Expression/Mechanism of ROR1 in healthy tissue ROR1 is currently under investigation as a therapeutic target for cancer (1). A number of studies show different cancers may have their metastatic potential reduced, or become apoptotic through targeting or abrogation of ROR1 (1-3). ROR1 itself is show to have a number interactions (either through crosstalk or interaction) with some known tumorigenic markers; these include c-Met, PI3K, Akt, Wnt5a, EGF, c-Src (4-7). In terms of metastatic potential, interactions with vimentin, Snail/Slug, cadherins, ß-catenin, and CXCR4/CXCL12 were also identified (1, 8). Some of these are via expression of CREB. In terms of ROR1 is tissue, abnormalities that lead to death were noted in newborn mice that has ROR1 knocked down (9). A notable mechanism for ROR1 in development was in neuroprogenitor cells in which ROR1 regulation status determined whether these cells differentiated into neurons or not (10). It's also found that neural, heart, lung and kidney tissue in adults express some form or another of ROR1 (11). More recent studies suggest ROR1 downmodulation may present toxicity for some subsets of normal tissues (12).

The question, now: Are there any empirical studies that illuminate the potential mechanism of ROR1 in healthy, adult tissues? This is from a treatment toxicity standpoint, since the subsets of affected cells seem to be rather slim. I can understand why the effect on metastatic potential can be significant from the fetal neural cortex development (the need to migrate the neurons into position). We also see a truncated version of ROR1 in some instances. If anyone can shed some light, thank you in advance!

References

Cui B. et al. Targeting ROR1 inhibits epithelial-mesenchymal transition and metastasis.      Cancer. Res. 73, 3649–3660 (2012).
Hojjat-Farsangi, M., Ghaemimanesh, F., Daneshmanesh, A. H., Bayat, A. A., Mahmoudian, J., Jeddi-Tehrani, M., … Mellstedt, H. (2013). Inhibition of the Receptor Tyrosine Kinase ROR1 by Anti-ROR1 Monoclonal Antibodies and siRNA Induced Apoptosis of Melanoma Cells. PLoS ONE, 8. doi:10.1371/journal.pone.0061167
Daneshmanesh AH, Hojjat-Farsangi M, Sandin A, Khan AS, Moshfegh A, et al.. (2012) Monoclonal Antibody Against ROR1 In Chronic Lymphocytic Leukemia Cells Induced Apoptosis Via PI3-kinase/AKT/CREB pathway. 54th American Society of hematology (ASH), Atlanta, USA, 8–11 December.
T. Yamaguchi, K. Yanagisawa, R. Sugiyama, Y. Hosono, Y. Shimada, C. Arima, S. Kato, S. Tomida, M. Suzuki, H. Osada, T. Takahashi. NKX2-1/TITF1/TTF-1-induced ROR1 is required to sustain EGFR survival signaling in lung adenocarcinoma. Cancer Cell, 21 (2012), pp. 348–361
Fukuda T, Chen L, Endo T, Tang L, Lu D, Castro JE, Widhopf GF, II, Rassenti LZ, Cantwell MJ, Prussak CE, et al. Antisera induced by infusions of autologous Ad-CD154-leukemia B cells identify ROR1 as an oncofetal antigen and receptor for Wnt5a. Proc Natl Acad Sci USA. 2008;105:3047–3052. doi: 10.1073/pnas.0712148105.
Gentile A, Lazzari L, Benvenuti S, Trusolino L, Comoglio PM. Ror1 is a pseudokinase that is crucial for Met-driven tumorigenesis. Cancer Res 2011;71:3132–41.
Zhang S, Chen L, Cui B, Chuang HY, Yu J, Wang-Rodriguez J, et al. ROR1 is expressed in human breast cancer and associated with enhanced tumor-cell growth. PLoS ONE 2012;7:e31127.
Teicher BA, Fricker SP. CXCL12 (SDF-1)/CXCR4 pathway in cancer. Clin CancerRes. 2010;16(11):2927-31.
Nomi M, Oishi I, Kani S, Suzuki H, Matsuda T, Yoda A, et al. Loss of mRor1 enhances the heart and skeletal abnormalities in mRor2-deficient mice: redundant and pleiotropic functions of mRor1 and mRor2 receptor tyrosine kinases. Mol Cell Biol 2001;21:8329–35.
Endo M, Doi R, Nishita M, Minami Y. Ror family receptor tyrosine kinases regulate the maintenance of neural progenitor cells in the developing neocortex. J Cell Sci 2012;125:2017–29.
Reddy UR, Phatak S, Pleasure D. Human neural tissues express a truncated Ror1 receptor tyrosine kinase, lacking both extracellular and transmembrane domains. Oncogene 1996;13:1555–9.
Linked in text.

Examining the literature it'd seem that the ROR pathways incl. ROR1 and ROR2 are critical for developing tissues in the majority of cases. We also see relevance in the expression of ROR1/2, more specifically ROR2, in cases where taxic cell types are required to migrate, branch, etc. Most of the literature determines much of this occurs through a noncanonical Wnt signaling pathway.

Wnt5a–Ror–Dishevelled signaling constitutes a core developmental pathway that controls tissue morphogenesis

Ror2 Receptor Mediates Wnt11 Ligand Signaling and Affects Convergence and Extension Movements in Zebrafish

Ror2 regulates branching, differentiation, and actin-cytoskeletal dynamics within the mammary epithelium

Notwithstanding the abnormalities we see in neonates with knocked down ROR, is it wrong to assume we'd see developmental defects of branching tissues in developing (or juvenile) organisms such as lung, mammary, neural, glandular tissue, etc.? Some data in that respect would be interesting, but it's also illuminating given the presence of ROR in cancer metastasis and EMT events.


Heart rate vs body size It is known that large animals have lower heart rates (beats per minute) than small animals. Is it the same situation in humans?

That is: if we have a group women, about the same age and fitness, and if we record for each women her body size (relevant indicators of body size are height, weight, BMI, body surface area) and her heart rate, will we see a trend that the heart rate decreases as size increases?

References to paper and studies about this issue are also welcomed.

The paper you link finds that there is not a significant correlation between body mass and resting heart rate in humans. While there is a well known negative correlation across mammals:

This is the ever-popular mouse-to-elephant curve that is found in one form or another for lots of physiological measurements.

I'll suggest, but have no evidence, that the lack of a significant correlation in humans is simply a result of there not being enough range in body mass among humans to allow finding a significant result. When the range of one variable is small, the association between that and another variable necessarily lessens. For example:

Although the linear relationship between the two variables is largely similar, when the range of x is truncated, the coefficient of determination, $R^2$, decreases. The correlation goes from 0.97 to 0.7. In this case, that might still be "significant", but I suspect that in humans that variation is much greater in resting heart rate.

It would have been nice if that paper included the actual data on HR, but they act like it doesn't exist just because it was not significant.


What happens when we eat excess fat? The fats in our body are stored in fat cells. When we over eat fats does the size of our fat cells increase, are more fat cells generated, or do we "throw out" excess fat?

The number of fat cells, or adipocytes, in adult bodies remains constant. Therefore, consuming more fat only increases the size of the fat cells not the number. After reaching the age of about 20 years the average number of fat cells is closely related to body mass index.

On the other hand, the adipocytes in children increase in number as more fat is consumed. This explains why people who became fat as children have a harder time shifting their weight as adults.

A study on obese adults who went through surgery to decrease the amount of food intake showed a reduction in their body weight by 18%. While the average size of the fat cells decreased, the number of fat cells remained the same.

This doesn't mean that the same fat cells are active throughout your lifetime. Adipocytes normally die off and are replaced by new cells. One study shows that fat obtained from liposuction of people who were exposed to radioactive materials from atomic bombs in the Cold War showed a decrease in radioactive material stored in the cells which indicates replenishment of fat cells over the years.

So when adults intake excess fat, their fat cells increase in size. The average number of their fat cells is correlated with body mass index. However, when children eat excess fats they exhibit an increase in the number of fat cells.

For more information see: http://www.nature.com/news/2008/080505/full/news.2008.800.html


RNAse activity review I was searching for any review unravelling the structure-function motifs responsible for RNAse activity. Or at least a well-composed review of RNAse superfamilies that are described nowadays (with linkage to their functional activity). My PubMed search performed didn't give any valuable results for that.
Any specialists to comment?

Thanks in advance!

I did a few searches, just for fun, but all I came up with was:

  Yuhong Zuo and Murray P. Deutscher "Exoribonuclease superfamilies: structural analysis and phylogenetic distribution"
  (2001) Nucl. Acids Res. 29 (5): 1017-1026. doi: 10.1093/nar/29.5.1017

Not very recent, but it's open access. It might be possible to search for more recent papers that have cited this. Although I haven't tried it myself, I found suggestions for doing this at https://www.bc.edu/libraries/help/howdoi/howto/pubcitation.html.


What is this bird of prey? I recently took a picture of this bird flying around Geneva, Switzerland:

In the beginning, and because it was bright and the subject was against the light, I though it was simply another Buteo buteo as there are many around here. Now by tweaking the brightness and contrast a bit in Lightroom, I can be 99% sure that it is not a Buteo buteo and my mind goes more to a Pernis apivorus, which is another bird of prey present in the region in summertime (May-Sep).

Can anyone tell me if I am correct and what field marks can be deduced from my picture to be sure that it is the right bird?

Nice photo - Yes, I would agree with you the bands on the tail and the wings suggest that it is a Honey Buzzard Pernis apivorus

http://www.birdwatch.co.uk/categories/articleitem.asp?item=995
http://www.gobirding.eu/Photos/HoneyBuzzard.php

Photo by Dominic Mitchell http://www.birdingetc.com


What species of spider is this? I'm trying to find out what kind of spider is this little fellow:

It really seems to like our garage and is the bane of my girlfriend (as evidenced by all the screaming when on two occasions one got into our home somehow). I was never able to spot this kind outdoors, which is rather odd (there are plenty of Araneus diadematus spiders in the area which are fairly easy to spot).

It's hard to tell on the photo, but these spiders seem rather big (at least as far as spiders in Poland I was able to spot go)... somewhere around 5cm at least (legs included)? They really do make for rather large, black spots against an otherwise white garage wall.

I'd really like to find what kind of species this is so that I can, hopefully, convince my GF that it's harmless to humans. Unless it isn't, in which case I'll start getting scared of walking into our garage. ;)

PS. We live in Poland, Poznań.

I think this is just
Tegenaria domestica. I am from Czech republic and this is really big and kinde everywhere. Specialy in garages.


What is the difference between the glycolate pathway and photorespiration? I came across the definition of photorespiration as a process that forms CO2 from O2 in the presence of light. However, the CO2 is released only when the plant cell undergoes the conversion of glycolate to PGA, i.e in the glycolate pathway.

Most textbooks seem to use the term photorespiration and glycolate pathway interchangeably, but then they seem to say that the glycolate pathway evolved to regain the energy lost in the formation of glycolate, whereas photorespiration is wasteful. How is this possible?

Shouldn't photorespiration be a conservation pathway as well? It is trying to regain lost energy from glycolate, isn't it? or Have I got the two terms completely confused?

Please Explain

The simple answer to the question posed in the title of the question is as follows. The glycolate pathway is the series of reactions converting phosphogycolate to reusable carbon intermediates + CO2. Photorespiration is the combination of two processes:

The oxidation of the enodiolate intermediate on Rubisco to phosphoglycoate + 3-phosphoglycerate.
The processing of the phosphoglycolate produced by the glycolate pathway.

You cannot use the two interchangeably as there is no respiration (use of oxygen) in the glycolate pathway. The glycolate pathway is just the latter part of photorespiration. I'm not sure what the text books are that confuse the two, but Stryer presents this quite clearly in Figure 20.6 and 20.7 at http://www.ncbi.nlm.nih.gov/books/NBK22344/#A2795.

I am not familiar with the term "conservation pathway" in your final question. I would call the glycolate pathway a "salvage pathway" (although this term is more commonly used for recycling the skeletons of the products of macromolecular, esp. DNA, degradation). It does not salvage all of the carbon skeleton of phosphoglycolate as some carbon is lost to the atmosphere as CO2.


Is there anything that is completely non-toxic to humans at any dose? Lately I have seen a number of unrelated "scientific" debates over whether certain substances should be outlawed because they are toxic to humans. My initial, informal reaction is usually to respond that anything is toxic to humans if you give them a sufficiently large dose.

However, formally I don't know if that's really true for everything a human being could ingest in some way. I started to wonder if there were some substances that our body could handle unlimited amounts of without any negative consequences.

As this question has been (correctly) identified as a bit vague, I'll try to explain what i'm looking for. For the purposes of this question, I'm willing to ignore the limitations of actually ingesting a given substance in "the usual way". For example, if you can't physically drink enough of some liquid fast enough to kill you without your stomach filling up and vomiting, but that same liquid injected intravenously could be lethal, I could consider that toxic. I also recognize that the body can only physically contain a certain volume of stuff, after which sheer pressure would cause it to fail; I'm more interested in "biochemical toxicity" as opposed to any physical damage (I just don't know the term for what I'm looking for.)

In other words, one of my goals is to learn if, under laboratory conditions, a properly motivated researcher could always find a dose that would be toxic, regardless of the impracticality of a real person ingesting that dose under normal circumstances.

So, with that qualification, my ultimate question is:

Is there any substance we know of that is completely non-toxic to humans at arbitrarily large doses ingested over an arbitrarily short period of time?

I’ll answer this theoretically, since that’s how it has been posed. And if we’re ignoring practicalities, we may as well posit that the substance in question will be introduced directly into the bloodstream (This is, of course, simple to do in reality, but not how most people consume their non-toxic substances.) The easiest way to show that any unspecified substance can be toxic at an unlimited volume is to invoke the human body’s mechanisms for volume homeostasis.

As mentioned in this answer, the human kidneys functioning optimally can produce up to ~ 25 L/day of urine.1 This would require complete suppression of ADH (anti-diuretic hormone, a.k.a. arginine vasopressin), which would occur only if the “toxin” load were markedly hypotonic (think water).2  There is therefore a theoretical maximum volume of any substance that can be dealt with by the body, which is something less than 25 L per day. (For any substance other than water, the maximum will be lower because ADH will not be as fully suppressed by a less hypotonic load.)

A volume of any substance introduced into the bloodstream (including a product precisely mimicking the constituents of the bloodstream itself!) will overwhelm the body’s homeostatic mechanism. This will result in edema which is unpleasant and, in the case of pulmonary edema, certainly pathologic - a “toxidrome” in your scenario. In the case of hypotonic fluids, serum osmolality will also fall causing hyponatremia with all of its consequences.

Summary: No, the human body can not tolerate an unlimited volume of anything, therefore there is no substance that is non-toxic "at any dose."

1. Christopher Lote. (2012). Principles of Renal Physiology. Springer New York.

2. No, you may not drink 25 liters of water per day. For one thing, urine can not be made with a tonicity of 0 to balance this (more like 60 mOsm/kg minimum). Additionally, ADH can rarely be completely suppressed, yielding a somewhat more concentrated urine and therefore lower tolerance for hypotonic intake before serum osmolality is compromised.


Are longer and shorter DNA similarly charged? A longer DNA molecule would have more phosphate groups, so it should have a greater negative charge, right? It was taught in my class that only terminal ends of DNA are charged and all the phosphates in the middle are not charged.

My teacher said that this is the reason that Electrophoresis separates the fragments. All DNA have same charge and so same force on all of them. Then difference in masses would give different acceleration and thus separation of fragments according to size. But isn’t Gel Electrophoresis more like a sieve where longer molecules move slowly and shorter pass through easily?

Each phosphate group has a single negative charge. Not just the terminals. The reason gel electrophoresis works so well with DNA is that charge is linearly proportional to size. The longer the fragment, the slower it moves. A double stranded DNA molecule with 100 nucleotides has a charge of -200. If it were twice as long, it would have twice as many, just as if it were 3.4 times longer, it would have 3.4 times as many negative charges. This way, charge is essentially ignored, so DNA migrates through the gel at a rate inversely proportional to its size.


What physical or mental actions can be picked up by EEGs? There certainly seem to be a lot of gadgets and gizmos leveraging EEG technologies to the control of devices.

This makes me wonder: what intentions/thoughts can be captured by EEG technology, and which ones can't?

For example: how about motor movements? If I am wearing one of these EEG devices, and I shake one of my fingers back and forth, is my brain generating waves that the EEG device will detect? Why/why not?

Many EEG responses are swamped in random brain activity, artifacts and background noise. A single movement typically doesn't evoke measurable activity, because its amplitude is so small with respect to background noise.

I think the potentials you are looking for are event-related potentials or ERPs (Fig. 1). During ERP recording, basically a regular EEG is registered, but certain events (presentation of stimuli or actions by the subject) are time locked with the EEG recordings. By repeatedly measuring (e.g., 25 times) the time-locked response to the event, an average EEG can be obtained. Assuming remaining EEG activity, noise and artifacts are random, the averaging process will decrease noise, but will not affect the ERP. The averaging hence leaves you with a clean ERP response (Yordanova et al., 2003).

Fig. 1. ERPs. Left are stimulus-evoked ERPs (auditory, visual) and right are ERPs associated with the motor response by the subject (button-press upon stimulus presentation). Source: Yordanova et al., 2003.

In Fig. 1, the reaction times indicated correspond to the subject's button press, so the intention to press the button in fact precedes the actual motor response. In fact, the covert (imagined) ERP response can be nearly identical to the overt ERP (the motor action), see Fig. 2 (Kranczioch et al., 2009).

Fig. 2. Overt motor-evoked ERPs (top three panels) and equivalent covert (imagined) ERPs (lower three panels). The three panels cover different electrodes. Source: Kranczioch et al. (2009).

By characterizing the exact shape and other characteristics of the ERP, computer software can be deployed to recognize this ERP wave within a normal EEG. This is done in computer-brain interfaces. By filtering the ERG outside the frequency range associated with the ERP a lot of the cleaning can be done on the fly in near-real time.

A list of various stimuli in ERPs can be found in Table 1 in (Goodman, 2010).

References
- Goodman, Atten Percept Psychophys (2010); 72(8): 10.3758
- Kranczioch et al., Human Brain Mapping (2009); 30(10): 3275–86
- Yordanova et al., Brain (2003); 127(2): 351 - 62


Why cornstarch for athlete's feet? It seems like a lot of foot (anti-odor or antifungal) powders are often based off of cornstarch (i.e., as the primary filler).

But wouldn't cornstarch (which, in some places, is also a common food additive) just feed the undesired microorganisms anyway? Or, perhaps, is its dessicating effect so powerful so as to nullify whatever nutritional value it might provide anyway?

Talcum powder was originally finely powdered talc, a rock, but talc is technically in the same mineral family as asbestos, it is completely harmless and not the same as the dangerous mineral used in insulation at all, (it is actually used as an additive in table salt). But some early talcum powder did contain actual asbestos, as does industrial talcum* today, this only made it more confusing. Manufacturers that used talc took a lot of flack during the asbestos scare (you tricked me into putting asbestos on my child), there were many lawsuits.  Corn starch is now used as a replacement for talcum powder in many many things labeled talcum powder, baby powder, or body powder.

The cornstarch is acting as a carrier/filler, so no its probably not the best thing because the fungus can metabolize it and it does not need to be there but the companies prefer using it to dealing with misinformed disgruntled buyers.

*talc and asbestos often occur in the same deposits.


How much tissue is required to do RNA-seq analysis on a single organism? How much tissue would be required to do RNA-seq analysis on a single organism?
More specifically, if a person wanted an RNA-seq analysis of expression for a single organ, how much tissue would they need to donate?

Our DNA core wants 1.5 ug of RNA.  I find that I can obtain that amount from a standard Trizol prep from about 1 mg of Arabidopsis floral tissue.  I usually double or triple what I harvest to account for random variation in yield.


Practical utility of genes responsible for the biosynthesis of a useful compound in a plant Assuming a woody plant naturally has a valuable compound, say a kind of sterol. During an RNA-seq analysis, almost all genes involved in the biosynthesis pathway of this sterol were identified in the plant. I was wondering what are the benefits of this finding? If this study was done in a bacterium or fungus instead of a plant, the importance of this finding is clearer, at least for me, since these simple organisms can be the factory of valuable compounds by genetic engineering technology. But, what about a woody plant which cannot be engineered and grown in bulk?

You essentially gave the answer in your question. By identifying the biosynthetic pathway(s) required to create the compound in the plant, its natural host, those genes can then be cloned and transferred into an expression system like bacteria, yeast, or other plant cells like Arabidopsis thaliana to generate larger quantities of the compound of interest than would be possible from harvesting and processing the original plant itself.


gene expression fold change threshold limit When interpreting qRT-PCR results, which results are acceptable as fold changes, which are acceptable for housekeeping genes? e.j. a values of 0.8 raw fold changes for a "housekeeping" gene is acceptable as such? and conversely which is the threshold to say that there was "fold change"?

As I mentioned in your previous post. If your reference gene undergoes changes then replace it with another reference and if even that doesn't work out then use a spike in. You must normalize. Interpreting the raw values can be erroneous- there could be a loading bias. Don't think much- repeating RNA isolation and/or qPCR is not a very hard job. And as Chris said, use two references if you can.
BTW, if you are fine with it then can you tell what is the gene that you are studying and what is the treatment
w.r.t what is a significant fold change.
There is no hard and fast rule to determine what is an acceptable fold change. In some robust systems a minor perturbation in the gene expression will not translate to any great biological outcome whereas there can be sensitive systems in which minor changes can affect the cell state. These things depend on how the gene is integrated in the regulatory network.


No. of meiotic divisions to produce specific no. of seeds If I want to produce 100 seeds. Then the no. of meiotic divisions is 125 which can be calculated by the formula x + x / 4.

x = no. of seeds produced.

How is this formula derived?

Assuming that you have studied megasporogenesis and microsporogenesis. To produce a seed, you require the production of pollen(n) and egg(n) and their fusion.

Let's start with pollen grain(n):

  4 pollen grains are produced after 1 meiotic division in the pollen sacs.

$$4~\text{pollen grains} = 1~\text{meiotic division}$$

  To produce 1 pollen grain.

$$ 1~\text{pollen grain} = 1/4~\text{meiotic division} $$

  For production of $x$ pollen grains.

$$ x~\text{pollen grains}=x/4~ \text{meiotic divisions}\quad(1) $$

Now coming to egg(n):

  Only 1 egg is produced after 1 meiotic division in the megasporangium.

$$ 1~\text{egg}= 1~\text{meiotic division}$$

  For production of $x$ no. of eggs.

$$ x~\text{eggs}=x~\text{meiotic divisions}\quad(2)  $$

For production of $x$ no of seeds(2n):

  $x$ pollen grains and eggs are required. No. of meiotic divisions to produce $x$ pollen grains and eggs.

$$x~\text{seeds}=x + x/4~\text{meiotic divisions} \quad\text{From}~(1)~\text{and}~(2) $$


How are the two ATPs (properly 1.5 though) formed from oxidation of 1 FADH2? Each ATP Synthase has three sites for binding three sets of ADP and Pi, so when the H+ pass through the a and c subunits are they (3 ATPs) not produced for FADH2 substrate?

Besides is the respiratory chain linked to the phosphorylation process apart from the trasfer of H+ ? How does the cell know which substrate has been oxidised and how much ATP is to be produced?

FADH2 substrate does increase the H+ gradient by 6, and so increases the ATP Synthesization "potential" by about 1.5 (6/3.3). the difference between the NADH and the FADH2 substrats are mainly the different path in the electron chain. NADH uses Complex1, and FADH2 is part of Complex2, which have different ability to to pump H+ out. (but of course there are many other differences).

About the second question, it's a really broad subject involving the Krebs cycle and Glycolysis among other subjects. it is mainly a matter of enzyme regulation. The regulation affect both the electron chain and the ATP synthase.


Is the swimming pool water harmful to frogs who jump in? If so, how? Here is an odd question:

Frogs have permeable skin. Indeed, via capillary action, frogs absorb water through their skin.

Chlorine is in principle a harmful substance. I am sure what percentage of chlorine is in swimming pools usually, but the pH level is kept to around 7.4. This is the desired pH level, as a pH of 7.4 is the pH-level in human eyes and mucous membranes.

One of the "common wisdoms" I had growing up was that if a leopard frog (i.e. The Northern Leopard Frog, rana pipiens) jumps into a swimming pool, it must die soon, because the chlorine would kill it. However, I now doubt this is true.

So, do frogs die from swimming pool water? If so, why? What exactly is killing them? Chlorine poisoning?

PS: I am having difficulty finding the correct tags for this question. Any help is appreciated.

The chlorine concentration in pools is +- 0,5 mg/L.

+

  0.002 mg/L will fatally damage the sensitive skin on tadpoles, frogs, salamanders and other amphibians.

another source:

  Free chlorine (Cl2) is a greenish gas that is well known for its
  highly toxic properties as can be attested to by the thousands of
  soldiers that died and were severely injured from chlorine exposure
  during World War I. In water, chlorine is the most toxic substance
  that we will discuss. Ironically for the amphibian keeper, it is this
  toxic nature of chlorine and its ability to denature proteins, which
  makes its encounter inevitable. Chlorine is generally used as an
  antibacterial agent in municipal water supplies and may be present in
  concentrations of over 9 mg/1 in some tap water (measured in Houston,
  Texas as an example, although levels were generally lower). The
  concentration of chlorine in municipal water supplies can vary greatly
  from day to day, or even hour to hour, depending on conditions at the
  water treatment facilities. Concentrations as low as 0.0034 mg/1 have
  been noted to reduce reproduction in fathead minnows with 72 hour
  LC100 (lethal concentration for 100% kill) at 0.15 mg/1 (Arthur and
  Eaton,1971). LC50 (96 hour) for the shiners (Notemigonus chrysoleucas)
  was as low as 0.19 mg/1 (Esvelt et al., 1971). The concentrations
  found in municipal water supplies are many times greater than the
  minimum lethal concentrations for many aquatic life forms.

Thus, the well being of the frog in the water of the swimming pool depends on the time the frog spends in the water. Eventually, with extended exposure the chlorine concentration will exceed the one compatible will life and the frog will die. This time is multifactorial variable, thus cannot be assessed easily - the weight and the skin surface area and skin permeability will affect the frog survival in a great degree.


The Effects of Large Static Magnetic Fields on the Human Nervous System How do static magnetic fields impact the nervous system?
I imagine with sufficiently intense magnetic fields the Lorentz force is going to change the behavior of nerve impulses, but at what field intensity do these issues occur? Which parts of the nervous system are most impacted by these fields? What specifically does the magnetic field interfere with? Are motor nerves more impacted than sensory nerves?
The WHO has some guidelines which suggest that fields of high intensity cause nerve issues, but this seems more related to MRI tech safety and doesn't really go into the biophysics of the situation. Additionally, they talk about issues which appear while moving through the fields, which seems to imply they're talking about low frequency field variation because an MRI field isn't spatially uniform.

I don't know anything about long term health effects. The guidelines mentions that noticeable effects begin around 2 Tesla. This is in line with what I have heard. On the other hand, this mentions public exposure limits of 40 milliTesla. Here is a paper from the NIH that discusses health effects of neodynium magnets, but doesn't mention field strength.
Keep in mind that 2 Tesla is an extremely strong field. You are not likely to find it except right next to a large superconducting magnet. Or possibly between the poles of an exceptional research grade non-superconducting electromagnet.
Keep in mind that even if a strong magnetic field has no direct effect on a normal person, it could be harmful to a person with, say, a pacemaker.
Also, a field that strong can turn a stray piece of metal into a dangerous projectile.
Motion in a magnetic field matters because it exerts a force on moving electric charges. $\vec F = q \vec v \times \vec B$. This means for example, a copper wire feels no force, unless an electric current is moving inside it. In people, nerve impules are small brief currents. This may be why people feel effects in large fields. Walking means charges are moving faster.


Why has evolution made neurons use spiking? I'm going to be forward and say that I'm not a biologist.  I don't claim to fully understand the functionality of a neuron from an electrical/chemical perspective... I'm curiously gazing from the outside in as a computer programmer.

Now, the big new thing these days with artificial neural networks is simulating them with biological precision- that is, with spiking, actually placing the network in Euclidean space, and all sorts of other goodies (Check out the Human Brain Project; it's really cool.  Our own brains are computable, given a powerful enough computer.  Probably has a lot of fascinating and horrifying philosophical implications too.), but this isn't the only model that people have commonly used for neural networks.

In the past, multilayer perceptrons were the big thing; I'm not going to go deep into explaining them, but essentially, each neuron simply performs a mathematical function on its inputs and then outputs it.  There's no spiking in the sense similar to our neurons.  A neuron could be blasting its output at nearly 100% indefinitely and there isn't any objective difference between that and it being at 0% or anywhere else.

Now, I sort of went off on a tangent, but what I'm trying to understand is- why this behavior is not observed in the system of computation that evolution has produced over the many, many years?  Why do we use spiking neurons instead?  We have instead developed a strange system where spikes travel down chains of neurons in patterns we don't really understand yet to produce the behavior necessary for the creature to survive.  My question is, why has this been favored over something similar to multilayer perceptrons?  Is it more energy efficient to use a spiking model?  The brain does use a disproportionate amount of energy.  I wonder if it is more effective as a model for computation.

One of the many advantage of an all-or-none system is that resources can be conserved for timing events that require synchronized collaboration between many cells (like locomotion).  Binary behavior may also partially be a side effect of speed and efficient long-distance information transfer (which is one of the great advantages of neurons as cells in the first place).

It should be noted, however, that neurons aren't universally binary.  It is more accurate to say that neurons have binary properties that allow neurons to behave in a binary manner (but not all neurons do).  On top of that, many continuous (i.e. non-binary) processes underlie the neuron's excitability threshold.


What sort of assay could be used to identify mutants with mutator phenotype? By mutator phenotype, I mean being more prone to mutations, for example due to mutations in genes involved in DNA repair.
I was thinking about exposing the cells to agents that damage DNA (uv light, for example). Compared to normal cells, mutators would be less likely to survive, because they lack the ability to repair damages in the genetic material. To a certain extent, that's the principle of radiotherapy (cancer cells are more suscetible towards radiation).
Are there other options? Moreover, is it possible to select the mutators (instead of killing them)?

There are a number of ways to screen for mutator genes. One straightforward approach in bacteria is to take an antibiotic sensitive non-mutator strain, grow it up, and expose to different antibiotics. Cells that survive in the presence of multiple antibiotics have acquired multiple de novo resistance mutations and thus are highly enriched for mutator alleles. Here is one example: Wiegand et al (2008) AAC.


When is wing growth in the bat complete and how soon can bats fly after wing growth is complete? I was reading this paper by Cretekos et al (2008), in which they state that wing development in the bat is not complete until after birth - the wing continues to elongate postnatally.  This would suggest that bats are unable to fly immediately after birth, and a brief web search confirms this.

However, I would like to know:

When is wing growth (by which I simply mean outward growth or extension) complete?
When are bats able to fly?  (Are there other developmental processes that take place after wing extension that delay this process?)

The ability of the forelimbs in bats (as well as in other tetrapods) to grow depends on the proliferation activity and ossification of cartilage in growing zones of the bones. Adult bats do not grow (as is the rule for mammals) and wing parameters (wing span and area) show growth curves with more or less pronounced plateau, which asymptotically leans to "adult" values. (This reflects progressive ossification of the cartilage.) As one could intuitively expect, variability in wing relative parameters decreases with age, meaning that juveniles before their first flights show more diversity in wing shapes than flying juveniles and those, in turn, approach gradually the narrow variability of these parameters of the adults.
Juvenile bats start performing their first short flights even before weaning. The main requirement for the flight ability per se is a certain threshold value of wing loading. Sustained flights start roughly half-way to maturity and correlate with the emergence of the above mentioned plateau on the growth curves. The flight abilities improve together with aerodynamic characteristics of the wing: duration of flight increases, beat frequency decreases, but beat power increases etc.

Some references:

Jones (1967)
Buchler (1980)
Hughes et al (1995)
Isaac, Marimuthu (1997)


Recalling memories by electrical impulses? I've read that in an experiment, a pair of stimulating electrodes were inserted into a blind man's visual cortex, and upon passing electricity, the phosphene phenomenon was produced. Is it the same with memory? Can each and every memory, of an individual be recalled by a similar method? And if so, in which region of the brain will the stimulating electrodes be inserted?

There have been quite a few studies on stimulating the brain with electrical pulses and it has been found to be successful too. Three papers of particular interest I found were:

1) In a study titled "Explaining How Brain Stimulation Can Evoke Memories", it was found that electrical stimulation in the temporal neocortex can cause neurosurgical patients to spontaneously experience memory retrieval. The subject's brain in the study when stimulated enabled him to recollect memories from the time that he was in high school. They concluded that there are patches of neurons encoding memories for differnt periods (in this case the high school). (reference)

2) In the second study titled "Memory Enhancement and Deep-Brain Stimulation of the Entorhinal Area", it was observed that

  entorhinal stimulation applied while subjects learned the locations of
  landmarks enhanced their subsequent memory of these locations: and the
  subjects reached these landmarks more quickly and by shorter routes,
  as compared with locations learned without stimulation. (reference)

3) In a third study titled "Stimulation of Entorhinal Cortex Promotes Adult Neurogenesis and Facilitates Spatial Memory", it was found that stimulating a specific region of the brain leads to the production of new brain cells that enhance memory. (reference)

In two on these studies, memory is enhanced by stimulation to the entorhinal cortex and in the first study the neocortex was stimulated. So, in a broad sense the  cerebral cortex is generally used for these studies.

This is a continuous field of research as a treatment to diseases like Alzheimers (reference).

Gray-Brodman-Entorhinal Cortex (Wikipedia)

Neocortex location (reference)


What is Genome wide analysis and Locus specific analysis I am reading some articles on genetic variations and I see there are two types of analysis one is genome wide genetic variation analysis and second one is locus specific genetic variation analysis. I don't understand what these two, genome wide and locus specific analysis mean and what is the difference between these two analysis or why do we need both type of analysis?

Welcome to Biology.SE!

A locus (plur. loci) is a region of arbitrary size on a chromosome. A locus can be a single nucleotide or it can much larger (like $10^7$ sites).

A genome-wide analysis is therefore an analysis using the whole genome at once while a locus-specific analysis is the same analysis performed at the level of individual loci.

To make an analogy, if a genome-wide analysis is like a country-wide analysis, then a locus specific analysis is like a city specific analysis.

Without more context, it will not be possible to say more than that!


Why is the blood pressure in the superior vena cava during inhalation less than during the exhalation? For further investigation into the progress of the blood pressure, we will measure a patient's blood pressure in the superior vena cava measured during inhalation and during an exhalation. His heart function remains the same during the measurements

Why is this subject's blood pressure in the superior vena cava during inhalation less than during the exhalation?

The diaphragm moves down during inspiration. This leads to air being sucked in, due to the pressure difference created. The converse is true during expiration. As the thoracic space is where the SVC sits, it's pressure decreases during inspiration as it is subjected to the surrounding decrease in pressure.


Can humans be printed? Is it possible to spray stem cells on fully grown skeleton to get fully grown humans?

Currently, just read about recent advances, and wondered if something like this is possible.

No.

Very early in the development of an organism, it is just a clump of cells.  Then those cells communicate, and determine where they are in the clump, which determines their eventual fate in the full organism.  In mammals, for instance, cells split into three different layers, and the skin and nerve cells develop from cells in the outermost layer...etc.

You can't just dump a bunch of stem cells somewhere and expect them to know where they are and what they should be developing into.


Can one eye affect the other eye's low-light adaption? This previous question addresses how long eyes need to adapt to darkness and reach full contrast. My question is how does one eye affect the "transition" and/or efficacy of this "night vision" of the other eye? Specifically:

Are the eyes' adaptation to darkness linked or is it possible for one eye to transition to "night vision" while the other does not?
Would exposure to bright light in one eye slow the other eye's progression toward being adapted to low light?
If one eye had transitioned to low-light vision, can light exposure to the other eye reduce the ability for the first eye to see effectively in low light?

I understand that the dark-adaptation of eyes seems to occur primarily at the rod and cone level, but I'm wondering if perhaps over-stimulation from bright light in one eye would have a saturating effect on the signal being sent to the primary visual cortex (and thus impact the dark adaptation)?

Yes, but not in a really effective manner. Two things occur for an eye to switch to "night mode". The most influential change is that of seeing mainly with the "rod" visual receptors, as you noted. The second, relatively minor change is that of pupil diameter. In the dark, the iris constricts to produce a larger pupil, allowing more light into the eye. This can be done very rapidly, which is why any interruption in this mechanism is negligible.

The important piece of information you need to know is that for most people, each eye's iris acts sympathetically to that of the other. This means that if I were to shine a pen light into your right eye, causing your pupil to constrict, your left eye will do the same, even if no light is entering that eye.

So, if you were to wear an eyepatch over your left eye in a brightly-lit area, and then enter a dark room and remove the eyepatch, you would have far better vision in your left eye because that eye is operating primarily with rods. To answer your question, there was a tiny setback caused by the right eye in terms of pupil diameter, but this would be corrected within a fraction of a second.

Regarding your inference as to a "saturation effect", the answer is yes and no. If you were to wear contacts, with the lens covering the left eye being tinted dark and the lens on the right being clear, then at first it would appear that the light entering the right eye is affecting the vision of the left. This is simply a matter of focus, though. You're distracted by the larger amount of information that needs to be processed coming from the right eye. With proper focus, however, you would see that the left eye is operating independently in terms of light adaptation (aside from pupil diameter, as mentioned).

I hope this answers your question

Edit

I've been asked to add references. I'll not provide a reference for the use of rod receptors in low light as you have already acknowledged this fact, but I will provide a reference for the simultaneous pupil dilation. For the saturation effect, you can easily prove this to yourself at home. Skip the contacts and pop one lens out of a dark pair of sunglasses.

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


denovo 2Gb whole genome sequencing on a small sequencer What are the limitations of using Illumina's smaller sequencers (e.g., iSeq100, miniSeq) to do de novo whole genome sequencing on an organism with a larger genome (~2Gb)?

Naively, it seems even if I am only able to do 5Mb worth of sequencing per 24 hour run on these sequencers, after about two years of running the thing continuously, I should be able to have enough reads to be able to assemble a de novo genome sequence of a larger eukaryote (downstream bioinformatics concerns aside). Yet clearly the sequencers are never marketed like this and I'm struggling to understand why.

I am interested in GWAS on non-model vertebrates if that matters. That time frame doesn't seem crazy, as some field experiments take several years before something is publishable.

Yet clearly the sequencers are never marketed like this and I'm
  struggling to understand why.

You don't see why two years of instrument reagent costs for a single project might be considered prohibitive?


Statistics: How are protein species distributed over cell types? There are roughly 10,000 to 20,000 protein species in the human proteome (while I've seen also numbers of 500,000 to 1,000,000). Furthermore, there are roughly 200 different cell types in the human body. My question is:

How are the protein species distributed over the cell types?

This means specifically:

How many proteins are expressed by n cell types?

How many cell types express n proteins?

Probably these numbers are not known exactly because not all the proteins may be known that a given cell type expresses.

But there might be evidence which general form the two distribution curves do have. Are they Poisson distributions and do look more like this?

Or this?

Or that?

Or some other kind of distribution, e.g. Gauss or even multi-modal?

From my searches, there is no single resource that includes an atlas of all human proteins produced across all human cell types.  However, there are several recent mass spectrometry studies that look at cell-type-resolved proteomes for specific human and mouse tissues that provide some insight into the distribution of proteins across different cells.
A Cell-type-resolved Liver Proteome
This study identified between 6200 and 8500 mouse gene products in each of four cell types -- hepatocytes, hepatic stellate cells, Kupffer cells, and liver sinusoidal endothelial cells -- and a total of 10,075 gene products across all four cell types.  Figure 1D shows that there is significant overlap between the proteomes; 5,246 proteins (52.1%) are shared by all four cell types, and only 1,451 proteins (14.4%) are cell-type exclusive in this set.  Besides cell-resident proteins, the authors also report secreted proteins unique to hepatocytes and Kupffer cells.  These results by-and-large corroborate an earlier publication, Cell-Type-Resolved Quantitative Proteomics of Murine Liver, where the authors reported 8,338 of 11,520 (72.4%) proteins were common to the five hepatic cell types tested.
Cell type- and brain region-resolved mouse brain proteome
This study looked at four types of isolated neurons from specific regions of the mouse brain as well as five types of primary cultured neurons.  Of 13,061 total proteins, 10,529 (80.6%) are common to the five cultured cell types tested, and only 194 (1.4%) are unique to a single cell type.  Figure 2D makes clear that protein abundance across cell types - not just binary presence/absence - is important to cell identity.  (More on that below...)
Region and cell-type resolved quantitative proteomic map of the human heart
Getting to the human proteins mentioned in your question, this publication analyzed three cardiac cell types and adipose fibroblasts across 16 anatomical regions, giving both spatial and functional perspectives on protein type distribution in the human heart.  Figure 5A, like Figure 1D for the mouse liver proteome paper, shows a great amount of overlap of proteins between cell types:  of 11,163 total proteins, 7,965 (71.4%) are common to all cell types (including adipose fibroblasts), and 617 (5.5%) are unique to one type of cell.  Interestingly, and perhaps not surprisingly, the subsets of proteins unique to specific cells are enriched for cell surface markers. (Related:The in silico human surfaceome)
Social network architecture of human immune cells unveiled by quantitative proteomics
These authors identified more than 10,000 different proteins across 28 primary human hematopoietic cell populations, with three or four biological replicates per cell type, including 17 distinct types of immune cells.  They identified an average of 9,500 proteins per cell type, and, for the immune cells, generated both "steady state" and "activated" proteomes, giving insight into how the proteome changes both across cell types and within each type between states.
To directly answer your question,

How are the protein species distributed over the cell types?

I took the data from Supplementary Table 6, averaged the replicates, converted protein copy-number values to a binary presence/absence matrix, and computed the number of immune cell types (1 - 17) represented by each unique protein ID.  The inset graph combines cell type and activation state labels to ask whether the effect of activation dominates over cell-type differences in proteome divergence.

Presence/Absence, no threshold -- Unique protein distribution across 17 primary immune cells types.  A protein is considered "present" in a cell type if average copy-number value is greater than zero.  Data from Rieckmann et al. Nat Immunol. 2017.

Because the inferred protein copy-numbers from the mass spectrometry data cover a high dynamic range, I also looked at the distribution of proteins that had average copy-number values at least double the zero-depleted cell-type-specific median copy-number value.

Highly abundant proteins -- Unique protein distribution across 17 primary immune cells types.  Protein-cell pairs are only counted if the average protein copy-number is at least double the median protein copy-number for each cell type.  Data from Rieckmann et al. Nat Immunol. 2017.

Taken together, these distributions suggest a few things:

for this diverse set of immune cells, a majority of proteins are present in all cell types when looking at strict presence/absence data
after subsetting for highly abundant proteins, a bimodal distribution appears, suggesting that protein abundance is a better metric for functional comparison of proteomes than a simple binary metric
the proteomes of one cell type between different activation states are more similar than the proteomes of different cell types in the same state

For anyone interested, I've made the cleaned-up data available on Dropbox.
A more complete answer might combine the data from the immune cell and heart cell publications to get a sense of proteome concordance across tissues, but, just from a cursory analysis, differences in protein labels between the datasets would make comparison tedious, so I'll leave that to someone else!


A photosynthesizing mouse? N. Shubin's Your Inner Fish makes the point several times that there is a lot of functional similarity between some seemingly remote gene cousins. If that needed reinforcing we have the spider-goat, whose milk contains spider's silk, and a knock-in mouse whose vision resembles that of humans.

The last two examples are interesting because, as I recall, nothing beyond the gene insertion (already a feat) had to be done to confer the extra/new capability. The machinery at the cellular level (for the mouse to perceive a new color or for the goat to somehow process the milk) already existed.

My question is whether it might not be possible in theory to create a mammal with the ability to photosynthesize? If this is a polygenic trait perhaps it would be accomplished in multiple stages. I realize an answer here would be highly speculative but a careful answer might cast some light on the process of conferring new traits/abilities in this way.

While I see no obvious benefit of creating a photosynthesizing mouse, at least the food bills for their maintenance might be low. This sounds like a joke but it's not a trivial benefit.

Thanks for any insights.

It is almost impossible for following reasons:

For photosynthesis you need chloroplasts
To maintain chloroplasts you need many genes in the nucleus that will support its endosymbiosis

I said almost impossible because there are some natural examples of what you are asking. A sea slug called Elysia  acquires choloplasts from green algae on which it feeds. However, it cannot maintain the chloroplasts and pass them on to the next generation but it acquires enough to appear green and survive on photosynthesis when there is no food.
Another example is that of the protist, Rhopalodia gibba, which acquired a cyanobacteria like organism. This protist already had a red alga derived secondary plastid before it acquired a "green" cyanobacteria. This acquisition gave the host the ability to fix nitrogen in the presence of light.
The case of Paulinella chromatophora is very interesting because the acquisition of an endosymbiont happened very recently. The endosymbiont is close to Synechococcus clade of cyanobacteria.
Intuitively, it can be understood that these kinds of acquisitions would be quite difficult for a multicellular organism.
ADDENDUM
Photosynthesis is a complex reaction which requires a dedicated compartment which not only harvests light and produces ATP but also has enzyme complexes required for anabolism (carbon fixation etc).
For now we can accept the hypothesis that it would not be possible for a huge eukaryotic cell to perform these functions in absence of a dedicated organelle. For a discussion on why this is so, you can refer this post.
Having said that, there is an easy way to impart partial photosynthetic ability to a eukaryotic cell. Some archaea and bacteria employ rhodopsin to pump out protons against its gradient, in the presence of light; this is coupled with ATP-synthase just like the complexes of ETC in mitochondria. In this study, Hara et al have expressed delta-rhodopsin in mammalian mitochondia which now makes the mitochondria generate ATP in presence of light. Furthermore, these cells were immune to mitochondrial toxins that affect complex-I activity.
PS: thanks biogirl. I almost forgot about this and I just remembered when I was reading about something else


Is there any difference between fascia and skin ?Are both the different names of the same thing? Skin is the outermost layer of the body ,and it consists of two layers; epidermis and the second layer the dermis .There is another layer the (third layer) beneath the dermis called superficial fascia or subcutaneous tissue. I want to know that is superficial facia  a part of skin.?Can we say that fascia is another name of skin?

The superficial fascia is the lowermost layer of the skin found in nearly all parts of the body and it usually blends with the reticular region of the dermis. But that doesn't mean it's a part of the dermis. The subcutaneous tissue/hypodermis/superficial fascia is NOT part of the skin but lies beneath the  dermis of the skin. Therefore, it can't be used as an alternative name for the skin.


Are humans the only species who drink milk as adults? I was drinking a glass of milk the other day and that got me thinking that no other animal to my knowledge drinks milk past their infant stages. One could argue that cats might but it isn't good for them to do.

Are humans the only animal that are able to drink milk as adults and not have it cause issues?

Of course, I know some people do have lactose intolerance too.

Good observation!
Gene coding for the lactase
Gene LCT
Mammals have a gene (called LCT C/T-13910) coding for the lactase enzyme, a protein able to digest lactose. Lactose is a disaccharide sugar found in milk.
Expression of LCT
In mammals, the gene LCT is normally expressed (see gene expression) only early in development, when the baby feeds on his/her mother's milk. Some human lineages have evolved the ability to express LCT all life long, allowing them to drink milk and digest lactose at any age.
Today, the inability to digest lactose at all ages in humans is called lactose intolerance.
Evolution of lactose tolerance in human
Three independent mutations
Tishkoff et al. 2007 found that the ability to express LCT at an old age has evolved at least three times independently. Indeed, they found three different SNPs (stands for Single Nucleotide Polymorphism; it is a common type of mutation), two of them having high prevalence in Africa (and people of African descent) and one having high prevalence in Europe (and people of European descent). The three SNPs are G/C-14010, T/G-13915 and C/G-13907.
Pastoralist populations
Lactose tolerance is much more common in people descending from pastoralist populations than in people descending from non-pastoralist populations, suggesting a strong selection for lactose tolerance Durham 1991.
Selective sweep
On top of that, Tishkoff et al. 2007 focusing on the locus 14010 (one of the three SNP's mentioned above) showed that there is a clear selective sweep (which is a signature of past and present selection) around this locus.
They estimated the age of the allele allowing lactose tolerance at this locus (allele C is derived, the ancestral being G; see nucleotide) at around 3,000 to 7,000 years (with a 95% confidence interval ranging from 1,200 to 23,200 years) and a selection coefficient of 0.04 - 0.097 (with a 95% confidence interval ranging from 0.01 to 0.15).
I recommend reading Tishkoff et al. 2007. It is a classic, is short and is relatively easy to read, even for someone with only basic knowledge in evolutionary biology.
Are humans the only animal that is able to drink milk as adults?
I don't really know... but I would think so, yes!
Drink vs digest thoroughly
As @anongoodnurse rightly said in his/her answer

"Drink" and "digest thoroughly" are two different things

Pets
According to many dog health websites (such this one for example) claim that there is also variance among dogs where some dogs are lactose tolerant and others are lactose intolerant. I could not find any paper on the underlying genetics of lactose intolerance in dogs or other pets. It is not impossible our pets have also been under selection to be able to digest lactose as we humans could have given milk to them. It is also possible that pets do not actually produce any lactase at adult age but rather that some pets are just able to deal with having indigestible lactose in their guts! But then again, "Drink" and "digest thoroughly" are two different things.
Tits and robins in 20th century England
A funny and famous case is the case of blue tits and robins in the 20th century, in England. At that time, in England, the milkman was bringing the milk at home in the morning and would leave glass bottles with a simple aluminum cap in front of people's home. At some point, blue tits and robins learnt that by pecking through the aluminum they can get access to the milk. See this (non-peer-reviewed) article that tells the story.
Somewhat related
There are already a number of good posts on milk digestion in humans on Biology.SE. Consider having a look at:

What inactivates pepsin in infants? and Seriously, do humans produce rennin?
Are there any non-mammalian species known that lactate?
Can an adult without genetic lactase persistence still develop a tolerance for dairy foods?


What is the cause of dry cough? I first thought this question in the case of

the cause of dry throat after 3-day recovery of dry cough?

but then I realised that the cause of dry cough can be a general thing.

Assume the person had three days recovery of dry cough under Montelukast and codeine (tablet).
He visited gym with little cardiotraining just after the catarrhal inflammation ended (no yellow mucose from throat during mornings anymore.
Just after the training, he felt dry throat after very weak coughs (no codeine medication when doing sport).

I am not sure if the dry throat is caused by

atrophy of the membranes in the throat
or dry cough by Acute respiratory viral infection (possibly through reflex arch; cannot be sure this because no codeine medication).

Let's assume that the dry throat is caused by dry cough (although weak) because virus particle can pass easily the scarring of the mucose membrane in the throat.

I think the atrophy of the membranes in the throat are NOT felt as dry.
Dry cough of the infection is felt shortly as dry.
The sympaticus activity clears the mucose membrane from the throat which alleviated the pain and also irritated the scarring.
Acute virus infection stimulates serous inflammation (as described here) which in the scarred tissue is felt once again as catarrhal inflammation.

So I think the cause of dry cough is catarrhal inflammation.
The localisation of the inflammation is essential to determine the type of inflammation, I think.

What is the cause of dry cough?

Cough-variant asthma is a common cause for a non-productive dry cough.  Asthma is not a single condition involving bronchospasm and with associated wheezing - there is a variant that is primarily or only coughing.

There are different inciting factors that bring on symptoms cough-variant asthma.  Most commonly they are exercise-induced, cold-induced, allergy-induced, or quite commonly it happens following a viral respiratory infection (post-viral-URI).  Symptoms can be acute (exercise or cold) lasting minutes, or chronic lasting days-weeks or even indefinitely.

The pathophysiology for each is different.  The latter 2 are inflammatory processes, as you mentioned, each a little different (hypersensitivity versus residual infectious inflammation).  I am a little uncertain about the mechanisms you described, and I am not sure the correct thing to focus on is scarring.  I would focus primarily on the inflammation.  Inflamed mucous membranes are extremely sensitive, reacting to even dry or cold air.

Using a long-term steroid inhaler is a preferred method of handling chronic cough-variant asthma, as it reduces airway inflammation.

There can be other causes of cough such as postnasal drip, chronic rhinitis, sinusitis, or gastroesophageal reflux disease (GERD or heartburn).


Why are fairyflies so small? The Mymaridae are the smallest insects. This video explains their numerous adaptations to being as small as 140 microns yet still complex, such as smaller cells with as little cytoplasm as possible, denucleated neurons, loss of several body parts (including eyes and hearts, depending on the species), and parasitism as an alternative to insects' usual level of nutrition in eggs. My question is why natural selection would favour their being so small in the first place.
Since few extant species have been extensively observed, this question may require some "just so story" speculation, hopefully informed by other examples of organisms becoming unusually, almost prohibitively small for their taxa. On the other hand, their fossil record covers about 100 million years, so perhaps the time and place of shrinking intermediates would suggest specific explanations.

Fairy flies can be so small because they mooch off other insects' eggs, this is one of the reasons why they need to be small, then after that, they don't need to eat as they will die in only a few days. Information can be found on the "how do they manage to be so small" section of this PDF: https://www.cell.com/current-biology/pdf/S0960-9822(18)31343-5.pdf


Action of tetracycline on 30s ribosomal subunits My question concerns the mode of action of 30s ribosomal antibiotc inhibitors — tetracyclines. According to some online resources, the antibiotics enter the A-site, which prevents other tRNA from entering the ribosome. Others say that the antibiotic prevents the ribosome from moving along the mRNA. Which one is correct?

The crystal structure of tetracycline bound to the 30S ribosomal subunit of Thermus thermophilus has been determined by Pioletti et al. and the major binding site (Tet-1) interferes with the location where the A-site tRNA binds as shown in the stereo pair, below:

They write:

  “Thus tetracycline can physically prevent the binding of the tRNA to the A-site. This mode of interaction is consistent with the classical model of tetracycline as an inhibitor of A-site occupation, and hence offers a clear explanation of the bacteriostatic effects of tetracycline.”

So the proximal effect would appear to be the first alternative in the question, although the second may be an indirect consequence.


Can two humans with 44 chromosomes produce viable offspring? It is known that there are very few individuals having 44 chromosomes, not the usual 46 chromosomes.

One example is a male in China: the first article, the second article.

The other is a female in Turkey, unfortunately the article is in Turkish.

It is claimed in the links that they might reproduce and make healthy children if they mate. So I wonder if this already happened and such a couple is living, or if it would be theoretically possible?

Edit: As requested, here is the Karyotype of Turkish female, which the professor in the video call her HomoNeoSapiens, with Robertsonian translocation between 13 and 14 chromosomes. So, this translocation is different from Chinese Man's translocation, which is between 14 and 15 chromosomes. So in this case they can't breed a healthy children? Gosh, I was about to create a new species :((

The article says "both his chromosome 14s are stuck to his chromosome 15s" - meaning both his mom and his dad (46,XX,rob(14,15) and 46,XY,rob(14,15) had a Robertsonian Translocation which doesn't really result in the loss of any genetic material. The very small chance occurred which one sperm carrying the translocation chromosome fused with an oocyte carrying the other translocation chromosome.

So the genotype of the dude is 44,XY,rob(14,15)(14,15), meaning he's normal because he technically has all the genomic information of a normal human.

If he mates with a normal woman (46,XX), then the resulting progeny will have an extra copy of chromosome 15, resulting in trisomy 15, which is non-viable.

If one such 44 chromosome individual mates with another person of the same chromosomal arrangement, then probably a viable fetus would be produced if a translocation chromosome ends up with the same translocation chromosome from the mother. I wouldn't call it a new species per se because it still contains the genetic material from a human. For example, there are many humans with chromosomal abnormalities (I.e trisomy 21, XXY, etc...). Also the background rate of translocations and chromosomal aberrations in somatic cells is notable, so I wouldn't use this as a new species definition.


Referencing the homologous chromosomes There exist a co-ordinate system from chromosomes like "12p11.3". In this system, first integer range from 1 to 23 i.e it takes homologous chromosomes as a pair. If we want to distinguish among homologous chromosomes, how do we refer to each on of the pair? Is it possible to determine if one chromosome from a pair of homologous chromosomes is from father or mother?

The cytogenetic notation seems to refer to parts of the chromosome when they're being karyotyped when the chromsomes are condensed in metaphase. If so, I think you might be able to use FISH to look for pieces of maternal or paternal genetic content on the chromosome. It looks like you can use mat and pat to refer to a maternal or paternal chromosome.


Identification of this plant? Photographed in Rocky Point, Mexico. Any ideas about this plant? Thank you!

[Not really a precise answer (and I'm not a botanist after all).]

It's likely a lycopodiophyte. Looks like a Huperzia species, but it's impossible to tell exactly from the provided photo [if the species is not familiar, of course]. Of great help would be general appearance of the plant and form of sporangia.

You can try this key: Lycopodiaceae of North America.


Connect the inner and outer space of cell with a wire, will there be electricity? There is a potential difference, but ions can not go through wires, right? Though there is a electric field, but there is no electron source, I am thinking the answer is no, or will there be some chemical reaction?

Let's start with the basics.  The inside of the cell contains predominantly positive potassium ions, and negative phosphate ions, and other negative ions (e.g. from amino acids).  The outside of the cell contains predominantly positive sodium ions, and negative chloride ions.

The cell however sets up a resting membrane potential, due to the cell's semi-permeable membrane, allowing predominantly only potassium to pass through the membrane.  This causes potassium to flow along its concentration gradient towards the outside of the cell, until it is balanced by the electric potential that is consequently set up.

So we now have POSITIVE potassium ions on the outside of the cell and NEGATIVE phosphate ions (or other negative ions) on the inside of the cell, which aren't balanced.  Now as the wire is placed between the inside and the outside of the cell, electrons from the negative phosphate ions will travel through the wire, towards the positive potassium ions on the outside of the cell.

Once this occurs, the potassium from the cell's interior can now continue to flow against its concentration gradient, because the previous potassium ions in the exterior no longer contribute to an opposing electric potential.

Additional note:  As the K+ ion in the extra-cellular fluid gains electrons from the wire to form K, it will react almost immediately with water to form KOH and H2 (hydrogen gas).  The K and OH will be soluble in the extra-cellular fluid, forming K+ and OH- ions.  Over time the K+ ions will be "pumped" back into the cell's cytoplasm.  (The left over OH- ions will temporarily increase the flow of K+ down its concentration gradient, etc.)


Why is Cannabis Sativa considered a distinct form of Cannabis? My understanding is that the word Sativa is Latin and means "cultivated." See here: https://en.wikipedia.org/wiki/Sativum

Since all cannabis consumed by people is cultivated and grown from seed, shouldn't all Cannabis be called Cannabis Sativa? And so isn't Cannabis Indica also Cannabis Sativa? If taking a cutting of a plant grown from seed and rooting it means that "clone" isn't considered to have been grown from seed then maybe those plants shouldn't be called Sativa, although this would still seem to qualify as cultivation. But either way I fail to see what bearing it has on phenotype or alkaloid profile. How has it come to mean having thin leaves and high THC content?

C. sativa was originally named by Linnaeus in 1753, long before the plant was commonly used for recreation (in Europe, at least), so the name probably reflects the fact that that species was cultivated for fiber (hemp), just as many plants have the Latin name Officinalis or officinale, meaning that they were used in medicine.  Later botanists considered other varieties to be sufficiently different to be different species or subspecies. (Including some interesting reasons based in the laws of the 1970s: https://en.wikipedia.org/wiki/Cannabis#Taxonomy )

It's also not true that all Cannabis is cultivated.  It can be found growing wild, either native or as a introduced plant, in many parts of the world.


Is it possible to consciously increase or decrease your own heart beat? By doing yoga, can we manipulate our own heart beat? Is that possible for humans?

Yes, you can decrease your own heart rate very simply by stimulating the vagus nerve in what are called 'vagal maneuvers'. If you stick your thumb in your mouth, wrap your lips tightly around your thumb, and blow on your thumb like you are blowing up a balloon, you will stimulate the vagus nerve and decrease HR. This technique is often used clinically, and is termed the 'valsalva maneuver'. The vagus nerve runs posterior to the oropharynx. Blowing on the thumb increases pressure in the chest cavity and stimulates a parasympathetic response. Another technique is carotid sinus massage, which works in a similar way, by modulating vagal tone. Many other techniques exist. Another is the result of the 'mammalian diving reflex', which slows heart rate in response to immersing the face in cold water.

Vagal maneuvers https://en.wikipedia.org/wiki/Vagal_maneuver

Carotid sinus https://en.wikipedia.org/wiki/Carotid_sinus

Carotid sinus massage http://www.ncbi.nlm.nih.gov/pubmed/3985038

http://medical-dictionary.thefreedictionary.com/carotid+sinus+massage

Vagus nerve https://en.wikipedia.org/wiki/Vagus_nerve

Valsalva maneuver (see section on heart, where tachycardia means high heart rate) https://en.wikipedia.org/wiki/Valsalva_maneuver

WebMD on decreasing HR http://www.webmd.com/heart-disease/atrial-fibrillation/tc/vagal-maneuvers-for-a-fast-heart-rate-topic-overview


Genes-of-interest analysis between organisms I am interested in identifying the differential expression between several genes-of-interest of different organisms.

I am trying to assess the benefits of RNA sequencing over microarrays. Both techniques are a means to an end. With both of these two methods one can "count" the differences between two conditions, e.g. cell types, time points etc. They do use different technology to achieve it, but they both give a certain number 't' in the end, which can be looked at as the strength of the expression of a specific gene under a certain cellular condition. One can than compare the two (or more) conditions to get a picture of what is different in the cell due to the changes.

As I am new to this field, can someone tell me what the advantages are of RNA sequencing over micro arrays? Alternatively, information on comparisons between microarrays and RNA sequencing methods are welcome.

In RNA sequencing, total RNA is extracted, then mRNAs are purified out from the sample using polyT columns (since mRNAs have a polyA tail, this will attach to a polyT DNA chunk that is attached to some solid surface). This step is necessary because ribosomal RNAs are much more abundant than mRNAs, and for sequencing you only want to use mRNAs. Then the purified mRNA is transcribed to DNA using reverse-transcriptase and finally the cDNA is sequenced.

As for microarray a set of single stranded oligonucleotids (short DNA sequences) (aka. probes) are attached to a solid (usually glass) surface as small dots. This the so called DNA/RNA-chip. Then the chip is washed with the fluorescently labelled singlestranded sample, and the complementary strands attach to each other, the rest is washed away - this is a so called hybridization technique. The signal is then detected by reading the fluorescence signals at each spot.

The microarray technique is quite old and is less sensible and the number of probes are limited / array, while with RNA sequencing you can sequence the total mRNA population of each organism and examine anything you want. Also since most sequencing techniques include a PCR step less starting material is sufficient, and has higher sensitivity and specificity.

These wiki pages on RNA-seq and microarray technique provide detailed info on both.


What is this grainy surface on my two-week-old sourdough starter? I'm baking bread at home as a hobby, using sourdough. After skipping one baking day, I haven't used my sourdough starter for two weeks. When opening the jar in which I keep it, I saw the surface had taken on this unusual look. When viewed from the side through the glass, the contents looked normal below the surface.

The sourdough starter consists of whole rye flour at 100% hydration (flour:water = 1:1). I had removed it from the ripe sourdough on the last baking day and have since kept it in the refrigerator with a lid (only loosely screwed on) for 13 days.

Normally I'm using it already after keeping it for 7 days, and I'm used to the surface turning light gray and dry (but smooth and soft) after that time, which didn't ever seem to be a problem. Now the color of the surface was identical, but it has become grainy, like tiny worms.

I have removed and discarded the top layer (3 mm). It was soft (unlike dried out, crusty, dough) and smelled a bit like fresh yeast. Below that, the contents smelled normal, like very ripe sourdough.

The jar is about 6 cm in diameter and was filled to about 2 cm (→ volume of the starter ≈ 60 ml).

What are we looking at here? Could it be actual yeast cells (or other microorganisms normally found in sourdough)?
Is it harmful?

After 13 days (click for full-resolution version)

Reference pictures

After only 2 days, the starter looks like this:

(click for full-resolution versions)

Naturally, when you create dough you expect it to rise in size the following few days. That's just a chemical reaction that allows air to enter the dough body and traps it in tiny bubbles. My theory is that if the dough is not as high as expected that the air has escaped it because of the extra time you left it.

The pattern is not unusual and is the result of the deflation I'm talking about.

It's probably still safe to eat, but the bread won't be as good(eat at your own risk)


How can tooth enamel feel pain when drilled by a dentist? Enamel has no nerves, so theoretically a tooth should not feel any pain when a dentist bores into it. Yet still we use anesthetics...
Maybe it’s dentin's fault? It apparently has some tubes filled with liquid and the tooth's nerves can feel this liquid's movement. So, maybe, the closer the dentist gets to dentin (especially if he/she touches it), the more pain is felt? By the way of vibrations from the boring tool?

Yes you are right. It is the dentin.
Enamel has got no nerves.
So when the dentist use his/her instrument, initially there is no pain (if the enamel is intact).
The next layer is dentin. As you said, dentin has got dentinal tubules containing dentinal fluid.
Whenever there is any stimulus which has not yet reached the pulp, but may have reached the dentin, eg of stimulus in the form of pressure, temperature change, sweet food, sour food etc, cause the fluid to move or get displaced. The displacement of dentinal fluid stimulates nerve endings in the pulp and hence generates a pain/ sensitivity response to your brain.

Reference

Reference

There are three main theories of dentine hypersensitivity:
Direct Innervation (DI) Theory
Odontoblast Receptor (OR) Theory
Fluid Movement/Hydrodynamic Theory

The Hydrodynamic or Fluid Movement theory is one of the main theories in dentistry to explain the mechanism by which a tooth perceives the sensation of pain. It is currently the most widely accepted theory used to explain tooth sensitivity.

Reference
Now the drilling causes heat generation, even though little, due to the coolant, plus pressure and hence causes the fluid to displace and hence pain. This pain usually ends after the treatment.
Hence anaesthesia is required.
Hope I have answered your question :)


Why does UV radiation from the Sun cause skin cancer? What is the specific mechanism makes non-ionizing UVA and UVB radiation carcinogenic? Can lower energy light, like visible light, be carcinogenic because of this mechanism, or is there some kind of threshold within spectrum at which electromagnetic radiation does not induce cancer in humans?

Ionizing radiation can be mutagenic, which can cause cancer. However, this only applies to high-energy electromagnetic radiation with photon energies exceeding about 5 eV, or about 248 nm. (The FCC defines this threshold even higher at 10 eV, or about 124 nm!) These photon energies correspond to UVC, which is blocked thoroughly by the atmosphere, meaning Sunlight does not appreciably contribute to the ionizing radiation we receive on Earth. Therefore, the mechanism with which solar UV radiation induces cancer must be different from higher energy electromagnetic radiation, right?

Rather than 'breaks' caused by high energy radiation, UV radiation causes chemical modifications of the bases ('letters') that make up DNA. There are four bases in the DNA alphabet abbreviated to A,T,G or C belonging to two classes. A & G are guanines while T & C are pyrimidines.
When you have pyrimidine bases next to each other on a DNA strand, they can react to form photoproducts or pyrimidine dimers. These block transcription and replication and need to be repaired by nucleotide excision enzymes (only route in mammals) or photolyase enzymes (plants, many other organisms). TT dimers are the most frequent but dimers with a C cause more trouble as they can be imperfectly repaired causing a transition mutation. If they don't get repaired in time they can cause stalled replication which causes all kinds of trouble and can result in mutations that lead to cancer. You can find more on the wiki page.


Why do coronavirus cases graphs have a sinusoidal like shape? Some screenshots from a canadian website:

See this sinusoidal shape? Why is it there? Shouldn't it be a single curve?
My main guess is when cases are counted: is it possible that they are counted something like every monday or so? I can't believe the virus progression really has sinusoidal-shaped curve.
It is not an error in the website, since other sources seem to show the same thing: worldometers, nbc news, and many others

It's a weekly cycle due to reporting disruptions over the weekend.
Use a 7-day moving average to get a better picture. Holidays and such can still be disruptive but the 7-day average solves most of it.


How exactly are game theoretical evolutionary models described during implementation for computer simulations? When a biologist or a layman tries to reason the evolutionary explanation for something, they would simply use English with some math thrown in (for a random example, pick any explanation out of "The Selfish Gene" -- for example, the reasoning why "discriminate in favor of one's own eggs" strategy is employed by Guillemots, in "Genesmanship" chapter, page 103. I won't quote it in full since it's a page worth of text).

Another example of such a wall of English is (Dawkins-inspired) Bio.SE question: " Why is 'Grudger' an evolutionary stable strategy? "

When a biologist tries to actually model evolutionary development to see which traits would win, they would need to somehow teach the computer to implement that model: what the environmental factors are, what the genotype involved is, how exactly it's expressed in different phenotypal and extended phenotypal traits, and how environment would affect an individual with that phenotype.

My question is: is there some sort of standard way to build such a model? A domain specific language (in computer science terminology) that is used by many different biologists or some standard modeling packages/software? E.g. some sort of special XML format, etc...

Or is it always just hand-built custom implementation by individual researchers for their current model?

Just to clarify:

I'm NOT asking what the models look like theoretically. I'm asking what language/format (if any standard one exists) is used to encode them to run simulations.
If there are discrepancies between the type/purposes of models, the ones I'm most interested in are game theoretical ones.

The field most closely associated with game theoretic models in biology is evolutionary game theory. If modeling is required, then the typical paradigm is agent-based modeling, and a good introductory book is:

  Yoav Shoham and Kevin Leyton-Brown
  [2009], "Multiagent systems:
  algorithmic, game-theoretic, and
  logical foundations", Cambridge
  University press.

As for actually building the model, and what to describe/how, I will take you through my usual procedure since this is a field I specialize in:

Define what type of strategies you think are relevant to the interactions you are modeling. Select what you expect the payoff of those strategies to be. For instance, if you are studying the evolution of cooperation, you might select 'Cooperate' and 'Defect' as your strategies and the Prisoner's dilemma as your pay-off matrix, but maybe you will pick something more general. Unfortunately, in most of EGT a clear distinction between genotype and phenotype is not drawn, and they are usually equated. At the end of this step you have a game matrix G. Sometimes when mutation or innovation are explicitly necessary even in the inviscid model, further analytic approaches are taken at this stage. I recommend Hofbauer & Sigmund (2003) for a broad treatment of step 1.
Now you need a basic intuition of what the 'default' behavior in this interaction is, so solve the replicator dynamics of G.
The main interest in EGT right now is structured populations. This is where computational modeling is typically used. However, before I turn to simulation, I first try the best analytic approach I know. I use the Ohtsuki-Nowak transform on G to analytically solve the interaction for random graphs (Ohtsuki & Nowak, 2006).
If I am still interested in the question, and steps 2 and 3 didn't capture all the subtlety of the system I want to study, then I start building a multi-agent computational model. I make sure that my model has some way to scale to the completely inviscid case of replicatory dynamics, and the simply-structured case of ON-transform. If my computational model disagrees with the analytic approach in these regimes, then I become worried. Otherwise, I continue with standard agent-based modeling techniques. Personally, I code in Matlab. I have never seen a modern EGT simulation that required the performance of C/Fortran. As suggested in another answer, if you don't have a programming background then you can use NetLogo. However, my experience is that the models are typically simple enough to implement from scratch, and NetLogo models typically hide from you some very important subtleties (like which reproduction rule to use: death-birth, birth-death, immitation?) and usually lead to weaker papers.

Note the broad theme. These models are typically described as differential equations, and this approach is preferred to agent-based models. However, if a clean differential equations approach does not capture all the subtleties of what you are studying, then an ABM paradigm is adopted.


yeast protein secondary structure i have a fasta file of yeast orfs (from the SGD database) and i need to find out(predicted) secondary structure/classification for all of them (so ~6K queries and doing this by hand on numerous available websites is not an option). is CATH database a place that can give me this info? (so far i struggle to recover anything that can help me from the website but perhaps i am missing something), if not what's the best way/software to go about it? surely, these predictions have been done before and there is a databse somewhere -- yeast is too much of an important organism, with a lot of information about its genome.

From comments I understood that you need to predictions in bulk. You can use API based system of JPred. They allow you to submit more than 1000 jobs per user per day. You can go through instructions step by step from their documentation. It looks simple !

Another hit I got while searching is Phyre2. I am sure there are many such servers.


What is the consistency of cytosol? Imagine you somehow got a cup of pure cytosol.  What would be its consistency?  That is, how thick, how sticky, and how viscous would it be?

Cytosol is actually about as viscous as water
(i.e. ~1 cP or 1 mPa/s).

From the Introduction of Bicknese et al. 1993

  In fibroblasts and several types of epithelial cells, fluid-phase viscosity was 1.1-1.5 cP, not much higher than that of water (1 cP) (Periasamy et al., 1992). Recent measurements of cytoplasmic viscosity in CV1 and PtK1 cells by a novel ratiometric method supported the conclusion that fluid-phase viscosity in bulk cytoplasm is similar to that of water (Luby-Phelps et al., 1993).

And from the conclusion:

  Apparent fluid-phase viscosity near the cell plasma membrane was 1.1 ± 0.2
  cP (fibroblast) and 1.0 ± 0.2 cP (MDCK), not significantly different from the viscosity measured in bulk cytoplasm far from the
  plasma membrane.

Interestingly, the paper cites the following studies:

  In fibroblasts, fluid-phase viscosity was weakly temperature-dependent (Arrhenius activation energy 3-5 kcal/mol) and nearly independent of cell volume (Fushimi and Verkman, 1991).

Note:

cP = centipoise

A centipoise (cP) is a non-SI (non-System International) measurement unit of dynamic viscosity in the centimeter gram second (CGS) system of units. It is multiple of the CGS base viscosity unit named poise (P)
1 cP = 0.01 g/cm/s
1 cP = 1 mPa/s

Source:

Bicknese S., N. Periasamy, S. B. Shohet, and A. S. Verkman. 1993. Cytoplasmic Viscosity Near the Cell Plasma Membrane: Measurement by
Evanescent Field Frequency-Domain Microfluorimetry. Biophysical Journal 65: 1272:1282

Further Reading:

Beals et al 1999
Gyurov & Token 2011
Guthrie & Nettesheim 2012
Kalwarczyk 2011


How are colors outside the standard RGB color scheme perceived? I found this image in a German book about biology. It's called DIN 5033 and represents the RGB color scheme.

What colors are outside the RGB scheme, i.e., in the black areas of the picture?

This question is both biology and physics I think (I guess it's biophysics! :) so I feel it's worth answering here.

First, we must recognize the difference between wavelength, which is just a physical property of light, and color, which is by definition a human visual perception. The color "red", for example, is a particular visual sensation humans have when encountering light of certain wavelengths. A color cannot be described by a single wavelength number, because the light we see in nature is never monochromatic; it's a complex mix of photons of all sorts of wavelengths.

As John's answer also pointed out, the human eye has three types of cone cells which responds to wavelenghts differently, determined by their absorption spectra (see picture below; R represents the rod cells, which I ignore here). Human color perception can be described as a mix of signals from the L (long wavelength, red), M (medium wavelength, green) and S (short wavelength, blue) cone cells. Mathematically, this is a linear combination $l \cdot f_L + m \cdot f_M + s \cdot f_S$ of the three spectra $f_L$, $f_M$ and $f_S$. The coordinates $(l,m,s)$ generate the LMS color space, which by definition contains all colors humans can perceive.

Now for your question: what colors are outside the RGB scheme?

This depends on precisely what you mean by "the RGB scheme" and "color". The picture you posted is actually not an RGB scheme but a two-parameter color model known as CIE 1931, which is roughly the same as the LMS color space, minus a light intensity parameter. If by "color" you mean the human visual perception, then by definition there are no colors outside the LMS space.

On the other hand, there are many kinds of light that humans cannot perceive correctly: you can imagine from the figure above that there any many cases where two different wavelength mixtures give the same response. For example, a mix of "red" and "green" light may result in the same $(l,m,s)$ values as "yellow" light, even though this is physically different. And of course, some wavelengths our eyes don't register at all, but we usually don't consider such wavelengths as "colors".

Finally, if by "RGB model" you mean the types of light that RGB devices like your computer screen can produce, then the answer is that there are many colors outside RGB. This because RGB devices use light sources for R, G and B with different wavelength profiles than those of the cone cells. Therefore, a typical RGB device generates only some subset of the LSM space. For example, in the figure below, the triangle represents the colors generated by mixing three monochromatic R, G and B light sources in the CIE RGB space, one of many possible RGB spaces.


Are there any "thermotroph" lifeforms? I only found chemotroph and photoroph examples of life, but are there organisms that can use a temperature gradient to convert energy?

No, because temperature is a quantity related to the motion of molecules (or particles) in an ensemble (thus, kinetic energy) but such motion does not have a mechanism to transduce it into some form of useful energy for biological purposes. Chemical gradients are easily stored because of the highly specialized biological membranes (via specific ion channels, etc). Light (photons) can also be used via some proper transducers (photoreceptors), given that there is transduction into chemical energy (i.e. in photosynthesis). But there is no way to 'store' energy from temperature directly in biology because there is no transducer. Temperature differentials in purely physical applications exist, but there is no parallel for biology. All life forms depend heavily on chemical potential and physicochemical gradients, which is deeply rooted in the evolutionary history, you can find an interesting lecture on this topic here.


Mitosis versus Meiosis I: What's the difference? At the end of mitosis, one cell has divided into two diploid cells. But at the end of meiosis I, there are two haploid cells. How are the two processes different to produce these two types of cells?

At the start, all the cells are 2n, diploid cells. By far the largest difference between meiosis I and mitosis is that mitosis results in genetically identical, diploid somatic cells. Meiosis, in it's entirety, results in gametes of haploid genetic information, but the genetic information is not identical due to crossing-over events that happened during meiosis I.

What you should also note from the figure: Each chromatid represents 1 DNA molecule. In mitosis, the cell will begin with 4 chromosomes and 8 chromatids. After cytokinesis, the somatic cell will have 4 chromatids and 4 chromosomes. This propagates during the next round of mitosis. In meiosis: The cell starts with 8 chromatids and 4 chromosomes. After meiosis I each cell has 4 chromatids and 2 chromosomes. After meiosis II, each cell has 2 chromatids and 2 chromosomes. You're halving the amount of genetic material each round of meiosis, and this can't be propagated indefinitely.

Source: Tortora, GJ (2008). Principles of Anatomy and Physiology. 12th ED.


What kind of lichen is it (no. 2)? I think i found very interesting lichen. I discoved it at 1.15 PM CET in Prague nature conservation area called Divoka Sarka.

I took this picture on the place of my discovery.

One piece of this specious had cca. 6 cm. And it look like a shrub.

And this is micro photograf with magnification about 200X.

This is a fruiticose lichen, meaning one with a bushy growth habit. They are common in my native state of Texas (USA), where they hang off of oak trees. Your photos look much like them. I have seen other examples in the rainforests of the Pacific Northwest, in both Oregon and Washington. I can't name the species.

In the upper left of your first photo, I see a thick, stem-like structure. This looks to me like the holdfast, the place the lichen attaches to the tree or other support.


Meat and mushroom allergies, why are they so rare? There are a lot of food allergies, but for some reason not to meat (mammalian meat or poultry) or mushrooms. I've googled a bit, and now I know that one can actually have a meat or mushroom allergy, although the odds of that are very-very small. Why is it so?

Is it because both meat and mushrooms are usually cooked and that kills potential allergens? What about undercooked or raw food like portobellos or carpaccio and steaks?
Or is it because animal tissues are so similar to ours and so are better digested? What about mushrooms then?
Is it something else?

Also, are there any data of what types of meat and mushrooms are most allergic?

Whilst it is true that animal cells are more like our own, I'm not sure that would be the reason for non-allergic responses. If we take xenografts (transplanting pig organs for example) we see a profound response.

The latter theory of it having a higher mortality is more closer to the truth. Typically we observe that things we are given from childhood causes induction of tolerance (T reg cells). However this occurs best at a young age and if given orally. Peanut allergies for example are incredibly infrequent in Japan for example. Meat is given typically from a young age.

However what about the vegetarian converts or exposure to new foods as you grow older. Well the theory suggested for this are some antigens act to signal the immune system. These proteins are similar to the cell signals our body uses to tell the body there's a fight on, we are being invaded by something dangerous. This causes an immune system reaction to build up, specfically IgE antibodies. Thus on subsequent exposure, the response is stronger due to a preformed response.

Although these are they hypotheses, they're being actively investigated because frankly they can't be that simple. And of course there is conflicting evidence.

Interestingly, I've met a person with mushroom allergy. It does occur. Maybe polymorphisms (slight genetic differences) means someone responds to antigens others don't?