necessary for meiosis and spore formation
  and for survival in stationary phase [34]. It is thus a functional
  prion.

[SMAUG+] is another example of a non-amyloid yeast prion which has beneficial effects (Chakravarthy et al., 2019 and Itakura et al., 2019; Jarosz group). Unlike Prb1p, [SMAUG+] actually forms self-propagating aggregates.

My summary

Many known prions are amyloidogenic and can switch to amyloid form. However, as per the definition, prions are "infectious" or in other words, self-propagating proteins.
What qualifies as a prion depends on our definition. Mode of action of most known prions is catalyzing a change in the protein fold. Wickner et al (as quoted above) reason that the original definition does not explicitly include the mode of action and hence proteins that activate themselves via proteolysis should also be considered prions. Jarosz's group has shown an example of a non-amyloid prion that forms self-propagating aggregates. It quite likely that more such proteins will be discovered in near future.

In any case, "amyloid" is a structural property whereas "prion" is a functional property and they cannot be considered a sub/superset of one another, even if they happen to be correlated.

The bottomline is:
Amyloid is a form of supramolecular protein structure which is often formed by many prionic proteins. However, not all amyloid forming proteins are prionic and not all prions necessarily form amyloids.


Yes, normal DNA extraction protocols fragment genomic DNA.  In my experience, extracted DNA tends to have a size distribution on the order of 10 - 20 kilobase pairs (kbp), independent of the protocol and source organism (assuming a chromosome size >> 20 kbp).  This seems to be corroborated by what I can find online -- see the gel below from Successful tips of DNA extraction and PCR of plants for beginners

Figure 1. Agarose gel electrophoresis of DNA samples extracted from horticultural plants. M, molecular weight marker. Modified from Kasajima et al. (2013)

as well as this gel from ThermoFisher

Genomic DNA purified with the Genomic DNA Purification Kit
Agarose gel (0.7%) electrophoresis analysis of undigested (odd lane numbers) and EcoRI digested (even lane numbers) DNA samples.
M – Lambda DNA/HindIII Marker [top band is 23130 bp]
1, 2 – human blood
3, 4 – human lymphocytes
5, 6 – human placenta
7, 8 – mouse liver
9, 10 – Hedera helix
11, 12 – Haemophilus influenzae
13, 14 – E.coli ER2267
15, 16 – Bacillus subtilis

The consistent size of extracted genomic DNA across organisms is a physical constraint rather than a genetic one.  When unwound and unprotected by the cell and nuclear envelopes, chromosomes are subject to the shearing forces of pipetting and vortexing.  Consider a mile-long length of high-test fishing line.  Coiled in the box or around a reel, the line is strong and stable.  If you laid the line out end-to-end, however, there would be many places along its length where the line gets snagged, knotted, and torn.
As hinted by canadianer, DNA fragmentation is necessary for most sequencing methods (specifically whole-genome shotgun sequencing, not sequencing of specific PCR amplicons).  As an example, Illumina sequencing platforms generally require libraries with fragment size distributions between 300 and 600 bp, and fragments larger than 1000 bp are sequenced inefficiently.  So, after DNA extraction, additional steps are required to further reduce the average DNA fragment size prior to sequencing adapter ligation.  The most common method of genomic DNA fragmentation for short-read sequencing is sonication, though enzymatic methods are also used in some kits.
Recently, long-read sequencing technologies have been developed to overcome the difficulty of assembling short reads.  Nanopore platforms can sequence DNA fragments that are 100s of kbp long.  To prepare these extremely long libraries, special care must be taken to not shear the DNA during extraction.  The Journal of Visualized Experiments provides a good guide on how to extract and process high-molecular-weight DNA:
Gong, L., Wong, C. H., Idol, J., Ngan, C. Y., Wei, C. L. Ultra-long Read Sequencing for Whole Genomic DNA Analysis. J. Vis. Exp. (145), e58954, doi:10.3791/58954 (2019).


Is it possible to identify this microscopic particle?

This is an plain old ice crystal. Welcome to the microscopic world! When water evaporates, high-energy molecules escape, leaving low-energy molecules of water. The droplets cool this way, and they freeze - the dirt or debris in the crystallizing droplets make curious patterns. Here are some in my samples I made last week, for comparison:

How about a close-up?

Here's one I made by accident, this time featuring a fluorescent dye.

Notice how cooling droplets never freeze the same way twice. You'll never find two identical crystallized droplets!

If you want to avoid these, prevent evaporation by putting nail polish or glycerol around and between your coverslip and slide, so that water cannot escape.

OFFTOPIC: You should also encourage your kid to try make some of his/her own crystals. You can use food dyes to make beautifully patterned art. Good moment to teach your kid about nucleation; why water doesn't freeze at 0° C, but rather at temperatures that tend to decrease as the volume of the water decreases and as the water impurity increases. And maybe sneak in a funfact about how the freezing of small water droplets into ice is an important process in cloud formation.


I would say that the left part of the picture depicts 2 stages of the development of cysticercoid, while the right part shows the consecutive stages in the development of cysticercus. These two parts represent different species of tapeworms in the same stage of their developments.


I don't really know what you mean by "abandoned children".  Adopted children?  Children in the wild?  Have you read the Wikipedia article on the subject?  If you want to know how it was studied, just take a look at the references, it's pretty straightforward.

Heritability simply means how much variation in a trait is due to genetics, which is usually easiest to test in monozygotic twins.  Here's a good example where they did just that - they compared identical (monozygotic) and fraternal (dizygotic) twins raised apart or separately, finding:

  General cognitive ability yielded a heritability estimate of about .80 in two assessments 3 years apart as part of the Swedish Adoption/Twin Study of Aging. This is one of the highest heritabilities reported for a behavioral trait. Across the two ages, average heritabilities are about .60 for verbal tests, .50 for spatial and speed-of-processing tests, and .40 for memory tests. For general cognitive ability, the phenotypic stability across the 3 years is .92 and stable genetic factors account for nearly 90% this stability.

Here's another example doing basically the same thing.  The rest of the enWiki article gives a good breakdown of all the various factors involved in making this such a complex issue, as well as what was studied.


I think this is an Egyptian Goose (Alopochen aegyptiacus), see the image (First from the Wikipedia article, the second from here, interestingly taken in Irvine):

You can see the distinctive spot around the eye and also the colored feathers on the back. Also, this bird is too big to be a duck.


Can neurotransmitter concentrations in the synaptic cleft add up if there are several impulses in quick succession?

The answer by bpedit is a good explanation of temporal/spatial summation, which can be partly a postsynaptic phenomenon (due to membrane time constants or second messenger sytems, for example).

Your specific question is about whether extracellular neurotransmitter levels sum over time. This definitely occurs regularly with "neuromodulatory" neurotransmitters like serotonin (others that behave similarly include dopamine and norepinephrine/epinephrine). "Faster" neurotransmitters like glutamate and GABA are cleared more quickly, though there are complicating factors there as well that are outside the scope of this question.

Although the summation has been shown many times, I looked quickly for an example and found the paper by Bunin and Wightman, 1998. Figures 2-6 all show extracellular serotonin concentrations that are elevated for seconds after release (let me know in the comments if you can't access this paper at your institution), and they show the changes in extracellular concentrations with multiple stimulus pulses (see in particular Figure 3).


Alpine flower identification — Italy/France

This is not Jasione montana, but Phyteuma orbiculare, another member of the family Campanulaceae. Except for the different flowers,
Jasione has no leaves on the upper part of the stem. This plant has. And these leaves are toothed and have a heart-shaped base, unlike Jasione.
And finally: Phyteuma is resticted to calcarious soils, whereas Jasione prefers non-calcarious soils.

https://en.m.wikipedia.org/wiki/Phyteuma_orbiculare


The cells never died in the sense that they kept replicating, individual cells still died. They were safely cultured in petri dishes before Henrietta Lacks died. The cells came from a tumor that developed from her cervix. The cervical cancer cells had developed high telomerase activity. Telomerase builds telomeres on the ends of DNA, protecting the chromosomes. In normal cells, telomeres tend to get shorter as the cells divide, eventually the DNA is damaged and the cells die. HeLa cells are protected because their telomeres are well maintained.

There was nothing special about Henrietta lacks that made her tissues immortal, so digging her up wouldn't be worth it. Her family would probably get mad too.


what is this mushroom and how to grow this mushroom?

This is an Ascomycota from the genus Morchella, called morel:

Morels are edible: despite the Wikipedia page I linked above saying that Morchella has hydrazine, according to Ammirati, Traquair and Horgen (1986):

  There is no evidence that Morchella species contain gyromitrin* or related compounds.

* A hydrazine compound.

Source: Ammirati, J., Traquair, J. and Horgen, P. (1986). Poisonous mushrooms of the northern United States and Canada. 1st ed. Minneapolis: University of Minnesota Press.

PS: Your second question ("how to grow this?"), however, seems to be off topic here at Bio SE.


What do trans-fats do when in human body?

In Ascherio & Willen (1997) it is mentioned that, and I quote:

  [...] Trans fatty acids increase plasma concentrations of low-density lipoprotein (LDL)
  cholesterol and reduce concentrations of high-density lipoprotein (HDL) cholesterol relative to the parent natural fat. [...] [T]rans fatty acids increased the plasma ratio of total to HDL cholesterol nearly twofold compared with saturated fats. On the basis of these metabolic effects and the known relation of blood lipid concentrations to risk of coronary artery disease, we estimate conservatively that 30 000 premature deaths/y in the United States are attributable to consumption of trans fatty acids.

The US Heart Foundation explains in more layman's terms the same principles:

  Trans fat is a type of unsaturated fat that behaves like a saturated fat because of its chemical structure. It increases our risk of heart disease by increasing the “bad” LDL cholesterol, while also lowering the “good” HDL cholesterol in our blood.

And from the Better Health Channel Australia we learn why LDL is 'bad':

  Too much cholesterol circulating within LDL in our bloodstream leads to fatty deposits developing in the arteries. This causes the vessels to narrow and they can eventually become blocked. This can lead to heart disease and stroke.

Reference
Ascherio & Willen, Am J Clin Nutr 1997;66(suppl):1006S-lOS.


Why does the pET- expression vector contain a LacI gene additionally to the one in the genome?

According to this article, a single lacI gene copy gives rise to about 10 copies of lacI protein per cell, and we can conclude, therefore, that this is the amount required to keep a single lac operon repressed.  The article also mentions the lacIQ mutation in the promoter of lacI that results in a ten-fold increase in the level of lacI protein.

If a lac expression construct is present at more than 100 copies per cell the result will be leaky repression, and this can result in selection for mutations in the gene of interest if it has deleterious effects on the host bacteria. The easiest way around this problem is to put a lacI (or lacIQ) gene on the expression plasmid so that repressor levels are commensurate with the number of copies of the lac operator, as in the pET vectors.


Has the most recent common ancestor of all living birds lived after dinosaur mass extinction?

I suppose that by the mass extinction, you are referring to the Cretaceous–Paleogene extinction event that happened 66 mya. The Most Recent Common Ancestor (MRCA) of all birds lived about 113.3 mya (early Cretaceous, according to this in oneZoom.org).

So yes, the MRCA of all birds is definitely older than the Cretaceous–Paleogene extinction event. As you said, this also mean that some ancient dinosaurs are/were more related to some extant birds than some extant birds are related.

You (the OP) might not need it but some other readers might need clarification about phylogeny with the post If dinosaurs could have feathers, would they still be reptiles?


How does a fungus protect itself from digestion by other fungi?

In general fungal cell walls are resistant to whatever enzymes or compounds they are excreting to break material down for consumption. Conceptually, it is a little like your stomach lining being resistant to stomach acid. For a more detailed answer you may have to head over to your local university and find a Mycologist.

There is ongoing research on how fungi actually "eat." You can look up fungal endocytosis if you wish to research it more. There may be other mechanisms as Shigeta mentions.


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


Does probiotics bacteria from yogurt live in the mouth too? Does it populate the mouth/throat or just the gut?

of course they do... the question is for how long.
Probiotics will tend only to affect the microbiome in the digestive tract for a while.  For yogurt supplemented with probiotics subjects microbiomes drifted back within 48 hours.  Depending on your diet the individuals can hang out for a while or persist.  Children, who tend to drink more dairy have a more persistent Lactobacillus signature.


Help identify this insect with a fan tail

This is the nymph stage of a planthopper, an insect in a suborder of the hemipterans.

The "fiber-optic-like" tail is actually made out of wax! From Wikipedia

  Nymphs of many [planthoppers] produce wax from special glands on the abdominal terga and other parts of the body. These are hydrophobic and help conceal the insects. Adult females of many families also produce wax which may be used to protect eggs.

The fact that there are about 12,5000 species of planthoppers and I am fully unfamiliar with the fauna of Colombia, I can only provide a quick image confirming that it is a planthopper. (Perhaps you have a field guide or key available to you to help ID to genus or species)

 Credit: Malcolm Burrows, source

You can find an aditional image of a species more similar to yours here.


What is the meaning of the word 'bin' in the context of RNA-Seq?

It's talking about things like "TSS_up_1kb", which is a "bin" of 1kb upstream of the gene. A bin is a somewhat generic term that in this context means "a region of some given size". Another example where you might see the term is with histograms. There, values are grouped into bins, with each bin then being represented by a separate bar in the graph.


How is the Energy Systems Language used in ecology?

Energy systems language is definitely still used in systems ecology, ecosystems ecology, and ecological engineering. It can be used in other aspects of ecology depending on the approach of the ecologist, some ecologists appreciate it more than others. For a broad snapshot of how science is currently building upon Odum's 1983 Intro to Systems Ecology, check out a Google Scholar search for the latest papers citing that text by Odum.

In my experience with it, energy systems language and energy flow diagrams introduced by Odum are used as helpful conceptual tools: understanding and organizing complex systems qualitatively and then potentially quantitatively; putting useful constraints and guidelines on brainstorming the effects of adjustments to complex systems; etc. This can be done in a teaching context, helping students understand systems and bridging the fields of engineering and ecology. It can also be done in a high-level professional context, sorting out the intricacies and potential solutions of very complex environmental problems.

I find that energy systems language is used most wherever the study of complexity and ecology intersect. This is especially true in the study of ecological complex adaptive systems and in studying agro-ecology. Even in those cases it depends on the ecologist in question: those with more of an engineering background tend to appreciate Odum's framework, whereas those without an engineering background may rely on other frameworks.


How are Thyroid Stimulating Ab destroying thyroid tissues?

Thyroid stimulating antibodies (sTRAb) don't destroy thyroid tissue. To the contrary, they have a TSH-like effect on thyrocytes and therefore lead to hyperthyroidism and thyroid growth resulting in goiter. The exception is Graves' disease with Hashimoto component. Here, the thyroid is also affected by cytotoxic T cells and antibodies directed against thyroid peroxidase, which gives rise to destruction of the thyroid. But even in this case, it aren't the sTRAb, which destroy tissue.

Perhaps healthy tissues refers to extrathyroidal tissues. Due to unknown reasons several tissues including skeletal muscle, heart muscle, adipose tissue and skin have TSH receptors, and they are affected by sTRAb, too. Hypertrophy results from cross-talk of TSH receptors with IGF-1 receptors in Graves' disease.

References

Dietrich JW, Landgrafe G, Fotiadou EH. TSH and Thyrotropic Agonists: Key
Actors in Thyroid Homeostasis. J Thyroid Res. 2012;2012:351864. doi:
10.1155/2012/351864. Epub 2012 Dec 30. PMID 23365787.
Krieger CC, Neumann S, Place RF, Marcus-Samuels B, Gershengorn MC.
Bidirectional TSH and IGF-1 receptor cross talk mediates stimulation
of hyaluronan secretion by Graves' disease immunoglobins. J Clin
Endocrinol Metab. 2015 Mar;100(3):1071-7. doi: 10.1210/jc.2014-3566.
Epub 2014 Dec 8. PMID 25485727.
Krieger CC, Place RF, Bevilacqua C, Marcus-Samuels B, Abel BS, Skarulis MC, Kahaly GJ, Neumann S, Gershengorn MC. TSH/IGF-1 Receptor Cross Talk in Graves' Ophthalmopathy Pathogenesis. J Clin Endocrinol    Metab. 2016 Jun;101(6):2340-7. doi: 10.1210/jc.2016-1315. PMID 27043163.
Yoo WS, Chung HK. Recent Advances in Autoimmune Thyroid Diseases. Endocrinol Metab (Seoul). 2016 Aug 26. PMID 27586448.


How to search for a DNA sequence in a genome on ENA (European Nucleotide Archive)?

While it is much better/easier to download and do the exact search on your own, it is possible to do something similar, online. You can use NCBI-BLAST and increase the word length and mismatch/gap penalty. It also allows restricting the subject space; you can even align two sequences. The BLAST on ENA does not have much flexibility (subject restriction/word length). Perhaps you can look for a duplicate sequence on NCBI.

If this genome is available on UCSC genome browser then you can use BLAT too. However, it only accepts sequences larger than 19nt.


Why is the hexose monophosphate shunt called a direct oxidative pathway?

This answer is based on a 2002 autobiographical account of the work of Bernard L. Horecker entitled The Pentose Phosphate Pathway. Here he refers to “direct oxidative pathway” but does not unambiguously explain this, so I shall summarize my interpretation and then provide evidence in terms of quotations.

Summary of my interpretion of Horecker’s account

When what I shall initially refer to as the hexose monophosphate shunt (HMS) was being elucidated in the late 1930s and the 1940s it was thought that its main purpose was the same as that was envisaged for aerobic glycolysis — to oxidize glucose to provide energy — and was merely an alternative way of doing this. The term ‘direct oxidative pathway’ was used to distinguish it from the glycolytic pathway (then refered to as the Embden–Meyerhof–Parnas pathway), presumably because six cycles of the oxidative phase e could completely oxidize one molecule of glucose 6-phosphate to carbon dioxide, whereas glycolysis only oxidized it to pyruvate. Presumably this was regarded as ‘indirect oxidation’ because complete oxidation required the further metabolism of pyruvate using the tricarboxylic acid cycle.

The term ‘direct oxidative pathway’ fell out of use as it was realized that the main functions of the pathway were to provide pentoses for nucleic acid synthesis and NADPH for synthesis of fatty acids, steroids, and reduction of oxidized glutathione. It was for this reason also that the name most commonly used for the pathway changed to the pentose phosphate pathway, transfering the emphasis to one of the products.

Quotations from Horecker

  …Haas arrived from Warburg’s laboratory in 1939. Haas asked me to join
  him in the search for an enzyme that would catalyze the reduction of
  cytochrome c by reduced TPN (now NADP). This reaction was thought to
  be the missing link in the electron transport chain from substrate to
  oxygen and marked the beginning of my interest in what was then
  thought to function as a direct oxidative pathway for the metabolism
  of carbohydrate but is now known as the pentose phosphate pathway…

  …These observations gave rise to the hypothesis that the oxidative
  pathway was really a cyclic mechanism for the direct oxidation of
  carbohydrate. With each turn of the cycle one molecule of carbon
  dioxide would be produced, and the pentose phosphates formed would be
  metabolized back to hexose phosphates to start another cycle. Six
  turns of the cycle would result in the complete oxidation of one
  molecule of glucose…

  …The function(s) of the new
  pathway, however, turned out to be quite different from the pathway
  for the direct oxidation of carbohydrate that we had expected. It
  provides two mechanisms for the production of ribose 5-phosphate. One
  is the “oxidative branch” of the pathway, which also generates 2 eq of
  TPNH (NADPH). Ribose 5-phosphate can also be formed directly from
  hexose and triose phosphates by the non-oxidative rearrangements
  catalyzed by transketolase and transaldolase. Where large quantities
  of NADPH are required, as in the synthesis of fatty acids or sterols,
  the excess pentose phosphates produced would be recycled back to
  hexose monophosphates.

[My emphasis]

Google Books ngrams of term usage


Is water movement across cell membrane purely diffusive or it always requires channels?

Water across cell membranes occurs due to osmosis( which is based on a concentration gradient). so water diffuses through the cell membrane. sometimes water channels called aquaporins can be found.
https://www.anaesthesiamcq.com/FluidBook/fl1_2.php
https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/aquaporin
In the loop of Henle, the water, and Na+ & Cl- exchange occurs due to the counter-current principle takes place. the interstitial fluid has a certain sodium chloride concentration. the filtrate that is entering the descending limb of the loop of Henle, has a particularly low NaCl concentration.so because of that water moves from the loop of Henle to the interstitial fluid.simultaneously, at the ascending limb of the loop of Henle just adjacent to that particular point, water concentration is high in the interstitial fluid. so because of that NaCl moves to the interstitial fluid (Na+ actively, and for ion balance, Cl- passively.) this happens along the length of the loop of Henle. what restricts water movement from the ascending limb of the loop of Henle is that that limb has no aquaporins and the descending limb has numerous (with relative to other places in the nephron). anyway, here's a link for you.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3468499/


Are cortical columns restricted to somatosensory cortical sections?

Cortical columns (also called minicolumns) are not limited to the somatosensory cortex. As shown in this paper (which discusses how the miniucolumns change in response to aging), it is also present in the associative cortex.

However, it should be noted that "minicolumn" in this paper is defined as neurons that are close together and form a minimum spanning tree, as shown below.

Connectivity doesn't seem to be analysed, probably because connectivity information is really painful to collect, but I'm not sure given I'm an amateur when it comes to neuroscience.


Alternatives to ethidium bromide for staining small nucleic acids?

A list of dyes is available here and a list of dyes specific to nucleic acids is available here. I think you have two choices the SYBR Gold nucleic acid gel stain (S11494) which can be detected under UV light (not sure if it can be used with polyacrylamide gels). Your other option which can be used with polyacrylamide gels is the SYBR Green II RNA gel stain (S7564, S7568, S7586), this stain can be detected with UV light post-electrophoresis. It states RNA in the name but it can also be used for ssDNA.

Hope this helps


How does energy conversion happen (chemical to mechanical?) in moving body muscles?

The conversion from chemical to mechanical energy is in general done by molecular motors which perform a power-stroke, using the hydrolysis of adenosine triphosphate (ATP) or more rarely of GTP to power a change of their conformation while bound to cytoskeletal elements.

Molecular motors include myosins, which is the molecular family powering muscles in interaction with actin filaments but also other cells e.g. for their motility or for morphogenesis. animation  of muscle contraction

There are also kinesins and dyneins, not used for muscle function, but which perform e.g. transport of "cargo" organelles along microtubules.

An alternative way to produce mechanical energy is via ion pumps, as is the case in flagellar rotors.


Can TGF beta family induce all somatic stem cells?

Signalling in the TGFβ pathway normally puts a brake on the progress of cells through the cell cycle - it counteracts the action of myc for example, partly by regulating the expression of myc. In Burkitt's lymphoma myc escapes this regulation because of a chromosomal translocation, tipping the regulatory balance over to uncontrolled cell growth.

This anti-proliferative action of TGFβ signalling is so critical that you might expect it to be ubiquitous in cells, and the expression atlas entry for the TGFβ receptor is consistent with this.


What is this Sacrificial Reproductive Strategy Called?

It is called Semelparity.

From wikipedia:

  Semelparity and iteroparity refer to the reproductive strategy of an organism. A species is considered semelparous if it is characterized by a single reproductive episode before death, and iteroparous if it is characterized by multiple reproductive cycles over the course of its lifetime.

You see semelparity as suicidal but it is more interesting to generalize survival after reproduction in all kind of species and ask why would an individual survive if it won't reproduce anymore anyway?

Why would an individual survive if it won't reproduce anymore?

From an evolutionary point of view, there is no point to keep living after the reproductive age. You will note a few interesting exceptions to the rule though, including Homo sapiens, where the female keep living relatively long after her reproductive age. Of course, modern medicine is part of the explanation but we tend to think that modern medicine alone is not sufficient. Another explanation is based on kin selection and is called the grandmother hypothesis. In consequence, semelparous species die right after reproduction.

Evolution of semelparity/ieroparity

I don't think this point can be summarized in a few words. In consequence, I will just invite you to have a look at wikipedia for an introduction on the subject.

How common is semelparity?

Iteroparity is more common. However it would be wrong to think semelparity is extremely rare or that it exists only in salmon species (in plural).

In invertebrates, Many insects (butterflies, cicadas, and mayflies) are semelparous as well as some arachnids and moluscs (some squids and octopus). In vertebrates, semelparity is rarer, but there are some frogs (i.e. gladiator frog), fishes (smelt, capelin), lizards (i.e. Labord's chameleon) and marsupials (such as the famous opossum). Finally there are semelparous plants (some agave and some bamboos). In unicellular species (and some multicellular species, such as some trees for example), the concept of semelparity/iteroparity may well not apply easily and depend on a philosophical discussion of the identity of an individual.


Are specialized cells considered to have life?

Life is defined in many ways.
Common definitions are usually simplified definitions. Under some definitions it would be "life" under others it would not be. But it doesn't matter. The problem you are having is thinking definitions of life are anything more than artificial categorization. Really there is no difference between living things and the rest of chemistry, or at least there is a smooth gradient connecting them, but we humans can't easily think that way, so we create descriptive but imperfect definitions to help our thought processes. There is a lot of gray area for any definition of life, and you have found one.


Vitiligo is a loss of skin pigmentation that causes patches of lighter skin as the immune system attacks melanocytes. It can eventually progress to cover the entire body.

Edit:

Ongenae, K., Van Geel, N. and Naeyaert, J.-M. (2003), Evidence for an Autoimmune Pathogenesis of Vitiligo. Pigment Cell Research, 16: 90–100. doi: 10.1034/j.1600-0749.2003.00023.x


If there is a stimulus at E, there will be depolarization (membrane becomes relatively more positive). It is just that no action potentials are fired. Therefore, if a strong stimulus does arrive, it will depolarize the membrane to an extent depending on its strength. It will increase the height of the succeeding B phase or reduce the dip of the succeeding E phase. If it is strong enough, it might persist above the threshold till the refractory period is over, and then an action potential can be fired.


How do paper wasp larvae not fall from their nest?

Social wasp larvae hatch from an overhanging egg, and they grow up through a series of skin moults, typically 5 in number. The shed skins accumulate terminally behind their pointed anus, where the egg chorion peduncule remain. These wasps have a special body construction and skin texture (e.g. abdominal lobes, numerous spikes) that allows for pressing against the cell walls.

You can see these traits from high-resolution images shown in the larval descriptions:
Florida Entomologist, 95(4):890-899 (2012) https://doi.org/10.1653/024.095.0411
Sociobiology 63(3): 998-1004 (2016) http://dx.doi.org/10.13102/sociobiology.v63i3.988

Finally, it should be minded that gravity doesn't affect small insects in the same way it affect larger mammals like humans. This means it way takes less effort and sticky secretions for these bugs to hang onto walls than we typically imagine by common sense.

I don't know of any dedicated estimations on fallen larvae, but I guess the event isn't common, unless perhaps in abnormally structurally-challenged nests.


How long is one generation for a mosquito?

According to this information page from the American Mosquito Control Association, the generation time for a mosquito at 70${}^\circ$ F is about 14 days. The precise generation time depends on temperature and access to nutrients, but yes, it seems reasonable that mosquitos can go through 10 generations or more in a year.


Can upper motor neuron lesions cause hypotonia?

The rule-of-thumb you (and I) were taught reflects the role of the central and peripheral nervous systems in establishing muscle tone. Deprived of CNS regulation, alpha motor neurons increase in their responsiveness to spindle afferents, resulting in hypertonia. Deprived of PNS regulation, muscle spindles are less able to react to input, resulting in hypotonia.

Beyond this rule-of-thumb, things aren't as black-and-white. As you have pointed out, there is such a condition as central hypotonia. In fact, the NINDS includes the CNS as an area where damage can cause hypotonia:

  "Hypotonia can happen from damage to the brain, spinal cord, nerves,
  or muscles." (source)

Purves et al. also note that upper motor neuron syndrome involves an "initial period of 'hypotonia' after upper motor neuron injury" (Neuroscience, 2012, p. 395).

To your question: Yes, the rule-of-thumb is not always accurate and upper motor neuron lesions can cause hypotonia.

If you're looking for a hypothetical mechanism, consider this: Purves et al. also state that hypertonia is "probably caused by the removal of suppressive influences exerted by the cortex" (p. 396). So it is conceivable that overstimulation of these inhibitory control systems by some sort of unique upper motor neuron lesion could result in hypotonia.


Why some muscles have more tendons than others?

If you observe the general structure of the locomotor system, you will be able to roughly separate muscles in two main groups:

the muscles used for static work and position maintenance.
those exclusively used for manipulation of the external world.

You will also notice that most muscles with extensive tendinous attachments reside on the axial skeleton (i.e the trunk). This is because they are used for maintenance of the upright position, and examples of those are: Trapezius, Latissmus dorsi, Rectus abdominis, and many more... Given their static nature, they contain a lot of slow muscle fibers, allowing them to keep working over extended periods of time without rest. However, this does not make them weak. If the postural muscles were to have a structure similar to more peripheral muscles, for example biceps brachii, they would require an enormous number of different circular tendons extending in every direction to account for all the different body positions they act to maintain. To build a progressive example:

the biceps brachii is a fusiform muscle including two main parts. It is designed to pull hard in a limited range of movement types (i.e arm flexion). For that, it has evolved a small number of strong tendon attachments.
the serratus anterior was designed for a more extensive panel of moves. It therefore possesses several main bodies of muscles extending in different directions, with their own tendon attachment on the ribs.
the trapezius muscle has been designed to allow the head to keep its upright position (among other functions), and therefore is used as a positional link to guarantee the positional relation between head and shoulders. Its a static muscle and must be able to pull efficiently in a wide range of different directions, so its tendinous apparatus is extensive.

There are also special cases. If you take the digastric muscle of the neck for example, the tendons are used as attachments, but also as a kind of hinge to redirect the directional strength of the muscle.


why do sodium channels close with excessive extracellular potassium ions in cardiac myocytes?

Short Answer

Depolarization block keeps sodium channels in a different state where they aren't available to open.

Longer Answer

The answer here applies equally to cardiac myocytes and neurons, and has to do with the gating properties of sodium channels (calcium channels have some similar behavior, which is also important).

Voltage-gated sodium channels at rest are pretty much all in a 'closed' state. The probability of a channel switching to an 'open' state increases with increasing voltage. However, those channels don't simply stay open indefinitely: they transition to third, 'inactivated' state. 'Inactivated' channels can't reopen. This helps keep sodium-mediated excitation brief and saves a lot of metabolic energy versus 'forcing' a cell to repolarize by only overwhelming the sodium conductance with potassium conductance.

Channels will stay in the inactivated state if the membrane remains depolarized. The probability of a channel switching from 'inactivated' to 'closed' (and therefore 'ready to open') increases with decreasing voltage. If a cell does not repolarize sufficiently, many sodium channels will stay in the 'inactivated' state. Further, channels that do switch to the 'closed' state could open, but not in synchrony. The eventual result is an equilibrium with a mix of sodium channels in open, closed, and inactivated states. There aren't enough 'closed' channels around to switch to open, there aren't enough 'open' channels to depolarize the membrane more, and as 'inactivated' channels switch to 'closed' there are other channels switching from 'open' to 'inactivated'.

This whole condition is referred to as 'depolarization block.'

Here's a helpful review on voltage-gated sodium channels that contains information covering what I discussed in my answer:

Catterall, W. A. (2000). From ionic currents to molecular mechanisms: the structure and function of voltage-gated sodium channels. Neuron, 26(1), 13-25.

You can also find lots more information in textbooks and elsewhere if you look for the term 'depolarization block.' Note also that I have simplified the gating transitions for voltage-gated sodium channels for the purpose of this answer, so some sources might explain a more complicated system; the general principles still apply to the question, though.


As far as I am aware, there are no commercially available re-usable microarrays. The reason for this is most likely that the arrays are really sensitive and you run into the trouble with false positive signals. I have once seen a microarray which has been stripped and still delivered quite some signals in areas which had a strong signal before.

You have to make sure to strip all the hybridized samples from the chip without damaging the probes which are bound on the surface. I think the trade-off between "everything is off" and "some sample is still bound" is not good enough. Who wants to risk false positive signals and possibly retract publications on this basis? You may also loose weak signals which are hidden under false-positive signals.


Normal position of Electrical axis only in the III lead?

Let's consider the definition of the electrical axis.
The text does not specify which type of electrical axis and of what.
For instance, Guyton discusses Mean Electrical Axis of the Ventricular QRS only.
However, Guyton says that the mean electrical axis of the normal ventricle is 59 degrees.
In many pathological conditions of the heart, this direction changes markedly, sometimes even to opposite poles of the heart.

So the original author must have considered the Mean Electrical Axis of Ventricular QRS.

I would change the paragraph to

  Mean Electrical axes of the Ventricular QRS

  Excitatory processes have definite direction and magnitude and could
  therefore be represented as vectors. At any moment there are two
  points in the heart with the biggest potential difference, which is
  called electrical axis, characterized by the angel α.
  Under normal
  conditions -> 30°< angel α < 90°
  The Mean Electrical axis of normal ventricles is 59 degrees, which gives information
  about the position of the heart, and it represents the biggest amplitude in the lead III.


Heterochromatin profile is of course different in different cells but I am not sure if absolute heterochromatin content will vary greatly. This DNAse hypersensitivity region data is for human cells but same principles apply to all organisms. If I have to take a guess then I would say that quiescent cells are likely to have more heterochromatin. Heterochromatin production is regulated by different epigenetic mechanisms but I cannot comment (I feel it is unlikely) if there is a mechanism to control absolute heterochromatin content.


Does difference in expected life duration between men and women have biological nature?

There are several explanations. Probably these are all true to some degree and thus combine to give the general longer life expectancy of females.

Most of these statistics are from Annex 2 of the WHO Health Report 2004 (found through Wikipedia)

Males are more likely to get lung cancer, liver damage and other drug-related illnesses (implied would be that males are more often alcohol/tobacco/drug users).
Males also die more often as a result of work-related injury, especially as soldiers
Males are usually larger. There seems to be a small inverse correlation between size and life expectancy
Mitochondrial DNA is passes from mother to child. As such, mutations harmful for men are less effected by natural selection.
Men have one X chromosome, while women have 2. The y chromosome is very small and contains almost no genes. Thus if there is a genetic defect on the X chromosome the female might have a healthy X chromosome to compensate while the male does not have one. Among others this makes males more likely to have hemophilia or color blindness.