Search engine for biological/medical/epidemiological science literature I hope this question is appropriate for this exchange (I think it is too specific for meta?).

We are looking for a search engine that is capable of performing a search of all available biological/medical/epidemiological scientific literature (So more on the scope of Google than Elsevier or similar subscription services) and providing as many as possible of the following features:

Keyword search
Range of dates
Boolean terms (AND NOT etc.)
Option to download and sort
Email alerts.

Does anyone know of a search engine or service that has these capabilities? (A paid subscription is fine).

Thank you in advance for your patience.

Yes, this exists. The portal is called "Pubmed" and looks like this:

This portal allows you to search (have a look into the search-Faq) in various ways as well as getting email alerts, download your searches in different formats and so on. It indexes most (but not all) scientific literature for medicine, biosciences and all related topics and is probably the biggest database in this field. And its free.

Another possibility would be Google Scholar, which is focussed on scientific literature and can also be adapted to your personal needs. However, I usually prefer using Pubmed, but sometimes it is useful as well to use Google Scholar.


How is ATP converted to adenosine? I am familiar with adenosine diphosphate (ADP) and adenosine triphosphate (ATP), how one relates to the other, and how each is formed in cellular respiration and photosynthesis, but I am confused as to how regular adenosine is formed.

I was reading an article on caffeine which stated:

  Caffeine is structurally similar to adenosine, a neuromodulator, whose formation is dependent on the relative rates of ATP breakdown and synthesis.

From this I concluded that ATP can be changed to regular adenosine, and adenosine back to ATP, but I cannot find anything else on the internet to support my conclusion. I was also wondering when and why your body would change ADP into adenosine instead of ATP. I assume that AMP plays a role in all of this, and possibly ADA.

I only have a high school level education in biology, so please bear with me. If you do not mind, please include a source in your answer so I can further research on my own. Thanks!

For a full understanding I refer you to the KEGG pathway map which is fairly comprehensive in showing all the metabolic processes that CAN produce Adenosine.
It's a bit daunting but if you find it on the map here it is interactive and you can see the enzymes and pathways involved. If you drill down it brings you to a host of papers and references in primary literature to back things up.

However the dominant process is as follows:

   2 ADP <=> ATP + AMP

enacted by an adenylate kinase then:

   AMP + H2O <=> Adenosine + phosphate

enacted by adenosine 5'-monophosphate phosphohydrolase (a 5'-Nucleotidases )


Can Dpn1 digest hybrid PCR product with only one methylated strand? In Site directed mutagenesis using PCR, after a cycle we obtain a hybrid molecule with one parental strand and other newly synthesized unmethylated strand. This is followed by Dpn1 digestion. Does this digestion just cut the parental strand leaving behind single strand of newly synthesized product?
Does this means that Dpn1 can use ds methylated DNA( both strands methylated) as well as ds hybrid DNA (with one methylated strand and other unmethylated strand) as substrate?

According to the NEB website FAQ, yes, it can, but less efficiently.

"DpnI cleaves hemi-methylated dam sites 60X more slowly than fully methylated."


What's the name of this bug? A friend of mine found this bug in Germany. He sent the picture and asked if anyone knew what kind of bug it is. Since no one knew and I didn't find anything similar via google search, I decided to ask it here. Since he only sent me the image I can't really give good information regarding size.
So can anyone identify what type of bug this is?

It looks like it's the other way around to me. More likely a member of Auchenorrhyncha, which includes cicadas and leafhoppers. I say this judging from the leg structure, abdomen shape, and the eyes. It is however missing wings... perhaps they were removed by another organism?

It somewhat looks like Philaenus spumarius, the "meadow froghopper" which is found in Germany. As for the green tail bit, I am not all that sure.


Do camels pose an environmental threat to kangaroos? Camels, once used for transport across the Australian outback, were set free, and are reproducing at an uncontrolled rate in the empty interior of Australia.

Do the ecosystems of camels and kangaroos overlap?

Are camels competing with kangaroos for what little vegetation there is, and if so, what is the impact on kangaroo demography?

Feral camels have environmental, economic and cultural impacts in Australia's Northern Territory (Dept of Land Resource Management, Australia).

In central Australia, camels feed on more than 80% of the available plant species. Feral camels severely defoliate and suppress the recruitment of some shrub and tree species, with such impacts being greatly exacerbated in drier years (Dept of Land Resource Management).

Feral camels have a noticeable impact on fragile salt lake ecosystems and waterholes, which are important sites for Aboriginal people and for native fauna (Dept of Land Resource Management).

However, its impact on kangaroos may be the last of our worries. There are other, typically smaller, marsupials that cover the endangered species list in the NT, including the Western quoll, bandicoots and wallabies (Dept of Land Resource Management). Kangaroos thrive in the agricultural farmlands that now dot the nation.


Mating patterns and genetic superiority In peacocks and peahens, the peahens prefer mating with peacocks having a large and bright tail. But how is having a large tail an indicator of genetic "fitness" (in survival terms) ? If having a large and bright tail is not related with genetic superiority, then what is the point of having the mating ritual?

Darwin thought quite a bit about this. He even said "The sight of a peacock makes me sick". https://www.ncbi.nlm.nih.gov/pubmed/10824193
He added to his ideas about natural selection to include sexual selection. Traits selected by females, even when they are non-adaptive for males, will increase the males fitness (as defined by his number of offspring). There is also the idea that perhaps possessing such an outrageous and non-adaptive tail proves that you a good mate, the same way we would think that a guy who could win a sprint while carrying barbells must be superior.


Can neurotransmitter depletion cause short-term drug tolerance? I'm curious to know if neurotransmitter degradation factors into drug tolerance and neural conduction and, if so, to what extent. As I recall from textbooks I read as an undergrad, one mechanism of drug tolerance works by increasing the necessary thresh-hold at a synapse such that larger concentrations of neurotransmitter or more-frequent action potentials in the upstream axon were required to depolarize the membrane and propagate the signal. It seems to me that the same effect would occur if there were fewer available molecules of the required neurotransmitter.

Does over-stimulation of a neural pathway (through the use of a drug or other stimuli that up-regulates a given neurotransmitter) shorten the half-life of the neurotransmitters it uses?

Could a diet which is poor for necessary precursor nutrients cause a person's neurotransmitter concentrations to drop and reduce signaling along specific neural pathways?

Could lack of sleep or other physiological stressors have a similar effect?

I am not a neuroscientist so please correct (and forgive) me if I'm using any terms incorrectly or am flat-out wrong in any of my assumptions.

As I recall from textbooks I read as an undergrad, one mechanism of drug tolerance works by increasing the necessary thresh-hold at a synapse such that larger concentrations of neurotransmitter or more-frequent action potentials in the upstream axon were required to depolarize the membrane and propagate the signal.

Yes - usually through a reduced expression of receptors on the surface. Increasing the drug dosage merely increases the probability that one of the molecules will find the receptor. Chronic exposure of increasingly large doses can dramatically reduce receptor expression. In time, sans the drug, the receptor count will climb back up.

This is why a common cause of chronic drug addicts who have just gone through rehab is overdose: After months in rehab or free of a drug they immediately go back to the amount of drug they were doing before rehab - with some severe side-effects at the least, death at the worst.

  Does over-stimulation of a neural pathway (through the use of a drug or other stimuli that up-regulates a given neurotransmitter) shorten the half-life of the neurotransmitters it uses?

No. The half-life of a neurotransmitters is not a major concern; your body will construct them from stored resources if necessary, and healthy neurons have a significant store of neurotransmitters to prepare for multiple firings.

A neuron can be artificially over-stimulated and the neurotransmitter pool emptied (or all the neurotransmitters is bound to its receptor) - but only for Ach receptors at neuromuscular junctions. It hasn't been observed naturally, and not for other types of synapses. This does not result in the muscle no longer responding, but rather it will not respond any faster.

  Could a diet which is poor for necessary precursor nutrients cause a person's neurotransmitter concentrations to drop and reduce signaling along specific neural pathways?

Yes, but by that point you're not in good shape, if not courting death. Neurotransmitters are either very common in the diet - like ions - or are constructed from very common constituents of a normal diet - like Glutamine, the most common amino acid.

It would not be a therapy to treat drug addiction.

  Could lack of sleep or other physiological stressors have a similar effect?

You would die of lack of sleep first. Your body generally keeps a 30 day supply of absolutely essential vitamins and minerals, and will easily digest itself for precursors to construct neurotransmitters out of.

I have not heard of any physical or mental stress which has reduced the amount of neurotransmitters released into the synapse beyond absolute starvation or artificial scarcity.


Is it possible to grow E. coli K12 with algal amino acids as the sole carbon source? Instead of glucose or glycerol, is it possible for E coli to grow on an amino acid mixture as the sole carbon source and, if so, what should the concentration be?

E.coli can do that and in fact does this a lot in a commonly used bacterial medium: The popular LB Medium. This is composed of three components:

Tryptone, a peptide mix made by digesting milk casein with the peptidase Trypsin (10g/l)
Yeast extract, made by autolysis of the cells (5g/l)
Sodium chloride (10g/l)

The original formulation of Bertani from 1951 (see reference 1) also contains 1g/l Glucose, which was later discarded, since the handling is easier without it (glucose cannot be autoclaved as it degrades).

Since the medium does not contain any other utilizable sugars as a carbon source, the bacteria use free amino acids (and small peptides up to 650 Da in size) for their growth. The reason for this limit is the exclusion size of the bacterial porin channels which allows the uptake of the peptides and free amino acids (see reference 2 for details).

Once these are exhausted, the growth stops, which is the reason why LB Medium is actually not very good suited to get really high densities (that's why SOC media are used for some applications). Read the excellent paper in reference 3 and the also excellent article in reference 4 if you want to know more about the topic.

I don't think it matters from which source your amino acids are coming. Regarding the concentration I haven't found any data, but in reference 4 it is estimated that only about 25% can be used by the bacteria. Since the mixture contains about 15 grams of protein lysate, this would roughly mean about 4 grams of free amino acids or more.

References:

Studies on Lysogenesis I.
Size Restriction on Peptide Utilization in Escherichia coli
Escherichia coli Physiology in Luria-Bertani Broth
The Limitations of LB Medium


Do different chiral centers on ligands cause different confirmational changes and effects in their target proteins? Say pathogenic bacteriaA makes toxinA, which had D-amino acids instead of L-amino aids, does this difference in chirality cause a different conformational change in the receptor or enzyme, thus leading to either deactivation of the enzyme or signal transduction pathway or activation of a different pathway?

I understand what chirality is in the concept of organic chemistry — rotating plane polarized light, ingold-prelog system etc; however I never leaned what structural feature of chiral molecules changes the way they react inside a cell.

I do NOT understand HOW changes in chirality can be associated with cellular toxicity.

links:
https://www.ncbi.nlm.nih.gov/pubmed/24752840

http://www.jomb.org/uploadfile/2014/0113/20140113053743849.pdf

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3960212/

There a few things you have to take care of with chirality in biological systems:

First note, that for amino acids we usually use L and D instead of r and s nomencalture.

In chemistry the difference between chiral enantionemeres is usually really just a difference in light polarisation like you described, otherwise they can be thought of as identical, since they have identical chemical properties. This way of thinking does not apply to biochemistry - the moment enzymes (large molecules with very defined 3D structures) are involved the structural difference between the two forms becomes very important for each and every biological reaction.

In the case of single amino acids this means that D amino acids are toxic to eukaryotic cells, because their similarity to the D form allows them to interact with some of the enzymes that usually bind it, but the binding is not a perfect match so the enzymes get inhibited, which makes the D form toxic. (This is already described in the second paper you linked:)

  In animal studies, administration of D-amino acids to rats and chicks resulted in growth inhibition [18]. In addition, serious damages such as suppression of the synthesis of glutamate oxaloacetate transaminase, glutamic pyruvic transaminase, and lactate dehydrogenase resulted from D-amino acids accumulation in animal tissues [18].

Now in your question you are asking about the difference between a toxin made from the 'wrong' amino acid. The thing is, this change of the protein will most likely mean, that its not a toxin anymore. A protein toxin is toxic because it can interact with other proteins, based on its 3D structure. This structure is based on the chemical and structural properties of the amino acids building it. If you change the underlying structure of every amino acid it will fold differently and you will get completely different protein - and not a mirrored version of the original protein/toxin.


Difference between "transcriptional activity" and "RNA expression" I am working with a network object where the nodes are different events in molecular biology.

Specifically;
Catalytic activity of X,
RNA expression of X,
GTP-bound activity of X,
Kinase activity of X,
Oxidoreductase activity of X,
Phosphatase axtivity of X,
Transcriptional activity of X,
Phosphorylation at residue Y.

What is the difference between RNA expression and Transcriptional activity? And which is the one that an Affymetrix microarray is measuring?
eg.;
transcriptional activity of KLF2, transcriptional activity of ATF2 RNA expression of HSPA1A RNA, and expression of CYP1B1

In your case, RNA expression and transcriptional activity probably differ in the stage of processing. Transcriptional activity refers to the binding and processive activity of RNA polymerase. There are different ways to measure this experimentally, but with a microarray you are measuring the amount of actual transcripts relative to the control array.

RNA expression usually refers to the amount of mature transcripts but is often used interchangeably with transcriptional activity. The distinction is made at the sample extraction stage and whether or not the RNA was selectively recovered using poly-A selection or other methods that isolate mature transcripts.

What your microarray will measure depends on the probe library constructed on the array and whether you are applying total RNA or selective RNA. Probes matching mature transcripts report for RNA expression. Probes matching immature or nascent transcripts can be used to measure transcriptional activity.

Careful probe design is required to distinguish between the different levels of processing.


How do muscle relaxants work? Do they act directly on the muscle and actually relax muscle tissue and ease spasms, or do they just prevent your brain from receiving signals that inform you of tight muscles?

In the latter case, it seems like your brain would sort of become "immune" to the pain even though the muscle is still in a spasm.

I'm obviously not a biologist, just curious about this.

How do muscle relaxants work?

Check out the muscle relaxant article on Wikipedia, it's pretty straight forward.  In short, there are two main types: Neuromuscular blockers, than act at the junction between the neuron and the muscle; and spasmolytics/antispasmodics, which (mainly) act on the central nervous system to reduce excitation or increase inhibition.  Most of the ones I've heard of, such as diazepam, are in the latter category.


What is the lowest common denominator of cancer? What is the lowest level attribute that all cancers share? Also, what is the highest level attributes that all cancers share?

Hanahan and Weinberg's "Hallmarks of Cancer" articles should answer your question.

Their original, highly cited (14k+ citations), [Six] Hallmarks of Cancer article list these six common attributes of all cancers:

Sustaining proliferative signaling
Evading growth suppressors
Activating invasion and metastasis
Enabling replicative immortality
Inducing angiogenesis
Resisting cell death

The new article, Hallmarks of Cancer: The Next Generation includes additional "emerging hallmarks" and "enabling characteristics" (Figure 3) common among cancers:

The capability to modify, or reprogram, cellular metabolism in order to most effectively support neoplastic proliferation; and
The ability to evade immunological destruction, in particular by T and B lymphocytes, macrophages, and natural killer cells.


Are we evolving as fast as the oxygen is depleting? How much oxygen saturation have we lost in the last 100 years? As oxygen levels dwindle and industry, deforestation,  and population increases, at what year and saturation will the low levels of oxygen become a problem in human development? Would living or sleeping with higher levels of oxygen increase cognitive or physical ability?

Good estimates from ice core samples put the decrease in oxygen concentration at 0.7% over the last 800,000 years. At sea level, currently, inspired $P_{O2}$ is (760 mm Hg - 47) * 0.21, approximately 150mm Hg. Human physiology easily adapts to lower $P_{O2}$ levels, with approximately 140 million people living at elevations over 2500 m, with inspired $P_{O2}$ at 108mm Hg, and many permanent human settlements higher than 5000 m, with inspired $P_{O2}$ approximately half what it is at sea level (see West Respiratory Physiology, Ch. 9). A 0.7% decline over 800,000 years isn't going to be much of a challenge.


What is the datatype of dna sample? What is the type of data you get when analyzing dna of a person? If you want to store them in a database, what type of field you will need (text,number,hex)? And what should be it's length?

Assuming that you are looking at data used to describe the differences for a new individual, as opposed to a human reference genome build:

A fastq file is the typical format of data from a sequencer.

It would require a text field of some sort as they can be quite large, even for single reads.  If you had a specific sequencer in mind with very short read you might use a fixed length field for the data column, but its probably not worth it.

After the data is processed, then the data is currently usually exchanged in the form of Variant Call Format files (a vcf file) which only documents differences versus a reference genome build.  This fits nicely into an SQL table with relatively small columns.


What advantage does lactose have as the main sugar in milk? Most organisms have lactose as their main sugar in their milk.

What advantage does lactose give have over sucrose (Which is a common sugar in the plants, so it makes sense for it to be present in milk)

Is lactose synthesis easy? Or is the enzyme B-galactosidase easy to make?

Or is it more easily digestible, allowing mammalian infants to get energy faster?

Yes it is thought to provide safer milk, less vulnerable to every bacteria that respires and multiplies on sucrose, and which lets the baby grow faster due to higher sugar content.

Milk has evolved from pouch mucus, antimicrobal secretions of the immune system, Lysozyme in mucus is a glycoside hydrolase which ruptures bacteria cell walls. So the origins of milk are very different than for plants.

Lactose is a larger molecule than sucrose, so it exerts less osmotic effect per unit mass, allowing more carbohydrate to be included in am isosmotic secretion such as milk.

for example:
marsupials have mostly longer oligosaccharides and their milk contains 11-14% sugar,
zebras and and horses with only lactose achieve 7%
humans and other primates achieve 8-9% using milk and polysaccharides.

Another advantage is that it's a molecule rarely produced in nature, and fewer bacteria have evolved the enzymes required to digest it, upgrading the lac-operon to produce galactose-permease, save for beneficial lactobacilli, e-coli, and other mostly mutualist species.

full text.

It is thought that milk evolved from secretory glands in the synapsid egg pouch which helped to protect parchment eggs, with moisture and antimicrobial secretions. In fact, lactose is thought to have come from mucus sugars, which are used to encapsulate and neutralize microbes in the body, "Because α-lactalbumin evolved from lysozyme before the division of amniotes into synapsids and sauropsids (see Figure Figure1),1), the capacity to produce lactose was an ancient trait that preceded its utility in milk synthesis"

Intro to synapsid and sauropsid precursors of lactose.


Why do drugs which are hormones have long half-life? Hormones normally have short half-life.

How is it possible that they have long-life in drugs?

The question is a bit vague, but in general a drug formulation is made of the active principle plus a series of other non-active compounds call excipients.

Excipients have multiple roles such as:

They act as fillers to add volume to the drug. Often only very small amounts of the active compound are present in each pill/capsule/etc. and it would be complicated for the patient to handle these very small amounts.
They act as binders to keep everything together and avoid the pill to crumble.
They can modify the pharmacokinetics of the active principle by speeding up or slowing down its release.

(there are many more resons to add excipients, see the relevant Wikipedia page for a longer list)

This last point is what you are looking for. If the hormone (or any other molecule, it doesn't really matter) is complexed with excipients it will be released in the blood or metabolized slower/faster depending on the specific molecules/formulations/mode of administration.


A mutation question from the Indian National Biology Olympiad DNA was isolated from wild type (Gal+) and mutant (Gal-) E. coli cells and separated by density gradient centrifugation technique. DNA from Gal- strain acquired a lower position. This indicates that the mutation is caused by:
(a) deletion (b) insertion (c) mis-sense mutation (d) point mutation

Me and my friends had an extended discussion on this question and we all agreed that since the Gal- strain acquired a lower position, it was obviously more dense than Gal+ strain. Now, one of them claimed that if the volume were to remain constant, then mass is directly proportional to density hence the insertion mutation should cause increase in mass corresponding to a similar increase in density. I am not convinced by this explanation. They also said that, "Keeping the volume constant is a necessity since the experiment would lose its meaning otherwise". I am curious to know how far these assertions are correct.
After doing some research on this topic on the internet, I found a paper related to this question :
Mutations caused by the insertion of genetic material into the galactose operon of Escherichia coli
The answer given by the organizing committee of the 2nd Indian National Biology Olympiad was (b) insertion.
What could be the possible explanation for such an occurrence? Me and my friends are still unable to grasp the logic behind it even after going through different papers and books.

Now, one of them claimed that if the volume were to remain constant,
then mass is directly proportional to density hence the insertion
mutation should cause increase in mass corresponding to a similar
increase in density.

I don't think that's quite how it works.  You don't worry about the volumes being used.  In those experiments (I don't know that anyone does them anymore)  the DNA is in a solution of really salty water.  Larger molecules get pushed more to the bottom of the tube, so the mutant DNA is larger, since it was close to the bottom.
https://embryo.asu.edu/pages/equilibrium-density-gradient-centrifugation-cesium-chloride-solutions-developed-matthew#:~:text=Density%20gradient%20centrifugation%20enables%20scientists,molecules%20based%20on%20density%20alone.

Thus, centrifugal force pushes the larger components of a mixture
farther from the rotor and closer to the bottom of the tube.

Larger DNA means an insertion.  Point mutations are not detectable with this method.


Can the regeneration mechanism of lizards be used in humans? Is there any mechanism or specific protein which helps lizards to regrow their tail? Can the mechanism of regeneration be used in humans to regenerate our limbs? Is there any other animal which has this kind of ability?

Actually there are some studies to find out your answer. Some of the studies claim that they have found a special enzyme and some say micro RNAs give salamanders the capacity of regeneration. But until now, humans couldn't use salamander's regenerative ability. Maybe you would like to know there is a mammal (african spiny mouse) with special regenerative capacities which include regeneration of its skin and cartilage without scarring.

References:

'Skin shedding and tissue regeneration in African spiny mice (Acomys)' Ashley W. Seifert,   Stephen G. Kiama,   Megan G. Seifert, Jacob R. Goheen, Todd M. Palmer & Malcolm Maden
Microarray analysis of microRNA expression during axolotl limb regeneration.
For further studies I recommend searching "salamander and regeneration", "african spiny mouse and regeneration" in pubmed ;)


Organelles present in sieve tubes I know that sieve tubes do not have ribosomes, nuclei and cytoskeletal elements.
What other organelles does it not have? Does it have a cytoplasm?

The sieve tubes of the phloem in angiosperms consist of sieve tube elements or members. These are cells which lose their nucleus, ribosomes, and vacuoles at maturity.  They of course have cytoplasm, and it is connected by channels to companion cells (which do have these organelles).  The sieve tube elements retain mitochondria and plastids. See the Wikipedia page and this page for more details.


What is the brain's preferred energy source? Glucose or ketones? As with all cells in our body, I know that the brain can get fed from both glucose and ketones, so my question is, given both of them, which one would the brain prefer to utilize first?

First of all, for those readers with less knowledge of the general principles of biology, I want to state an important, even if obvious, point: The brain doesn't
"prefer" anything. Despite being the smartest organ in the body, it is subjected (like any other biological system) to changes in the concentrations of the substances in question, that is, glucose and ketone bodies.
According to a study in rats from 2010, it seems that ketone bodies suppress glucose metabolism in order to conserve glucose when its concentration is too low for the body to be used regularly. Therefore, the ketone bodies are regarded as neuroprotective, since their metabolism prevents the brain cells from starving.
Another study in rats from 2013 emphasizes this point further. Please note the following excerpt from the discussion section:
The brain's ability to switch from glucose oxidation towards ketone bodies requires a type of ‘cerebral metabolic adaptation'. This process is not well understood but is thought to be highly associated with the duration and level of ketosis. Ketones are considered to supply up to 70% of the total energy demands once maximal metabolic adaptation occurs. Blood ketones become elevated during prolonged fasting or with a ketogenic diet reaching a state [of] ketosis and glucose sparing. During this process, monoca[r]boxylic transporters upregulate at the blood–brain barrier with increasing demand for ketone utilization by brain. Recently, investigators have recognized additional therapeutic properties of ketosis, such as neuroprotection after stroke or injury. What remains unclear is whether the neuroprotective or therapeutic properties of ketosis is as a result of changes in the regulation of metabolic signaling pathways...
This means that when the balance of concentrations shifts toward the ketone bodies, they will have precedence over glucose in order to conserve the latter. The mechanism is probably upregulation of ketone bodies receptors and transporters that increase its transport into the brain, as stated above.
Therefore, when the brain is given both ketone bodies and glucose (which actually happens in the fasted state - ketone bodies transport and metabolism in the brain begins when blood glucose is low, not zero), there will be "preference" for the ketone bodies, but this depends on the glucose concentration. If it shifts back, above a certain glucose concentration glucose metabolism is supposed to be renewed.


Insect identification: white spotted beetle 3 pairs of legs, a pair of antenna, wings absent, compound eye, 4-6 centimeter approx. in size.
I found this beetle at my door, in Pune, India.

It is a longhorn beetle (Cerambycidae), most certainly from the subfamily Lamiinae (flat-faced longhorns). The overall apparence with a downward-pointing face, partially divided eyes, robust build and spined pronotum fits well with Lamiinae.
The beetle in you picture is very similar to species in the genus
Batocera, for instance Batocera rufomaculata (also called Mango trunk/stem borer), and the red spots on the elytra fit relatively well. This species is considered a pest on mango plantations in India and Nepal (Hill, 2008 and Insects in Indian Agrosystems), so it's probably not all that uncommon.

(picture from Insects in Indian Agrosystems, from the National Bureau of Agricultural Insect Resources.)
However, there are probably hundreds of species in Lamiinae found in India, and I cannot give you a certain answer.
The striped elytra with raised lines doesn't fit with the species I've seen in Monochamus (suggested in the other answers), so I don't think that is the correct genus.
References:

Hill. 2008. Pests of Crops in Warmer Climates and Their Control


Is there a genetic reason explaining the difference of the height of male and female? The male and female height difference seems to be around 1.08 if all cultures are counted from these stats: https://en.wikipedia.org/wiki/Human_height

Can this ratio, 27/25, be explained by genetics and is there any research to explain how genes affect the growth of a man and woman? I assume there are a lot of factors that affect height and it might be very difficult to say if environmental and selective reasons or genetics are behind this factor.

ADDED:

GIANT study reveals a giant number of genes linked to height (October 6th, 2014)

  “Height is almost completely determined by genetics, but our earlier studies were only able to explain about 10 percent of this genetic influence.”

https://www.broadinstitute.org/news/6119

Short answer:

There is strong evidence that height is a heritable trait with a strong genetic component. The genetic mechanism could be higher expression of an X-chromosome gene that, expressed in high levels, inhibits cartilage development, perhaps causing lower height. The increased expression seems to be caused by incomplete X inactivation in females. Furthermore, there is differential selection for height between human males and females likely causing the differences we see in modern human populations.

Long Answer:

Genetic basis of height

The genetic variants analysed by Wood et al. (2014) account for ~29% of the phenotypic variance and 60% of the heritability of height.

Due to this high heritabilty (and the fact that there are still expected to be more unknown variants affecting height) there most likely is a genetic reason explaining the difference of height in human males and females. Thinking about the nature of this difference is a bit difficult. It is good to know that the trait has a high heritability and therefore a strong genetic component as this allows us to have a look at how natural selection affects height.

Selection on height

Height is a polygenic trait that is under recent and strong natural selection (Field et al., 2016 - preprint) leading to height increase in both human males and females (Fig. 3D in Field et al. (2016)):

What does this tell us in terms of the genetics underlying the height differences in human males and females? First, we have to understand that natural selection (at least mainly) affects individuals, not species. Then, we can understand that natural selection can affect males and females of a species differently. And Field et al. (2016) have shown exactly that for height. In their analyses, you can see that male and female height show (mildly) differing signals of natural selection (Fig. 4C in Field et al. (2016)):

But selection needs heritable genetic variation that allows this differentiation between the sexes. So what is the mechanism?

Genetic mechanism of height differences between human males and females

As pointed out by @tsttst in the comment differences between sexes are usually caused by genes on the X and Y allosomes. There is evidence that the height differences between human males and females are related to the X-chromosome (which also explains some of the missing heritability of the GWAS study by Wood et al. (2014)), reported by Tukiainen et al. (2014). They write

  In one of these three associated regions, the region near ITM2A, we observed that there is a sex difference in the genetic effects on height in a manner consistent with a lack of dosage compensation in this locus. Further supporting this observation, ITM2A has been shown to be among those chrX genes where the X chromosome inactivation is incomplete.

They also give a molecular mechanism how this hypothesised increased expression of ITM2A can cause the height difference. They report that the ITM2A gene is
involved in cartilage development (van den Plas et al., 2004) and that the height-associated ITM2A variants change expression of the ITM2A protein. This is interesting as increased ITM2A expression in mesenchymal stem cells of adipose tissue seems to inhibit cartilage development (Boeuf et al., 2009). Tukiainen et al. (2014) conclude:

  As the allele associated with shorter stature associated with increased expression of ITM2A (sic), this suggests the allelic effect to height could be mediated through the capacity to generate cartilage and bone.

Finally, how can this be interpreted from an evolutionary point of view?

Evolutionary interpretation of height differences in human males and females

Differences in height (but also other traits) between sexes of a species are refered to as sexual dimorphisms. Sexual dimorphism (at least in primates) in height is strongly related to differences in mating behaviour and a sign of aggression and/or dominance-based mating patterns (Wynn and Coolidge (2011, p.82), sorry for that poor referenc link). The counterpart to this is pair-bonding, or in human terms marriage: a primate example is our pretty close relative, the Gibbon, that is (at least socially) monogamous and as expected does not have a height-related sexual dimorphism. Great apes including humans do have this polymorphism even though pair-bonding in humans is widely spread. Therefore, it was not surprising to find a reduction in height dimorphism from Australopithecus over Homo erectus to Homo sapiens (Wynn and Coolidge, 2011, p. 83, see also this, especially the last paragraph of this chapter).

Update on the main source

One of the papers I mainly used for this answer - to illustrate selection on height - was a preprint. It is now published in Science: Field et al. (2016).


Do we vaccinate sick people? As I understand, vaccination helps the human body to create antibodies and stimulate immune system to react against specific antigens. If someone gets sick, do vaccines help to stimulate immune system? If so, do we vaccine sick people for some specific disease?

Yes. Sick people are occasionally administered vaccines. But you need to keep in mind the mechanism of action of vaccines.

Broadly speaking, there are two types of vaccines.

Active immunization works by exposing the immune system of an individual with a pathogen (be it organism or derived proteins, etc). This type of immunization results in development of adaptive immunity in the individual, with long lasting effect; but it can days or weeks to fully develop.

On the contrary, passive immunization works by directly administering protective agents (antibody, etc). This will provide the individual with almost immediate protection; but will not lead to development of adaptive immunity, and thus will be short-lived.

You may find this wikipedia article informative.


What are these tiny dark red insects? I found these creatures stuck to a leaf on my tomato plant in the greenhouse/glasshouse, in early June, in south Oxfordshire in the United Kingdom.

They are each about 1-2mm in size. They didn't move much, even when gently nudged, although some did crawl tentatively.

I would be very interested to know what these are, especially if they are a beneficial species or a pest!

These little creatures look a lot like White-margined Burrowing Bug or Sehirus cinctus nymphs.

Very interesting thing about the Sehirus cinctus is their brooding behavior. The female watches the eggs and even feeds the young for a few days. Have a look around. You might see it.

AFAIK they don't harm your plants.

More info:
http://polyploid.net/bugs/bugs.html
https://en.wikipedia.org/wiki/Sehirus_cinctus


How does cholesterol affect the fluidity of a plasma membrane? I was previously taught that cholesterol affects the fluidity of a plasma membrane. At high temperatures, cholesterol decreases fluidity and at low temperatures cholesterol increases fluidity. The Khan academy and Wikipedia pages below say the same thing.

https://www.khanacademy.org/video/cell-membrane-fluidity
 https://www.wikiwand.com/en/Membrane_fluidity

Yet, in a current college course, the textbook ("Molecular Biology of the Cell 6th" by Bruce Alberts et al.) says that cholesterol reduces the mobility of the first few CH2 groups of a phospholipid's two fatty acid chains. In this way, the cholesterol makes the lipid bilayer more rigid and decreases the lipid bilayer's permeability to small, water-soluble molecules. However, it says that cholestrol does not actually make the membrane less fluid.

Is the textbook from my current course just a more nuanced explanation, or have I misunderstood something else?

Cholesterol certainly affects plasma membrane fluidity. In 1978 Cooper found that increasing the ratio of cholesterol to phospholipids decreased the membrane fluidity. This also reduces membrane permeability and reduces the survival of the cells (red blood cells in that case). I imagine this is where the textbooks draw their conclusions.

More recently Rog et al., 2008 demonstrated the importance of the hydroxyl group in the cholesterol by replacing it with a ketone. This affected fluidity and flip flop rate.


How are chromosomes counted at the end of mitosis in a plant cell? Page 89 of the Study Guide for Campbell Biology, 11th Edition has the following question:

  A plant cell has 12 chromosomes at the end of mitosis. How many chromosomes would it have in the G2 phase of its next cell cycle?

  a. 6

  b. 12

  c. 24

  d. 48

Page 449 states that the answer is b.

As far as I understand, the number of chromosomes a cell has in G2 phase is double the number of chromosomes as it has after mitosis (which would imply the answer is c).

For (b) to be true, the plant cell must have had 6 chromosomes at the end of mitosis, but the question states it had 12. The only way I can imagine this to be true is that the question assumes that "a plant cell [...] at the end of mitosis" represents both daughter plant cells before the cell plate & cell wall has fully split the two daughter cells up, but doesn't "the end of mitosis" imply that the cell wall has completely formed and there are two cells (each with 12 chromosomes)?

I think I know what is confusing you.
A chromosome can have one or two chromatids. If you have two chromatids, you don't necessarily have two chromosomes. This is what happens during S-phase, during replication. Before the S-phase each chromosome had one chromatid, after the replication, it has two. So the number of chromosomes stays the same.

In the karyogram (the picture with all chromosomes), each object is one chromosome. Usually those will be double-chromatid chromosomes, and you will see a nick (like here). After these chromosomes divide, you get two separate objects → two identical chromosomes.


Beginning of the urogenital system Are any invertebrate nephridia (proto/meta) homologous with vertebrate kidneys in the sense that embryologically they also begin together with the genital system?  When did the embryologic association between reproduction and osmoregulartion/metabolite elimination begin in terms of evolution?

The urogenital system as a cohesive functional unit probably evolved very early in vertebrate history. Hagfishes and lampreys have separate systems for reproduction and excretion. More derived groups of fishes use kidney tubules and ducts for sperm delivery outside the body (Helfman et al. 2009).

The vertebrate nephron may be homologous to the invertebrate nephridia (Ruppert 1994). The genetics underlying the development of vertebrate female reproductive organs shows many homologies with invertebrate reproductive organs (Kobayashi and Behringer 2003)

I would hypothesize that the both the reproductive and extrectory systems of vertebrates show corresponding homologies to invertebrate organ systems (at least genetic and developmental homologies) but evolution of the urogenital organ system did not evolve until the early vertebrates.

Literature Cited

Helfman, G.S. et al. 2009. The Diversity of Fishes. Biology, Evolution and Ecology. Wiley-Blackwell, Oxford, UK.

Kobayashi, A. ad R.R. Behringer. 2003. Developmental genetics of the female reproductive tract in mammals. Nature Reviews Genetics 4: 969-980.

Ruppert, E.E. 1994. Evolutionary origin of the vertebrate nephron. American Zoologist 34: 542-553.


How long is one generation for a mosquito? For instance, humans are said to have an average generation time of 20 years. I've heard that mosquitos go through 10 generations in a year. Is that information correct?

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


Which Enzymes are Responsible for the Biodegradation of Noladin Ether? Which enzymes degrade the CB1-specific endogenous cannabinoid 2-arachidonyl glyceryl ether? (Noladin ether)

Noladin is an endocannabinoid. The best-characterised members of this family of molecules are Arachidonoylethanolamine (AEA; anandamide) and 2-arachidonoylglycerol (2-AG). The degradation of these endocannabinoids is reviewed in:

  Pamplona, FA et al. (2012) Psychopharmacology of the endocannabinoids: far beyond anandamide. Journal of Psychopharmacology 26:7-22

These endocannabinoids are inactivated via a reuptake system that is present in both neuronal and glial cells, although the protein responsible has apparently not been identified.

AEA is then metabolised to arachidonic acid and ethanolamine by fatty acid amide hydrolase, while 2-AG is converted to arachidonic acid and glycerol by monoacylglycerol lipase.

Because of its ether linkage, noladin cannot be a substrate for either of these enzymes. However the review also describes other possible pathways of endocannabinoid metabolism involving oxidation by cyclooxygenases, lipoxygenases and P450 cytochromes. These are the best candidates for the further metabolism of noladin, but there is apparently no direct evidence for this.


Genetic analysis of one sibling relevant to other My sister, my only sibling and I have literally no physical traits in common. Whatever trait I inherited from one parent she inherited from the other. We're thinking of using one of those genome analysis services to learn information about our mysterious geographical ancestral origins.

We're wondering if, despite our differences in appearance, if only one of us submitted our genome for analysis, the geographic origin results would still be accurate for the other. Because our parents may both have diverse lineages, the answer might not be so cut and dried.

Understand, please, that we are not so much looking to find out the general "where" of our origins as we are to have each of us know what our individual genetic heritage is.

If you are siblings, then, outside the Y chromosome (if you are a man, otherwise, you both only have X chromosomes), the results should be very similar. There might be some slight variations of course but it is unlikely to come out as important.

If you are not siblings (e.g. you might be half-sibling if your mother is hiding an affair; sorry for suggesting this possibility but that's no so unusual), then the results might well be quite different.


What is the body density of insects on average? What is the body density (in $\text{g}/\text{cm}^3$) of insects and is there a list of animals and their value of body density?

A recent studya measured the volumes (using a 3D scanner) and masses of 113 different insect species. They found the following relationship between the mass of the insects and their volumes ($V[mm^3]$ and $m[mg]$):

$\ln (V) = 1.019 \ln (m) + 1.46$

$\Leftrightarrow V = 4.30596 m^{1.019}$

Thus, since $\rho = \frac m V$

$\rho(m) = \frac m {4.30596 m^{1.019}} = \frac {0.232236} {m^{0.019}}
 $

Figure: Scatter plot of the measured masses and volumes

Reference:

a Kühsel, S., Brückner, A., Schmelzle, S., Heethoff, M. and Blüthgen, N. (2016), Surface area–volume ratios in insects. Insect Science. doi:10.1111/1744-7917.12362


What does conditional analysis of a SNP in a GWA study entail? I am familiar with the use of tag-SNPs in genome-wide association studies to identify gene loci involved in complex traits, but I keep seeing the term "conditional analysis" used without any explanation. Is it some sort of mathematical manipulation in which the significance of a tag-SNP is reduced to zero, to see if other SNPs are directly associated to the phenotype in question?

In GWA studies you tend to analyze your "lead" SNPs in regions where genotypes are correlated (known as linkage disequilibrium).

If you find an association between another SNP with the outcome, and this SNP is correlated with the original variant, you can perform a conditional analysis where you adjust for the original SNP in the model. This is to test if the association between the 2nd SNP is independent of the first, or whether it is just because they are correlated (in LD).

So performing a conditional analysis is just seeing if the association observed is an independent signal.

At least, this is how I have interpreted it perviously!

E.g. SNP-A is found to be associated with increased risk of type-2 diabetes (T2D).

SNP-B is later found to be associated with risk of T2D as well.

SNP-A and SNP-B are correlated.

To see if the association between SNP-B and T2D is independent of the first association, you would adjust for SNP-B in the model (a conditional analysis).

First model: lm( T2D  ~  SNP-A + confounders)
Second model: lm( T2D  ~  SNP-A + confounders + SNP-B)

If the association between SNP-A (and/or SNP-B) and T2D is still significant then they have some independent effect on risk of T2D. If the association disappears then they are only both associated because they are correlated in the individuals.


Accessing Expression Levels for Genes of Interest from GEO Experiments I have a list of 100 lncRNAs (long non-coding RNAs). For each of these RNAs, I would like to query GEO to find any experiments that used a high throughput sequencing platform and detected expression levels of that RNA in FPKM. To filter further, I'd like to have those expression levels found in controls only. The last filter is to find experiments which found the specific RNA's expression in smooth muscle tissue.

Here are some example lncRNAs:

CDC37L1-AS1
LCMT1-AS1
FLJ21408
CDIPT-AS1
LINC00920
TAT-AS1
SUZ12P1

Is there any way to do any of this? Any help would be appreciated.

Thanks.

You could look at supplementary and methods section of "The Landscape of Long Noncoding RNAs in the Human Transcriptome" paper. They've collected RNASeq samples from TCGA, ENCODE and MCTP and processed it with their pipeline (most of it are filtering and GSEA) to detect novel lncRNAs and associate them with cancer pathogenesis. Their statistics, processing and cross-validation look clean and accurate.
To extract signatures from GEO, you could use GEO2Enrichr. Then calculate the differential expression of tissue-specific libraries in Enrichr. Also, you could submit gene list to Enrichr's Crowd libraries and find GEO entries with a reasonable number of mapped genes first.


Does Cas9 require a nuclear localization signal (NLS) for it to work in a Eukaryote? I'm trying to establish if it's required to add a NLS to Cas9 when expressed (or transfected) in a Eukaryotic cell.   Several papers report using a viral NLS, but is it absolutely necessary?   Could Cas9 be trafficked to nucleus without addition of a NLS?

The transport from cytoplasm to nucleus is mediated by importin family. Importion family recognize NLS and transport proteins such as transcription factors into nucleus. So, NLS is necessary for cas9 to be transported into nucleus.


What does 'proper' mean in the anatomical context? I've seen the word 'proper' in websites, lectures, etc., in the context of human anatomy. But I'm unsure as to what its definition is. For example, the 'oral cavity proper'.

This use of proper is simply using one of the normal English meanings of the adjective proper: "In the very strictest sense of the word or phrase".  Thus, while 'oral cavity' generally might be taken to include, in part, the space between the cheeks and the teeth, the term 'oral cavity proper' refers to a stricter definition which excludes that space.


When was it understood that a male haemophilia sufferer can't pass it on to his sons? Haemophilia A and B are both X-chromosome mutations, so a sufferer necessarily inherits the disease from his mother. She won't have serious symptoms unless both of her X chromosomes have the mutation, which is very rare. Since sons of a sufferer necessarily inherit his Y chromosome, they can't inherit the disease from him.

I'm trying to find out when it was understood that sons of a sufferer could not inherit the disease from their fathers. The relationship between chromosomes and heredity was clearly demonstrated in 1915. The idea that females were usually carriers and sufferers usually male had been understood since 1813. The XY sex-determination system was discovered in 1905.

However, it is not clear to me when this would all have been put together and become part of normal biology and medical courses. I think the crucial points are:

There are sex-linked genetic conditions.
Haemophilia is one of them, and is an X-chromosome recessive condition.
Men are XY, women are XX.

Can anyone help with when all of that became normal knowledge for doctors and biologists?

Titles and authors of biology textbooks from the 1920s to 1945 would help, since I'm quite prepared to seek out old books, if I know what to hunt for.

Using Google Scholar, I've found the oldest publication on this item.
1911 - "The pathogenesis of hereditary haemophilia".
In this article you'll find a complete synthesis of all the works done about haemophilia till 1946.

OP adding a summary, in case of future link rot: The linked article is from 1946, based on research in the late 1930s and early 1940s into the statistics of haemophilia. It's attempting to estimate the mutation rates of X chromosomes in males and females, and to test if X-Y crossover allows the haemophilia mutation to skip generations. It assumes the knowledge that leads to the conclusion that a male sufferer can't pass it onto his sons.


What do the names of Immunoglobulin subtypes mean? What is the exact meaning and full form of  IgM, IgG, IgA, etc? What is the rationale behind the names of the isotypes, if there is one? For example, what does "M" mean in IgM?

Ig stands for immunoglobulin. The isotype names have various origins. This paper provides an interesting story:

Black CA. 1997. A brief history of the discovery of the immunoglobulins and the origin of the modern immunoglobulin nomenclature. Immunol Cell Biol 75:65-68.

A brief summary, in order of characterization and naming:

IgG - named gamma globulin because it migrated in the gamma band of electrophoresed blood plasma (the bands were named in order of mobility: alpha, beta, etc)
IgM - named macroglobulin because it sedimented faster than IgG (ie was larger)
IgA - found in the beta and gamma bands of electrophoresed plasma and initially named β2A and γ1A, later renamed to alpha globulin
IgD - named by process of elimination: IgA was taken, murine immunoglobulins were expected to be named beta, the letter C has no Greek equivalent
IgE - named because it was most reactive with a fraction of pollen proteins (fraction E because it induced erythema)


How to interpret Percent identity matrix created by Clustal Omega? I did a multiple sequence alignment using Clustal omega. checked similarity for 3 protein sequences : aspartyl aminopeptidase [Homo sapiens], aminopeptidase P (APP) [Plasmodium falciparum 3D7], yeast aminopeptidase (S000001586)APE1. I got Percent identity matrix as

Percent Identity  Matrix - created by Clustal2.1

 1: PF3D7_1454400              100.00   16.18   20.35
 2: gi|5902181|gb|AAD01211.2|   16.18  100.00   29.66
 3: S000001586                  20.35   29.66  100.00

My doubts:

I would like to know how to interpret this matrix result
Coming back to sequence alignments results, when I click on 'Show colors', the alignment summary is colored in 4 colors - red, green, blue and pink. Can anyone help me in decoding the color reference of alignment summary?

Thanks

Gene-1   Gene-2    Gene-3
Gene-1  100.00    16.18     20.35
Gene-2  16.18    100.00     29.66
Gene-3  20.35     29.66    100.00

Gene-1 and Gene-1 have 100% similarity (and all the other diagonal elements). Gene-1 and Gene-2 have 16.15% similarity, and so on. Therefore the matrix is symmetric M(i,j) = M(j,i).

You can also show just the upper triangular part of this matrix and that would be sufficient.

        Gene-1   Gene-2    Gene-3
Gene-1  100.00    16.18     20.35
Gene-2           100.00     29.66
Gene-3                     100.00

The colours basically denote the type (molecular nature) of residue. Have a look at this and this.


Do bacteria exist which live exclusively on non-organic matter? Are there bacteria which consume exclusively non-organic matter? Meaning that they do not require organic matter from other organisms to stay alive and reproduce? A completely pacifistic bacterium.

Or phrased differently, are there bacteria which can stay alive and reproduce indefinitely with only non-organic matter present (plus sunlight or thermal vents etc.)?

I'm asking specifically, to name one or more bacteria species which can do this.

Sulfate reducing bacteria get their energy converting sulfate to hydrogen sulfide. They are relatively common and may have been the source to turn some oil/gas deposits "sour". Specifics in Wikipedia.


Is it easy to test human Flicker Fusion Threshold? How would you go about testing human flicker fusion threshold? Is the testable rate consistent in humans over time or volatile?

Flicker-fusion rates are very easy to test in humans: you provide a flickering light-source, set it to flicker at different speeds, and get the people to tell you whether the light is flickering or constant. This paper (from 1952) achieved a flickering light by putting a rotating disc with holes in it in front of a projected light source. A more modern testing unit is demonstrated here.

The human flicker-fusion rate does not appear to be a constant. In addition to being influenced by attributes of the light source (such as its wavelength, how much the brightness changes, etc), it also appears to be influenced by factors such as stress and fatigue (pdf).


Did most pandemics originate from Asia/China? This question may be on the borderline of well-posed-ness. Let me ask it. Then please tell me if or where it can be improved.
Is it statistically true that the majority of the pandemics or epidemics originate from Asia particularly China? If not, is there a geographic concentration of the origin of pandemics? If so, why?

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


How long does the Ebola virus remain infectious on contaminated items or surfaces? I'm sure there will be variation depending on what the contaminated item or surface is made of - linens, I could imagine, would remain dangerous for longer than a door-knob. But if the items are not decontaminated in some way, how long can the virus survive outside a host?

This really depends on the environment, one study (listed below as reference 1) found that the Ebola virus can survive under ideal conditions on flat surfaces in the dark for up to six days - see the figure from the same publication.

However, the virus is quite sensitive to UV radiation (see reference 2 for all the details) and most viral particles are likely to get inactivated within relatively short time. It might still be possible to get positive tests for Ebola from really sensitive PCR-based tests, but these are most likely not infectious anymore. The CDC lists common bleach (or any other routinely used disinfected) as a good way to get rid of Ebola viruses.

References:

Persistence in darkness of virulent alphaviruses, Ebola virus, and
Lassa virus deposited on solid surfaces
Sensitivity to ultraviolet radiation of Lassa, vaccinia, and Ebola
viruses dried on surfaces


Pharmacology: Drug Administration Why is the enteral route seem by far the most common way to administer a drug to the body?

Let's review drug administration routes, and see for yourself:

transdermal/ionophoric: expensive, unreliable release concentrations (which makes it expensive because of the extensive research needed for controlled release), noticeable to others ("why do you have that skin patch, mom?" Er...)
Sublingual: quite similar to oral route, however absence of first pass hepatic metabolism can result in completely different blood concentrations between the two routes. Impairs speech. Could cause mouth irritation (quite disabling). Requires patient compliance.
intravenous: quite unpractical in outpatient settings. Invasive measure.
intramuscular/intradermal: hurts. As all things using a needle. Usable, but impractical in the outpatient setting. Can lead to skin lesions (insulin injection in diabetes, for example)
rectal: culturally unacceptable to some, unreliable release.
vaginal: similar to rectal, but only for women obviously
spinal/epidural: very invasive, only in inpatient settings.
topical: usually only acts locally, can cause discomfort (eyes)
oral/enteral: well known pharmacokinetics, mostly invisible to others, practical in the outpatient setting, requires limited patient compliance, well known excipients. Of course there can be secondary effects, but that is the case for all administration routes. Most common side effects are abdominal discomfort and nausea, but no one can see you in the water closet. Plus people are used to see pills as medication, something which might not be the case for other routes, depending on the cultural background of the patient.

This answer is of course somewhat subjective, however the importance of the patient's perception and his/her view of what the administration route implies socially cannot be overemphasized.


How to calculate the geometric mean titer (GMT) of titers from a haemagglutination assay (influenza)? I got a list of Influenza-specific antibody titers from a hemagglutination inhibition assay.

They look like this:

40
640
160
<10

One site says: “The swine influenza HI scale is geometric: 20, 40, 80, 160, 320, 640 (successive values increase by a factor of 2). The geometric scale is logarithmic. It is best to express an average influenza HI titer as a geometric mean. A geometric mean is calculated by averaging the logarithms of the test values and then converting the mean to a real number. This prevents a few obviously high positive values from making the mean unrealistically large.”

What does that mean for my sample? How do I deal with <10 in this calculation? This is surely not rocket science, but honestly I don’t get it right now.

Typically "<10" is converted to a number that is below the limit of detection; often "9".  After that simply following the instructions you have yields a GMT of 77.9.  If you are using spreadsheet apps such as Excel or Google Sheets, they almost certainly offer "GEOMEAN" functions which will give the number directly.


Is there any evidence of causation for breathing rate to affect blood pressure in a human? I did some research and trials, and with 5 trials for a normal heart rate and 5 done 45 seconds into breath holding, the results came back showing that my heart rate of 116/65 mmHg increased to 138/90 mmHg. I was interested in the cause of this, but couldn’t seem to find any evidence online to explain why this happens, exepct for some simple studies that showed that their is a correlation.

So my question is: has there’s been any studies that hypothesize or found a reason for breath holding to affect blood pressure?

Interesting question, it has been studied because sleep apnea is associated with hypertension in humans.
It's not my field of research, so I read a few sources to give you an answer.
There is a open-access review here (https://doi.org/10.1152/jappl.2001.90.4.1600) on the topic of episodic hypoxia, which is similar to the experiment you conducted. Two studies in dogs (https://doi.org/10.1152/jappl.1996.80.3.773 and https://www.jci.org/articles/view/119120) showed that neural reflexes, but also arousal, explain a part of the acute increase in blood pressure but here caution has to be used, as acutely holding breath may have different mechanisms on blood pressure elevation than the chronic hypoxia induced by sleep apnea.
Finally, a review (https://doi.org/10.1038/ajh.2009.43) in 2009 summarizes the evidence between sleep apnea and hypertension.

Overall, there seems to be multiple mechanisms. First, there is a sympathetic discharge during asphyxia, releasing catecholamines which can induce elevation in blood pressure by activating the baroreflex.  These are supported by studies of denervation in multiple organs. Secondly, there is activation of the renin-angiotensin-aldosterone system, a central player in blood pressure regulation. Thirdly, the animals studies show that arousal is an important factor in the acute blood pressure elevation ; in other words, being conscient of holding your breath itself induces blood pressure elevation. I cannot find the exact mechanism linking arousal to blood pressure elevation, though.


Does size correlate with sensory abilities? On average, do smaller animals have senses inferior to those of bigger animals?  I ask because it seems like a somewhat logical assumption: smaller eyes would in theory collect less light, and smaller ears would in theory collect less sound.

Or is size just irrelevant?

Size is not likely to have anything to do with sensory acuity. A simple example can be seen in the fact that rodents have much more sensitive sense of smell than humans, and some birds have much sharper visual senses than humans. It has much more to do with the number of olfactory/light sensors, sensory pathways to the brain and how that information is processed by the brain (i.e how much priority is assigned). Sensory organ size per se is less relevant (think of elephant ears).


Why is the prefrontal cortex called such? Pre means before. Frontal means front.

What does cortex means? Brain?

Is it the front most part of the brain? Is it located at the most frontal part of the brain and that's why it's called prefrontal cortex?

Is morality processed at ventro medial pre frontal cortex or at anterior singular cortex?

My background: I am a programmer. I just want to understand humans brain the way a programmer understand computer. It seems that we don't have CPU. We have huge analog based memory. And we got registers instead of tons of abstract variables. Understanding why certain part of the brain is named under certain things will help me a lot in remembering where exactly that thing is and why. It's something very useful in my ways of learning math and programming.

Basically there are 2 theories.

Prefrontal cortex is named as such because it's before (or in front
of) prefrontal lobe.
It's because it's behind prefrontal bone (the
way other brain lobes are named)

Some people told me to just look that up on wikipedia. If you can show me something in wikipedia explaining the exact answer I am looking for I will be very happy.

The prefrontal cortex (PFC) is a part of the frontal lobe (Fig. 1).

Lobe means

  [A part] demarcated from the rest of the organ by a fissure (crack), sulcus (groove), connective tissue or simply by its shape. For example, there are the frontal, parietal, temporal, and occipital lobes of the brain.

Cortex means

  The outer or superficial part of an organ or bodily structure (such as the kidney, adrenal gland, or cerebellum or a bone); especially: cerebral cortex

The frontal lobe is called as such, because... it's in the front of the brain.

The prefrontal cortex is called that way because it forms the frontmost part of the frontal cortex. Prefrontal means

  anterior to or involving the anterior part of a frontal structure

Anterior meaning

  situated before or toward the front

Indeed Siddiqui et al (2008) mention:

  The anterior part of the frontal lobe referred in the literature as ‘pre’-frontal lobe has been simultaneously referred to as ‘frontal granular cortex’ and ‘frontal association cortex.’ The anterior most portion of the frontal lobe is occupied by the PFC...

Reference
- Siddiqui et al., Indian J Psychiatry (2008); 50(3): 202–8

Fig. 1. The frontal lobe includes the prefrontal cortex (PFC). source: Socratic


Sequencing a specific region of a genome First off, I'm new to bioinformatics and I am learning about DNA sequencing.

Let's say that I knew that a specific region of a genome which contained information about a disease (whether it a person had the disease or not).

It would make sense that we would only want to sequence that part of the genome in order to make a detector for this disease.

Would it be possible to 'cut-out' this region of the genome and only sequence that part (so we don't have to sequence the entire thing)? If not, how would we sequence only this part of the genome (it doesn't make sense to sequence the other parts as they don't give us information).

Thanks in advance.

Yes, it is possible to sequence a specific region of the genome. The method, as you mentioned, is called targeted sequencing. Resequencing is basically sequencing something that has already been sequenced. This means that instead of assembling all of your sequence reads from scratch, you can just align them to the reference sequence (in your case, the entire human genome has been sequenced). Targeted resequencing means you're sequencing a specific region, such as a gene. This requires concentration of the specific DNA you wish to sequence and can be done by PCR amplification (using primers that flank your desired sequence) or hybridisation (using probes complementary to your desired sequence that are fixed to a surface), among other methods.

For information on methods for enriching a DNA sequence, give this a read:

Mamanova, L. et al. Target-enrichment strategies for next-generation sequencing. Nat. Methods. 7, 111-118 (2010).


Does blood clot reduce blood flow? I read that blood clot reduces blood flow from few website and from doing an A level biology question; and if this blood clot is formed in pulmonary thrombosis, this can reduce gas exchange in lung.

However, how are we so certain this is true? If there is a blood clot, then blood pressure around that region increases I believe thus implying the blood will travel faster in that region? If so, then we can't firmly conclude blood clot will reduce blood flow as although blood clot will reduce the lumen of the vessel, the blood will also be travelling faster.

A blood clot can nearly completely or completely block an artery, in which case the blood flow will be reduced or stopped.

How do we know this?

Pulmonary Embolism (Merck Manuals):

  Pulmonary infarction is when some of the lung tissue does not receive
  enough blood flow and oxygen and appears on imaging studies to die due
  to blockage of a lung blood vessel by a pulmonary embolus.

An embolus is a blood clot that usually develops in the leg veins in individuals with deep venous thrombosis, detaches and travels to a certain pulmonary artery and blocks it.

Similarly, atheroma (atherosclerotic plaque) that builds up within the artery and only partially blocks it, can reduce the blood flow to the target organ. For example, a partial blockage of a coronary artery can result in decreased blood supply to the heart and consequently in angina pectoris or myocardial infarction. It is then the investigation called coronary angiography that can show that a certain coronary artery is partially blocked.

When a clot interferes with blood flow (Harvard.edu):

  In venous thromboembolism, a blood clot slows or stops the flow of
  blood through the veins...


How do migrating birds know where to migrate? Migrating birds return to the same spot, year after year. These locations are often thousands of kilometers apart. How do the birds know where to fly to?

So far I have found that the birds tend to follow a leader. Like Canadian Geese flying after one bird in a V shape. It seems that this leader is the one who 'knows' where to fly, but how?

Why do birds migrate?

The primary reasons for why birds migrate are food availability and nesting locations. There are many other factors that can also play a role in why a bird migrates; too name a few, it includes responses to weather patterns, geography, and day length.

Since you use Canadian Geese as an example, I’ll use North America as the example region. There are over 650 migratory birds in North America and many scientists are studying individual species and learning that different factors have a variety of importance when it comes to migration. Generally birds can be classified into residents (non-migratory), short-distances migrants and long-distance migrants.

Residents are able to find food year-round and there is no need to migrate. Short-distance migrants tend to respond to food and weather (1). Long-distance migrants are more complex, but it is thought that response to day length and hormonal changes are important influences in their decision to migrate.

Now how do birds know where to go?

The most important factor is genetic predisposition, which can be composed of many variables such as moult, reproduction, and physiology (2). Just because there is a leading Canada goose, doesn’t mean the others don’t know where they are going. They can all have the same genetic factors affecting their decisions. There also can be cases where a young Canada Goose, doesn’t know where he is going, but he joins the V-formation and learns where to go from others in which he can then pass this knowledge on to future generations (I’m just using Canada Goose as an example for birds in general).

Navigation cues can also play a role such as geography, suitable habitat, landmarks, sun position and earth’s magnetic field. Geography can play a role in migration by acting as a barrier or a funnel, in North America, migratory birds can be limited as to where they travel. For example, they will not cross the Rocky Mountains or Atlantic Ocean. Suitable habitat also plays a role, for example North America has a variety of habitats, but to classify them simply there are: deserts, plains/ prairies, deciduous forests, boreal forests and mixed forests. The bird in question will be looking for these locations to nest or spend its winter. Many birds exhibit a step-wise migration where they stop at sites along their route to feed and regain strength and these areas are frequented annually.

As you can see, there are many answers to why a bird migrates which can create even more questions and led to many different explanations. Here's a website with a nice summary and a good starting point to learning about migratory behaviour that could help you understand further:

https://www.allaboutbirds.org/the-basics-how-why-and-where-of-bird-migration/


Melatonin production, sleep, and "cyan light"; how might this finding be possible? The BBC News article Cyan colour hidden ingredient in sleep describes research that suggests melatonin levels as measured in saliva could be affected by the presence or absence of cyan color in a displayed screen, even when the color balance was adjusted so that the difference was not visibly perceptible.

The colour cyan - between green and blue - is a hidden factor in encouraging or preventing sleep, according to biologists.
University of Manchester researchers say higher levels of cyan keep people awake, while reducing cyan is associated with helping sleep.
The impact was felt even if colour changes were not visible to the eye. (emphasis added)
The researchers want to produce devices for computer screens and phones that could increase or decrease cyan levels.

Is cyan going to keep you awake?

I am guessing that this even possible because color perception comes through the sensitivity of three (or four?) color channels and so two different spectra can appear to be the same color. An example might be that a green wavelength might appear to be the same color as the mixture of a blue and a yellow wavelength if properly adjusted.
But if the two stimuli are adjusted to have the same or similar mix of signals in the individual's color receptors, how might the melatonin production still be affected?
edit: According to Wikipedia, monochromatic light would have a wavelength in the range of 490 to 520 nm, and if you wanted to create a visual impression of cyan, you'd use a mixture of Green and Blue channels:
Wavelength    490–520 nm
Hex triplet   #00FFFF
sRGBB         (r, g, b)   (0, 255, 255)

Melatonin production is in response to photoreceptors in the eye, in part, the same photoreceptors in rods and cones that process and transmit information about the wavelength of light (eventually) to the visual cortex for vision. However, @uhoh was right to wonder whether there might be a separate receptor input for melatonin production.

There is an additional opsin (photosensitive protein), found in the ganglion cells rather than the rods and cones, that is sufficient for responding to light and causing the production of melatonin by the pineal gland (mediated by the suprachiasmatic nucleus of the hypothalamus). Processing of light signals by the circadian system is quite separate from processing by the visual system. This is discussed briefly in Chapter 47 of Kandel's Principles of Neural Science, but you can read more about it in this review.

The pathways involved in receiving and processing light as an input to the circadian system were discovered relatively recently. Consider that the optic tract was discovered in the 3rd or 4th century BC, and the retinohypothalamictract was discovered in 1971.


How deep does water have to be so a mosquito can lay viable eggs in it? I read about this idea for a mosquito trap (with a rather tactless name) where the idea seems to be that because the water available for the mosquito eggs is so shallow, they will die somehow or not be viable. Mosquitos are pretty small though, wouldn't they not need much water for the eggs to hatch?

Many mosquitoes, such as Culex quinquefasciatus, lay their eggs on the surface of fresh or stagnant water. The water may be in tin cans, barrels, horse troughs, ornamental ponds, swimming pools, puddles, creeks, ditches, catch basins or marshy areas. Mosquitoes prefer water sheltered from the wind by grass and weeds (reference). There are mosquitoes like Aedes taeniorhyncus (floodwater mosquitoes) which can even lay eggs in moist soil (because the eggs need to dry out before they can hatch) which then waits for the rainy season for hatching. These eggs are capable of surviving through summer, winter and spring to find the right time to hatch (reference). Water is necessary during the life cycle of a mosquito but how much is never an issue. Even the top of some mushrooms can be a place for mosquitoes to lay eggs (reference).


Is it possible to clone a Neanderthal? As Neanderthal DNA has been sequenced, is it possible to create a living Neanderthal?

Not any time soon.  By far the greatest challenge is getting the DNA sequence from the computer into a form that could be implanted into an embryo.  Craig Venter's team was able to build a bacterial genome from scratch, but that was incredibly painstaking work, requiring the assembly of many small fragments of DNA into a single circular chromosome.  With current technology that process becomes prohibitively difficult for a human-like genome.  You would have to build each chromosome from scratch, these chromosomes are linear, and you'd need to associate with them the various histones and other proteins help tightly fold them together.

Another huge problem is epigenetics.  The next generation sequencing methods used for the neanderthal genome just give you DNA sequences, not what epigenetic modifications are present on that DNA.  Genomic imprinting in mammals is very important, and presents problems even in normal cloning efforts where genomes are taken wholesale from live animals.

Not to mention that 1% of the current genome is contaminated with human DNA (not meant as a criticism, its amazing what they have been able to do with a toe bone if this work stands up to peer review).

And none of this takes into account the ethical problems associated with this.  Would you clone it in a human?  Chimp?  Either way its got serious ethical questions.

Dont take my word for it though, here is the leader of the project commenting on this question a few years ago:

  Paabo said because the Neanderthal DNA was scattered in imperfect
  fossils, the notion of cloning a Neanderthal was far-fetched.

  "Starting from the DNA extracted from a fossil, it is and will remain
  impossible," he said. "There is not really an improvement on current
  technologies that would make that possible.


Why is leucine amino acid used the most in proteins and tryptophan the least? The amino acid leucine, is used in proteins more than others. Leucine with 9.1 percent (its average in more than 1.150 different proteins) is used most and tryptophan with 1.4 percent is used less than all other amino acids.

Why is leucine used more than tryptophan?

This is a guess.

Tryptophan is a bulky amino acid. Having a lot of if would make the protein bulky. It is anyways hydrophobic and cannot be present on protein exteriors; high tryptophan may distort hydrophobic core possibly because of its bulkiness and ability to form pi-stacking interactions.
However, tryptophan is an essential amino acid and cannot be made de novo in humans. Indeed, it has only one codon perhaps because of its limited usage.
Nonetheless, tryptophan, despite its low abundance, is important in stabilization of protein structures such as β-hairpin [1] and it is also required for synthesizing serotonin.

Leucine is present in the hydrophobic core and β-regions. It also surrounds active sites which causes exclusion of water; this in turn facilitates catalysis by allowing polar residues to bind to the substrates [2].

I don't have any comment on why not isoleucine or valine instead of leucine.


What is the minimum water consumption for Arabidopsis and other plants? I'm working on a project to design a self-contained plant growth environment for germinating and growing plants in space. It's important to know the absolute minimum amount of water and nutrients required to keep the plants alive and healthy over the course of 30 days, since we have very little space to store the water.
The plan is to use a single water reservoir to feed three separate growth chambers by injecting nutrient-rich water directly into a soil medium, similar to the ISS Veggie environment. We want to find out how much water we need to inject and how often.
I've looked over the literature as to what previous astrobotany projects have done. While they are typically very clear about the nutrient composition of the water, I have yet to find one that clearly states how much water the plants were given, and how often.
I focused my search on Arabidopsis thaliana to start, but ideally we would like to know water requirements for all major groups of small plants.
This seems like it shouldn't be a difficult question to answer. What am I missing?

The plant will intake water to keep constant internal water pressure to compensate for evapotranspiration. However, the evapotranspiration will not be a simple universal number.
The evapotranspiration rate strongly depends on temperature, air humidity, water tension inside the plant you want to keep (may it wilt?) and also the radiation received by the plant (PAR - photosynthetically active radiation) and also the air flow. In longer time that will also depend on the ventilation of air in your box. That means how fast water vapour escapes the air from your box and whether any of it condensates.
Also, how much water evaporates from the soil itself? That depends on soil properties, air temperature and also air flow.
A common model for evapotranspiration is by Jarvis and Stewart but is most often used for trees. You can read about interesting measurements of evapotranspiration at Whole plant open chamber to measure gas exchange on herbaceous plants.


How to replace intron region in a plasmid? I'm considering working with the plasmid pRFHUE-eGFP and would like to replace the gpdA intron (which is the eGFP promoter region) with a promoter from another organism.
What would be a good strategy for replacing the intron if I already have the other gene in-hand?
Would I cut out the fragment between the SalI and SmaI restriction sites and then insert the new promoter with compatible overhangs there?

Your strategy would work, but if possible you might be better off using XmaI rather than SmaI, as the latter is a blunt-end cutting enzyme.
Furthermore, your strategy would not replace the entire gpdA promoter, if that's what you're after. You might wanna refer to their paper, where it's clear from Fig. 1 that the promoter region is much longer than the region between SalI and SmaI:


why is DNA antiparallel? Can it be parallel? My biology textbook mentions that DNA is antiparallel and it got me wondering... Can DNA be parallel? What would happen if it was parallel? could DNA still replicate right?

Interestingly the answer is yes. The problem with parallel strands is that the DNA is not pairing in the known way it does when it is combined anti-parallel (or Watson-Crick-pairs).
I have found different images illustrating the problems:

Both images are from this blog post (originally from a publication cited there which is not available online). Both pictures show a distorted DNA structure.

This article ("NMR structure of a parallel-stranded DNA duplex at atomic resolution") shows a more schematic solution of this problem by showing the single pairings. C and G cannot build up 3 hydrogen bonds as they do this in the Watson-Crick-pairing.

Subfigure A and C show the Watson-Crick-pairs, the others come from parallel bindings.

This changes in structure disrupts the function of the DNA (which for example depends on the reverse strand for proof reading). Enzymes which replicate, transcribe, repair etc. DNA will not work on this changed structure, as their function depends on the structural features of the DNA.


Organisms in food deposits I have just discovered that my kitchen sink pipe has been leaking for quite some time (possibly months) which has resulted in water and food deposits collecting in my cupboard.

I smeared some of the residue onto a slide and looked at it under my microscope. I could see a large number of translucent organisms (visible at 40x magnification, they are roughly 100 µm in length). They all appeared to be of the same species although they varied in size and developmental stage. The 'adults' are quite long and look similar to maggots; they scrunch their bodies into balls and then stretch out in order to propel themselves.

Unfortunately I lack the equipment to take a photo of it but here's a rough sketch of what it looks like moving to the right:

Don't take the features too literally.

Can anyone hazard a guess as to what it might be?

It seems like Euglena but I need more parameters than what you have provided.

(source: eastmarinedrive.com)

https://www.youtube.com/watch?v=ZHZZKwrYm4g

you can narrow it down by this:

http://goo.gl/XTEZ7S

Or

You can find them in commonly found microorganism in kitchen:

http://www.colorado.edu/eeb/EEBprojects/FiererLab/Flores_etal_2012_kitchens.pdf

Or

http://www.plosone.org/article/info:doi/10.1371/journal.pone.0078866.t001/largerimage

Source: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0078866


How long can C. Tetani survive in soil? Clostridium tetani (C. tetani) is a bacterium commonly found in soil and is excreted in the faeces of many animals (both mammals and birds) and serves, by means of the exotoxin, tetanospasmin, causes the life-threatening condition tetanus.

Soon after asking this question I found a reliable source, the National Institutes of Health. It can survive for over 40 years.


Vitamin A Deficiency I have a quick question regarding Vitamin A deficiency.

The photoreceptor molecules in both rods and cones have the same general structure which is retinal which is bound to a protein called opsin and depending on the photoreceptor opsin changes but the retinal is always the same. And it is the retinal that makes the opsin light sensitive and so it is highly important.

My question is, why is it that when researching the symptoms of vitamin A deficiency one of the most common ones is night blindness. I understand that if not enough retinal is formed not enough rhodopsin is formed and so the patient would suffer from night blindness but wouldn't it also mean that the patient wouldn't be able to produce enough of the other photoreceptors as well and so doesn't only suffer from night blindness but from complete blindness?

Good question! As you write Vitamin A is quite important vision as it is an integral part of the light sensitive rhodopsin protein. Rhodopsin is necessary for a type of photoreceptor, the rod. It is located in outer segment of the photoreceptor. Vitamin A is also required to other opsins that are needed for the cones to function.

When someone has Vitamin A deficiency it does not mean that they have no Vitamin A. For example instead of having i.e. 100 Vitamin A you only have 30 (arbitrary numbers!).

In the retina, you have the very light sensitive rods and the less light sensitive cones. Rods need a lot of rhodopsin (and hence Vitamin A) as they have to detect small levels of lights (it is thought that a rod can detect a single photon!).

Cones, on the other hand are not so sensitive to light. During the day there are tons of photons*. Since you need less Vitamin A for cones to function, you will see the symptoms of Vitamin A deficiency later compared to rods.

Hence, when you still have a bit of Vitamin A but not enough (e.g. 30 instead of 100) you will first notice it in systems that need Vitamin A the most. It turns out that this are the rods. And yes, if you had 0 Vitamin A you would be blind. But since Vitamin A is needed for many other processes, you will probably be dead at that point.

*Personally, I find it hard to grasp just how large the difference in Illuminance (and hence photon numbers) is for example between day and night. See here for a comparison. As you can see, our visual system has to deal with an enormous dynamical range of illuminance. The fact that we usually don't even think about these differences in light intensities in everday live is testament to how fantastic our visual system is in dynamically adapting to the huge differences in input.


What do we call this adjustable platform used to ensure that something is positioned strictly level in a lab? This is an adjustable platform. Such a platform is used, for example, to make sure that a gel electrophoresis cassette is level relative to the earth. A passage in a procedure description which I'm translating says that the gel caster (the two glass plates between which we will pour the solution) should be put on top of this platform, after which the platform is adjusted "using a level". The text describes a vertical SDS-PAGE procedure.

I wonder what such benchtop lab platforms are called. In my Russian text it is called "заливочный столик" (pouring table, casting table).

I remember using those for agarose gels as an undergraduate, though using them for PAGE doesn't make a lot of sense unless your bench is seriously out of level. Anyways, they can be called levelling tables and are used to promote uniform migration across the gel. Casting table also seems reasonable.


What are the differences between carnitine forms? I've heard of L-carnitine, acetyl L-carnitine and L-carnitine L-tartrate. What form(s) occur in meat? What form does the human body manufacture?

Is L-carnitine just a shortened name for L-carnitine L-tartrate?

Carnitine tartrate is a salt between carnitine (cation) and tartrate (the conjugate base of tartaric acid, anion). So in this case, tartaric acid is not covalently bound to carnitine.

The salt formulation is a little tricky, because carnitine is itself a zwitterion at physiological pH (it has both a positive and negative charge) and so is overall uncharged in pure form. I think the tartrate salt is formed because tartaric acid is more acidic (first pKa = 2.89) than the carboxyl group of carnitine (pKa = 4.09), which leads carnitine to become protonated and therefore +1 charged in a concentrated mixture. The formulation sold by Lonza (which seems to be a major provider) appears to be a ratio of 2 cartinine (68%) to 1 tartrate (32%), which would indicate that tartrate acts as a -2 anion in this mixture (this is a bit surprising as the second pKa of tartaric acid has pKa = 4.40, but maybe I'm missing something).

You can recognize that this is a salt from the naming: the form tartrate indicate a conjugate base of an acid (as in lactate, acetate), and when used in a two-component name like carnitine tartrate (or, sodium acetate) refers to a salt. On the other hand, a carboxylic acid covalently bound to another group is given the suffix -yl, so tartryl carnitine would indicate tartaric acid bound to carnitine, as in fatty acid oxidation.


What are these two nerves running parallel to the spine called? I was looking for a human body nervous system, and often times i found a picture like the one below, where there are two nerves running parallel to the spinal column. I searched for it, but nothing came up.

Can anyone tell me what are the names to these two nerve column parallel to the spine and what are their functions?

From this closeup image, you can see there is more than one nerve on each side that is parallel to the spine.

Source: imgur.com

First, they are the right and left sympathetic trunk that run from the base of the skull to the coccyx.

Image source: Earthslab.com

Additionally, they could be the right and left long thoracic nerve, which innervate the serratus anterior muscles in the chest wall. In your image they appear like running along the spine, but in reality they run vertically and laterally in the chest wall.

Source: Semantic Scholar


Storing Apples at 30F? This article about storing apples for the winter says:

  You do not want the apples' temperature to fall below 30°F (-1.1°C), however,
  because that will make them freeze and turn to mush when they're
  thawed. Their cell walls will all collapse.

  Therefore, apples are best stored somewhere around 30-35°F (-1.1 to 1.6°C), in a humid environment.

I don't understand why you should keep the apples below the freezing point of water. Why would damage only occur below 30°F (-1.1°C)?

Is the article correct?

This temperature range would be a compromise between a very low temperature needed to limit natural decay or decay triggered by micro-organisms (the lower the temperature, the lesser the decay) and the formation of destructive ice crystals.

Only pure water freezes at 0°C (32°F) under atmospheric pressure. But the content of apple cells and cell walls is a rather complex aqueous solution, containing many natural cryoprotectants, among which the fruit's sugars. Therefore, the freezing point of apples might be as low as 30°F.


Why do we have two of some organs, but not all? We have two eyes, but we don't have two hearts.
Why do humans have two of some organs, but not all?

Here is my overly succinct answer.

I doubt we will ever know this for sure. But, it basically comes down to ancestral bilateral symmetry in development; this defaults to two organs and is broadly symmetrical except where the organs are central. See this article for a more thorough answer regarding bilateral symmetry.

Further exceptions to symmetry occur where evolution pressured the body into not bothering to grow the second of an organ due to a waste of resources for the body, or functional advantages emerged from asymmetrical evolution. I always like the ears of an owl for an excellent example of two asymmetrical features that provided a discrete advantage when it comes to locating the source of a sound.