These are Scuttle Flies (Order Diptera, Family Phoridae) (the wing venation, best seen on the lower left individual of the top photograph, is characteristic); the group has several hundred species in America north of Mexico.  So far as I am aware, the generic key in Manual of Nearctic Diptera, Volume 2 (available online here, pages 25 to 48) will still yield useful results, but cannot be used on these photographs.  The 30 pages in bugguide.net's gallery (starting here) eliminate a few of these, but not nearly enough to go further on the evidence we have.


What is/are the molecular differences between HDL and LDL cholesterol?

First of all, we should specify that there is no such thing as "HDL-cholesterols" and "LDL-cholesterols". On the same note there is no such thing as "good cholesterol" and "bad cholesterol": cholesterol is just one molecule, with this chemical structure

What blood tests generally report is HDL-C and LDL-C, that is the amount of cholesterol in HDL or LDL respectively (again, cholesterol is always the same molecule, whether in an HDL or in an LDL).

HDL (high density lipoprotein) and LDL (low density lipoprotein) are lipoproteins, aggregates of proteins and lipids that can carry, amongst other things cholesterol.
There are 5 major types of lipoproteins, called chylomicrons, VLDL, IDL, LDL, and HDL and are distinguished by their size, density and the proteins they are composed of.

The main function of lipoproteins is that of carrying lipids (=fats) around the organism in the blood. The problem is that lipids are not soluble in water (try to pour some oil in a glass of water) and blood is mainly composed of water. Lipoproteins, on the other hand, have a hydrophilic (="water-loving") exterior and a lipophilic (="fat-loving") interior, like this:

In the picture, the "balls" represent proteins, called apoproteins, and the C represent cholesterol and T tryglicerids, which are both lipids.
As you can see, all the fats are inside the lipoprotein, but the exterior, being soluble in water can be easily dissolved in the blood.

The biochemistry of lipoproteins is quite involved and I will not go into details here (but please leave a comment if you want further explanations) but, to simplify things:

HDL bring lipids from the periphery back to the liver
LDL bring lipids from the liver to the periphery

It is very important, at this point, to note that lipids are a physiologically important part of our organisms. All the cells in our body contain lipids: the membrane of each cell in the body is made up of lipids (called phospholipids) and also contain cholesterol. In fact, cholesterol is extremely important for the correct functioning of the body as, for instance, it is used as the base to make many hormones (the so-called steroid hormones, such as estrogen, progesterone, cortisol, testosterone etc).

However, too high levels of lipids, particularly cholesterol, are not beneficial, as high cholesterol levels have been in fact linked to many cardiovascular diseases, which we hear a lot about these days.

So, because HDL tend to remove the lipids from the circulation and bring them back to the liver they can be considered as some sort of "cleaners", that remove excess cholesterol from circulation.


Is a species lifespan affected by meat consumption?

I don't think that the theory is very reasonable, because animals drink from stagnant ponds (i.e. savanna wells , forest puddles) and have lots of vectors of infection other than rotten meat: cuts and grazes, tract infections, parasites like mosquitoes and nematodes.

The olfactory sense is also very sharp in many carnivores and they can gage the decomposition state of meats. Even humans have a very strong sense of the age of meat using smell, although I can't find  research on it.

The fun thing is to see the age of other animals, i.e. birds and bears. The oldest zoo birds:

Flamingoes, seagulls, vultures, 50-70
parrots 90-120 years.

the oldest panda: 37
the oldest grizzly and polar bear: 40 and 42

Oldest reptiles:
lizards crocodiles and tortoises: 50-100 years
giant tortoise: 150-250 years.

Other herbivores with slow senescence: donkey 60, bison 50, gorilla 60...

research papers don't include any evidence to correlate carnivory and lifespan. It's mostly body mass and ecology, i.e. predation rate.

Carnivores have must stronger stomach acid also which mitigates some of the risk.


Where does this equation in the electrophysiology literature form come from?

They chose that equation mainly because of numerical simplicity. It can fit the rates $\alpha$ and  $\beta$ for all the ion channel particles in the model.

The theoretical foundation for the equation, as in the H&H model, are loose. It resemble the equation derived for the movement of a charged particle in a constant field. But it is not an equation derived from the ion channels biophysics. We can't blame them, considering that at that time (1952) they don't even know for sure that ion channels where proteins.

In page 183:
 In order to simplify the reporting of the actual values used in this model, we have expressed the alphas and betas entirely in terms of a generalized function, with eight defining coefficients. Table 1C gives the equation, and the defining coefficients for al rate constants.

For the generalized function note that in every case at least some of the coefficients are zero: this generalized formula is just a way to collect both possible forms for the H&H rate constants.

I have read papers using Eyring equation for a theoretical formulation of transition rates, based on thermodynamics.


What's the difference between a free chromosome fragment and an extrachromosomal array?

I asked my professor, and the answer appears to be differences in both the generation and the final product.

Free chromosome fragments are created through irradiation/other damage of the germline in one animal.  Through a series of crosses, it is possible to introduce individual fragments (containing a duplication of your gene of interest, as well as a marker) into a mutant background.  The extrachromosomal fragment will be lost during mitosis at various points in development, and in a mosaic analysis, you can look for the loss of your marker (and therefore the loss of the wildtype allele), and see if yfg product is required in certain cell types for a wildtype phenotype.

Extrachromosomal arrays are created by cloning, and you typically have many copies of both the gene and marker.  It's the same principle as free chromosomal fragments in terms of mosaic analysis, but it's very powerful, as you can easily clone individual genes (versus irradiating and hoping to discover yfg on a fragment) and markers (and now you can use non-endogenous markers like GFP).

Even though extrachromosomal arrays are comparatively easier to generate, the problem is that you end up with many copies of the gene, which leads to non-endogenous dosage levels. Even if this doesn't cause a completely different mutant phenotype in the cells, it is possible that enough of these proteins could segregate at mitosis into the daughter cells, such that even if the fragment is lost, you could still have your gene product around in the daughter cells (if your marker protein didn't also segregate like this, you might draw erroneous conclusions about the necessity of yfg product in those particular cells).


Neural coupling between Pinsky-Rinzel (reduced Traub) neuron with a Wang-Buzsaki neuron?

There is no straightforward answer to this.
It completely depends on the properties of the neurons and the network they are in.

I would recommend you to study Central pattern generators. Those are usually small networks that can create a repetitive pattern of action potentials. However, the exact pattern they generate depends on how they are connected (number and type of synapses, network structure,...) and a presumably large number of neuronal properties (like the conductance, the shape of their dendrites, the expression level of various ion channels and all kinds of intracellular messengers/peptides/proteins/molecules). For example, there are "leaky" ion channels that can cause a neuron to spontaneously depolarize (and fire action potentials) regularly without requiring any synaptic input. This means that you can have a regularly firing neuron even without network feedback mechanisms. example

There are many different rhythms in the brain and they are all generated by smaller and/or larger networks of neurons with different properties. Neurons can even participate in multiple different rhythms, depending on the situation (e.g. theta rhythm vs. SPWs in the hippocampus). Thus, even the same neurons in the same network can generate different rhythms.

So, the rhythms that you can build depend on how you tune the neurons' properties and the way they are connected. With just the information you provided (simulated excitatory and inhibitory neurons, but no info on their excitability, network,...) I can't tell you what the resulting rhythm will look like.

I'm afraid I didn't really answer your question, but I hope this was still helpful.


Can someone identify this brown spider in California

It looks a lot like a Kukulcania hibernalis, or southern house spider. This one appears to be a female and if it were to bite you then it would be painful, but not dangerous. These spiders typically keep to themselves so unless you find one hanging in a really bad place it's better just to leave them alone.

For further information you can look here:

https://spiderid.com/spider/filistatidae/kukulcania/hibernalis/


Why spermatogenesis is an independent process while formation of ovum is dependent on fertilization by sperm?

This can only be answered logically. Imagine bellow paragraph.
If secondary oocyte does not require fertilization for completing 2nd meiotic division then it will become an ootid (female gamete). Once formed lots of hormonal changes occur in female example individual's diet increase, mammary glands differentiate and all necessary changes for pregnancy which will be unnecessary at end of every month.
I hope u understood and comment if u want to ask about above imaginary paragraph.


Why can't I smell things that aren't there?

Couple of contributing theories:

The olfactory system does not project to the thalamus, which serves as a relay to other higher processing areas.
Lack of a specialized working memory subsystem; we have fairly robust subsystems for movement,visual and auditory buffers of information, what is normally called working memory, things we can hold on for a little while, but it seems they are not as developed or engage the same areas for smell. see for instance:Working Memory in Another Dimension
It is not as useful,used or adaptive ( beyond recognizing odors) as the other senses, there is a relationship in between how much we use something ( could also be the above working memory systems )and the cortical real state devoted to it's processing, this is a competitive part of the brain and in comparison to other senses like vision the portion of the cortex devoted to olfaction is small.
Another way of looking at it, is that we do have the capability to imagine smells and gustation, but they are not as developed as the others since we don't use them as much.
Anectodally, I would argue that people whose jobs revolve around combining nice smells or tasty things do develop certain abilities like those in vision as well as for those who have been exposed to the same odor repeteadly and can imagine it at will.


How do we sweat immediately after drinking water on a hot day?

Not everyone sweats in seconds after drinking water in summer.

Also, sweating in seconds after drinking water is not likely due to water being absorbed (Nutrition Reviews, 2015):

  Ingested fluids are not immediately available for assimilation into
  the body. They are initially stored in the stomach, and there is
  little net absorption of water or solute across the gastric mucosa.

There are a lot of receptors, including stretch receptors and various chemoreceptors, in the stomach, so your stomach will likely recognize water as water and signal the brain via the nervous system, probably via the visceral afferent fibers.

One of two things may then happen:

Your brain can perceive a sudden appearance of water in your stomach as stress and react with sweating, like when you are embarrassed or excited.
When dehydrated, you sweat less to prevent further dehydration; when your brain recognizes there is new water in your stomach, it can now allow the signals coming from warm skin to trigger sympathetic nerves to release some sweat to cool you down.


How likely is to develop an infection from a single virion entering a single cell?

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology! I'm glad we encourage such questions from curious people who want to learn more.

This is called the Independent Action Hypothesis, described here:

  The Independent Action Hypothesis (IAH) states that pathogenic individuals (cells, spores, virus particles etc.) behave independently of each other, so that each has an independent probability of causing systemic infection or death.

Zwart et al. (2009) tests this theory, and their results support the hypothesis that a single virus particle can infect a cell:

  The ‘independent action hypothesis’ (IAH) states that each pathogen individual has a non-zero probability of causing host death and that pathogen individuals act independently. IAH has not been rigorously tested. In this paper, we (i) develop a probabilistic framework for testing IAH and (ii) demonstrate that, in two out of the six virus–insect pathosystems tested, IAH is supported by the data.

The modeling done in this paper may be worth reviewing.


How do I interpret this depiction of dopamine neuron signaling?

From the figure caption for that figure:

  Each line of dots shows one trial, the original sequence in each panel being from top to bottom.

The bars at top are a summed histogram. Dots mark the time of spikes (this is called a "raster"). Each line is a different single trial from the same neuron.

(also note: this type of paper is called a 'review' paper, i.e., it isn't original research, although the original research might have been done by the same author. That doesn't mean anything bad, reviews are an excellent place to start understanding a topic, but you should be aware that the figures here are just representative examples or in some cases schematic diagrams. There is a lot of other data behind the conclusions drawn besides these single examples)


What is the minimum sample size to get reliable results in haplotype and nucleotide estimations?

I'm still a little unclear on what the analysis looks like, but I'm going to assume for the sake of this answer that it's a single locus sequenced across multiple populations, with some number of individuals per population, and that the concern is that some of these populations are represented by only a few individuals. I'm also going to assume that the individuals are diploid, so you in fact have a little more data than it appears.

All the same, this paper indicates that n<5 individuals in a population leads to quite noisy estimates of $\pi$ and $h$ (section "The effect of sample size on haplotype and nucleotide diversities"). This is of course specific to a certain ~500bp region that they collected sequences for. That doesn't mean that you can't compute these metrics, only that they may not be very reliable.

For reference, the early Neanderthal genome papers compute some measures based on only the two copies present in their diploid genomes- of course, they are assisted by a large amount of modern human data for making comparisons. If you have supporting data from other populations, you may still be able to say something about the populations with few individuals. But you will likely have to use measures other than $\pi$ and $h$ to do so.

Some other tools that you might use to "borrow" information from other individuals outside those groups are ordination analyses such as PCA, or clustering tools like STRUCTURE. One way of thinking about how this works is that you can "embed" your populations with few individuals in the population structure of your overall dataset. This allows you to still learn from those populations even if the number of individuals is small. The Neanderthal papers implement versions of this, but with much more elaborate statistical frameworks, for a whole genome rather than just a single gene.

I'm not sure if DnaSP can carry out these analyses, but there are a lot of tools that do similar things, one tutorial here. Of course looking at the DnaSP manual is probably a good idea to see what you can do with your current tool.

Depending on your goals it may also be interesting to compute F-statistics across your populations, this is done by most population genetics tool suites. I used GenePop many years ago to do this, it appears to still work, though I am sure there are better alternatives now.

An important note is that most of these measures are purely descriptive, not inferential. Low sample size makes descriptive statistics noisy, but doesn't invalidate them. Inferential statistics are a bit more dangerous.


Looks like this is a follow up to this question on this forum.

The short answer to your question is you will not be able to indicate that a cell or colony on an agar plate is dead even with a microscope unless you are using fluorescent dyes (i.e., some form of live/dead staining). There are quite a few ways to do this, but they will all require that you have access to a microbiology laboratory.

Now, if your objective is to simply show that UV light kills microorganisms, this is easily done as an experiment with one target microorganism (i.e., one species). I'm going to obfuscate details aplenty here, but I'll offer you a description anyway.

You'll need replicate plates of agar colonies inoculated with the same quantity of the microorganism--this is typically achieved by propagating the microorganism in liquid medium and depositing equal quantities of the medium onto multiple agar plates. Once your plates have been incubated to obtain some colonies, retain one plate as control (this will not be exposed), and expose the remaining plates to your UV source. [Ensure that you've counted the number of colonies in every plate--including the control--before you subjected them to UV irradiation.]

Now comes the hard part. You will need to re-suspend the colonies from your plates in liquid media and re-plate them on agar. You can either choose a single colony from each plate (ideally, colonies that are similar in size across plates) for re-suspension, or you can re-suspend all colonies visible to the naked eye. Either way, re-suspend your colonies in liquid media, and deposit them on agar thereafter, and incubate the agar plates.

If everything went right, the number of colonies you would observe in the re-plated control plate should be higher than the number of colonies in the UV-exposed "re-plates." What that indicates is that at least some of the colonies that were exposed to UV irradiation died, and thus did not show up as colonies upon re-plating. This would loosely "prove" that exposure to UV irradiation kills microorganisms (with many, many caveats).

All that being said, I would not attempt this at home. To the best of my knowledge, this shouldn't even be doable at home without spending a significant amount of money to obtain some of the necessary equipment (which I have not described here). Further, doing this experiment in the format I described would likely yield very noisy results--the way I've described it is more back of the envelope experimentation than something proper.

If you are keenly interested in this topic, find the nearest microbiology department, and talk to a subject expert. They might even let you try this experiment out for yourself in their lab.

Edit - the core methodology I've described here is CFU counting (CFU - colony forming units).


Mechanisms and Assumptions of the Species-Area Realtionship

Dengler 2009 would be a good start.

I'm sure this paper, his citations and papers citing Dengler's paper will get you well on your way.


Why did humans evolved the scratch reflex?

With about 20 square feet of skin constantly exposed to potential irritation, itching must serve an important protective/defensive function.

The "scratch reflex" (I'm not sure I would call it that) is necessary to life and limb. Itch is a major somatic sensation, along with (and different from) pain, temperature, and touch. Itch can be an acute sensation, e.g. a mosquito bite, or a chronic condition (peripheral or internal disease).

Research on itch signaling is still at its infancy, and basic mechanisms by which the itch sensation is transmitted and regulated have yet to be fully understood. It is meant to give us information about how we are interacting with our environment. Loss of such fine sensation, such as occurs with Hansen's Disease - aka leprosy, where patches of skin become painless and do not itch, so are ignored by the patient - leads to festering wounds and resultant problems.

As @MattDMo stated in a comment, sensation allows us to respond appropriately to irritants which, if ignored, might lead to festering wounds: thorns and other foreign bodies, sucking or biting insects (parasites or other, which can act as disease vectors as well), etc. It allows us to learn how to avoid and treat such irritants.

Various types of itch can be classified by the origin of the itch, which could be skin-related, neuropathic, systemic, or psychogenic. The most common cause of itching is dry skin; tiny cracks in the skin cause an inflammatory response, which (within reason) is not a problem in and of itself. The response to the itch, though, can be beneficial or damaging. One can treat dry skin, wash off irritants, treat infections, avoid causes, etc.

Scratching can be benign if done sensibly, or it can injure the skin, allowing infection, etc. However, the benefit of having such sensation under normal circumstances certainly outweighs the inconvenience.

That is not to say that pathological conditions that cause itching are not problematic. They are, and one might reasonably curse the sensation under those circumstances.

Edited to add: Itching, or pruritus, is defined as an unpleasant cutaneous sensation that serves as a physiological self-protective mechanism to prevent the body from being hurt by harmful external agents. (Nature, 2007)

Scratching is simply a reasonable response to itching from any source and is not necessarily harmful. It's not a reflex per se. You can avoid scratching. Some animals must actively seek out a way to scratch. This takes it well outside of the terminology of reflex as neurologically understood.

Itch Signaling in the Nervous System
Pruritus
When you have an itch, what is happening under your skin?


What shows how healthy someone is by their heart rate?

A healthy heart and cardiovascular system distributes oxygenated blood more efficiently than a less healthy one. Therefore, for a given level of exertion, a healthy heart will need to pump fewer times than a less healthy one to provide the same quantity of oxygenated blood to the rest of the body.

It's pretty much that simple.

However, the whole patient has to be considered. A low heart rate in and of itself doesn't mean someone is fit since there are many drugs and medical conditions that can create a low heart rate. Person A sitting in front of you appears fit and healthy, is on no relevant medications, and has a heart rate of 50? Fitness almost certainly explains it. Person B sitting in front of you is overweight, on several meds and not very fit? Fitness almost certainly doesn't explain it.


Correlations between tool use and evolution

This is a very confusing question! You have many sentences that end in question marks but then you answer them yourself, ending with a final question mark which is basically "are there references that show I'm right" but which is phrased in a way that makes the answer rather trivial (yes, of course our ancestors show a decrease in canine size, I'm not sure how else you would expect to get from there to here. Strength is harder to measure in fossils I think).

I'll address a few points. First I think this question makes humans to be much more hapless and vulnerable than we are:

  We humans would be nearly defenseless against large predators without weapons.

Humans are large predators. It's a nitpick because your other points about the relative strength of great apes and how we use weapons are correct, but I think it's relevant to the "oh us poor squishy defenseless humans" trope. We tend to think of our size as normal but we're actually among the biggest animals.

  Even small mammals can outrun humans.

Not for long they can't. One hypothesis that seems to have some credence in the field of human evolution today is the Endurance running hypothesis, which points out that almost no other animal shares our capacity to run for a very long time and that hunting stragegies based on this may have been a significant aspect of our evolution, that would explain many aspects of our physiology.

Of course this kind of hunting would likely involve weapons, but as you point out humans and proto-humans have been using tools for a long time.

You seem to have an image of weak proto-humans inventing weapons to turn the tables on the large predators that would eat them, but how would they have survived before? I had a similar one about hairlessness and clothes; probably we tend to think of human bodies as immutable human attributes, and all our tools as optional. When the truth, as you said yourself, is that humans as a species aren't separable from our tools and intelligence; our bodies, minds and behaviors all co-evolved. There never was a weak, naked human with no tools; before tools our ancestors weren't weak or naked and with tools of course we are neither. Also, intelligence and social behavior count for a lot; a single human might be vulnerable to a large predator where a coordinated band of hominids, probably armed with sticks and stones and some understanding of how to use them, would be another story.

But you want actual references and evidence, which is harder. I linked to the Wikipedia page on the evolution of canine size but strength isn't so easily measured in the fossil record. I think this paper might be the closest thing:

Body mass and encephalization in Pleistocene Homo

Relevant quote from the abstract:

  On the basis of an analysis of 163 individuals, body mass in Pleistocene Homo averaged significantly (about 10%) larger than a representative sample of living humans.

That's assuming body mass is a good proxy for strength, which isn't clear to me.

The following paper confirms that humans are indeed weaker than other apes and that the genes related to skeletal musculature have changed a lot since our common ancestor with them but doesn't give a timeline:

Exceptional Evolutionary Divergence of Human Muscle and Brain Metabolomes Parallels Human Cognitive and Physical Uniqueness

That paper goes with the hypothesis that loss of strength was caused by diverting resources to our brains, but other papers suggest there could be a trade-off between strength and fine motor control, like here:

The strength of great apes and the speed of humans

  More than 50 years ago, Maynard Smith and Savage (1956) showed that the musculoskeletal systems of mammals can be adapted for strength at one extreme and speed at the other but not both. Great apes are adapted for strength--chimpanzees have been shown to be about four times as strong as fit young humans when normalized for body size. The corresponding speed that human limb systems gain at the expense of power is critical for effective human activities such as running, throwing, and manipulation, including tool making. The fossil record can shed light on when the change from power to speed occurred. I outline a hypothesis that suggests that the difference in muscular performance between the two species is caused by chimpanzees having many fewer small motor units than humans, which leads them, in turn, to contract more muscle fibers earlier in any particular task.

(note that this paper mostly seems to be proposing a hypothesis and not demonstrating it, and it isn't very cited... but a lot of the papers citing it look interesting. Including this entry in the "could pre-humans hunt with weapons" column:

Clavicle length, throwing performance and the reconstruction of the Homo erectus shoulder

  These data (...) suggest that the capacity for high speed throwing dates back nearly two million years.

)

I think the question of how human strength evolved in their evolutionary history is probably very answerable with modern genetics, I've been looking for papers along the line of this one, which is about jaw muscles not upper-body strength:

Myosin gene mutation correlates with anatomical changes in the human lineage

  Using the coding sequence for the myosin rod domains as a molecular clock, we estimate that this mutation appeared approximately 2.4 million years ago, predating the appearance of modern human body size and emigration of Homo from Africa.

but I haven't found any; it's possible this specific question just hasn't been answered yet.


What are primary reasons for the failure to localise/anchor sequences in genome assemblies?

I'm going to re-interpret this question slightly to make it easier to answer:

"Why do genome assemblies frequently consist of large numbers of short contigs rather than a relatively small number of long chromosomes (or full replicons of other types)? And how could I make my assembly better?"

De novo sequence assemblies (usually) consist of a set of contiguous sequence fragments ("contigs") that have been derived from shotgun sequencing by some heuristic. If sequence assembly did a perfect job, we would expect that these contigs would be full chromosomes. Instead, what we observe is lots of sequence fragments with uncertain relationships to one another. In this common case, we think that some of the contigs could be stitched together ("localized", "anchored", "scaffolded") meaningfully into chromosomes, but we aren't sure how.

For de novo sequence assembly, there is no ground truth to compare to. So all of the information for generating assemblies comes from the starting sequences (which are usually "reads", small shreds of sequence that come off of a sequencing instrument). The heuristics that generate contigs from reads consist of finding overlaps between different starting reads and trying to extend them into the largest possible partially overlapping groups of reads, using some assumptions about rates of error in the sequence of the reads (and other variables). See wikipedia or this paper (figure inset) for a little more information on this.

It turns out that there is a body of statistical theory that governs how large these overlaps will be, and therefore how big/complete your contigs will be. This body of theory says that the size and number of contigs is predictable to some degree from the size of the genome you're trying to assemble, the length of the reads, and the number of reads you have.

Some genomes, like maize, wheat, or the human genome, are also harder to assemble because they are "repetitive". This means that there are lots of very similar sequences in different places in the genome. So when you take a read from one of these places, you are uncertain which one of these very similar regions it comes from. These repetitive regions are hard to resolve unless you have very long reads or some parallel information, so they also lead to gaps in sequence. Such regions will also tend to be "collapsed", meaning that you only have one contig representing a repeat that should actually be present as several contigs with different locations in the assembly.

Sources of parallel information that are helpful are proximity ligation (methods such as Hi-C), genetic maps from crosses, or optical mapping. These orthogonal sources of information express relationships between contigs in terms of their closeness on a chromosome. Here is a paper with more information on these topics. Recently, long read technologies such as PacBio or nanopore sequencing are starting to read through large repeats, but they are still usually not reliable enough to fully assemble even smallish genomes "telomere-to-telomere".

So, if there is a recipe for localizing/anchoring/scaffolding fragmented assemblies, here is roughly what can be done:

get more reads
get longer reads
get orthogonal information about contig placement (e.g. proximity ligation, genetic maps, a closely related assembly, etc.)

Hope that helps.


What kind of insect is this? (seen in Goma, Democratic Republic of the Congo)

Common name is "Giant Water bug". These are hemipterans, in the family Belostomatidae. Images can be found here: https://bugguide.net/node/view/12796


When describing mutations, $\Delta$ usually stands for deleted sequences. In this case it means the exchange of 4 cysteine residues in the NCAM protein by serines to disable palmitoylation and the association of the protein to lipid rafts. If you search for this specific mutation, you will find the paper from Niethammer et al., 2003, which describes the mutation. Figure 2a (below) shows a schematic view of the locus and is described as following in the caption:

Mutation of NCAM140 palmitoylation sites abolishes NCAM140 raft association.
(A) Schematic diagram of the structure of NCAM140 and
NCAM140Δ. The plasma membrane is indicated by the pair of vertical
lines. The semicircles represent the five Ig-like domains. The two
fibronectin type III–like domains are shown as black boxes. The
expanded segment shows the NH2-terminal sequence of the cytoplasmic
domain and the four cysteines that were mutated to serines in the
NCAM140Δ construct to remove all sites for palmitoylation.


Where can I find the genome of the L-strain coronavirus and the S-strain coronavirus?

Article links to this publication which has all the information needed:
https://academic.oup.com/nsr/advance-article/doi/10.1093/nsr/nwaa036/5775463

It is mentioned in the paper that:

  Although we found only 4% variability in genomic nucleotides between
  SARS-CoV-2 and a bat SARS-related coronavirus (SARSr-CoV; RaTG13), the
  difference at neutral sites was 17%, suggesting the divergence between
  the two viruses is much larger than previously estimated.

Their results highlight evolutionary changes in the development of new variations in functional sites in the receptor-binding domain (RBD). These developmental variations have a spike in changes to the RBD of SARS-CoV-2 and viruses from pangolin SARSr-CoVs

How do they define S and L variations?

They did population genetics on 103 available SARS-CoV-2 genomes.
These two major types are well defined by two SNPs which show complete linkage across the viral strains.

It also important to mention that SARS-CoV-2 was found to have 96.2% similairty to a bat SARS-related coronavirus (SARSr-CoV; RaTG13) but not very similar to SARS-CoV (79%) or MERS-CoV (50%).

How do we know that there's two type?

We know there's two types because from the 103 sequenced genomes two SNP locations show significant linkage. These are SNPs at location 8,782 (orf1ab: T8517C, synoniumous) and 28,144 (ORF8: C251T, S84L).

If you have a "CT" (as in base pairs) haplotype SARS-CoV-2 you've got the L-type ("L" type because T28,144 is in the codon of Leucine). Otherwise, if you've got a "TC" haplotype you have the S-type (C28,144 is in the codon of Serine).

They found that S-type is the ancient (less aggressive version) by aligning it with other older viruses. In fact for each variant of the virus the ancestral state was inferred by alignments of SARS-CoV-2 (NC_045512), RaTG13, and GD Pangolin-Cov.

So to be more precise on my answer for finding S and L types. You sequence the genome of an infected individual (you can find these online on NCBI) align it with the current reference sequence (MN908947, NC_045512), look at the SNPs and figure if they have a "CT" or "TC" haplotype to determine S or L type.


Is pith a ground tissue with no specialized function?

Short answer: it's not the greatest question.

Long Answer:

So there are three primary tissues in a plant: ground tissue, dermal tissue, and vascular tissue. See below for how they sort out:

However, some sources refer to the tissues of plants slightly differently, and indicate that the three basic tissue types are parenchyma, collenchyma, and schlerenchyma.

Example: "Botany: A Lab Manual" by Pfluger 2014:

  The three fundemental tissues of plants are parenchyma, collenchyma, and sclerenchyma

Since these are all "ground" tissues, this approach to classifying plant tissues would suggest that all plant parts consist of some kind of ground tissue (including all the plant parts you mention in your post). In fact, this is often the case...

Again, from Pfluger 2014:

  They [parenchyma] can be found in virtually any part of the plant and are the most common cell type in a plant.

Of the parts you mention, xylem is "specialized" to move water through the plant via tracheids, pits, and vessel elements; phloem moves sugars/sap through sieve tube cells which are supported by companion cells; cambium acts in secondary growth of wood and bark via the vascular and cork cambia; and bark is a water-proof protective layer.

However, "pith" is simply the central parenchyma cells in the stem, and therefore are primarily just used for storage like "all unspecialized" ground tissue.

As for cambium: from here:

  Interfascicular cambium differentiates from parenchyma or collenchyma cells located between the vascular bundles (mainly in stem)


With only a microscope, you might be able to find the bacteria, but how do you know what kind of bacterium it is?

Taking Listeria, under a microscope, it looks like a small rod. Well, so do lots of other bacteria. If you only see that one bacterium, you can't take it and do any further tests with it, you can only see it.

So we do cultures, where bacteria multiply and form colonies. Whether they even grow under these conditions already tells you a lot - a lot of bacterial species won't grow colonies on The type of colony is another factor in determining what bacterium we are looking at - does it have fuzzy or clear edges, what color is it, is it "shiny"?

And then, with that culture, further tests can be done, like what chemicals the bacterium in this colony can break down, what they produce, whether they can be stained with certain dyes, etc. Many times this is needed because bacteria look very much alike (round or rods).

For Listeria specifically, there are special plates used as a growth medium that has certain chemicals added that makes their colonies appear red-violet. Other bacterial species won't show this color even if they do grow on the plates.


Looking for a database of plant features

-- Traits --

TRY

TRY is a Plant Trait Database. More formally, it's a network of vegetation scientists headed by DIVERSITAS/IGBP, and the Max Planck Institute for Biogeochemistry, providing a global archive of curated plant traits.

BioTraits

This is an online resource for empirical data on how biological traits respond to environmental drivers such as temperature, light, and salinity.

Nate Swenson

Nate and his collaborators have compiled a ton of traits for species all over the world (though focused on the tropics).

Coyle et al. 2014

Appendix 2 of their 2014 Ecography paper lists primary literature sources and publicly available trait databases they used to examine 3 traits: leaf nitrogen, seed mass, and wood density.

-- Images --

Morphbank

An international Web database that contains thousands of high-resolution photographs and other images of plant and animal specimens.

Botanical Images Databases

This site provides dozens of links to databases containing plant images. There are also regional databases provided (e.g., Pflanzenphotos.de).

Botany.ch

This site contains both text sources (e.g., lectures and essays) as well as links to morphology picture databases (e.g., Botanical Image Database of the University of Basel).

See also FAO Online Catalogues for a number of morphological sources in both English and German.


Why does the ring finger not move independently?

The reason for this phenomenon is in both the muscular structure and neural connections of the little and the ring finger. Lets start with the following diagram:

As you see (click on the image to see full version), the fingers contain extensor muscles for movement. However, the index finger and the little finger have separate extensors, because of which they can move more independently as compared to the middle finger and ring finger, which contain a common extensor muscle called extensor digitorum. Some people lack the interconnections between these extensors, and can thus move their ring finger quite easily. One can also achieve this through practice.

Now, as to why the ring finger moves easily when moved along with another finger, have a look at another image:

The fingers are connected to brain via two nerves:

radial nerve, which connects with thumb, index finger and one side of middle finger
ulnar nerve, which connects with little, ring and the other side of middle finger

As you see, the branching between these nerves is what causes dependence of the fingers on each other for movement. Since the nerves for ring finger and little finger are intertwined, it becomes difficult to move each of these fingers separately. Similarly, you may find it easier to move your ring finger along with your middle finger. But you can easily move your middle finger independently because it gets signals from radial as well as ulnar nerves.

Thus, it is the combined effect of muscular and neural anatomy of ring finger which causes this effect.

PS: Since the effect is due to the neural and muscular anatomy of the ring finger, I don't think surgery would help in this case.

References:

Wikipedia contributors. "Extrinsic extensor muscles of the hand." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 29 Jan. 2017. Web. 27 May. 2017.
Ross and Lamperti, 2006, p. 300
Flexor Tendon Anatomy - Medscape
Wikipedia contributors. "Median nerve." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 1 May. 2017. Web. 27 May. 2017


What if a Point Mutation is seen in only half the coverage for its location?

I don't know, whether the organism you are working with is diploid, but suspect it's an animal (or even a mammal), so the most parsimonious explanation would be that you have homozygotes and heterozygotes at this SNP-position.


The answer is that they will do either or both, depending on conditions: this is one of the things that has caused complex systems scientists to be so interested in things like using slime molds in modeling optimization problems.
In good nutritional conditions, the cells will happily multiply. At the same time, they will flow and reshape themselves to spread and migrate in search of food when nutrients are not uniform.


Brain capacity of Cro-magnon man vs Modern man

Some of the possible explanations are summarized in Selection for smaller brains in Holocene human evolution. It's a blog post (but from a well-regarded anthropologist and heavily referenced), but I'll excerpt a few quotes here:

  Less well known is that the terminal Pleistocene and Holocene (ca. 30,000 years ago to present) witnessed a substantial decline in endocranial volume ... This decrease of approximately 240 ml in 10,000 years is nearly 36 times the rate of increase during the previous 800,000 years.  ...

He considered one possible explanation, that the smaller brain size is due to smaller stature, and determined that it's not likely:

  Here, I apply a quantitative genetic model to test the hypothesis that Holocene evolution of brain size may be explained by reductions in body size. ... The net change in endocranial volume, roughly 130 ml from the terminal Pleistocene to late Holocene skeletal sample would predict a reduction in stature of 13 cm, if the brain size had changed only because of correlated changes in stature. That degree of stature reduction is not biologically impossible although it would be extreme. ... The evidence suggests substantial reductions in brain size in some recent human populations, more than can be explained by correlated changes in body size.

He then lists six possible alternate explanations, which are not mutually exclusive:

Chance.
Plasticity.
Climate.
Nutrition.
Function.
Development.

He spends some time discussing each but concludes that at the present time the cause can't be definitely determined.

Here's his conclusion:

  The available skeletal samples show a reduction in endocranial volume or vault dimensions ... This reduction cannot be explained as an allometric consequence of reductions of body mass or stature in these populations. The large population numbers in these Holocene populations, particularly in post-agricultural Europe and China, rule out genetic drift as an explanation for smaller endocranial volume. ... Therefore, smaller endocranial volume was correlated with higher fitness during the recent evolution of these populations. Several hypotheses may explain the reduction of brain size in Holocene populations, and further work will be necessary to uncover the developmental and functional consequences of smaller brains.


How could one calculate the gene flow between two populations?

Theoretical Background

From Slatkin 1991, at equilibrium

$$F_{ST} = \frac{1}{1+4Nm\left( \frac {d}{d-1} \right) ^2}$$

, where $N$ is the per island population size, $m$ is the migration rate and $d$ is the number of islands ($d$ stands for "deme"). As $d \rightarrow \infty$, $\left( \frac {d}{d-1} \right) ^2 \rightarrow 1$ and Slatkin equation becomes the standard Wright's equation $F_{ST} = \frac{1}{1+4Nm}$.

From the above, it is easy to show that

$$m = -\frac{(d-1)^2(F_{ST}-1)}{4 d^2 F_{ST} N}$$

For 2 islands, it becomes

$$m = -\frac{9}{16} \frac{(F_{ST}-1)}{F_{ST} N}$$

In consequence, in a 2 island model the expected $F_{ST}$ is almost twice as low $\left(\frac{9}{16} = 0.5625\right)$ than in the infinite island model.

The above equation is an approximation that assumes...

low mutation rate (would not apply to microsatellite data)
relatively low migration rate (there is a $m^2$ term that is dropped)
symmetric migration rate (backward and forward migration rates are equal)
equal population size per island
equilibrium!

Further Reading

I recommend reading this paper (Slatkin 1991), it is IMO one of the best on the study of $F_{ST}$. I would also recommend Nei 1973, Slatkin 1985 and Whitlock and McCauley 1998.

The specific software to use depends on the kind of data you have. In any case, if you average $F_{ST}$ over a number of loci, make sure to use Weir and Cockerham 1984 method.

Bioinformatics

The first step for you is to calculate your $F_{ST}$. Assuming you have a number of SNPs, you will want to use Weir-Cockerham estimate of $F_{ST}$. There are a number of solutions to compute such estimates. One solution to calculate this is vcftools. The following (Bash) will do the job

./vcftools --vcf MyFile.vcf --weir-fst-pop individual_list_1.txt
--weir-fst-pop individual_list_2.txt --fst-window-size 800 --fst-window-step 100

, where MyFile.vcf are your data in vcf format (you might eventually want to use PGDspider to reformat your data). individual_list_1.txt and individual_list_2.txt are files containing the list of individual names (seperated by \n) belonging to the first and second population, respectively. The options --fst-window-size and --fst-window-step allows you to compute the estimate over a sliding window. I chose arbitrary numbers above. EggLib is another good alternative.


How can calcium be a kept as a local signal in the cytoplasm?

As @BryanKrause says in his comment, net flux of calcium would not ever be from inside the cell to outside the cell. There is a large gradient the other direction. Per Berg, the cytosolic concentration of calcium in a resting cell is on the order of 100nM, while extracellular concentration is in the mM range.

Signalling occurs when channels open up and allow $Ca^{2+}$ to diffuse down that very steep electrochemical gradient (from extracellular or topologically similar sources, e.g., the endoplasmic reticulum).

At least part of your question seems to involve a concern that the signal would not be very long lived. Though your concern about it diffusing out of the cell isn't warranted, the question about the time dynamics of calcium signalling is interesting. Calcium signals are, in fact, often very brief (though in other cases they last much longer). This is actually a benefit, and is one reason these signals can have very localized, very brief effects. For localized membrane fusion events, e.g., exocytosis, the signal lasts on the order of microseconds. The control of the time and position of a calcium signal involves a large number of players, including sequestering proteins, various compartments and stores, and tight control of the balance between calcium on and calcium off signals. It is discussed in this nature review, and summarized in this simplified figure:

You might also be interested in looking at some videos of calcium signalling. There are a number on youtube. This is one example


Why aren't gene drives extremely common?

I have a feeling that the OP is confusing naturally occurring so-called selfish, or parasitic genetic elements and the CRISPR/Cas9-based gene drives that have been making news as potential tools to eradicate disease vectors like the aedes mosquito. My answer is working from that assumption.

The big difference between naturally occurring "parasitic" genetic elements (including bacterial CRISPR elements and things like transposons) and the gene drives that are being tested as vector control revolves around what we put inside the latter class of gene drive.

The OP hit on this difference in his question, when he mentioned the decrease in fitness caused by engineered drives. In the naturally occurring drive-like elements, there is rarely ever a decrease in fitness in the organism and when it does occur, it is unlikely to be passed on to future generations.

Transposons, for instance, are largely active in somatic cells, whose DNA is not passed on to descendants. Semi-randomly occurring genetic changes are sometimes passed on, but this is relatively rare and evolution favors those that are either neutral or that increase fitness. A brief search doesn't turn up, and I can't think of, any cases of naturally occurring deleterious genetic alterations caused by something like a transposon having been found to remain in a population long enough to be studied.

Engineered gene drives, on the other hand, particularly in the cases of those meant to combat mosquitos, are purposefully designed to reduce the fitness of their target host.

The last question, of what keeps naturally occurring drives at low levels, requires either a rather vague, or a very long answer. I'll go with vague and provide some links to longer ones. Briefly, our genomes have evolved a lot of ways to maintain genomic integrity, in the forms of proteins responsible for proof-reading DNA, repairing breaks, and destroying any "free" pieces of DNA found outside of a chromosome. We've also evolved a lot of mechanisms to maintain genomic integrity through small non-coding RNAs.

Here are some good papers (without paywall) on the subject:

How p53 restrains mobile genetic elements
Proteins that function to restrain mobile genetic elements in rice
Good review of transposons in general
Finally, how people are engineering gene drives to combat malaria

Hope that helps!


Why is amyloplast produced by some plant cells but not other cells?

Amyloplasts are non pigmented organelles responsible for plant sugar storage, release and gravity perception (or tropism). This being the case they are commonly found in root caps (for gravity) and storage sites like tubers, fruits and grains.

So due to cell differentiation, it is not possible for these plastid organelles to be present in all cells the same way chloroplasts (another type of plastid) is not present in the stem (with the exception of small plants and succulents) and most of the root cells (Reece Urry et al, 2011).

Reference

Reece J.B., Urry L.A., Cain M.L., Wasserman S.A. et al (2011). “Campbell Biology 9th ed” Pearson Education, Inc., publishing as Pearson Benjamin Cummings, 1301 Sansome St., San Francisco, CA 94111.


Advantage of GCPRs over RTKs or other receptor protein kinases

I think GPCRs are evolutionary more older since tyrosine kinase signalling is relative recent evolved system. This could be one explanation for why their is more diversity in GPCRs

By the way GPCRs can actually signal g-protein independent, for example via B-arrestin. Also their are many types of g-proteins witch can all induce signaling via different signaling pathways. So GPCRS are actually quite versitile.

And then their is also a lot of crosstalk between GPCRs and RTKs


Could there be a pathogen which does not activate an immune response?

"I think, though am not at all sure, that pathogens need to invade cells to be dangerous."
True in the case of viruses and some bacteria.
Hiding within the cells of the host is the intracellular pathogenesis.
But other "tricks" are possible. Four examples:

biofilms
surface proteins that "catch" antibodies
fast mutation of surface epitopes, like the (in)famous HIV
using host molecules (the HIV again)

Source: Extracellular Immune Avoidance (LibreTexts)
Also interesting: How bacterial pathogens colonize their hosts and invade deeper tissues (Microbes and Infection
Volume 17, Issue 3, March 2015, Pages 173-183).


Short answer - you will need to use a nonionic detergent. These will dissolve lipid membranes but leave most protein complexes intact, and many proteins in active form.

However there are many of these available and finding the right one for a particular job is a black art.

The usual approach is to start off with something widely-used and not too expensive like Triton X-100. Detergents with glycoside head groups are also widely-used but tend towards the expensive.


Identification of an Australian pigeon in the NT

Your bird appears to be an Imperial Pigeon of the Ducula genus. Based on the limited angle of the lone picture of your specimen, my best guess as to the species is the Torresian Imperial Pigeon (Ducula spilorrhoa).

The species is a relatively large, pied species of pigeon found in various habitats (forest, woodland, savanna, mangrove and scrub) in Australia (including in the Northern Territory where you saw your specimen), New Guinea and nearby islands.
You can see more pictures, videos, and calls here, as well as additional info here.
Your specimen is unlikely the closely related  Pied Imperial Pigeon (Ducula bicolor) because:

D. bicolor is a  Southeast Asian species

D. bicolor has a bluish grey beak, whereas your specimen and D. spilorrhoa both have a yellow beak.
Note: Your specimen is also unlikely Ducula subflavescens because the feathers are white and not yellow, and it is unlikely Ducula luctuosa because that species is endemic to only a few islands.


Are there any known health benefits / risks from milliampere current (0.1-2 mA) on forehead?

Interesting question!

You ask 3 questions if I am correct:

What is tDCS;
What are the adverse effects of tDCS (at 0.1 - 2 mA);
What are the health benefits (enhanced focus);

I will answer your questions one by one:

(1) What is tDCS: tDCS devices are TransCranial Direct Current Stimulation (tDCS) devices. They send direct current through (trans) the skin and skull (cranial) to the brain.

(2) Adverse effects: EDITED: A review by one of the leaders in the field (Nitsche et al. Transcranial direct current stimulation: State of the art 2008; Brain Stim. (1) 206-23) mentions that current densities between 0.029 and 0.08 mA/cm2 are regularly applied in humans, with session durations of up to 40 min. Side effects are summarized in Table 1 in the cited review. Side effects are mostly nonexistent, though quite a few studies report some itching or tingling sensations under the electrode surface. Very rarely headaches or more serious side effects are reported. The authors predict that the limits will probably increase in the coming years (i.e., after 2008).

A more recent review, however, mentions a slightly lower upper limit of regularly applied current densities, namely 0.066 mA/cm2 in humans, using stimulation times of up to 20 min.

The highest upper safe current limit I could find is mentioned in a 2009 paper by Bikson et al. that mentions 0.14 mA/cm2 based on animal data.

Note that it is not current level per se that determines safety, it is the density of the current that matters. Moreover, the duration of stimulation will be an important factor to take into account.

To go back to your device: in case of 3.5 x 3.5 cm square electrodes (i.e., 12 cm2) as mentioned in the question, the current level range (0.1 - 2 mA) represents a current density range of 0.008 - 0.16 mA/cm2. However, I skimmed the website and they mention 3 cm square sponges or 3.5 cm diameter circular sponges, which brings the upper limit to 0.22 and 0.28 mA/cm2, respectively. The website says the device can be used up to 40 min.

In all, based on this literature review on tDCS and despite the company claiming their device is safe, I would conclude the upper limit of 2 mA not advisable, as its assciated current density exceeds the upper limits that I was able to find (Note, my answer is by no means a comprehensive review on safety of tDCS !). Dependent on the exact electrode surface you could calculate your own safety limit based upon the references cited.

(3) tDCS and enhanced focus: Health benefits in terms of ability to focus: I searched Google Scholar using the search term "TransCranial Direct Current Stimulation attention", which yielded no useful hits.

Another way to go for your focus question is to look at what cortex is situated underneath the 'forehead' that is stimulated by this device. Basically it is the prefrontal cortex:

Stimulating the prefrontal cortex reportedly increases working memory (Fregni et al., 2005) and motor learning (Nitsche et al., 2003). Working memory basically allows a person to use acquired information (let's say seconds or perhaps minutes ago) in subsequent tasks. Motor learning is essentially training of motor skills. Both motor learning and working memory are essential in gaming(!). However, one should carefully read the cited articles (and perhaps related ones, I gave just a few) in terms of effect size, electrode placement and stimulus conditions (including, but not limited to: current level, stimulus duration, stimulus waveforms, stimulus frequency, session duration etc.) to extrapolate their findings onto your device.


What spider is this? Is this invasive or dangerous?

That appears to be a zebra jumping spider (Salticus scenicus). It is fairly widespread throughout North America. It does not post any kind of threat to people or to the environment:
Here is a map of iNaturalist observations for zebra jumping spiders.

And here is a gallery of photos you can view: https://inaturalist.ca/taxa/68901-Salticus-scenicus/browse_photos


What Conditions must Drugs satisfy for them to be Deliverable via the Transdermal route?

Whether a drug can be delivered transdermally?  I think that carriers can be formulated to carry a small molecule through the skin into circulation, so I don't even know about lipophilicity. I believe if you spend enough money, you can overcome many of these problems.  I think that pharmacology might be just as important.

I think the first condition of a transdermal administration is that the drug cannot be effectively administered orally.  This is the most cost effective route go get a pharma compound into the body. It requires no devices, no fancy coatings or vaporizors.

Reasons that a pill (or its less popular cousins the suppository and sublingual tablet) cannot be used as the delivery system for a drug include effect of pH and other degradation of the compound in the GI tract, absorption rate from the GI tract and other factors such as effect of food in the system, other drugs which might interact in the system.

Another advantage of absorption through the GI tract is that this is the physiological system which is meant to be ingested and introduced into the body - its relatively fault tolerant, even if less of the drug actually reaches the blood stream.  There's more, but that's not a bad outline.

After pills and the like, the second choice is intravenous administration, which puts 100% of the drug into the circulatory system.   This has its own disadvantages, requires a clinical setting and the needle and breaking of the skin are not ideal in many cases.

If the drug needs continuous and non clinical administration there are many other means of drug delivery, including transdermal administration.  Differentiating these methods often includes making sure the drug is available specifically to the part of the body that needs it.  E.g. topical administration; putting on a medicated cream for a skin condition or use of an inhaler which delivers the drug directly to the lung for an asthmatic condition.

Transdermal administration has its own specific advantages; continuous distribution of the compound over long periods of time.  Disadvantages include: poor ADME properties for biologicals like antibodies and other proteins, low delivery concentrations where you need a large amount added (epinephrine, and maybe antibiotics come to mind).

Examples of successful transdermal delivery are testosterone gels and the nicotine patch.  Both of which apply continuous controlled low dosage that is important there.

There are three typical routes of drug absorption in transdermal delivery.  The drugs can diffuse through the membranes of dead cells of the stratum corneum, which works if the drugs are lipophilic enough.  They can diffuse around these cells, through the intercellular spaces, which can work for more polar drugs although this path is not usually as efficient.  The most extreme means are patches which contain tiny needles that can deliver straight through the protective layer of the skin.  With enough economic investment probably any sort of compound could be introduced through a patch.

Most of this is just cribbing off the notes from this lecture on coursera: Fundamentals of Pharmacology.  Its probably outlined on any pharmacology text.


It's an Ipomea also known as a Morning Glory. There are 600 species of Ipomea including the sweet potato. There are many colors of mixed Ipomea, your one is probably a fairly random hybrid. It is perhaps most similar to Ipomoea Rubriflora and Ipomea Coccinea:


Biological siblings possible with <9 months age difference?

What do you mean by siblings?

If by siblings, you accept cases of individuals having the same father but not the same mother, then of course, it is possible! Below, I will assume you are referring to full siblings (eventually twins).

Age gap between twins

According to the huffingtonpost, there is a case of two twins that were born 87 days apart. On average, the age gap between two twins is rather of the order of 15 minutes (Rayburn et al., 1984).

Cousins that "look like" full sibs

Imagine family A has a pair of homozygotic twin daughters. Family B has a pair of homozygotic twin sons. If the sons of family B mate with the daughters of family A, then the offspring will be cousins but will have a relatedness of two full siblings.

One can of course extend this kind of crazy scenario to any number of generations apart.

Superfetation

I discovered the concept of superfetation in @froimovi's answer. From wikipedia

  Superfetation (also spelled superfoetation and superfœtation – see fetus) is the simultaneous occurrence of more than one stage of developing offspring in the same animal. It is not believed that it occurs naturally in humans. There have been 10 reported cases of possible superfetation in humans.

As @1006a rightly pointed, the two babies might well be delivered during the same labour though. If they are delivered during the same labour, then they will have the same age counting from birth but different age counting from the time of fertilization.

Uterus didelphys

See @Bakuriu's answer!

Human intervention

Other alternatives would require some human intervention. For example, fertilization could have happened in vitro and the eggs were implanted in two different wombs. One womb could be a surrogate mother and the other one could be either another surrogate mother or the woman who actually donated the ovules.

Plenty of cloning techniques could yield two full siblings to be less than two months apart. Also, techniques of ex utero pregnancy could be used (although I am not sure we have the technology ready for that). Note that human cloning is illegal in many countries.


It's Verbena hybrida Voss (See here; the page is in French though).

It belongs to verbena genus in the family Verbenaceae. It's about 10 to 50 centimeters tall with a squarish stem and opposite leaves.The flowers are small with five petals, and borne in dense spikes on the top. Verbena hybrida Voss is always used as ornamental plant. They are drought-sensitive, tolerating full to partial sun, and enjoy well-drained, average soils. It's always plant in warm and dry and sunny environment. About why a flower with two colors in one petal, it's because there are always two kinds of pigment in the petals. The pigments in different temperature and different acid alkaline environment present  different colors. When the flower is open, the acid-base property changed will lead to petals present different colors (K. Yoshida et al., 2009).


What was the evolutionary reason for cross lateralization of the brain?

The theory developed by Cajal more than a hundred years ago hasn't been challenged, according to a recent article in Molecular Neuroscience. Making it simple:

At a certain point in the phylogeny, decussation is favored for the optical pathways. Since the images are inverted on the retina, the crossing is necessary in order to build a coherent and continuous image on the cortex.
Decussation of the motor pathways appears next, and it is supposed to make the flight response more efficient. If a danger is perceived visually at the left hand side of one's body, it is processed in the right hemisphere and the motor signal is sent to the left hand side muscles, which are the one that can propel the body to the right, thus escaping the danger. The efficiency resides in that the interpretation of the danger and the signal for the reaction happen in the same hemisphere.


Why should we preceed neostigmine by atropine in tubocurarine toxicity?

Tubocurarine is a non-depolarising neuromuscular blocking aqgent, that is, it acts as a competetive antagonist of Acetyl Choline at the Nicotinic receptors.(Toxicity/Effect: $-N$)

Atropine is a competitive antagonist of the muscarinic acetylcholine receptor, classified as an anticholinergic. (Effect: $-M$)

Neostigmine blocks acetylcholinesterase, increasing the concentration of ACh at, and stimulating both muscarinic and nicotinic receptors. (Effect: $+M+N$)

Hence, to counter the only nicotinic deficiency of ACh, we give Neostigmine, which will also stimulate the muscarinic receptors, leading to muscarinic side effects. To counter the latter, atropine is given. A similar formulation is used in a disease like Myasthenia Gravis, with a functionally similar lesion.
$$(+M+N)+(-M)+(-N)=0$$


What genes are required to make E. coli photosynthetic?

I think the crux of the answer is only hinted at in WYSIWYG's answer. The crux of photosynthesis is partitioning coupled reactions.

Photosynthesizing plant cells have sub-cellular structures called chloroplasts; their membranes are especially important for the compartmentalization of different functions and chemical processes for the entirety of photosynthesis to even be possible. Partitioning is difficult to achieve in E. coli, and that to me seems a necessity for achieving true heterologous, truly ectopic photosynthesis... Even photosynthesizing cyanobacteria (photosynthesizing prokaryotes) possess thylakoids, membrane-bound compartments where the magic happens. Photosynthesis though can certainly proceed and be made more efficient in single cells (example).
That leaves us with a simple answer: engineering E. coli with thylakoid-like structures is not really practicable. Why not simple use cyanobacteria instead?
Further reading: review on single cell photosynthesis in single cells.


Gene duplication and subfunctionalization

Suppose a gene performs two distinct functions 1 and 2, both of which are essential. We'll call this gene A, for ancestral gene.

A duplication copies A to another locus. Now there are two genes, A and B, that perform the same two functions. At this point, if either A or B is deleted, the organism is fine.

Over evolutionary time, A and B undergo genetic drift to become A' and B', respectively. Let's say that B' loses function 1, and that A' loses function 2. This isn't a problem for the organism since A' still performs function 1, and B' still performs function 2. In other words, the two genes complement each other.

However, now A' can't be deleted without losing function 1, and, similarly, B' can't be deleted without losing function 2. The result is that both genes are fixed in the genome by evolution.

This means that now, after hundreds of millions of years of relevant evolution and genetic drift, we many duplications like A' and B'. The key to this is that through genetic drift with no selective pressure, it's very easy to lose function but extremely difficult to gain it.

As for your second question, I'll look for a paper on gene duplications that I think would be the most helpful, but there are many.


As already pointed out by Remi, you can identify the sex from a tissue sample only if there is a genetic (such as chromosomal) sex determination system (by using techniques such as PCR or in-situ hybridization). However, different species of fish employ different mechanisms of sex determination:

  Focus on or attachment to genetic systems involving X and Y
  chromosomes must quickly be shed in studies of sex determination in
  fish due to the diversity of mechanisms utilized, and, by doing so,
  the researcher can explore alternative regulatory mechanisms that hold
  important clues for understanding sex determination in general. The
  biology and ecology of fish is sufficiently diverse to provide unique
  examples of sex-determination mechanisms, yet they possess many of the
  same processes and pathways that are used in other vertebrate systems.

   Devlin, Robert H., and Yoshitaka Nagahama. "Sex determination and sex differentiation in fish: an overview of genetic, physiological, and environmental influences." Aquaculture 208.3 (2002): 191-364.

Though Devlin and Nagahama comment (above) that fishes also employ the same signalling pathways as other vertebrates for sex determination, study of these pathways to determine the sex would be extremely difficult as you may be aware that the cell-signalling and the gene regulatory networks are highly complex.

Fishes are highly sexually dimorphic (including Discus) and the sex can be easily identified (with some practice) by visual inspection. Microscopic identification would be both money and time consuming. Morphology based identification can be automated (when the machine is trained sufficiently). You can have a look at this article1 which is about using image analysis to score salmons.

1.    Merz, Joseph E., and William R. Merz. "Morphological features used to identify Chinook salmon sex during fish passage." The Southwestern Naturalist 49.2 (2004): 197-202.


How can TMS induce enough depolarization to cause an action potential?

I think my mistake was to believe that the electric field has to be somewhat perpendicular to the membrane, so that it can directly apply a voltage difference across the membrane, and that the resistance inside and outside the axon was the same, so that a tangential field was useless.

In fact these are false : depolarization and action potential creation happen where the axon is parallel to the electric field and where the gradient of the tangent field is the bigger.

Here you have a complete explanation but I think we can make a simplified one :
http://stbb.nichd.nih.gov/pdf/Nerve_Fiber_Stimulation_Model.pdf

Let's look at a membrane model (Hodgkin-Huxley) :

As we said if we try to apply an electric field $\vec{E}$ along $\vec{y}$ , it should be incredibly strong to produce a trans-membrane potential $V$ strong enough to create an action potential.

In between the inside an the outside of the membrane you have all the channels and the capacitance of the membrane. but I think the crux of the matter here are the resistances inside and outside : the small surface of a section of axon limits the conductivity, whereas the outside is supposed to be bigger so that its resistance is negligible.

As a result if you apply a gradient $\frac{dE_{x}}{dx}$ you can create trans-membrane current and potential:
because of the gradient, the fields $E_{1} = E(x)$ and $E_{2} = E(x+\Delta x)$ are different : $E_{2} = E_{1} + \frac{dE_{x}}{dx}\Delta x$.
Then using electricity laws :
$$i_{m} = I_{1} - I_{2}$$
$$i_{1} = -\frac{ E_{1} \Delta x}{R}$$
$$i_{2} = -\frac{ E_{2} \Delta x}{R}$$

then :

$$i_{m} = \frac{\Delta x}{R} (E_{2}-E_{1}) = \frac{\Delta^{2} x}{R} \frac{dE_{x}}{dx}$$

This trans-membrane current will produce a potential across the membrane which will be proportional to $\frac{dE_{x}}{dx}$, electromagnetic stimulations shows that TMS can easily produce gradients strong enough to create actions potential.


How close genetically is the most human-like chimpanzee to the most chimp-like human?

You may be interested in this 2005 Nature paper from the Chimpanzee Sequencing and Analysis Consortium: Initial sequence of the chimpanzee genome and comparison with the human genome. It breaks down the most common categories of genetic variation:

  Single-nucleotide substitutions occur at a mean rate of 1.23% between copies of the human and chimpanzee genome, with 1.06% or less corresponding to fixed divergence between the species.

So if we accept their analysis, ~1% (it says "or less", but elsewhere in the paper they estimate a lower bound of ~0.96%) of the genome difference consists of fixed single-nucleotide differences between species.

  Small insertions and deletions: On the basis of this analysis, we estimate that the human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total ~90 Mb. This difference corresponds to ~3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions; this confirms and extends several recent studies.

So another ~3% comes from small insertions and deletions, which gives around a ~4% fixed divergence between populations. This rough estimate of the fixed genetic distance between humans and chimpanzees is probably a reasonable estimate of the distance between the nearest human-chimpanzee pair.

If you also want to know how far apart the two furthest humans are, as @Remi.b mentioned, the populations we've sequenced don't span the whole diversity of our species, but it is likely much smaller. You could look at some of the HapMap or Human Genome Diversity Project papers. For reference, when Watson's genome was sequenced, they reported around 0.1% of the sequence to be different from the reference genome, but that isn't a particularly diverse comparison.

You may also be interested in this paper comparing the human, chimpanzee, and bonobo genomes: http://www.nature.com/nature/journal/v486/n7404/full/nature11128.html.


Why clotting does not occur during Menstruation

The endometrium changes throughout the menstrual cycle in response to hormones. During the first part of the cycle, the hormone estrogen is made by the ovaries. Estrogen causes the lining to grow and thicken to prepare the uterus for pregnancy. In the middle of the cycle, an egg is released from one of the ovaries (ovulation). Following ovulation, levels of another hormone called progesterone begin to increase. Progesterone prepares the endometrium to receive and nourish a fertilized egg. If pregnancy does not occur, estrogen and progesterone levels decrease. The decrease in progesterone triggers menstruation (the shedding of the uterine lining). Once the lining is completely shed, a new menstrual cycle begins. (ACOG)

The uterine lining secretes an anti-clotting factor during periods to assist the blood flow. If the substance is not sufficient to overcome the natural clotting factor menstrual blood clots can form, a process known as hemostasis. Flow may slow down toward the end of a period, and blood can clump. When women are reclining for a time, such as while sleeping, the discharge will pool, and blood clots will be dislodged when upon standing. The blood darkens as it sits and sometimes looks brown or black.
During menstruation, the endometrial cells that line the uterus strip away and leave the body. As this happens, the body releases proteins that cause the blood in the uterus to coagulate. This coagulation prevents the blood vessels in the uterine lining from continuing to bleed. The blood that the body has already shed also contains these coagulation proteins. When the flow is most substantial, the coagulation proteins within the blood may start to clump together, resulting in menstrual clots. This generally occurs when menstrual blood pools in the uterus or vagina before leaving the body.
Menstrual blood clots can be caused by an imbalance in the clotting and anti-coagulating factors in blood or by hormonal changes. Fibroids and endometriosis contribute to excess buildup of the uterine lining, which breaks free as clots.

Under normal physiological circumstances menstruation is a highly regulated, complex process that is under strict hormonal control. During normal menstruation, progesterone withdrawal initiates menstruation. The cessation of menstrual bleeding is achieved by endometrial haemostasis via platelet aggregation, fibrin deposition and thrombus formation. Local endocrine, immunological and haemostatic factors interact at a molecular level to control endometrial haemostasis. Tissue factor and thrombin play a key role locally in the cessation of menstrual bleeding through instigation of the coagulation factors. On the other hand, fibrinolysis prevents clot organisation within the uterine cavity while plasminogen activator inhibitors (PAI) and thrombin-activatable fibrinolysis inhibitors control plasminogen activators and plasmin activity. Abnormalities of uterine bleeding can result from imbalance of the haemostatic factors.
Endometrial haemostasis is a vital process for the control and cessation of menstruation. It is influenced by systemic clotting systems that react to the hormone induced shedding of the endometrium, forming the haemostatic platelet plug and fibrin deposition. Local factors within the endometrium are paramount to ensure the process is highly regulated, with adequate blood vessel occlusion, breakdown of thrombus, and tissue regeneration.
Davies, J., & Kadir, R. A. (2012). Endometrial haemostasis and menstruation. Reviews in Endocrine and Metabolic Disorders, 13(4), 289-299. doi:10.1007/s11154-012-9226-4

Coagulation & Fibrinolytic Pathway in 5 minutes - Simple and Easy

Fibrinolysis Wikipedia


Why are eyes more sensitive to flicker in periphery — contradictory answers

I think the most likely explanation is that ambient lighting conditions in the room where OP was sitting, as described in the original question, might not have been bright enough to saturate the rods. Under mesopic conditions, both rods and cones are active. Hence your statement that

  ...since the light from CRT mentioned in the question pointed to by the first link above is quite above the photopic threshold.

may not hold. Since rods indeed have quicker responses, the periphery may be more sensitive to the flickering of a CRT or light bulb.

Note, however, that cones have flicker fusion frequencies of up to 90 Hz (reviewed by Perz, 2010), and CRT screens and light bulbs flicker at frequencies following the mains (50 or 60 Hz). Hence, cones may still be able to pick up the flickering. Since OP reports on an anecdote, experimental conditions may have been suboptimal and their report might have been unreliable. So we cannot exclude OP was using photopic vision, regardless their report.

Reference
- Perz, Master's thesis, Eindhoven University


Why isn’t Haemoglobin a plasma protein, rather than being encompassed by the erythrocyte?

To the man with a hammer, everything looks like a nail.

The poster’s hammer seems to be kidney function. Mine is the biochemistry of the erythrocyte (red blood cell). Others, no doubt will be able to provide yet different perspectives.

From a biochemical point of view the erythrocyte has a limited repertoire of metabolic pathways compared with other tissues. However it does have an extremely active pentose phosphate pathway (not universally found in tissues) and the function of this is to provide the reducing cofactor NADPH, which is needed to maintain glutathione in a reduced state. The importance of reduced glutathione in these oxygen-carrying cells is that it provides protection against reactive oxygen species — something that could not be done — or at least not controlled so well — in the blood plasma.

Another feature of haemoglobin is that the equilibrium between the oxy- and deoxy- forms involves the small triose molecule, 2,3-bisphophoglycerate. This is described in the answer to another question. The ability of the erythrocyte to synthesize this molecule allows the sophistication of this control.

I imagine there are many more examples. (Any added in comments will be added.)

One could argue that these metabolites are not indispensable for organisms (glucose phosphate dehydrogenase deficiency does cause haemolytic anaemia in man), and this presumably explains why the simpler organisms you mention (and about which I know little) can dispense with red cells.

But a question certainly worth asking.


Significance of basal lamina for outer layers of epithelium

The basal lamina, a specialised type of extracellular matrix (ECM) that differs between cell types, acts as a base for stratified epithelia cells to layer on top of and therefore has a supportive role as well as providing a base for attachment (for the layer of cells immediately on top of it) 1. Layers of epithelial cells on top of further strata of similar cells with no differing tissue composition underneath would have no support and cell types would be able to mix freely within tissues. The different cell types within tissues are kept seperate by this ECM to maintain areas for specific functions. The importance of this can be seen through studying epithelial cancers, where the epithelial cell layer breaks through the entire basement membrance and invades the surrounding tissue. This can cause massive disruption of tissue function.

Yes, it seems that the layers of cells are attached by various junctional complexes, the desmosomes (maculae adherentes) being the most abundant for stratified epithelia.

Referenes

1 http://www.histology.leeds.ac.uk/tissue_types/connective/con_basal_lam.php


Consensus symbols in multiple sequence alignment

The use of these symbols in output of the type shown below is purely presentational, to help you inspect the alignment and identify regions of partial conservation.

                  51                                                 100
          CCPC50  SEEGFK.YGE GILEVAEKNP DLTWTEADLI EYVTDPKPWL VKMTDDKGAK
          CCRF2C  TYPEFK.YKD SIVALGASG. .FAWTEEDIA TYVKDPGAFL KEKLDDKKAK
          CCRF2S  TQADFKGYGE GMKEAGAKG. .LAWDEEHFV QYVQDPTKFL KEYTGDAKAK
          CCQF2R  HKDNYA.YSE SYTEMKAKG. .LTWTEANLA AYVKNPKAFV LEKSGDPKAK
          CCQF2P  TFAGYS.YSP GYTVMGQKG. .HTWDDNALK AYLLDPKGYV QAKSGDPKAN
       Consensus  t...%k.Y.e g..e.gakg. .ltWt#..l. .Yv.#Pk.fl .ek.gD.kAk

This is quite independent of the logic (algorithm) of the program, which is indicated by the documentational comments:

  Symbol comparison table: blosum62
  Gap weight: 12
  Gap length weight: 2

This also gives a reference to the original paper you should read to find more information about the program.

You would also be advised to read the Wikipedia entry on Multiple Sequence Alignment and on Sequence Alignment in general. I would mention that this is an old method (as the appearance of the site also indicates). If it gives useful results, fine. Otherwise you might try the more popular and more frequently updated Clustal, which is available online or as a standalone program.


What is (are) the medium of conduction for an electrical current with an external source in the human body?

Electric current flows rather rather easily through water that contains ions, which are electrically charged atoms. Since the human body is more than half water, and that water is filled with ions such as sodium, chlorine, potassium, etc., the body for the most part conducts electricity rather well.  The skin can have a high resistance to the flow of electricity, but it varies substantially, particularly being reduced when the skin is moist.  Medical electrodes, as for heatbeat measurements, are typically applied with conductive paste to overcome most of the skin's resistance.  You may want to look at this "Electricity And Human Body" page, or the article "Conduction of Electrical Current to and Through the Human Body: A Review".


Effect of testosterone hormone on cell signalling and behaviour?

Steroid hormones produce a slow response because they do not have secondary messenger
It's true that steroids don't have secondary messengers because they don't need them - they can go directly into a cells nucleus and affect transcription there.  This wouldn't slow down the response by much, however.
Slow response is due to lack of cell membrane receptors and amplification enzymes
This is just the inverse of the first option, which again isn't really a cause of slowing down the response.  Steroids are amplified in that they act directly on DNA at the very first step of the synthesis pathways so don't need much amplification.
Movement of this hormone is very slow in blood
 Again I don't think there is much to this option, the difference in speed of distribution of steroid and peptide hormones is likely to be minimal

This leaves us with:
 4. None of the above

I would personally have gone with this answer.  Steroids have a long time of action because they require the new transcription of genes that they activate.  This process takes time and consistent doses are needed to maintain the effect.


How do disulphide bonds in hair cause curling?

Nice question. I must say it took me many hours to get satisfactory answer.
Hairs are made of keratin molecules, which contain cysteine. Cysteine has thiol (-SH) group, by which it can form disulfide (-S-S-) bond with another cysteine of another keratin, causing bending of hair. See this image from here:

Curling of hair can be justified on both microscopic and macroscopic level.

Microscopic level: See this post from here:

Curly hair has to do with the chemical bonds in the protein that makes up hair - $\alpha$-keratin. Keratins, particularly $\alpha$-keratin, have long sequences of amino acids (often more than 300) which forms a helical structure.
Pairs of these helical structures then coil about each other in a left-hand coiled-coil structure. These are then attracted to another coiled coil so two keratin helices will stick together. These four-chain structures then associates with another four-chain structure to form the hair filament. One of the amino acids which make up these chains, is cysteine which has a sulpher group which is able to make connections with other sulpher groups on other coiled coils.
The more interactions a filament has with another filament, the more tightly coiled the coiled-coil becomes. Hence, curly hair has more interactions than straight hair. The process of `perming' hair introduces more accessibility of the sulpher on the amino acid, cysteine, to make these connections. Finger and toe nails have many many bonds between filaments and are thus, very hard.

For example, see how hairs are curled artificially via perming.

Source
This change in location of bonds is what causes curling of the hair (look again at the first diagram and notice the orientation of disulfide bridges). Those vertical strands now get curled due to change in these bonds. Here, the required mechanical tension for bending is provided artificially.

Macroscopic level: Shape of hairs is also determined by its macroscopic structure. Look at this article:

All hair, whether curly or straight, has two major components: the shaft and the follicle. The shafts are the visible, flowing strands that we see on our heads. The follicle is the part of our hair that resides within the skin, or dermis, of our scalp. Each of these structures plays a role in determining our overall hair shape.
Let’s start at the root of the issue (pun 100 percent intended): the follicle. It turns out that the shape of our follicles is a major determinant of our hair texture. If you were to look at the follicle of straight hair, you would find it is perfectly round. The follicle of curly hair adopts an oval shape. The flatter the oval is, the curlier the hair will be.
Another contributing factor to a hair’s curl is the way the follicle tunnels into the scalp. Follicles of straight hair tunnel vertically down from the skin’s surface into the dermis. If the follicle angles into the dermis then the hair will curve as it grows causing it curl. Although, this curving of the follicle can lead to gorgeous curls it causes one major drawback that all curly-haired persons can attest to, dryness. Within the dermis, special glands line the follicle to secrete oil, called sebum, to lubricate the hair. Unfortunately, when follicles curve sebum isn’t able to travel the length of the hair as well leading to dryness of hair that doesn’t get lubricated.

Source
Although how shape of follicle determines structure of hair strand is probably not known, the major contributing factor likely is how hair emerges from the scalp. When it emerges in a bent shape, it faces a lot of tension from the scalp, which causes it to bend in the shape of the follicle to form curls. Since straight-emerging strands don't face such forces, they do not lead to curled hairs.
In this way, hair curls are a consequence of large number of disulfide bridges between keratin molecules and how the hair emerges from the scalp.


Will plants accumulate toxins from soil contaminated by toxic substances like paint thinner/lead paint?

You could use other plants to extract harmful substances from the soil. There are plants which are called hyperaccumulators which absorb high amounts of contaminants from the soil.
Have a look at at Phytoremediation where the process of phytoextraction is described in detail.

Normally phyotextraction needs several generations of plants to be grown in order to be effective. Consequently you could just plant your vegetables as usual but take samples and test them for heavy metals or other contaminants of concern.


Lac operon: How can lactose enter the cell in the absence of lactose permease?

Introductory textbooks will not get into the details of the lac operon.

Basically, the operon is expressed constitutively at a low level that means that Beta Galactosidase and Lactose Permease are expressed at low levels by the bacterium. This is because it takes a little bit of time to build up the concentration of LacI in the cell before it can start to bind the operator.

The LacI repressor only binds the operator in the absence of Lactose in the cell's environment due to the fact that allolactose allosterically binds the LacI repressor and affects that molecule's ability to bind the operator. So RNA polymerase can bind the promoter of the Lac operon at some low rate and continue to produce the protein.

When the cell no longer has glucose, it generates cyclic AMP, which induces the CAP protein to bind to the CAP site, just upstream of the promoter of the Lac Operon. CAP associates with RNA Polymerase, and this makes the promoter very active. Beta Galactosidase and Lactose Permease levels increase rapidly.

Where you see the full effects of the LacI repressor is when neither Glucose nor Lactose are present in the environment of the cell. At this point the repressor binds to the operator and blocks transcription by DNA Polymerase.

I hope this helps. I have an entire book that covers the Lac Operon, so even though this is a bit expanded of an explanation from a basic textbook, it is still a summary.


No, if you use only centrifugation to separate proteins from other parts of the (bacterial) cell, you need very high centrifugal forces. The actual speed (in rpm) you need to separate soluble proteins from the rest of the cell is mostly dependent on the rotor of the centrifuge, because both together determine the acceleration you get, which should be
in the order of at least 10,000 - 100,000 g.

If you do not have a (working) ultracentrifuge available, you could try to precipitate your proteins from the lysate, which would allow you to use a normal centrifuge to collect it. However, this won't be an option if your protein can't be properly re-folded and you need it functional.


Myoepithelial cell contraction initiates glandular release from most exocrine glands developed from the ectoderm. These are the cells that exist in the glandular epithelium.

At the distal end of the glanduar coil, an isotonic plasma filtrate gets actively transported into its lumen. As you move down the coil, close to where it connects to the duct, absorptive cells remove NaCl to make sure the sweat is hypotonic when it reaches the surface of the skin. If you view these cells where staining for alpha tubulin or beta actin, you will see they have abundant levels of myofillaments, something uncharacteristic of epithelial cells. Hence Myoepithelial.


Poxviruses, such as variola (the causative agent of smallpox) and vaccinia (the active constituent of the vaccine that eradicated smallpox), are very large, complex DNA viruses that replicate in the cytoplasm, rather than the nucleus. Because of this, they must carry enzymes with them to accomplish tasks that occur in the nucleus of the eukaryotic cells they infect. This includes all the proteins necessary for mRNA synthesis (e.g., a DNA dependent RNA polymerase). The enzymes for DNA replication are encoded in the poxvirus genome and are transcribed and translated as part of the "early" stage, directly after adsorption and penetration.

So, yes, poxviruses bring their own preformed RNA polymerase with them. They don't bring their own DNA polymerase with them, but they do produce it shortly after infecting a cell.

You can read more about this in Murray Medical Microbiology Chapter 54.


Is there a biological urge to have children in women?

The biological urge to find a mate means that an innate desire for children is unnecessary. Having sex with a partner pretty much guaranteed children before contraception was available.

It's hard to imagine why an urge to have children would exist, but that's not the same as saying it doesn't -- but I also can't imagine how you'd be able to pull apart biological vs social pressures in such a complex and core part of being human.


At night you can actually see further than during the day. At night you can see stars that are many light years away, but during the day the furthest thing you can see is probably the sun, which is 8 light minutes away. There's probably no definite answer because the brighter and bigger the object (and the darker the surrounding and the clearer the air), the greater the distance from which you can see it.

According to Sky and Telescope, the most remote stars (as part of Andromeda Galaxy) you can see with a naked eye are 2.5 millions light years away.

Talking about the objects on earth, at half-moon, you could see to "the end," that is to the horizon.


The term was pioneered by Mendel, who had no knowledge of chromosomes, so definition 1 would perhaps be the best answer. However, we now know that definition 1 arises from definition 2 (chromosomes are inherited independently of each other) and from the fact that chromosomes recombine (cross-over).

That said, independent assortment does not apply to linked genes, which tend to be inherited together. That is, they are not independently assorted.


One premise of the full proposal is that the freezing process should avoid the formation water crystals which prevent structural damage of membranes and proteins and keep the integrity of the life organism being frozen under high-pressure cryonics.

I have not seen a discussion on the thawing process which I always thought was a problem for example when thawing cells for in vitro cell culture.

For the design I would try small with for example mammalian cells like HeLa. Maybe full organisms like worms or flies for "tissues" and "full organisms".


According to Minami et al. (2003)1 (open access) the early gestational sac can be located by ultrasound, and usually is high in the uterus, more often on the left or right than in the middle.  They provide an illustration of the distribution.

 1. Minami, S., Ishihara, K. and Araki, T., 2003. Determination of blastocyst implantation site in spontaneous pregnancies using three-dimensional transvaginal ultrasound. Journal of Nippon Medical School, 70(3), pp.250-254.