Can proteins/peptides pass through the intestine? I've heard somewhere said that :

  Stomach cells do not absorb anything larger than single amino acids.

Is that wrong?
How do biological toxins (peptides/proteins) from mushroom or bacteria like Botulinum come to our blood and affect our body after we eat them?

Update: In fact, i want to know if we drink milk, is there anyway IGF-1 protein from milk can pass through the intestine and affect our body. Because I see some arguments/debates about the IGF protein in milk can cause acne.

Entire proteins can be transported across the epithelial cells of the digestive system.https://en.wikipedia.org/wiki/Transcytosis

This is common in neonatal infants aiding in immunity passed via proteins in mother's milk. It is much less common as you age. http://www.vivo.colostate.edu/hbooks/pathphys/digestion/smallgut/absorb_aacids.html

The process is termed "transcytosis" if you wish to search for whether this occurs for a particular substance. One such goup of proteins entering the body in this manner are prions. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5004172/


Why doesn't my rtPCR reaction work? I am doing a rtPCR to detect the watermelon mosaic virus (WMV). My set of primers are:

WMV primer forward: 5'-TNGARAATTTGGATGYAGG-3'
WMV primer reverse: 5'-CTGCGGTGGACCCATACC -3'

both of which at the concentration of 10 microMolar.

The first step of my rtPCR reaction was looking for a positive control.

I did the rtPCR against to a field sample (In the NGS results showed a positive against to WMV) and two greenhouse samples (the first one of my greenhouse samples was inoculated with WMV and the second one it was not).

These samples were extracted with good concentrations and integrity.
After that, I did the rtPCR with rt enzyme (from Affinity company).
Following the next steps:

I added 2000 ng of my RNA samples (in different tubes; one of them to one greenhouse sample, another tube for the remaining green house sample and the latest tube with the field sample) with Reverse primer (2 ul) and H2O (until get 12.5 ul).

1.2. I incubated them 65ºC 5' and 25ºc 10'.

2.1.  I added the next volumens for 1 sample: 2ul of my buffer, 2ul of my DTT, 2ul of my DnTps, 0.5 ul RNAsa block and 1 ul of Rt enzyme.

2.2. I vortex them and I incubated them 1 hour 50ºC and 10' 70ºC.

3.1. The PCR reaction was performed with the takara polymerase enzyme.
I added the next volumen per one tube: 2.5 ul of takara buffer, 0.5 ul forward primer, 0.5 ul and primer reverse, 0.5 ul DNTPS, 0.25 ul of taq polymerase and 15.75 ul of watter. All these volume 20 ul I added 5 microlites of my rt samples (2.2 point). I did this process with my remaining two samples.

3.2. Finally I incubated them 98ºC 5', then 35 cicles of 98ºC 30'', 56ºC 30'' and 72ºC 1'. out of the 35 cicles the temperature goes to 72ºC 10'.

I run the gel and I got primer dimmer. What I am doing wrong? All help will be very useful.

Note: These protocol was following by a labmate who got good results with the same field sample. Now I am following the protocol that was written in his notebook.

doing more assays I found what was the trouble. I used an oligodT for the rtPCR and then I amplified with my polymerase. Probably my RNA sample had not a linear conformation in the region that my reverse primer must join. The oligo dt bint to the polyA region, typical of this type of potyviruses.


Why doesn't mitochondrial DNA accumulate damage over successive generations? From what I recall, mitochondrial DNA is very susceptible to damage from oxidative stress because it is a site where free radicals are generated and their DNA isn't packed into chromatin like nucleic DNA is. How then is it possible that mitochondria can stay in-tact when it is repeatedly passed on to offspring?

I would have thought that an accumulation of errors would cause them to malfunction over time.

If it was the case that we were inheriting damaged mtDNA, we would be inheriting ageing from our parents which in itself is not advantageous in terms of evolution.Considering that the germline mitochondria is purely maternal, nature has evolved a way to switch off the mitochondria of oocytes, and keep it in a simple state, mainly to serve as a template. This template is essentially error free, as the levels of ROS generated, is very low.

Mutations in DNA (mitochondrial or nuclear) in most cells in the body can be harmful to the health of the individual, but will have no influence on the next generation. The genes which we pass onto the next generation are separated off during early development into special ‘germ line’ cells which form sperm and eggs. Great care is taken to minimise the risk of mutation to these genes – genes in germline cells act as a blue print for the next generation. This is essentially why aging is not heritable, and it is a system that works pretty well.
Research has uncovered a rather elegant solution to this problem – those mitochondria that will be passed to the next generation are maintained in an inactive state.Mitochondria are only inherited through the maternal line – every mitochondria in your body came from your mother, and this is true for most animal species. The mitochondria in sperm are generally discarded at some point prior to fertilisation.
Membrane electrical potential, a measure of the activity of the electron transport chain, was reduced in oocytes compared to both sperm and the surrounding tissue. Further, ROS production was 50- and 100-fold lower in the eggs of fruit flies and zebrafish respectively. Finally, they confirmed that oocyte mitochodria in both species exhibit a simpler structure, indicative of reduced activity. So, it seems that in both fish and flies, the mitochondria in egg cells represent little more than a blueprint, ready to be passed on to the next generation error-free. By deactivating ovarian mitochondria, the fidelity of information is ensured across generations, and aging is not heritable.

Taken from: http://blogs.ucl.ac.uk/gee-research/2013/11/11/damage-and-fidelity-the-role-of-the-female-germline-in-mtdna-inheritance/
You can read the article here: de Paula, Wilson BM, et al. "Female and male gamete mitochondria are distinct and complementary in transcription, structure, and genome function." Genome biology and evolution 5.10 (2013): 1969-1977.


What is this insect with scary antennae? I encountered with this insect on the wet floor in Sri Lanka. Is it dangerous?

Actually, the antennae of that insect are not scary at all!

In your image, the antennae are pointing down; those forceps-like structures pointing up are part of abdomen, and are called cerci.

That insect (probably a male) is an earwig, from the Order Dermaptera. In the image below, the antennae are at the left, while the abdomen and the cerci are at the right:

Narrowing down the the Genus of your specimen is more complicated, but here is a list of earwigs from Sri Lanka: https://en.wikipedia.org/wiki/List_of_Dermapterans_of_Sri_Lanka

Regarding the danger: earwigs are not dangerous. The cerci may be scary, but they normally are not capable of hurting a human. Also (and I hope you don't believe urban legends), they do not lay eggs in human ears: http://www.snopes.com/horrors/insects/bugear.asp


Obvious phenotypic inheritance markers in humans In humans, are there phenotypic markers that prove parenthood? For example, if mother and father have <trait characteristic> (let's say, specific ear lobe form), then any child will have <trait characteristic>. If the child does not exhibit that characteristic, than either father or mother or both are only alleged, not actual.

No. To determine the genetic relationship (if any) between two individuals requires molecular evidence based on genetic markers in their somatic DNA. Using phenotypes could be misleading because a genetic marker (an allele) can have variable penetrance (the percentage of carriers who actually have the phenotype) and variable expressivity (the severity or degree of the phenotype). Some of this variability can come from gene-environment interactions, and some could come from epigenetic effects (ie non-heritable).


Where do butterflies sleep? Do butterflies (insects) sleep, and if so, where??

I have googled for information but didn't get an exact answer.

It would be better to say that they go into an inactive, low metabolic state. This low metabolic state is often driven by the temperature in the air itself; ectothermic butterflies require outside heat-energy to become active. Basically they use this time to digest their food and produce sperm/eggs. (reference). At night, or during inclement weather, most butterflies perch on the underside of a leaf (this provides them with a bit of shelter from the rain and makes them less noticeable to prey), crawl deep between blades of grass or into a crevice in rocks, or find some other shelter to rest (reference).  In short, I would not call it sleeping but just a state of rest. Butterflies cant even close their eyes from the lack of eyelids (reference).


Plant identification — Phuket, Thailand Found in Phuket, Thailand. White flower, five petals, 5 stamens. Strings of flowers hanging down from red stems. Buds white, tear-drop shape.

RHA, Here are the leaves. The flowers hang from a bush about 6 foot (2 metres Tall)

Bli, thanks, but not honeysuckle. No scent.

This is Clerodendrum schmitii similar to C. wallichii (Bridal Veil). It is commonly called Chains of Glory and is native to Thailand.

It belongs to Verbenaceae family.

  Chains of Glory is a shrub to small tree, multi-stemmed, with hanging branches. Each winter it grows long, pendent, dark red racemes, 1.5 ft long, of delicate white flowers. The cascading white fragrant flowers are held in loose hanging clusters, similar to Bridal Veil. The white flowers on long dark red flower stalks look very attractive against the dark green leaves. Chains of Glory is native to Thailand.

(from flowersofindia)

  The genus is native  to tropical and warm temperate regions of the world, with most of the species occurring in tropical Africa and southern Asia, but with a few in the tropical Americas and northern Australasia, and a few extending north into the temperate zone in eastern Asia.

(from wikipedia)

Picture reference:

  Chains of Glory $^1$

 Bridal Veil $^2$

$^1$ (Source: tuoitre.vn)

$^2$ (Source: Cebuano wiki)


Need to make a library of mammalian coding sequences I want to clone ~100 different coding sequences from human or mouse into an expression vector to analyze phenotypes in tissue culture. I can do all of the steps, but I'm not sure what I should use as the template for my reactions. Ideally, I would purchase a pool of full length cDNAs from a bunch of organs, and amplify from that. Less ideally, I can generate cDNAs myself, from multiple organs and pool them. Does anyone have suggestions on a template source?

Verify where these transcripts are generally present (this should not be difficult for common organisms)
If they are all expressed in a certain tissue use cDNA from that tissue
If not then pool the cDNAs from different tissues such that all genes can be amplified
cDNA libraries (including whole organism) are also available and you may obtain them from the nearest repository (I guess NCBI also provides).

Some other things you can do:

Ask the primer synthesis company to provide primer sets it in a
96well format.
DNA synthesis is also a decent option (it takes something like $0.5
per base pair), but that can be expensive if your cDNAs are huge.


Can geckos climb a wet surface? We know geckos can climb vertically or even upside down a surface like glass. But can they do that on wet glass?

Short answer
Yes they can, but with less efficiency.

Background
Efficiency of sticking to a glass surface decreases about 20-fold when the gecko's feet are wet (Stark et al., 2012). On dry glass, Gekko gecko holds on with about 18 N, which is about 18 times their own body weight. Hence, the gecko attachment system is over-designed (Knight, 2012). Wetted toe pads reduce the adhesive force significantly down to 0.9 N. A wetted glass surface does not significantly affect the grip of Gekko gecko, except after the gecko takes multiple steps. Hence, geckos can cling to wet surfaces, but only when their feet are not getting too wet.

Note that gecko attachment is not based on suction, such as the suction cups seen in octopus. Instead, geckos cling to surfaces with Van der Waals forces. Van-der-Waals-based adhesive systems take advantage of weak intermolecular forces between two surfaces. Upside is that these forces are not surface specific, allowing geckos to climb trees, rocks, walls and even glass windows.

Geckos achieve their strong attractive force to the substrate by utilizing small hair-like structures on their toes called setae, which are made primarily of keratin (Fig. 1). Setae contain flexible spatulae which make intimate contact with rough and even dirty surfaces.

Fig. 1. Left panel: Close-up of the underside of a gecko's foot as it walks on vertical glass. Source: Wikipedia. Right panel: Images of (A) dry and (B) wet setae using the same digit of an individual tokay gecko (Gekko gecko). The image in A was taken prior to exposure to water and the image in B was taken after 30 min of soaking in water. Source: (Stark et al., 2012).

The drawback of using Van-der-Waals forces for grip is that the Van-der-Waals forces only exist across surfaces very close together, and an intimate contact between the spatulae and the substrate is required for van der Waals forces to be effective in the gecko adhesive system (Stark et al., 2012). Wetting of the feet decreases the Van der Waals interaction with the surface.

References
- Knight, J Exp Biol 215, i
- Stark et al., J Exp Biol; 215: 3080-6


What Evidence Do We Have For the First Mammal? Edited for a less broad question, I've retained my original question in the event anyone wants to try to answer it

Narrowed down question

According to evolution we should all share common ancestors, straight to the very first cell. I am trying to find evidence for these ancestors. So therefore as a start, what fossil evidence do we have for the first official mammal to roam the earth? What was the defining moment and change from whatever it was before to a mammal?

Original question

I'm just doing some research for my biology class and I was wondering
what evidence we have for the elusive "change of kinds" question? And
for clarification, I define kinds as the branches of life (essentially
birds, reptiles, mammals, amphibians, fish, etc etc). Do we have
evidence for the common ancestors that link the vastly different
species we have? Because obviously a human, tortoise, jellyfish, and
say tarantula are vastly different, each their own distinct "kind",
but according to evolution there should be common ancestors and many
distinct species leading up to them. We all came from one thing. Man
and primates came from one thing. Mammals came from one thing. Where
do we get that distinct change of a kind, from say a fish to mammal?

There should theoretically be tens of thousands of in between links
and species that were what led to everything today, correct?
Therefore, we should have mountains of fossil evidence to support it,
yet from what I've researched I've found very lacking evidence and
generally just see posts insulting creationists and skimping the
question. So by asking the question myself hopefully I'll get a
legitimate and clear answer that is the truth.

Obviously, it's impossible to point to "the" earliest mammal; dividing lines are pretty much arbitrary. However, a reasonable representative of a very early mammal or very late mammaliaform is Arboroharamiya jenkinsi, described in A new arboreal haramiyid shows the diversity of crown mammals in the Jurassic period, from roughly 155-160 million years ago.  That shows a number of fossils, including this quite nice one:

The supplementary information shows some cranial features, including this:

A related species from roughly the same time period, Haramiyavia clemmenseni, had CT scanning done on this fossil mandible:

yielding images like this:

Similarly, the euharamiyidans were either very early mammals or very mammal-like cynodonts, which are known from a number of quite nice fossils including these three (described in Three new Jurassic euharamiyidan species reinforce early divergence of mammals):


Do drugs' levo isomers have a better interaction with the receptors in our body than dextro isomers? Examples of levo drugs include levothyroxine, levocitrizine, and levodopa. Is there any specific reason why the receptors in our body exhibit this stereoisomerism and hold a high preference for the levo isomer form of any drugs?

This is purely coincidental. The term levo simply means the direction that the pure enantiomer of the compound rotates plane polarized light at a specific wavelength and has no direct bearing on the interactions with biological systems. A quick search of the Dictionary of Drugs database gave 6845 compounds with optical rotation >0 (dextro-compounds) and 8406 compounds with optical rotation <0 (levo-compounds). So there are plenty of chiral drugs that rotate plane polarized light each direction.

The inclusion of 'levo' (or 'dextro' for that matter) into the name of the compound was done to distinguish enantiomers of chiral compounds. This naming convention as fallen out of favor due to the improved ability of chemists to know the absolute stereochemistry (e.g., R/S) and distinguish enantiomers based on their structure.

Dextroamphetamine (Adderall) and dextromethorphan (Robitussin) are a couple of examples of drugs with 'dextro' in their names.

With respect to the stereochemical nature of HTS and fragment libraries, most compounds are achiral (do not rotate plane polarized light). I'm not aware of any library biased toward optical rotation, and I'm not aware of any chemist making any selection of compound based solely on an optical rotation measurement. In fact, chiral compounds are often studied first as the racemate. If there is activity, the individual enantiomers are tested.


Why a repeat wasp sting cause an anaphylaxis shock? I understand that an anaphylaxis shock caused by a huge dose of histamine. But why the first sting does not cause an anaphylaxis shock like the second sting? As i think there may be a relevant between antibody and histamine because the victim already have antibody presence in the second sting, is that right and what is it?

The reason is the way anaphylactic shock is caused by massive release of certain cytokins as well as inflammatory mediators such as histamine by two types of white blood cells: mast cells and basophils. This release is triggered by the binding of immunoglobulin E (IgE) to the antigen (the foreign substance provoking the allergic reaction). Antigen-bound IgE then activates so-called FcεRI receptors on the mast cells and basophils. IgE molecules specific to the allergen provoking the allergy are not present in the blood in sufficiently large quantities until after the first (several) exposures to this foreign material. Initial exposure triggers IgE production by specific B-lymphocytes. Only once one or more exposures to the antigen have occurred will there be sufficient quantities of the relevant IgE to trigger this excessive mast cell and basophil reaction.


How should lentil roots grow in a microgravity system? I recently executed an experiment in which I collocated 20 lentil seeds in independent Petri boxes with an agar agar solution, all of it located in a clinostat (a slowly rotating device used to simulate microgravity conditions, where they rotated perpendicularly to the ground (gravity). The objective was to see in what direction did the roots grow under the effects of microgravity, since geotropism didn't have a fixed direction to head to. At the end of an entire cycle, the forces (gravity in 360°) applied to the seeds would turn out to be equally strong, in opposite directions, so it would come down to nearly zero.
However, after many executions, without having any functional problem with the clinostat, the seeds simply didn't grow roots while being in the agar agar in the Petri boxes. I tried different agar agar solutions, different concentrations, more & less quantity so that the seeds would have a thin air layer; and I also added copper sulphate to prevent fungi from appearing, also varying its concentration. Afterwards, I tried using an already germinated seed so that the radicle had direct access to the solution and to the air layer. Nevertheless, after several executions, only a few seeds grew their roots and I din't find a concrete explanation for this experiment not being successful.

I expected having the roots in the experimental group to grow in many different directions, not being constant. As in the other hand, I expected the control group to grow roots in the same direction, going downwards, being in the same system (clinostat) without having the rotations going on.

It sounds like your first issue is with seed germination. I am assuming you are doing a seed sterilization. You may want to try allowing them to imbibe water for about an hour after the sterilization process, and then wrapping them with aluminum foil and placing them in a fridge for a day or two. I've done this with Medicago, which is another legume. However, not sure if it works for your lentils.

The root may also have trouble developing given the micro-nutrients in the media. I am curious what recipe for media you are using, as the amount of agar may also affect the ability for these roots to penetrate the media. I have had trouble germinating legume seeds when there were 100+ seeds in a plate as they inhibit each others growth.

It's hard to give a clear answer, but try optimizing your seed sterilization protocol and media recipe and best of luck!


Cooperativity of haemoglobin and oxygen dissociation curve of haemoglobin Haemoglobin shows positive cooperativity with oxygen. When an oxygen atom binds to one of hemoglobin's four binding sites, the affinity to oxygen of the three remaining available binding sites increases; i.e. oxygen is more likely to bind to a hemoglobin bound to one oxygen than to an unbound hemoglobin. This is referred to as cooperative binding.

Haemoglobin reaches 50% saturation when the partial pressure of oxygen reaches about 28 mm Hg. Now partial pressure had to be increased by about 70 mm Hg for haemoglobin to reach maximum saturation. If haemoglobin is a cooperative molecule, once haemoglobin reaches 50% saturation it should be easier to attain ~100% saturation. But it is taking a difference of 70 mm Hg. Whereas 50% saturation requires only 28 mm Hg.
Hope this makes sense.
Please answer this and correct my understanding.
Thank you

As you may notice from the graph you provided, there actually is no such thing as true 100% saturation: there is always an asymptotic approach to 100%, regardless of cooperativity.

Let's think, though, of what is actually plotted in that graph: $p_{O_2}$ effectively oxygen concentration, versus number of total percentage of binding sites that have an $O_2$ bound.

However, this also means that as you go up on the y-axis, the number of sites available to bind also goes down. So even if those sites have a high affinity for oxygen, there aren't as many of them open!

That's one big problem with the type of plot you show: it doesn't highlight the cooperativity very well. Therefore, people sometimes plot this information in a "Hill plot", with an algebraic shuffling and log scaling like this:

See Wikipedia

...where $\theta$ represents the fraction of receptors bound to ligand, and $L$ is the (unbound) ligand concentration. $n$ is the Hill Coefficient, i.e., the cooperativity.

When plotted this way, you can easily see the effect of the cooperativity of hemoglobin versus myoglobin (which has cooperativity of 1, because it has a single binding site):

http://cbc.arizona.edu/classes/bioc462/462a/NOTES/hemoglobin/hemoglobin_function.htm via Fig. 7-13, Nelson & Cox Principles of Biochemistry, 3rd ed., 2000


What kind of fish is this (Florida, USA)? What kind of fish is this? It was caught in Florida (USA) in a canal and was in a group. It was about 5 or 6 inches in size.

So after much more time on this than I should have, I am pretty confident this is a silver jenny (Mojarra).

Silver Jenny, Eucinostomus gula

  "The Silver Jenny, Eucinostomus gula, whose common Spanish name is
  mojarra Española, is a species in the Mojarra or Gerreidae Family,
  known collectively as mojarras in Mexico. Globally, there are eleven
  species in the genus Eucinostomus, all of which are found in Mexican
  waters, seven in the Atlantic and four in the Pacific."

Dorsal fin structure, tail fin split, location of ventral fins and gill fins all match up, as does color.  So does the faint stripe from top of gill to back of fish. The last clue was the protrusible mouth.

I'm surprised you found it in a canal, as it is a saltwater fish. Were you close to the ocean?  From the link above:

  The Silver Jenny are an abundant schooling species that are found
  seasonally in shallow coastal waters over mud bottoms in mangrove
  lined lagoons and creeks in waters that are between 11oC (52oF) and
  28oC (82oF) at depths up to 175 feet. Juveniles are found in seagrass
  beds. They may also enter freshwater. They are known to make seasonal
  migrations to off-shore warmer waters during the cooler months for
  wintering and hibernation returning to coastal waters in the spring
  for breeding. They reach a maximum length of 23 cm (9.1 inches). They
  are benthic feeders that probe the bottom with their protrusible mouth
  consuming bivalves, crustaceans, ostracods and detritus. They are a
  poorly studied species and very limited information is available about
  their behavioral patterns.

Last Link here


Why do cats meow when they are adults? Meowing for kittens is similar to a baby crying. As human adults grow, they stop crying, but as kittens grow up they continue to cry. Why is this?

I could not find a peer-reviewed paper, but there is a widespread popular belief that adult cats only meows to communicate with humans but never with other cats. Meowing allows a cat to obtain the attention of its human owner and eventually get what it wanted.

See this webpage from the american society for prevention of cruelty to animals for example or this quora post.


Is Covid-19 likely to mutate into a deadlier form? When the Spanish influenza hit in 1918, it struck in two waves. The first wave was typical for a flu virus, targetting mainly elderly people, but the second wave was far deadlier and killed far more young people. How likely is it for something similar to happen with the current coronavirus? Also, wikipedia states that people who contracted the virus during the first wave were immune to it in the second wave. I thought when a virus mutates it usually avoids detection, hence why we need to usually get an up to date flu vaccine annually. Why was this not the case for the spanish influenza?

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology! I'm glad we encourage such questions from curious people who want to learn more.

Mutations are mostly deleterious to begin with. This means that mutant copies of virus only very rarely survive and proliferate. A virus that is deadlier will already be less likely to reproduce, having killed more hosts.

The current estimated mutation rate of the SARS-CoV-2 virus is 24 bases per year. Of those mutations, those to be most concerned about are those which would mutate the proteins specific to this virus. Vaccine development will aim to train the immune system to target those proteins, particularly the S or spike protein.

Mutations to those proteins can make potential vaccines less effective. This is why influenza ("flu") vaccines, which are produced ahead of the flu season, may not always line up against the more prevalent strains which result.

A recent comment was published in Nature, authored by life scientists and epidemiologists, which goes into your question in more detail, as regards to the novel coronavirus:

  In this case and that of SARS-CoV-2, mutations consume the narrative, even though individual mutations seldom become fixed during outbreaks nor modulate complex virological traits. Rather, mutation is a humdrum aspect of life for an RNA virus. Because these viruses employ an intrinsically error-prone RNA polymerase for replication, their genomes will accumulate mutations during every copying cycle. Moreover, these cycles can occur on the order of hours, ensuring that a diverse virus population will be generated within a single infected host. While this amazing capacity to mutate fuels the engine of evolutionary change, most mutations adversely impact some aspect of virus function and are removed by natural selection. (emphasis added)

Further, and more to the original point of your question:

  These warnings will probably not halt the question as to whether mutations will arise in SARS-CoV-2, enabling it to spread more efficiently between humans or generate a higher case fatality rate. In response, we can look to the 2002–2003 SARS-CoV epidemic. Large deletions in the open reading frame 8 (ORF8) region and mutations in the spike (S) protein were discovered during the early stages of the outbreak and eventually dominated the epidemic, suggesting that these were adaptations to humans12,13. Based on this observation, some hypothesized that virus genetic changes in part drove the SARS epidemic, but this claim is unsubstantiated14. So, could SARS-CoV-2 adapt in the same way? Yes. Will adaptation precipitate more deaths? Unlikely. (emph. added)


What is the eye muscle status when you stare at distant view through a glass wall? The book said when you look at object close to you, the eye muscles contract and vice versa. I wonder what will be the status of the eye muscles when I stare at distance view (such as a mountain) inside an office through a glass wall. The mountain is far away but the glass wall is close to us. In this case, does the eye muscles relax?

In the situation you describe, the eye would be focused on the distant mountain.  This would mean that the lens would be stretched and thin in order to minimize the focussing power of the eye.  Therefore the ciliary muscles would be relaxed.

When you are looking out of the window, it is possible to make a conscious decision to focus on the window pane itself (thus adjusting the focus to be more powerful as the ciliary muscles contract), however then the distant object will be out of focus and uncomfortable to look at.

This is because the light rays reflecting from the mountain are barely affected by the pane of glass, hence its transparency.


How do scientists kill the bacteria they themselves made resistant? I was reading this article on researching bacteria resistance to silver by removing some of their genes.

  Researchers then used "colony-scoring" software to measure the differences in growth and size of each plate's bacterial colony. E. coli strains with genes deleted involved in producing sensitivity, or toxicity, to silver grew larger colonies. Strains with genes deleted involved with resistance grew smaller colonies.

Once you end up with some resistant bacteria and you're done researching it, you can't just flush it down the toilet. How do you safely dispose those colony plates in a way that ensures those bacteria don't get out into the wild and reproduce?

You are absolutely right, flushing down the toilet (or the sink) or simply throwing them into the normal waste doesn't work for biosafety reasons. And it is also not allowed, depending on the country you would do this in, this can lead to hefty fines.

Biologically contaminated lab waste can be inactivated (=all potential dangerous organisms are destroyed) by two ways: Either by heat or chemically. Which ways is used, depends on the kind of waste.

The most commonly used way is autoclaving, meaning treating the waste with steam at high temperatures at higher pressure. The temperature used here is usually 121°C, the exposure time depends on the volume of the waste, since the temperature needs to be reached and kept for at least 20 minutes. See the references for more details.

Liquid wastes (like culture media) can also be inactivated chemically by adding chlorine bleach to decompose the cells. Bleach can also be used to decontaminate surfaces, although here more often alcoholic solutions (70% Ethanol or Isopropanol) are used. After chemical inactivation, the remaining solutions should not be autoclaved as the emerging fumes are either unhealthy (bleach) or explosive (alcoholic solutions) and this is unnecessary, too.
Liquid wastes can also be autoclaved to inactivate them.

Autoclaving has the main advantage that it is rather simple (put the waste into the autoclave, close it and run a appropriate program), the waste can afterwards simply be discarded as normal waste, which may not be the case for chemically inactivated waste, which may need special precaution for disposal.

References:

Decontamination and Sterilization
Decontamination of laboratory microbiological waste by steam
sterilization.
TECHNIQUES FOR STEAM STERILIZING LABORATORY WASTE
Decontamination of Laboratory Microbiological Wasteby Steam Sterilization


Where does crop biomass come from? Each year, large volumes of crop are harvested from fields.

Where does this biomass get replenished from?

The matter in plants is mostly carbon, hydrogen, oxygen, and nitrogen, with various metal ions and some sulfur and phosphorus. The carbon, hydrogen, and oxygen are taken from carbon dioxide in the air and water from the soil through photosynthesis. Nitrogen is taken up from the soil as ammonia or nitrates, or fixed from nitrogen gas, but this only happens in legumes. Phosphorus is also part of a nutrient cycle. Metal ions such as sodium, potassium, magnesium, and calcium are taken up through the roots with water.

If you're asking about how this material is replenished, fertilizer is an important answer. For centuries, nitrogen was a limiting nutrient in farms because it would get removed faster than it was replaced, especially if crop rotation was not used or legumes weren't grown. Thanks to the Haber Process we can produce humongous amounts of ammonia from nitrogen gas, this has greatly increased the amount of nitrogen available for plants, but has also resulted in nitrate pollution in waterways and algal blooms and eutrophication. Phosphate and potassium are also used in fertilizer and are usually mined, however phosphorus reserves are limited.


What is a Archival Tumor Tissue ? For What Purpose is it collected? Over the course of Conducting trials various tissue and tumor samples are collected  from the patients.

One such sample is the Archival Tumor Tissue.
Could someone kindly clarify what is the meaning of the term archival tumor?, and what data is gleaned from it.

When a tumor is removed from a patient, it is usually send to the pathology the make sure that it has been excised completely to make sure there are no residues. Often this tumor is also used to analyze the mutation status of the tumor to determine, which further treatment is possible. For example, this is routinely done for melanoma where the mutation status excludes some drugs for further treatment.

Afterwards these tumors are important material for the scientific tumor research to isolate fresh cell lines or analyze them further. Parts of it are usually stored either frozen or as formalin fixed tissue to build tissue banks. These can be used for later research on this type of tumor and have a high value.

These tissues can then be cut and stained with antibodies or used for nucleic acid extraction (either DNA or RNA) or to test new ideas or methods which where not available to the time when the samples was archived.

Another famous case (although not from tumors) are tissues samples which have been archived from people deceased from the spanish flu in 1918, where parts of the virus was reconstructed using these samples decades later.


Species-ID: What kind of bug is this? What kind of bug is this?

Size: About the size of a pencil tip

When was it found: spring time

Where was it found: In northeastern USA, inside the bathroom of our house

It could be a cockroach nimph. Distinctive characteristics:The overall shape and size, the long antenae, the segmented abdomen and the visible rear cerci.


Which are mobile and immobile elements in plants? I am confused with this element or nutrient classification in the plants, since some authors set elements like $\ce{S}$ and $\ce{Ni}$ as mobile and other as immobile elements (Citation 1, 2, 3, 4, 5). Then, I would like to know if there is a fixed and official classification.

I found a classification only for those elements:

Mobile: $\ce{N}$, $\ce{Mg}$, $\ce{P}$, $\ce{S}$, $\ce{K}$, $\ce{Ni}$

Immobile: $\ce{B}$, $\ce{Ca}$, $\ce{Mn}$, $\ce{Fe}$, $\ce{Co}$, $\ce{Cu}$, $\ce{Zn}$.

And what about the rest of elements like $\ce{Sr}$, $\ce{Mo}$, $\ce{Ba}$, $\ce{Pb}$, etc?

What does it mean for an element to be mobile or immobile in plants?

Generally speaking, mobile elements are those that can be moved from older to newer tissue in the plant, while immobile ones cannot be.  For example, calcium is incorporated into the cell wall, so it is immobile; it cannot be relocated later.

Plants with a deficiency of mobile elements (e.g. nitrogen) will exhibit damage to older tissues as the nutrients are moved to new growth.  Conversely, plants lacking immobile elements (e.g. calcium) will exhibit stunted new growth while the older tissues stay healthy.  Some elements (e.g. sulphur) fall somewhere between these two extremes.

To illustrate this concept, here is a plant with nitrogen deficiency (source).  Notice how the older leaves are dying while the newer leaves are relatively normal.

Is there an official list of mobile and immobile elements?

No.  You will probably have to survey the literature yourself to come up with such a list.

Why are some elements not mentioned in the sources?

Elements like Pb or Sr do not appear in either list because plants generally do not use these elements at all.  Only a few elements are present in any appreciable quantity in plants.  The main elements used are C, H, O, P, K, N, S, Ca, Fe, and Mg. Additionally, some other elements such as Cu, Mo, Al, and Cl are used in trace amounts as enzymatic cofactors.  Si is used for structural purposes in some plants.

However, even for "useless" elements, it is possible to study how these elements are absorbed transported through a given plant.  For instance, Rediske and Selders (1953) studied the absorption of strontium by bean plants using radioactive labeling, and concluded that the element was not relocated once absorbed by the plant.  This would make it an immobile element.

References

Feldman, Lewis J. (23 February 2015). Water Relations, Mineral Nutrition, Fruit Development (YouTube). Biology 1B. UC Berkeley. At 32:20.
Lewis, Helen (9 January 2012). "Mobile vs Immobile Nutrients". Mastering Horticulture.
Rediske, J. H. and Selders, A. A. (October 1953). "The Absorption and Translocation of Strontium by Plants". Plant Physiology 28 (4): 594–605. PMC 540423.


How is "firing together" detected in Hebbian learning? I assume, that the signal that forces a synaptic receptor/ion channel complex to change its behaviour (i.e. strengthening in the course of upregulation) must be the combination of the state of the complex ("occupied" or "open" or any other state except the ground or rest state) and an extraordinarily high membrane potential at the complex (caused by a retrograded action potential).

The not-ground state indicates that the presynaptic neuron recently has fired, the potential indicates that the postsynaptic neuron recently has fired. According to the rule "fire together, wire together", both conditions must be fulfilled for Hebb-like strengthening to occur.

I assume further that the membrane potential that triggers the upregulation of the complex must be significantly higher than the typical post-synaptic potential generated by the synapse, otherwise activation of the synapse alone would suffice for strengthening to occur, which violates Hebb's rule.

Is this way of thinking essentially correct? Or is strengthening triggered by other signals than the ones mentioned above?

The dynamics of Hebbian or associative synaptic plasticity are thought to be governed primarily through the function of the NMDA glutamate receptor. The short answer is that you are basically right on all counts.

Figure of the NMDA receptor present the nervous system.
By Blanca Piedrafita [CC BY-SA 1.0 or CC BY-SA 2.5], via Wikimedia Commons

The NMDA receptor is a non-selective cation ionotropic receptor. The reversal potential of the NMDA receptor is around 0 mV, in contrast to the resting membrane potential of a 'typical' excitatory neuron which is around -70 mV. This means that a pretty strong stimulus is required in order for the NMDA receptor to be activated. Whereas some current can pass through the channel upon binding of its preferred ligands (glutamate or glycine), the pore is normally blocked by a magnesium ion. This mechanism confers some degree of voltage-dependent regulation of ion flow through the channel. When a strong stimulus raises the membrane potential at sufficient levels the magnesium block is lifted, allowing more current to pass through. The slow kinetics of the NMDA receptor allow the temporal integration of incoming signals. This makes the NMDA receptor function as a coincidence detector or AND gate. There are many more known details about the mechanisms involved but the above should suffice to answer your specific question.

Further reading: https://en.wikipedia.org/wiki/NMDA_receptor


Multi-nucleated cells: advantages and examples? This question arises because I saw that monocytes and leukocytes are commonly called 'mononuclear cells' in the scientific literature. The implication of course being that other immune sub-types are multi-nuclear!

I know of granulocytes (e.g. neutrophils) that are classed as 'polymorphonuclear' because their nuclei are segmented, and can alter their shapes, and muscle cells that fuse together to form one long cell (muscle fiber) with multiple nuclei. What other examples of multi-nucleated cells are there?

I am also interested in the advantages gained by cells having multiple (or segmented) nuclei?

Muscle cells are the only cells I know of that are polynuclear. With respect to monocytes, a concise review of their nomenclature can be found in this paper by L Ziegler-Heitbrock, P Ancuta, S Crowe, et al. (Blood, 2010). Apparently it has had quite a complex and confused biochemical characterization, but the article states the name indeed derived from its single lobed, mononuclear morphology. This is in distinction to other phagocytes which have multi-lobular nuclei (polymorphonuclear cells).

With respect to advantages, a multinucleated cell makes sense when the speed of intracellular signalling is important (e.g., calcium diffusion). It may also be useful in the case of cells when the cell needs to coordinate the synthesis of large amounts of protein.


Why plants (eg. parsley) can keep vitamin C despite all the sun? I have read that vitamin C is highly sensitive to light. So, how could parsley, for instance keep its vitamin C as it's flooded with sunlight?

UV light promotes the photo-oxidation of ascorbic acid (AsA) to dehydroascorbic acid (DHA).

DHA can be reduced to AsA by a specific dehydrogenase using reduced glutathione as reductant. I'm pretty sure that all cells are able to carry out this recycling of ascorbate.

Interestingly, in plants it appears that ascorbate acts as an electron donor to photosystem II (which is equivalent to it being oxidised).


Do hormone drugs affect whether a person feels sexual attraction to males or females? I know that ingesting testosterone and other hormonal drugs may stimulate libido and increase sexual desire.

But I wonder, if a man ingests female hormones such as estrogen, will he experience sexual desire towards other men or not?

Similarly, the other way around, whether a female ingesting male sexual hormones will experience desire towards other women?

The question is motivated by the interest to know whether transgender people, particularly, the MtF transsexuals engaged in prostitution experience genuine attraction to males.

There is no evidence that postnatal hormone exposure can change the sexual sexual preference of an individual. However atypical hormonal stimulation of the fetus can induce homosexuality.

Homosexuality does not develop without a variety of social factors which are up-to-date mostly unexplained. But can develop without hormonal stimulation.

As real life examples there are a androgen antagonists for the treatment of of prostate cancer, which reduce the testosterone level in males. Under treatment the men often turn softer and more emotional, as described by their wifes. And there is beer which contains oestrogens and can induce the growth of female breasts in men. But none of this mechanisms has been observed to turn males homosexual.

Further Reading (second text is free fulltext):

[1] http://www.ncbi.nlm.nih.gov/pubmed/23397798

[2] http://endo.endojournals.org/content/152/8/2937.long


A study found that the hepatitis C virus can live on surfaces for six weeks. Did they end the study before the seventh week began? A study once found that the hepatitis C virus (HCV) can remain infective for six weeks on ordinary household surfaces. You can see the free full text, or a summary for busy clinicians.

What happened in the seventh week? Did the virus cease to remain viable, or did the study just end suddenly?

From part B of this figure, it looks to me like the study just ended suddenly. But I'm not a biologist, so I'd like to hear your opinion.

The place to find this information would be the Methods section of the paper.

  We spotted 33 µL of plasma spiked with HCVcc on the 24-well plates. They were either immediately tested for viable virus or stored at 4°C, 22°C, and 37°C for up to 6 weeks before testing.

They tested their samples for (up to) 6 weeks. At the time of the 6th week they still found infectious virus. They did not test samples beyond 6 weeks so they can't say anything about infection past that time.


What makes a DNA sequence motif a DNA sequence motif? I've read about DNA sequence motifs, but still don't understand what makes some sequence a DNA sequence motif. Is this a well-defined concept? For, example,
What are DNA sequence motifs? says:

  Sequence motifs are short, recurring patterns in DNA that are presumed
  to have a biological function. Often they indicate sequence-specific
  binding sites for proteins such as nucleases and transcription factors
  (TF). Others are involved in important processes at the RNA level,
  including ribosome binding, mRNA processing (splicing, editing,
  polyadenylation) and transcription termination.

For example, I've been working with Recombination Signal Sequences (RSS), which are important in immunology. However, from what I can tell, RSS are not themselves motifs, but they do contain motifs. E.g. Conservation of sequence in recombination signal sequence spacers
says

  Previously, the RSS has been described as possessing both a conserved heptamer and a conserved nonamer motif.

So, apparently, the heptamer and nonamer component of the RSS are themselves motifs, but the RSS itself is not. Can anyone explain why? Thanks.

Motif means a pattern. For any array of objects to be called a pattern, it has to have at least more than one instance.
To define more precisely, a motif should have significantly (statistical) higher occurrence in a given array compared to what you would obtain in a randomized array of same components (expecting at random).

[Here i use the term array to mean an arranged set such as a genome (array of nucleotides with their position in the sequence) or a protein structure (array of amino acids with their vector positions). A randomized array with same components is generated by shuffling the elements and their values; for e.g. assign the same collection of nucleotides to random positions]

RSS nonamers/heptamers are called a motif because they are a pattern of sequence which a) has more than one occurrence b) the occurrence is significantly higher than a random expectation. Generally in sequence motifs randomization is not usually done because the genome size is too huge. In such conditions if your sequence has >= 2 occurrences throughout the genome it may be considered a motif. Lets assume a 10bp sequence. Its random probability = 1/4¹⁰. Therefore in 1048576 bp (1Gb) there is a likelihood of finding one instance of that sequence on random. So I assumed that if that sequence has >=2 instances it can be called a motif. However, I am not sure about this.

RSS is not a motif because the entire RSS is not conserved; the conserved 'motifs' are interrupted by sequences. This is analogous to lets say a promoter which is a functional region of the DNA. Promoter can have binding sites for different transcription factors and these operator sites (TFBS) can constitute a motif (if they are conserved) but not the entire promoter.


How to measure the total number of cells in an average human body? I have got one assignment to calculate the approximate sum total of all cells in the human body. How to tackle this problem? I know that the current statistics is $10^{13}$ cells. I wanted some hints.

This is a classic Fermi estimation problem. The usual approach is to estimate the volume of a body, estimate the volume of a cell, and divide one by the other, remembering of course to have both volumes in the same units.

My quick attempt gave 1013 to the nearest order of magnitude.


Are more animal species edible than plants? While grocery shopping I was thinking that we restrict ourselves in regard to which animals we eat. I surely don't want to eat spiders and ants, for example, but I know that this is just because of my upbringing. But a lot of plants are actually inedible. So, is my idea correct that we can eat far more animal species than plant species? And if so, why? The reasons why certain plants are inedible seem to me also as rather diverse, like most plants
developed their own special molecule(s) to avoid being eaten by us. :)
I would be interested in some more educated opinion on this thought than mine. Thx in advance.

It is estimated by some that on earth there are

  7.77 million species (of which 953,434 have been described and cataloged) of animals
  298,000 species (of which 215,644 have been described and cataloged) of plants
  611,000 species (of which 43,271 have been described and cataloged) of fungi
  36,400 species (of which 8,118 have been described and cataloged) of protozoa.

with 6.5 million species found on land and 2.2 million (about 25 percent of the total) dwelling in the ocean depths.[1][2]

Despite the existence of toxic plants and animals, from the numbers alone it is clear that there are more animal species we can eat than plant species.

This does not take into account population or individual sizes, just species.

[1] How Many Species Are There on Earth and in the Ocean?
[2] How many species on Earth? About 8.7 million, new estimate says


Analyzing Messy Data Files I was writing some code scripts to analyze some plasmodium spp. using this database. However the names assigned to the various epitopes and other items on the list is very very very disorganized. In some places there are acronyms and other places the full name. Sometimes hyphens replace the spaces for the same epitope name. So I was trying to collect lists of all the different names that are actually synonyms of each other. However there were some words that were added on sometimes that I wasn't sure would count as synonyms:

"xxx" and "xxx, putative" synonyms?
"xxx" and "xxx like antigen" synonyms? (this one made little sense to me as both are epitopes
"xxx" and "xxx 1" synonyms?
"xxx" and "xxx partial" close enough to    be synonyms for sake of
grouping?

I'm rather new at analyzing these sorts of databases. I'm sure I'll find other such messy naming issues and was wondering how to approach such a problem and solve such discrepancies.

It’s not the fault of the database, it’s the fault of the individual scientists that described the epitopes. O.K. in a perfect world the curators would have gone through the entries and tried to standardize the descriptions. But they probably lack the time or expertise. I sympathize with them.

So what can you do? You have to use your own expertise or that of experimental scientists you are working with and make your own decisions, some of which will be incorrect.

This is a general problem with databases compiled from papers or individual submissions, and is a headache for data mining: misspellings, spaces or no spaces, hyphenated or not, different names for the same entity. Unfortunately there’s no fairy with a magic wand to solve the problem for you.


What is an example of a plant species that is a halophyte with seeds that germinate quickly? I’m doing an experiment on the effect of salt concentration on the germination of seeds from halophyte plants. What would be an example of a species that is suitable for such an experiment? I would prefer a species the seeds of which germinate relatively quickly under not very difficult conditions.

It turns out that your research question about halophytes has been asked many times before. You should learn from your predecessors...

Seed germination in halophytes displays a high degree of inter- and intra-specific variability. However, Khan & Gul (2006) report that germination patterns respond to a number of environmental factors (including temperature, NaCl concentration, and presence of different regulating chemicals).

Their paper has over 100 citations, many of which cite germination studies of numerous halophyte species. I'd recommend you start your search there.

You'd also probably benefit by perusing the sources in Ungar (1978) and Panuccio et al. (2014).

Citations

Khan, M.A. & B. Gul. 2006. Halophyte Seed Germination. In Halophyte Utilization and Regional Sustainable Development of Agriculture. pp.11-30
Panuccio, M.R., S.E. Jacobsen, S.S. Akhtar and  A. Muscolo. 2014. Effect of saline water on seed germination and early seedling growth of the halophyte quinoa. AoB PLANTS 6: plu047
Ungar, I.A. 1978. Halophyte Seed Germination. Botanical Review 44(2): 233-264


A and AB blood types from B and O? My grandma is O- blood type, my grandpa is B+, but my mother is A+ and my aunt is AB+.

Is that possible?

I've just looked at different sources like this and all of them are saying that from O and B, comes only B or 0, and A and AB are forbidden.

How can my mother be a child of my grandparents and how my aunt can be a child of my grandma at all? Or can we 100% say that they are not the real children of those parents, assuming that all blood types are correct?

It is correct that O- and B+ parents cannot produce biological children with A+ and AB+ blood groups, with the exception of a few rare edge cases.

Firstly, as noted in the other answer, your grandmother may have the Bombay phenotype. However, this is unlikely, due to the fact that she has been previously hospitalised and it was not noted.

Another unlikely possibility is that your grandmother is a genetic chimera. This means she would have two sets of genes, and her bone marrow hematopoietic cells had the O- genotype and phenotype, while her reproductive cells had an A allele.

If we exclude the rare edge cases, then it is strong evidence that your mother and aunt are not the biological children of your grandparents, and you should consider performing genetic testing to verify this if you wish.


How T-Cell recognizes a cell infected by a virus? According to few articles I read (like BBC about The people with hidden immunity against Covid-19 ):

starting out about four or five days after infection, you begin to see T cells getting activated, and indications they are specifically recognising cells infected with the virus,” says Hayday. These unlucky cells are then dispatched quickly and brutally – either directly by the T cells themselves, or by other parts of the immune system they recruit to do the unpleasant task for them – before the virus has a chance to turn them into factories that churn out more copies of itself.

When virus just entered a cell, but had no chance to churn more copies: Is surface of the cell any different? How T-cell can distinguish infected cell from non-infected?
I am no biologist, but I am fascinated about biology now, and curious to learn more. Sorry if I am not using proper terminology.
I found How do T-cells determine which cells they've already inspected? , but T-cell activation is mentioned only in the context of dendritic cells and lymph nodes. IIUC, T-cells should attack lungs cells to eliminate cells infected by covid-19 there.

All cells chew up internal proteins all the time - it's part of the normal activity of cells to recycle those proteins into amino acids to be rebuilt into other proteins. The first step is chopping up the protein into peptides by the proteasome.
When a virus infects a cell, one key thing it needs to do to replicate is to have the cell start making viral proteins. However, some of these get chewed up, too.
Some of the peptide fragments get bound to major histocompatibility complex class 1 (MHC-1) molecules. These are then transported to the cell surface. This is the cell advertising "hey, this is what I've found in the trash lately."
Sort of like antibodies, T-cells only bind certain antigens, and during development the immune system learns which antigens are self versus foreign by process of elimination: if you detect it during development, it must be yours. Everything else is fair game to attack. When a killer T-cell binds strongly to the MHC-1:peptide complex, it recognizes that this is a foreign peptide and the cell presenting it must be infected or damaged in some way, and this starts a cascade that leads to apoptosis of the infected cell.


The ring formation of ringworm I know ringworm is caused by a fungus on the skin, nails or scalp but what causes the rash to form as a ring instead of like a normal spread out rash?

dermatophyte fungi

Ringworm is caused by a several species of Trichophyton fungi (T. rubrum, T. tonsurans, T. interdigitale, and/or T. mentagrophytes); and a couple others are well known (Microsporum canis, and Epidermophyton floccosum).

The ring pattern is not unique to ringworm causing fungi. (Fairy) Rings are totally common with fungi because mycelium grows outward from the center; and as the mycelium grows, the inner mycelium often dies (from starvation, age, attack by immune system?, or it is cannibalized) leaving only the outer ring of mycelium, which may continue expanding.

Unfortunately the medical world doesn't spend much time on the problems that they can already solve (like with an antifungal ointment or pill), so there hasn't been much effort devoted (to my knowledge) toward answering the mechanistic questions of ring formation of dermatophytic fungi. But it is known that some Trichophyton species sexually reproduce and Trichophyton rubrum also probably does reproduce sexually (ie., plasmogamy, karyogamy, and gametangia). I don't have any grounds for mentioning it (besides logic), but sexual reproduction is probably "age" related in fungi as is growth- so, a ring may be more pronounced in an area where fungal hyphae conjugate... much like the expression of fruiting bodies of other mushrooms.


Evolution of the Redundancy of the Genetic Code In short

Looking at the genetic code, it appears that most redundancy is on the third letter rather than on the first or the second letter of the codon. Why has it evolved this way?

Longer version

In order to compare the relative redundancy accounted by each letter of the codon, let's assume that that every codon occurs at equal frequency. It is probably wrong but useful for the sake of the calculations. Using observed frequencies of codon usage in a given population would change the following probabilities but the question of why some positions in the codon has more redundancy than some others still hold.

A substitution of the first letter of the codon has a probability of $\frac{1}{2048}≈0.00005$ (Stop codon) to be synonymous. A substitution of the second letter of the codon has a probability $\frac{3}{256}≈0.012$ (nucleobases U and G) to be synonymous. A substitution of the third letter has a probability of exactly $\frac{2}{3}$ to be synonymous.

Probability of a substitution to be synonymous given that it occurred on the...

First letter: $\frac{1}{2048}≈0.00005$
Second letter: $\frac{3}{256}≈0.012$
Third letter: $\frac{2}{3}$

Why are there more redundancy on the third position than on the second (which has more redundancy than the first position) in the codon?

To fully comprehend the concept of wobble base-pairing we need to consider the nucleotide sequences of the anti-codons in the tRNAs that have to "read" the genetic code when the mRNA is being translated on the ribosome.  The nucleotide in the anti-codon's wobble position is, for example, often inosine.  Under the rules for wobble base-pairing an Inosine can potentially base-pair with three other nucleotides.

In real terms that means a cell can use less than 63 unique tRNA genes to decode mRNAs carrying messages made of the 63 different "words" (codons).

In an active cell the Ribosome's A-site, where the charged tRNA binds, is occupied by the incorrect tRNA most of the time (based on the law of mass action where any charged tRNA can randomly diffuse into the binding site).  With tRNAs that can recognize multiple codons (which is what the wobble hypothesis gets us), any given protein can be translated faster (assuming  that correct charged tRNAs are limiting for the polypeptide polymerization reaction).

So those are the practical ramifications of the table that you presented, but the explanation, as for most why based questions about biological evolution, is a retrofit.  Natural selection can only work with the materials at hand, and so we can infer that during the period when this genetic code was finalized that the organisms who used it were more successful than the others.  And the current code is based on whatever the previous one looked like. "Descent by modification" is the original description.

[whoops, sorry about the pedantic voice on the "how selection works" bit, I just looked at your profile and realized you can likely teach me on this subject]


Pangenesis and Lamarck's theory of inheritance of acquired characteristics I've read that Darwin had split ways with Lamarck's evolutionary ideas. Yet his theory of pangenesis seems to support Lamarck's theory of inheritance of acquired characteristics. What am I missing?

Pangenesis and Darwin's Gemmules theory suggests a mechanism so that the body's information can travel to and be transmitted by the gametes. Today we know that the information is present in every cell.

Stephen Gould estimates that Lamarck was the first to develop a truly coherent evolutionary theory.

Lamarck's biological and metaphysical theories comprised entirely correct premonitions, 70 years before Darwin. His book was "Philosophie Zoologique" and Lamarck was not illustrious in his lifetime. His lack of evidence made him an impious, profane author, of the pre-enlightenment style of Voltaire, Rousseau, and prior to Emile Zola and Jules Verne.

Scientists have recently attacked Lamarck with great energy, in favor of Darwin:
http://www.textbookleague.org/54marck.htm

Basically Darwin emulated Lamarck's skeletal theory, perhaps independently, and fleshed it out in a modern writing style. He also discovered the foundations of an entire scientific field of his own which tied into Lamarck's, and he fought the church and the science institutions with it.

The evidence of Darwin was copious and meticulous, completing the work of Lamarck (with lesser or greater brilliance, for you to judge).

Lamarck's speciation theories were correct, and his trait-inheritance theory was metaphysical.

First law
Life by it's own force, tends to increase the volume of all organs which possess the force of life, and the force of life extends the dimensions of those parts up to a extent that those parts bring to themselves;

Second law
The production of a new organ in an animal body, results from a new requirement arising. and which continutes to make itself felt, and a new movement which that requirement gives birth to, and it's upkeep/maintenance;

Third Law
The development of the organs, and their ability, are constantly a result of the use of those organs.

Fourth Law
All that has been acquired, traced, or changed, in the physiology of individuals, during their life, is conserved through the genesis, reproduction, and transmitted to new individuals who are related to those who have undergone those changes.

Darwin convinced many scientists and wrote about it continuously from his 30's till his 70's non-stop, sent letters to everyone, and used evidence to define a scientific and mechanical reality to the theory of adaptive radiation. Darwin also coined catchy phrases:

The English and French view of Lamarckism differ.

The English view slights his status, due to lack of evidence and some alchemical bases for the selection process, even though Lamarck is the father of adaptive radiation theory, in the age of the printed book.

The French view gives him more influence, firstly because he may have inspired Darwin as an eloquent writer on the topic of adaptive radiation, the father of the adaptive radiation theory, and secondly because a glimmer of Lamarckism can be found in the new discoveries of Epigenetics, non genetic inheritence.


Would prehistoric humans have been considered negroid or australoid by modern standards? What are your thoughts about this?

For myself I think that the subject statement is rather obvious isn’t it, since Africans, & especially Australian Aboriginals, have the most archaic features & share the most traits with prehistoric humans & other primates within modern humanity? Africans have neotenized greatly, culminating with the khoisan people, whereas australoids don’t have any neotenous traits which the other races have been developing & don’t lack archaic traits which the other races have devolved.

Which of the great races, the highest general division of humanity, mongoloid, caucasoid, negroid, australoid, etc. would prehistoric humans have been considered both by layman’s perceptions, & classified as more scientifically, by contemporary standards, if the choice had to be made, or at least considered closest to or most resembling?

What we’re probably thinking of then are remains going really far back enough to not be of obvious contemporary racial categories aren’t we?

Since prehistoric humans are said to not resemble any modern race, this question may end up being more about opinions rather than hard answers, might it?

Please explain & fill in details regarding your opinion & knowledge. But please do answer the main question first before adding in more details, even if to explain how this subject statement has no merit!

Not sure how much merit this book holds, but do have a look at the tables in ‘Section II: Traits of Living Populations’ for a nice summary:
https://analyseeconomique.files.wordpress.com/2012/12/richard-d-fuerle-erectus-walks-amongst-us.pdf

Here’s the tables themselves. The site’s in French but you can translate it in google. You can also click on the images & save them:
https://analyseeconomique.wordpress.com/2011/11/20/erectus-walks-amongst-us-richard-d-fuerle-section-2/amp/

The first question to answer might be: Has phenotypic diversity in humans increased or decreased since prehistory?  It might be the case that prehistoric humans were as diverse as modern humans, or more so, since there have been a number of diversity-reducing bottlenecks in our evolution.


What is the likelihood of a single human gene to the same gene from the other human? The human genome comprises 3,234.83 Megabases and contains ~ 19,000 genes. It has been estimated that the genomes of humans are 99.9% identical. How likely is it that any single gene might vary from one individual to another? Assume an average length for a gene of 3 kilobases.

Is it still 0.01%, the same as for the whole genome? Why then we have the number of genes in this exercise, together with an approximate length?

Assumptions

Let's assume that we can perfectly align all human genome and therefore calculate such statistics of identity.

Let's assume that the probability of identity of 99.9% is the same for neutral sequences than for coding sequences. This assumption is most likely wrong but there is no other way to answer the question with the data that are given to us.

What is the question exactly?

Your homework question is a little unclear unfortunately. I don't know what is meant exactly by

  How likely is it that any single gene might vary from one individual to another?

Does it mean

  You randomly sample two humans and randomly sample one gene. What is the probability of perfect identity a this gene?

or does it mean

  You randomly sample one gene, what is the probability that all humans are identical for this gene?

I will assume it means the first one.

Step by step

I will go by subquestions to guide through the thought process! Try to answer the following questions one by one and you should be able to get to the final answer yourself

Randomly sample two individuals and randomly consider one nucleotide in their genome. What is the probability that this nucleotide is the same?
Randomly sample two individuals and randomly consider two nucleotides in their genome. What is the probability that these two nucleotides are the same?
Randomly sample two individuals and randomly consider n nucleotides in their genome. What is the probability that these n nucleotides are the same?
Randomly sample two individuals and randomly consider n nucleotides in their genome. What is the probability that these n nucleotides are different?
Randomly sample two individuals and randomly consider 3000 nucleotides in their genome. What is the probability that these 3000 nucleotides are different?

What answer did you get? If you got stuck somewhere, please let me know where!

Hints

No point about using a calculator, it will return Infinite or 0 at some point anyway!
Don't worry too much if you're not using all the numbers that are given to you!


Help identifying plant I saw this plant during the summer in Yorkshire, in the north of England. It was found near in a lowland area not too far from a river, but not in a boggy / marshy place. I’ve also seen them ok roadside verges as well.
I think it’s possibly related to a Lily, but I’m not sure at all about that.
Does anyone know what species this might be?

This plant is a bellflower. Either a Campanula Takesimana or a Campanula Alliariifolia


How to choose secondary Antibody? when isotype of the Primary antibody is IgG2a (from Mouse) and IgG2b (from Rat), how to choose secondary Antibody against these Primary isotypes?
Does secondary Antibody is that much specific to detect IgG2a/2b? What is the logic behind choosing secondary antibodies? A detailed note in this regard will highly be appreciated.

You are not telling, what you do, but I think itis western blot - and for this application it is not important to know which isotype your antibody has. The secondary antibody (which is supposed to bind the primary) has to be directed against the isotype (IgG for example) and the species in which the primary antibody was made, in your case this would be this would be anti-mouse or anti-rat IgG. Since most commercially antibodies in the lab are IgG people usually don't think about it.

The reason is that the secondary antibody is directed against the Fc part of the primary antibody (which has a species specific sequence) and even with the differences in the sub-classes due to different assembly of the light and heavy chains this will not be detected by the secondaries. See the figure (from here) about the schematic differences:

With a careful selection of the peptides used for immunisation it is possible to generate secondary antibodies which can be used to distinguish between sub-classes.


Gap junction turnover Gap junction proteins, connexins, are known to form intercellular hemichannels, between two adjacent cells. These junctions are maintained cell adhesion proteins (cadherins), yet the turnover of connexins is fairly rapid. As these connexins are being turned over, do the replacement connexins re-form the channel at the same location as previously existing channels, or is the pattern stochastic? Put another way, if we know cells in culture have formed gap junctions, and for any one cell, does it have different connected neighbours with time?

This is an interesting question.
Reading this two articles linked below, it seems very much that the connexins are turned over and degraded with the channel more or less staying at the same place (the figure is taken from the first paper, but the second has a similar):

Following this, the connexins are synthesized and then subjected into the ER and then the Golgi for proper protein maturation and oligomerization into hemichannels (misfold proteins are subjected to proteasomal degradation). They are then exported from the trans-Golgi in small vesicles to the cell membrane, transported to the sarcolemma where they form complete gap junction channes with hemichannels from another cell. Single channels aggregate into gap junction plaques.

The connexins are degraded in the proteasome and the lysosome. It is discussed that post-translational modifications as phosphorylation and ubiquitination play an important role here.

The degradation seems to take place at the formed channels. This was tested in two ways: When the export of new proteins to the membrane is inhibited, then the connexins in the membrane and the junctions get lost over time. If the proteasome is inhibited, the number is growing. And when both pathways are inhibited (export and degradation) the number is approximately constant. See paper 3 for more details.
This shows that the process of forming the junctions and degrading the connexins is a permanent and that cells, which form junction with each other stay in the same place.

References:

Connexin Expression and Turnover
Pathways for degradation of connexins and gap junctions
Degradation of connexin43 gap junctions involves both the proteasome
and the lysosome.


Have there been any "chopstick gene" mistakes in genetics? I've heard of the "chopstick gene" fallacy - wrongly assuming an association between genetics and some characteristic, confounded by non-genetic factors.

Has this fallacy happened in real life?

I'm not really interested in cases deliberately focusing on race, where people have argued that there's an innate difference between people of different races based on certain genetic differences, such as the putative "warrior gene" ("warrior allele"?) being described as more common in Maori people. As far as I can tell, the "chopstick gene" isn't about arguing that Asian people are better with chopsticks because of genetic differences between Asians and non-Asians.

I'm more interested in research that was done in good faith, which ignored the possibility of genetic variations having different frequencies in different groups, that produced erroneous conclusions.

Have a look at this time article from a couple years ago.

A concept that you should think about is nature vs nurture. You can think of nature (your genetics) as controlling part of the potential of what you could become (for example, many long distance athletes have genetics that are beneficial for their sport) where as nurture encapsulates the environment that you grow up in (a nutritionally deficient child will not reach maximum potential height that you might predict based on genetics alone).

When scientists are studying a gene in relation to a phenotype, they statistical methods to determine how much a genotype contributes to a phenotype. This process would minimize these types of fallacies since different alleles in different populations would be considered. However, sampling biases can occur and most human variation studies are done on people of european, asian, and african descent.


How do porcupines keep from pricking each other while mating? How do porcupines keep from pricking each other while mating? It seems like they would constantly be scratching each other.

The female stood with the tail held sharply to one side, and the quills on
  the back lying very flat.  The male stood on his hind legs, while the
  front legs grasped the sides of the female. There was no repetition  of the act.

The male's urethra is 115-120 mm long, and his penis is 75 mm, so the he doesn't need to be as close to the female as one might think.  The retractor muscles are attached to the lower portion of the pelvis, which is likely well below the level at which the male's quills end.

Apparently, a dozen or so porcupines will den up in close quarters for the winter, so one can probably guess they have a good sense of whether their spines are hurting another, but that's only conjecture.

I suppose the take-home message is, nature will find a way.

Struthers, P.H. (1928) Breeding Habits of the Canadian Porcupine (Erethizon dorsatum).  Journal of Mammalogy, 9(4), 300-308. http://www.jstor.org/pss/1374084

Mirand,E.A., Shadle,A.R.(1953).  Gross anatomy of the male reproductive system of the porcupine
Journal of Mammalogy, 34(2), 210-220. http://www.jstor.org/pss/1375622


Denaturation of protein Exposure of native protein to heat leads to partial denaturation of the protein due to breaking of-
a. S-S bonds
b. H-bonds
c. Hydrophobic interactions
d. Peptide bonds

After a bit of surface googling I understand peptide bonds are not broken in the process of denaturation and di-sulphide bonds are not broken either (by heat) but by reducers like $\beta$- Mercaptoethanol. These reducers are added in experiments to ensure that the bonds which contribute largely to the tertiary structure are broken.
So either H-bonds or hydrophobic interactions are affected. I cannot make out which one would be the most affected/first one to be affected since the question says partial denaturation, meaning, it was not heated for long.

If you think about the boiling of water, I'm sure you can understand that heat breaks hydrogen bonds. Next consider that the hydrophobic effect is driven entropically and so, by the equation $\Delta G=\Delta H-T\Delta S$, its strength increases with temperature (to a point). See here and here for further explanation. Also, this paper for a more empirical view.


Can siRNA induce DNA methylation in mammalian cells? Some years ago Hiroaki Kawasaki and  Kazunari Taira published an article called "Induction of DNA methylation and gene silencing by short interfering RNAs in human cells" in Nature:

  In plants, dsRNAs targeted to CpG islands within a promoter can also
  induce RNA-directed DNA methylation3, 4, 5, 6, 7, 8; however, it
  remains unclear whether gene silencing mediated by DNA methylation can
  be induced by dsRNAs in mammalian cells. Here, we demonstrate that
  short interfering RNAs (siRNAs; 21–25-nucleotide RNA molecules) induce
  DNA methylation and histone H3 methylation in human cells.

This paper seemed to show that siRNA can also induce long-term silencing of genes by DNA methylation in mammalian cells, which hasn't previously been observed. Unfortunately, the paper was retracted later, calling the results into question.

I found the paper very exciting at the time, as it suggested the possibility to perform gene therapy, to silence specficic genes, just by using RNA interference.

What is the current scientific consensus here, is there any convincing evidence that siRNA-induced DNA methylation is possible in mammalian cells? Was anyone able to replicate the results from Kawasaki and Taira?

From a brief survey of the literature, it seems Kawasaki and Taira have been largely vindicated by the community before and since their paper. The retraction was by Taira alone, Kawasaki refused to co-sign because he maintained the data were valid. From the retraction it seems the reason for the retraction was a lost lab book.

Prior to the Kawasaki and Taiga paper, there were already several other papers describing RNAi-induced epigenetic modification in mammals:

Castanotto, D., Tommasi, S., Li, M., Li, H., Yanow, S., Pfeifer, G.P. & Rossi, J.J. (2005) Short hairpin RNA-directed cytosine (CpG) methylation of the RASSF1A gene promoter in HeLa cells. Mol Ther. 12 (1), 179–183.
Morris, K.V., Chan, S.W.-L., Jacobsen, S.E. & Looney, D.J. (2004) Small Interfering RNA-Induced Transcriptional Gene Silencing in Human Cells. Science. [Online] 305 (5688), 1289 –1292.

Then there was another paper the next year by Kawasaki & Taira, which was not retracted:

Kawasaki, H. & Taira, K. (2005) siRNA Induced Transcriptional Gene Silencing in Mammalian Cells. Cell Cycle. [Online] 4 (3), 442–448.

And it seems the idea is now generally accepted and supported by quite a few other studies, mainly looking at germline cells. For example:

Carmell, M.A., Girard, A., Kant, H.J.G. van de, Bourc’his, D., Bestor, T.H., Rooij, D.G. de & Hannon, G.J. (2007) MIWI2 Is Essential for Spermatogenesis and Repression of Transposons in the Mouse Male Germline. Developmental Cell. [Online] 12 (4), 503–514.

There is no review that I could find which really ties it all together convincingly, but there are several reviews on RNAi directed histone and chromatin modification in general which mention that the fact is now established in mammals:

Joshua-Tor, L. & Hannon, G.J. (2010) Ancestral Roles of Small RNAs: An Ago-Centric Perspective. Cold Spring Harbor Perspectives in Biology.
Volpe, T. & Martienssen, R.A. (2011) RNA Interference and Heterochromatin Assembly. Cold Spring Harbor Perspectives in Biology. 3 (9).


What would happen if nerves didn't have refractory period? What would happen if nerves didn't have refractory period? And, what part of his nervous system or neurons are not needed?

Refractory period returns the repolarization period to the nerve's resting potential . it's the time taken for recovery of a neuron to generate another impulse being excited by another stimulus . so if nerve doesn't have refractory period they wouldn't be able to return to its resting potential & generate new impulse . moreover the repolarization potential further exceeds its value and cause hyperpolarization , so its badly necessary to restore to resting potential by expelling na+ and taking k+ in . unless it would be impossible to restore the resting potential & be ready to get excited to transmit another impulse via the electrochemical pathway . one more benefit of refractory period is that it causes unidirectional impulse conduction.
I didn't get the 2nd part of your question. What are you trying to mean , make it more clear.


Concentration dependent cellular processes Are there any famous biological processes that depend strongly on a chemical concentration reaching a particular value, like some sort of switch?

E.g. if concentration of chemical x reaches concentration y at cell location z (membrane, organelle etc) then a particular biological process will occur?

Thanks

There are several, but I guess the most well known is the neuron action potential, where the concentrations of Na+, K+, and Cl- ions determine the membrane potential of the cell. When the potential reaches a certain level, it triggers the action potential. You can read about this in much more detail on wikipedia, https://en.wikipedia.org/wiki/Action_potential .

But to be pedantic about it, almost every cellular process is concentration dependent.


Can Naegleria fowleri enter through your ear? Is it possible to get infected with the amoeba, Naegleria fowleri, through your ears, or is the nose the only way it can enter to cause infection? How commonly is it found in your stool as well?

Ears? No. The tympanic membrane (eardrum) is a watertight barrier between the outer ear and middle ear.

  Exposure to the organism is extremely common due to its wide distribution in nature, but thus far lacks the ability to infect the body through any method other than direct contact with the olfactory nerve, which is exposed only at the extreme vertical terminus of the paranasal sinuses; the contaminated water must be deeply insufflated into the sinus cavities for transmission to occur.

In short: Don't huff warm lake water too deeply through your nose, and you'll probably never get it.

You shouldn't find it in your stool. Other amoebic infections can be found in your stool, as they can attack the lining of your intestines, but Naegleria, specifically, will reside in your sinuses and brain until you die or receive treatment.


Is there a known glucosepane cross-link breaker? I read the following on wikipedia:

  There is, however, no agent known that can break down the most common
  AGE, glucosepane, which appears 10 to 1,000 times more common in human
  tissue than any other cross-linking AGE.

(AGEs are related to oxidative stress, aging and chronic diseases.)

I was wondering maybe the article is out of date, and there is a glucosepane cross-link breaker available. Do you know anything of that, or a current research which aims to find that?

Unfortunately at this time, there are no known glucosepane breakers which can feasibly be used in a living organism.  There is a small (very small) amount of research being done on the topic by Yale university in cooperation with the SENS foundation, but the focus is extremely early stage - nothing more than synthesis and detection of artifical glucosepane and precursors.

It is a rather frustrating situation, as there are very good arguments indicating glucosepane as an almost universal 'bad thing that should be fixed', and the molecule itself isn't particularly complicated.  It seems that this would be a low effort/high reward research area.


How to recover all protein ses into refseq database I'm actually trying to download all the virus protein sequences available in the NCBI database.

I guess the link is this one: ftp://ftp.ncbi.nlm.nih.gov/genomes/refseq/viral/

How could I get all the protein sequences in fasta format into one file ? Does someone have codes to do that easily?

Thank you very much.

As with most things, there are multiple ways to do this. Here are two of them:

Download from the NCBI Assembly portal

Go to https://www.ncbi.nlm.nih.gov/assembly/ and search for 'Viruses[Organism]'. For our purposes, I am going to restrict this search to Virus assemblies that are latest RefSeq and reference genomes. The query for this will be: "Viruses"[Organism] AND "latest refseq"[filter] AND "reference genome"[filter]. It will return 46 results.
To download the protein FASTA sequences for all of these, click on the big blue Download Assemblies button, choose RefSeq as source and Protein FASTA as File Type.
Click the Download button and a tarball with FASTA files - one for each assembly - will be created for you to download. You will then have to combine them all into a single file.

Download using wget

Go to ftp://ftp.ncbi.nlm.nih.gov/genomes/refseq/viral and download the assembly_summary.txt file. This is a tab-delimited file with information about every RefSeq viral assembly located in that FTP path. Column 20 has the FTP path for the assembly which you can parse out and use wget to download the protein FASTA file for each assembly, followed by combining them into a single gzipped file as shown below:

## download the assembly_summary.txt file
wget ftp://ftp.ncbi.nlm.nih.gov/genomes/refseq/viral/assembly_summary.txt
## download the protein FASTA files
grep -v '^#' assembly_summary.txt \
    | cut -f20 \
    | while read -r url ; do wget $url/*_protein.faa.gz ; done
## combine all files into a single one
zcat *_protein.faa.gz | gzip > all_viral_proteins.faa.gz


What are the functions of magnetic bacteria? I'm trying to understand why are bacteria "equipped" with magnetosomes ("intracellular organelles in magnetotactic bacteria that allow them to sense and align themselves along a magnetic field") and why and for what do they need such organelles.

You can find a detailed discussion of this topic here.

Magnetic bacteria contain chains of magnetic crystals (magnetite or greigite) which cause the cells to be oriented in a magnetic field.

It was originally proposed that magnetic bacteria use their magnetosomes to ensure that they swim downwards into the sediment (everywhere on earth, except at the equator, these lines of force have a downward component vector.) However, the current view is more complex than this: magnetic bacteria are microaerophilic and occur in stratified aquatic environments (i.e. ones where there are zones of oxygen concentration at different depths). In this view the magnetic "sense" is not a true taxis, but rather is used to keep the cells oriented in the magnetic field while they adjust their position by sensing oxygen (aerotaxis). As you may be aware, the standard way that Gram-negative bacteria operate is to perform a biassed random walk in three dimensions. The alignment of cells with the magetic field will reduce the dimensionality of the movement, which is more efficient.


What are the effects of caffeine on the mammalian circulatory system? A friend of mine told me an anecdote about his mother, who drank too much caffeine, to the point she became hypotensive and would pass out. Because caffeine acts as a stimulant, I'm assuming the decreased blood pressure was some kind of tolerance effect.

How exactly would caffeine have disrupted her circulatory regulation and caused her normal pressure to decrease?

I can't speak to the causes of hypotension, but you are indeed correct, caffeine is a stimulant. As a stimulant, there is a well documented acute period of hypertension that lasts for up to 4 hours. Interestingly, there is no causal link established between caffiene consumption and chronic hypertension leading to cardiovascular disease (see here and here).

Having said that, caffeine is also a diuretic, which could cause someone who is already fairly dehydrated to exacerbate that state. It's possible to faint from a result of severe dehydration but I think it would have to be pretty severe.

It's possible someone is prone to fainting for non-medical, purely physiological reasons, such as standing for long periods, standing up too quickly, hypoglycemia, or some other predisposition.


Is there a comprehensive list of human circadian-like processes, hormones or gene expressions? I'm reading this article onblood sugar and circadian rhythms and the following question popped into my head: a lot of articles mention various diurnal or circadian rhythmicity of biological processes. Is there a "master" list of hormones, gene expressions and other processes that the modern science recognizes as "circadian"?

In other words, is there something that can give reader a clear picture of what's happening at a certain (biological)time for a human and is expected to happen tomorrow at similar time?

It would be great to take a look at such list and see what are the major processes that recur on a time-sensitive basis in humans.

There isn't a central/master website that I'm aware of, as it's still an area of active research.  I did a bit of work in the field about 10 years ago, and at that point we were still working out the circadian rhythms in the yeast mating cycle.

Since then, the field been enumerating more and more involved processes: mRNA expression, mRNA degradation, micro RNA, mRNA transport and translational regulation, then protein translation and protein regulation... Given that any single gene can be regulated at one or more of these points, and that there are at least a few different circadian cycles and they can even conflict... well, it's a bit of a mess.  Oh, and don't forget that different organs and cell types have different responses, so then you have to cross check 50 cell types.

I'd start with this review paper, which can give you an idea of what kinds of papers to search for.  If you decide you want to know about individual genes, a lot of scientists in the field have made their datasets available online in various gene expression databases.  There are several databases running currently, and maybe one of them will be specialized in circadian expression.

Circadian topology of metabolism
Joseph Bass
Nature 491, 348–356 (15 November 2012) doi:10.1038/nature11704
Published online 14 November 2012
http://www.nature.com/nature/journal/v491/n7424/full/nature11704.html


Production of processed Insulin in bacteria Genetically-engineered bacteria are used to produce insulin in industry, but as far as I know, the bacteria can produce only proinsulin. Why is that? What happens in the human body in order to make functional insulin, that can't happen in some microorganisms? In the body proteases cut some at amino acids, and cleave the polypeptide while other enzymes create disulfide bonds.  Why is there no bacteria in the industry that can do the same? It's not possible for some reason or in other words — can such a bacterial strain not be engineered?

Insulin is processed from proinsulin by folding the peptide and forming 3 disulfide bonds before cleaving the peptide in 2 positions, leaving 2 peptide chains held in place by the disulfide bonds. This process is summarized in this image:

This only works because the peptide is packaged in a secretory vesicle during synthesis. This protects the peptide against the reductive environment of the cytoplasm, where glutathione is likely to reduce the disulfide bonds that hold insulin together.

When industrial insulin production moved from extracting the hormone from animal pancreases (pancreai?) to bacterial production of human recombinant insulin, glutathione was likely to cause a problem because simple protein production in bacteria just builds the protein in the cytoplasm, where glutathione is present. It is possible to export the protein into the periplasm during synthesis, similar to how proinsulin is moved into the endoplasmic reticulum during synthesis in human cells, but this can complicate protein purification (larger volumes of media, if protein is inside cells you can spin the cells down and work with a smaller volume).

Note that more recent methods use yeast to make insulin, potentially allowing production of actual insulin instead of proinsulin. And modern purification methods can extract insulin from animal sources that is just as good as recombinant sources.

I know from personal experience that it can be very hard to produce proteins with multiple disulfide bonds in bacteria. We attempted to produce mutants of bee venom PLA2 in E. coli, but the protein was misfolded and wound up in inclusion bodies. We purified the inclusion bodies, unfolded the proteins, then slowly refolded them by dialysing the protein in a glutathione solution. We aimed at making a protein with a free thiol for later chemical modification, but that free thiol just picked up a glutathione we couldn't remove without ruining enzyme activity.

Also please note that I am not fully aware of how insulin is made on the industrial scale and I could be wrong. That's why this was originally a comment.


Creatinine excretion Creatinine accumulates in blood if kidneys fail to excrete it.  Does this unexcreted creatinine ever get thrown out of body? What prevents creatinine from continuously rising in the blood?

Creatinine is formed irreversibly and non-enzymically from creatine and phosphocreatinine and is usually assumed to be metabolically inert in humans (Wyss & Rima Kaddurah-Daouk, 2000, Creatine and Creatinine Metabolism): no human enzyme is known to metabolize creatinine, and this compound is normally eliminated from the body via the kidneys

  In chronic liver failure, however, "a significant quantity of creatinine is excreted into the gut, as is true of urea and uric acid, and is metabolized by gut flora" (Jones & Burnett, 1974, Creatinine Metabolism in Humans with Decreased Renal Function: Creatinine Deficit.

This was 'news to me', and the observation about urea is also surprising, but it looks to be a very good paper.


Reference for the bite force for Nile Crocodile The (maximal) bite force of the Nile Crocodile (Crocodylus niloticus) is estimated around 22,000 Newton (refer to YouTube interview with Ofer Kobi, a crocodile conservation ranger and croc farm owner, time 7:50-8:00, Hebrew , where he estimates the bite force as above 2 metric tons). However, I didn't find a proper reference for this. Dr. Gregory Erickson measured the bite forces of a 5.2 meters long Saltwater Crocodile (Crocodylus porosus) and obtained a value of about 16,000+ Newton and estimated a 6.7 meters long Saltwater Crocodile can exert a bite twice as strong (about 34,000 Newton). See Paper by Gregory Erickson et al. Interesting to note that Erickson measured small Nile Crocodile (total body length < 3 meters) so it does not represent the bite force of a full adult big crocodile.

Remarks on units of force:

1 Newton = 1 kg * 1 meter / sec^2

$1 \ \mathrm{Newton} = \frac{\mathrm{kg} \times \mathrm{meter}}{\mathrm{second}^2}$

1 Newton = 0.224808943 lbf = 0.225 lbf (pound-force)

10,000 Newton is approximately 1 tonne-force (1 tonne = 1 metric ton = 1000 kg)

Here is a video by Brady Barr (video in YouTube) measuring 5000 lbf for an adult Nile Crocodile. This is equivalent to 22.24 kN (more than 2.2 tonnes of force). This result is also refered here (Getty Images).

 Source: Gianfranco Gori, Wikipedia


Please give information about this insects I took this photo of a small insect which I found near to my house (Maharashtra state, India). What insect is this?

It looks like an insect belonging to the family Cicadidae. Further information is needed to identify this cicada species.