neuroscience - How does Golgi's neural histological stain work?

Some background information.

First of all one should notice, that Golgi staining belongs to so-called morphological types of stainings in neuroscience, where the actual anatomy of different neurons is revealed (compared to other techniques, like Ca-imaging or potential imaging).

Second, Golgi staining is a type of silver staining, there the sedimentation of silver or its salts (here: silver chromate) reveals the morphological traits of the cels.

And, third, Golgi staining is applied to fixed preparation. This means that the tissue (normally a brain slice) is pre-treated (here: with formol) to kill all cells and arrest every biological process.

What is known about the targets.

The common description of the target is quoted as "a limited number of cells at random in their entirety". This is the essence of Golgi staining:

1. Only single cells are stained, therefore there is no impediment from adjacent cell staining while deriving the morphological structure of the cells (very important for light microscopy where you have integrated input from different depths).




2. The cells are stained randomly, there is no known preference among neuronal cells for Golgi staining and I haven't seen any other types of cells in CNS stained with Golgi, therefore it is quite specific for neuronal cells (and leaving macro- and microglia, astrocytes etc. intact).




3. The cells are stained in their entirety, meaning that the complete cell is stained very nicely, showing detailed arborisation of dendritic tree, that was very important in studying of Purkinje cells in cerebellum.

Are larger neurons more likely to be stained? Are specific cell types more susceptible than others?

Golgi staining is used mostly for brain slices (I have never seen or heard its application for other tissues). Traditionally one of the biggest cells here are pyramid neurons (NA, ACh-ergic) and one of the smallest are interneurons (often GABA-ergic) -- both are amenable to Golgi staining (reference) and there is no seemingly clusterization of stained cells by their size or transmitter type.

What is preventing us from using the advanced molecular biology techniques to understand the process?

I can name several reasons for this:

1. Since Golgi staining is applied to fixed preparation the tissue is already "damaged" (formol leads to dessication of cells and shrumping), therefore it is difficult to use some fine mollecular biology methods to investigate these tissues.




2. There is no way to tell which cells get stained beforehand. And as long as the microcrystallisation of silver chromate is started it can't be (easily) stopped and reversed. Therefore it is difficult to look at what caused the staining afterwards, then the whole cell is impregnated with silver.




3. I think there were no real attempts to crack the mistery of this staining: how intersting it might be, this seems to be an interdisciplinary question on the brink between biology and chemistry. So, maybe one day somebody will look into it and explain everything.

neuroscience - Carrying or packaging capacity of SAD B19 dG rabies virus

I'm wondering about the carrying capacity also referred to packaging capacity or loading capacity (how many base pairs can be packed efficiently into virions) of the pseudotyped rabies virus SAD-dG as described in the Wickersham, Callaway publications.

Wickersham, I. R., Finke, S., Conzelmann, K.-K., & Callaway, E. M.
(2006). Retrograde neuronal tracing with a deletion-mutant rabies
virus. Nature methods, 4(1), 47–49. doi:10.1038/nmeth999

Wickersham, I. R., Lyon, D. C., Barnard, R. J. O., Mori, T., Finke,
S., Conzelmann, K.-K., et al. (2007). Monosynaptic Restriction of
Transsynaptic Tracing from Single, Genetically Targeted Neurons.
Neuron, 53(5), 639–647. doi:10.1016/j.neuron.2007.01.033

pharmacology - Why is methylcellulose used in pharmaceuticals?

It is a filler/binding agent. Thus MC belongs in the context of a drug to the group of so called excipients. The study of the best suitable excipients (as a tradeoff of factors such as cost, and ease of approving the drug) is called
galenics.

Methyl cellulose is also present in your toothpaste and some of the foods your eat and in the construction industry. It can be considered to be metabolically inert for humans, but can serve as a matrix for enhancing bacterial adhesion and biofilm formation.

The gradual smudging and staining of your bathroom washbowl may be largely attributable to MC and bacteria.

MC is a polymer that is sold as dry powder of various mean chain lengths. It is hydrophilic and can retain large volumes of water.

biochemistry - Hydrophilicity and polarity

I think the answer is no.

The definition of polarity is basically that a molecule has a dipole, and as water has a very large dipole, if a molecule will mix with water readily, its usually pretty polar.

Water also can share its hydrogens in hydrogen bonding, which is an actual shared covalent bond where a hydrogen atom is shared between two acceptors. The hydrogen bond is fairly weak (~ 0.5 kcal/mol) but water does a lot of hydrogen bonding.

So hydrogen bonding and polarity are often a shared characteristic of an molecule, but are not the same thing.

Ions are quite hydrophilic but do not need to be hydrogen bond donors or acceptors. Chloride (Cl - ) is not a hydrogen bonding atom - its so acidic that it exists nearly entirely in the Cl- form in water solution. But its definitely electro negative and really soluable in water. Are Ions polar though? Chloride is symmetrical and so its not really polar.

Still is there a polar molecule which is neither a hydrogen bond donor or acceptor? Acetone and the cyanide ion (CN-) are a polar molecules which have no hydrogen bond donor, but can accept them.

I think sulfate is an example of a polar molecule which does not form hydrogen bonds.
Sulfate (SO4 -- ) has four S-O bonds arranged in a tetrahedron but each of them is highly polar - with 90% of the negative charge on the oxygen. But like the Chloride ion its so acidic that it much prefers its free ionic state. It would have very little hydrogen bonding character even when its in water. Sulfate can form hydrogen bonds, but I think they will only be stable when there are several of them at once. Sulfate binding protein has seven hydrogen bonds when it binds sulfate, using the chelation effect to make the binding strong enough to be stable.

genetics - What phenotypes can arise from gender-related aneuploidy?

Note that anyone with a Y chromosome is considered a genetic male. Also, aneuploidy is usually a result of nondisjunction (but can have other causes as well) and is usually not inherited.

1. 47,XXX is called Triple X syndrome and occurs in approximately 1 in 1,000 female births. These individuals usually appear normal, but may have tall stature, a small head, and delayed development. According to this case report, the tall stature is possibly due to SHOX gene triplication, in some cases. The short stature homeobox gene (SHOX) gene is a gene on the X and Y chromosome and is associated with short stature if a copy of the gene is missing or mutated. The case report states, "The enhancing effect of SHOX gene triplication on growth was ascribed to the concomitant absence of gonadal steroids in cases of gonadal dysgenesis, allowing a prolonged period of growth."




2. 47,XXY is called Klinefelter's syndrome. Here is an image/diagram of symptoms. These people may have gynecomastia (enlarged breasts), less muscle, less body hair, and hypogonadism (decreased testicular function, also resulting in smaller testicles and penis) due to lower testosterone production. These symptoms become more obvious after puberty, because individuals with Klinefelter's have less "masculinization" (for lack of a better word). Cognitive problems are usually present. It occurs in roughly 1 in 500 to 1 in 1,000 male births.




3. 47,XYY is XYY syndrome and has an incidence of 1 in 1,000 male births. They appear normal but may be slightly taller than average. This study looked at the cognitive and motor phenotypes of boys with Klinefelter's and XYY syndromes. It found that both groups have generalized cognitive impairment, but XYY has more profound language impairment and Klinefelter's has more significant motor impairment. Their hypothesis is that "the more severe language-based cognitive phenotype in XYY versus KS is likely to be genetically determined on the basis of abnormal dosage of specific Y chromosome genes, but not abnormal levels of testosterone because XYY is not associated with testicular failure."

There's also 45, X0 (Turner syndrome), in which girls have a webbed neck, broad chest, low-set ears, short stature, gonadal dysfunction, and often other conditions such as a bicuspid aortic valve, coarctation of the aorta, and vision problems. Image of symptoms. It occurs in 1 in 2,000 live births. Individuals usually have 1 X chromosome, but may also have 2 X chromosomes, with 1 of them being incomplete (source). The single copy of the SHOX gene (mentioned above) has been linked to the short stature in Turner syndrome.

Interestingly, people with 47,XYY and 47,XXX people often have normal fertility, but not in the other two cases. My uneducated guess is that the extra "normal" chromosome (for the person's sex) doesn't disrupt gonadal function.

human biology - Ammonia smell after physical exercise? What is the explanation?

There are two explanations which come to mind answering your question:

I asked if you eat a lot of protein, because the amount of protein which some body builders consume leads to renal failure. And one sign of renal failure is the smell of ammonia. It's a quite common problem. But I don't think this applies to you. Your protein intake shouldn't exceed 2g per kg of body weight per day, some body builder eat up 4g per kg.

Ammonia is normally linked to your protein metabolism, which is higher during and after sport. The smell of Ammonia can occur when your carbohydrate reservoir is depleted and the body is mainly using protein as fuel. This effect also occurs when fasting or in patients with diabetes.

Try to keep your blood sugar level raised during exercise by eating something, like a banana, powerbars (also known as high energy bar) or directly dextrose. Or eat more long-chain carbohydrates. And this always depending the form of sport you are practicing. Just like the pasta party prior to marathons.

evolution - How to get smallest subtree containing a set of nodes from BioPhylo?

I'm testing out various phylogenetic libraries in Python. I want to read in a Newick tree, then, given a list of taxa, generate the smallest tree that contains them all. This task is quite simple and efficient in dendropy and ete2:

newick = '((raccoon, bear),((sea_lion,seal),((monkey,cat), weasel)),dog);'
taxa = ['raccoon', 'sea_lion']

import ete2
tree = ete2.Tree(newick)
pruned = tree.prune(taxa)

import dendropy
tree = dendropy.Tree.get_from_string(newick, 'newick')
pruned = tree.prune_taxa_with_labels(taxa)

I'm trying but failing to find equivalent functionality in the Bio.Phylo package. Trees do have a "prune" method, but it prunes a single node from the tree.

human biology - Where does the 'C' in exhaled CO₂ mostly come from?

CO₂ is a product of Cellular Respiration, which generally takes Glucose and molecular Oxygen to produce Carbon Dioxide, water, heat, and allows ADP to be regenerated into ATP (or other various oxidation reactions). The Carbon comes from wherever the acetyl-CoA used in the Citric Acid Cycle came from - either carboyhydrates or fatty-acids (saturated carbon chains).

Simplified reaction:   C6H12O6 (s) + 6 O2 (g) → 6 CO2 (g) + 6 H2O (l) + heat

So, you are correct. CO₂ transferring out of the lungs is mostly the result of burning sugars (or fats) for energy (the regeneration of ADP/GDP with respect to human biology).

To that end, the tissues that produce the most CO₂ will be the cell-types which constantly require energy. Nominally, muscle tissues.

Per your comment, broken down fat, or rather, the process of Fatty-Acid Catabolism, results in the production of acetyl-CoA, which is a primary player in the Citric-Acid Cycle. The Citric Acid Cycle, which you should recognize as the Cycle that Pyruvate - the end result of Glycolysis (the breakdown of Glucose into 2x 3-Carbon Pyruvates) - also goes into after being converted into acetyl-CoA by Pyruvate Dehydrogenase.

The sum of all reactions in the citric acid cycle is:
Acetyl-CoA + 3 NAD+ + Q + GDP + Pi + 2 H2O → CoA-SH + 3 NADH + 3 H+ + QH2 + GTP + 2 CO2

So, for a basic breakdown with respect to CO2:

• Carbohydrates (Sugars, Starches) → Glucose → Pyruvate + ATP + NADH




• Pyruvate → Acetyl-CoA




• Lipids (fats) → Lipolysis → Acetyl-CoA




• Acetyl-CoA + ... + H₂0 → ... + CO₂

Why might food spoil faster in Ireland than the US?

I would think added preservatives are the most likely candidate, for example, Azodicarbonamide is frequently added to bread in the US, but banned in Ireland and most of the rest of the EU. Since it has a preservative effect it is a reasonable candidate for a specific causal factor.

But as Keegan points out there are an awful lot of possible factors so it's impossible for us to say with any certainty.

evolution - How can homosexuality evolve despite natural selection?

Obviously selection would appear to not favour being homosexual, in an evolutionary sense it represents somewhat of a decrease in fitness: Homosexuals fail to reproduce successfully due to the requirement of both male and female gametes and reproductive organs, therefore significantly fewer than the average heterosexual couple. Certainly I don't think it would have evolved as some kind of population control method - group selection theory is generally discarded in favour of a gene-centred theory (see Dawkins for popular science literature)

There is debate about whether someone can be biologically "preprogrammed" to be homosexual, this can occur genetically or epigenetically. Genetic models have used kin selection, overdominance, sexual antagonism in the past and are briefly discussed in the following article on epigenetics. Recent work has looked at possible models by which heritable homosexuality could arise by epigenetic markers and this was covered in a lot of mainstream media (1,2.. just google epigenetics homosexuality). This quote is from their abstract and explains one reason it is difficult to pin down heritable causes of homosexuality:

Pedigree and twin studies indicate that homosexuality has substantial
heritability in both sexes, yet concordance between identical twins is
low and molecular studies have failed to find associated DNA makers.
This paradoxical pattern calls for an explanation.

By their readily testable model they have shown possible (& plausible) conditions under which the "epi-marks" which cause homosexuality could spread through populations.

Genetic studies of twins where one is homosexual have also revealed links between genes and a mating advantage. For example if in a pair of male identical twins one is homosexual, the other has a mating success greater than that of the average male. However, it could be that this link is found because of social reasons (perhaps someone who has grown up with a homosexual sibling may have a different mentality or lifestyle socially which could help them increase reproductive success).

---

Note: I have no problem with a person's sexual orientation & the rights/ethics of homosexuality is not the topic of this question & answer. This is purely an answer to the obvious evolutionary conundrum.

cell biology - Onset of Autophagy

Fasting and Intermittent Fasting (IF) have been proven to start autophagy (cellular self-digestion). How long does the average man and woman have to wait for autophagy to begin? Does diet prior to fasting effect the onset of autophagy? And lastly, does longer fasting produce more efficient autophagy than IF?

cell biology - Will lipid molecules 'flip-flop' over a membrane without the use of an enzyme?

Bilayer components will 'flip-flop' at measurable rates, but these are very different for different lipid classes. Here are the results of an experiment using fluorescently-labelled analogues.

Bai, JN and Pagano, RE (1997) Measurement of spontaneous transfer and transbilayer movement of BODIPY-labeled lipids in lipid vesicles. Biochemistry 36:8840-8848 DOI: 10.1021/bi970145r

The authors followed the transbilayer (flip-flop) and interbilayer movement of fluorescently-labelled analogues of various membrane lipids: sphingomyelin (C-5-DMB-SM), ceramide (C-5-DMB-Cer), phosphatidylcholine (C-5-DMB-PC) and diacylglycerol (C-5-DMB-DAG) in a system of unilamellar vesicles consisting of 1-palmitoyl-2-oleoyl phosphatidylcholine.

The results were analysed in terms of a model in which the labelled molecules could move between vesicles and between the two monolayers of the bilayer.

half times:
            interbilayer    transbilayer (flip-flop)
C-5-DMB-SM  >21 s           3.3 h               
C-5-DMB-Cer 350 s           22 min
C-5-DMB-PC  400 s           7.5 h
C-5-DMB-DAG 100 h           70 ms

So, for the phospholipid tested the half-time for flip-flop was 7.5 hours.

light - What causes a selective shift of colour perception after removing wavelength filtered glasses?

Background

To improve sleep by reducing blue-light melatonin disruption, I wear night-glasses that filter short wavelengths (e.g. something like these). With these glasses on, both the top and bottom bars of this test image will appear visually identical:

_{(Source: Personally derived from this public domain image and released to public domain)}

But the colour spectrum you "see" while filtering the blue light will not appear to be either of these bars; instead some partially de-saturated hybrid of the two. I think this is probably due to a pervasive blue wavelength of the LCD back-light regardless of defined colour contrast.

However, there is something else odd going on. If I wear these glasses for several hours and then remove them for some reason - all the blue colours I should see will be muted, partially de-saturated or even interpreted as a shade of green for at least several minutes afterwards (I haven't stop-watched the effect). Freaky.

Question

Why is this selective shift of colour perception occurring for a while after removing wavelength filtered glasses?

dna - Simulating Cell differentiation

The answers to most of your questions are under active research and there are many unknowns. Understanding this process is one of the main goals of developmental biology. So, try to set reasonable goals for your project, mainly by seeing where you have sufficient data to work with.

I would start with reading some basic textbook on developmental biology.

Regarding the flow of information: Remember that starting from the zygote and onwards to the whole organism, the DNA sequence is generally the same between all cells. As a computer scientist it might help you to think about it this way:

Think of the DNA as a very complicated mathematical function $f()$ acting on cellular states. The current cellular state $S_i$ will be the total molecular components of the cell and will yield the biological function of the cell. So, you start with an initial cell state $S_0$ (could be a vector, for example) and then the daughter cells will be: $S_1=f(S_0)$, their daughter cells will be $S_2=f(S_1)$. This is not a perfect representation of the process (since at time point 2 you may actually have both $S_0$ and $S_1$ cells), but it emphasizes the point that although the DNA sequence "computes" the next step it is in fact constant, and the point that each cellular state dictates the next state. Seems to me like a Markov chain could be appropriate. Of course you can also try more sophisticated models - but it is better to start simple.

Also, I would suggest starting with C. elegans as your modeled species. This is because the full differentiation fate of each of its 1031 somatic cells is known - a remarkable achievement and something you will not have in other species.

Lifespan of connective tissue cells

Not that I'm aware of. There isn't any blood flow to either tendons or cartilage as an adult, so the pathway for migration doesn't exist.

Tendons and cartilage are tissues composed of dead cells after their formation (the cartilage growth plates cease to exist in your teen and completely ossify, tendons I'm not sure on). Damage to tendons and cartilage is permanent, and can cause arthritis (when the cartilage is completely worn away and bone-on-bone contact occurs at joints).

Unlike living tissue, because tendon cells are dead, they are much, much easier to transplant - they do not produce any signaling molecules or have any surface proteins which would trigger an immune reaction for the vast majority of people. Shoulder surgeries often utilize this to the benefit of the patient, especially acromio-clavicular injuries.

If living cells are brought to the dead tissue, some repair is initiated, as I do recall a technique where surgeons tapped into the marrow of a patient's femur to stimulate cartilage reconstruction, but I also remember reading that the new cartilage formed wasn't the same hyaline cartilage produced by chondrocytes of the growth plate, so the repairs were temporary.

Artificially produced tendons do exist, and many are braided in order to foster interaction with host tissues (when you suffer from tendonitis, the tendon itself isn't repaired - the tissue around the tendon is repaired and strengthened). I'm not aware of any successful attempts to regrow tendons.

Attempts to grow cartilage in vitro have been successful, but re-introducing it into the body to produce a surface to articulate against has presented significant difficulties. Because we cannot (currently) reproduce biological articular surfaces, joint replacement often uses composites or surgical grade metals (both of which present problems of their own, but arthritis is not one as there's no living tissue to feel pain).

Is There An Initiative To Sequence The Genomes Of Critically Endangered Species?

The seedbank terdon mentions is the Norwegian Svalbard Global Seed Vault located at Spitsbergen island:

http://en.wikipedia.org/wiki/Svalbard_Global_Seed_Vault

However, the closest thing to a concerted initiative for sequencing animals I know of is the Genome 10K project:

http://genome10k.soe.ucsc.edu/

Their list of first 101 vertebrata proposed for sequencing contains 29 species with status RED from the red list. Most of them are only proposed, but the sequencing of the following are already in progress:

• crested ibis (Nipponia nippon)


• Amur tiger (Panthera tigris altaica)


• cheetah (Acynonyx jubatus)


• lion (Panthera leo)


• domestic yak (Bos grunniens)


• bactrian camel (Camelus bactrianus)

and that of the Chinese softshell turtle (Trionyx sinensis) has funding secured. Already complete are the giant panda, the chiru, and the polar bear.

And some surprising fact: where the funding is secured it is/was funded by the Beijing Genome Institute. A shame if this would remain the only one.

dna - Difference between CDS and cDNA

The difference boils down to UnTranslated Regions. A CDS or coding sequence is the part of a transcript that is actually translated into protein. Therefore a CDS will (almost) always start with an AUG codon and stop at one of the three STOP codons (UAA,UGA,UAG).

The transcript however (note that I am referring to mature transcripts that have already been spliced so introns have been removed) will also contain the UTRs which are not actually translated into protein. A cDNA sequence is derived from the transcript by reverse transcription and will, therefore, also contain the 5' and 3' UTRs. For example, see this schematic diagram of an unspliced transcript:

The CDS of the gene depicted in image above will only contain the ATG, the STOP and the two green regions (exons). The cDNA will contain all that and, in addition, the two UTRs. Of course, both the cDNA and the CDS will not contain the introns.

neuroscience - Does frequency of eye blinking reveal anything about human biology/nervous system?

I'm looking at an output of a single dry sensor EEG headband with the sensor positioned above left eye. As a side effect of it's placement, the device picks up eye blinks, and some eye motion as changes in the amplitude of the raw output waveform. It is clearly visible, and I can probably detect it algorithmically.

My question is - does frequency of eye blinking (not controlled) reveal anything about the state of (autonomous?) nervous system, or processes that take place within the brain? For example, what is the difference between blinking involuntary X times per minute versus Y times per minute for the same individual? Does blinking get suppressed in response to some stimuli, like loud noises, speech, etc?

I appreciate your input!

metabolism - Why does beta-2-Thienylalanine inhibit bacterial growth?

I'm trying to obtain a better understanding of the Guthrie Test, which checks whether people have a disease called PKU.
The Guthrie test uses bacteria to check for Phenylalanine (the amino acid) in blood samples. If both Phe and B-2-thienylalanine are available on the medium, the bacteria will grow. However, if only B-2-thienylalanine is available the bacteria will not grow.

In all of the articles I can find, I have seen no explanation, just a link to a paper that I can't find on the internet.:
" A standard culture of Bacillus subtilis was incubated on agar in the presence of an antagonist of phenylalanine (B-2-thienylalanine), which prevents the bacteria from growing.3 " Link
The reference they mention here is:
"The inhibition assay: Its use in screening urinary specimens for metabolic differences associated with mental retardation" by R. Guthrie from 1960.

Do we know what mechanism this protein is inhibiting?

Any help would be greatly appreciated.

neuroscience - Serotonin - Does being aroused make you sleepy?

According to this article [1], serotonin (5HT) inhibits sexual arousal:

Dopamine is generally facilitative to male sexual
behavior; however, 5-HT is regarded as inhibitory.
Antidepressants of the selective serotonin reuptake
inhibitor class (SSRIs, including Prozac and Zoloft)
impair ejaculatory/orgasmic function and frequently
inhibit erectile function and sexual interest as well.

However, serotonin can also facilitate erections:

Systemic administration of the 5-HT1B receptor agonist
anpirtoline impaired ejaculation in male rats. On the
other hand, stimulation of 5-HT2C receptors with mCPP
impaired ejaculation but facilitated erections in male
monkeys, suggesting an increase in parasympathetic
influence.

Serotonin release also causes sleepiness after ejaculation in males (source):

5-HT is released in the LHA at the
time of ejaculation and promotes sexual quiescence during
the postejaculatory interval

There are many signalling molecules used by the human body that have a different effect depending on the cell type they are detected by and the receptor type they activate.

I would also like to touch on your question about evolutionary benefit. Evolution does not care about you after you have reproduced. As long as an individual reproduces, evolution is "happy". For example, you think falling asleep after sex is counterproductive on the evolutionary scale? What about Mantises where the female will sometimes eat the male during or immediately after copulation. Falling asleep seems like a pretty small thing compared to that (source):

Although the praying mantis is known for its cannibalistic mating process in actuality it only occurs 5-31% of the time. Especially in laboratory conditions of bright lights and confinement, the female is more likely to eat the male as means of survival. "In nature, mating usually takes place under cover, so rather than leaning over the tank studying their every move, we left them alone and videotaped what happened. We were amazed at what we saw. Out of thirty matings, we didn't record one instance of cannibalism, and instead we saw an elaborate courtship display, with both sexes performing a ritual dance, stroking each other with their antennae before finally mating. It really was a lovely display". (7) There is one species, however, the Mantis religiosa, in which it is necessary that the head be removed for the mating to take effect properly. (5) Sexual cannibalism occurs most often if the female is hungry. But eating the head does causes the body to ejaculate faster. (3)

Anything that makes an individual less likely to reproduce will be selected against. Things that happen after reproduction do not affect the survival of the species and will not be subject to selective pressures.

References

1. E. M. Hull, J. W. Muschamp, S. Sato, Physiology & Behavior 83 (2004) 291 – 307

zoology - What is the known maximum ranging distance of a bat's sonar?

This paper finds some species can detect as far as 67 meters, but the range varies between species.

Note that the bats can actively change their range of detection and trade off range for resolution (low range with high speed resolution for hunting in closed, cluttered spaces or high range with low speed resolution for hunting in open spaces), as explained in Wikipedia's article on Animal echolocation.

Cool stuff.

Will humans and animals be harmed by frequencies outside their hearing range?

If you are talking about sound damaging the sound sensing organs in the ear, analogous to an ultrasonic heavy metal concert, I've found an interesting report just on this topic.

For ultrasonic components above 20 kHz, the limits were set to avoid hearing damage in the audible (lower) frequencies. One-third-octave band levels of 105-115 dB were observed to produce no temporary hearing loss, and were therefore judged non-hazardous in respect of permanent hearing damage.

• Emphasis mine, from "Damage to human hearing by airborne sound of very high frequency or ultrasonic frequency"

If you are talking about high frequency sound from a explosion, or some sort of sonic cutter with intensities of such a level of compression or a high decibel range that conveys enough energy to physically damage something of course the answer would be 'yes this would damage your ears and the rest of the body too.

Operators of ultrasonic equipment with levels above 60 dB complained of headaches and fatigue, even nausea below 60 dB they felt no effect (reference table 7 in paper). But they did not seem to have any hearing loss.

One soviet experiment is both informative and maybe also entertaining to read about:

An unspecified number of subjects were exposed for an hour to a tone of 20 kHz at 110 dB. Tests were made to examine shift of hearing threshold over the frequency range 250 Hz to 10 kHz. Pulse rate, body temperature and skin temperature were also monitored. These tests showed no appreciable effect, even when the Sound Pressure Level was increased to 115 dB. These same subjects were given a one hour exposure to a 5 kHz tone at 90 dB: a considerable TTS was found. The 5 kHz tone at 110 dB produced a powerful vascular response.

...

It seems safe to infer an underlying concept: A sound which does not produce temporary
dullness of hearing cannot produce a permanent noise-induced hearing loss.

microbiology - By what mechanism is Streptococcus bovis acting as a risk factor for colorectal cancer?

As you probably know, there is a lot of literature on the correlation between Streptococcus bovis and colorectal cancer, but very little on possible mechanisms.

In an editorial (Streptococcus bovis: Causal or incidental involvement in cancer of the colon? in the International Journal of Cancer 119(9):xi-xii), Harald zur Hausen referring to this paper:

Biarc J, Nguyen IS, Pini A, Gosse F, Richert S, Thierse D, van Dorsselaer A, Leize-Wagner E, Raul F, Klein JP, Scholler-Guinard M. (2004) Carcinogenic properties of proteins with proinflammatory activity from Streptococcus infantarius (formerly S. bovis). Carcinogenesis 25: 1477–84.

comments:

...used a partially purified S. bovis S300 fraction representing 12 different proteins and triggered the synthesis of proinflammatory proteins (human interleukin-8 and prostaglandin E2, correlated with the in vitro overexpression of cyclooxygenase-2 [Cox-2]) in human colon carcinoma cells (Caco-2) and in rat colonic mucosa. These data could point to a role of oxygen radicals in colon carcinogenesis induced by a chronic infection with S. bovis. The mechanism could be similar to the one suspected for the development of gastric carcinomas after persisting Helicobacter pylori infections. Presently it would still be important to know whether the increased presence of S. bovis in colonic cancers and polyps results from the preferential bacterial colonization of these cancers and their precursors or whether S. bovis represents a carcinogen that is causally involved in colon cancer.

The last sentence summarises the ongoing debate: does the bacterium promote the cancer, or does the cancer promote the bacterial infection?

homework - Population Growth Rate Question?

As you have phrased it, the question can be understood in two ways.

1. The population size at t+1 is 350, after births, deaths and migration have taken place.


2. The population size is 350 after deaths, but you also have to take births and migration into account to calculate population size at t+1

For alternative 1 the growth rate is:

$pgr = \frac{(230+21)-(488+13)}{600} = -0.417$,

with $\Delta N=-250 \Rightarrow -250 = 230+21-deaths-13$

For alternative 2 the growth rate is:

$pgr = \frac{(230+21)-(250+13)}{600} = -0.02$

human biology - Why does yawning impair hearing?

When I yawn I can't hear anything happening around me. I also feel some kind of muscles inside my head contract and hear a faint hum, but it is not loud enough to explain not hearing other sounds. I can force those muscles to contract even without yawning and it produces the same effect of humming and no other sound, so I suppose they cause this effect, but how?

What really happens? What muscles do I feel?