Photosynthesis - Light Intensity Say I was conducting an experiment for photosynthesis. If I moved light closer to the plant, what effect would this have on the process of photosynthesis?

The rate of photosynthesis varies from plant to plant. Some plants require more light and some require less. If you move light closer to the plant, in most scenarios the rate of photosynthesis is likely to be increased. For some plants a minimal light is enough for their photosynthesis, so for those plants, moving light source closer or further will have less effect.


Can epigenetics have positive impact on the genes are development? I know that epigenetics have capacity to affect and degrade the genes thereby inducing problems/illness/degradation in body functions.

Can they also make better genes or have positive impact on genes or body? If yes, can someone give some examples?

First, let me qualify the idea of "problematic" epigenetic modifications by saying that the impact of a modification on an organism is often dependent on the environment.  That is to say that outcome is dependent on the interaction of genetics (or epigenetics) and the environment in which the associated genes are expressed; e.g. a mutation or modification that confers an advantage in a nutrient-limiting environment may be detrimental when nutrients are plentiful.

Second, it is helpful to think of epigenetic modifications as reversible switches rather than entities that "degrade the genes".  In fact, the etymology of "epigenetic" implies that such changes work at a level above that of the gene sequence, i.e. gene expression.  Canonically, DNA methylation and histone modifications (acetylation and methylation) modify the expression of a gene by regulating the ability of RNA polymerase to access that gene, either by directly influencing transcription factor binding or modulating the associations of nucleosomes and DNA. Read up on facultative heterochromatin.

As for examples, I point you to a set of papers that show associations between human starvation, epigenetics, and disease / mortality outcomes across generations.

DNA methylation as a mediator of the association between prenatal adversity and risk factors for metabolic disease in adulthood

  [DNA methylation] at six CpGs, including at previously [serum triglyceride]-associated CpGs at TXNIP and ABCG1, mediated the association between famine exposure and [serum triglyceride]. [DNA methylation] at these CpGs was likewise associated with the expression of genes implicated in cell growth and energy metabolism.

Note that the authors present caveats to their analyses in the discussion. The New York Times also covered this publication.

Paternal grandfather’s access to food predicts all-cause and cancer mortality in grandsons

This publication is essentially a replication of the published works concerning transgenerational epigenetics in the Överkalix cohort.  They give a concise summary of how epigenetic changes caused by environmental stress may be heritable:

  An intriguing aspect of these studies is the conjecture that an epigenetic pathway, carrying information across generations, may open up just before puberty, during the so-called slow growth period (SGP). Pre-puberty may be one of several “windows” for germline reprogramming in response to nutritional signals. A number of mechanisms for transmission across generations have been suggested, usually involving DNA methylation, chromatin formation or small noncoding RNAs. After fertilization, in the preimplantation embryo, epigenetic modifications acquired early in life are then usually erased, but not fully. Imprinting on specific loci may resist the post fertilization wave of reprogramming, eventually causing changes in offspring phenotype that are not driven by changes of the DNA sequence.

If you're looking for more examples, research genomic imprinting.


Why does crossing over take place at all? I already know that crossing over causes genetic variation. My question is that since DNA is a stable molecule, why would it undergo process like crossing over during which it becomes so unstable and develop a chance of mutation?

Crossing over is believed to be beneficial for evolution. It does not cause only mutations, it allows for the switching and mixing of genetic information. Thanks to crossing over entire protein families evolved, like the hemoglobins. Indeed it is one of the mechanisms that shaped the chromosomes.
Some in-silico simulation proved that, in general, adaptation take place faster if crossing over is applied.

Here some extra references for further readings.

https://www.ncbi.nlm.nih.gov/pubmed/28565671

https://www.ncbi.nlm.nih.gov/pubmed/28564047

https://www.ncbi.nlm.nih.gov/pubmed/28563027

https://www.ncbi.nlm.nih.gov/pubmed/28557225

https://www.ncbi.nlm.nih.gov/pubmed/28555659


Evolving a smaller brain In Kurt Vonnegut's novel Galapagos, a certain mammal species, due to drastic and peculiar environmental changes, evolves (among other features) a smaller and smaller brain.

Has this ever happened? Are we aware of any species whose ancestors had remarkably bigger brains?

Brain size vs intelligence

Of course brain size and intelligence are two very different things. Sure these two characteristics are correlated (assuming we manage to define intelligence in any intelligible way). The sperm whale has a brain that is 8 times larger than the human brain for example and the Brown thrasher (small bird) can learn thousands of songs while other birds can memorize the location of thousands of seeds. So really size is not the only thing that matters.

You might want to read about brain-to-body mass ratio and the encephalzation quotient.

Evolution toward smaller brain size

I am pretty sure such examples should exist but it might be hard to come up with good citation on the subject because

It is hard to tell other than through fossil record how big was the brain of a certain ancestor
It is quite a specific question

Someone might well come up with good answers. Of course, most examples of evolution toward smaller size (such as through insular isolation as pointed out by @user137) will result is reduction in brain size however, I am not sure these example would satisfy your needs/curiosity.

Evidence of metabolic cost of brains

In the meantime, I would like to point to a few among many evidences that brain comes at a fitness cost (that might be compensated by benefits of learning and other "brain abilities"). Those evidence mainly comes from experimental evolution in labs but some comes from comparative genomics as well. In short:

Brain consumes a lot of energy (Magistretti 2013). There are evidences in Drosophila (Mery and Kawecki 2003), birds (in this review I think: Nowcki et al. 2001) and guppy (Kotrshal et al. 2013) that evolution of learning abilities comes at an important metabolic cost. Johnston (1982), and more recently Snell-Rood et al. (2009) made reviews on the cost and benefits of learning abilities that you might want to have a look at.


Why would a plant evolve to produce an addictive chemical? It seems kind of anti-productive in terms of survival for a plant to produce an addictive chemical as that plant will constantly be sought after by animals that ingest it. In this instance, I'm looking for a possible general & inclusive answer here that would describe most plants that make this. Not a specific instance (although if provided as an example would be a plus).

To appreciate the scope of this is terms of number of plants producing potentially addictive compounds - see this compendium:

compendium of botanicals reported to produce toxic, physchoactive or addictive compounds

It's a matter of perspective. Most of the chemicals that are addictive to us humans (particularly alkaloids), and may be addictive for some other animals as well, are also insecticides. Lots of plants that we consider poisonous are good food for other species, and lots of plants that insects would consider poisonous are treats for us.

This is a great example of the aimless nature of evolution. The plants that could successfully defend themselves against insects stabilize on a solution that happens to be bad for them in certain ways. Although, you would be hard pressed to find a better way to guarantee reproduction than being addictive to humans.

Background reference

Plant-insect coevolution and inhibition of acetylcholinesterase
The defensive role of alkaloids in insects and plants
Exploration of nature's chemodiversity: the role of secondary metabolites as leads in drug development

Also of interest

Bees prefer foods containing neonicotinoid pesticides


Is there a resource that has quantitative data about cell proteins? I am a MSc student working in mathematical biology. In my thesis I am modelling diffusion of a protein that can bind to cell surface receptors. In order to simulate this I need some rough figures about the binding rates, degradation rates, diffusion rates etc. of components involved in this system. I have managed to find some information about these things, but they have all come from reading papers - biology papers where I only barely have enough knowledge to grasp the key concepts and (lets face facts) barely have the patience to read.

Is there a better way to find this quantitative data? Ideally I would love to come across a database that had this kind of data in it, but I'm not holding my breath.

What techniques do people in my position use to find this kind of information?(short of trawling through incredibly dense biology papers)

I'll list the papers that I obtained these parameters from. BioNumbers is a very useful resource and some of these papers that I cite have been obtained from the reference mentioned in BioNumbers. So BioNumbers should the first place to look for things like this. If you are not satisfied then start googling around :)

You should, however, keep in mind that simulation using exact parameters may not be very helpful. You can try varying the parameters in some given range and see the effects. Some parameters actually vary a lot.

Protein translation rate: 11 amino acids per second. Assume some steady state concentration of mRNA. This parameter is highly variable as there can be multiple ribosomes per mRNA [1]. Also see Schwanhäusser et al. (Supplementary excel sheet) [2]
Protein degradation rate: Take an average or one of the values reported by Schwanhäusser et al. (2011) [2]
Association/dissociation rates: See table shown by Zhou (2003). It lists different known interactions.[3]
Protein diffusivity: This differs for cytoplasm and water. You can assume diffusivity in ECF to be same as that in water. See Arrio-Dupont et al. (2000) [4]. They report it for specific proteins. You can extrapolate for other proteins using the Stoke-Einstein relation which says that diffusivity decreases inversely with the radius of the particle.

[1] Siwiak, Marlena, and Piotr Zielenkiewicz. "Transimulation-protein biosynthesis web service." PloS one 8.9 (2013): e73943.

[2] Schwanhäusser, Björn, et al. "Global quantification of mammalian gene expression control." Nature 473.7347 (2011): 337-342.

[3] Zhou, Huan‐Xiang. "Association and dissociation kinetics of colicin E3 and immunity protein 3: convergence of theory and experiment." Protein science 12.10 (2003): 2379-2382.

[4] Arrio-Dupont, Martine, et al. "Translational diffusion of globular proteins in the cytoplasm of cultured muscle cells." Biophysical journal 78.2 (2000): 901-907.


What is the name of this berry producing tree? I live in Middle Tennessee (USA) and came across this tree while I was hiking through the woods. I'm curious as to what type of tree this is and if the berries have any uses or are poisonous.

The tree is rather short, and I was unable to see any more distinctive features given that the tree was surrounded by other brush. I can supply a better picture in a day or two if necessary.

This is some type of Sumac in the genus Rhus. Probably either Rhus glabra (Smooth Sumac) or Rhus typhina (Staghorn Sumac). The berries of those two species are supposedly not poisonous. But they are closely related to other poisonous plants such as poison ivy and poison sumac. Poison ivy and poison sumac are in the genus Toxicodendron, but used to be in the genus Rhus.

A photo of Smooth Sumac


Did Mendel believe that proteins are hereditary substances? Scientists first thought that proteins, which are found in chromosomes along with DNA, would turn out to be the sought-after genetic material. Proteins were known to have diverse amino acid sequences, while DNA was thought to be a boring, repetitive polymer, due in part to an incorrect (but popular) model of its structure and composition.
Was Mendel (1822-1884) one of these scientists?
Note that in 1869, Friedrich Miescher isolated "nuclein," DNA with associated proteins, from cell nuclei. He was the first to identify DNA as a distinct molecule.

The first person to directly indicate a linkage between the hereditary material and enzymes was Garrod in 1902, based on the observation of the hereditary enzymatic disorder alkaptonuria. This is after Mendel's death.
The tetranucleotide hypothesis (i.e. DNA is not informative) that you refer to seems to have been formulated around 1910. So there is no way that Mendel knew about that.
It was not even proposed that proteins were composed of amino acids before 1902. No protein was sequenced before 1950. So Mendel had no idea what sequences or amino acids were, for any biopolymer.
It is formally possible that Mendel knew at some point about Miescher's result, but I'm not aware that he was at all interested in the chemical nature of Mendelian factors (what we now call "genes"). I agree with commenter @jamesqf on this point.
It was not immediately obvious to anyone that there was a discrete mapping between phenotypes and specific agents such as proteins. The major theories of inheritance at the time came from biometricians such as Galton, who believed that inheritance was driven by a blending-like mechanism (more or less), based on phenomena such as regression to the mean. They weren't really interested in the chemical basis either.
Mendelian genetics was only rediscovered around 1900 (Mendel was basically ignored during his lifetime), after which the debate started to consider the question of discrete genetic factors.
In short, I don't think that there is any evidence that Mendel had any interest in chemistry or the chemical relations of the organismal characters he studied.


Assembling small DNA parts using Golden Gate Background
I've always been told that DNA assembly can be tricky when using very small DNA parts due to low efficiency. I've also seen this when using 3A biobrick assembly to assemble promoters and RBSs together. However, there doesn't seem to be any information that I can find which definitively shows what the minimum DNA part size is that can be used before the efficiency becomes so low that assembly is unfeasible. The most I can find are warnings that small DNA parts are problematic (e.g. https://blog.addgene.org/plasmids-101-golden-gate-cloning).
The Question
What is the minimum DNA part size that can be used in DNA assembly before it becomes unfeasible? I'm specifically interested in Golden Gate assembly, but information for other digest-ligate assembly methods could also be helpful.

Purely going off experience here having used golden gate assembly methods for 5+ years now, there is a definite lack of literature regarding small part assemblies. In my current lab, we use CIDAR MoClo (a golden gate method) and have assembled 100's of constructs successfully with parts as small as ~ 70 bp. However, when we assemble smaller parts we tend to increase the amount of this part compared to bigger parts. For example, we dilute each part to 10 fmol ready for assembly as a basis for all assemblies, this then allows us to play with the ratios and quickly optimise reactions. So as a standard, when the part is small we automatically start with at least a 3:1 instead of 1:1, where we put 3x the volume of the small part compared to others in the assembly. This usually helps, but on top of that we try to increase transformation efficiency by using SOC media and generally avoid building parts < 100 bp. e.g. we don't tend to use promoters and RBS separately we make larger combined parts containing both.


Synapses of inhibitory neurons I sometimes read of "inhibitory synapses". But I understand that when the neuron is inhibitory, all of its synapses will be inhibitory (so it is a property of the neuron, not only the synapse) - is that correct?

How is this experimentally tested? I did not find an estimate of how many outgoing synapses inhibitory neurons typically have, but I assume that it might be thousands. So how do we know for all of its synapses that they are inhibitory?

I think the definitions of inhibitory and excitatory neurons are currently defined as a matter of convenience based on observations made by synaptic staining, electrical feature and its morphology.
In other words, neurons with more inhibitory synapses are inhibitory neurons, and neurons with more excitatory synapses are excitatory neurons, and so on.
By detecting inhibitory and excitatory synaptic-specific staining in different colors on the same section, we may be able to determine whether all synapses in a single neuron are inhibitory or excitatory.
Also, I think there are events happening in the process of neural differentiation that distinguish excitability/inhibition, but we don't seem to know how they are happening.
It may be determined by signals from neighboring neurons, Ca++ concentration, etc.
If, at the neuronal precursor stage, the differentiation mechanism that determines excitability/inhibition could be confirmed at the level of gene expression, it might explain why inhibitory neurons only make inhibitory synapses.
22th June 2020 added;
I find a good example of Excitatory synaptogenesis on dendrites of hippocampal-mediated (inhibitory) neurons, here;
https://www.nature.com/articles/ncomms1736
In short, this article shows what will occur after generating spine on inhibitory neuron.
(A)The synapses move along the microtubule from the tip of the process to the shaft. (B) Morphological changes in parallel fibers of cerebellar granule cells during synapse formation. When the parallel fibers come into contact with Purkinje cells, the neurexin-Cbln1-δ2 glutamate receptors A complex of synaptic vesicles is formed and synaptic vesicle accumulation occurs. Synapse matures after microprojections extend from the parallel fibers and encircle the spine to form an annular structure. (C) In early postnatal hippocampal pyramidal cells, DCLK1 accumulates at the tip of the process to promote process elongation and Inhibition of synaptic maturation.


Is there a scientific name for the field of study focusing on the hemispheres of the brain and their control of opposite sides of the body? I'm assuming this field of study would focus on motor controls, movement, and exercise, but it could also focus on activities which strengthen the corpus callosum or stimulate a specific half of the brain.


What's the name of this tree? I photographed this flower on the street in Los Angeles.
It looks like a lilac, but I am not sure.

This is probably a crape myrtle, a plant from the Genus Lagerstroemia.

Here is another photo for comparison:

And here another photo, showing the whole tree:


Is there any documented evidence for suicide among vertebrates other than humans? Is there any documented evidence for suicide among vertebrates other than humans? Lemmings not accepted !

Well, there are certain behaviors that may qualify. The clearest example I know of would be sexual cannibalism, and more specifically (source):

  The redback spider is one of only two animals to date where the male
  has been found to actively assist the female in sexual cannibalism. In
  the process of mating, the much smaller male somersaults to place his
  abdomen over the female's mouthparts. In about two of three cases, the
  female fully consumes the male while mating continues. Males which are
  not eaten die of their injuries soon after mating.

That sounds pretty suicidal to me...

A less flagrant but commoner example is that of mothers dying to nourish their offspring. Again often seen in spiders, the best example I know of is the giant pacific octopus (Enteroctopus dofleini). The female will chose a den and lay her eggs. She will then spend her last weeks tending her young, never leaving the lair to hunt. Eventually she dies of hunger and her body nourishes her young. My source here is the wonderful BBC life documentary series.

Neither of these are vertebrates of course but still, I thought the suicidal little spider was interesting.


Is there a scale suitable for continuous tracking and recording of plant weight? I want to measure water transpiration and evaporation in a bonsai tree, and measuring the weight of the tree in its pot is my proxy for water usage.  This has worked well with manual measurements, but I want to go to the next level.
I would like to monitor the weight of something continuously (e.g. once a minute) and access the data easily via a phone app.  Is there something like that?
There are numerous options for similar devices if you want to measure ambient temperature and humidity (e.g. https://www.amazon.com/SensorPush-Wireless-Thermometer-Hygrometer-Android/dp/B01AEQ9X9I).
But all my searching for balances with similar functionality have failed.  I've found many lab balances and kitchen scales, and body weight scales.  Only the body weight scales interact with apps on your phone, but they do not record continuously.
If you know of one, or just have better google-fu than me and can suggest a more precise search term, any pointers would be appreciated.

maybe this company  https://www.industrial-needs.com/scales-and-balances/recording-scales.htm

Our scale software allows a real-time measurement on a computer and
depending on the weighing data, they can also be saved with a date
stamp as a TXT file on the computer


When does the Cas9 nuclease stop? If I understand correctly, the steps of gene editing with CRISPR-Cas9 are roughly as follows

Cas9 nuclease and guide RNA form a complex.
Cas9+guide RNA complex scans genomic DNA and recognizes the sequences homologous to the guide RNA
Induces a double strand break in DNA upstream of the PAM sequence (only breaks when the homologous sequence of the guide RNA is in the vicinity of the PAM).
Genetic modification using the mechanism of DNA repair (NHEJ, HDR) after double-strand break.

If so, in the gene editing with CRISPR-Cas9 , gene editing is likely to continue as long as the Cas9 does not lose its activity, am I right?
My question

When does the Cas lose its activity?
What was the logic of the experiment that identified the timing? / If the matter itself is unexplored, what kind of experiments could be done to find out the timing when the Cas lose its activity?

As this movie shows, if the gene editing occurs successfully, it will indeed introduce a mutation in the target gene.
However, even if it does,-this is just my guess from here on out- it is likely to remain complementary to the target gene, at least upstream of the guide RNA. However, even if the target gene is mutated, there is likely to remain complementary sequence to the guide RNA, at least upstream of the mutation. So, even if one successful gene edit is completed, I think it's possible that gene editing could happen again in the same location. Moreover, even if the targeted site is successfully edited, there is still the possibility of subsequent off-target editing elsewhere. That's why I think the tools exist to stop CAS.

A guide RNA binds to the target gene that has been bitten by CAS. The strand opposite the strand to which the guide RNA was bound has just been cleaved.
Quoted from this video.
An idea for an experiment to detect when CAS goes quiet
If a single cell colony was created from a gene-edited population and there was genetic variation in the cells born from that colony, then I think that would mean that there would have been Cas9 activity even after the single cell colony was started in culture. Is this idea correct? Could there be a smarter experiment?

Regarding the loss of Cas9 activity, you are already touching on the answer in your question. Cas9 as a nuclease/enzyme is always active, and will continue to cleave double-stranded DNA as long as there are complementary target sites and guide RNAs to guide it there. If the target site is not mutated or completely removed after cleavage, Cas9 can indeed cleave the same site again.

However, even if the target gene is mutated, there is likely to remain complementary sequence to the guide RNA, at least upstream of the mutation.

I'm not sure if I misunderstand the point you are trying to make here, but the introduction of mutations is usually enough to prevent recurrent cleavage of the same site (although studies of off-target effects clearly show that this is not always the case):
Both Streptococcus pyogenes and Staphylococcus aureus Cas9 cleave their target sites between positions -3 and -4, counting from the end of the 20-nt guide sequence (see attached figure below). The double-stranded break can then be repaired either via non-homologous end joining (NHEJ), or via template-driven homologous recombination (HR).

In the former case (NHEJ), double-stranded breaks are sometimes repaired with small errors. These errors usually accumulate near the break site (read about NHEJ to understand why), and such mutations will typically destroy the gRNA recognition site. Note, however, that not all (in fact, very few) NHEJ repair events will result in the introduction of mutations, and "perfectly repaired" breaks both can and will be re-cleaved by Cas9. But since repeated cleavage is lethal to the cell, there is a selective advantage for mutations that prevent re-cleavage of a target site. Also note that the introduction of mutations (and thereby gene editing) via NHEJ is a random process, with no direct control by the researcher.
In the latter case (HR), the DNA template used for repairing the double-stranded break can typically be chosen by the researcher. It can for example be a chemically synthesized DNA fragment or PCR product with at least some sequence homology to regions flanking the cleavage site. But since there is no specific sequence requirement for the region in between the homology regions, this interspacing region can be designed such that it partly or completely replaces the original recognition and/or PAM sequence (violet region in figure below).


Can intron become exon in alternative splicing? From this image

We can see several exons that are actually introns in other genes. It's not a really a different gene, it's an alternative splicing of a gene. My background is not biology so is it possible for alternative splicing to behave like this? I only know that alternative splicing is just exon skipping and introns will just stay introns and not become exons. Can someone explain this to me and give any suggestions on which part of biology (or genetics) I need to learn. Thank you.

Most of the transcripts you show have different transcription start sites. In other words, this happens because of alternative transcription start sites. So this is not typical alternative slicing. Some genes have different transcriptional start sites, but the case you show has exceptionally many start sites.


Seeing with one eye, why intensity doesn't get half? Today I just closed one eye(for finding blind spot), and as usual some of the visual field is lost, but I wonder why is not intensity of light(brightness) reduced to half?
Shouldn't it be since our brain is now getting only half impulses?

Does our brain instantly reduces the threshold of rods and cones when one of the eye is closed?

Think of eyes as cameras producing an image at a given framerate. If you have 2 cameras and shut 1 of them off, that doesn't change the amount of light incoming to the other camera.

Your question is one of signal interpretation rather than receiving signals and adding them. Given that the 2 cameras have different perspectives, adding their respective pixels makes no sense. Instead, the dual images (if both cameras are on) are post-processed for spatial reference relevant to perspective.

In the case where a camera is shut off, then the spatial reference becomes a null picture and the post-processing can be skipped.

(For reference, if you took incoming data from both eyes and added them, the result would be an incoherent and largely unusable mess)


Why didn't humans evolve to reproduce identical twins all the time? According to the selfish gene theory, it seems like because identical twins sometimes get produced, a mutation to a gene that says, "if you have an identical twin, be fully altruistic towards them" would get selected for when ever it happens to arise in an identical twin. After humans evolve to be fully altruistic towards identical twins, wouldn't a mutation to a gene that makes a woman more likely to produce identical twins also be selected for because if it happens to appear in a a child who has a non-identical sibling, that gene might be discontinued from reproduction by the partial selfishness of the sibling but if it appears in an identical twin, the other identical twin will preserve that gene with their altruism.

What you describe could have happened under the right conditions. However, there are a few things you haven't considered.

Because humans are especially altricial, always having twins would double the cost of children on parents.
The benefit of sexual reproduction is immune diversity. So a population like this could be far more vulnerable to disease.

So as far as this thought experiment goes, genes can't be too selfish or they dramatically reduce their own fitness. It's something worth simulating computationally to see what happens.

References

Sexual reproduction as an adaptation to resist parasites (a review)


Voluntary actions of Autonomic Nervous System Somatic motor activity is always voluntary, while ANS motor activity is usually involuntary. pgno:762

This indicates the possibility of voluntary activity by ANS.
So, what are the voluntary actions by ANS?

My Attempt:
Wikipidea says:

Most autonomous functions are involuntary but they can often work in conjunction with the somatic nervous system which provides voluntary control.

So, is right to say that Flight or Fight response is the voluntary activity of ANS?

I have no idea what the author has in mind, but their statement is wrong from the beginning: somatic motor activity is not always voluntary. Reflexes are a good and obvious example.

"Fight or flight" response is basically half of the entire ANS (the sympathetic part), so that's incredibly broad. Parts of that response are definitely involuntary.

I think it's more likely that Wikipedia is thinking of things like breathing, which is normally under ANS but you can also manually control your breathing. They may also be thinking of things you can do to directly influence your autonomic responses, for example, if you start running, you are voluntarily moving your muscles, but the autonomic nervous system will also participate (for example, by increasing your heart and breathing rates).


Impact of latitude on agriculture? I live in southern California, where the difference between seasons is mild, and the dominant limitation on agriculture is the lack of water. (Spring is whenever it rains, not a place on the calendar.)

In my early education, as is usual, I learned the growing season is shorter in more northern latitudes. The natural deduction is to expect less effective agriculture, further north.

Recently, I spent a week in early April in Vancouver (Canada). The weather was very (very!) nice, much warmer than I expected, and the hours of daylight longer. On reflection, all this was obvious ... but I was surprised at the time.

Northern latitudes may have shorter growing seasons, but the hours of daylight during that season are much(!) longer. What is the potential agricultural productivity of more northern latitudes?

Much of the past century of agricultural research was centered on the American mid-west. How much is possible if we further optimize agriculture for more northern latitudes, and higher levels of technology?

As the Earth warms, large expenses of Russia and Canada will thaw. Seedlings started early in artificially warmed and lit greenhouses could jump-start crops. (Or transported from more southern latitudes.) If we took full advantage of the longer hours of daylight in northern growing seasons ... what is the limit to agriculture?

With global warming, could Canada and Russia become the bread-basket of the world? Can agriculture as a technology be adapted to more northern latitudes, and take best advantage of a shorter season with longer daylight?

(In imagination, I see seedlings started in greenhouses, and robot-planters placing seedlings in just-warm fields, to capture every hour and day of longer sunlight.)

Do we know how to best take advantage of long northern days for agriculture?

I know this response is coming a bit late but in case you're still curious I have a response!

I'm a M.Sc. student working in Agricultural entomology in Northern Canada (between 55 and 59 degrees North). You are correct, up at more Northern latitudes our short growing season mainly limits what crops we can grow, but less so our yield. We are also restricted in where we can farm by soil conditions as the further north you go the more you are on the Canadian Shield - so less fertile. If you look at growing regions in Northern Alberta, North West territories, etc. you'll see that they tend to stick fairly close to rivers. Further south in Canada, moisture conditions play a much bigger role in determining yield. Mainly we stick to crop species and cultivars that can produce a good yield in a short time - canola, wheat, barley, peas (although corn and soybeans have some large acreages in the Eastern prairies and Ontario).

Climate wise, the comment about light intensity is not really accurate in the summer. The longer daylength definitely compensates for any differences in light intensity. Even at 59 degrees latitude it can get well into the 30's (Celcius) in the summer.

Canada already produces a large amount of wheat and canola, we are the 6th largest exporter of wheat according to a quick google search. So I would argue that while Canada may not be the bread basket of the world it is pretty close already.

It's tough to say how climate change will affect agriculture, because it's really tough to determine how climate change will affect local climate. The changes to weather patterns (changes in amount and timing of rain and moisture, changes in spring or fall frost timing) will have a large impact on agricultural outputs.


Unlike humans, why do plants not have something blood-like to transport $O_2$ throughout their body? Since plants have a large number of stomata at different parts of their body, they can get $O_2$ at almost every part of the plant and so, they don't need to transport it throughout the whole body whereas in the case of human beings, they can only intake $O_2$ through their nostrils, but a large number of organs throughout their body require it. So it needs to be transported. And for this reason, blood is present.

Let me know if I'm wrong and what the actual answer is.

In plant cells, O2 enters through stomata or lenticels. Then, the O2 molecules are transported to the cells through the process of diffusion. Stomata and lenticels are found all over the surface of plant body, i.e., leaves, stem and root. Because of this, plants don't need blood like connective tissue to transport O2 and CO2.


Can you tell the name of this spider? This image has been posted on the Wikimedia Commons

This spider is about 3~4cm long. It was found in the middle of tomatoes plants in a garden, in the center of France, Clermont-Ferrand. Photo taken in the early days of August. It would be interesting to specify the species on Wikimedia Commons.

Please let me know if you need other information.

This is a wasp spider (Agriope bruennichi)

See here: Wasp spider

The link leads to a German Website showing the belly side of a wasp spider

Or see here: Wasp spider II


What is the relationship between W, X, Y and P, M retinal ganglion cells? In Guyton and Hall Textbook of Medical Physiology (12e) the retinal ganglion cells (RGCs) are classified into W, X, and Y types. However, in Gray's Anatomy (40th ed.), RGS are subdivided into midget and parasol cells. What is the relationship between the W-X-Y versus midget-parasol classifications?

Summary of the WXY classification as in Medical Physiology:

About 40% ganglion cells are W cells. They are the smallest (<10 μm), and the slowest (8 m/s) to transmit signals, but they have the broadest receptive field. They receive signals from rods and detect directional movement.

About 55% are X cells. They have medium size (10~15 μm) and transmission speed (14 m/s). Their fields are small. They transmit color vision.

About 5% are Y cells. They are the largest (<35 μm) and the fastest (35 m/s) to transmit signals. They have broad fields. They respond to rapid changes in the vision.

Short answer
X = P = midget = β
Y = M = parasol = α
W = γ

Background
First off, P and M cells are not equal to parasol and midget cells; on the contrary - P cells are midgets and M cells are considered to be parasols.

X, Y and W cells are used to denote different retinal ganglion cells in cats, as proposed by experiments Enroth-Gubel & Robson (1966). As you already indicate, these cells have different physiological response properties. X and Y cells have the standard center-surround distribution of their receptive field, X cells having linear additive response properties in center and surround and Y cells nonlinear properties. X cells therefore have predictive responses such that responses can be predicted to be maximal (e.g. light shining on the ON center and no light stimulation on the OFF surround). Y cells tend to respond in more complex ways. W cells do not have a center-surround structure (Bruce et al, 1996).

Based on morphology, retinal ganglion cells in the cat have been labelled α, β and γ cells, which are thought to correspond to the physiological classes of Y, X and W cells, respectively (Boycott & H. Wässle, 1974).

The P and M division was introduced by De Monasterio & Gouras (1975) based on monkey experiments. P and M refer to the parvocellular and magnocellular connections retinal ganglion cells in monkeys make in the LGN of the brain. Both types of cells have a center-surround receptive field structure like X and Y cells in the  cat. P cells show color opponency and respond to specific wavelengths of light, and are involved in color vision. P cells respond to a range of wavelengths and respond most vigorous when different light intensities illuminate the center and surround (Bruce et al, 1996).

P cells are considered to be mostly midget ganglion cells, and equivalent to β cells of cat. M cells, on the other hand are considered to be mostly parasol cells and resembling α cells (Kolb, 2001).

References
- Boycott & H. Wässle, J Physiol (1974); 240(2): 397–419
- Bruce et al, Visual Perception (1996); 3rd ed. Psychology Press
- De Monasterio & Gouras, J Physiol (1975); 251(1): 167–95
- Enroth-Gubel & Robson, J Physiol (1966); 187(3): 517–52
- Kolb H. Webvision (2001). Salt Lake City (UT): University of Utah Health Sciences Center


Which processes are during the latent period of ventricular contraction? The latent period is the time between the start of depolarisation and the start of contraction.
I know that the contraction of ventricles starts after sufficient influx of Ca2+ and threshold potential is met.
The influx of Ca2+ is at start of Phase 2, so Phase 0 and 1 are included in the latent period.

Comparing to electrocardiogram is not simple, since there is always at least some time lag between the event and the recording.
I think there not much sense to compare cellular model events to ECG recordings here.

Which cellular processes does the latent period include?

During the latent period of ventricular contraction, excitation-contraction coupling takes place.

There may be other processes, but I think most are these from Wikipedia:

An action potential is initiated by pacemaker cells in the Sinoatrial node or Atrioventricular node and conducted to all cells in the heart via gap junctions.
The action potential travels along the surface membrane into T-tubules (the latter are not seen in all cardiac cell types) and the depolarisation causes Ca2+
to enter the cell via L-type calcium channels (also known as Dihydropyridine receptors) and possibly sodium-calcium exchanger during the early part of the plateau phase. This Ca2+
influx causes a small local increase in intracellular Ca2+
.
The increase in Ca2+
is detected by ryanodine receptors in the membrane of the sarcoplasmic reticulum which releases Ca2+
in a positive feedback physiological response. This positive feedback is known as calcium-induced calcium release and gives rise to Calcium sparks.
The spatial and temporal summation of ~30,000 Ca2+
sparks gives a cell-wide increase in cytoplasmic calcium concentration.
Contractile mechanism similar as in skeletal muscle about cytoplasmic calcium binding to troponin C and so on.

Note that to fully answer this question you should include figures about mechanisms of excitation-contraction coupling, cardiac action potential -figure and permeabilities of different ions.


Thoughts precede neuron firing or vise-verse? I am at the verge of submitting a paper on 'scientific explanation of reality' to an international philosophy body. First submitted draft was returned by the evaluation expert, asking me to re-submit it, after re-checking the validity of my  assertion that 'science (biology) believes that neuron firing always precedes thought'. Can any one provide answer on biology's clear stand on above question ?

I think the only way to interpret these kinds of questions biologically is to assume that "thought" means "the perception of a thought occurring." The perception of a thought, like all perception, arises from neuronal firing.

The interesting biological (rather than philosophical) questions arise when we look at the relationship between the neural firing that gives rise to the perception of intent to act and neural firing that carries out the "intended" actions.

This paper is relevant. The authors are trying to argue that the initiation of a motor action comes before the perception of intent for that action. I'm not a cognitive neuroscience person, though, so I'm not very familiar with their techniques and personally have a hard time determining if they draw valid conclusions.


How much can you learn about species variation from a skeleton? I just read about the discovery of the 1.8-million-year-old human skull in Georgia, and how it suggests that early humans were all one species instead of distinct ones. Would an archaeologist unearthing dog bones a million years from now know that a Great Dane and a Chihuahua are the same species?

It seems as if this article is purely speculative. They didn't mention any DNA testing, but instead discussed physical features.

There are two "types" of archaeologists: clumpers and splitters. Clumpers (like the author of this article) believe that there is wide variety among members of the same species, and so it is often wrong to categorize every new hominid fossil as being a different species. Splitters like to "split" their findings into new species, even though there is no evidence that speciation had ever occurred; they just decide that since the remains look different, they must have speciated.

In the future, I hope that archaeologists will have more sophisticated means of sequencing the DNA of ancient remains, allowing them to construct an accurate phylogeny


How many (taxonomic) families are there? Approximately, how many families have been identified?

I've often often come across figures for the total number of species on Earth. Recently, I found myself wondering about the encompassing ranks above them, specifically family, but I can't recall any figures on family and it's a little difficult finding what I want by typing "family" into a Google search. ;)

The NCBI Taxonomy statistics page displays the following information:

There are currently 73540 genera, 331418 species, and 23127 taxa of higher order. Since the number of taxa decreases with the genericity of the taxon, there are probably around 20000 families, give or take a few thousand.


What is this tiny insect? I took this picture in central Mexico. The insect is about 1mm in size. I found lots of these dead on a desk, so many that at first I thought they were just dust. I assume they came from a plant that was above the desk.

Does anyone know what it might be?

EDIT:

I found the culprit walking nearby! I guess that verifies what others pointed out: It seems to be the molted cuticle of an aphid. (sorry for the poor quality of the pictures)

Thanks a lot!

Since you suggest they come from a plant, they might be dried aphids. These insects usually feed on plant sap, and I already noticed some tiny, white, and apparently dead ones on plants.

As suggested in the comments, these are actually not dead aphids, but only the cuticle they leave after moulting, or ecdysis.


Bioinformatics : Drawbacks of using ORA(Overlap Analysis) What do you think are the potential drawbacks/weakness of using ORA to explain distinction between two phenotypes.

I identified a few which were the dependencies of DE and the statistical method used to filter the starting DE list.

Any other weakness?

Thanks

It really depends on the specific methods you're using. If you're using a pathway-based methodology, I'd strongly recommend reading Khatri et al (2012) (1), which provides a good overview.

The main issue that's not touched on in that work is that pathway-based methods are highly dependent on the pathway definitions used, and the contents of the pathways are not always what you might expect in terms of their topology (a good example is KEGG's Neuroactive ligand-receptor interaction (2), which contains a huge number of events that look like 'single ligand binds to receptor', with no downstream events).


ATP stoichiometry of the Na+/K+ pump The Na+/K+ ATPase pump exports 3 Na+ for every 2 Ka+ imported. This process is ATP dependent, but I have not been able to find how many ATPs are required in each translocation. What is the stoichiometric ATP cost of this reaction?

Sodium/potassium-exchanging ATPase (EC 3.6.3.9):

  An enzyme from the plasma membrane of animal cells that catalyzes the efflux of three Na(+) and influx of two K(+) per ATP hydrolyzed.

You can read about the mechanism on Wikipedia:

  The pump, after binding ATP, binds 3 intracellular Na+
  ions.
  ATP is hydrolyzed, leading to phosphorylation of the pump at a highly conserved aspartate residue and subsequent release of ADP.
  A conformational change in the pump exposes the Na+
  ions to the outside. The phosphorylated form of the pump has a low affinity for Na+ ions, so they are released.
  The pump binds 2 extracellular K+ ions. This causes the dephosphorylation of the pump, reverting it to its previous conformational state, transporting the K+
  ions into the cell.
  The unphosphorylated form of the pump has a higher affinity for Na+
  ions than K+
  ions, so the two bound K+
  ions are released. ATP binds, and the process starts again.


What determines the colors and patterns of a clam shell? Earlier this week I was looking at some bivalve shells that had ornate patterns which ranged in color from a light orange-pink to a deep orange-red. Here is an image I found online that seems to be of the same type of shell:

The friend who was with me said, "I wonder where the color comes from." We were trying to look for two shells with similar colors, patterns, and approximately equal sizes, and it was hard, even though we were looking through a large collection of similar shells.

What determines this ornate pigmentation? Is it influenced by environmental factors such as the minerals in the water? Does it have anything to do with the age or health of the organism? Or is it purely genetic? Is this determined by the same basic biological principle that determines the color of human hair, or is there something different at work in shells?

This post is pretty well written and seems to say that the evolutionary forces that produce shell color like this is not known.  There are suggestions that the color is camoflage or the result of metabolic byproducts or that the pigments serve to strengthen the shell.  Its hard to believe some of these theories given that some shells do fine without coloring (at least that humans can see).

Structurally, shells are living things.  [They consist of many layers of thin irregular calcium carbonate hexagonal plates that make the mineral portion of the shell. The plates are held together by a protein glue and renewed by cellular action][3].  Whatever their evolutionary motivations, the colors are biomolecules which are in the biomatrix binding the plates together. This is a reason that shells that are left out to dry in the sun can become bleached and brittle.

I wish I had some better references about the shell structure, but I'm remembering a lot of this from a one afternoon book report given in a class, not from any intensive study on my part.

This has influenced some ideas about things like tank armor, by the way.  At least there is funding for biomaterials research by agencies interested in tank armor.  Lamellar armor made of segmented plates can withstand tremendous impacts at a single point like a shell being dropped from a great height by a seabird or a shell hitting a tank. Plates just a few microns wide and a fraction of a micron deep shaped like irregular hexagons are hard to make if you aren't a mollusc so far though.


What are the main mechanisms of interaction between the nervous and immune systems? We know from pop science that our psychological states have an effect on our immune systems ("worrying ourselves sick", etc.), but what are the actual mechanisms through which our nervous systems pass information to the immune system?

Cell mediators come to mind, but where in the body would a nerve cell release an interleukin or other factor? (Put another way, are neurons releasing these factors as a part of their normal cell metabolism and the side effect is a communicative effect with the immune system?)

It is not only the immune system that prevents us from getting ill. Worrying much in my opinion won't make you catch a cold; rather, you can get problems with your cardiovascular system (arrhythmias, hypertension, angina pectoris) or limbic system (panic attacks, sweating attacks etc.).

The connections are many; here are some possible ones:

There are many glands in our body that are either densely innervated (like the thyroid gland) or are a part of nervous system (like pituitary gland, epiphysis). They can release hormones directly to our blood and make our hormone profile unstable, hence also impacting the immune system.
Sympathetic/parasympathetic nervous system is under direct control of the CNS (N.vagus, carotide sinus sinus etc.) and can dramatically change the peripheral resistance of our vascular system by constricting (=> angina pectoris, hypertension) or dilating (swellings, bowel movements problems -> constipations etc.) the small vessel. This alone can start so many different mechanisms resulting not only in being ill, but also being dead.

Speaking about connection between the nervous and immune system we must consider that:

Many neuromediators, like adrenaline, for example, have clear effects on immune cells.
The mediators and humoral factors released by nerve endings can easily diffuse outside of the synaptic cleft and act locally, attenuating immune response.


What are the "stars" we see after a bump on the head? Sorry  if this might appear funny. When I close my eyes for a longer time, and suddenly open  it, I see some twinkling white small circles, and when i concentrate on anyone of them it disappears, as if the image is falling on the blind spot.

This also happens when I am struck on my head sometimes accidentally. I would see thousands of tiny objects floating. What are these and why they appear shiny ?

"Seeing stars", or as it formally is called, "phosphene", is caused by stimulation of the visual cortex or retina by causes other than light hitting the retina.
http://www.oubliette.org.uk/Three.html


How was it discovered that flouride helps stop tooth decay? Apparently flourinated water helps stop tooth decay. So I have some quesions about this.

Firstly how does it stop tooth deacy?

and

Secondly, how was it found that out of all the chemicals, it is flouride that stops tooth decay and nothing else?

There is an interesting historical story of fluoride use in prevention of dental caries.
Interestingly the journey started with a "mysterious disorder-fluorosis."

In 1909 Dr. McKay (r) persuaded the Colorado State Dental Association to invite Dr. Green Vardiman Black (l), one of the nation's most eminent dental researchers, to attend 1909 convention where McKay's findings were to be presented. The two men began joint research and discovered other areas of the country where brown staining of teeth occurred.

Fluoride research had its beginnings in 1901, when a young dental school graduate named Frederick McKay left the East Coast to open a dental practice in Colorado Springs, Colorado

McKay collected the samples. And, within months, he had the answer and denouement to his 30-year quest: high levels of water-borne fluoride indeed caused the discoloration of tooth enamel.

Dr Dean recalled from reading McKay's and Black's studies on fluorosis that mottled tooth enamel is unusually resistant to decay. Dean wondered whether adding fluoride to drinking water at physically and cosmetically safe levels would help fight tooth decay.

This finding, considering the thousands of participants in the study, amounted to a giant scientific breakthrough that promised to revolutionize dental care, making tooth decay for the first time in history a preventable disease for most people.

These are excerpts from the article
Another reference
In 1802, Sir James Chrichton Browne suggested the probable cause of dental caries as a change in bread, which did not have bran or husky part of wheat containing fluorine.
Now your next question on fluoride stopping the tooth decay.
So yes apart from preventing tooth decay, research has found that fluorides like silver diamine fluoride can be treatment of choice for dental caries.

The silver component provides an anti-bacterial effect while the fluoride promotes remineralization of tooth structure.

I hope I have answered your question :)


Why is the null hypothesis of trait evolution Brownian motion? Many models of continuous trait evolution assume that traits evolve according to Brownian motion. What is the biological or physical basis for this choice?
I realize there are models that do not assume Brownian motion, but what I am interested in asking is why the null model is so often chosen to be Brownian motion.

I think that the simple answer to this question is that the present comparative methodology was largely established by Felsenstein 1985, American Naturalist. For mathematical convenience, he suggested Brownian motion as a null hypothesis, because "...the variance of the distribution of change of a branch is proportional to the length of time of the branch...", and then "...it is easy to see that the differences between pairs of tips... must be independent." Also: "...after one unit of time, the contrast [between a pair of tips] has expectation 0 and [easily defined] variance..."
He explicitly discusses whether Brownian motion is a reasonable model in the section "What if we lack an acceptable statistical model of character change?"
I would suggest reading that paper in more detail if you are interested in the details of Brownian motion applied to phylogenies.
A recent historical perspective on this influential paper can be found here.
For a more extensive bibliography/more details you can see here.


Where do transamination and deamination take place? The only information I know is about deamination is that it occurs in the liver and kidney. But in which part of the cell does deamination occur? To which tissues is transamination specific, and in which part of the cell does it occur?

I have searched Google and Google books and have come across some information like L-Glutamate dehydrogenase occurs in both cytoplasm and mitochondria and transamination occurs in the cytoplasm of all cells. But they were not from authentic sources, so I am asking it here.

According to David H. Vroon and Zafar Israili aminotransferases (transaminases) are widely distributed among tissues, and are found in both cytoplasm and mitochondria, although this may vary between different aminotransferases:

  Aminotransferases catalyze the redistribution of nitrogen between
  amino acids and corresponding oxoacids participating in both protein
  metabolism and gluconeogenesis. They are ubiquitous in their cellular
  distribution.

  Tissue activity for AST (aspartate aminotransferase) is as follows in decreasing concentration:
  heart, liver, skeletal muscle, kidney, pancreas, spleen, lung, and
  erythrocyte. Two distinct forms have been identified: a cytoplasmic,
  or soluble isoenzyme, and a mitochondrial isoform...

  The distribution and relative tissue concentration of ALT (alanine aminotransferase) is similar
  but importantly different. Highest activity is found in the liver,
  followed by kidney, myocardium, skeletal muscle, pancreas, spleen,
  lung, and erythrocyte. ALT activity is found in the cytosol; organ- or
  organelle-specific isoenzymes have not been demonstrated. The
  concentration of ALT in hepatic cell cytoplasm is comparable to AST;
  however, a mitochondrial ALT isoform is not found. In all other
  tissues, ALT activity is significantly less than AST.

As regards deamination, there is a Wikipedia page for glutaminase, which indicates that it is found in the mitochondria of a variety of tissues. There are two isoforms, one especially active in the kidney, and the other in liver (although both are found in other tissues).


In adverse effects of Heparin, why is bleeding from deeper organs more common? The reason given in my book is that it i because it interferes with the secondary hemostasis..but i did not understand how that implies that bleeding from deeper organs is more common..

Skin is extraordinarily tough compared to much of our internal tissues; it has to be to protect us. To bleed, skin integrity must be breached, which usually involves sharp objects.

Think for a moment that most splenic or hepatic injuries (even complete ruptures) occur from blunt force trauma without breaking the overlying skin. For a more common example, if someone hits your thigh with a baseball bat, you will get a large bruise, maybe even a broken bone, but the skin will usually remain intact (if badly bruised) from blood vessel damage beneath and within the skin.

Many organs are delicate, and damage within them is not rare. Bleeding within/from some bodily organs is fairly common: runners bleed from their kidneys, and many, many people bleed from somewhere in their GI tract. High blood pressure may cause bleeding in the brain (a stroke) but it won't cause bleeding from the skin.

Just add to all the above the effect of anticoagulation (what heparin does.) I hope that explains things. If it doesn't, please leave a comment.


Is it ok for Chili pepper plant's fruits to fall into its soil? I wonder if Chili pepper's fruits which fall into the soil near the plant will harm it, since the peppers are so spicy for people.

As @MCM says, the capsaicin molecule isn't intrinsically damaging - its effect upon us is mediated through the TRPV1 (Transient Receptor Potential Vanilloid 1) receptor in the membranes of cells whose function is to sense noxious stimuli such as heat. The binding of capsaicin to this protein causes transmembrane movement of Ca2+ ions which depolarises the membrane, triggering an action potential - a signal to the brain. Heat has the same effect on the TRPV1 protein. In this way the presence of capsaicin mimics the effects of heat, causing a painful sensation.

Have a look at this SE.Biology question.


cellular respiration What are the effects of addition of these chemicals to actively respiring cells ?
Which of them would lead to INHIBITION of aerobic respiration ? Would cytochromes be actually taken up by cells ?

a.addition of CO

b.addition of CO2

c.addition of cytochromes and flavoprotein

Carbon Monoxide "CO" would definitely inhibit aerobic respiration. This is in fact the mechanism of the toxicity of compounds such as carbon monoxide and cyanide, namely, carbon monoxide binds (coordinates) with an affinity several orders of magnitude greater than oxygen to the heme group of mitochrondrial cytochrome oxidase, thus inhibiting the enzyme. When the respiratory electron chain is no longer drawn by the reduction of molecular oxygen, the hydrogen ion gradient across the mitochrondrial inner membrane is depleted, and ATP production halts.

Carbon dioxide would not effect the electron transport chain directly, but is rather involved in the reactions of the citric acid cycle, although, in all likelihood, the cell would die of acidosis before CO₂ concentrations became great enough to reverse the citric acid cycle. Cytochromes and flavoproteins are complex molecules that if the cell were to endocytize them, it would simply digest them.

I do not know your degree of experience in biochemistry, but if you wish, search on the internet for protein structural images of cytochrome oxidase or hemoglobin bound to oxygen and carbon monoxide. Oxygen binds the iron of the heme group at an angle, while carbon monoxide binds directly perpendicular to the heme ring. This difference in geometry is partially responsible for the differential affinity of the two species for heme.


Why Does Salt Water Help Sore Throats? I am having some trouble understanding how salt water, a simple solution, could so effectively remove the pains of a sore throat.

I do believe that the answer is closely related to hypo/hyper-tonic solutions, but why is this so, and how does this work?

Salt water may have anti-septic properties due to the effect it has on water potential.  Pure water has a water potential (Ψ) of zero.  A concentrated salt solution has a lower (more-negative) water potential.  The water potential of the salt solution is likely to be more negative than that of the pathogen's cytoplasm; the salt solution is therefore referred to as hypertonic.  Therefore water osmoses out of the cell (osmosis being the net movement of water from a higher water potential to a lower water potential across a semi-permeable membrane).  The loss of water from the pathogenic cells causes osmotic crenation - the cell becomes shrivelled and dies.

A hypotonic solution (for example cells placed into pure water) would cause the opposite effect - osmotic lysis.  This is the bursting of the cell due to the movement of water into the cell.  The bacterial cell wall would first have to be damaged (e.g. by penicillin).  This would not be the process by which a salt solution has effect, however.

The fact that the salt water is warm in order to improve solubility may also have the side-effect of causing vasodilation around the infection, increasing the rate at which white blood cells can arrive at the infection site.

It has been more difficult to find a theory as to why a salt solution would have analgesic properties, see the comments below & previous versions of this answer.


How can promoter binding sites be determined? I have been trying to find out which sigma factor is responsible for the transcription of RNA polymerase subunits $\alpha$ (rpoA) and $\beta ^{\prime}$ (rpoC) in Bacillus subtilis. I would expect it to be the housekeeping $\sigma^A$. However I have found out from the Bacillus subtilis transcription factor database, that $\sigma^A$ binding sites have been found in the promoters of $\beta$ (rpoB) and $\delta$ (rpoE) subunits, and a whole bunch of alternative $\sigma$ factors, but it says nothing about $\alpha$ or $\beta ^{\prime}$.

So I want to know if there is a way for me to find out, without entering a wet lab!

Firstly; how do we know that something is a transcription/sigma factor binding site? What is it about the region? And how do we know which TF/SF it is a binding site for? Could the same transcription/sigma factor have multiple different binding site motifs?

Secondly; Since the genome for B. subtilis is available, would I be able to find out binding site motifs for all the sigma factors, and then determine which is/are contained within the promoter for the $\alpha$ subunit? I.e. if I know the TF/SF sequence, is there a way of finding out which promoters it can bind to?

Finally; the main purpose of this question is to find out how rpoA is transcribed, and I know that in general sigma factors are required in bacteria for specific transcription initiation, but could it be that rpoA transcription is non-specific, and that the sigma factor is just not involved in its transcription?

Please let me know if there is anything I can do to improve my question, I can provide references if it would be a good idea. Thanks!

I don't have a definitive answer, but I can perhaps offer some insight. Given the necessary function of rpoA, I would be willing to bet that SigA is the factor responsible for its transcription, so I will focus my discussion there.

Predicting promoters without experimentation can be very challenging given their immense variability. The idealized core promoter consists of a -10 region, a spacer and a -35 region. Recognition of the promoter by a sigma factor is done at the -10 and -35 regions: each sigma factor recognizes a different consensus sequence. Bacillus subtilis SigA recognizes the consensus sequences TTGACA (-35) and TATAAT (-10). They key word there is consensus however, as it is rare that a promoter will actually contain these exact sequences. In reality, 3/6 nucleotides matching could be considered reasonable. Between the -10 and -35 regions is a spacer with conserved length. In the absence of transcription activators, SigA requires a 17 +/- 1 nucleotide spacer. This is due to thermodynamic constraints. Very briefly, promoter melting (at -10) is dependent the angle between the -10 and -35 regions. Given the helical nature of DNA, this angle is in turn dependent on the distance between the -10 and -35 regions. If the angle is just right, the untwisting of the DNA to align the promoter elements and thus allow sigma binding provides the energy to melt the promoter. If the angle is too large, the regions can never align. If the angle is to small, alignment will not provide enough energy for melting. Complicating this are non-standard core promoters and various flanking sequences that all play a role in transcription initiation. As a direct answer to one of your question, a single sigma factor can bind to many different DNA sequences with some conserved regions.

Fortunately, the B. subtilis genome has been sequenced. Your search for the promoter might involve looking for the -10 and -35 regions 5' to the rpoA gene. This however doesn't take into account that rpoA might be part of a polycistronic operon and thus under the control of a promoter further upstream. Suh et al. (1986) did basically this and reported:

  Our DNA sequence analysis suggests further experiments to study regulation within the rpoA region. Because inhibition of polycistronic message translation by free protein S4 is one of the chief controls of alpha operon expression in E. coli (16, 23), the apparent absence of S4 from the B. subtilis alpha region suggests different regulation. Although the close coupling of the rpsM and rpsK genes in our sequence (Fig. 3) supports the notion of a translational coupling similar to E. coli, the putative rpoA promoters in the relatively large intercistronic distance following rpsK are also different (28, 29). However, the apparent absence of a rho-independent terminator in this region could indicate that significant transcription occurs from additional upstream promoters in B. subtilis as well as in E. coli (28).

Albeit this is an old paper, but I was unable to find more recent studies in my quick research. Basically they compared the B. subtilis rpoA gene to that of Escherichia coli, where it is located in an operon with ribosomal proteins rpsM, rpsK, rpsD and rplQ (under the control of a single promoter). They found both similarities and differences. They were able to find two possible SigA core promoters in the region between rpoA and rpsK (the next gene 5' to rpoA in B subtilis). There was also a relatively large distance between the two genes, suggesting that they are not part of the same operon. Furthermore, they were able to find a ribosome binding site (Shine-Dalgarno sequence) between the hypothetical promoters and the translation start site. On the other hand there is no transcription terminator between rpsK and rpoA which suggested that a promoter further upstream regulated rpoA expression. After their sequence analysis, they suggested that further experimentation was required.

In conclusion, it's hard to find promoters just by looking at the sequence. Even if you do find a possible promoter, it's impossible to say whether or not it is utilized without experimentation. That said, given that the alpha subunit is necessary for cell function, that the rpoA gene appears to be transcriptionally tied to ribosomal proteins (which are also necessary for cell function) and that SigA is the predominant factor in log phase B. subtilis, I feel that it is very likely that SigA is ultimately the factor responsible for rpoA expression

I also thought I'd mention that there are various online bioinformatics tools that attempt to predict promoters, but I will not comment more on them because I have not used them.


Are there testosterone receptors in female mammary tissue? Does female mammary tissue have receptors for testosterone hormones?

Do male hormones influence female mammary glands, as female hormones influenced the male mammary tissue, such as in gynecomastia?

The female mammary gland tissue contains androgen receptors (testosterone is an androgen). So this tissue is sensitive to androgens, and they inhibit the estrogen-induced proliferation. The inactivation of the androgen receptor on the other hand leads to an accelerated growth of the pubertal mammary gland and to the upregulation of estrogen receptor α expression in female mice. See references 1-3.

And the androgen receptor also seem very important in the formation of the nipples, as testosterone here directs apoptosis in the forming breast tissue. Mice without a functioning androgen receptor were born without nipples. See reference 4 and 5 for details.

To answer your question shortly: Yes, androgen hormones (among them testosterone) have a profound influence on the female mammary gland.

References:

Testosterone inhibits estrogen-induced mammary epithelial
proliferation and suppresses estrogen receptor expression.
Minireview: The Androgen Receptor in Breast Tissues: Growth
Inhibitor, Tumor Suppressor, Oncogene
Androgen receptor inactivation resulted in acceleration in pubertal
mammary gland growth, upregulation of ERα expression, and
Wnt/β-catenin signaling in female mice.
Hormone Action in the Mammary Gland
Specificity of tissue interaction and origin of mesenchymal cells in
the androgen response of the embryonic mammary gland.


Why do birds move their heads abruptly? When we humans look around, we pan smoothly from one side to the other. Birds on the other hand seem to point their head in one direction for a while, then abruptly point their head in another direction and stay in the new position for a while. Then they continue with the abrupt movement. Why is that?

Most species of birds have 2 foveas, the temporal fovea and the central fovea.

  temporal fovea, which is like ours in the sense that it looks straight
  ahead and offers binocular vision (i.e. the temporal foveas of both
  eyes point in the same direction). But birds also have a central
  fovea, which points sideways and is, obviously, monocular (i.e., the
  central foveas of both eyes look in opposite directions).

So the bird has a choice of which fovea it wants to look through.

  It can look straight ahead with its temporal foveas, to the left with
  the central fovea of its left eye, or to the right with the central
  fovea of its right eye. And this is not a hypothetical possibility:
  Birds actually do switch between foveas all the time! This is why they
  tend to swing their heads erratically in turns of about 90° (reference).


What was the evolutionary reason for cross lateralization of the brain? In the human brain the right hemisphere controls the left side of the body and the left hemisphere controls the right side of the body. What led to this development? Why doesn't the left side of the brain control the left side and vice-versa?

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

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


Alpine flower identification — Italy/France I have been using the internet to try to identify alpine flowers photographed in July 2007 on a shortish walk above Chianale (1800 m), in the Italian Valle Varaita (bordering the French maritime alps).

I have managed all except the blue/lilac one shown below. It looks a bit like a scabious or perhaps a knapweed, but neither seem to correspond properly. Anyone know?

Group of flowers

Close-up with triply split petals indicated by red arrows

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

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


Species ID: Cape Town mystery insect This insect bumbled into my bedroom last night - can someone ID it for me? I'm mainly curious because I'd like to know if it poses any danger to my cats (who were very eager to add it to the menu).

It was about an inch and a half to two inches long, and when I picked it up to toss it outside it made a loud squeaking noise. I live just outside of Cape Town, South Africa (but I'm not a native, so I don't know all the species here).

It appears to be a longhorn borer beetle. A more comparable picture is found here. Are there fig trees nearby?

Here you will find numerous images of Longhorn beetles.


What is the name of this yellow bumble bee that I photographed in New York City? Does anybody know the name of this bumblebee? (For categorization on Wikipedia Commons: 1 and 2)

It's a Brown-belted Bumble Bee (Bombus griseocollis).

Details: http://bugguide.net/node/view/3538


Why doesn't sugar spoil? Sugar contains a lot of easily accessible chemical energy. Why seemingly nothing likes to grow on it?

Our food mostly gets spoiled by bacteria and / or fungi. There are 2 main reasons for sugar crystals not getting spoiled.

1- Lack of sufficient amount of water to sustain metabolic processes by microbes.

2- Even if sufficient amount of water is present , then due to high osmolality of the fluid formed, will cause plasmolysis or cell shrinkage.

Some technical data:

  Microorganisms differ widely in their ability to resist salt- or sugar-induced reductions of aw. Most disease-causing bacteria do not grow below 0.94 aw (roughly 10 percent sodium chloride concentration), whereas most molds that spoil foods grow at an aw as low as 0.80, corresponding to highly concentrated salt or sugar solutions.

Source: https://www.scientificamerican.com/article/how-do-salt-and-sugar-pre/


How did butterflies evolve to have eyes on their wings? Some butterflies, such as the UK native Peacock butterfly (Google Image Search) have markings on their wings that look just like eyes, complete with a white fleck to imitate a convex, transparency effect, as though the "eye" is reflecting sunlight.

Presumably, this pattern is designed to deter prospective predators, because the predator will see a creature with massive eyes looking at them and think twice before attacking.

But how did the pattern evolve?  Was the first one a fluke / a genetic mutation that happened to work, or is there another explanation?

For possible bonus points, is there any way of telling when this occurred, and therefore making a guess as to which creature's eye is being imitated?

You're correct with the genetic mutation bit. A basic explanation would be:

Some gene or genes became mutated that lead to the coloration you see, and the end result was that the butterfly or butterflies with the mutated gene were able to produce more offspring or offspring which survived better than the eyeless versions.

There are ways of dating genetic mutations by comparing one organism's genes to another, but accuracy can be an issue without some significant genomic study to confirm mutation rates and other aspects.

However, the butterfly wouldn't be purposefully imitating another creature's eye. It may be by chance and/or predator behaviors that the eyespots look like the eyes of another creature, but the adaptation wasn't a willful act. It was a random genetic mutation or mutations that lead to beneficial coloring, and the eyespots may have improved over time as more mutations occurred.


What happens during the fermentation process of the eco-enzyme? introduction about the eco-enzyme
I have tried to make several ones at home, no matter what I am using, lemon or pineapple peels with brown or white sugar, the final products all show the similar brown colour.
It seems to me that no matter what type of fruit peel or sugar used as the material, would all lead to a similar brown colour.

So I am curious about:
Why the colour of the final product is different from normal homemade fermentative fruit or vegetable?
Are the microbes  involved in fermentation have some difference between the both? Is this because of the difference between enzymes that are produced by bacteria?

I have tried to find the appropriate and availible resource about microorganisms that may take part in the fermenting process of fruit and vegetables, but I am still not sure which one would take part in which step of the eco-enzyme.
(In my observation, some white tiny spots and big speckles began to float on the the surface of the liquid after a week, before opening the container to release gas and make it become aerobic).

What could be the role of fruit peels aside from being the source of microbes,if it will also produce enzymes to influence the chemical reaction?

Is the eco-enzyme really an enzyme?

The recipe is using yeast to convert the sugar into alcohol (ethanol). All of the proposed cleaning effect is from the dilute alcohol (and also some vinegar).  The citrus peel provides some aromatic oils. There may be low levels of some particularly hardy enzymes released from the rotting fruit and dying microbes, but it is difficult to imagine that any of those proteins have any effect on removing dirt from clothes, dishes, or surfaces. The solution is also acidic from the fermentation and the dissolved CO2 gas--just like if you used grape pulp and skins you would make a primitive wine with this recipe, and that wine would then turn into vinegar (acetic acid, HOAc).  Mixing some vinegar and alcohol would give you the same cleanser.

The enzyme concentration should be similar to the amount of active enzymes present in homemade beer or wine--would you use either of those for cleaning?


Is there a photobleaching-resistant, cell-permeant viability stain in the far red part of the spectrum? I am looking for a live-cell–impermeable dye for viability. (The cells cannot be permeabilized and fixed in this experiment.)  I would prefer with excitation and emission spectra similar to Cy5, but I can be flexible here as long as the spectra are far away from Hoechst.

I have tried TOPRO3, but it seems to lose its brightness after a few exposures, so I would like something more resistant to photobleaching.

You could try SYTO Orange. Unlike SYTOX, which is a fixed-cell marker, SYTO works with both live and fixed cells.


Lifetime of secondary messengers such as Calcium or IP3 Can anyone suggest me literature on the lifetime of secondary messengers such as calcium or IP3? A book would be preferred. What I am specifically looking for is a validation that secondary messengers have a certain lifetime and undergo degradation. I need not know specifically how long their lifetime is but rather interested in the fact that they do undergo biodegradation.

[EDIT]: Replaced the word 'biomolecule' by 'secondary messengers' as per the suggestion of @WYSIWYG to narrow down the answer.

The lifetime of Calcium can be considered infinite in biological time scales, it is not a real biomolecule. The half-life time of other biomolecules like IP3, PIP2, receptors, hormones, etc. is species-dependent and within the species strongly depending on the cell and its metabolic state.

Short answer: There is no overview for lifetimes of biomolecules. It is easier to search for a specific molecule in a specific cell. Perhaps you are lucky and somebody measured it.

Update to the comments:
All known second messengers, like Ca2+, IP3, PIP2, change their concentration in response to a stimulus, e.g. activation of muscarinic receptors causes activation of phospholipase C which cleaves PIP2 in DAG and IP3. IP3 causes release of Ca2+. Ca2+ never gets degraded or synthesized but the intracellular concentration changes. PIP2 gets degraded, i.e. its concentration becomes lower, while the concentration of its cleavage products, IP3 and DAG, increases. Those changes are temporary, after removal of the stimulus the 2nd messengers get degraded as well or e.g. Ca2+ is taken up into intracellular compartments.

A general overview about second messengers.


Does food continue to stay sequential once it is inside my body? I may be very off on many scientific details here, but I'm always all ears.

As far as I understand, any food that is eaten goes to the stomach, gets broken down even further into smaller food molecules, and after a period goes through the intestines where nutrients are absorbed out of this... stomach-output.

Let's say I eat food A sometime, and it's gone down and is now sitting in my stomach, waiting for the stomach to start breaking it down. After a while, I eat food B.

When digestion occurs, is it possible that the stomach only starts breaking down food A's material first before it gets to food B?
Is it possible that food B's output goes into the duodenum before food A's output?

Please help break any of this down if it's obvious I've been living in a cave. Thanks!

In general, food is not kept in any particular sequential order.  The stomach has a lot of smooth muscle which churns the food, very rapidly erasing any "order" to the food.  Beyond that, the stomach digests "the food in the stomach," in parallel.  Whatever is in it, it digests.

Now, in general, food eaten earlier will digest into chyme (the digested slurry which enters the intestines) sooner, but that's a very general pattern and doesn't account for any differences in how long it takes to digest various types of foods.

I don't have any sources to back this next claim up, but I do believe that if you were to chew some steak poorly, and then follow it up by more steak chewed properly, the later steak would actually digest first because it would take less mechanical processing in the stomach to get the digestive enzymes to where they need to be to work.


Meaning of some unit of measurement of kinase activity I need help knowing what $cpm \times 10^3$ means in Figure 4(C) of this paper (https://www.sciencedirect.com/science/article/pii/S0022202X15323149#f0010). It appears to be a unit of kinase activity.

It is not a specific unit of kinase activity, rather a general approach taken for following reactions where there is no change of colour. The abbreviation cpm stands for counts per minute and is a measure of radioactivity.
In this particular example a radioactive phosphate has been incorporated in the ATP of the protein kinase assay. If the protein kinase is active with the substrate, the phosphate will be transferred from the ATP to the substrate peptide/protein. If the sample mix is loaded on a SDS-PAGE gel, a scintillation counter can be used to measure the radioactivity of each band and one will be able to  show how active the protein kinase has been in phosphorylating it's substrate.


Lateral corticospinal tract and termination I'm studying the motor pathways of the brain and I'm a bit confused about how the lateral corticospinal tract descends.

From Neuroanatomy: Text and Atlas by Martin, J. H., 4th edition, right before Figure 10-4:

  Some of these [terminating] axons descend ipsilaterally; many descend
  contra-laterally and re-cross midline within the gray matter in lamina 10.
  The function of these ipsilateral axons is not well understood.

I understand that the axons cross over at the Pyramidal decussation, but this paragraph is really confusing me. What descent is being referenced here? Is it descending in the spinal chord? Alternatively, is the paragraph implying that some axons don't decussate in the pyramidal decussation?

The answer ends up being on the next page when discussing the ventral corticospinal tract.

  Many ventral corticospinal tract axons have branches that decussate in
  the spinal cord, similar to the re-crossed lateral coticospinal tract
  axons described earlier.

In other words, some axons of the lateral corticospinal tract ignore the pyramidal decussation, join the anterior corticospinal tract (which then synapses bilaterally later at the spinal commissure).


Where can I find the data on the geographical distribution of the species of Drosophila within various areas of the world? Let X denote an arbitrary geographic area where drosophilas occur in the wild. I will need the answers to the questions of the following type:

  What is the three most occurring species of the genus Drosophila within X?

Where can I find the data on the geographical distribution of Drosophila species within various areas of the Earth?

Source: pinterest.com
I have been unable to find data on a global scale, for now here's a map on the USA.


How can potassium rich foods reduce blood pressure? How come sodium increases blood pressure, but potassium, which has to some extent similar properties helps lower it?

potassium is really the main guy in charge of everything that happens involving action potentials which in turn govern homeostasis such as blood pressure.

k+ lowers blood pressure due to making it harder to get an action potential going, which in the macro scale causes the heart to pump less.

too much k+ kills the person as it stops the pumping of blood (lethal injections are just lots and lots of k+ along with some pain killing drugs)


Text or source (preferably free) for learning developmental biology I might have to take a graduate level course in developmental biology, of which I have never taken a course in before. The course website lists no recommended texts. Therefore, I assume we will be doing a more independent study, and I would want to have a book or source to better facilitate that study.

Any recommendation, free or not free, is welcome.

Gilbert's Developmental Biology is an excellent text. It is in the 11th edition, though the 6th edition is available free on NCBI bookshelf.


identifying OTU interactions / hubs I would like to know how can i run a network analysis for identifying major OTUs hubs. I wish to build a network of co-occurring OTUs found in different soils samples.
I've started going through the VEGAN R package but i'm not sure it's what i'm looking for.
any recommendations network analysis packages ?
thank you!

I am going to assume you have a count table that you are starting with. Every tool you decide to use is going to have its own respective instructions so let me get you pointed in a direction to find one that works for you.

I wrote a simple R package for my lab awhile back but there are much better ways to put together Co-occurrence networks (in no particular order):

SparCC
CoNet
MENA
Spiec-Easi
MDiNE

Now speaking specifically about "hubs", "connectors", and other keystone organisms, I would recommend reading more about what they are and how they were developed. Again, I have a brief summary here but the original "hub" came from a paper on bee pollination networks


What is "beto carotene" and how can it turn lakes pink? The BBC News article Pink lake in Australia attracts and delights tourists describes an artificial salt lake in Westgate Park, Melbourne, Australia that tuns pink around February and then in "late Autumn, until cooler temperatures restore it back to blue."

I am not sure about the autumn part as it's in the southern hemisphere, but my question is about the color change.

Could they mean beta carotene rather than beto carotene?
And if so, does the pigment stay inside the algae or is it released into the water to produce this color change?
And why pink, rather than the orange color we associate with carrots?

  In those conditions, the lake's algae produces a red pigment called beto carotene

  The lake's pink colour typically lasts through to late Autumn, until cooler temperatures restore it back to blue.

The "beto" is a typing mistake. Beta is an organic chemistry label referring to a beta-ring of 6 carbons that exists at either end of a carotenoid polymer C40-Hx.

It is localized in the chloroplast. The plants don't really have a mechanism to release pigments, they can re-metabolize chlorophyll. The volvocalean algea Dunaliella salina is used to harvest beta-carotene in Karratha, Western Australia, from salt lakes. The can have 12% beta-carotene as dry-matter content, the highest of any known source.  The squares are probably salt.

the algea afterwards:

There are over 1,100 known carotenoids of which at least 700 have been identified in plants. They include carotene and xanthophylls, and carotene include beta-carotene. The plants and algea use it to protect themselves from intense sunlight and UV's. It is an anti-oxidant.

Pink doesn't actually exist as a color. It is imagined when green and blue light is sensed by the eye, while red is at a maximum. In the lakes, we know there is 80% red and 20% green pigment in the algea. All that is required would be 20% blue to percieve pink. I don't know where the blue color comes from, the sky/water.
Orange is complex for the eye, and so is pink, because we can only see red green and blue.


What is actually systematics? What is the difference between it & taxonomy? In the last century, even during the past decades of the present century, students of systematics could not have thought of any fundamental distinctions among Taxonomy & Systematics . These terms appeared to them more or less synonymous and hence often misunderstood until G.S.Simpson(1961) analysed each of the terms separately & gave a comprehensive definition of each term and its workable areas so that their underlying fundamentals became clear.

This is what I found in my book. But what is actually Systematics? And what is the difference between it and taxonomy??

Systematics studies the diversification and relationships of past and present living forms. Taxonomy is only a part of systematics as defined by Michener et al. in 1970:

  Systematic biology (hereafter called simply systematics) is the field that (a) provides scientific names for organisms, (b) describes them, (c) preserves collections of them, (d) provides classifications for the organisms, keys for their identification, and data on their distributions, (e) investigates their evolutionary histories, and (f) considers their environmental adaptations. This is a field with a long history that in recent years has experienced a notable renaissance, principally with respect to theoretical content. Part of the theoretical material has to do with evolutionary areas (topics e and f above), the rest relates especially to the problem of classification. Taxonomy is that part of Systematics concerned with topics (a) to (d) above.

Source: Michener, Charles D., John O. Corliss, Richard S. Cowan, Peter H. Raven, Curtis W. Sabrosky, Donald S. Squires, and G. W. Wharton (1970). Systematics In Support of Biological Research. Division of Biology and Agriculture, National Research Council. Washington, D.C. 25 pp.

via Wikipedia contributors, "Systematics," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Systematics&oldid=635316421 (accessed November 30, 2014).


Duplicity Vs. Singularity of Mammals Organs Are there known evolutionary reasons why mammals contain 2 of some organs (such as lungs and kidneys) and only 1 of some (such as liver)?

It's just how we evolved. At some point in the past, a distant ancestor of ours had two lungs, two kidneys, one liver etc.( maybe then there was a pretty good reason for this). We evolved following that pattern and now we ourselves have two lungs, two kidneys, one liver etc.

Snakes, for example, have just one functional lung because their elongated form doesn't cope well with having two full-grown lungs. Humans on the other hand have a body shape that works very well with two lungs, so we didn't have to sacrifice one lung.

There are other examples of different organ distribution, like the octopus which has 3 hearts. Usually the more different the internal symmetry, the more distant the common ancestor.


Why do some people have cold hands and some have warm? I've known people who have warm hands even in the most chilling weather and also those having cold hands in a relatively hot climate. Why does this happen?

Though I haven't heard of people having warm hands in cold temperatures (unless your using a hot pack or something), there are biological explanations for cold hands.

  Having cold hands even when you're not in a cold environment is
  common. Often, having cold hands is a part of your body's natural
  response to regulate your body temperature and shouldn't be cause for
  concern.

  But if you have persistently cold hands, particularly if accompanied
  by color changes, it could be a warning sign. For example, having cold
  hands could mean you have a problem with the nerves or blood
  circulation or a problem with tissue damage in your hands or fingers.
  If you are outside in extreme cold weather and you have cold hands,
  you should watch for warning signs of frostbite.
  - MayoClinic

Other than frostbite, there are also reports of the Reynaud's disease.

Sources:
Clinic
CNN