Sunday 29 June 2008

homework - What is the total number of rounds of cleavage during mammalian embryonic development?

It's not a totally answerable question, since some types of cells are going to divide more times than others. But for an estimate, take as a starting proposition that there are 1 trillion cells in the adult human body. [1] The average weight for a human is 62kg. [2] Average birth weight is about 3.4 kg. [3]



So that implies roughtly (3.4/62)* 1 trillion = 55 billion cells in a newborn.



You then take the log base 2 of 55 billion, which gives you the exponent you have to hang on 2 in order to get 55 billion, which is about 35. Then add one for that additional cell division to get from one to two cells == 36 divisions.



Of course I'm just using math, not biology, so your actual reality may vary. Certainly some cells will reproduce more often than others, maybe cells actually grow in mass instead of dividing (i.e., baby cells might have less mass than adult cells) so the baby-cell-count could be off, lots of possible sources of error.



[1] http://www.nichd.nih.gov/publications/pubs/fragileX/sub3.cfm



[2] http://en.wikipedia.org/wiki/Body_weight#Average_weight_around_the_world



[3] http://en.wikipedia.org/wiki/Infant#Weight

Friday 27 June 2008

human biology - If body temperature is 37°C (98.6°F), why are most people more comfortable at around 21°C (70°F)?

This is due to the fact that skin is the interface where heat is lost.



Our body due to constant functioning, produces heat constantly as a by-product (due to exothermic reaction of ATP break mainly). The excess heat needs to be conducted away from the body, or it will cause a decrease in the body metabolism to prevent temperature rise.



Heat is lost mainly through the skin by:



  1. Sweating - Through evaporation

  2. Radiation - As heat waves (IR rays - That's why IR camera captures people at night)

  3. Conduction - Directly through objects that touch skin

  4. Convection - Through air circulation

When the ambient temperature rises, the heat lost through radiation, conduction, and convection drastically decreases. And often when the temperature is high, there is a accompanying rise in the relative humidity which decreases the heat loss through sweating (as the amount of water vapor is high in the atmosphere, the sweat does not evaporate, so no heat is lost).



So the heat which is not lost is felt as the "hot sensation". It relieves by stopping any activity, seeking shade or a cool place, etc... all of which increases the heat lost or decreases the heat produced.




You have to note that the temperature of skin is lower than the body temperature.



enter image description here



The Skin temperature is lower than the core body temperature for two reasons:



  1. The skin acts as a medium through which the external temperature is measured - as such the skin temperature is at equilibrium with the external temperature. The brain regulates the core-body temperature in response to temperature measured through skin. If a person is exposed suddenly to cold environment, skin looses much of its heat in the form of radiation (radiation is direclty proportional to the temperature difference) this will cause perception of cold and the body starts shivering even though no actual heat loss has occured from the core body thermal load (only skin looses heat, not the body core). The brain anticipates that the core will loose its heat when exposed to such low temperature for prolonged periods and starts the warming mechanism before the actual cooling occurs such that the cooling is either prevented or minimized. This is called Anticipatory control and the temperature of skin being close to the ambient temperature within physiological limits is needed for this.


  2. Skin is the medium (almost the only medium) through which the excessive heat produced by the body core during activity is expelled. The skin temperature is lower so that a constant gradient can be created between the body core and body surface to maintain the flow of heat. (Heat losses through urine and feces is minimal)


For more details see this question. All the answers in this question are good and will increase your understanding of what actually happens.

Tuesday 24 June 2008

zoology - Color of the Fur coat of Polar bears

The fur coats of polar bears are in fact clear tubes - not white fur as is often believed. It is their skin that is black, to absorb the most warmth from the sun (and the clear tubes allow the majority of the light to pass through to the skin).



I recently watched the BBC's Frozen Planet TV series (with David Attenborough), where I heard the above answer. If you haven't already, I recommend watching it.

Tuesday 17 June 2008

molecular biology - What is causing my problem with very low yields when isolating a 42kb yeast plasmid?

I've successfully used the Zymoprep kit, but only for smaller plasmids in 2-hybrid experiments. So their cell lysis enzyme/buffer system works well, but I'd guess that your 42kb plasmid is precipitating out with the genomic DNA.



The standard Qiagen midi columns are capable of capturing large constructs. This has worked wonders for me when I was purifying large BACmids from E. coli - and gets the cost down to $10/sample (it does require additional buffer, but that's a minor expense). It might be worth trying the Qiagen yeast DNA protocols for the midi kit and see if you can isolate your large plasmid?

Saturday 14 June 2008

Is Batesian Mimicry a form a parasitism? To what extent is the species with real defenses harmed by the defenceless species?

In my own opinion, I would not classify this as parasitism, as more unpalatable species are eaten with Batesian mimicry (and eating causes death). Parasitic organisms often do not kill the host, whereas in this case, it does. However, you are correct in stating that a unpalatable species with aposematic coloring is detrimented by the presence of a palatable Batesian mimic.



Predators often recognize the aposematic coloring of an unpalatable or dangerous species. They "train" themselves not to eat that particular prey, as it is detrimental. The presence of a Batesian mimic which is palatable or not harmful, in simple terms, "untrains" predators of the harmful nature of that particular aposematic coloring. Predators are "confused", and are thus more likely to eat preys with that aposematic coloring, and results in more death of the species being mimicked, while providing protection to the species that is mimicking.



As far as I'm concerned, within an ecosystem, this phenomenon happens with any Batesian mimicry to some degree. Factors that may influence this degree is the recognizability of the aposematic coloring, as well as the ability of a predator to recognize this coloring.



I hope this clears things up.

biochemistry - Solution based measurement of Solvent-Accessible Surface Area of macromolecules

I only know of one method, but here it is. You create a sphere the diameter of the VdW radius of water, and then 'roll' it along the surface. I know this as a Richards-Lee surface, wikipedia has another name for it.



enter image description here



This looks complicated, but its not. you move the probe sphere along the surface of the molecule in the XY plane until it just touches the vdW radius of the protein, keeping the center of the sphere as the surface, all the way around the molecule. If you like, you can color the surface by the charge of the position too, which is useful for discussing solvent interactions.



Then you translate along the z axis and do another contour until you run out of protein. Apparently jmol and other packages will do this for you.



Wikipedia references a more mathematical method LCPO, which I am not so familiar with.



Is this accurate? As usual with such calculations its more of a guess than an answer. You can do the calculation on any structure or any ensemble of structures (like NMR gives). It doesn't understand how the molecule might be flexible or dynamic. If you read up on your physical chemistry you see that proteins breathe and can allow diffusion into the core rather readily. If I recall right, you can get rather large molecules quenching heme flouresence in hemoglobin at room temperature.



If you are looking to dock 2 proteins, SAS might be more useful. Its an important piece of information, but not an ultimate answer. I'm afraid with proteins that doesn't happen so easily.



@bobthejoe asked about SAS for which no structure exists.
This is an extremely difficult thing to even guess at. The non helpful answer is that the surface of the protein goes as the cube root of the molecular weight of the protein.



By getting a solution of the protein and shooting it in a syhcrotron, you can get a mean radius of gyration pretty easily which will give you an ellipsoidal volume (and surface area) for a protein. Again most of the particulars would be lost and this could easily be off by 25% for an irregularly shaped protein. For a regular globular protein it might give an answer similar to the power law above.



I have seen physical chemistry experiments that look for changes in osmotic pressure when the salt concentration in a solution of the protein changes substantially (Adrian Parsegian's work at NIH in the late 80s).



I doubt you will find any of these answers useful as their mean error is going to be very large (20-200%) and also assumes the protein is soluable and amenable to the experimental conditions.



Solvent probes can help too. For instance exposing the protein to D20 then doing mass spectroscopy on the protein. This is still only going to give you a general idea of how much of the peptide is surface exposed. Protein structure is still pretty necessary to getting any accurate measurement of SAS I think.

homework - Do humans have Coelom?

Kimball Biology 5e says




Coelom is the main body cavity of many animals. It is lined with an epithelium derived from mesoderm.




Gilbert Embryonal Biology 9e says




Coelom is the space between the somatic mesoderm and splanchnic mesoderm that becomes the body cavity. In mammals, the coelom becomes subdivided into the pleural, pericardial, and peritoneal cavities, enveloping the thorax, heart, and abdomen, respectively.




Then my lecture materials and the research site say




Coelom is the secondary body cavity.




Finnish Wikipedia says that Coelom is only with invertebrates.
Again the Wikipedia page about peritoneum suggests that human has abdominal cavity and no coelom, and other mammalians coelom.



Does human have Coelom?



The confusing thing is the use of the word "OR", since I am not sure whether people are using it in different pages like "XOR" or like "AND" in normal speaking.

Friday 13 June 2008

molecular biology - How do proteins and genes participate in learning?

The storage of memories in cells is rarely thought of on the protein level of the cell. Cells are usually given a developmental state, but no memory. A cell may become a liver cell, cancerous, or diabetic, but this is not memory, but a physiological change in the cell which is usually not reversible to a previous state.



For example cancer treatments are entirely focused on identifying the cancerous cells and killing them. Internally the genomes of cancer cells often have deletions and duplications. They are cancerous, they have not learned to be cancerous. Though not as dramatic, it is now thought that cellular differentiation which creates different types of cells is heavily influenced by epigenetic modification of the genome; the DNA is marked by methyl groups which dictates the state of the cell by modifying the gene. This is mediated by proteins for sure, but is quite complex and not well understood at this time. Epigenetic markers can even change gene behavior between generations of offspring as well, though that is not usually called memory.



How is information stored in the brain? This is thought to be reflected in the organization of the neurons in the brain. There are many kinds of neurons. They can be distinguished by the sorts of axons and dendrites that emanate from the cell body. They can also be distinguished by the chemical variety of neurotransmitter they use (there are a score of different molecules). So to a great extent the type of cell and the specific proteins it chooses to use to mediate information is very important.



That being said, information is currently thought to highly related to the placement of the axons and dendrites connecting the neuron to sometimes scores of other cells, sometimes touching the cell body, other times other dendrites or neurons. As neural activity ensues, the cells will reconfigure their connections by physically moving them.



More recently, investigators have tried to understand the genes which internally modulate the neural signals within the cells. This nobel prize lecture discusses how the CREB/MAPK pathway can modulate Long Term Potentiation - the shape of the neuron response to a signal over time (days or hours).



Taken as a whole, you can see that memory is likely to be stored on several levels at once - the kinds of cells (dictated by differentiation) involved, structural arrangement of the neurons (axons and dendrites connecting to various cells and places on cells), as well as internal signaling circuitry that generates and modulate the electrical and chemical activity within the cell.



"Marker protein" only refers to a protein that you can follow to see some sort of activity in the cell. A typical example is Green Fluorescent Protein, which is colored, fused with a protein of interest. It has no specific meaning regarding learning I think.

microbiology - Is it plausible that eukaryotic organelles like flagella and cilia are the result of endosymbiosis with spirochetes?

This was a claim by Lynn Margulis explained over at this link.




The sense organs of vertebrates have modified cilia: The rods and cone
cells of the eye have cilia, and the balance organ in the inner ear is
lined with sensory cilia. You tilt your head to one side and little
calcium carbonate stones in your inner ear hit the cilia. This has
been known since shortly after electron microscopy came in. Sensory
cilia did not come from random mutations. They came by acquiring a
whole genome of a symbiotic bacterium that could already sense light
or motion. Specifically, I think it was a spirochete [a
corkscrew-shaped bacterium] that became the cilium.




And why would our bodies incorporate spirochetes as part of our basic functionality?




There are many kinds of spirochetes, and if I’m right, some of them
are ancestors to the cilia in our cells. Spirochete bacteria are
already optimized for sensitivity to motion, light, and chemicals… If
I’m right, the whole system—called the cytoskeletal system—came from
the incorporation of ancestral spirochetes.


Thursday 12 June 2008

homework - What are all possible vectors for unicellular human parasites?

I got the given question. They want the following pieces of information about protozoological human parasites:




disease - parasite - vector.




There are 10 proteogenic diseases at the Wikipedia. I added the corresponding parasite and the vector next to them:



  1. Malaria - Plasmodium - Apicomplexa

  2. Amoebiasis - Entamoeba histolytica - sarcomastigophora

  3. Giardiasis - Giardia lamblia - no vector

  4. Toxoplasmosis - Toxoplasma gondii - no vector

  5. Cryptosporidiosis - Cryptosporidium - Apicomplexa

  6. Trichomoniasis - Trichomonas vaginalis - no vector

  7. Chagas disease - Trypanosoma cruci - insect

  8. Leismaniasis - Leishmania donovani - sand fly vector

  9. Sleeping sickness - Trypanosoma brucei gambiense - tsetse fly vector

  10. Dysentery - Entamoeba histolytica - sarcomastigophora

I am unsure what I should answer to the question since it is asking "all" possible vectors for unicellular human parasites.
There are many possible diseases, much more than the given ten in my opinion.
It seems also that there are many possible ways of getting the infection for each disease.



I hope that I am wrong in my statements.
It is my first course in Parasitology.



What would you answer to the given question?

Sunday 8 June 2008

How does a veggie-less diet affect the human body?

You'd be deprived of the vitamins and minerals which are found only in vegetables, but you'd live. There are vitamins and minerals in meat and other foods, plenty of them, and your metabolism would adapt to produce the proteins which are missing. Human body is a wonderful organism.



You wouldn't have a higher risk of cancer because cancer is a byproduct of life (the DNA repair mechanism and programmed cell death) and you can't get it by consuming meat or by not consuming vegetables.



You wouldn't gain weight if you're not consuming too much food. The math is simple, if you need 2000 calories, you'll gain weight if you're consuming 2050 calories of vegetables and lose weight if you're consuming 1950 calories of meat.



Your risk of heart disease wouldn't increase.



The only things which would change in this case would be the ones directly related to the nature of carbohydrates, proteins and fat. The carbohydrates in vegetables release energy slowly over a longer period of time, so if you'd eliminate vegetables you'd possibly be hungry more often. However, fat - and the glucose produced from it - would keep you going.



And you might have digestion problems because of lowered intake of fibers until your metabolism adapts.

bioinformatics - Too few transcripts from transcriptome assembler Oases

I am trying to run Oases for transcriptome assembly. The result is far from expected, so I would like to ask whether I am running it in a right way? Thanks.



Here is my running command:



python scripts/oases_pipeline.py -m 25 -M 29 -o output -d " -strand_specific -shortPaired data/reads.fa" -p " -min_trans_lgth 100 -ins_length 300"


My library is strand-specific and pair-ended with length 67bp. The reads are shuffled as:



>0(left_mate_forwarded)
ACTC...
>1(right_mate_reverse_complemented)
TATA...


I got some transcripts, but are far from the transcripts annotated, also far from the result of Trinity. The longest contig from Oases is ~2500bp (vs. ~10000bp from cufflinks and ~6000bp from Trinity). The N50 value is also low. It only reports 20 contigs those cover full-length of some transcripts from Cufflinks (totally ~4000), while Trinity reports ~650.



The dataset I am using is a subset of S. pombe. Does it matter?



Could somebody help me point out whether something wrong here?

Friday 6 June 2008

human biology - Why don't teeth glow?

Just to add a little more on the interface between optics and dentistry:



Whilst teeth do not phosphoresce, they do in fact autofluoresce.



The differential auto fluorescence of healthy tooth and carious tooth has been used for the early diagnosis of caries. (Gugnani N, Pandit IK, Srivastava N, Gupta M, Gugnani S. Light induced fluorescence evaluation: A novel concept for caries diagnosis and excavation. J Conserv Dent 2011;14:418-22 and http://www.opticsinfobase.org/boe/abstract.cfm?uri=boe-2-1-149)



To see teeth glow, or rather, fluoresce, they should be illuminated with short wavelength light, like blue light (wavelength 450 nm) and the teeth will glow green, which will be visible if the the blue light is filtered out.



Also see http://www.inspektor.nl/dental/qlfmain.htm#QLF%99%20Basic%20Principle

Wednesday 4 June 2008

human biology - Why is the Patellar reflex not triggered when the tendon is extended slowly?

This effect you are observing has to do with the nature of the afferent neurons (Ia fibers), which carry a signal into the spinal cord and synapse onto motor neurons directly. See this text (scroll down to section 1.10) for a diagram. At their other end, these Ia fibers penetrate into the muscle and wrap themselves around the body of the muscle spindles, "[which] are specialized receptors that signal (a) the length and (b) the rate of change of length (velocity) of the muscle."



Because the main role of these spindles is to monitor the muscles for very rapid changes in length, the neurons have a static range which is optimized for these quick jerks (rather than firing over a wide range of velocities). When you are stretching the muscle slowly, the Ia fiber is not building up a sufficient depolarization to fire off an action potential.