Will you stop sweating if you exercise in a cold enough room?

Apparently you can sweat even in a cold enough room, without even doing exercise! The main causes of sweating include, among exercise and high body temperature, stress and anxiety. This condition is called cold sweating. See this article:

  The body normally produces sweat as a way to help keep cool. Sweating normally occurs with exertion such as when exercising or in high temperatures. However, there are other reasons for sweating. Sweating can be triggered by fear or anxiety, and this is often referred to as a cold sweat. It comes on suddenly and results in cool, damp skin. It is the body's reaction to stress as part of the "fight or flight" response that helps us to react in a dangerous situation.

So, even if you just think about doing heavy exercise, you might get sweat in hands or feet.

But cold sweating is not the only cause. It may also be caused by a more severe condition known as hyperhidrosis. See this article:

  Normally, your sweat glands produce perspiration that’s carried to the skin’s surface when the air temperature rises, you develop a fever, you’re exercising, or you’re feeling anxious, nervous, or under stress. When those factors are no longer an issue, the nerves that signal sweating are put on hold. For the 2% to 3% of the population who have hyperhidrosis, however, the sweat glands don't shut off. They sweat even when the circumstances don’t call for it: when they’re in air conditioning, or while they’re sitting and watching television. Some people even tell their doctors that they sweat in a swimming pool.

So, one might start sweating even in a cold enough room, if not because of body heat, then because of anxiety, hormones or medical conditions. Also, this condition does not work the way you are speculating. When the surrounding environment is very cold, the body prefers to shut off blood supply to skin than to cool it down through skin i.e. sensing cold environment, the body shuts off blood supply to skin and diverts it to core of the body. This is what causes more urination in cold environment and is called cold diuresis. Have a look at this answer for more information on this point.


What keeps organs suspended in the body?

Most of the organs are attached to the abdominal wall by a fold of peritonium called mesentary.
Mesentary is a membranous tissue arising from the posterior wall of the peritoneal cavity and is responsible for keeping the organs at their designated places.Mesentary wiki


Have there been multiple aboriginal species of dogs?

That's one of — quite a few, we have to say — the mistakes Darwin made in his edition from 1859 (I have to confess that this is the only edition I've read, and I reckon this is the only edition anyone should read). This mistake is even more contrasting if you realize that he failed to apply the very same reasoning he had made just a few pages earlier, when discussing variation in pigeons: he explained that, even if counterintuitive, all different pigeons with all different features descend from the same wild species. Then, when he talks about dogs a few pages later, he incomprehensibly makes the same mistake he had just accused his readers of commiting.

Darwin is not the only one: Lorenz made the same unfounded claim, namely that the domestic dog would have two different origins, one from Canis lupus and another one from Canis latrans. We have to agree that Lorenz was way more bold than Darwin when it comes to making unfounded claims.

The fact is that, today, we're pretty sure (the scientific and statistical meaning of sure is being used here) that all domestic dogs (Canis lupus), from the chihuahua to the german shepherd, descend from a population of wolves (also Canis lupus) from east Asia.

Here is a Nature paper from Peter Savolainen, one of the best researchers on this subject: Wang, G., Zhai, W., Yang, H. et al. Out of southern East Asia: the natural history of domestic dogs across the world. Cell Res 26, 21–33 (2016) doi:10.1038/cr.2015.147


What is this insect that showed up after I left food out? How can I get rid of it?

It is likely a fruit fly, a Drosophila melanogaster.

I've tried different methods to trap then but the most effective way I found is this. You need a container (pan, jar, bowl, whatever), vinegar (I use any type), a drop of dish soap, and plastic wrap over the top with holes poked in. Then the flies cannot stand on top of the liquid but also have issues escaping through the holes in the plastic wrap.


Why does capsaicin irritate mammals and also kill fungi? Are the two related?

Recent study has shown that capsaicin indeed has antimicrobial properties. For example, see this article:

  Two pungent compounds found in Capsicum species (capsaicin and dihydrocapsaicin) were also tested for their anti-microbial effects. The plain and heated extracts were found to exhibit varying degrees of inhibition against Bacillus cereus, Bacillus subtilis, Clostridium sporogenes, Clostridium tetani, and Streptococcus pyogenes.

In one of the attempts to study its mechanism, a study on yeasts suggested that it works in following ways:

Detoxification of capsaicin by a PDR-type ABC
superfamily of multi-drug resistance transporters
Osmotic stress response and damages in membrane
structure caused by the capsaicin treatment
Genotoxicity of capsaicin to yeast cells
The effects of the deletions of the genes those were
induced by the capsaicin treatment
Mechanism of capsaicin in the growth inhbition to
yeast cells:

The DNA microarray analysis of antimicrobial
mechanism of capsaicin shows that capsaicin induced
an osmotic stress element, the key genes for membrane biosynthesis, and the PDR network and repressed the genes for ribosomal components
and cellular growth. The growth characteristics of
deletion strains suggest that PDR5 is important for
the resistance to capsaicin. These observations that
the PDR network may pump out capsaicin from cells
are the first findings. The contribution of the PDR
network also suggests that capsaicin enters to the
cells and capsaicin functions as a toxic substance to
the yeast cells. This toxicity is possibly to the
mebrane structure and/or as osmotic stress.

Full article (PDF) here.

Though in mammals, its mechanism of action is quite different; it acts on ion channels to give a burning sensation. See this article:

  The burning and painful sensations associated with capsaicin result from its chemical interaction with sensory neurons. Capsaicin, as a member of the vanilloid family, binds to a receptor called the vanilloid receptor subtype 1 (TRPV1). TRPV1, which can also be stimulated with heat, protons and physical abrasion, permits cations to pass through the cell membrane when activated. The resulting depolarization of the neuron stimulates it to signal the brain. By binding to the TRPV1 receptor, the capsaicin molecule produces similar sensations to those of excessive heat or abrasive damage, explaining why the spiciness of capsaicin is described as a burning sensation.

However, it is toxic for mammals too. Capsaicin is a highly irritant material requiring proper protective goggles, respirators, and proper hazardous material-handling procedures. Capsaicin takes effect upon skin contact (irritant, sensitizer), eye contact (irritant), ingestion, and inhalation (lung irritant, lung sensitizer). The LD50 in mice is 47.2 mg/kg.

Though its mechanisms are different, it performs quite similar functions: protecting the plant from predators and infections i.e. a defense system.

It seems like quite a coincidence, unless capsaicin has some general destructive properties.

It is neither a coincidence nor capsaicin has general destructive properties. In fact, capsaicin is being used as an analgesic too. See this article:

  Capsaicin is a chili pepper extract with analgesic properties. Capsaicin is a neuropeptide releasing agent selective for primary sensory peripheral neurons. Used topically, capsaicin aids in controlling peripheral nerve pain. This agent has been used experimentally to manipulate substance P and other tachykinins. In addition, capsaicin may be useful in controlling chemotherapy- and radiotherapy-induced mucositis.

Its mode of action is, seemingly, somewhat similar. See this:

  The mechanism of action of topical capsaicin has been ascribed to depletion of substance P. However, experimental and clinical studies show that depletion of substance P from
  nociceptors is only a correlate of capsaicin treatment and has little, if any, causative role in pain relief. Rather, topical capsaicin acts in the skin to attenuate cutaneous hypersensitivity and reduce pain by a process best described as ‘defunctionalization’ of nociceptor fibres. Defunctionalization is due to a number of effects that include temporary loss of membrane potential, inability to transport neurotrophic factors leading to altered phenotype, and reversible retraction of epidermal and dermal nerve fibre terminals. Peripheral neuropathic hypersensitivity is mediated by diverse mechanisms, including altered expression of the
  capsaicin receptor TRPV1 or other key ion channels in affected or intact adjacent peripheral nociceptive nerve fibres, aberrant re-innervation, and collateral sprouting, all of which are
  defunctionalized by topical capsaicin. Evidence suggests that the utility of topical capsaicin may extend beyond painful peripheral neuropathies.

(P.S. substance P is a neuropeptide, a potent vasodilator & iniates expression of almost all known cytokines.)

Pay attention to the last line 'utility of topical capsaicin may extendbeyond painful peripheral neuropathies.' i.e. capsaicin may have more effects on body than known!


Looks like an orb-weaver ..

I agree! This spider definitely belongs to the genus Argiope, though, due to the angle of your provided image, it's difficult to be more specific than that (if I had to guess, A. anasuja).

The confidence in my genus suggestion comes from the stance the spider is displaying. Spiders within the Argiope genus carry a common nickname of "signature spiders", due to the fact that they'll intertwine additional webbing within their web, called stabilimentum, that, given the design of the support webbing and the spider's stance, will allow for the spider to appear much larger than it really is.

If you can provide an image that reveals the top of the abdomen, a more confident species suggestion may be possible.

  Is this a common garden spider?

From the looks of it so far -- yes, this is a common garden spider.


Strange looking mushroom found in a dead tree

Possible Species: California Fungi - Gymnopilus luteofolius

Source:

http://www.mykoweb.com/CAF/species/Gymnopilus_luteofolius.html

http://mushroomobserver.org/174362?q=28kZM


Parasite? or a possible home infestation?

It is a minute pirate bug, in the family Anthocoridae. https://en.wikipedia.org/wiki/Anthocoridae They are generally thought to be beneficial insects, in that they are predators of pests. Do you have some house plants that may be infested with something else they are feeding on (like aphids)? Unfortunately, minute pirate bugs do bite, and the bite is painful. https://hortnews.extension.iastate.edu/2017/10/minute-pirate-bugs-are-biting-argh
But these are not human parasites, and I would not be concerned. Just find what they are feeding on, and take care of that.


How a person can transmit COVID-19 while his COVID-19 is still in incubation state?

The incubation period is the time it takes from the infection of a patient with a disease until he develops symptoms. How fast this happens depends on the disease.

According to the references the main difference is that SARS 2003 replicates in the lung/lower airways, while SARS-CoV-2 also replicates in the upper airways and sheds high viral loads there early in the course of the disease.

Since both diseases are transmitted by droplets, it is much easier to have a sufficient viral load in infected cells from the upper airways compared to the lower ones.

References:

Severe Acute Respiratory Syndrome Coronavirus Infection of Human
Ciliated Airway Epithelia: Role of Ciliated Cells in Viral Spread in
the Conducting Airways of the Lungs
Virological assessment of hospitalized patients with COVID-2019


From the limited information, I can provide the following but I am not sure if this is what you are looking for. Also, I still don't see the statement where the author concludes we get the Linear regression model $E(q_i) = Aq_i + C$ which is odd notation since it says the expected value is a linear regression. In fact, if it is a linear regression, it should say $q_j = Aq_i + C$.
$$
A = \frac{\text{cov}(q_i,q_j)}{\text{var}(q_i)}\quad\text{and}\quad C = E[q_j] - \frac{\text{cov}(q_i,q_j)}{\text{var}(q_i)}E[q_i].
$$
Now, we can write the variance and covariance as
\begin{align}
\text{var}(q_i) &= E[q_i^2]-E^2[q_i]\\
\text{cov}(q_i,q_j) &= E[q_iq_j]-E[q_i]E[q_j]
\end{align}
where the expected value of a discrete random variable $X$ is calculated as
$$
E[X] = \sum_{i=1}^Nx_ip_X[x_i]
$$
where $p_X[x_i]$ is probability of $x_i$ and $N$ can be countable infinite.

The mean of conditional PDFs comes up in optimal prediction where the minimum mean square error is $E_{Y\mid X}[Y\mid x]$. This optimal prediction covers linear and nonlinear. For the standard Gaussian PDF, the optimal prediction will be linear since $E_{Y\mid X}[Y\mid x]=\rho x$ where $\rho$ is the correlation coefficient. I am going to short hand $E_{Y\mid X}[Y\mid x]$ to $E[Y\mid x]$
$$
E[Y\mid x] = \mu_Y + \frac{\rho\sigma_Y}{\sigma_X}(x-\mu_X)
$$
where $\mu_i$ $i=X,Y$ is the mean and $\sigma_i$ is the standard deviation. If $X$ and $Y$ are not Gaussian, then the model can be nonlinear. Are there examples of non Gaussian be linear probably.


Evolutionarily speaking, why do humans have 46 chromosomes

I think the OP is asking why we have one less chromosome pair than chimpanzees (for example) [23 pairs instead of 24].

The is an abundance of evidence, as alluded to above by shigeta, that human chromosome 2 is the result of a telomere-to-telomere fusion of two ancestral chromosomes (IJdo et al., 1991).  This event did not occur in our closest ancestors, hence we have one less chromosome pair.  In fact the sequence of human chromosome 2 contains the relic of an ancestral telomere-telomere fusion (IJdo et al., 1991).

The pdf of this key reference is freely available to all from PNAS

Reference

IJdo, J.W, Baldini, A, Ward, D.C, Reeders, S.T, Wells, R.A. (1991) Origin of human chromosome 2: an ancestral telomere-telomere fusion  Proc Natl Acad Sci U S A., 88 9051-9055.[pdf]

Actually it has now been shown that Neanderthals and Denisovans also exhibit the same chromosomal fusion as humans - http://m.motherjones.com/politics/2014/02/evolution-creationism-bonobos-neanderthals-denisovans-chromosome-two


Is 100% accuracy in DNA sequencing possible?

Current DNA sequencing techniques are based on shotgun sequencing, randomly breaking the chromosomes into small pieces, sequencing the pieces (by various techniques), and then computationally reassembling the pieces by looking for overlapping patterns. This depends on sequencing each piece of DNA multiple times; the more coverage or depth, the more reliable the results. However, especially with long repeating base sequences, 100% coverage is uncommon with small genomes, and almost impossible with large genomes.


Examples of how the presence or absence 2'-hydroxyl groups influence physicochemical properties of DNA and RNA

As user137 said, the general base abstracts a proton from the 2'OH and subsequently the 2'O- renders a nucleophilic attack on the δ+ Phosphorous, leading to the hydrolysis of the phosphodiester bond. There can be slight variations in the mechanism and the intermediates; for details see this review.

After hydrolysis both 2'- and 3'- phosphates can form.
RNA is not thermodynamically unstable; apart from being unstable in the presence of a strong base RNA is biochemically unstable too. This is because there are several RNAses and most of them degrade RNA by a mechanism similar to alkaline hydrolysis (they cannot act on DNA). Also see this post.


How to search for organisms by criteria such as growth substrate and overflow metabolites?

Some of the criteria, I guess are difficult to find (Also for my lack of understanding of those terms). For the rest you can search these databases:-

Growth substrate: I don't really know what you are asking here — growth rate in minimal media/optimal growth medium ? Nevertheless, see the Media Database
Methanogenesis: Ortholog Table - KEGG MODULE M00567
Nitrogen fixation: Ortholog Table - KEGG MODULE M00175


The creatures in the video do indeed show the shape, size, coloration, and typical behavior of ostracods ("seed shrimp"), a type of freshwater crustacean (class Ostracoda) that is distributed worldwide (Martens et al. 2008). They lay eggs either on plants or directly in the water as plankton. Some researchers consider them to be potentially useful as bioindicators (e.g. Ruiz et al 2013), or even keystone species (Lawrence 2002). You can find many photos of ostracods on the Internet.

Lawrence, J. et al. 2002. Microb. Ecol. 44: 199
Ruiz, F. et al. 2013. Int. J. Environ. Sci. Technol. 10: 1115
Martens et al. 2008. Hydrobiologia 95:185


What is the difference between transpiration and evapotranspiration?

Essentially, evapotranspiration is the sum of evaporation and plant transpiration from the Earth's land and ocean surface to the atmosphere.

Here are some links to articles about transpiration: https://biolympiads.com/plant-anatomy-and-physiology/


How to manage fat-gluten oxidation in celiac disease?

Gluten is a protein. The textbook answer is that protein is not stored in fat cells.

Proteins are hydrolyzed into amino acids through digestion; some amino acids are ketogenic, and can contribute carbon towards fat biosynthesis. So some of the carbon that originates in gluten may be incorporated into a fatty acid. But the carbon has no 'memory' of its previous role in a gluten molecule, and could not act as gluten when the fat is subsequently oxidized.

One can imagine an undigested gluten molecule (or its peptide fragments) binding to the exterior of a fat cell, but there's no mechanism for it to get incorporated into fat as an intact protein.


Why do some bacteria have most genes on the leading strand of the genome?

The pattern we see in B. subtilis is quite common in prokaryotes. The origin of replication is shown at the top of the genome diagram. DNA replication proceeds bidirectionally from this point. In the B. subtilis diagram, most genes are located along the leading strand in each direction. Even in E. coli, by the way, important genes, including all rRNAs, tend to appear on the leading strand.

Why is that? Rapidly growing bacteria are replicating their genomes most or all of the time, so you've got replication and transcription happening at the same time.  If genes are on the lagging strand, RNA transcription proceeds in the opposite direction from DNA replication, and the DNA polymerase will often collide with the RNA polymerase. If the genes are on the leading strand, however, RNA transcription proceeds in the same direction as replication and collisions are minimized. Hence the selective advantage to positioning most genes along the leading strand.

Some genes may also be on the lagging strand in order to target them for mutagenesis (Paul et al. 2013, Million-Weaver et al 2015). This goes back to the concept of transcription-replication collisions where the head-on collisions are worse than co-directional collisions. Head-on genes actually have a higher mutation rate and incidence of convergent mutations which suggests that they are mutated and evolve faster than leading strand genes. This is a controlled process in that it only occurs in lagging strand genes, and only when the gene is transcribed (i.e. when it is needed). It was argued that this is a way bacteria can control and ratchet up or down the rate of evolution in a controlled way. This was argued against by Chen and Zhang based upon computer based modelling. It is an interesting concept that has been hotly debated.

EDIT for additional clarification and references:

This diagram from Chen and Zhang (2013) helps show what is going on:

Caption: "Schematic drawing of a collision between a working DNA polymerase and a working RNA polymerase in bacteria. (a) Codirectional collision when a gene is encoded on the leading strand. (b) Head-on collision when a gene is encoded on the lagging strand. Arrows show the directions of movement." (Chen and Zhang 2013)

A few references

The original idea goes back almost 40 years to Nomura M. and Morgan,E.A. (1977) Genetics of bacterial ribosomes. Annu. Rev. Genet., 11, 297–347.
An early paper about highly transcribed rRNA on the leading strand: Ellwood M. and Nomura,M. (1982) Chromosomal locations of the genes for rRNA in Escherichia coli K-12. J. Bacteriol., 149, 458–468.
A recent overview: Rocha, E. P. (2004). The replication-related organization of bacterial genomes. Microbiology, 150(6), 1609-1627.
Why some genes remain on the lagging strand: Chen, X., & Zhang, J. (2013). Why are genes encoded on the lagging strand of the bacterial genome?. Genome biology and evolution, 5(12), 2436-2439.
Paul, S., Million-Weaver, S., Chattopadhyay, S., Sokurenko, E., and Merrikh, H. (2013). Accelerated gene evolution through replication-transcription conflicts. Nature 495, 512-515.
Million-Weaver, S., Samadpour, A.N., Moreno-Habel, D.A., Nugent, P., Brittnacher, M.J., Weiss, E., Hayden, H.S., Miller, S.I., Liachko, I., and Merrikh, H. (2015b). An underlying mechanism for the increased mutagenesis of lagging-strand genes in Bacillus subtilis. Proc Natl Acad Sci U S A 112, E1096-1105.


Is it possible to directly uploaded controlled imagery into a person's conscience?

In principle there's no reason why we shouldn't be able to do so. In practice, we do not seem to be anywhere near able to do so.

We are barely able to decode natural images from fMRI information, and before you can hope to induce imagery you should usually first be able to decode it.


what happens to rna length if we have a termination site in additional to the original one

Assuming that by termination signal you mean transcription termination signal (and not a stop codon), you would have one shorter RNA molecule. You can have two shorter RNA molecules if there is another transcription start site after the termination signal, but there is no reason to assume this will be the case.

In some cases the RNA polymerase will skip a base and frameshift while transcribing a new RNA strand. This is known as transcriptional slippage, and it is taken advantage of by some viruses in order to make their genomes more compact by having several different mRNAs overlap each other.

In this rare case, having a termination signal does not necessarily mean transcription will terminate, it might be able to skip through parts of the termination signal and continue to the next termination site.


How does 2,3 biphosphoglycerate works to release oxygen bound to the hemoglobin?

You've answered your own question. The association/dissociation of oxygen is an equilibrium reaction. If you stabilize one state, you move the equilibrium to that state. 2,3-BPG helps release oxygen from Hb exactly by binding and stabilizing deoxy-Hb.


How are light sheet microscopy 3D images and their computed sections built up from stacks of 2D images?

According to their website dispim.org they are using registration software like the ImageJ Multiview-Reconstruction Plugin. Judging from the descriptions, this plugin uses the alignment of multiple points in the different angle images (like fluorescent beads that have been introduced to the medium or the cell nuclei) by rigid transformation and then deconvolves the 3D information using the point spread functions.

Knowing your optical system (microscope lenses etc.) you can calculate how the image of a point light source would look like in the image. This can be used to reversely calculate the actual position of your light source from the image and reconstruct an image without the distortions.

From that they get a volumetric image that can be projected into any coordinate system. I recommend watching the videos on the plugin page to get an idea how this works.


Why do some plant species have lobed leaves, while similar species in the same habitat don't?

This is a question for which, I think at the moment, we don't have a clear answer.

It is important to bear in mind that the leaf plays a number of important roles in the plant (photosynthesis, thermoregulation etc.) so leaf shapes probably evolved through a process of successive trade-offs. This may make it difficult to identify the exact selection processes operating on any one species. In contrast, something like the eye has a well-defined single function, which in principle at least, makes it easier to understand the link between form and function.

From Niklas (1988):

  Life history and optimisation theory suggest that the number of
  phenotypic solutions that allow for different equally successful trait
  combinations increases as the number of trade-offs increases – a
  conclusion that applies to traits within the leaf (e.g. for shape) as
  well as to leaf–branch relationships.

However, there are a  number of ideas to explain leaf shape diversity which include:

Thermoregulation

It has been shown that by adding lobes to leaves, the rate of heat transfer across a leaf is greater than that of an unlobed leaf of the same area (e.g. Gurevitch and Schuepp 1990). So, lobed leaves may be selected for under certain environmental conditions.

hydromechanical constraints

Lobed leaves may have greater hydraulic efficiency. For smaller veins, hydraulic pressure increases as they present an increased resistance to water flow. This places stress on the deliate outer leaf tissues. If  lobed leaves have relatively less mesophyll tissue than large, highly conductive veins, they may have reduced hydraulic resistance compared  unlobed leaves (Sack and Tyree 2005).

optimization for photosynthesis
adaptations against herbivorous animals
random (non-selected) variation. This is a possibility, although probably unlikely due to the importance of the leaf in plants.

So, some or all of the above possibilities (which are not necessarily mutually exclusive) may shape the leaves of species which may appear to have undergone very similar selective pressures.

This is a good read by Nicotra et al. (2011) which summarizes the state of play.

Gurevitch J, Schuepp PH (1990) Boundary layer properties of highly dissected leaves – an investigation using an electrochemical fluid tunnel. Plant, Cell & Environment 13, 783–792. doi:10.1111/j.1365- 3040.1990.tb01094.x

Nicotra et al., The evolution and functional significance of leaf shape
in the angiosperms, Functional Plant Biology, 2011, 38, 535–552

Niklas KJ (1988) The role of phyllotactic pattern as a developmental constraint on the interception of light by leaf surfaces. Evolution 42, 1–16. doi:10.2307/2409111

Sack L, Tyree MT (2005) Leaf hydraulics and its implications in plant structure and function. In ‘Vascular transport in plants.’ (Eds NM Holbrook, MA Zwieniecki) pp. 93–114. (Elsevier Academic Press: Burlington, MA, USA)


You true randomness definition is partially wrong! Something does not need to be fundamentally random to be beyond known science.

Also, it is unclear what process you are referring to when talking about a child's trait. I would assume you are thinking about crossover but then, summarizing crossover positions by "child's trait" shows that you misunderstand a number of things!

To my knowledge, outside of quantum physics, in no field of knowledge has it been shown that true randomness has any measurable effect. So, no what chromosome an individual inherits is only random in the sense that it would be necessary to know exactly the position of every molecule in the cell to know where the crossover will happen.


How much energy takes C4 photosyntesis to make glucose?

Yes,C4 plants use 30 ATP molecules to make one molecule of Glucose.See since you have stated in your question that you know very less about biology and got some similar vibes from looking at your profile so I'll sum it up in a nutshell but hopefully this might help.In flowering plants,all of them follow a basic pathway know as the C3 cycle to make glucose from CO2.Now,in that process about 18  ATP is used.But apart from CO2, there's O2 also present in the atmosphere which interferes with the compounds taking part in C3 cycle and instead of CO2 participation O2 participates in the reaction and the consequence is that glucose is not produced and the plant wastes some energy in the form of ATP.

Now to prevent that from happening,some plants evolved themselves and made some chemicals which bind only with CO2.But the thing is that they also require energy to function and for each molecule of glucose produced they require 12 ATP this making net amount of ATP required to be 30 in a C4 plant.You can in a way visualise this C4 pathway that the plant placed some guards in the form of chemicals that combines with CO2 and makes sure it reaches its destination and to prevent traitor O2 molecules to disrupt plants from making glucose.But we all know that that guards would require some fee and so that fee is 12ATP.And visualise C3 pathway as some some sort of glucose making factory which makes glucose from CO2 and the production cost from raw materials is 18 ATP.


How is e-value calculated in BLAST 2 sequences (BLAST+)?

You do not need the nr database for BLAST to calculate an E-value.
It will be calculated based on the alignment of n sequences.
The exact procedure is mathematically complex but if you want to read the original paper it is here:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC53667/pdf/pnas01031-0226.pdf

a simplified version you will find here:

http://homepages.ulb.ac.be/~dgonze/TEACHING/stat_scores.pdf


In Kabash and Sander's paper related to DSSP (Biopolymers 1983 vol. 22 (12) pp. 2577-637) the following appears in the abstract:

We have developed a set of simple and physically motivated criteria for secondary structure, programmed as a pattern-recognition process of hydrogen-bonded and geometrical features extracted from x-ray coordinates. Cooperative secondary structure is recognized as repeats of the elementary hydrogen-bonding patterns “turn” and “bridge.” Repeating turns are “helices,” repeating bridges are “ladders,” connected ladders are “sheets.”

It seems from this that they are using the term bridge to mean one hydrogen bond of the type found in a beta-sheet, ladder as two protein strands joined by many hydrogen bonds, and sheets as beta-sheets — more than two protein strands joined by many hydrogen bonds. The term beta-bridge in the DSSP documentation (http://www.cmbi.ru.nl/dssp.html) is presumably equivalent to a bridge in the paper

In the DSSP files residues that are in ladders or beta-sheets are designated E, and B is used for instances where there is a single hydrogen bond. The former are very common, wheres the latter are quite rare — some proteins have none. I have prepared an image of an example for residues 74 and 79 (side-chains omitted for clarity) in a loop in the protein 1PPR.pdb (a light-harvesting protein). The other loop residues 75-78 are designated as T (turn) in the DSSP file, whereas residues 73 and 78 have no structure designation. Hence the hydrogen bond between Ser-74 and Val-79 is an isolated singleton and designated B.


What causes the human body to “jump” when we get a shock?

This is similar to many other reactions humans have when scared, such as freezing, feeling like as if your heart is beating out of your chest, shaky legs, or the feeling that hair stands up on the back of your neck.

Fear starts with a trigger, and in your example, it is the sudden loud sound of the cannon. That stimulus signals to your brain that you might be in danger. Whether the stimulus is touch, sight, or sound, the scary signal quickly reaches the thalamus at the center of the brain and travels down to the amygdala, at the base of the brain.

From here a neurotransmitter called glutamate then carries the signal even deeper into the brain. This is what causes us to freeze, or involuntarily jump, and put humans through what is know as the "fight or flight" response.

These two reactions are automatic and involuntary because the deep brain is ancient in terms of evolution. We have little control over it. The reason is because a fight-or-flight response unleashes powerful hormones that affect the entire body.

When frightened, your body floods with the hormone adrenaline, skyrocketing your heart rate and blood pressure. The hormonal surge also causes your heart to pump blood more forcefully to the muscles. That's why you might feel a little shaky or unsteady when you're scared — the extra blood is getting your body ready to sprint away from the danger or stand and fight if you need to; hence the name fight or flight response.

Our bodies can reverse the fear response fairly quickly, though. If it turns out we aren't in a life-threatening situation, the parasympathetic nervous system (PSNS) kicks in to counter the fight-or-flight instinct, primarily by stopping the flood of adrenaline and lowering our heart rate back to normal. That's why every time we jump during a scary movie, or in your case a cannon sound, we don't run out of the theater/parade screaming; after the initial reaction, our PSNS helps us recognize the threat is not real and calms us down.

On a side note, part of the reason the PSNS exists is because adrenaline can actually be toxic in large amounts. If too much adrenaline floods into the heart, it can lead to the failure of that organ and death. You cannot control the fight or flight response, however you can limit it through meditation.

Hope that helps <3,

Jess


What would happen if you combined the world's deadliest diseases & viruses?

Viruses in the same cell can recombine (although they don't always do). This can happen by crossing-over of the genomic strands or reassortment of genomic segments. Therefore, you can get a new virus out of the fist two. The new one is not necessarily deadlier than the first two. If there's no recombination, the test subject will enjoy both diseases until the deadliest one kills him.


Why do nerve gas victims have chronic neurological issues?

Most of the nerve agents (and quite a number of commercially used pesticides) fall into the class of organophosphates (OP). Their mechanism of action is the inhibition of the acetylcholin esterase which leads to the build-up of acetylcholine in the body and thus a permanent activation of mucarinic and nicotinic acetylcholine receptors.
Irreversible inhibitors of AChE may lead to muscular paralysis, convulsions, bronchial constriction, and death by asphyxiation - and organophosphates can act as these. See here for some more information.

According to reference 1, four different toxic effects can be differentiated:  The cholinergic syndrome, the intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP) and chronic organophosphate-induced neuropsychiatric disorder (COPIND).

The cholinergic syndrome is happening in the acute phase of the OP poisoning and can be explained by the inhibition of the acetylcholin esterase.

All quotes are from reference 1:

  In cases of human poisoning, general acute symptoms of peripheral
  nicotinic and muscarinic intoxication are clearly apparent.
  These symptoms include miosis
  (unreactive to light); sweating, rhinorrhea, lacrimation, and
  salivation; abdominal cramps and other gastrointestinal symptoms;
  respiratory difficulties and cough; dyspnea, constriction sensation in
  the chest, wheezing; twitching of facial muscles and tongue, tremors,
  and fasciculations; bradycardia and ECG changes, pallor, and cyanosis;
  anorexia, nausea, vomiting, diarrhea, and involuntary urination and
  defecation. These signs and symptoms are accompanied by central
  effects such as dizziness, tremulousness, and confusion; ataxia;
  headache, fatigability, and paresthesia. Finally, seizures,
  convulsions, twitching, coma, and respiratory failure may also occur.
  If the subject survives the first day of poisoning, personality
  changes, mood swings, aggressive events and psychotic episodes
  including schizoid reactions, paranoid delusions, and exacerbations of
  preexisting psychiatric problems may also ensue.

The intermediate syndrome happens after the acute phase, around 7,7% of the patients develop it.

  The term Intermediate Syndrome (IMS) was first described by Senanayake
  and Karalliedde (1987) because it appeared in the interval between the
  end of the cholinergic crisis and the onset of OPIDP. Following
  exposure to various OP pesticides, clinical manifestations of IMS
  typically occur within 24–96 h, and affect patients without
  fasciculation or other cholinergic signs. The reported incidence of
  IMS ranges from 7.7% to as high as 84% (Shailesh et al., 1994).
  Although IMS is well recognized as a disorder of neuromuscular
  junctions, its exact etiology, incidence, and risk factors are not
  clearly understood. IMS generally occurs among patients with prolonged
  and severe inhibition of AChE, although not every patient with severe
  AChE inhibition develops IMS. Other risk factors of IMS include
  delayed metabolism of OP pesticides due to toxicokinetic factors or
  impaired organ function, severity of poisoning, elevated muscle
  enzymes, plus adequate or late oxime therapy. IMS has been linked with
  exposure to specific OP pesticides displaying the dimethyl phosphate
  moiety (e.g. fenthion, dimethoate, monocrotophos, dichlorvos,
  methylparathion) but has also developed after exposure to parathion
  (ethyl phosphate) and methamidophos (phosphoramidate; De Bleecker et
  al., 1993; Yang and Deng, 2007).

The organophosphate-induced delayed polyneuropathy (OPIDP) cones later and has been connected to the phosphorylation and subsequent ageing of the neuropathy target esterase by the OP (see reference 1 and 3).

  OPIDP is relatively rare neurodegenerative disorder in humans that is
  characterized by loss of function and ataxia of distal parts of
  sensory and motor axons in peripheral nerves and ascending and
  descending tracts of spinal cord. The early neurological symptoms
  usually are sharp, cramp-like pains in the calves, tingling in the
  feet and hands followed by distal numbness and paresthesia. Pain and
  weakness in muscles spread rapidly and patients become unsteady and
  unable to keep their balance. Progressive leg weakness occurs,
  together with depression of tendon reflexes. Symptoms may also appear
  in the arms and forearms. Sensory loss may be mild. Muscle tonus of
  the limbs gradually increase and spasticity appears in the lower
  limbs. Physical examination reveals distal symmetrical and mainly
  motor polyneuropathy, with wasting and flaccid weakness of distal limb
  muscles, especially in the lower limbs. In severe OPIDP quadriplegia
  with foot and wrist drop were observed as well as mild pyramidal signs
  (Lotti, 1992). There may be some functional recovery in less severe
  cases with more distal involvement and sparing of spinal cord axons,
  but pyramidal and other signs of central neurological involvement may
  become more evident with time. The recovery affects only sensory
  nerves, while motor neurons may permanently lose function as indicated
  by Morgan (1982) who described the lack of improvement over 47 years
  in 11 patients poisoned with TOCP.

The chronic organophosphate-induced neuropsychiatric disorder (COPIND) happens to persons with a chronic exposure to OP and is most likely caused by permanent damages to the central nervous system (CNS), but the real cause is not known yet.

  The most common symptoms of COPIND include cognitive deficit
  (impairment in memory, concentration and learning, problems with
  attention, information processing, eye-hand coordination and reaction
  time), mood change (anxiety, depression, psychotic symptoms, emotional
  lability), chronic fatigue, autonomic dysfunction, peripheral
  neuropathy and extrapyramidal symptoms such as dystonia, resting
  tremor, bradikynesia, postural instability and rigidity of face
  muscles

References

Neurotoxic effects in patients poisoned with organophosphorus
pesticides
Long-term health effects of nerve agents and mustard
Neuropathy target esterase (NTE) and organophosphorus-induced
delayed polyneuropathy (OPIDP): recent advances


Dopamine and other neurotransmitter release during music listening

Here is an article I found on google scholar. It links an increase in 5-HT a serotonin neurotransmitter when listening to pleasant music.

https://link.springer.com/article/10.1007/s004060070031


A strain of my hair has a grey spot in the middle, how is this possible? And why does it happen?

Your hair gets its color from a compound known as melanin, produced by special cells called melanocytes. There are two versions of melanin - one that produces dark pigmentation and the other that produces light pigmentation. If your natural hair color is brown/black, then it normally has a specific amount of dark vs light pigment. The middle section of this hair is grey because there was an absence of melanin production when the hair was still growing. There could be multiple factors (including stress , as described on the library of congress site), but it's nothing to worry about. Your melanocytes started to normally produce melanin again, which is why the newest hair growth (closest to the roots) is dark in color (dark brown/black).


Each codon codes for one amino acid and every codon contains 3 nucleotides.


What are the fibers and small droplets on the surface of dividing HeLa cells in the figure?


Go for the  link below, you will find an article on "How do marine bacteria produce light, why are they luminescent, and can we employ bacterial bioluminescence in aquatic biotechnology?"

www.biology-online.org/articles/marine_bacteria_produce_light/abstract.html

From this article :

  The question remains whether quorum sensing regulation of bacterial
  luminescence is a kind of a ‘social behaviour’ in which cells
  ‘predict’ the possibility of increased mutagenesis where conditions
  allow for efficient metabolism leading to extensive bacterial growth.
  Such conditions may cause the appearance of large quantities of
  metabolites, including mutagenic agents. Thus, one could speculate
  that enhanced light emission at a high cell density may ensure more
  efficient DNA repair in response to potentially increased
  concentrations of mutagens. Alternatively, quorum sensing may be
  needed for another role of bacterial bioluminescence, besides
  stimulation of photoreactivation.


We had to do this frequently. What I would first recognize is that all of your current methods only work for at the small scale and that for you to purify mg quantities of DNA, you need to work with mg scale equipment.

First of all, you should examine your "upstream" process. Are you doing your PCR at scale? Typically, we have scaled out by going with multiple PCR reactions rather than one large PCR reaction. Generally the reactions max out at 50uL depending on your thermocycler. If you're getting around 1ug/10uL, scale up to a 96 well plate with 50 uL reactions and get ~500 ug of material. Make sure that you mix your dNTPs! Scale-up accordingly.

To start, the DNA Clean and Concentration is designed for really small reactions. It's much better to use the next level of purification by maxiprepping everything. The  The binding capacity of those columns go up to 1 mg. Using the QIAEX II slurry works but you should make sure that you scale up correctly. Make sure that you complete your regeneration. This protocol works well.

Alternatively you can ignore the column and just ethanol precipitate everything to remove your nucleotides. I suggest following Ethanol precipitation of nucleic acids from OWW. We had to make a lot of linear template and for most applications this works great.

As with all things related to molecular biology, there is a lot of voodoo. Some things that supposively work is to chill your ethanol mixture at -20C for at least an hour (or overnight), generally, you'll see your DNA fall out of solution and that's your sign that things are working. At this scale you should be seeing your DNA pellet; that's a good sign if things are working. While eluting anything from the columns, we would warm up our elution buffers. Thermodynamically this would make sense since it would reduce the barrier for unbinding. You would also get away with a lower residence time.

I would frankly avoid using FPLC unless you're working with gram quantities of DNA. You're not Moderna.


Cell evolution: immortality vs reproduction

You'll see that in many cases, when any sort of cell enters a zone of intolerance or zone of physical stress, the replication machinery gets put on the backburner (and thus replication). Expression of stress-response proteins like heat shock proteins is increased as a result (1). If a cell isn't within acceptable parameter to undergo division at G1 or G2 (anoxic environment, etc.), you'll find mechanisms like G0 phase or sporulation are preferred until the environment returns to something less stressful (2). I wouldn't say cells would rather be immortal, per se, but longevity or even apoptosis/entosis/etc. would be preferable to replication if nothing is going right (3, 4).

To be clear, when we're talking about evolution that's a tough one. Sure, some sort of stress-response transient signal could induce some lasting cell memory selecting toward a specific function. I simply don't have the data to quote you in that aspect, however.

Biology of the heat shock response and protein chaperones: budding yeast (Saccharomyces cerevisiae) as a model system.
Slonczewski, J., & Foster, J. (2011). Microbiology: An evolving science (2nd ed., p. 143). New York: W.W. Norton.
DNA damage-induced apoptosis
Cellular Stress Responses: Cell Survival and Cell Death

As a footnote, while replication does occur in sporulation, the replicated chromosome is destroyed in the process of forming the actual spore.


According to this article appearing on the website of the American Association of Neurological Surgeons, gunshot injuries to the head are fatal in 90 per cent of cases. Many victims die before reaching the ER, and the 50 per cent who survive the initial trauma die in the ER.


Validity of Acoustic Weapon Effects on Biological Organisms?

There are a few things which can lead to miscommunication regarding the potency of acoustic weapons, but there are two main things to consider: source levels and duration.
Most organisms can tolerate loud sounds, within reason, for a short period of time. However, no matter how short, at certain levels acoustic weapons can cause temporary or permanent hearing loss, nausia, gagging, and disorientation.  Weapons with a lower source level played over a longer duration will be easier for organisms to initially ignore, but exposure to weaponized source levels over time will lead to internal issues with health, including a decrease in fecundity and nutrient digestion.
Often military and sometimes scientific reports will focus on one particular type of weapon used for a specific purpose, and deem its use acceptable or not. Many scientific studies take more factors or variations into consideration.
Ultimately, its risky because we don't have enough data about the long-term effects acoustic weapons can have on a population, and they also don't appear to be particularly effective when it comes to humans. The Acoustic Weapons (chapter 7) in 'Non-Lethal' Weapons1 by Neil Davison sums it up nicely.
Reference:
1: Davison, N. (2009). 'Non-Lethal' Weapons. Springer.


What is a good identification key for European mushrooms?

There are various types of Mushroom identification Sites. you can take help from:

Mushroomexpert
Rogersmushrooms
MycoKey 4.0

Source: MycoKey 4.0


Infer gene frequency within a species over time

There are really two ways to infer past genetics.

Sample the past.

Only really works if you have well-preserved uncontaminated archaeological samples, but works surprisingly well, considering. The accuracy and completeness goes down fairly quickly as you go back in time but thousands of years to hundreds of thousands of years is roughly possible. You won't have many samples so it's hard to say anything about population genetics. Don't do this. It doesn't work very well and it's very hard.

Molecular clocks.

Same-sense mutations that affect nothing accumulate in genes over time as they're passed down. Genes that have a distant common ancestor are more different than genes that are just a generation or two apart. This is essentially how phylogenetics works as a whole, but you can use age differences between nearby genes to detect selection in this way. If gene A is nearly identical in every individual in a population, but gene B has thousands of pretty distinct variations, it's clear gene A does something important and has been powerfully selected for. Don't just count the number of kinds of alleles for gene A, calculate the average relatedness between all the alleles you find. If the relatedness for gene A is much lower than for other genes, gene A is being selected on. This is what the text means by 'reduction in genetic diversity', bringing down the average relatedness.

You can't work out allele frequencies at arbitrary times in the past without a time machine(even ancient sampling, you can't really be sure you're getting an accurate sample of the historical population), but phylogenetics can hint at what happened by detecting the signatures of evolution.


Where to start understanding chemical principles of human body?

If you want to start from the chemistry upwards I'd recommend you to either look into a biochemistry textbook (buy or borrow one/get a used one, since they are quite expensive) or look for some (online) courses in that field.

The textbooks I know from university studies are:

Biochemistry (Stryer, Berg, Tymoczko) [possibly downlaodable from here]

Biochemistry (Voet & Voet)
Lehninger Principles of Biochemistry (Cox, Nelson)

The MIT offers quite a few (free!) online courses and there seem to be quite a number of biochemistry ones (I haven't looked into any of them, but I reckon the MIT courses aren't too bad).


Effect of spaying on the female cat organism and health

From the standpoint of the skeletal system, spaying is definitely not good for her health. Removal of the ovaries mimics what happens at menopause, when circulating estrogen levels fall. Estrogen is necessary for maintenance of bone mineralization. Without estrogen, bones start to demineralize (the same process that happens in human females after menopause, leading to osteoporosis).

Then again, some animals, if they do not get pregnant, will cycle indefinitely until they get anemic and die. Ferrets are an example. So it's better to have these spayed.


How does HBeAg change to Anti-HBe in acute hepatitis

I'm not sure that I have understood the question but ...

HbeAg is a secreted variant of HbcAg (the core antigen of HBV). Unlike HbcAg, HbeAg is found in the blood. I believe that it is produced as a result of a splice variant of the corresponding RNA.

The phenomenon described in these Figures is an example of seroconversion. Before seroconversion the antigen is detectable in the blood but there is no antibody directed against it; after seroconversion there is antibody but no antigen.


Why we can't feel the different parts of ear during hearing which is mentioned in all biology books?

Going to be productive instead of posting unhelpful snarky comments and downvoting.

You can only perceive what you have nerves for. Considering humans are unaware of all the rattling going on between the eardrum and inner ear, the only logical explanation is that there are no nerves in the region made to perceive said rattling.


How to retrieve full gene names list and Entrez gene IDs and other annotation information from HUGO gene name list (in R or any)?

I would recommend just downloading the database, which HUGO allows you to do free of charge.

The HUGO website has a "downloads" tab at the top that takes you to the following page

http://www.genenames.org/cgi-bin/statistics

You will see a table of statistics relating to how many protein- or non-protein-coding genes there are catalogued, etc.

Under the tables is a section called Complete dataset download links -- this is the section you want (unless you only want a subset of the data - but why not get it all!)

This plain text file (once uncompressed) can be loaded into R (or any other language) to be parsed and analysed as per your requirements.

It is worth updating the version you download quite regularly, as they update the HUGO database with new/updated info quite regularly.


Statistician confused about exact SNP data type

SNP is not a specific data type but rather a biological phenomenon. The abbreviation "Single Nucleotide Polymorphism"  only means there is a variability (between individuals) in a single letter in a specific position in DNA sequence. It depends on the speaker how they decide to describe the variability; wether they choose to focus on the possible sequences and say for example "There is only A or T in this position" or they focus on possible human genotypes and spells out all combinations (AA, AT, TT).
What constitutes as SNP data depends entirely on research question, used organism (diploid/haploid/polyploid) and experimental design.
Article you link in your comment uses oat lines and not individuals from outbreeding population. Oat like arabidopsis is naturaly highly self polinating so creating highly homozygous inbred lines is relatively easy. In this case it is reasonable for the researches to expect only AA or aa genotypes in each line.
Edit: Since you asked for more examples where the researcher chooses to focus on alleles instead of genotypes. Many SNP genotypes distribution fit Hardy-Weinberg equations. If that is the case, the frequency of genotypes can be calculated from an allele frequency in population. The researcher might ask: "Is the frequency of allele a different in population/group 1 from population/group 2?" They collect data from indivuduals in group 1 (AA, AA, Aa, Aa, aa) and group 2 (Aa, Aa, aa, aa, aa). They decide to treat each allele as independent measurement (not dependent on individual it comes from) and poll the data: group 1 (AAAAAAaaaa), group 2 (AAaaaaaaaa) and then they do simple binomial test to answer their question.
Note: Even if Hardy-Weinberg equilibrium is not met, the questions about of allele frequency are is still valid biological questions (with slightly different use/interpretation down the line).


To what extent is eating and nutrition important in recovery from minor illness like viral fever?

During infection a body has to produce absolute masses of immune cells, raise your temperature via increased metabolism, repair tissue damage, migrate components of the immune system including proteins and cells, produce masses of antibodies and probably lot's more.

A lot of protein components need to be made which require protein synthesis and energy. Metabolism of fats and carbs goes up too. Also, importantly, vitamins are a key part of the immune system serving to migrate the immune system  such as vitamin D aids migration of cells to the skin. Vitamin C is required for collagen synthesis in repair. Minerals are required for the metalloenzymes. However your dependency on each component depends on the type of infection, your immune response, your natural state including your reserves of everything.

How important is it? Very. I've listed what the things are needed for which gives an indication of how important they are. If starved, the body will do the best it can by focussing its resources on the thing it deems most important.


The boy is holding a couple of smoked/barbecued cane rats, also known as "grasscutters".  These are commonly hunted as bushmeat in West and Central Africa and have recently been farmed as well.

You can see some similar photos here:

http://members.virtualtourist.com/m/p/m/178963/
http://westafricaadventure.blogspot.com/2011_04_03_archive.html
http://www.fionaleonard.net/2012/04/rodents-of-unusual-size.html
http://2summers.net/2015/01/23/pop-up-travel-cane-rats-in-ghana/


Remi.b and Potterbond007 have put forward excellent answers. Would like to add something..

One of the reasons that Myopia (near sightedness) happens is because of use of eye in work like reading, which requires working with close objects. I don't think there was much working with close objects in the past. So very few people with myopia might have been present (and of course, they may have had disadvantages in catching prey.)

Other common disease is hypermetropia which generally occurs during old age, past the reproductive prime, so it could not have much evolutionary impact.


Behavior of plant guard cells: open or closed stomata

I found a paper and this is the link https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258058/  it says that Stomatal opening is induced by low CO2 concentrations, high light intensity and high humidity. By contrast, closing is promoted by high CO2 concentrations, darkness, drought and the plant hormone ABA.
Another paper, Open or Close the Gate – Stomata Action Under the Control of Phytohormones in Drought Stress Conditions https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3652521/
During the night, elevated levels of CO2 in the leaves were observed due to respiration. It has been proved that CO2 has a positive effect on the stomatal closure process


species ID

I feel reasonably confident this is a late-instar Acanthocephala declivis nymph (that is, almost-but-not-quite-adult).

Compare your pictures with those on bugguide of a similarly-aged individual, or the bugguide ID page. Also see the key here; which gives three characters for declivis

  Humeral angles of pronotum broadly expanded, extending laterally well beyond maximum lateral abdominal margin. Distal dilation of hind tibia broad until apex, then curving in at right angles to tibial shaft. Anterior pronotal lobe with 2 small shining blunt tubercles along midline

If you look at your pictures, you'll see that you're three for three here: the broad 'shoulders' (pronotum), the right-angle in the leg flange (dilated tibia) just above the the 'ankle', and the two rounded bumps on the pronotum (visible in photos 1 and 3).

original answer / working towards the ID

You're right on track, it definitely looks like a true bug (Hemiptera/Heteroptera). Possibly immature if it looks wingless. Maybe some kind of Assassin Bug (Reduviidae)? They don't all have burly forelimbs. You might also want to consider Coreidae, for instance the genus Leptoglossus (pdf on Leptoglossus in Georgia).

You could try this key to Florida bug families, it looks pretty user-friendly.


What signals a ribosome to stop production when the cell is out of available amino acids?

When cells run out of amino acids, more and more of their tRNAs remain uncharged. This elevated ratio of uncharged/charged tRNAs trigger complex signalling pathways that control amino acid biosynthesis, general reduction of translation, halting ribosome biosynthesis, autophagy (includes ribophagy - digestion of ribosomes) to recycle cells' components, etc. This can be clubbed into general amino acid control (GAAC) and involves the super important regulatory kinase protein called as Target of Rapamycin (TOR) and other transcription factors. The regulation of amino acids level is one of the most basic and important features of cellular metabolism and can be found conserved from yeast to humans. In addition to GAAC, there can be pathways for some specific amino acids as well.

There is not shortage of scientific literature. To start with you can read following article:

http://www.cell.com/trends/cell-biology/abstract/S0962-8924(14)00036-1
http://jcb.rupress.org/content/206/2/173.full


Scientific name: Camponotus compressus

Common name: Common Indian black ant

Camponotus compressus tending soft scale insects growing on a stem

Source:

Common Indian black ant
Wikipedia

Cannibalism is common in social insects. It is a way through which they control the population of the colony and conserve nutrients. Members of Hymenotpera (this ant being one) are very quick to consume injured eggs, larvae and pupae. It has been experimentally observed that when a colony of Zootermopsis angusticollis(a species of termite) was kept on a diet full of cellulose i.e. deprived of protein, they attacked their own kind. But cannibalism dropped to zero when casein was introduced in their diet. So it is safe to  assume that these ants too engage in cannibalism for the same reason, proteins.

Reference: This book.


Can you Transfer Cancer Between People via Saliva or other Bodily Fluids?

Although transmissible cancer has been found in some species, such as Tasmanian Devils and clams, it is quite rare in most species. Certain viral and bacterial agents that cause cancer, however, can be transmitted. One example is HPV, which can cause cervical cancer


The two plasmids have to have different origins of replication. Two plasmids from the same incompatibility group cannot survive together in the same cell.

This quote is from the Wikipedia entry on plasmids:

  Plasmids can also be classified into incompatibility group. A microbe can harbour different types of plasmids, however, different plasmids can only exist in a single bacterial cell if they are compatible. If two plasmids are not compatible, one or the other will be rapidly lost from the cell. Different plasmids may therefore be assigned to different incompatibility group depending on whether they can coexist together. Incompatible plasmids normally share the same replication or partition mechanisms.

This is a nice definition/explanation from an OpenAccess article:

  A formal scheme of plasmid classification is based on incompatibility (Inc) groups (Novick, 1987). The procedure for incompatibility grouping is based on the introduction, by conjugation or transformation, of a plasmid of an "unknown" Inc group into a strain carrying a plasmid of a known Inc group. If the resident plasmid is eliminated in the progeny, the incoming plasmid is assigned to its same Inc group (Datta and Hedges, 1971). Plasmids with the same replication control are "incompatible", whereas plasmids with different replication controls are "compatible". On this basis two plasmids belonging to the same Inc group cannot be propagated in the same cell line (Datta and Hughes, 1983; Couturier et al., 1988). Inc group identification has been frequently used to classify plasmids. The method has been an important tool to trace the diffusion of plasmids conferring antimicrobial resistance and also to follow the evolution and spread of emerging plasmids (Anderson et al., 1977).

A synopsis of the Datta & Hedges article sited above:

  Classification
  In 1971, Hedges and Datta proposed a plasmid classification scheme based on the stability of plasmids during conjugation (incompatibility). The first incompatibility (Inc) groups were IncI, IncN, IncF, and IncP. Currently, 26 Inc groups are recognized in Enterobacteriaceae including six IncF (FII to VII) and three IncI (I1, Iγ, I2) variants. Major plasmid families occurring in Enterobacteriaceae are HI2, HI1, I1-γ, X, L/M, N, FIA, FIB, FIC, W, Y, P, A/C, T, K, B/O, FII, FIII, FIV. IncF plasmids are low- copy-number plasmids, often carrying more than one replicon with at least one replicon strongly conserved.

One way to think about it is: if one prepares a plasmid cloning vector to accept foreign inserts, and ligates in a "shotgun" collection of fragments from some DNA of interest. After transformation, selection and growth on plates, none of the colonies whose plasmids carry inserts ever contain more than one unique plasmid.  In other words, it may be possible for two different inserts to be inserted during ligation into the same vector backbone, but it is not possible to find a single pure colony that contains cells harbouring two different plasmids, each carrying a different insert.

If a cell gets transformed by two different plasmids from the same inc group only one plasmid will "win."

Examples of compatible ori's commonly encountered:

pMB9 (pBR322, pUC, etc., etc.,)
F (fosmids)
bacteriophage lambda (some cosmids)
bacteriophage M13 and relatives (also yields ssDNA phage useful for Sanger sequencing)
bacteriophage P1
pSC101

Here is a nice table, but I cannot vouch for its accuracy.


Does it make sense to make my own DNA copy (kind of backup) while I am young?

While your DNA gets damaged, not every single cell will have the same damage.  Your consensus DNA sequence will not change.


This is a pond heron or paddy bird. The de-facto source for identifying Indian birds is Birds of the Indian Subcontinent by Richard Grimmett, Carol Inskipp and Tim Inskipp. The book is remarkably complete and contains the vast majority of species found in the Indian Subcontinent.


Did most pandemics originate from Asia/China?

According to Merriam-Webster Dictionary a Pandemic is:

an outbreak of a disease that occurs over a wide geographic area and affects an exceptionally high proportion of the population : a pandemic outbreak of a disease

Epidemics are considered a smaller scale version of a pandemic affecting a smaller region, community or population. Epidemics are obviously more common than Pandemics for that reason.
COVID-19 is believed to have become a pandemic event because it has affected multiple continents and most if not all Nations of the world. These extent of pandemics though rare in the past may become increasingly frequent as our world continues to become more globalized if further precautions are not continuously developed.
According to this list, Around 5 of the world's Pandemics have likely started or been mainly spread from and within China, They are:

Third Plague - 1885
Asian Flu 1957
Hong Kong Flu - 1968
SARS 2002
Coronavirus Disease - 2019

These are 5 out of the 20 pandemics in the list. Would that count as a majority? Depends on how you look at it. For one country to start so many does make it unique and a possible majority but we must also consider the size of the country's population relative to the rest of the world. For such a large country (currently 1.4 Billion people which is about 18% of the world's population) with a large portion of the population being poor it is almost expected that China suffers more epidemics than most countries.
Pandemics and Epidemics start for a wide variety of reasons (some quick-search articles that explain: 1, 2, 3) and many of these pandemics develop because of unique environments or pathogens existing in 'coincidence' with each other.
Generally, lack of hygiene, low economic wealth, lack of healthcare products including vaccines coupled with a high population are common societal trends for the beginning of an epidemic. However the pathogens have their own characteristics that make them effective at causing an outbreak. This includes but definitely is not limited to: rapid mutation rate, easy transmission such as through air (e.g. SARS) or water sources (e.g. ebola virus), and zoonotic capabilities (being able to infect more than one species such as swine flu).
Two sources that must be strongly suggested to check out for anybody interested in these sort of topics are the Center for Disease Control and Prevention and the World Health Organization


is having more copies of gene better then having it less? if it's why is it ?

I was learning about elephants rarely getting cancer and learn that elephants have 40 copies of genes while human only has 2 copies of genes each from parents.

Where did you read that? Please always include your sources.

What you're saying is unclear but I suppose you are referring to ploidy variation among species and not to CNV (Copy Number Variation) for specific genes. It is also possible that you mistake alleles for genes but it is impossible to tell where your misunderstanding is without reading from your source. I will assume you talked about ploidy variation.

Elephants are diploids, just like humans. So, the claim appears flat wrong.

  so I wonder if it's better to have more copies of the gene then having 2

There is no general rule. Because having a single working copy is often enough, high ploidy can be a pretty good defense against loss of function mutations but that's only valid for some time just after a recent polyplodization event as the relaxation of selection pressures against such mutations will lead these deleterious mutations to higher frequencies (at mutation - drift - selection equilibrium).

Note that doubling or halving the number of gene copies often yield to issues in dosage of mRNA and protein expressed. Related to that you might to read about dosage compensation


What is a good introductory book on plant genetics for an outsider?

I am in a PSEO class for plant biology and ecology and I found a book online I believe you would find useful.

Click here

I've used this book to study many times even though it wasn't supplied to me. It does a great job explaining overall concept of plant microbiology. This book will introduce concepts that someone would be new to. I recommend that you give it a read, then after you read it, move to a book specifically on plant breeding.

Hope this helped!

-Sartoaster


What is the scientific name of this tree?

It is Lagerstroemia, perhaps Lagerstroemia indica, the common crape myrtle.

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

Myrtle in french means blueberry: "From Medieval Latin myrtillus, diminutive of Latin myrtus (“myrtle”), from Semitic: Arabic مُرّ (murr, “bitter”), Hebrew מֹר (mor, “bitterness") ." Myrtle is an unrelated family with tough spicy seed pods which are used as a condiment including eucalyptus.

Crape, refers to the frilly flowers, from Latin Crispus, Crispy: frilly, crèpe is often used to refer to frilly fabric and it also means pancake in french, which is a chapatti with butter and milk and an egg from the bible.

Because you said it is common, I checked google images for "india frilled pink flower tree", it was about 20 images in. There should be a Hindi/Indian script of the wiki page, with the Indian derived name.


Ventricular Filling : Systole or Diastole?

Ventricular diastole is a period in cardiac cycle during which the ventricles are filling with blood. During this period, the atria are contracting and the ventricles are relaxed.

The diastole consist of this: atrioventricular valves open, atria contract (atrial systole), blood flows from the atria to the ventricles, the atrioventricular valves close.

When the term systole or diastole is used without saying is it atrial or ventricular, it means it is ventricular. For example, systolic blood pressure is the blood pressure during ventricular systole and diastolic during ventricular diastole.


Is NADPH salt still usable after an hour at room temperature?

In my experience, half an hour at room temperature will make absolutely no difference.  Boehringer Mannheim (now part of Roche), who at one time supplied the best NADPH, used to recommend storage at 4o C.

By A340 callibration, NAD(P)H is typically about 85% 'pure' based on dry weight measurements, and Sigma will try to tell you that the remainder is mainly water.  That is, if you calculate a concentration based on the dry weight, the A340 will be about 85% what you expect.

Even if some water is absorbed from the atmosphere, this will make little difference as you are probably going to calculate the concentration based on
the A340.

As User 243 has pointed out, if you are concerned that the NAD(P)H is degraded or oxidized, then an A340
measurement will probably set things right.

If you are concerned that all the A340  absorbing material is not NAD(P)H, or that a significant proportion is in the α-form (Oppenheimer & Kaplan, 1975) or is otherwise enzymically inactive, the best thing is an enzymic calibration.

This is done by adding limiting amounts of NAD(P)H to an assay system containing excess substrate and calibrating enzyme, and measuring the total decrease in absorbance (Racker, 1957).

A popular calibrating enzyme for NADH is aldehyde dehydrogenase (EC 1.2.1.3), as the reaction is practically irreversible, and it makes it easy to 'drive' the calibrating reaction to completing (and you don't have to worry about equilibria).

As I said in a previous post, NAD(P)H is UNSTABLE IN ACID (Oppenheimer and Kaplan, 1974). To put it crudely, 'the head (nicotinamide moiety) falls off', causing a bleaching of the absorbance at 340nm.  Making 100mM acetate, pH 5, 100 micromolar in NAD(P)H produces a very significant decrease in A340 absorbance with time (which may be very easily monitored in a spectrophotometer).

Just because all the A340 material is due to NAD(P)H, this does not necessarily mean that the commercial preparation is pure.  In fact, far from it.  Dalziel (1963) showed that commercial preparations of NADH then available contained a competitive inhibitor of many dehydrogenases, most probably adenosine diphosphate ribose.

Accepting Dalziel's value of 17 600 M-1cm-1 for the extinction coefficient for NADH at 260nm, and assuming that NADPH has an identical value, then highly purified samples of NAD(P)H should have an A260/A340 ratio of about 2.83, and values higher than this may indicate the presence of impurities that absorb at 260nm, but not at 340nm. ADP-ribose is a prime example, but NAD(P)+ is another possibility.

I notice that in one of the links given by AliceD, Sigma quote a A260/A340 ratio of 2.32. So is the higher value due to the presence of residual NAD(P)+, or something else (a breakdown product?), or both?

You may need to use chromatography, typically on an anion-exchange resin, to obtain NAD(P)H free of impurities.

References

Dalziel, K. (1963). The purification of nicotinamide adenine dinucleotide and the kinetic effects of nucleotide impurities.  J. Biol. Chem. 238, 1538 - 1543.  [pdf]

Oppenheimer, N. J. & Kaplan, N. O. (1974). Structure of the primary acid rearrangement product of reduced nicotinamide adenine dinucleotide (NADH). Biochemistry 13, 4675 - 4685.[pubmed]

Oppenheimer, N. J. & Kaplan, N. O. (1975). The alpha, beta-epimerization of reduced nicotinamide adenine dinucleotide.  Arch. Biochem. Biophys.166,  526 - 535.

Racker, E. (1949). Aldehyde dehydrogenase, a diphosphopyridine nucleotide-linked enzyme.  J. Biol. Chem. 177, 883 - 892. [pdf]

Racker, E. (1957). Spectrophotometric enzymatic methods for the determination of aldehydes and ketoaldehydes.  Methods Enzymol. III, 293 - 296.

Other References

Ciotti, M. M. & Kaplan, N. O. (1957). Procedures for determination of pyridine nucleotides.  Methods Enzymol. III, 890 - 899

Horecker, B. L. & Kornberg, A. (1948). The extinction coefficients of the reduced band of pyridine nucleotides.  J. Biol. Chem. 175, 385 - 390. [The definitive determination of the extinction coefficient at 340nm] [pdf]

Kornberg, A. & Pricer, W. E. (1950). On the structure of triphosphopyridine nucleotide.  J. Biol. Chem. 186, 557 - 567.
[This paper shows that the 'extra' phosphate in NADP(H) is attached to the  2' position of a ribose.  In Coenzyme A, of course, the phosphate attached to the ribose is on the 3' position. [pdf]

Pullman, M. E., San Pietro, A. & Colowick, S. P. (1954). On the structure of reduced diphosphopyridine nucleotide.  J. Biol. Chem. 206, 129 - 141 [pdf]


Any studies on the effects and/or benefits of oil pulling?

This is a classical pseudoscientific claim: It is supposed to help against everything, including AIDS, Diabetes, Bronchitis, Cancer and so on. See for example this table I found online:

First, there is no real mechanism, and it is rather implausible to have an universal cure-all drug for all these completely unrelated diseases. There seems to be some weak evidence for the dental hygiene claims, but as the first reference writes, study groups where too small, not effectively blinded, so there is no final clue if this is true:

  Oil pulling’s positive effects are based entirely on anecdote and not
  at all on clinical research – because there’s been very little. Pubmed
  lists six clinical studies related to oil pulling, all performed in
  India, and their quality and results seem all over the map. Some do
  indicate mild improvement in gum health, comparable to mouthwash use.
  But they’re not well blinded, use very small sample sizes and involve
  oil pulling only as part of a proper oral hygiene regimen. So it’s
  impossible to tell what’s causing said improvement.

What clearly does not happen is the detoxification, as this is a pseudoscientific myth itself. Our detoxification is done pretty efficiently by liver and kidney, so there is no need to remove whatever toxin by a treatment.

See references 1-3 (especially 1) for background on the "oil pulling" and reference 4 for the detoxification.

References:

Oil Pulling: Miracle Treatment or Woo Mouthwash?
Oil Pulling Your Leg
Is Oil Pulling Effective for Curing Medical Ailments?
Fashionably toxic


Are there any drawbacks to having a fixed-Köhler microscope?

IMHO: there's hardly any reason why you should't use Köhler illumination. It's the method of choice to achieve bright and even illumination, in the entire FOV, permitting max. resolution. In a well designed system.
Köhler has only one drawback: often it turns out to be impossible to achieve even illumination at low power in the entire FOV. Usually, but not aways, the manufacturer has made provisions to achieve propper illumination at low power at the condenser level.
Allow me to add that I'm not a fan of the Primostar stand, which is a microscope build on order for Zeiss, probably by Meji.
Compared to the older Black, grey and white Zeiss Standard stands, it's a toy...


Does the brain store information and personality traits in different areas?

I think your confusion comes from the fact that you take traits and memory to be distinct from each other. The brain processes information and we know that some of the connections between its cells are altered in the process --some call that memory. You are convinced that this is the only way that traits form, through experience at some developmental stage. You are then asking if cells in areas other than those that change during the formation of traits are affected more by the experience of forming a trait. If that were true, they would by definition be included in the areas that are associated with the trait in the first place. Can you see the problem in the logic of the argument?

Many people have followed similarly flawed reasoning, including trained neuroscientists that have been indoctrinated to believe in extreme forms of functional specialization of the brain, a more subtle version of the now debunked theory of phrenology.


Here in Australia there are more cases of vitamin D shortage than in England. Given the double amount of sun hours per annum here in Down Under, that's quite counter intuitive. In fact, an estimated 31% of adults in Australia have inadequate vitamin D status, increasing to more than 50% in women during winter–spring and in people residing in southern states (Nowsen et al., 2012).

It turns out that in Australia people are, rightfully, careful of sun exposure due to the thin ozone layer and the resulting high incidence of skin cancer. As a result, people here wear long-sleeves on the beach, use high-factor sunscreens, wear sun hats, use umbrellas to evade the sun etcetera. The Australian  Cancer Council supports the famous "slip, slop, slap" slogan:

  Slip on a shirt, slop on sunscreen and slap on a hat, Slip, Slop, Slap! You can stop skin cancer [..]!

Hence, folks here in fact often take vitamin D supplements, despite the large amounts of sun hours.

Reference
- Nowsen et al., MJA (2012); 196(11): 686-7


Short answer

The exact mechanism behind tinnitus (ringing in the ear) is unknown.

Background

Of the two theories you pose here, to the best of my knowledge the second one is the most widely accepted. It is a generally accepted phenomenon that whenever neural systems are being deprived of input, they start seeking new input, or even generate it themselves. For example, blind folks rarely have no visual perceptions at all. In contrast, they often perceive spontaneous visual sensations. For example, many blind folks report perceiving a persistent grayish background hue. In other words, it is never black in the eyes of a blind person. They also often see spontaneous spots of light. The most striking example, however, being Charles Bonnet syndrome, where the blind person may perceive complex scenes with faces and objects (Bhatia et al., 2013).

In the case of tinnitus, the perceived sounds are mostly not complex, but repetitive and simple in nature ('ringing', beeps etc.). It is thought that the deafferented auditory cortex actively starts generating sound perceptions. However, many other explanations have been brought forward, such as spontaneous activity in the hair cells in the cochlea and spontaneous activity in the auditory nerve fibers (Luxon, 1993). I will sum up a list of potential causes mentioned in Han et al. (2009):

Peripheral mechanisms

(1) Spontaneous otoacoustic emissions
Spontaneous otoacoustic emissions (SOAEs) are small acoustic signals generated by the electromotile activity of outer hair cells (OHCs) in the cochlea. While normally inaudible, SOAEs may be perceived as tinnitus. Tinnitus due to SOAEs is mild and is more common in subjects with functional hearing.

(2) Discordant theory
Tinnitus may be induced by the dysfunction of damaged OHCs while inner hair cells (IHCs) are still intact. For example, intense noise and ototoxic agents initially damage OHCs in the basal turn of the cochlea, and subsequently, if continued or repeated, affect IHCs, because IHCs are generally more resistant to such damage. IHCs are the receptor cells for sound transduction. In contrast, OHCs work as mechanical amplifiers, enhancing weak sounds by providing up to 50 dB, which can be evaluated by measuring OAEs. When OHCs die, cells in the dorsal cochlear nuclei (DCNs) show increased spontaneous activity due to the fact that IHC input is relatively normal, but OHCs input is decreased due to damage to the OHCs. This spontaneous activity is perceived as tinnitus.

Spontaneous activity in neurons can occur through a host of mechanisms. Basically, a depolarization beyond a certain thresholds sets the neuron off to fire. In case of the disinhbited DCN neurons, the input from the OHCs is taken away. OHC input to the DCN is inhibitory,m as it is believed OHCs activate inhibitory interneurons. The exact mechanism is unknown, but a central inhibitory neurotransmitter is GABA. GABA can activate GABA-A receptors, that open up a Cl- channel, which in turn leads to Cl- influx into DCN neurons and hyperpolarization. When this input is taken away, you can imagine that DCN neurons depolarize and when this depolarization reaches threshold, the DCN neuron may increase firing Kaltenbach et al. J Neurophys 2002;88:699-714. Hence, as you question whether, in the absence of neurotransmitters, cells can fire action potentials, I say: **yes*. In fact, many neurons have spontaneous spiking activity, often with very regular frequency. These oscillating behaviors are often mediated by cation channels that gradually depolarize the cell up until its spiking threshold.

(3) Crosstalk theory
Nerve compression (e.g., due to a tumor) may cause artificial synapses to be formed between nerve fibers of the cochlear and vestibular nerve  (crosstalk). The breakdown of the myelin insulation of the nerve fibers may further enhance coupling. Hence, spontaneous activity in the auditory nerve may be generated through vestibular activity.

Central mechanisms

Some patients may still perceive tinnitus after the auditory nerve is transected. Hence, tinnitus in this subgroup must be caused by mechanisms located more centrally from the auditory nerve.

(4) Auditory plasticity theory
Damage to the cochlea enhances neural activity in the central auditory pathway, specifically in the temporal lobe in the auditory association cortex and inferior colliculus. This theory was touched upon further above in the first paragraph. Basically, when neural tissue is deafferented, it tends to look for new input or even generate activity de novo.

(5) Somatosensory system
The activity of the DCN is also influenced by stimulation of nonauditory structures and the somatosensory system has been implicated in development of tinnitus. Somatic tinnitus can develop as somtaosensory input may disinhibit the DCN.

(6) Limbic and autonomic nervous systems
The aforementioned theories cannot explain why some people suffer from tinnitus while others do not. More than 80% of those perceiving tinnitus for the first time do not associate the sound with any negative meaning and experience spontaneous habituation. However, if the first perception of tinnitus induces high levels of annoyance or anxiety by association with unpleasant stimuli or with periods of stress and anxiety, tinnitus might develop into a problem.

References
- Bhatia et al. Delhi Psych J 2012;15:423-4
- Han et al. J Clin Neurol 2009;5:11-9
- Kaltenbach et al. J Neurophys 2002;88:699-714
- Luxon, BMJ 1993; 306:1490-1

Further reading
- Action potentials in the absence of neurotransmitters: how-does-optogenetics-work


How were the first genes isolated from genomic or cDNA libraries without already knowing a hybridization probe?

The following is based on a chapter on Cloning DNA in the 10th edition of The Biochemistry of the Nucleic Acids (RLP Adams et al.) published by Chapman & Hall in 1986. (This is probably more pertinent than the 11th and final edition, which was published in 1992 and had a more contemporary treatment.) Apologies for the fact that it will be difficult to find.  It should be available from some university libraries and through inter-library loan systems in certain countries. Section A.7.3 gives a taste of the methodology used at that time.

Protein properties that could be used as the basis of a cloning strategy

In attempting to clone DNA for a particular protein for which there were no pre-existing clones to use as hybridization probes, one had to consider the properties of the protein one is able to exploit. These might include:

Amino acid sequence
Antibodies to the protein
Biological activity
Particular physical properties, such as size

(Clearly if one had no such ‘handle’ to the protein one was not in a position to try to clone its cDNA or gene.)

Three general approaches

There seemed to be three general approaches:

No expression
Indirect expression
Direct expression

The approach that one might take was also governed by whether the protein is particularly abundant in a specific tissue, when one might expect less sophisticated more labour-intensive approaches to stand a chance of success.

Another point to emphasize is that, at least with eukaryotes, one would look for a cDNA clone first, and only try for a genomic clone after one had this to employ as a hybridization probe.

1. ‘No expression’ approaches

In the no expression approaches one relied on the amino acid sequence to identify the cloned DNA. One such approach was to use hybridization probes against stretches of amino acids, the codons of which had limited redundancy (Met and Trp have a single codon, and some other amino acids only two) using low stringency hybridization conditions. This required luck. Alternatively one could sequence random clones and hope to find one that correlated with the amino acid sequence. At that time DNA sequencing was slow and labour intensive, so that this was only applicable to proteins that were relatively abundant in the tissue from which the libarary was prepared.

2. Direct expression approaches

Direct expression generally entailed using a bacterial expression vector which produced a fusion of a bacterial protein with a part of the eukaryotic protein. (Statistically only one in six of clones would have the correct reading frame in a fusion protein.). This approach was favoured if one had an antibody, which did not require a complete protein.

3. Indirect expression approaches

By indirect expression was meant using immobilized cloned cDNA to select corresponding mRNAs (‘hybrid selection’) which could be expressed in a cell-free system. This was appropriate if the distinguishing characteristic required a full-length protein, as in the case of biological activity or size.


How can one relate in vitro studies of caffeine (dose expressed as concentration) to dietary intake of caffeine (dose in mass)?

In the mentioned study, they tried to support the evidence from earlier studies in which caffeine consumption was associated with skin aging and slow wound healing:

  Our research confirms our earlier observations that caffeine may have
  an adverse effect on the wound healing process, as well as on the
  aging process, of the human skin.

...and by "earlier observations" they mean another in vitro study.

In the study, they used 1, 2 and 5 mM caffeine solutions. 1 cup (~250 mL) of brewed tea can contain 95-165 mg caffeine (source), which makes it 2-3.4 mM, so much like the solutions used in the study. When you drink 1 cup of coffee (let's say, 2 mM caffeine solution), the caffeine, which is water- and lipid-soluble (StatPearls), will be dissolved in the body water and fat, which can together make ~50 kg in a 70 kg person. So, you would need to drink ~200 cups of coffee (~20 g caffeine) in ~2 hours (caffeine half-life is ~5 hours - source) to achieve 2 mM caffeine solution in the skin cells.

I haven't found any actual human clinical trial in which caffeine consumption would be associated with adverse effects on the skin. In a recent review: Coffee consumption and health: umbrella review of meta-analyses of multiple health outcomes (BMJ, 2017), they don't even mention skin or wound healing and regular drinking of 3-4 cups of coffee per day was not associated with an increased risk of various health conditions (except in pregnancy).


How do we know if a neuron is inhibitory or excitatory?

In my naive understanding, a neuron was inhibitory or excitatory depending on the neurotransmitter it releases onto its postsynaptic partners.

This is mostly correct. What remains a question is what makes a given neurotransmitter inhibitory or excitatory. To some extent, that depends on the post-synaptic receptors, but also depends on other conditions: one case mentioned in the linked Q&A that I'll repeat is that GABA is actually excitatory at some times, including during development (and the same thing can happen in certain causes of epilepsy). In that case, the reason is because GABA-A receptors are chloride channels, so the reversal potential for chloride is what matters. If the reversal potential for chloride is more hyperpolarized than threshold, GABA-A is an inhibitory receptor; if the reversal potential for chloride is more depolarized than threshold, GABA-A is an excitatory receptor. Chloride ion concentrations are different during certain stages of development so the role of GABA changes (in development it seems like it is important for development of eventually inhibitory circuitry).

I digress a bit, but I think you've really already encountered all you need to know: labels like "excitatory" and "inhibitory" for a neurotransmitter itself are generalizations that satisfy human preferences for heuristics. It's convenient to talk about GABA as an inhibitory neurotransmitter, because in most cases the major systemic effect of GABA is inhibition. Same with glutamate in the direction of excitation.

Most of the inhibition caused by glutamate is the presynaptic inhibition type discussed in a previous Q&A; that is, it is suppressing the release of glutamate itself. In that sense, glutamatergic inhibition is only as effective as glutamatergic excitation is: the net effect of glutamate will always be excitatory in that system.

Therefore, it is straightforward to consider GABAergic and glutamatergic cells inhibitory and excitatory, respectively.

  how can we be sure that the presynaptic's cells action are not mediated by other cells, and the observed inhibition/excitation is not rather a network effect?

The principle way is by pairwise recordings: you record from the presynaptic and postsynaptic cell at the same time, activate the presynaptic cell, and measure the voltage in the postsynaptic cell. These sorts of pairwise recordings are a common tool in neuroscience.

Cancedda, L., Fiumelli, H., Chen, K., & Poo, M. M. (2007). Excitatory GABA action is essential for morphological maturation of cortical neurons in vivo. Journal of Neuroscience, 27(19), 5224-5235.

Owens, D. F., Boyce, L. H., Davis, M. B., & Kriegstein, A. R. (1996). Excitatory GABA responses in embryonic and neonatal cortical slices demonstrated by gramicidin perforated-patch recordings and calcium imaging. Journal of Neuroscience, 16(20), 6414-6423.

Thomson, A. M., & Deuchars, J. (1997). Synaptic interactions in neocortical local circuits: dual intracellular recordings in vitro. Cerebral cortex (New York, NY: 1991), 7(6), 510-522.


What is phenotyping of blood during transfusion process?

In response to the above q. many have commented that the process is only limited to Middle Eastern countries....I think the term 'only' will be better substituted by 'mainly', the reason to which , is explained later ....

Now, the main clarification lies in the fact that,

  ....there are more than 600 known antigens besides A and B that
  characterize the proteins found on a person's red cells. A combination
  of some of these less familiar but commonly occurring antigens are
  absent from the blood of an extremely small percentage of the
  population. There are also a few antigens that almost all people have
  on their red cells but that some lack. - One In A Million
  American Rare Donor Program

Now patients receiving a 1st time transfusion normally do not show any reactions or cross-matching problems with these blood subgroups but during repeated transfusion process like in case of thallaesemia , the receiver's blood gets sensitized against the donor's blood & the problems ensues...

  Dr Therese Callaghan said, “All other antibodies are unexpected and
  are of two distinct types, alloantibodies (which target an antigen
  that is not present on your own red blood cells) and autoantibodies
  (which target an antigen that is present on your own cells).

  “Patients receiving a transfusion for the first time do not normally
  have problems with matching blood types and antigens. However it is
  during subsequent transfusions when more care needs to be taken. If,
  during a later transfusion, the blood contains the same antigens as an
  earlier one, the patient’s immune system recognises the transfused
  blood cells as ‘foreign’ and the antibodies (formed after the first
  transfusion) will destroy the blood cells the patient has been given.
  This is called a transfusion reaction and can cause serious illness or
  even death if not treated quickly. That is why matching the blood
  phenotype is so important.”

Now coming to "Why mainly in Middle-East ??"

These rare blood groups are distributed into major 30 discrete system, which mainly  are present in different ethnic groups & communities...mainly living in Middle-Eastern states & Asia...& also in African countries...
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3353626/table/T3/

Intersted people may also check the following articles (or simply search Google)

To Provide Phenotype-Matched Red Blood Cells or Not – That is the Question!

13.3: Pre-transfusion testing- Joint United Kingdom (UK) Blood Transfusion and Tissue Transplantation Services Professional Advisory Committee

& for a complete picture plz browse through- Immunohaematology


What is titratable acid? Why is ammonium not titratable acid?

Titratable acidity is a total amount of acid in the solution as determined by the titration using a standard solution of sodium hydroxide (titrant). In other words, it is the maximal capacity of the solution to "neutralise" base solution.

H$^+$ produced from CO$_2$ and H$_2$O is actively transported into the distal tubular lumen.
Titratable acidity is the amount of the H+ which is buffered by bases present in the tubular lumen. Mostly by phosphate (the highest concentration).

When the urinary pH change other molecules can gain the ability to buffer H$^+$.  For example creatinine (pKa about 5.0) or ketoacids (pKa about 4.8)  may contribute to the titratable acidity.

Standard measurement of the titratable acidity with the standard solution of sodium hydroxide spans pH range up to 7.4. Therefore:

  Ammonium is not measured as part of the titratable acidity because the high pK of ammonium means no H$^+$ is removed from NH4$^+$ during titration to a pH of 7.4.

Source


What dinosaurs live during cretaceous period?

Wikipedia has a nice summary: https://en.wikipedia.org/wiki/Category:Cretaceous_dinosaurs


What's the exact species of this African Giant Snail?

I am not sure how to handle this.
The answer is the content of this page, which (I guess) should not be entirely copy / pasted here for copyright reasons.
So based on the texture of the skin, you have a variety of Achatina.
If I receive advice about how to make this answer comply more with the rules of the site, I will edit my answer.


Which DNA polymerase can use a nick as priming site?

It sounds like you are looking for a DNA polymerase that can perform nick translation. NEB maintains a chart listing the properties of their polymerases, including nick translation and extension from nick.  Without additional details, it looks like Taq would work for your purpose.