Can RNases/DNases survive in strong acid/base solutions of around 10M?

You are safe here.
RNase is much more stable than DNase (of any flavor). Extreme pH would destroy even RNase, especially considering time (it has to sit in the bottle with all that acid/base..)
Also, consider this: it is highly unlikely that high-tonnage chemicals like HCL or NaOH could be contaminated with organic enzymes.
If you have a problem with RNase/DNase contamination I would look elsewhere for the source of it.


The term "non-immune immunoglobulin" is both confusing and non-standard in the immunology field - "pre-immune" is sometimes used, but not always accurate. A negative control is as they describe - the same diluents and components of the sample incubated with the antibody of interest, only they use a non-specific antibody of the same isotype that is not expected to bind to any targets in an "immune-dependent" manner - the "usual" way you think of an antibody binding to a target antigen. However, antibodies can bind samples in an immune-independent manner, via protein-protein interactions (the sample was insufficiently blocked) or to Fc receptors, for example.

The non-specific antibody can be from several sources - a pre-immunization bleed from the animal that generated a polyclonal primary antibody, an antibody to a target not expected to be present in the sample, such as KLH or GFP, or a monoclonal antibody engineered or screened to not bind to anything.


It looks to me like one of the Amaurobiidae - the Hacklemesh weavers, often called Lace Spiders for their fluffy, cottony silk snares/shelters that they spin under rocks and logs.  It's an adult male from the big boxing glove pedipalp structures in front of the face, which is presumably why it was out in the open; it was looking for love.
As to which one it was, I'm not entirely sure - these are not a group I'm too familiar with, and I don't even know what species are found in Minnesota.  It looks a bit like a male Amaurobius ferox (an introduced European species that is spreading across the country from eastern N. America), but even lightening the photo doesn't help reveal the abdominal pattern, I'm afraid.  I'll just go with "probably Amaurobiidae" and suggest you send the photo to Bug Guide for the attantion of the pros over there:  https://bugguide.net/node/view/6/bgimage

Here's a representative male A. ferox for comparison, but note that this is a well-lighted photo so you can see the pattern on the abdomen.  Also note that there is a fair amount of individual variation in these (as in most) spiders, so some are darker, some are lighter, some have obvious patterns, some are more poorly-defined, etc.


Is it better to receive a certain dose of radition gradually or all at once?

The period of time over which a dosage is given matters critically. You probably have experienced this in your daily life. If you are out in the bright, summer, sun for 8 consecutive hours on a single day, you are likely to get a sunburn. If you are out in the sun for a total of 8 hours spread evenly over a month, you're very unlikely to get sunburned.

You body has mechanisms that can repair radiation damage or limit it's effect, but these processes take time. A particularly important processes is apoptosis. A cell can detect if its DNA has been critically damaged, and self-destruct before something else goes wrong. If the exposure is acute, there my not be time for the apoptosis mechanism to take effect before it is damaged itself, possibly transforming the cell into a cancerous state. There is considerable evidence that lower dose rates do give rise to fewer cancers.


Parts of the brain pivotal for maintaining consciousness

The minimal neural mechanisms that are jointly sufficient for consciousness (conscious percept, thought, memory, etc.) to occur, under constant background conditions, are called the neural correlates of consciousness (NCC) [1]. The background conditions are enabling factors that must be present for the NCC to be able to function (e.g., the heart must beat and the lung must exchange air to supply the brain with oxygenated blood, the blood levels of sugar and other blood constituents must be in normal ranges, the ascending reticular activating system (ARAS) must be functioning, etc.), but they are not the NCC.

The ARAS is the neural network in the core of the brain extending from the rostral pons to both thalami and the basal forebrain, and from there it sends extensive axonal projections to the cerebral cortex, including the consciousness neural network (which is the anatomical part of the NCC). The ARAS is responsible for the alertness of consciousness, but it is not responsible for the content of consciousness. So, it is not part of the NCC proper. However, there can be no consciousness if there is no stimulation from the ARAS, even if the consciousness neural network is intact and able to function, such as in the case of extensive brainstem hemorrhage, infarct, and trauma. And the level of conscious alertness depends on the activation from the ARAS – the more activation, the higher level of alertness. This results in various conscious level’s states, such as (from lower to higher level of alertness) coma, stupor, drowsiness, normal alertness, and heightened alertness [2]. So, the answer to question #2 – why this oldest part (the brainstem) is pivotal in maintaining consciousness – is that it is the way the consciousness neural process has evolved to be dependent on the ARAS for its level of function (i.e. its alertness).

On the contrary, if the ARAS is working normally but the consciousness neural process is not, there can be alertness without, with minimal, or with some awareness. The degree of impairment of awareness depends on how much the consciousness neural process is dysfunctional. For example, in the case of damages to the consciousness neural process from diffuse cerebral hypoxia, extensive bilateral cerebral infarcts, or diffuse cerebral cortical injury, the results can be various abnormal conscious awareness’s states that range in severity of abnormal conscious awareness, depending on how much the consciousness neural process is impaired, such as (from mild to severe) acute confusional state, akinetic mutism, minimally conscious state (MCS), and vegetative state (VS). In the latter two categories, which are severe conditions, the patients can open eyes and have some reflex responses, such as blinking, chewing, and yawning, but show no (in VS) or minimal (in MCS) signs of conscious awareness of self and the environment (by clinical testing or by special investigations such as EEG, evoked potentials, and fMRI) [2].

Regarding the neural circuits of consciousness, as far as one can conclude from the evidence at present, it seems very likely that the Default Mode Network or Resting State Network [3], which includes the medial prefrontal cortex, posterior cingulate cortex, precuneus, hippocampal and parahippocampal cortex, retrosplenial cortex, and some parietal and temporal cortices, is the network of the consciousness neural process when the mind is in the state of passive internal mentation, not performing cognitively demanding tasks, and not attending to outside stimuli. This network overlaps with the network that functions for access consciousness (consciousness of episodic stimuli, not consciousness of continuous stimuli as in the former case). At present, evidence shows that the network of Global Workspace theory proposed by Baars [4] or the network of Global Neuronal Workspace hypothesis of Dehaene [5], which includes the cortico-thalamic (C-T) core and a network of neurons with long-range axons densely distributed in the prefrontal, fronto-parietal, parieto-temporal, and cingulate cortices, is the network of access consciousness. So, the complete neural network of consciousness that functions to be conscious of continuous events and episodic events is likely to be some form of combination of these networks, such as the neural network in the extended theory of global workspace of consciousness proposed by Song [6].

The complete neural circuit of consciousness, whatever it is finally found to be composed of, and the way it functions will constitute the complete NCC. The complete NCC is necessary and sufficient for consciousness to occur. Even if we do not have the complete NCC now, the above current models that we have are fairly well supported by experiments. I hope this answers question #1.

References.

Tononi G, Koch C. Consciousness: Here, there and everywhere? Philos Trans R Soc Lond B Biol Sci. 2015 May 19;370(1668):20140167. DOI: 10.1098/rstb.2014.0167.
Ukachoke C. Chapter 6 – Consciousness. In: The Basic Theory of the Mind. 1st ed. Bangkok, Thailand; Charansanitwong Printing Co. 2018.
Andrews-Hanna JR. [The brain’s default network and its adaptive role in internal mentation.(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3553600/) Neuroscientist. 2012 Jun;18(3):251–270. DOI: 10.1177/1073858411403316.
Baars BJ, Franklin S, Ramsoy TZ. Global workspace dynamics: Cortical “Binding and propagation” enables conscious contents. Front Psychol. 2013;4:200. DOI: 10.3389/fpsyg.2013.00200.
Dehaene S, Charles L, King JR, Marti S. Toward a computational theory of conscious processing. Curr Opin Neurobiol. 2014 Apr;25:76–84. doi: 10.1016/j.conb.2013.12.005.
Song X, Tang X. An extended theory of global workspace of consciousness. Progress in Natural Science. 2008 Jul 10;18(7):789–793. DOI: https://doi.org/10.1016/j.pnsc.2008.02.003.


Howe and Smallwood (1982) provide a nice review of the many methods of seed dispersal that have evolved in plants. The review is broad but they do have a section on frugivory.  They highlight hypotheses developed by McKey, and Howe and Estabrook (see Howe and Smallwood for citations) that suggest plants may use one of two strategies.

One strategy is the "high investment model." Plants invest lots of resources to produce large seeds and nutrient rich fruits. THe hypothesis is that these types of fruits tend to attract relatively few but specialized frugivores that are will to invest the energy necessary to find these types of fruits and their associated nutritional reward.

The second strategy is called the "low investment model." In this model, plants invest little in individuals seeds and fruits but produce an abundance of them. The hypothesis is that these types of fruits will be eaten by as many different potential seed dispersers as possible. These tend to be very small or starchy although they can still be colored as you describe.

Other factors also come into play. For example, tropical fruits tend to have large seeds and nutrient rich pulp while temperate fruits tend to be smaller and offer less nutritional reward.  All of this is placed in the context of the community diversity of frugivores. The Howe and Smallwood paper was an interesting read.

A paper by Gatier-Hion et al. (1985) looked at the characters of fruit choice and seed dispersal mechanisms by tropical forest vertebrates. The showed the relationships between fruit characteristics and the corresponding frugivores. They looked at 122 different fruit species and the frugivores that consumed them.  Their results showed that fruits tended to separate along one of three axes:

Heavy, indehiscent fruits with fibrous flesh and well protected
seeds vs light, dehiscent fruits with unprotected seeds. Many of
small fruits are red,
Lots of seeds produced (typically the the large indehiscent) vs few
seeds produced, and
Juicy and brightly colored fruits vs dry and dull-colored fruits.

Figure 2 from Gautier-Hion et al., shown here, shows the relationship between different frugivores and the fruit types.  Notice that small granivores, which are frugivores, don't eat large, juicy fruits. They consume lots of small green or brown grains that are easy to manipulate and produced in high quantities.  Squirrels are similar.

Thus, as you suspected, fruits and seeds have evolved in response to their frugivores but the fruits do not always have the traits you listed. I think, but do not know for certain, that the fruit traits you list are the result of selection being driving by the frugivores. The sugars provide lots of quick energy, which is necessary for active animals. The carbs probably provide a much greater nutritional reward than salts or proteins (which are present anyway). The colors may help the fruits to stand out against the green foliage (for organisms that are not red-green colorblind). These traits probably provide the greatest reward (lots of energy) with the lowest energy investment by the frugivore (easy to find).

Throughout, I've assumed natural conditions and not fruits modified by artificial selection for human consumption.

Literature Cited

Gautier-Hion, A., et al. 1985. Fruit characters as a basis of fruit choice and seed dispersal in a tropical forest vertebrate community. Oecologia 65: 324-337.

Howe, H.F. and J. Smallwood. 1982. Ecology of seed dispersal. Annual Reviews in Ecology and Systematics 13: 201-228.


What is the connection between exercise and muscle growth

Muscle growth and development is mediated by "trophic factors" not biochemical reactions (ATP) or muscle contraction directly. The best method of releasing tropic factors is exercise and not electrical stimulation or biochemical reactions (ATP) or biomechanical contraction.

Nerve ending release growth or tropic factors which stimulate muscle growth and for example if the nerves die off either due to injury or disease (ALS) the muscles will atrophy.

Not all of the tropic factors are as of yet known, but it is these tropic factors that stimulate muscle growth, not the biochemical or biomechanical reaction of the muscle (contraction). One can not as of yet stimulate muscle growth by delivering electrical energy to the muscle, for example (it has been tried to in an effort to maintain muscle mass in critically ill patients).

There is a review of the trophic factors here - http://neuromuscular.wustl.edu/lab/trophic.htm

And a review of electrical stimulation - http://www.medword.com/MedwordStore/PCP/EMS_truth.html

There are many claims of benefit for electrical stimulation, such as regeneration of the facial nerve in facial paralysis, such as Bell's palsy.

The "problem" is that the prognosis in Bell's palsy is very good, even without electrical stimulation, and so it is difficult to "prove" benefit with electrical stimulation:

  With or without treatment, most individuals begin to get better within 2 weeks after the initial onset of symptoms and most recover completely, returning to normal function within 3 to 6 months.

http://www.ninds.nih.gov/disorders/bells/detail_bells.htm

  Statistically, the natural history without treatment was described in a study of 1011 patients in 1982 [8]. One-third had an incomplete paralysis, and two-thirds had complete paralysis. Overall, 85 percent showed signs of recovery within three weeks, 71 percent had complete recovery, 13 percent had slight sequelae, and 16 percent had residual weakness, synkinesis and/or contracture. Patients with incomplete lesions had a 94 percent rate of return to normal function, while only 60 percent of those with clinically complete lesions returned to normal function.


What are possible reasons for a DNA template not giving amplification?

Lets summarize the comments into a real answer: When the only chemical changed in your reaction is the DNA, which came from a fresh Phenol/Chloroform preparation, I would suspect it. From there, we have a few possibilities, what could have gone wrong.

The most likely cause of an enzymatic reaction not working with
Phenol/Chloroform prepared DNA are left-overs (or carry-over) of the
organic solvents from the reaction. The inhibit (especially Phenol)
enzymatic reactions very efficiently. It would help to do another
round of DNA precipitation.
It is possible that your DNA didn't got dissolved after the drying
step in the precipitation. Depending on the conditions, DNA can form
a pellet which is hardly to see and even harder to dissolve. So your
DNA concentration would be too low to get amplification. To prevent
this measure the concentration of your DNA.
It is possible that the water you used is contanminated with DNAses
(although it shouldn't) and your DNA got degraded by them. Here only
new aliquots will help.
Depending on the size of your amplicon, it is possible that overly
harsh condition during the preparation led to the shearing of the
DNA leaving not enough intact DNA to get a proper amplification. If
this is the case, be more gentle with the extraction.

Additionally your primers can be a problem. It would be good to keep the 100x stock solutions permanently at -20°C and prepare 10x working solutions. These can undergo freezing and thawing (which will degrade them over time) but they can be replaced easily.
I would also try the new DNA prep (if possible side by side with one that is working) with new primers to test if they are the problem.


I would classify the neurological phenomenon of "taste" or "tastyness" as an emergent property (1), and therefore synergistic (i.e. not adequately explained simply by additive effects). For example, when something "tastes like chicken" that's a synergistic sensory pattern in your brain involving the specific ratios of the 5 basic tastes(2) on your tongue, along with your sense of smell, and the sensation of the food's texture in your mouth (is it moist, dry, viscus, etc). This helps explain why simply combining two tasty flavors (coffee+tea) does not necessarily yield something twice as tasty, and also why foods which might not be tasty on their own, can be tasty in the right combination (e.g. potatoes+onions+salt+oil+heat makes tasty hashbrowns, but none of those foods are especially tasty on their own).

Taste preference (tastyness) also involves a certain amount of neurological learning, which is partially why often people don't like the taste of something like coffee when they are young, but learn to enjoy it as they find it elicits a response from the reward centers of the brain.

In summary, "tastyness" is most likely an emergent and synergistic property of a system of complex sensory and neurological interactions, and not simply an additive.


Do changes in an organism's cell modify the genetic information it uses for reproduction?

In multicellular organisms there are specialised cells called gametes that are responsible for sexual reproduction (sperm/ egg cells). Mutations occurring in these cells can be passed on to offspring (germ line mutations). Mutations occurring in others cells affect only the given individual (somatic mutations).

Edit:
For unicellular organisms it is pretty straight forward, the daughter cells formed through fission are identical. As for multicellular organisms here are many forms of asexual reproduction, and even these may involve the formation of specialized cells (eg. spores). So my answer is: it depends on the type of asexual reproduction and the actual cell(s) that accumulate mutation(s). For example in parthenogenesis - where the unfertilized egg cell develops into a new individual - , a mutation can be inherited if it occurs in the germ line cells generating the egg cell, but any somatic mutation would stay in the parent. You can find detailed info on asexual reproduction with details on each form on this wiki page


What is the opposite of a mutation (the regular state)?

A mutation can be both the act of changing the genetic material (the process) or the changed genetic material itself (the result of the process). You're using the second meaning. See What is the definition of a mutation? for more info.

That being said, the opposite of a mutant allele is a wild type allele.

According to Pierce in his book "Genetics: A Conceptual Approach" (2012):

  The normal allele for a character is called the wild type because it is the allele most often found in the wild. (emphasis mine)

The same way, the opposite of a mutant phenotype is a wild type phenotype.

Besides that, you can sometimes find "wild" alone, without "type": wild allele, wild phenotype etc...

Source: Pierce, B. (2012). Genetics. New York, NY: W.H. Freeman.


What is the "stimulus" that initially triggers an action potential?

There are several possible answers, which is partly why the sources you are reading are being vague: they are discussing the chain of events that happen after the initial depolarization, the source of which doesn't matter much for that chain of events.

Receptor potentials

Sensory receptors consist of some machinery that eventually lead to ion channels opening, often cation channels. This machinery can be direct, where a stimulus directly opens an ion channel, or it can me mediated through g-protein coupled receptors. There are many many examples, but one favorite toy example is the TRPV1 receptor, part of the "transient receptor potential" family.

TRPV1 channels open when exposed to high temperatures or chemical agonists like capsaicin (which gives chili peppers their 'heat').

There are mechanically gated channels in the inner ear that are stretched open as sound waves pass; there are G-protein coupled receptors in the retina that are activated in response to light - when they are activated, they close channels which reduces neurotransmitter release and therefore changes the amplitude of the post-synaptic polarization.

Ligand-gated ion channels

Synaptic transmission between neurons is often mediated by ion channels that are gated by neurotransmitters. A presynaptic cell releases a neurotransmitter, for example glutamate, and that neurotransmitter binds glutamate receptors on the post-synaptic cell, for example AMPA receptors. These receptors are non-specific cation channels, and when they open sodium comes in and depolarizes the cell. Other neurotransmitters, including inhibitory ones, work a similar way.

Gap junctions/eletrical synapses

Although they only occur between particular populations of neurons in mammalian nervous systems (for example, some inhibitory networks in the brain and between cardiac myocytes), some cells are coupled through channels that allow ions to pass between cells. Therefore, depolarization in one cell can be transmitted by ions flowing through that gap junction and begin to depolarize the adjacent cell.

Intrinsic conductances

It doesn't really apply in the context of a "stimulus" but in some types of cell there are intrinsic conductances that can bring a cell to threshold and trigger an action potential. One example would be in the pacemaker cells of the sinoatrial node that initiate cardiac contractions.


Based on the location and picture I believe this a Goosander (Mergus merganser) which is the European name, the North American name is the Common Merganser.

You can find more information about them here.

They undergo two main molts, breeding plumage in December and eclipse plumage in May. Here is a description of the eclipse molt by Bent, 1923:

  In May the adult male goosander begins to assume its eclipse plumage.
  The adult male in August has the crown reddish brown, with a gray
  tinge; chin white, and the rest of the head and upper neck rich red
  brown.

By the looks of your photo, you either have 2 females during the breeding plumage phase (January - May) or either sex during the eclipse phase (June - December). It will depend on when the photo was taken.

Here is an image with a breeding plumage male (left) alongside some females:

References:

Bent, Arthur Cleveland. 1923. Smithsonian Institution United States National Museum Bulletin 126 (Part 1): 1-13. United States Government Printing Office


Apoptosis is very tightly controlled for obvious reasons. Setting it off without proper control would result in the uncontrolled loss of cells. Apoptosis is one of the major pathways which are either mutated or shut-off in cancers, preventing the body from eliminating malingnant cells. These two papers are interesting in this context:

Apoptosis: A Review of Programmed Cell Death
The role of apoptosis in cancer development and treatment response

In this context it makes no sense to have a shut-off mechanism once the apoptosis cascade has started. It is only set off when there is a real reason (and is well controlled), so I don't think there a "null-apoptosis" mechanism. It would of course still be possible to artificially make substances, that inhibit parts of the activation cascade. But besides for apoptosis research I don't see any use for it. There is actually some research going on to find out how to activate apoptosis again in cancers.


do prokaryotic DNA sequences contain enhancer elements

Yes: https://www.ncbi.nlm.nih.gov/pubmed/1776167

  other than the UAS(upstream activating sequence)

The Gal4/UAS system is borrowed from yeast, a eukaryote https://en.wikipedia.org/wiki/GAL4/UAS_system

  In addition, are enhancer elements like promoter-proximal elements and enhancer elements encoded directly within the DNA?

Yes. Enhancers are usually considered to be encoded directly within the DNA; e.g.: see the following recently published historic perspective on the discovery of enhancers by its discoverer, Walter Schaffner : https://www.ncbi.nlm.nih.gov/pubmed/25719310

Sidenote: Enhancers have originally been discovered in a virus, and thus neither in prokaryotes nor eukaryotes

  Or are they proteins that attach themselves to the strand of DNA in order to enhance transcription?

Enhances (often / ~always) exert their function though proteins. https://en.wikipedia.org/wiki/Enhancer_(genetics) Note that this doesn't necessarily affect the definition of enhancers.


Species identification; clusters of big plump red bugs in Taipei

I'm fairly certain these true bugs belong to the species Leptocoris vicinus, and carry the nickname of "soapberry bugs", which is specific to the subfamily Serinethinae. They're quite common in urban areas of Southeast Asia, which coincides nicely with where you encountered them.

Also, you had mentioned,

  There are plenty of birds around (this is quite a green area) but I didn't notice any interest by birds in eating them.

Soapberry bugs, as well as many other types of insects, are able to freely congregate in large numbers, and in such exposed places, due to their bright coloration. Having such a bright color may indicate to some predators that the prey in consideration is toxic, a phenomenon referred to as aposematism.

 source

 source

And then, here's a map of their distribution, with Taipei holding marker #37. (source)

An interactive version of this map can be found here.


Why does the oxygen produced in the photosynthesis come from water and not carbon dioxide?

You are missing some knowledge here for sure, photosynthesis is a little complicated at A level, so I will describe it in brief.

During photosynthesis electrons and protons (A hydrogen atom without the electron) are required for a process called the electron transport chain and proton motive force. This happens during the light dependent stage of photosynthesis, (there is also a second light-independent stage called the Calvin cycle, and that is where the CO$_2$ is used), I won't go into detail about what the protons and electrons do (unless you want me to) but you need to know that these come from a water molecule, the water is split using light (photolysis, literally: cutting with light) into two hydrogens and half an oxygen molecule (or an oxygen atom). The oxygen that was released in photolysis is not required for the rest of the pathway, so it diffuses out of the cell.

For why it doesn't come from carbon dioxide, you need to consider the Calvin cycle. In the Calvin cycle, carbon dioxide is converted to glucose by enzymes, using products from the light dependent stage, so 6CO$_2$ are combined over six cycles to form one molecule of glucose. So that is where the CO$_2$ is used as well.

Hope that helped! If you want me to go into any more detail please ask!


What do you call mRNAs that translate to the same protein?

This is by no means a consensus, but this paper from 2000 proposes a new term: Isotranscript.

According to the authors:

  Duplicated genes often encode distinct proteins that differ by only a few amino acids, such as the two mammalian S27 isoforms, S271 and S272, documented here and the yeast and Arabidopsis S27 isoforms identified previously. On the other hand, we have found that different S27 transcripts encode 100% identical proteins. This phenomenon has also been described previously for the histone subtype, H3.3, in which two different transcripts encode the same H3.3 amino acid sequence . We have chosen the terminology “isotranscripts” to describe such mRNAs. (emphasis mine)

Source: Thomas, E., Alvarez, C. and Sutcliffe, J. (2000). Evolutionarily Distinct Classes of S27 Ribosomal Proteins with Differential mRNA Expression in Rat Hypothalamus. Journal of Neurochemistry, 74(6), pp.2259-2267.


Here are some thoughts based on my own experiences purifying many proteins and running many SDS-PAGE gels:

(1) Resolution--how fast did you run this gel? Often if you run at higher than say 150V or so you can get bands that look like this. The resolution could also be related to..

(2) I would bet the streaking is due to salt in the sample--a lot of the time lysis/wash/elution buffers can have upwards of 500 mM or 1 M salt, and this invariably causes streaking. Load less sample in these lanes and keep the total volume the same to dilute the salt below 250 mM at least. Other things in your buffers could be causing the streaking, but salt is the most common (let us know the composition of your lysis/wash/elution buffers).

(3) Your purification of GST alone looks very good--often your preps will look much more like the lanes you have indicated, which are not entirely clean. This is quite common for a one step purification--often you need 2-3 for certain proteins to completely remove contaminants. There are several possible sources of these bands:

Endogenous proteins: Many bacterial proteins will non-specifically stick to the beads (this is why we wash), but even thorough washing can still leave some contaminants. These proteins also could be bound to your protein of interest and are co-eluted off of the resin.
Truncation products: Depending where your tag is (let's sat it is on the N-terminus), you can sometimes get incomplete translation products--they have the tag, but they are not full length proteins. These will still bind and elute from the beads because they have retained the tag. Ignore this point if you tag is on the C-terminus, as in that case the tag will only be on full-length protein.
Degradation products: This is related to your later questions--often during the purification your protein will be degraded by bacterial proteases. Did you include a variety of protease inhibitors in your lysis buffer? Keeping all of your samples on ice is also important for this reason.

(4) Understand that degradation products do not mean you get only your protein and the fused GST--they can be a variety of truncations due to degradation by proteases.

(5) I would bet this is just due to your running conditions or the salt in your samples. I think this is probably actually your single GST band.

(6) Glutathione will not show up on the gel--it's formula weight is about 300 g/mol if I recall meaning it's about 300 Daltons, so much smaller than anything that you'll retain on the gel. Further, remember than your stain is for proteins--Coomassie blue binds basic residues on proteins.

(7) I'm not sure which band you are referring to, but I think the very bottom band in your marker lane is simply the dye front. It could also be a degradation product of a protein in your ladder.

As far as the second gel goes--it is all due to the buffer level falling during the run. Without buffer covering the top of the gel there is no current flowing. Probably as the leak was occurring you had uneven distribution of the buffer. Strange things can happen when this occurs (unscientific, I know).


After finding some higher-quality images/videos with some views of the creature from the front, I can say that the image I linked is mostly accurate, if lacking in detail. There does appear to be a set of antennae, though they are significantly shorter than the legs, the front two pairs of legs are shorter than the others and end in small claws, and are positioned more 'underneath' than 'to the side of' the body relative to the other legs. The reason for the confusion seems to have been a combination of the different position of the front four legs, some pictures of other Phronima species misnamed as sedentaria, and that the antennae appear to be able to fold in close to the head, making them nearly invisible.


Do hornets remember and recognize a human? Do they have any (kind of) memory?

Most studies show that a hornet will give off a hormone that tells others in its hive that you or someone else is target and threat to the colony as a whole. They also are able to remember their surroundings near the hive or nest fairly well.


What percentage of the human genome hasn't been sequenced yet? If percentage estimates aren't precise, why is it difficult to estimate?

I answered a related question here that may be helpful.

Some initial notes:

Your first bullet point ("99%") is to my reading talking about not the total genome size but the data that they actually assembled- e.g. for 99% of nucleotides, we are 99.99% that the nucleotide at that position is not some other nucleotide, but there may be other positions not included in the denominator that are simply not in the assembly in the first place. In other words, the existence of the position in the assembly and our confidence of the accuracy of a nucleotide call for such a position are two different (though related) phenomena.
Also, you are comparing a 2003 estimate to a 2017 estimate. We learned a lot in those 14 years.

To answer the last and most specific question about why this number is hard to know, there are a variety of reasons why:

There is no single number that is the "actual" true sequenced percentage of the human genome. In this I strongly disagree with commenter Konrad Rudolph (technological change is now giving us telomere-to-telomere assemblies of human chromosomes! The question is not how much it's possible to sequence and assemble but more whether it's the worth the time and expense to do so.). No two genomes are exactly alike, and that means not only that the nucleotides are different but that the positions are different. So even if we sequence 100% of your genome, that may only include 99% of my genome. These variable regions are, as suggested in the comments, largely repetitive regions but also just big chunks that are missing; to learn more about this google "structural variation" (here is an older review on the topic).
As mentioned already, technological advances have changed how we view the linear sequence of the genome. Earlier estimates were limited by available technology of the time; now that we have 3rd-generation sequencing tech like nanopore and pacbio, we are learning more about the extent of our ignorance. In that sense, it is unsurprising that the denominator has changed/increased.
As commenter Jeppe Nielsen states, all of these are statistical estimates based on available data. As available data increase and the statistical models that we use to estimate change, thus do the estimated outcomes change.
Related to (1): Different populations have different chunks of genome that are unique. The initial sequencing project selected a small number of humans, who were not representative of all human diversity. Efforts to fully characterize the human pangenome are ongoing.
Sometimes contaminants sneak into genome assemblies, which have to be removed. So for every sequence in the human genome assembly, especially if it's fragmentary or recently added, there's a nonzero chance that it's not actually part of any human genome.


Absorption ratios 260/280 and 260/230 for RNA

DNA and RNA absorb at 260nm. Proteins absorb at 280nm. The 260/280 ratio is a good estimate of how pure your sample is. For RNA, the 260/280 should be around 2. If it is lower, this might be an indication from contamination or proteins, phenol, or other contaminants in your sample. The 260/230 ratio is a second measure for purity of the sample, as the contaminants absorb at 230nm (like EDTA). The 260/230 ratio should be higher than the 260/280 ratio, as it is usually between 2 and 2.2. Lower ratio might be an indication of contamination.

In your case, I would be worried about the purity of the sample which gave you 260/230 ratio of 0.98. If you are using nanodrop, looking at the plot can also be a good indication of the quality of your sample. For a pure sample, a well defined peak (no shoulders or wiggles) at 260nm is expected.

Take a look at the NanoDrop manual for more information.


What is the criticality of the ribosome binding site relative to the start codon in prokaryotic translation?

I found an oldish paper on this topic (from 1994).  Here's a summary:

Determination of the optimal aligned spacing between the Shine-Dalgarno sequence and the translation initiation codon of Escherichia coli mRNAs. by Chen, Bjerknes, Kumar, & Jay. Nucleic Acids Research. (1994)

Experiment

The authors constructed a series of synthetic RBS regions that varied the length separating a synthetic 5-nt Shine-Dalgarno sequence from the start codon.  The regions varied in size between 2 to 17 nt.  They assayed the activity of a downstream enzyme, chloramphenicol acetyltransferase.

Conclusion

The authors concluded that the optimal spacing between a consensus 5-nt Shine-Dalgarno sequence (5'-GAGGT-3') and the start site was 5 nt. Note: this synthetic SD was made of the last 5 nt of a 9 nt SD consensus sequence.  They also tested a synthetic SD made from the first 5 nt (5'-TAAGG-3')of the consensus SD.  In this case they found the optimal distance was 9 nt.

So the optimal distance depends on where your desired SD aligns with the consensus SD sequence, which optimally is 5 nt from the start.  Read on for more details.

Details

the RBS is considered to be large, extending 20bp on either side of a core Shine-Dalgarno (SD) sequence.  These days, I often hear of the RBS spoken of in sizes that are equivalent to the SD.  So in the parlance of the paper, you question is rephrased as "how does distance of the SD from the start codon effect translation?"
the canonical SD sequence referenced in the paper is 5'-UAAGGAGGU-3'.  It is 9 nucleotides long.  Distances between the SD and the start codon are defined as the number of nucleotides separate the 3' Uracil of the SD from the Adenine of the start AUG.
Example: the distance is 5 nt in the following mRNA

       5'.....UAAGGAGGUnnnnnAUG......3'

if the SD is not a complete 9 nt long, the distance is between the position of where the canonical Uracil would occur.  In the following example, the distance is still calculated as 5 nt:

       5'.....UAAGGAnnnnnnnnAUG......3'

the average distance between the SD sequence and the start codon varies considerably and on average is 7 nt. Other investigators have found "optimal" spacing (circa 1994) ranged from 5 to 13 nt.
the SD site complements with region on the 16s rRNA. The start codon complements to the anticodon of fMet-tRNA loaded into the ribosomal P-site.  So there are two distinct sites on the ribosome that contact the mRNA during translation initiation.

Also good to read

Designing Genes for Successful Protein Expression by Welch et al. Methods in Enzymology, Vol 498. (2011) (pdf)
Automated design of synthetic ribosome binding sites to control protein expression by Salis, Mirsky & Voigt. Nature Biotechnology. (2009). (pdf)

Note

I enjoyed researching this question because I found my own knowledge to be lacking solid empirical details. I do not have any direct experience besides this little lit review with this topic.


Are the alleles that code for the same phenotype all the same exact sequence?

No the same phenotypes do not mean the same sequence. For example some phenotypes are associated with alleles that are caused by non-functional gene products (like proteins). But there many ways to alter a gene to produce a non-functional protein.


Is there a maximum limit of connections between a pair of neurons?

There's several ways neuronal connections can strengthen: growing the spine, increasing the amount of vesicles that carry neurotransmitters at the synapse, sensitizing and increasing the amount of receptors and yes creating more spines and synapses also.

Roughly, neurons can make tens of thousands of connections to multiple neurons the size of each spine is estimated to be between 0.01 µm3 to 0.8 µm3.

You are correct in saying that as life happens the connection would tend to grow to max and not encode anything anymore, however the brain seems to re-normalize all of its connections during sleep through special membrane channels.

Check out:
https://en.wikipedia.org/wiki/Neuron (especially the connectivity part)

https://en.wikipedia.org/wiki/Long-term_potentiation

https://en.wikipedia.org/wiki/Long-term_depression

https://en.wikipedia.org/wiki/Ion_channel


Why I don't feel pain when I press the skin on my knee and elbow?

There is several types of nerves in the body.
Some nerves are specialized in sensing cold or hot temperature, some other to cuts and cell damage and others feel pressure and touch.

The answer to your question is that the nerves in your elbows and knees have less pain detectors and are in fewer number, thus with they are less sensitive.

Here's a funny little poster on BBC: Can you pinch yourself without it hurting?


Well, Sender, Fuchs, and Milo wrote a paper to discuss the total number of cells in the body and compare it to the number of bacteria in the body (http://dx.doi.org/10.1101/036103). Their discussion is quite in-depth.

There are a number of ways to calculate it, but an interesting one involved calculating mammalian cell density by a study measuring the DNA obtained from a 25 g mouse. Researchers were able to determine there were 3*109 cells in the mouse (Baserga, 1985). From this study we can simply divide to find a value for "typical" mammalian cell density--1.2*108 cells/g.

If you want to know the number of cells per mL, you'll need the density (g/mL) of the tissue you are measuring. As the comments have mentioned, this is typically around 1 g/mL and varies from person to person. There is a web page that has some tissue densities for various tissues.

Baserga, R. (1985). The Biology of Cell Reproduction (Harvard University Press).


Why we aren't making Darwin's theory a Law

Scientific Laws differ from Scientific Theories in that Laws do not posit a mechanism or explanation of phenomena. Scientific Laws are merely distillations of the results of repeated observation. As such, a law is limited in applicability to circumstances resembling those already observed, and may be found false when extrapolated.

Examples are like
Ohm's law only applies to linear networks, Newton's law of universal gravitation only applies in weak gravitational fields, the early laws of aerodynamics such as Bernoulli's principle do not apply in case of compressible flow such as occurs in transonic and supersonic flight, Hooke's law only applies to strain below the elastic limit, etc. These laws remain useful, but only under the conditions where they apply. Such laws do not explain how and why they work.

https://en.wikipedia.org/wiki/Scientific_law

Darwin's Theory of Evolution in contrast contains both observation, and a proposes an explanation of the phenomena of species formation.


Evolution: Can the genotype frequencies change, but the allele frequencies remain constant?

Where do you get that populations aren't evolving?
A population might be in HWE for a particular trait if there is no selection on that trait, but that doesn't mean that there is no selection or drift happening on any trait!


Do there exist publicly available Genome sequences of a family?

I know that 1000 Genomes has sequenced Mother-Father-Child genomes from populations around the world (I think at least some of these samples were obtained from HapMap) and their data is publicly available by following the links in their website.


Evolutionary distance between Canidae, Felidae, and Rodentia

Online Ressources

Here is exactly the kind of question where tolweb.org is your best friend. tolweb.org is one of the most updated phylogenetic tree online. It also contains tons of reference, very useful to understand controversy over some nodes. onezoom.org is another online source that offer you to seek through the tree of life. Also, onezoom shows only the tetrapods (incl. mammals, birds, amphibians, lizards, snakes, turtles). However, onezoom has an awesome display and is a great tool for displaying diversity (they use the total length (in years) of all branches within a clade) within a clade and the threaten index (IUCN (red list) categories).

Dogs, Cats and Rodents

You will find the placental mammals here (tolweb). As you can see, the cats and dogs are both carnivora, while a rodent is a Rodentia (as you said). This means that cats and dogs have a more recent common ancestor than does either the cat or the dog with any rodent. Stated differently again, cats are not closer or further to rodents than dogs are. There is exactly the same distance between cats and rodents than between dogs and rodents.

One onezoom, the carnivorans is presented as a sister group to the ungulates. I have no idea what representation is the most correct but in any case, cats and dogs are carnivorans and share a common ancestor that is more recent than the common ancestor shared by carnivorans and rodents. So again, there is exactly the same distance between cats and rodents than between dogs and rodents.


Mice (Mus) and rats (Rattus) are definitely separate species, by whichever definition of species you choose to use. They are genetically distinct, and both genera are members of the clade Muridae, along with Acomys ("spiny mice") and Gerbillus ("gerbils").

Moreover, what we call colloquially "mice" and "rats" encompass a great deal of variation within rodents. The genus Mus is one of several subgenera with ~15 species.

A recent phylogenetic study of rodents by Blanga-Kanfi et al. (2009), revealed that Mus and Rattus are sister groups, meaning that each is the other's closest relative. The image below from the paper above shows the complete tree. Muridae is about 2/3 of the way down in blue.


Why are the positions of simple sequence repeats at the gene and related transcript sequences different?

Because of Alternative Splicing, suppose an exon occurs neither the first nor the last, then the same exon will come at various positions in different transcripts of the same gene. Thus, if your SSR of interest exists in that exon, you will find the same SSR located in the various positions of different transcripts.


Does light from the left visual field reach the temporal left retina?

There is overlap between the left and right visual fields, as shown in Fig. 1. This overlapping part is referred to as the binocular field of view. The monocular field of view (FOV) is 160o (w) x 175o (h), and the binocular FOV is 200o (w) x 135o (h). The region of binocular overlap is 120o (w) x 135o (h) (Kolb, 2016). The visual disparity in the binocular FOV of the both retinal projections forms one of the most important depth cues that allows us to estimate the distance of objects.

Fig. 1. The left and right visual fields have an overlapping area, the binocular visual field. source: Harvey Mudd College

Fig. 2 below shows why only a certain part of the visual fields overlap. Firstly, the retina has a finite size and secondly, the anatomical location of the pupils restricts the angles of the visual field. The most eccentric parts of the left visual field simply cannot reach the temporal left retina (and vice versa), because the angle of the pupil with respect to the retina simply doesn't allow for it. The same holds for the most central part of the left FOV, which cannot reach the nasal part of the right retina; it can only project to the the temporal right retina because of the restrictions due to the localization of the pupil, the retinal size limitations, as well as the nose blocking a certain part of the FOV.

Fig. 2. The left and right visual fields have an overlapping area, the binocular visual field. source: Ohio State University

Reference
- Kolb, Facts and Figures concerning the human retina. In: Kolb et al (eds). Webvision, The Organization of the Retina and Visual System. Utah University (2016)


How does a glucose molecule enter the cell from blood vessel?

I think I understand your question, Natasha. In short, your own answer #2 is correct.
There are 3 spaces, and 2 pathways for glucose to pass from one to the next:

intracapillary plasma
extracellular fluid
the cytosol.

Ways glucose gets into the cell:

(2->3) To get from the ECF to the cytosol , glucose always needs a transport protein. These are the GLUTs. In two cases, the small intestine and kidney, these are part of a secondary active transport system based on the Na/K-ATPase. In the pancreas, it's GLUT2.

(1->2) To get from the capillary plasma to the ECF requires filtration, the process of applying hydrostatic pressure to the plasma and literally squeezing it like a sponge. The boundary of the "blood sponge" is the basement membrane. The membrane holds in the proteins, and lets anything dissolved in the watery serum (like glucose) through.

The Filtration Constant Kf is proportional to the percentage of the BM that is exposed in a given capillary, which varies by the type and other factors like histamine release.

Type 1 (continuous) has the lowest exposure of the BM (only the intercellular clefts). Type 2 (fenestrated)has the clefts and the fenestrations to expose the BM. Type 3 (sinusoids) have huge gaps between the cells, and importantly, an incompetent BM that allows proteins and cells through along with the watery serum.
Dynamic factors that change filtration rates:

Histamine causes the post-capillary venule's endothelial cells to contract, and exposes more of the BM allowing more serum filtration, but it also allows neutrophil extravasation, during which the neutrophils punch holes in the BM through which white cells can squeeze, which is why you get a proteinaceous exudate in Type I hypersensitivity.

Increase in blood flow Like a water balloon increasing its surface area with more blood flow, skeletal muscle capillary beds (Type I) increase their volume and surface area when engorged with blood during exercise. This doesn't change the Kf (the only exit for serum is still the intercellular clefts, but they're bigger now).

P.S. A 1985 morphometric study of pancreatic capillaries shows that the idea that endocrine glands need a boatload of bloodflow (high serum filtration) is valid. Even within a single capillary that feeds both an exocrine acinus and and endocrine islet, the side facing the endocrine islet had more fenestrae.


How are atoms in benzopyridines and benzopurines numbered?

This is a question of chemical nomenclature and the principle source for this is the IUPAC (IUBMB in case of biological molecules; but not in this case). You can find all hetero-ring nomenclature references on the IUPAC web site:

http://www.acdlabs.com/iupac/nomenclature/

http://www.acdlabs.com/iupac/nomenclature/79/r79_702.htm

(I'm skipping the actual naming step)

Numbering is actually done according to
http://www.acdlabs.com/iupac/nomenclature/79/r79_72.htm

That means, if you take the skeleton without hetero atoms, you start

  in a clockwise direction commencing with the carbon atom not engaged
  in ring-fusion in the most counter-clockwise position of the uppermost
  ring, or if there is a choice, of the uppermost ring farthest to the
  right, and omitting atoms common to two or more rings.

Now, if there are more than one possibility due to symmetry, you chose the numbering that gives the heteros the smallest possible numbers (this means your purines would be actually wrongly numbered if they weren't an exception---see the List of retained names).

So, we have finally in dxC and dxT the start at the lower nitrogen, going anti-clockwise (the other N at 3, methyl at 6, ribose at 8), and in dxA and dxG similarly the start at the lower right N, going anti-clockwise with other Ns at 3, 6, and 8, and ribose at 8, as well.


species ID: garden bush from Bangalore, India

Could be anything, if it's ornamental. However, it would appear to be some kind of Pinaceae or other evergreen conifer. Possibly a juvenile hemlock or araucaria. I know that in Northern India there is Tsuga dumosa

Maybe an Araucaria?


Would current-day human-initiated panspermia be effective?

Okay, there are technically four questions here, but I'm willing to have a stab anyway.

  [Are there organisms that c]ould survive [65,000 years], perhaps
  frozen or in a dormant state;

Probably/possibly (prossibly?). There are claims of the recovery of viable bacteria from samples that have been frozen for millions of years, and viable green algae have been growth from permafrost samples at least 5,000-7,000 years old. Dormant bacteria have also been  reportedly recovered from 25-40 million year-old amber and salt crystals formed 250 million years ago. Several of these results are controversial, since in some cases the organisms's genomes are suspiciously modern, and it's not clear whether they could represent sample contamination, but confidence in several of the ones in the range of 10-100,000 years seems to be fairly high (for example, this Carnobacterium recovered from 32,000-year-old permafrost . Using freezing methods optimised for viability, it should be possible to achieve better viability levels than occur naturally (but you'd have to test your samples after 65,000 years to make sure!).

It's also (with a fairly high degree of confidence) probably possible to create micro-environments containing viable bacterial communities that can survive for thousands of years without light or nutrients, but this looks like it would require liquid water, and the maximum lifespan of most radioisotope thermal generators (RTGs), which would be the lowest-maintenance form of heat generation, is only a few thousand years (I am not a physicist though - you might want to post this on Space.SE).

  [are there organisms that w]ould have a fair probability of surviving
  in the barren oceans (or land if preferred)

Yes, if you have liquid water and CO2. If you don't, you might need to engineer something. There are various currently-available technologies for inferring the atmosphere of exoplanets.

I'd recommend sending as many species as possible to encourage the formation of a complex ecosystem (and increasing the chance that one of them survives!). The gypsum-crystal samples mentioned above contained around 40 strains of bacteria plus several viruses, so that's a start. Maybe try freeze-thawing that first. Happily (pretty much by definition) any crystals proven to contain bacteria are water-soluble, so if the planet has an ocean of water then they'll eventually dissolve, releasing their (hopefully) highly invasive payload.

  [Are there organisms that would e]ventually have a change of evolving
  to more complex lifeforms?

This is the easiest one to answer: an unqualified yes. Any organism relying on error-prone information storage (so DNA, RNA, or pretty much anything else) is capable of evolution.

  If possible, give a rough estimate of how likely you think that would
  be -- would we need to send 10 probes for a good chance, or billions
  of probes?

This is the problem. The reasons go rather beyond this SE (again, maybe try Space.SE) but literally any machine you can conceive based on anything more complex than chemistry or melting points is going to fail after 65,000 years in space. Forget computers, moving parts, rockets, etc. So how do you do it? You really want something that starts to melt as it approaches the other star and releases tens of thousands of packets, each containing copies of everything you're trying to seed the planet with and capable of surviving re-entry (for this, you should post another question on Space.SE - those guys are going to love you). Even so, I don't have the figures for this (again, Space.SE) but I have a very, very strong suspicion that since you're basically throwing darts at a pinhead millions of miles away you'd need to build a moon-based factory or something and fire synthetic comets/meteors containing your payload every few minutes for thousands of years. But since that's trivial compared to the travel time, and that in turn is miniscule compared to the time it'd take for the arrivals to evolve into anything worth visiting, I imagine that's fine. Launch early, launch often.

(I have posted a related question on Space.SE)


In my view, we simply don't have good enough data to answer this question. The fossil evidence is too sparse prior to the Cambrian and the evidence that we do have suggests that the phyla were already too separated. Meanwhile, the depth of time and the different lifecycles and circumstances of the species involved mean that any "genetic clocks" we might use are likely to be too poor at keeping time and, indeed, different attempts have delivered different estimates of the time of divergence.


I don't want to comment about the nature of electric signals in neurons (as I know only little about physiology and neurophysiology). But here is a short answer that may already help you.

Neuronal electric signals are called action potential. If you register the voltage at a given location on the axon of a neuron through time you will see something like this:

This picture shows one action potential. Of course when you feel pain it lasts for more than 5 milliseconds. In such case, if you record the voltage for a longer period of time you will just see a series of action potentials. You should have a look to the wiki page for more information.


How does Halosulfuron-methyl kill nutsedge, while leaving lawn grass and most weeds undamaged?

Halosulfuron-methyl is a member of the family of sulfonylurea herbicides. Brown (2006) mentions in his abstract the following, and I quote:

  This class of herbicides acts through inhibition of acetolactate synthase [...], thereby blocking the biosynthesis of the branched-chain amino acids valine, leucine and isoleucine. This inhibition leads to the rapid cessation of plant cell division and growth. [...] Crop selectivity results from rapid metabolic inactivation of the herbicide in the tolerant crop. Under growth-room conditions, metabolic half-lives in tolerant crop plants range from 1–5 h, while sensitive plant species metabolize these herbicides much more slowly, with half-lives > 20 h. Pathways by which sulfonylurea herbicides are inactivated among these plants include aryl and aliphatic hydroxylation followed by glucose conjugation, sulfonylurea bridge hydrolysis and sulfonamide bond cleavage, oxidative O-demethylation and direct conjugation with (homo)glutathione.

Hence, metabolic inactivation activity differs between susceptible and insusceptible species. To get to your question: this means that the enzymes in lawn grass are also inhibited, but to a lesser extent, as the herbicide is metabolized and inactivated more rapidly in grasses.

Reference
Brown, Pesticide Science 2006;29:241–378


Does the nature of nervous impulses give us a finite number of things we can perceive?

I know we have sensors in the form of hairs that trigger a nervous
  impulse to the brain when they are stimulated. But as I understand it,
  each one can only send that on/off binary signal when they are
  triggered by a very specific level of sound.

Your overall question borders on philosophy and the biology of consciousness which is hardly understood at all. However, your picture of sensory input is a huge oversimplification. That's not really your fault, it's the sort of thing you are likely to pick up from pop science descriptions, which in turn are faulty because this is not a dead field where everything is understood to a T. Even the question of which parts of perception "are" digital and which "are" analog is still under investigation. However it makes your question hard to answer because it's sort of ill-posed since is assumes a purely digital model.

To address one oversimplification, our perceptions of the outside world are not necessarily binary on off bits. It is hypothesized that some neurons signal by changing the rate at which they fire. Is the rate continuously variable? It's not clear, but it certainly provides a much larger range of encodings than 1 and 0.

  Can we only perceive image A and image B with nothing in between, or
  can we perceive image A.012744 and A.064212454 And A.24545157845?

I don't know how this meshes with your statement that 'And I know we all have our personal reactions and even perceptions'. If you've ever looked into color blindness then you already know that some of your fellow humans can't distinguish between A.012744 and A.064212454, even if you can. It's not that they can't see them, they just can't tell that they are different.


Is the heart more relaxed when stretched or contracted, and how does it affect cross-bridge interactions?

The muscular portion of the heart is comprised of cardiac myocytes, elongated cells filled with bundles of actin and myosin called sarcomeres. These cells are similar in many respects to skeletal muscles, but are shorter, have only one nucleus, and slightly different isoforms (versions) of the proteins involved. The purpose of this cell, like the skeletal muscle cell, is contraction, or shortening on activation.

This image of cardiac muscle cells shows how full they are with long bands of proteins (proteins stain pink).

Because the heart is a muscular chamber, instead of simply a band of muscle (like the bicep), the relevant dimension for the organ is volume instead of length. Where your bicep gets shorter when it contracts (and pulls your forearm toward your upper arm, bending at the elbow joint), when your heart muscle contracts, it twists and squeezes against the fibrous part of the organ, decreasing the volume of the chamber.

Since there is no air in a healthy live heart, when the heart contracts, reducing the volume of the container, the blood is forced out of the heart (ejection) through whatever opening is available. This is called systole. When the heart relaxes, the volume of the container increases, and blood enters the container through whatever opening is available. this is called diastole.

Now, how is this related to cross-bridge interactions?

The mechanism for contraction itself, in both skeletal and cardiac muscle, is cross-bridge cycling. Those pink bundles of actin, myosin, and associated proteins in the picture above form bonds, change conformation, break bonds, change conformation, and form new bonds:

This cross-bridge cycling occurs during contraction when $Ca^{++}$ enters the cell as part of the cardiac action potential. Relaxation occurs when $Ca^{++}$ concentrations decrease, through the action of the $Ca^{++}$-ATPase, causing cross bridge interactions to decrease.


What is the purpose of the “No DNA control”?

No DNA controls (or water control, also "no sample control") are important to rule out false positives results due to contamination.

If your reagents/pipettes/equipment you use is clean, this reaction (I suppose in PCR) gives you no band. If you have a contamination, this will show up where no band should be and shows that you have a problem. In this case you cannot trust the other results as well.


Why are local field potentials generally band-pass filtered?

There is no physical limitation whatsoever on the frequency band you wish to record, other than the hardware limitations on the sampling rate.

Often electrophysiological recordings suffer from noise (mainly in the high-frequencies) and drifts in the baseline (low-frequency range).

In the end, you wish to filter out as much noise as possible, without throwing away the baby with the bathwater. In effect, prior knowledge about the frequency range of the responses of interest are vital. Anything outside that range can, and likely should be filtered out.

For example, FFT analysis of EEGs mainly focuses on bands limited to the frequency range of 1 to 50 Hz. The mains frequency is 50 or 60 Hz, often imposing sinusoidal noise when the room is not shielded. Hence, what reason would there be not to use a low-pass filter with a cutoff around 50 Hz to get rid of it?

Lastly, offline filtering methods are aplenty. My personal preference nowadays is, is to collect the raw data and filter offline. That way you have the baby and the water, and you can focus, with trial and error, on where the baby is and where the water.


Based on this line from the paper you linked, it seems like they are using intracellular retention to refer to proto-cadherins being taken up in to the cell via endocytosis.

It is possible that the effects of deleting the intracellular domain might be a result of loss of an organelle retention signal located in the cytoplasmic domain of the protein and/or a decrease in endocytosis of the protein accumulated in the membrane.

This paper also refers to intracellular retention of cadherins in the context of endocytosis of proto-cadherins: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3216661/
Based on this information, the quote from the Wikipedia page ("The cytoplasmic domain also mediates intracellular retention, a property which distinguishes the clustered protocadherins from the related classical cadherins.") seems to be saying that the cytoplasmic domain regulates proto-cadherins on the cell membrane being taken back up into the cell via endocytosis, hence retaining them intracellularly.


The role of antibodies interacting with cancer

This article on the University of Kentucky website is pretty good, it seems the cancer cells hide because they do not express CD80, a co-stimulating molecule. Co-stimulating molecules are often necessary for an effective immune response.

This is a big part of the article and I think they do a good job of explaining it so I'll just quote:

  "People once thought that cancer occurred because of a weakness in the
  body's immune system," says Yannelli, "but we have known for years
  that overall that is not the case. The immune system in cancer
  patients actually works quite well. Otherwise, they could not survive
  the disease for long periods of time nor could they fight off other
  viruses, which they routinely do. The problem is not that the immune
  system doesn't work; it is that the immune system doesn't recognize
  the tumor."

  According to Yannelli, for the body's defense system to work properly,
  key antigens must be presented in a specific way to lymphocytes, the
  cellular mediators of the immune system, which then kill the cancerous
  cells. Normally, antigens are tipped off by co-stimulating molecules.
  When the co-stimulating molecules are not present, the immune system
  does not "see" the cancer cell, and therefore does not act to destroy
  it.

  Scientists have discovered that lymphocytes have very narrow job
  descriptions, each one designed to attack only a specific molecule.
  The researchers have also discovered a wide range of co-stimulating
  molecules. A critical co-simulating molecule is CD80. Because cancer
  cells do not express CD80, they are invisible to the lymphocytes
  responsible for destroying them.

This paper has more on the function and mechanism of CD80.

Thanks to @Nico for pointing out that not all cancers are the same so the generalization discussed in this answer may not be true of all cancers.


Are there any animals that are both poisonous and venomous?

That is certainly an interesting question!

First, to clarify definitions:

To be considered venomous the toxic substance must be produced in specialized glands or tissue. Often these are associated with some delivery apparatus (fangs, stinger, etc.), but not necessarily.

To be poisonous, the toxins must be produced in non-specialized tissues and are only toxic after ingestion.

Interestingly, many venoms are not poisonous if ingested.[1]

I know of at least three species that produce both poison and venom. One is a snake (although not a rattlesnake, which are, in fact, edible): Rhabdophis tigrinus, which accumulates toxins in its tissues, but also delivers venom via fangs.[2] The other two are frogs: Corythomantis greeningi and Aparasphenodon brunoi, which have spines on their snout that they use to deliver the venom.[3]

[1] Meier and White (eds.). 1995. Handbook of clinical toxicology of animal venoms and poisons. Boca Raton, Fla.: CRC Press, 477p.

[2] Hutchinson et al. 2007. Dietary sequestration of defensive steroids in nuchal glands of the Asian snake Rhabdophis tigrinus. PNAS 104(7): 2265-2270.

[3] Jared et al. 2015. Venomous frogs use heads as weapons. Current Biology 25, 2166-2170.


Why does Nature use a 4-level system to encode information in DNA?

The current hypothesis is that RNA came first, DNA and proteins came later. So the reason that four bases are used might be related to the initial RNA world, and then DNA just reused the already existing RNA bases in a slightly modified form. In the RNA world, all functions had to be performed by RNA. Having more bases available than two would likely be important to be able to adopt various structures and create binding pockets or active sites for ribozymes.

You can't really think of the genetic code as an abstract data storage device. There are physical and chemical consequences to the choice of encoding. For example, proteins have to be able to bind to DNA and recognize particular patterns. With your binary code, the recognition sequence would have to be longer, because each basepair contains less information. The tRNA anticodons would have to be larger for protein biosynthesis to work with the binary code. Another issue that plays a role in some processes is that GC base pairs are more stable than AU/AT base pairs.

These are all just hypotheses. Evolution doesn't necessarily choose the best option, sometimes it is just the most convenient one that still works well.

I also found a review titled "Why are there four letters in the genetic alphabet?" that makes a similar point as my first one.

  All present models to explain the fact that we have four base types in
  our genetic alphabet hinge, in covert or overt form, on the assumption
  that the genetic alphabet evolved in an RNA world

Another factor I didn't think of that is mentioned there is that while more bases make better ribozymes, more bases also decrease the accuracy of  replication.

  In summary, two-dimensional RNA-like structures (and, presumably also
  the three-dimensional structures) become better defined as alphabet
  size increases, whereas the accuracy of replication decreases.


Can cognitive enhancement from exercise be replicated/replaced through prolonged standing?

Short Answer

Probably not.

Slightly longer answer

This fairly recent review shows little positive effect of standing desks and mixed results of treadmill desks for cognitive outcomes (note: this is a summary of 23 full studies). Only treadmill desks were actually studied for cognitive performance, and even those showed no effects.

There were some positive physiological outcomes for both standing and treadmill desks, but much more consistent with the treadmill desks. The treadmill desks seemed good for weight loss, though, especially in obese participants.

All in all, it doesn't seem like a mere standing desk is known to give direct cognitive benefits, though the existing studies are all fairly small. It probably won't hurt, although standing for long periods can be problematic, too.

None of these studies compared the effects of the standing desks to the effects of exercise.

References:

MacEwen, B. T., MacDonald, D. J., & Burr, J. F. (2015). A systematic review of standing and treadmill desks in the workplace. Preventive medicine, 70, 50-58.

There are studies, however, like this one:

Mehta, R. K., Shortz, A. E., & Benden, M. E. (2015). Standing up for learning: A pilot investigation on the neurocognitive benefits of stand-biased school desks. International journal of environmental research and public health, 13(1), 59.

...that purport cognitive benefits of standing desks. However, it is important to note that one of the authors has patents on standing desks that are licensed by companies that produce them, including some of the desks used in the study.


Is there are practical lower limit to gene length in E. coli?

In terms of naturally-occurring "genes" I think that the record is probably held by the attenuator peptides.

In bacteria, the regulatory mechanism known as transcription attenuation involves the ribosomal biosynthesis of very short peptides. In the trp operon, where the phenomenon was first described by Yanofsky's group, the peptide, MKAIFVLKGWWRTS, consists of just 14 amino acids. Other examples, described subsequently, are of comparable size.

Now that I have written this answer, I have reread your question and I see that you are really interested in transcripts. In the case of the attenuators, the peptides are encoded by the 5' end of a much larger transcript, so they probably don't count for you.


How can rooted and unrooted (phylogenetic) trees be distinguished from one another

In case of a drawn figure, either look for the a short stem to the left, or for an explicitly labelled outgroup. Trees derived from phylogenetic analyses are normally unrooted by default, you need to root them by either making an arbitrary (but hopefully informed) decision or by adding an outgroup.


Does the necessary Carbon Dioxide need to be in the atmosphere for mammals?

No it isn't necessary to breathe in CO2 from the atmosphere. For the buffer system your brain detects the amount of CO2 (H+ which is an indicator of excess or too little CO2) and adjusts your breathing automatically to compensate so that your blood's pH stays normal. No outside CO2 is needed. Your kidneys also play a similar role but the lungs are what provide a rapid response.


As I understand it, most, if not all genetic engineering uses a marker
  gene to identify transformed bacteria. This marker gene was/is usually
  an antibiotic resistance gene so the transformed bacteria will be the
  only ones that can grow on an antibiotic laced culture medium

Most but color markers (which gives the host cell a color that can be used for selection) are also used. More complicated selectable-counter selectable markers are also used (ie  HyTK gene). A counter selectable marker is a marker that kills a cells when it is present. A selectable-counter selectable marker is a hybrid marker that allows you to both select for cells with the marker using one selection agent and kill the same cell with a second selection agent.

  So, every (most) GMO will contain a copy of a bacterial antibiotic
  resistance gene.

Well not quite. GMO ie Genetic modified organism, includes both prokaryotes (bacteria) and eukaryotes (plants, animals, and yeast). The promoters which drives gene activity in prokaryotes and eukaryotes are different. So a eukaryote markers do not work in prokaryotes and vise versa.

Furthermore, genetic modification of eukaryotes is difficult. Hence modified viruses are often used. These viruses are made in such a way that their genome has been replace by desired DNA playload. And as the payload size is limited, often time any unnecessary DNA is also removed, like prokaryotic markers which have no function in a eukaryotic host.

Lastly due to public pressure, there has been a push towards cleaning up after genetic engineering work in GMOs that are to be marketed to the public (GMO crops). So things such a selection markers are removed (either by use of counter selectable markers followed homologous recombination or site specific recombinases).

  So, is it a fair question to ask if the unnatural proliferation of
  antibiotic resistance genes in the wild due to the commercial
  propagation of GMOs might be at least partially responsible for the
  increase in multiply resistant organisms that we are seeing?

Given the wide spread use of antibiotic in animal husbandry and by the public general, and move toward removing selection markers in commercial GMOs, I do not think GMOs are the cause of the increase in MR bacteria.

A more likely cause would simply be because we are using so much antibiotics and thus there is a selection pressure to aquire multiple resistance. Remember all our antibiotics resistance genes and most of our antibiotics were acquired from nature.

  Has anyone, for example, mashed up GMO matter, added non antibiotic
  resistant bacteria, grown the mix up overnight, added the antibiotic
  used as a marker in the GMO, incubated for a few days and then seen if
  any bacteria survived?

Yes, lots of times around the world to varying degrees of sucess. I have personally spent time doing this and so have my labmates. It will work if you prepare good quality DNA that has not been degraded by endonucleases, the bacteria are very transformable (ie the bacteria has been treated to take up DNA easily), electroporation is use (to force the DNA into the cell) and you have prokaryotic marker. A eukaryotic marker, is a marker that works in an animal cells will not work in bacteria. So you have to engineer your GMO animal to carry both a eukaryotic and prokaryotic marker.


Is there a complete connectome of a cortical minicolumn?

Perhaps the first place to look would be the Allen Brain Atlas
 (for mice, this is a paper about it), and also [this paper].(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4169118/)


How much of human's behaviors and preference can be explained by evolution?

What is heritability?

First of, please read about the concept of heritability. See for example the post Why is a heritability coefficient not an index of how “genetic” something is? You should be able to understand why all else being equal, why if environmental variance for a given phenotype increase it results in a decrease in heritability and why directional selection in a population decreases heritability.

Do you now know what heritability is and is not?... Good!

Your question is very broad...

As you now understand, heritability is a concept define for a given population in a given environment and most importantly for a given trait. There is no way to give a single answer for all traits one might want to consider.

By experience, it seems that, in humans, most behavioural traits that we decided to investigate has heritability estimates in the order of 0.05 - 0.6.

One example

I will consider just one of the trait you list, "preference for sweet foods". Sweet taste preferences appears to have a high heritability in humans with estimates of the order of 0.41-0.66 (Keskitalo et al., 2007). For heritablities about other food preferences, you might want to have a look at Reed et al. (1997; there are probably more recent papers that make better reviews though).

Preference for sweet foods


Comparing SIFT and PolyPhen to other methods

I will strongly suggest you:

PredictSNP: It's the best tool for nsSNP detection as it compares and throw out result from all the tools available.

http://loschmidt.chemi.muni.cz/predictsnp/

Paper: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3894168/


This looks like an ant, but I cannot say which species. Their small size, colour, bite and being found indoors made me think of Pharaoh ants (Monomorium pharaonis), but I haven't heard that they smell bad. Ghost ants (Tapinoma melanocephalum) are rather similar and have a foul smell when crushed, and have been found indoors in Europe. They usually have a dark head/thorax and lighter abdomen though. They can also be separated from Pharaoh ants by having a one segmented petiole (the Pharaoh ant has two). A closely related species to the Ghost ant is Tapinoma sessile, which also smells but has a uniform colour (usually darker than your specimen though, see picture at bugguide.net). The petiole not being clearly seen in your specimen points towards the two latter species, or other species with a short/hidden petiole (see hidden petiole at antkey.org). However, these are only a couple of suggestions, and there are probably many other possible species.

Termites have larger mandibles (jaws) relative to their size, and no distinct narrow division between thorax and abdomen (your specimen does). Your animal also has eyes (termites don't) and I think you can spot a long first antenna segment, which ants have (hard to see in the picture though).


There is no straightforward answer as to whether a "single cell" is irreducibly complex. Which cell are we talking about? Human mitochondria do not survive without their genome, but those of Cryptosporidium do persist without it. The Minimal Genome Project, led by biotechnologist Craig Venter, concluded with the creation of Mycoplasma laboratorium, the result of removing non-essential genes from Mycoplasma genitalium. This minimum cell had 382 genes.

Are 382 genes the minimum number of genes required for life then? No. That number refers to the total number of genes necessary for a particular organism, which happened to be Mycoplasma. Iterative trials of removing genes will reveal different numbers of essential genes for different organisms. Primates will require a high number of essential genes, whilst archaea could survive with fewer genes.

Regarding the transition from RNA-only to RNA-protein world, peptides function as cofactors for some ribozymes. Amino acids and peptides are known to have existed in the prebiotic environment and have been found in space (glycine has been found in comets, along with other 70 amino acids).

Regarding the formation of nucleotides, from Scientific American.

  A New Route
  In the presence of phosphate, the raw materials for nucleobases and ribose first form 2-aminooxazole, a molecule that contains part of a sugar and part of a C or U nucleobase. Further reactions yield a full ribose-base block and then a
  full nucleotide. The reactions also produce “wrong” combinations of the original molecules, but after exposure to ultraviolet rays, only the “right” versions—the nucleotides—survive.

This answer is not complete, I will add more information and provide citations in the future.


What photoreceptors are necessary to permit infrared vision?

The photoreceptors of the mantis shrimp (Fig. 1) are quite different from that of the human retina (Fig. 2).

Importantly, when light enters the units in the shrimp's eye, it must first pass through a crystalline cone, which lies over the receptors. These crystalline cones contain frequency-specific light-blocking substances called MAAs (mycosporine-like amino acids). These filters help to filter the spectrum and this means that less different opsins are necessary tod etect different wavelengths. In other words, a mantis shrimp does not feature 16 different opsins. Instead it utilizes the same opsins for various wavelengths by putting a filter on top of the cone (source: National Geographic).

Fig. 1. Mantis shrimp photoreceptors. source: Physiologizing

Fig. 2. Human cone cell. source: Wikipedia


What's the rationale behind freezing one's eggs if cells can be cloned?

Why Would You Freeze Your Eggs?

For 1, a woman may wish to freeze her eggs if she needs to delay childbirth. This page explores several reasons why, for example, "Women who want or need to delay childbearing in order to pursue educational, career or other personal goals.". Additionally, it explores some basic explanations of the process, if you are interested. If a woman has doubts about her fertility in 10 years time (using your final sentence as an example), such as if she is recently diagnosed with cancer, or needs to finish education but is ready to be committed to having a baby in more than 9 months' time, then she may decide to freeze her eggs for a time when she is more suited to have a baby, using a time when her body is more suited to producing eggs.

Does Freezing Have Adverse Effects?

As for your second question, the same page does mention successfully freezing an embryo for 10 years at -196 degrees Celsius, with no adverse effects on the eventual birth.

Regardless, exploring the risks reveals that the decision on whether the practice is seen as positive or negative is still on the fence - different parties argue for different opinions, as there appears to be no objective truth about proven adverse affects.

The risks described by this clinic are worth considering, albeit minimal compared to a risk of malformed children, however, it is still a popular choice, albeit put forward as 'experimental'. This study (2010, Rudick et al) showed how, in the US, cryopreservation was already being offered in 283 of 442 fertility clinics surveyed. 1/3 of the reasons for the choice was for women with cancer, and the other 2/3 was for women with 'advancing maternal age'.

The ACOG (American College of Obstetricians and Gynecologists), in 2013, stated that they do not endorse freezing of eggs 'for the sole purpose of circumventing reproductive aging in healthy women', however, the ASRM (American Society for Reproductive Medicine) lifted its label as being 'experimental' in 2012. The previously linked article describes a study conducted by the ASRM, which 'reviewed data from four randomized controlled trials and various observational studies that compared fertilization rates, embryo implantation rates and pregnancy rates of fresh eggs versus eggs that were frozen', and 'showed no increase in birth defects, developmental disorders or chromosomal abnormalities when in vitro fertilization cycles were conducted with frozen eggs, leading the society to declare the technique effective and safe'.

Conclusion

Your question is a slightly broad one, and can be answered by the subjective choice of the woman/women involved, however the ASRM still stresses that "we should proceed cautiously in using this as an elective technique", by making a clear line between 'need' and 'want'. However, there is no evidence to show that rates of abnormality are any higher using this method, but considering it is still a fairly new practice that is being marketed as a choice rather than a medical treatment, there is skepticism in the air around whether marketing scientific and medical designs as a mere 'choice' for older women will lead to this technology becoming better or worse.

Additionally, about your comment of it being 'less expensive', this website shows that the average cost of in vitro fertilization in the U.S. is currently about 10,000 - 20,000 USD, whereas the first website I linked (here) estimates the cost at about 10,000 USD to undergo an egg freezing cycle. Although, the prices will change from clinic to clinic. Regardless, the prices are still similar, and the choice lies in the woman choosing to pay and freeze her eggs if, for example, she has recently been diagnosed with cancer, or fears she will not be fertile in 5+ years time.

I hope this answer has been sufficient in answering your questions, and if you have any more questions, feel free to ask me :)

Sources:

http://uscfertility.org/egg-freezing-faqs/
http://www.mayoclinic.org/tests-procedures/egg-
http://www.sciencedirect.com/science/article/pii/S0015028210008009
http://www.ncbi.nlm.nih.gov/pubmed/24463693
http://edition.cnn.com/2012/10/19/health/egg-freezing/
http://www.advancedfertility.com/fertility-treatment-costs.htm


Nutrient limitation in terrestrial and freshwater ecosystems

The traditional explanation for this is that nitrogen compounds are more mobile than phosphorus compounds. As a result, nitrogen is more likely to flow through terrestrial ecosystems and accumulate in freshwater ecosystems, making P relatively more limiting than N in freshwater.
Phosphorus compounds (e.g., phosphate) are more "sticky" and tend to bind/sorb to compounds in the soil and aquatic sediments, e.g., ferric compounds. Thus, most phosphorus gets bound up in terrestrial ecosystems because it's less mobile than nitrogen, or gets bound up in aquatic sediments. As a result, nitrogen becomes relatively more limiting than phosphorus in terrestrial ecosystems, and the phosphorus that does enter freshwater ecosystems often becomes inaccessible to biological organisms like primary producers.
Note that this paradigm is a generalization, and is dependent on many other factors. Lake pH and concentration ferric compounds can regulate whether the sediments are sources or sinks of P; anoxic conditions can lead to denitrification, a loss of N that could offset N inputs. Anthropogenic additions of N and P (either to the freshwater system directly or to the terrestrial ecosystem that drains into it) could dramatically perturb the natural balance between N and P limitation in terrestrial and aquatic ecosystems in a way that does not conform to the paradigm.
Some references you might find useful:
Elser, J. J., Bracken, M. E.S., Cleland, E. E., Gruner, D. S., Harpole, W. S., Hillebrand, H., Ngai, J. T., Seabloom, E. W., Shurin, J. B. and Smith, J. E. (2007), Global analysis of nitrogen and phosphorus limitation of primary producers in freshwater, marine and terrestrial ecosystems. Ecology Letters, 10: 1135–1142.
Vitousek, P.M. & Howarth, R.W. Biogeochemistry (1991) 13: 87.


What winged insect is in this photo? Is it Axymyia furcata?

Great pictures.  First, fly or wasp?

In the second picture, under the head you don't see jaws of a wasp, but do see a bit of a tongue-like organ, like a fly.  Further down, you can see that there are only 2 wings.  Just below where the left wing meets the thorax, you can see what looks like a tiny wing or paddle.  That's a haltere, a reduced wing that vibrates to provide stability, like a gyroscope.  Flys have halteres.  Finally, in the first picture at the very end of the abdomen are 2 points.  That ain't a stinger, it's an ovipositor.  It's a fly, female, and from the size of the abdomen, gravid.

The closest I've gotten to identifying this one is Axymyia furcata http://bugguide.net/node/view/1216479.  Everything matches, as well as we can see from a photo, except the coloration.  Also, A furcata is associated with streams and is found in the north-east and north-central US, while, your bug was found on a lawn in CA.  For more information about A. furcata than you need, there is a master's thesis available:  http://lib.dr.iastate.edu/cgi/viewcontent.cgi?article=1882&context=etd.

I've looked at hundreds of fly pics to find the one I linked to above.  That's the only fly I found that matches the shape of yours.  Maybe it's a different fly within that genus, maybe it's just a color variation.

Their maggots live in rotten wood and decaying plant material, and the adults are mostly interested in more maggots, so this isn't a pest, just a neighbor.

Edit: furicata --> furcata, oops.


Influence of eating at late night on sleep

According to Crispim et al 2011, caloric intake late at night is correlated negatively with sleep quality:

  We conclude that food intake during the nocturnal period is correlated with negative effects on the sleep quality of healthy individuals. Indeed, food intake near the sleeping period (dinner and late night snack) was negatively associated with sleep quality variables.

The paper is an interesting read. Here's their figure 1 which shows the correlation between sleep latency (how long it takes to fall asleep) and nocturnal caloric intake:

Thick line: men
Thin line: women

Basically, it shows that people who eat more at night take longer to fall asleep, and other results show that it's also correlated negatively with other sleep quality indicators.


What are these needle-like plants growing in the ground?

What you have here is a Filaree/heron's bill/stork's bill (Erodium species). These are widespread in California, being plants of disturbed and unmanaged soils - farms, dunes, roadsides, etc.
Note that I'm not Californian, or even from North America, all I did was google "weed species california" (without the quotes) and hit the first link that looked reputable, then used a small bit of knowledge of plant forms (rosette in this case...) to follow the links inside - and found the species at the link I supplied.


Do rare earth metals actually repel sharks?

Short answer
Electropositive metals such as the Lanthanides generate electrical currents when they come in contact with (sea) water. This electrical activity may repel sharks by over-stimulating their lateral line organ. However, the effectiveness of lanthanides as shark repellent depends on many factors. For example, hungry sharks, or sharks engaged in a feeding frenzy may simply ignore the stimulus altogether.

Background
Rare earth metals are Lanthanides - metals with a low electronegativity. Metals with low electronegativity are called electropositive. Electropositive metals (EPMs) react vigorously with water when immersed and generate electrical potentials that are thought to overstimulate the sharks’ highly sensitive electroreceptors, the ampullae of Lorenzini.

Many electropositive metals fall in groups I and II of the periodic table and explosively react with water. Examples include sodium and lithium. The Lanthanides, on the other hand, contain some less reactive elements.

There is in fact a considerable body of primary literature on the use of EPMs to deter sharks, because the by-catch of sharks is a recognized problem of modern fishery. However, much of this literature shows very mixed results of EPMs, and therefore I have based my (second :-) answer attempt on a recent review article by Hart and Collin (2015), which is available on-line and cites some fifteen primary research articles on the topic:

EPMs are primarily intended as a mechanism to reduce shark bycatch and catch depredation in longline fisheries, without affecting the catch of non-electrosensitive target teleost fishes. As you indicate in the question, EPMs can be formed into shapes that are easily attached to a fishing line or hook.

Early tests in the laboratory with captive sharks showed that several EPMs (including magnesium and rare-earth lanthanide elements such as cerium, lanthanum, neodymium and praseodymium) were effective in repelling various shark species. However, more recently, several studies showed no such repellent effects other species of shark, and it was shown that aversive behavior was highly dependent on various factors such as duration of food deprivation prior to testing. Specifically, hungry sharks ignored the EPM, especially when feeding in groups (feeding frenzies).

The results of field trials with EPMs were also mixed, with some studies showing a reduction in the catch rate of various shark species, while other studies showed no such effect. The authors of the review article summarize a range of factors that may influence the efficacy of EPMs in repelling sharks, including the type of EPM used, the relative sensitivity of the electrosensory system, shark density and competition, hunger level, and differences in feeding ecology. Other impediments to large-scale adoption of EPM technology by commercial fisheries include the relatively high cost of the rare-earth metals (although magnesium may represent a cheaper alternative), potential toxicity to other marine animals, and the fact that they dissolve rapidly in seawater and, therefore, must be replaced frequently. The use of EPMs for personal shark deterrent devices is also hampered by the limited effective range (<85 cm) of the electrical field they generate.

Instead, for use in scuba dive gear a rechargeable battery-powered capacitor-discharge unit connected to two or four electrodes is sufficient as shark repellent. Also, electro-magnetic induction using permanent magnets may be a more suitable alternative (Hart and Collin, 2015).

Regarding the great white: this shark has a lateral line featuring ampullae of Lorenzini, so EPMs may repel it, theoretically.

Reference
- Hart & Collin. Integrative Zoology; 10(1): 38–64


Optimal pH of protein buffer? Basic principles to adjust buffers according method and analysis

The correct pH depends on the properties of the proteins that you are trying to exploit. These are a good deal different between extracting proteins from tissue and performing Western blots.

Extracting proteins means keeping them soluble in aqueous solution. Working at the pI of the protein might be the worst choice as the protein then has no net charge, typically reducing its water solubility. An extreme case would be the highly basic histone proteins with very high pI values but best extracted at low pH.

After proteins have been run on a denaturing gel and transferred to a membrane for Western blotting, they are already denatured and bound strongly to the membrane through hydrophobic interactions little affected by pH except perhaps at extremes. For the blotting, you want to exploit the interaction of epitopes on the protein with the antibodies against them. During antibody production, the interactions between the epitopes and the antibody-specific receptors on the antibody-producing cells occur at normal extracellular body pH, 7.4. Using that pH for the blotting best recapitulates the charge state of both the epitopes and of the antibodies as they existed when cells producing the best antibodies were selected.