What happens when a human ingests a large meal, and after a short time follows it up with a large amount of indigestible carbs? A human eats a large meal and indigestible carbs (IC) with such a timing that the IC arrive to the small intestine when it is already full and busy breaking down and absorbing the meal. What would happen to the IC? Would they stay there until the digestible meal is digested, or would they somehow be moved along? Would they start fermenting if they are stuck there for some time? Would they push the unabsorbed remnants of the meal out as the body tries to excrete IC? Would they hamper absorption or aid it?

Indigestible carbs are known as dietary fiber. They slow down gastric emptying, which results in slower absorption of the absorbable nutrients in the small intestine.

  Early research regarding soluble fiber demonstrated delayed gastric
  emptying and decreased absorption of macronutrients, resulting in
  lower postprandial blood glucose and insulin levels [44]. This is
  most likely due to the viscosity of soluble fibers inside the GI
  tract. Interestingly, different types of soluble fiber had varying
  effects on viscosity and nutrient absorption. Guar had the highest
  viscosity as well as the greatest effect at decreasing postprandial
  blood glucose. Therefore, it would be assumed that an increased level
  of soluble fiber would be associated with a decreased risk of
  diabetes. However, several recent studies have demonstrated the
  opposite showing no correlation between soluble fiber and a reduced
  risk of diabetes (Nutrients, 2010).

So, dietary fiber can slow down the absorption of macronutrients (carbohydrates, proteins, fats), but does not reduce the amount of macronutrients absorbed (at least not significantly).

Dietary fiber can be soluble (for example, stachyose and raffinose in legumes) or insoluble (for example, cellulose in fruit skins or grain hulls) (Linus Pauling Institute).

They are microbes, mainly in the large intestine (not in the healthy small intestine), that ferment soluble, but not insoluble fiber. Fermentation of a large amount of soluble fiber produces a lot of gas (flatulence), which typically occurs several hours after a meal.

Insoluble fiber can stimulate intestinal motility and thus help in constipation, but large amounts can be laxative, which could result in decreased absorption of nutrients; soluble fiber can trap some bile secreted by the gallbladder and may thus reduce the synthesis of cholesterol (Linus Pauling Institute).

Dietary fiber probably does not interfere significantly with the absorption of minerals and vitamins (Nutrients Review).


Are there any small peptides with protease activity? I'm looking for a very small protease to base an engineered protein on.  I did a search for "peptides with protease activity" but all the results seem to be as peptides to be used as protease substrates (eg in assays); I couldn't find any catalytic peptides.

What is the smallest protease or domain which has independent proteolytic activity?  (Ideally looking for something very short, a dozen aminoacids)

60 residues is the smallest I could find, ref below.

https://jbiomedsci.biomedcentral.com/articles/10.1186/1423-0127-19-54


Is COVID-19 claimed to get less deadly over time? If so, why? From a TV news report of a press conference from (I think) the German Robert Koch Institute, I remember hearing an expert declare that he was expecting COVID-19 to get less deadly over time.  Unfortunately, I don't know what press conference it was (I'm not sure if it was the Robert Koch Institute — it might also have been the Charité university hospital) and cannot find such a stated expectation on the internet.

Why would an expert express this expectation?

Is it because we're heading toward summer (at least where most COVID-19 cases have been reported), or is it a standard pattern, perhaps either due to people's immune systems or due to the virus evolving and becoming weaker?

While the data are much too sparse and noisy to give an answer about what is happening to COVID-19's virulence (the technical term for the "deadliness" of an infectious disease), or to forecast what will happen to its virulence in the future, there are indeed theoretical reasons that one might expect the virulence to decline in the future.

There is an entire theoretical literature on the evolution of virulence (e.g. see Read 1994, or see Wikipedia); Robert May and Paul Ewald are two researchers who contributed seminal ideas. The basic idea is that infectious 'organisms' (including viruses) may face a tradeoff between their ability to produce lots of infectious particles (e.g. by replicating faster within the host) and the length of time that they can stay in the host before it dies or activates immune defenses sufficiently to end the infection. In this case, some intermediate level of virulence may evolve.

Evolution of virulence in ways predicted by the theory has been observed in the real world in such diseases as myxomatosis (a viral disease of rabbits). The theory has also been suggested to apply in HIV and syphilis.

The actual forecast can depend on many details of the biology and epidemiology of a particular organism. If COVID-19 happened to have a higher-than-optimal virulence in humans at the time of emergence, we could expect its virulence to decline over time. It could also decline if epidemic control was applied in such as way as to differentially affect more-virulent strains; this has been suggested by Tang et al. on the basis of the pattern of mutations in different strains, although their logic has also been criticized on Twitter by an expert in genetic epidemiology, and now by a more official rebuttal by McLean et al. (with some back-and-forth discussion between the authors and critics).

This explanation doesn't include the possibility of host evolution, which is theoretically important but not really relevant to COVID-19 — it would only happen over many generations, and only if the epidemic was so severe that it was a significant overall cause of death or failure to reproduce ...

Tang et al. "On the origin and continuing evolution of SARS-CoV-2", National Science Review, nwaa036, https://doi.org/10.1093/nsr/nwaa036 .
Read, Andrew F. "The evolution of virulence." Trends in microbiology 2.3 (1994): 73-76.


Why Can't the passage of acquired behavior be considered acquired inheritance? While reading about a cross-fostering experiment conducted on Male California mice and Peromyscus californicus, I came across the fact that the behavior acquired by a generation of mice due to foster-parents is transferred to the next generation as the next generation also gets the same amount of parental-care and attention as the first.

As we can say that behavior is also a character in a way (and is influenced by genes as well as environment), wouldn't the transfer of such behavior over time (if the mice bred by foster parents were positively selected for) be considered 'inheritance of acquired characters?'

Yes, a behaviour is definitely a phenotypic trait.

Some acquired trait (typically behavioural traits but not only) can indeed be transmitted to a few future generations. But make sure to understand the mechanism. I can think of 3 different mechanisms:

epigenetics
covariance between parent fitness and offspring fitness (within one genotype and one environment) typically due to to parental care.
Transmission of tradition (in the broad sense). A tradition is also sometimes called a meme.

One will need a link to the specific paper you are reading to know what mechanism is in play in the study you are reading.


Does the body prioritise the use of available sugar before fat? Let's say you eat a very unhealthy snack that contains 90% sugar and 10% fat. Would somatic cells not start using the fat for energy until all the sugar is used up?

Does the body not use fat at all if there is more bio-available sugar to be used? Or is there always a proportion of fat being used for energy?

In a very simplified explanation  - the body usually picks the process which is easiest/ fastest which would be to absorb the glucose  then the fat would be used for energy as this takes longer to digest and absorb because it is a relatively complex molecule which also requires bile to emulsify it.

Starchy/ high glucose products will already be broken down in the mouth by amylase and absorbed in the intestine + pancreatic amylase etc. which takes around 20 mins-1hr whereas soluble fats are digested primarily in the small intestine (by enzyme lipase) for (very approx.) 1-4 hours depending on the amount ingested. Insoluble fats are broken down into soluble fatty acids and glycerol which can be absorbed into the blood.

The amount of either you use for energy just depends on how much energy you expend.


Why proteins are not visible on my membrane after ponceau staining? I have a problem in western blot that I can't resolve by myself.
When I am use to add 100 microgram of proteins for each sample but after running and transfer its impossible to me to see bands of protein.
What can be the reason of that?
Thank you for your help

From what you say, I can only give a few advices:

For the quantification, make sure your sample does not contain any substances which disturb the assay. The Bradford assay is for example sensitive against SDS or DTT. See here for more details. This prevents you from loading a sample without enough protein.
Make sure that you really have protein on your gel. Run a gel as normal and then stain it with Coomassie Blue (it cannot be used for western afterwards).
Don't loose your sample - this happens easier than most people think.
Make sure your transfer works. This can either be done by using pre-stained ladders (which are helpful anyway) or by doing Ponceau Red staining. This can be washed off with water and doesn't disturb downstream applications.
Depending on the type of membrane you are using, they might need pre-treatment. PVDF membranes are extremely hydrophobic and need to be activated in methanol.


Which is the reference 16S rRNA? Recently, I've stumbled upon a fact, which hasn't bothered me for many years. The fact is that all universal 16S primers are written as "[FR][0-9]+" (in regex notation), that is they have a position with respect to a reference. I've read through many papers, wherein these primers were introduced, and most of the time the authors say nothing but "E. coli 16S". Anyway, in one case I've found that it is in fact the reference K12 E. coli. But the problem is that it has 7 distinct rRNA operons: rrnA, rrnB, rrnC, rrnD, rrnE, rrnF, rrnG. Do you have a reference showing a particular operon used for the 16S position notation?

Edit

Figure 2. Hypervariable regions within the 16S rRNA gene in Pseudomonas . The plotted line reflects fluctuations in variability amongst aligned 16S rRNA gene sequences of 79 Pseudomonas type strains... (Bodilis et al., 2012)

As you correctly point out, designing an optimal primer pair for 16S-rRNA sequencing is a tricky affair because even the less-variable regions are not same between different strains and species. Sambo et al (2018) have even developed a bioinformatics software for optimal design of primers for 16S-rRNA sequencing for multiple bacteria.

  We propose here a computational method for optimizing the choice of
  primer sets, based on multi-objective optimization, which
  simultaneously: 1) maximizes efficiency and specificity of target
  amplification; 2) maximizes the number of different bacterial 16S
  sequences matched by at least one primer; 3) minimizes the differences
  in the number of primers matching each bacterial 16S sequence. Our
  algorithm can be applied to any desired amplicon length without
  affecting computational performance.

There is diversity in the 16S-rRNA genes within the same species i.e. the different copies are not exact duplicates (Větrovský & Baldrian, 2013).

  Větrovský & Baldrian (2013)

Interestingly, the different rRNA operons in E.coli have different promoters and are even differentially expressed during stress conditions (Kurylo et al., 2018).

However, Kitahara et al. (2012) found that 16S-rRNA genes isolated from soil samples, in place of the original E.coli gene, could support its growth. In other words E.coli is highly robust to mutations in its 16S-rRNA.

  After counterselection, ∼200 clones of KT103-derivatives (carrying
  pRB103 whose 16S rRNA gene was substituted with foreign genes) were
  obtained, from which 33 nonredundant 16S rRNA genes (A01–H03) were
  identified. Through multiple alignment of E. coli 16S rRNA and our
  metagenomically retrieved 16S rRNA sequences, it was found that at
  least 628 (40.7%) of the 1,542 nucleotides were variable, indicating
  marked mutational robustness of the 16S rRNA. Strikingly, the
  functional 16S rRNA sequences (except A10 and F02, which were 99.0%
  identical to E. coli 16S rRNA) obtained in this study showed only
  80.9–89.3% identity to E. coli 16S rRNA, which was well below the value reported thus far (Proteus vulgaris 16S rRNA, 94% identity to E.
  coli 16S rRNA)

For your question

  But the problem is that it has 7 distinct rRNA operons: rrnA, rrnB,
  rrnC, rrnD, rrnE, rrnF, rrnG. Do you have a reference showing a
  particular operon used for the 16S position notation?

I don't think any one of them is considered the reference. The complete E.coli 16S-rRNA sequence reported in NCBI seems to consider a "consensus" of different reported sequences:

  [5], [7] contain updated sequence data for the original work by the
  same laboratory [4]. There were too many discrepancies between [4] and
  [5], [7] to list each revision in our sites table. The sequence shown
  is from [7]. [4], [5], [7] point to a number of cistron
  heterogeneities. There is uncertainty, however, with regard to
  assigning these various heterogeneities to specific cistrons. The RNA
  method used by [4], [5], [7] gives the average of all the cistrons
  present in the cell [7]. The heterogeneities are classified by their
  relative proportions into major, minor and undetermined species. The
  sequence shown corresponds to the major species. The heterogeneities
  were annotated as variations in the sites table. It is not known which
  of the residues 'c' (base 633) or 'a' (base 641) undergoes a deletion,
  giving rise to the minor component 'atctg'. [7] suggests the existence
  of one or two mutated cistrons among the known seven cistrons of
  ribosomal RNA. With the exception of a single base deletion, this
  sequence is identical to the current 16S rDNA sequence for the E.coli
  rRNB gene.

The NCBI page also lists different polymorphisms and base modifications in the 16S-rRNA within and between different strains/"species".

NCBI has several partial sequences as well. When I checked for P.aeruginosa and B.subtilis, I could find only one or two complete sequences (rest were partial). Moreover, each entry indicated the strain that it was obtained from. Therefore I assume there is no single reference sequence.

I guess that people do consider the different variants while doing phylogenetic analysis (or simply just look for conserved "signature" sequences for a given species). I am sure that there are computational algorithms for doing the classification in an optimal manner (see Chatellier et al., 2014). Since, I don't have an expertise in this area I cannot say anything conclusively about the routine practice. In fact there is still ongoing research in improving the analysis (for example, Yang et al., 2016 and Sambo et al., 2018).


Can an electrocardiogram be recorded with a single electrode? Is it possible to do an electrocardiogram with one electrode? Or is it neccesary to have multiple electrodes? I do not understand much about EKG, so I am sorry if this question sounds naive.

Short answer
Any electrophysiological recording of potentials, including the electrocardiogram (ECG or EKG), measures a potential difference. Hence, two or more electrodes are necessary.

Background
The ECG measures the rhythmic voltages changes generated by the heart muscle. Voltage is defined as a potential difference between two points. Therefore, a voltage is always measured across two or more points. For example, when
you measure voltage when holding one out of two recording electrodes to one of the two poles of a battery, nothing will be recorded. This, because no current will flow through the potentiometer by connecting just one pole of the battery. Likewise, electrophysiology needs at least two recording channels to determine the voltage differential between the two. One channel is typically called the active electrode, the other the reference. The configuration of active and reference determines the polarity of the recorded voltage. Often a ground electrode is added to remove background noise.


Number and function of voltage-independent ion channels Googling for "voltage-independent" ion channels neurons doesn't give a good overview over the topic (and yields only approx. 50,000 hits, compared to 500,000 hits when searching for "voltage-dependent" ion channels neurons).

What I want to learn:

How many voltage-independent ion channels are there in the brain (or in specific parts of the brain, e.g. cortex) compared to voltage-dependent ion channels? (Rough estimate, order of magnitude: a tenth, a percent, ...?)
Which functional role do they play (compared to voltage-dependent channels which are mainly (?) concerned with the propagation of action potentials along the axon)?

Are there other (and possibly more concise) references than the one I found:
ROLES OF THE ION CHANNEL NALCN IN NEURONAL EXCITABILITY CONTROL (which states, that NALCN is "widely expressed in the nervous system")?

(I guess voltage-independent channels could support the mechanisms of Rall's model which doesn't pressume voltage-dependent ion channels but only modifiable membrane resistances, possibly realized by voltage-independent ion channels, right?)

Addendum: I made a bad mistake not pointing out, that I meant ion channels that are neither voltage- nor ligand-gated but just influence the membrane resistance passively. (Ligand-gated ion channels are of course examples of voltage-independent ion channels, but not the ones I wanted to ask for.) Are the voltage-independent ion channels I wanted to ask for possibly just what is called leak channels?

Those would be referred to simply as 'ion channels'. Voltage-dependent channels should get special mention.

This link from the Blue Brain Project should prove useful:

  http://channelpedia.epfl.ch/ionchannels/

A query for 'voltage-dependent' gives me results from 58
channels. According to the original
reference
there should be at least 187 channels in this database (out of the
estimated ~500 ion channels expressed in the brain). That should
give you at least the order of magnitude.

An additional resource can be: https://icg.neurotheory.ox.ac.uk/.
'Non-voltage gated' channels are used to depolarize and
hyperpolarize the membrane. That is as much as specific the answer can be when talking about all of the ion channels. Their specific compartment localization makes a big difference, though. Those that are located in synapses have different functions compared to those that are non-synaptic, for example.

No, voltage-dependent channels are not
solely found in the axon. That is what makes dendrites active
compartments as well. See this very good
review
and my
answer
to
How does a neuron change as you learn?.
In brief, voltage-gated channels facilitate the integration of
inputs on the dendrites independently from the integration at the
level of the soma. This is thought to extent the information
processing capacity of the
neuron.

PS: A lot of your questions suggest that you would be interested in the NEURON simulation environment, as previously suggested to you by @bryan-krause. Using this tool could save you some trouble of trying to re-invent the wheel, as you can start off by using a pre-existing model from ModelDB.


Never caught this fish before After catching a bunch of mangrove snapper using live shrimp, my son caught this fish in about a foot of brackish saltwater water off a dock near a rock wall in  Vero Beach at around 10:00 AM  on July 5th. Fish was about 6 inches long and had a wide mouth with  small pointy teeth and what appeared to be two small horns/bumps that protruded from behind its eyes. Never encountered it before.

Expanding my comment into an answer as no one else has jumped in-

This fish closely resembles a sculpin of some kind. This is a very large and diverse family, but many of them share distinctive features. The quite wide head and horns that you describe and show are common in this family. Where I am from (Northwest USA), the Red Irish Lord / cabezon is a gamefish sculpin that can grow to be quite large, and closely resembles this picture of yours (a rather small specimen shown in Figure 1).

Figure 1.

Based on where you are in Vero Beach (Florida?), I have looked a little bit and there is a chance that it is a Gulf Toadfish (Figure 2) based on its appearance and where you caught it. Here is another fisherman's account (with pictures) of a similar fish.

Figure 2.

Hope that helps.


Why social animals attack odd members of their own group? Some social animals are known for attacking odd members of their own group, for example, chicken:

  If you have a large group of one type of chicken, they will usually gang up on the one or two others that do not look like they do. They recognize color differences the most and will beat up on the odd chickens in a group.

Of course the same behavior is most commonly observed in humans, where any difference can be a reason for aggressiveness.

Why this behavior developed and still exists and how it is called?

Persecution is not a term often used in zoology, compared for example to the notion of social exclusion and hierarchy disputes/social animal hierarchy. That is because humans incarcerate animals which would otherwise flee to safe distance from the group if they are attacked. Wild Mammals, birds, fish, other animals with free movement can normally get safe distance from an aggressive group in order to be safe from persecution.
Fish and insects/island animals sometimes have restricted ranges, and "social exclusion of a mutant" - studies are difficult to find and perhaps won't give masses of information to know why it happens, for categorization and prevalence of different reasons.
I found only one research on social aggression based on appearance:Aggressive biases towards similarly coloured males in Lake Malawi.
Useful related terms for further research for your question are i.e.:

"social exclusion mutants traits aggression"
"social exclusion zoology"
"social exclusion injury zoology"
"social exclusion zoology mutation"
"hyerarchy disputes appearance zoology"

It's an interesting notion for research that you have found, for which a lot can be written, because it gives a complex range of potential reasons for the given behaviour: warding off a contagious individual, warding off a tribe from far away that could displace the current group, inability for the brain to average the mutant's appearance to associate with it, habituation of species to a type of social companion since their birth (i.e. birds sometimes think they are humans)
And so a research requires a broad understanding of juvenile establishment of appearance recognition of other individuals of the group, i.e. where humans search for an average appearance compared to the social group, and chimps recognize close relatives and mate with the most distant, chickens can adopt humans... and animal behaviour towards an ill individual, it's difficult and takes a while to gather actual sci documents for.
When you have found all the closest related research, the given write up would be very fascinating!!! i hope you can search the given topics and give a summary of some previous examples of vaguely related research.


History: Do evolutionary and ecological processes occur at the same timescales? Classically, it was thought that evolutionary processes occurred at a much slower pace than demographic/ecological processes. Nobody, ever thought about incorporating both processes into the same model as they were assumed to occur at different time scales. We slowly came to realize that this way of thinking is quite wrong and many demographic/ecological changes (demographic expansion for example) directly affect evolutionary processes and even more important that evolutionary processes can directly influence demographic/ecological processes. I take for example Kirkpatrick and Barton (1996) who investigated how dispersal load (fitness decrease due to maladaptive alleles brought to local populations by dispersal) affect the "evolution" of the species range limits.

Who (what) are the main authors (articles) that allowed for this switch in our viewpoint about the interrelations between evolution and demographic/ecological processes?

Dennis Chitty might have been an important author to establish the viewpoint that evolutionary processes can influence the probability of survival of a population. However, I know a little bit about his work only because he was professor at my department (way before I even arrived in the department) and he might therefore not be the most important author of all.

This doesn't directly answer your question but my current research is on building models that combine ecological and evolutionary processes. Thompson (1998) is one of the earliest papers to talk about rapid evolution on ecological time-scales. And also a recent paper highlighting the interactions was Schoener (2011).

Perhaps reading through these two papers and looking at their references will give you a better idea of when the shift in thought started.


Do ants know the direct (approximately shortest) path to their nest from the food morsel? I've been studying a bit on the foraging habits of ants, and one of the things I'm not clear on is whether ants know the shortest path from the food that they find to their nest. I understand that ants can leave different types of pheromones$^{[1,2]}$, they can change their behavior based on those trails, and those trails are often volatile. What I'd like to know is how do ants find their nest once they find a food morsel. In one of the papers,$^{[3]}$ it was shown that ants change their foraging strategy based on the number of encounters they have: they follow a straighter path when the ant density in an area is low, while they follow a more tortuous path if the ant density is high.
Considering a lower ant density, an ant will travel pretty far from the nest in search for food in a path that is not always straightforward. Assuming that the pheromone trails it leaves behind do not evaporate by the time it finds the food, will the ant travel back on the same path laid down by its pheromone trail, or will it actively find a more direct path towards its nest? I might also be missing something in the sense that ants always know where their nest lies when they are foraging, and thus can find the shortest path whenever they find any food. If so, any work reflecting such research would be of great help.
References:

Dussutour, A., Nicolis, S. C., Shephard, G., Beekman, M., & Sumpter, D. J. (2009). The role of multiple pheromones in food recruitment by ants. Journal of Experimental Biology, 212(15), 2337-2348.

von Thienen, W., Metzler, D., & Witte, V. (2016). How memory and motivation modulate the responses to trail pheromones in three ant species. Behavioral ecology and sociobiology, 70(3), 393-407.

Adler, F. R., & Gordon, D. M. (1992). Information collection and spread by networks of patrolling ants. The American Naturalist, 140(3), 373-400.

Terms that may help you research are dead reckoning or path integration. From Wikipedia:

In navigation, dead reckoning is the process of calculating one's current position by using a previously determined position, or fix, by using estimations of speed and course over elapsed time. The corresponding term in biology, used to describe the processes by which animals update their estimates of position or heading, is path integration.

There are many animals and certainly some species of ants that use dead reckoning/path integration for navigation. Here are some papers about the Cataglyphis genus by one scientist and some colleagues:
Wehner, R., & Räber, F. (1979). Visual spatial memory in desert ants, Cataglyphis bicolor (Hymenoptera: Formicidae). Experientia, 35(12), 1569-1571.
Wehner, R., & Wehner, S. (1986). Path integration in desert ants. Approaching a long-standing puzzle in insect navigation. Monitore Zoologico Italiano-Italian Journal of Zoology, 20(3), 309-331.
Müller, M., & Wehner, R. (1994). The hidden spiral: systematic search and path integration in desert ants, Cataglyphis fortis. Journal of Comparative Physiology A, 175(5), 525-530.
Collett, M., Collett, T. S., Chameron, S., & Wehner, R. (2003). Do familiar landmarks reset the global path integration system of desert ants?. Journal of experimental biology, 206(5), 877-882.
The last one on the list is particularly relevant because it seems to show that the ants are not using landmarks as markers of position, because moving landmarks doesn't alter their paths.
My intuition is that the extent of path integration will depend on the environment. Species living in a fairly "flat" terrain can gain a lot from knowing the direction towards their home. In a tree canopy, however, the direction "home" doesn't matter a whole lot if your path is constrained by paths down foliage, etc.
Therefore it's unlikely to be able to make any general statement about ants as a whole group, and better to investigate individual genera/species.
However, the Cataglyphis genus from the papers above live in a desert, and their dead reckoning abilities seem to be the ones most studied (there are many many more papers than the ones I pasted here, try searching Google Scholar for "path integration" ant or "path integration" Cataglyphis).


Are all mammals capable of sneezing? I only know dogs and humans sneeze... so do other mammals sneeze as well? Is it possibly an evolutionarily-determined immunological trigger?

This national geographic post discusses many mammals that sneeze. It doesn't come right out and say all, but suggests most mammals have a cough and sneeze reflex:

Mammal coughs and sneezes come from throat and nasal passages, respectively, says Bill Milsom, a comparative physiologist at the University of British Columbia.
Mammals, he says, are the only animals that process food in the mouth by chewing. In other types of animals, like reptiles, "food is swallowed whole or by chewing, and breathing is suspended during the event."

The same expert discusses non-mammals that sneeze, marine iguanas and fish.
You don't even need nerves or muscles to sneeze, per this Cell Press article

Sponges 'sneeze' without the benefit of nerves or muscles


In molecular docking, what is the difference between ligand and cofactor? In molecular docking aspect, what is the difference between the Ligand and Cofactor? Can a Cofactor be used like a ligand for docking with the target?

Ligand is an umbrella term for non-covalently bound anything. A cofactor, substrate, or allosteric regulator could be a ligand. This is a biochemical definition ligand, don't confuse it with a formal chemistry definition of ligand.

What's generally important about cofactors is they're not protein, but they're essential to the protein's biological activity. They could be a metal ion, organic complex, a vitamin, etc. Organic complexes that act as cofactors are also known as coenzymes. Cofactors that bind tightly or become covalently bound are called prosthetic groups. The protein without the required cofactors is called an apoenzyme, and with it's cofactors is called the holoenzyme.

Keep in mind to be on-topic for this site you need to do some research ahead of time and produce a focused, studied question. Wikipedia regularly provides the same answer verbatim!


Can box jellyfish see with their eyes? While normal jellyfish don't have any eyes, box jellyfish have 24 eyes.
Looking into my question on the internet, in one answer on Quora to the question Do jellyfish have eyes?, it is said that:

While box jellyfish have eyes, they cannot process images at all because they simply don't have the central nervous system to process images [Source: GRE Biology question I got right].

I heard somewhere though that box jellyfish do have a nervous system and they can see with their eyes.
I have found answers on Quora to be a bit hit and miss with their accuracy and wondered what the facts are.

This article from Live Science provides some insight (no pun intended) into box jellyfish eyes.
“Whereas we have one set of multi-purpose eyes that sense color, size, shape and light intensity, box jellyfish have four different types of special-purpose eyes. The most primitive set detects only light levels, but one set of eyes is more sophisticated and can detect the color and size of objects.”
This article from Science Daily may also help.
“The researchers examined the function of one of two types of "upper lens eyes," already known to form images, to work out just what those eyes can see and how well. It turns out that those four eyes cover precisely the visual field needed to see through the water's surface up into the world above.”


Up to date B cell review Where would I find an up to date (last 6-7 years max) review on B cells? I've tried searching through pubmed with filters, cochrane library, medline and various other resources including searching old questions. A textbook would be fine too, but I'm not sure which one would give me detailed information. I'm a BSc student studying immunology. I'm not trying to create a war of "best" answers, any answer that fits these criteria I will accept.

Cellular and Molecular Immunology by Abul Abbas et al. is pretty good, and you can't beat Charlie Janeway's Immunobiology either. Both will give a good introduction to B-cells, antibodies, BCR signaling, and how they fit in to the immune system's structure and function. I own earlier editions of both, and their different perspectives are good for getting a more holistic understanding of the field. Good luck in your studies, it's a fascinating subject!


Carl Sagan's ideas on the self-extermination of technological civilizations I've read (though I can't remember the source) that Carl Sagan speculated that intelligent life forms tend to evolve on various worlds, then exterminate themselves.

If true, then I'd like to learn more about this idea. Can anyone share any details on this? Do you know where I can read more about it?

It sounds like what you may be referring to is Fermi Paradox:

The Fermi paradox — or Fermi's paradox — is the apparent contradiction between high estimates of the probability of the existence of extraterrestrial civilizations, such as in the Drake equation, and the lack of evidence for such civilizations. The basic points of the argument, made by physicists Enrico Fermi (1901–1954) and Michael H. Hart (born 1932), are:

The Sun is a typical star, and there are billions of stars in the galaxy that are billions of years older
With high probability, some of these stars will have Earth-like planets, and if the earth is typical, some might develop intelligent life.
Some of these civilizations might develop interstellar travel, a step the Earth is investigating now.
Even at the slow pace of currently envisioned interstellar travel, the Milky Way galaxy could be completely traversed in about a million years.

-Wikipedia: The Fermi Paradox
In 1966, the book Intelligent Life in the Universe originally written by I.S. Shklovskii and extended by Carl Sagan "speculated that technological civilizations will either tend to destroy themselves within a century of developing interstellar communicative capability or master their self-destructive tendencies and survive for billion-year timescales."(4)
This review of the book written by E. J. Öpik, questions what, if any, factual information was presented.
In 1983, Sagan cowrote an article for the Quarterly Journal of the Royal Astronomical Society with William I. Newman entitled The Solipsist Approach to Extraterrestrial Intelligence that also addresses the issues of the self-extermination of technological civilizations.


What is the definition of Mitotic Index? Sometimes I find Mitotic Index defined as (i) the number of dividing cells over the number of non-dividing cells, other times as the (ii) the number of dividing cells over the total number of cells...

When reading a paper, which definition is more likely to be correct?

According to cancer.gov, it's the ratio of number of dividing cells to the number of cells not undergoing mitosis. This is equivalent to the number of dividing cells over the total number of cells.

Note that most papers, such as this one, report the mitotic index as a value from 0-100 (I.E. a percentage)


What is the exact definition of mitochondrial depolarization? As I understand as per literature reading and some khanacademy(https://www.youtube.com/watch?v=PtKAeihnbv0&t=315s):
Proton gradient := the gradient created when hydrogen ions moves to the intermembrane space from the mitochondrial matrix.
Mitochondrial membrane potential := the potential energy created by the proton gradient.
Does depolarization mean the loss of mitochondrial membrane potential? The lower the mitochondrial membrane potential, then the more depolarized the mitochondria?
So the way I defined proton gradient and mitochondrial potential is conceptually derived from the so-called proton-motive force used here https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2605959/ and also described here https://www.dummies.com/education/science/biology/the-proton-motive-force/ as an electrochemical force. Thus, my definition is from my rudimentary physico-chemical intuition.

The inner mitochondrial membrane is important for ATP synthesis (oxidative phosphorylation) to occur. Electron transport chains are situated on the inner mitochondrial membrane where electrons traverse the chain across proteins - causing protons to traverse into the mitochondrial matrix. Creating an electrochemical proton gradient.
This is a very interesting topic and is best understood with an explanation of the JC-1 Dye.
Explanation
Mitochondrial membrane potential changes - depending on cellular events.
The dye 'JC-1' is able to indicate mitochondrial membrane potential in different cells.

If there is a negative charge inside mitochondria then the monomers express green fluorescence.
If there is a positive charge inside mitochondria then the monomers form J-aggregates and now express red fluorescence.

The ratio between red & green florescence shows the mitochondrial membrane potential.

A low or negative mitochondrial membrane potential will show more green florescence.
A high or positive mitochondrial membrane potential will show more red florescence.

Example
One event that may influence mitochondrial membrane potential is an increase in reactive oxygen species.
Reactive oxygen species are molecules that damage cells but are also important to regulate cellular activities. Some examples are Hydrogen Peroxide or Superoxide.
In this image cells are stained with JC-1. The ratio of the dye is ~1:1 at basal. As the reactive oxygen species hydrogen peroxide is added and time continues, there is more green. Showing:

A low or negative mitochondrial membrane potential in each of the cells.


What is the "mucin net"? From Giulia Enders, Gut: The Inside Story of Our Body’s Most Underrated Organ

  Mucins are proteins that form the main constituent of mucus. They help provide hours of fascination and fun for young children who have just found out they can blow bubbles with their own spit. A more useful function is their ability to envelop our teeth and gums in a protective mucin net. We shoot them out of our salivary papillae like Spider-Man shoots webs from his wrists. These microscopic nets can catch bacteria before they have a chance to harm us. While the bad bacteria are caught in the net, antibacterial substances in our saliva can kill them off.

What is the mucin net the author refers to? No result is found when googling it.

From Wikipedia (emphasis mine):

  Mucins are a family of high molecular weight, heavily glycosylatedproteins (glycoconjugates) produced by epithelial tissues in most animals. Mucins' key characteristic is their ability to form gels; therefore they are a key component in most gel-like secretions, serving functions from lubrication to cell signalling to forming chemical barriers.

The "ability to form gel" is the key here. Also from Wikipedia:

  Gels are defined as a substantially dilute cross-linked system, which exhibits no flow when in the steady-state. By weight, gels are mostly liquid, yet they behave like solids due to a three-dimensional cross-linked network within the liquid.

So, a gel (and mucins are no exception) is composed of a liquid trapped in a 3D net, much like a sponge. This is the "mucin net" your book is referring to.


HIV and T helper cells As far as I know and could understand from reading about HIV, T helper cell is one of the main reasons to develop AIDS in patients infected with HIV virus, that because the absence of helper T cell suppresses the immune system because no T cell cytokines released to allow other white blood cells to attack or release antigens.

Q1. Did I understand it correctly?

Q2. Now if my understanding is correct, why don't scientists find a way to produce T cell cytokines in the lab? and then inject it to patients with HIV? wouldn't that in theory revive the immune system and perhaps heal them or at least make them live longer?

P.S. My knowledge is close to nothing in this topic, so excuse me if the question itself is wrong :)

Q1: Partially. T cells are important for the immune response through pathways other than cytokine release. Being activated by contact with another immune cell presenting their corresponding antigen, T cells proliferate and themselves activate their compatible B cell counterpart. These then produce antibodies specific to that antigen, the basis of the adaptive immune response (see figure below, from Wikipedia). The important part here is that this mechanism requires cell-to-cell contact, not simply cytokines. Without it, any pathogen for which memory B cells do not exist yet will not produce an adaptive immune response - and will persist if the infection is not cleared by the innate immune response.

Q2: I expect because merely injecting T cell cytokines would not be sufficient in order to replace the essential function of T cells. Aside from that, WYSIWYG's point about the general response is probably also true: the side effects would be horrendous.


Why does atheroma contain thromplastin/tissue factor? From my understanding, when the endothelial lining of arteries is damaged, atheroma is formed at the site of the damaged area. If the atheromas is ruptured, thromboplastin contained in atheroma is released into blood stream thus thrombus is formed after atheroma gets ruptured - this phenomenon is known as atherothrombosis. As a result, atheroma is characterised by its thrombogenic activity.

My question is, how come atheroma contains thromboplastin thus when it is damaged, thrombosis occurs? What was the source of this thromboplastin? Was it in the bloodstream? If thromboplastin was always present in the blood in which it entered into the atheroma during the formation of atheroma, why don't thrombosis occurs at the start when endothelial lining of the artery is damaged (without the need for an atheroma to rupture)?

I've read a couple papers and watched some videos on this topic. I've put one of my research below for reference to back up 'my understanding'.

  Rupture of the fibrous cap will typically release all the semiliquid
  material from the central portion of the atheroma. Because this
  material contains thromboplastin, it will trigger blood clotting, and
  a thrombus will develop at the site of intimal ulceration.

Tissue factor is present in subendothelial tissue and leukocytes - in this case this would be within the atheroma since the atheroma consists of damaged endothelium.

Tissue factor's presence in the subendotheilum in general implies that whenever the endothelium is damaged, tissue factor is released which promotes clotting at that site. Clotting starts after an atheroma ruptures because up until that point all the tissue factor is encased within the atheroma, protected from direct contact with the bloodstream - there is still no superficial injury to the endothelium to expose the underlying tissue factor that would signal the clotting cascade to begin. Therefore, clotting only starts after the atheroma ruptures and all the tissue factor stored within the atheroma is released into the blood vessel.

It is worth noting here that in homeostasis without any injury, the coagulation cascade and fibrinolytic pathways (the clot-lysis or pathways) are both active, but they balance out each other's effects. Disruption of this balance due to pathology, injury, or other insult causes an imbalance between the two pathways which the body seeks to rectify. The imbalance is what leads to clot lysis (in the case of wound healing - after the wound has healed) and clot formation (in the case of a new injury).

Sources:

https://www.ahajournals.org/doi/full/10.1161/01.CIR.94.6.1226
https://www.ahajournals.org/doi/full/10.1161/01.CIR.96.2.396
https://ascpt.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1752-8062.2011.00351.x


How does the sticky ends of foreign gene bind with its counterpart in the plasmid DNA if positions are not matching? Consider  a foreign gene with recognition sequence as GAATTC  for EcoR1. Now suppose that it is being cut at two palindromic sequence  to form sticky ends.

Here the sticky ends are formed such that its position is parallel to each other around the axis of DNA.

The plasmid DNA has a recognition sequence and is  being cut at a  site and as obvious would be  cut with the sticky  ends as  counterparts. If we join the foreign DNA to this vector DNA the problem of combining the DNA arises. How will we cope with this problem  or if I am going wrong can someone tell me where?

In the Google search engine I entered "ligation of sticky ends"; then I selected the "Images" tab. Here is the first result, which addresses your question exactly:

This originates from this website:
AddGene

Based on your question it sounds like you understand the basic rules of forming Watson-Crick base pairs; but your diagram and question omits the innate polarity of the sugar-phosphate backbone in DNA and RNA. The convention in depicting double-stranded DNA is that the "top" strand (sometimes referred to as "Watson") is written in the 5'-to-3' direction, reading from left to right. Since the two DNA strands are anti-parallel, it follows that the "bottom" strand (maybe nobody refers to it as "Crick" any longer?) is written in the 3'-to-5' direction -- if you are reading from left to right.  If you want to decode the biological information encoded in the bottom strand then you need to read it from right to left.

This is a long-winded way of saying that I usually note the 5' and 3'-ends on a drawing of DNA to emphasize this, and if I can figure out how to do so I will update the image.

Here is a slightly better version from Google:

Which is from this site: A WordPress Blog


How does yeast dissolve in sugar? There's this fascinating "kitchen experiment". Take a "brick" of baker's yeast (not dry yeast), and a couple teaspoons of sugar, put them together in a cup and stir together. There's no doubt both are solids: yeast is a firm block, you must use quite a bit of force initially to crush it and even then it should remain a rather thick paste. The sugar is crystals, nothing tricky about that. And then, within a minute or so of stirring, your cup contains only liquid - not entirely fluid like water, but not much thicker than cream. Solid+Solid -> Liquid.

What process leads to that? What happens with the baking yeast when it comes in contact with sugar, that it turns from solid to liquid, and releasing enough water to dissolve the sugar?

The whole process is called osmosis. In it there is the flow of liquid along a concentration gradient. Water then flows from the side which contains the low concentration of dissolved molecules (this can be salts or sugar for example) to the side with the higher concentration until it reached equilibrium. This principle is shown in the image below (all images from the Wikipeadia article on osmosis):

The blue dots are the dissolved material, the concentration is high on the right side and lower on the left. Through the dotted line in the middle (which is a semi-permeable membrane) only the solvent can pass to reach a concentration equilibrium. There is a pretty cool osmotic pressure simulator available on Molecular Logic which can also help understanding the principle.

And this is exactly what happens to the yeast cells. The sugar crystalls get dissolved (at least partly) by some of the humidity from the yeast block (this will not work with dried yeast) and form a highly concentrated sugar solution (also called hypertonic). The sugar concentration inside the cells is relatively low (called hypotonic). This leads to the effort to balance the concentration inside the cell and outside of it which then leads to a massive efflux of water from the cells. This goes so far, that the cell membranes break and the interior of the cells is released (nucleus, DNA, proteins and so on) and the sugar is completely dissolved in the released water. The reason why this mixture is so "gooey" afterwards is the DNA, which forms long, thick strains.

This method can be used in the lab to break up cells relatively gently without applying too much force.

When baking you should make sure, that your yeast is not coming directly into contact with undissolved sugar (or salt which works the same way), as this will kill a part of your yeast cells. However, for baking you usually dissolve the yeast in water or milk, so there is a huge excess of water which dissolves the sugar (or salt) and protects the cells. Addionally your yeast is much better distributed in the dough and gives better results.


How many ATP molecules are formed? What is the number of ATP molecules formed during the photosynthetic processes which consume 8 molecules of $\text{H}_2\text{O}$ due to noncyclic electron transport and subsequent photophosphorylation?

Assume that quinone cycle facilitates the transfer 4H+ to the lumen of thylakoid membrane for every two electrons passing through electron transport system and one ATP is formed for every 3H+ moving down the proton gradient by the mediation of F0F1-ATPase

MY ATTEMPT: In the lumen, due to hydrolysis 16 H+ are formed. Due to quinone cycle 32 H+ are taken from stroma and transferred to the lumen and NADP+ takes 48 H+ so in stroma there is deficiency of 80 and there are only 48 H+ in the lumen. If I assume that if there were initially hundred H+ on both sides then after non cyclic transport inside the lumen there are 148 H+ and in stroma there are 20 H+ so to have equilibrium then there should be 84 H+ on both side so total 64 H+ should travel then I am getting 64/3 ATP which is wrong. Where I am going wrong?

Screenshot of question paper

Sorry for the poor quality of the image, but its just as a reference for my answer.

You have made the question too complex. From the figure, we find that 1 H2O gives 2 H+ and 2 e-. 2 e-, through quinone cycle, provide 4 H+ i.e. total 6 H+ which form 6/3 = 2 ATP i.e.

1 H2O => 6 H+ => 2 ATP

Multiply this equation by 8 and you get:

8 H2O => 48 H+ => 16 ATP

So, 16 ATP should be the answer.

Reference:

Pradeep's: A textbook of Biology for Class XI, 2015, Vol. II, page IV/106


Can the human eye axial length decrease? I just have a quick question regarding the axial length of the eyeball.
I understand that the axial length of the eyeball grows up until your around 20 years of age which is why hypermetropia decreases with age but myopia doesn't. My question is, can the axial length of the eyeball decrease and does it naturally?
I know that certain conditions can cause the axial length to reduce such as very low pressure or disease but my question is regarding a normal healthy eye. I have found 2 studies which I will link below. In one of the articles it says that with current research we KNOW that the axial length decreases with age this same point was also in a different study based on the idea of a an emmetropizing mechanism for the adult eye but many people have criticised this study and due to this apparently the studies findings should be taken with a grain of salt but if this is the case why is it that many articles do say that the axial length reduces with age is there another study that shows this?
The other study that I will link below basically used lenses to create hyperopic and myopic defocus in participants and they measured the axial length of the eyeball after exposure to the blur. They found that the axial length did decrease in the case of myopic defocus and increased in the case of hyperopic defocus in order to create a clearer image by focusing the image on the retina but if this article provides definitive proof that the eye does in fact change its axial length then why is that people still say it doesn't happen?
Also do we know which mechanisms allow the eye to determine whether it is myopic defocus or hyperopic defocus that is presented to the retina?
Lastly, if the eye's axial length is able to reduce wouldn't myopia have a cure or at least a method to reduce it based on the reduction of the axial length of the eyeball?
Thank you for taking the time to read my question and I look forward to your answers!
https://www.karger.com/Article/Fulltext/317072
https://www.quora.com/How-can-the-axial-length-of-an-eye-decrease-as-they-say-that-it-does-with-ageing
https://iovs.arvojournals.org/article.aspx?articleid=2126435

Generally the axial length doesn't decrease:
graph
Although there is discussion of various conditions where it has been observed to decrease, i.e. nanophthalmos, microphthalmos, and retinoblastoma... A review of current research is here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5501611/ quote:
It is considered that the axial length reaches adult length by the age of 13 years, showing no further increase in length. Recent cross-sectional studies found that the axial length in older adults tended to be shorter, suggesting that it may decrease with aging. However, in a recent longitudinal study by He et al., slight increase of the axial length in adults (mean refractive error, −0.44 ± 2.21 diopters) was reported. Conversely, an increase in the axial length in adults with highly myopic eyes is common and has been previously shown in longitudinal studies [5–7]. However, to the best of our knowledge, there have been no studies directly comparing the increase in the axial length in adults with non-highly myopic eyes or highly myopic eyes. In addition, because previous studies on the axial length in highly myopic eyes have not compared between eyes with and without macular complications, their influence on the axial length remains unknown.
Can myopia be treated with a reduction in axial length? Presumably, yes it could, if opticians had figured a way to do it... Do you suggest that a drug or a medical intervention can flatten the entire eyeball a bit? perhaps a drug could but it would reduce the entire eyeball, you'd have to find a way to administer it. Apparently doctors haven't researched that option, but perhaps they will in future. Laser currently seems like a better way.
https://www.google.com/search?hl=en&biw=1706&bih=951&sxsrf=ALeKk01GuiHpl6-_fRp-Bg_UdsYOdqVzbg%3A1596509065944&ei=icsoX9aRObLMgweX6KboCQ&q=%22decrease+in+axial+length%22+of+optical
https://www.google.com/search?hl=en&biw=1706&bih=951&sxsrf=ALeKk03b75zOsA6CN_Ypqdv5v7hqfVWLbA%3A1596509091797&ei=o8soX8ySMIyqUP2dtvgI&q=%22reduction+in+axial+length%22+of+optical&oq=%22reduction+in+axial+length%22+of+optical


types of cells in a pharyngeal specimen I would like to ask what type of cells should someone expect in a pharyngeal smear, in a person, who is infected with a viral infection. Thank you a lot!

The tissue in the pharynx include:
Stratified squamous epithelium & mucus-producing glands.
However other cells that could be found would be other types of bacterial, is this what you're referencing?
Commonly scientists start with a gram stain to determine the classify the bacteria.
Gram+ bacteria have cell walls composed of thick layers of peptidoglycan. Gram+ cells stain purple when. Gram- bacteria have cell walls with a thin layer of peptidoglycan. Gram- bacteria stain pink.
The microbiome of a human consists of 100,000 billion bacteria. Therefore there are many types. E.g. Prevotella has been shown to be the most common type of bacteria in the human pharynx.
In a pharyngeal smear you would expect to find Stratified squamous epithelium, mucus-producing glands, bacteria and if a virus is present. Viral particles. This can be determined by RNA or DNA analysis.
E.g. COVID-19 is an RNA virus. If PCR analysis was completed on a sample obtained from a pharyngeal smear then we could confirm the presence of the aforementioned mammalian cells, bacteria and viral genetic material.


What is the genomic position of HLA-B*1502 variation? I've searched the position and SNP ID of HLA-B*1502 variation. However, I couldn't find that where this variant exactly located on genome or HLA-B gene.

HLA-B*1502 is not a SNP ID but rather, a name of an allele of HLA-B. This allele is made up of multiple mutations which can be found here.


How can skull size difference alone explain behavioral differences using evolutionary theory? I just started Robert Sapolsky lectures series on Youtube on Human behavior biology, and on the second lecture, at this point, he is explaining how evolutionary biology can be used to predict lots of animal behaviors just through the differences on the skull size of adult males and females.

He considers two groups of primates, one in which the skull of the adult male is quite bigger than the female and the other where they are about the same size. He then asks the student: "which group would display higher male aggression?" I am lost at this point. How can the size difference alone be used to answer that question? The students answer the question: "the first group (in which the males are bigger)", and the reason provided is that their body is built for it. Why and how?

Following up, the next question is: which of the species has more variability among males in reproductive success? The answer provided: "obviously, it is the first one because the males are aggressive for a reason, and that is they are competing for reproductive access." Couldn't it be that the second group had a biological variation in sperm productivity, that greatly outmatched the fight for reproductive access of the first group? I mean, how can it be this easy to conclude such a complicated process? Shouldn't you carefully consider millions of other things before concluding that one group will have higher reproductive variation simply because of differences in the size of the skulls?

Thanks!

Having a large difference between the sizes of the skulls between males and females is strong sign of sexual dimorphism, particularly of males that are larger in general.  Knowing which form of sexual dimorphism there is allows you to predict several other features. In particular large males is seen almost exclusively in animals in which the males fight each other for control of a harem AKA contest competition. This means high male aggression, since they are driving away other males. Since they drive away other males they have little to no sperm competition so they also don't need competitive sperm. These species also show drastic difference in male reproductive success, males with a harem produce many offspring males without one produce few to none.

https://www.intechopen.com/books/sexual-dimorphism/the-evolution-of-sexual-dimorphism-understanding-mechanisms-of-sexual-shape-differences


What happens in lasik operation? First of all,I am very bad at biology. So please bear if it sounds elementary.

I heard about lasik operation for reshaping cornea.

Assume the patient is suffering from myopia implying lens is thicker than expected.So if i think logically ,to correct the lens thickness ,lens must be reduced.

In lasik, do they cut the lens's tissue.If yes what happens to the part that is cut and if no then how exactly lens thickness is reduced?

There are two possible ways to perform refractive operation: first,  to perform the procedure on the cornea, the second - to exchange the crystalline lens with the artificial one.

The second approach is extremely rare, because the lens (1) is inside the eye and (2) it allows us to accommodate (=change the focus of vision). Thus, this method is relevant only to extremely high myops and people who have some degree of cataract (the clouding of the lens).

In "classic" myopia the eye is larger than "normal" one, and the lens thickness is less relevant in the terms of treatment.

Back to LASIK - the operation is performed on the cornea: for myopic eye the corneal thickness should be reduced, for hyperopic eye there are other protocols (special thickness reduction).


What type of genetic changes occurs when ovaries or uterus are removed from female body? I saw so many women which have present dermoid cysts in their ovaries or uteruses. Doctors operate and mostly the ovaries and uterus can not be saved and the doctors remove the ovaries or uterus.

Which type of genetic changes occur in such type of women?

welcome to biology stackexchange!

In the classical way we think of the body, there won't be a lot of genetic changes if the ovaries, uterus (or the testes for that matter) are removed from the body.

The main effect would be that the sex hormones that are produced in these organs would no longer be present and this would have a profound effect. So the broad answer might be 'no genetic effects but large endocrine changes'.  Endocrinology is the study of glands and their function in the body. Growing cysts, tumors as well as other effects seem like reasonable effects to see for such a drastic change in the body as removing the reproductive organs.

If I were hard pressed though probably this might end up with some small genetic effects compared to an individual who had never had the organs removed.  Mutations happen frequently in many of our tissues and also they respond to the environment to methylate the genome and modify it in non-genetic ways ( known as epigenetic effects).  This is purely conjecture but its also found that nearly everything has some effect on the cells.

hope this helps.


Horns in animals and birds Are there any carnivores with horns (whether extinct or currently alive)?

Do any flying creatures have horns?

By horns I mean horn like structure.

Males of the carnivorous Jackson's chameleon (Trioceros jacksonii) have three hornlike structures on their heads (also found in a couple of related species). From what I know, these are true horns, which means that they are pointed keratin-covered protrusions that have a core of living bone, see e.g. this website from Toronto Zoo (this page also claims that their horns show annual growth rings). However, there are many definitions of horns (some only consider the horns in Artiodactyla to be "true" horns), so you need to be specific in what you are asking for. Used casually, the antlers of Cervids or other similar structures, are often considered as horns.

As for birds, the closest thing to a horned bird I can think of are species of the Australian Cassowary (Casuarius). They have a bony crest on the top of their heads, which is covered by keratinous skin. However, the bony crest is supposed to be relatively soft and spongy, and can hardly be counted as a horn is the strict sense of the word.

(Southern cassowary, Casuarius casuarius, from Wikipedia)


Where does NADP+ come from? Trying to understand Photosynthesis better. I understand the NADP+ is reduced to NADPH in light dependent reactions and NADPH is then recycled back into NADP+ in the Calvin cycle. What I don't understand is where does the NADP+ come from initially?

Specifically I am asking with regards to its presence in the stroma within the chloroplasts of a plant cell. Where do plants get NADP+ from in order to assist in the production of sugar?

Niacin (better known as vitamin B3) and nicotinamide are both precursors of the coenzymes NAD and NADP in vivo. As you can see below, the biosynthesis of NADP+ proceeds as follows, when nicotinamide combines with a basic ingredient, a sugar phosphate:

The sugar phosphate precursor can also form AMP and GMP, also important molecules in the cell, when it reacts with the nucleobases adenine and guanine (A and G from the 'ladder' that bridges the DNA helix).

Just as an additional funfact, some bacteria such as Plasmodium falciparum and Toxoplasma gondii cannot synthesize nicotinamide themselves, because they lack the genes for it. Instead, they salvage the enzymes from eukaryotic hosts. This is an example of an incomplete biochemical toolkit giving rise to parasitism.


Why is the internal capsule dark in this transverse section of the brain? Why is the internal capsule dark in this transverse/horizontal section of the brain?
If it is white matter, then why isn't it white?

P. S. : Formalin was used for fixation.
Why the same color was not for remaining white matter.

Short answer
White matter is called white matter because it is relatively white compared to gray matter. However, in fixated specimens it is not as snowy white as in textbook pictures.

Background
The internal capsule is a paired V-shaped structure that is visible in horizontal brain slices (Fig. 1). It is a subcortical structure mainly consisting of fiber tracts connecting the cortex to the brainstem.

Fig. 1. Horizontal (transverse) brain slice showing internal capsule. source: Utah University

In Fig. 1 the structure is quite white'ish, but in the following two images you can see it is not always the case.

source: The Human Brain: Chapter 5: The Cerebral Hemispheres

Fig. 3. source: Medicos Notes

As you can see, the internal capsule is not always nice and white. Fig. 2 particularly shows a reddish taint of many white matter structures.

The internal capsule is well-vascularized (Schamann, 2003) and strokes in this region are associated with muscle weakness and loss in sensory sensitivity (source: Stanford Medicine). Hence, the red coloration may well be due to red blood cells that have not been completely washed out of the brain beore it was fixated. Also, non-specific coloring may happen over time in fixated specimens and many fixation artifacts can occur that lead to alterations in gross morphology (Chatterjee, 2014).

References
- Chatterjee, J Oral Maxillofac Pathol (2014); 18(S1): S111–6
- Schamann, Stroke (2003); 34: 2264-78


X-recessive disorders and genetic markers Please observe the following pedigree of a family with a x-recessive disease (bleeder disease).

The A's are genetic markers so close to the disease gene that recombination is negligible.

I understand it like this: They place markers that cut the DNA at the locus of the diseased gene. If you have the disease, your gene snip will be different in size than someone who does NOT have the disease and this will be visible on a gel.
So if A1 is the disease marker, how come II:1 is not affected? He only has 1 X-chromosome and has the A1 marker?

EDIT: Another problem:

Is the coming child affected? Here I don't understand how the mother A1,A1 is NOT affected when the child A1 is?! Obviously A1 is the diseased marker and the mother has two of them...So she should be sick? Unless it's spontaneous?

Am I misunderstanding something fundamentally?

Genetic markers don't cut the DNA. They're simply regions of DNA sequence that happen to be variable between individuals (see my answer to your previous question). They might be measured using restriction enzymes (i.e. RFLP) to identify the exact difference, but it's not the marker that's cutting DNA. Furthermore, they don't necessarily cause disease. They're used in pedigree analysis to find regions that are linked with various phenotypes, among which is disease. However, linkage does not imply causation, especially with so few individuals.

To answer your first question II:1 isn't in the affected family - he married into it. In the affected family, A1 has become linked with the disease mutation. It is not necessarily linked with the disease in other families.

This is also the answer to your second question. I:2 has A1 marker on one chromosome associated with the disease allele, and one that's not. II:3 presumably inherited an X chromosome with the disease allele.


Why do human ears have a lower boundary for the lowest energy perceivable signal than eyes? I am currently hearing a lecture about human machine interaction. The lecturer is not a biologist (neither am I, we are both computer scientists), but he makes some statements about biology which I think are questionable.

One statement was that the energy of the lowest perceivable signal for eyes is  and the energy of the lowest perceivable signal for ears is . He cites those values from the following (German) source:

  Schmidtke, H. et al. Handbuch der Ergonomie mit ergonomischen
  Konstruktionsrichtlinien und Methoden. Koblenz: Bundesamt für
  Wehrtechnik und Beschaffung (BWB)

  HdE (2002): 2.4.1, Abb. 2

  [KIT-Bibliothek: 2007 E 1808-1(2) (Präsenzexemplar)]

It is clear that those values vary from person to person. Assuming they don't vary too much, it is interesting to know why the human ear can detect signals with lower energy than the human eye.

According to my lecturer, the reason is because we can hear in all directions, but see only in one direction. He argues that hearing is much more important for this reason to detect predators, even if they are silent.

However, this argumentation seems very weak to me. I would rather think that there is a range in which "interesting" signals occur. If the interesting signals have lower energy for sound than for visual signals the ear adapted to this range.

I guess if the hypothesis of my lecturer is correct, then animals which can see in all directions would (always / very often) have much worse ears. If my hypothesis is correct, then there would be no significant difference in animals with "panorama-vision" and animals without in terms of lowest perceivable energy for ears and eyes (assuming fair comparisions; unfair would be comparing fish with land animals as the medium might play a big role).

Is there any source (written by somebody from biology, not form computer science) which makes a claim about this question?

Preamble. There is a lot of misunderstood science here and you are more than right for questioning the lecturers interpretation of these energy values; something the other answers do not discuss. The problem arises from a dodgy reference and a lot of conjecture.
In summary.

Light and sound cannot be compared energetically in a biological context.
Our ears probably don't hear lower energies than our eyes see to avoid prey.

Let us ignore the reference...
The reference is from BWB which is as far as I can tell a non peer reviewed federal technical publisher and that this is a textbook about ergonomics. But given its obscurity, it having never undergone peer review, it being not biologically scientific, it is safe to ignore from the context of a scientific biological topic. The fact it is in German doesn't help either.
If anyone can provide an open link to this reference or correct me on this I would be grateful. Google scholar turned up no hits other than a citation.
Let us give your lecturer the benefit of the doubt. This answer assumes that there are derived energy values for sight and sound as your lecturer suggested and that eyes sense higher energy than ears.
Is hearing omnidirectional to detect predation?
I'm going to use the term sensory setup to describe that our senses use fixed ears that hear omnidirectionally and forward facing directional eyes.

... hearing is much more important for this reason [omnidirectional] to detect predators, even if they are silent.

Let's flesh out this hypothesis so that it makes sense in practical terms.

A small movement is made by the predator. This generates some sound and some change in light. In the case of forward sighted animals, the sound is much more difficult to detect than the light would be as it contains less energy. The ears must compensate by detecting lower energy signals than the eyes would need to in order to detect the predator.

Before we question the physics, this biological hypothesis is very tough to swallow. Without citation I would say it is unreasonable conjecture.
Examples that contradict this hypothesis:

Gorillas have no natural predators or prey but have a very similar sensory setup to ours that helps social bonds.

Meerkats on the other hand rely on sentries that broadcast a series of bleats after spotting prey by sight. Other meerkats immediately hide when hearing this signal (interestingly, this call is mimicked by Drongos who steal the meerkat food that is abandoned in the panic) before checking if a predator is present. Meerkats have a similar sensory setup to ours.

There are other megafauna like deer that are prey for the big predators; predators that would have put ancestral humans on the menu. Deer-like prey animals rely heavily on near-omnidirectional eyesight and can angle their ears to focus on an area to hear stealthy predators. This is the "opposite" sensory setup that has the same conclusion of predator evasion.

Even those non-exhaustive examples makes the hypothesis questionable at best.

...there is a range in which "interesting" signals occur. If the interesting signals have lower energy for sound than for visual signals the ear adapted to this range.

This answer too is based on pure conjecture it seems, however it more aligns with how biology might work.
It is sensible to say evolution selected for animals that could detect noises and lights that, if reacted to, saved the organisms life to continue propagating. This hypothesis bypasses the idea that sound and light are comparable energetic signals too, which is good (discussed below).
This hypothesis also allows for various morphologies to have evolved depending on what an "interesting signal" is to that species.
Light vs Sound.
These aren't the same thing.
The elephant in the room of this question is that light and sound are non-comparable energies. This is due to source, speed, distance, medium, mechanisms for receiving the energy (eyes and ears) and most significantly in a biological context neural interpretation. These values are so abstract that even if an energy value is calculated, it is not in anyway quantitatively comparable in biological organisms. For example a really loud subsonic whale call is not the same as a small change of grass parted by a wolf as it sneaks up on you. One is absolutely essential for survival, the other is undetectable. Both could theoretically have the same "energy".
Note Frequencies are the biologically important part of the "energy" but must be considered as two different methods of acquiring sensory information. The difference between a chimp mating call and a territorial threat are very similar but for their frequency, and eating the delicious red berries compared to the toxic blue berries is also down to the frequency reflected from them!
There is little to no biological literature that uses energy values as sensory input. This would just obscure the actual important physical aspects of the sensory input values.

I hope that helped clear things up and accurately discussed your dis-satisfaction with your lecturers' hypothesis despite being months too late!


Do large animals often evolve into smaller animals? There are several examples where the largest animals were killed off preferentially due to a major ecological shift:

The KT extinction event
The Holocene extinction, as well as the major megafauna humans killed off

The common ancestor of modern mammals is thought to be "shrew-like" in size, and it differentiated into most of the large animal species in the world today.  I imagine that a similar statement can be made for dinosaurs.  In general it seems that a major extinction event is likely to be best weathered by smaller creatures which can later, over time, increase in size to fill the niche that larger animals, and evolution dictates it will be profitable to do so.

Does this limit large animals to only the branches of the tree of life?  Any given set of (Multicellular) species obviously share a common ancestor that is much smaller than them.  Is it possible for many species to share a common ancestor that is considerably larger than any of them?

Your question brings up several important issues with regards to the evolution of body size. The rationale for concluding that the ancestral mammal had a small body size is that all of the taxa in that area of the tree tend to be small. In contrast, if all of those taxa had been cow-sized, then the most parsimonious conclusion would be that the ancestral mammal was cow-sized.
Identification of ancestors is difficult
Identification of a fossil species as the most recent common ancestor of a pair of sister taxa is exceedingly difficult. The way that different species are diagnosed in fossils in by their unique derived characteristics (autapomorphies). So if a fossil is found with no autapomorphies, then it is plausibly an ancestor (i.e., at the split between two sister taxa). Some would argue that if you don't find any autapomorphies, then you just haven't looked closely enough.
Cope's Rule
The idea that lineages tend to evolve toward larger body size is known as Cope's Rule, named for the paleontologist Edward Drinker Cope. The success of Cope's Rule has been highly variable, with some lineages following and others not (Polly, 1998).
Some clades following Cope's Rule

Early reptiliomorphs (Laurin, 2004)
Pterodactyloidea (Hone and Benton, 2007)
Most Cambrian-Devonian marine invertebrates (Novack-Gottshall, 2008)
North American canids (Van Valkenburgh et al., 2004)
Mesozoic birds (Hone et al., 2008)

Some clades not following Cope's Rule

Early stegocephalians (Laurin, 2004)
"Rhamphorhynchoid" pterosaurs (Hone and Benton, 2007)
Mesozoic birds (Butler and Goswami, 2008)

Note that many results depend on the methods used.
Evidence from experimental evolution
Several studies have addressed body size evolution in vertebrates both directly and indirectly. MacArthur (1944a, 1944b) directly selected for large and small body mass in laboratory mice. Within 8 generations, mean body masses had increased or decreased by over 50%. Even when body mass is not directly selected upon, mass can change in a correlated way. Selection for high levels of voluntary activity has led to an approximately 25% reduction in body mass.
Based on these studies, evolution of body size (larger or smaller) is certainly possible within relatively few generations.


Can Alzheimer's disease be caused by Slow Prion infection? I found this claim in my study materials with explanation of amyloi plaques, in comparison to CJD (Creutzfeldt-Jakob Disease).

Its characteristic are

Long doubling time of at least 5.2 days (I think this means the time it takes to double the amount of prions in the target organ)
NO Cypopathic Effect (CPE) in vitro
Long incubation period (about 30 years)
Vacuolation of neurons, amyloid-like plaques
Deficient immunity
Deficient immunoresponse
Deficient Interferen (IFN) production

so this suggests me that the person with infection at a young age can have the disease then at an old age.
Other possible agent could be virus, but it seems that prion is the major one.

Can Alzheimer's disease be caused primarily by Slow Prion infection?

Dr Yong in the paper titled Prion, The unconventional slow Infectious agent states that the formation of amyloid plaque which is a major contributor to Alzheimer's disease is a unconventionally slow infectious disease (Prion). Some papers have also pointed out the similarities between Alzheimers and prion disorders (reference) Cerebral amyloid plaques have also been identified in scrapie which is caused by a Prion. Discovery of a novel prion disorder (reference) with peripheral symptoms have led researchers to believe that protein misfolding, is the basis for most neuro-degenerative diseases, including Alzheimer's disease and Parkinson's disease.

With regard to your question, Alzheimer's has not been completely classified as a prion disorder as of now, but seeing that amyloid plaque formation (reference) and Creutzfeldt-Jakob disease (CJD) (a form of dementia) (reference) have been identified as being part of Prion disorders, it is highly likely that Alzheimer's is too.


Quantitative Differences : DNA and Gene After HGP, we are not having many databases which consist of several notepad files of ATCG....

Can we distinguish quantitatively a given A,T,C and G stretch as DNA or Gene?

I interpret your question as: Given a stretch of DNA sequence, can we determine if it encodes a gene? My summary of the answer would be: "Sometimes".

The problem you ask about is called "Gene prediction" and is described in some detail by Wikipedia:  http://en.wikipedia.org/wiki/Gene_prediction

The most basic indication that a gene may exist is the presence of an "Open Reading Frame" (ORF). An ORF is a stretch of DNA from which a single protein may be produced.  However, an ORF is not strictly required for a gene (as not all genes encode proteins), and not all ORFs are genes. There are many software tools for gene prediction available which use different rules to predict if a given region of DNA is functional (contains a gene or a regulatory element). They may be usable on any kind of DNA sequence, or on sequences from certain organisms only, depending on the program.

Two commmonly used gene prediction tool are GLIMMER (http://www.ncbi.nlm.nih.gov/genomes/MICROBES/glimmer_3.cgi, used for microbial genomes) and GeneMark (http://opal.biology.gatech.edu/gmhmm2_prok.cgi). See also http://en.wikipedia.org/wiki/Gene_prediction

As a quick check, you may also use NCBI BLAST (http://blast.ncbi.nlm.nih.gov/Blast.cgi) to see if your sequence aligns to a known gene.


How many consecutive cell divisions are required to form the adult human body from the single cell zygote? The preferred question would have been what is the total number of cells in a full term human foetus and how many cell divisions are required to reach that number. However estimates of total cell numbers in foetus could not be found. From the abstract of the July 5, 2013 article published in Annals of Human Biology, the adult human body consists of approximately $3.72 \times 10^{13}$ cells (37.2 Trillion). The question is: what would be the approximate number of cell divisions required to reach that number (Ignoring the fact that different tissues may reach full differentiation at different times)?

Sounds like just a math problem if you allow that cells dying and different rates of division are not to be accounted for:

$2^N = 40 \times 10^{12}$

$log_2(40 \times 10^{12}) = N$

$N = 45.185$

so 45 or so divisions.

is that what you are looking for?


Last-ditch efforts to maintain thermal homeostasis I was in the gym's steam-room today and a thought occurred to me: have I truly thwarted all possible mechanisms for maintaining thermal homeostasis?

There's sweating, which is thwarted because the steam-room's atmosphere is as close to 100% humidity as possible, so there's almost no evaporative cooling.

There's convection, which is thwarted because the ambient temperature is above normal body temperature.

And I can't get rid of heat by exhaling, because every lungful of air I inhale is already above normal body temperature.

I think that, eventually, I should go into hyperthermia, but beside the above, are there any other last-ditch attempts to lower core temperature that my body could take?

Another factor at play here is the cardiovascular system.  Biro, Masudo, et al (2003) wrote an article about the benefits of the induction of systemic vasodilation for those with congestive heart failure.  This may be a short-term adaptation of the body stemming from the reduced ability to sweat in those conditions, or it may be a harbinger of the more serious circulation changes below.

Epstein and Roberts (2011) explain how the eventual results of heatstroke (which isn't the phenomenon that you are describing, but a sauna might induce some of the features of these same pathways) can cause a circulatory collapse due to an initial overtaxing of the circulatory system to compensate as well as the activation of certain heat shock proteins.

There are a lot of other references out there on sauna physiology, but many are not in evidence-based journals, so you can make your own decisions on those.

One factor that I didn't find mentioned explicitly was the basal metabolic rate.  It's probably safe to assume that the body will limit its own processes and reactions which produce heat.  I'm not clear on the extent to which factors such as the level of interleukins, etc. would play a role as they do in fever regulation.


If hands are folded with both index fingers parallel, they will come closer and touch eventually? I have a question out of curiosity. It is just something I found out/discovered:
if I fold my hands into each and let my two index fingers (see picture) be in parallel then they will eventually come closer to each other and touch.

How can this be explained?

Another thing I found out: if I fold my fingers on my left hand slightly and then with my right hand squeeze the wrist of my left hand (see picture), then the fingers of the left hand will fold more and more. Is this a coincidence of general?

The easy way to explai the first phenomenon is that at rest, your fingers - all of them - curl. Relax on your bed on your back. No matter what direction your hands face, they will curl inward as if loosely holding an egg. That's the anatominal position of the hands at rest, because the finger flexors are stronger than the extendors. So once you set the finfers up, you'll tire of keeping them extended, they'll start  to relax, and in doing so, will tough.

If I'm understanding the second example, that's because the flexor tendons for your fingers are actually in your forearm. Squeeze them and it shortens the tendons causing flexion.


Why some cells don't produce purines? It is said that erythrocytes, polymorphonuclear leukocytes and brain cannot produce purines. And the reason given as per this site is:

  Human brain tissue has a low level of PRPP glutamyl amidotransferase (reaction Image, Figure 33–2) and hence depends in part on exogenous purines. Erythrocytes and polymorphonuclear leukocytes cannot synthesize 5-phosphoribosylamine (structure III, Figure 33–2) and therefore utilize exogenous purines to form nucleotides.

My question is why do these cells don't produce the required enzymes for the synthesis of purines? What could be the functional significance for such absence?

My attempt : At first I thought that Erythrocytes as such don't have nucleus so they don't need purine synthesis for cell division , but I don't understand why then they need purines from external source( as said in the above site). Also brain cells are neurons and neuroglia, of which former doesn't divide( except in some areas of brain) but they too need purines.
 The later divide but they don't produce required enzyme. Why?

So my questions are:

Why do cells which don't replicate need purines?( May be for formation of Coenzymes , correct me if Iam wrong)
Why do the cells which divide too don't produce required proteins(enzymes)?

I am going to throw this idea out there. I was unable to find it stated anywhere so far.

There are several very ancient parasites that make their homes inside erythrocytes and neutrophils. Plasmodium is one, the causative agent of malaria. Trypanosoma is another. These things are ancient degenerate eukaryotes and their lifestyle as intracellular parasites is probably ancient too.

These things cannot make purines either but they need them and they need a lot of them, because they are reproducing fast. If the host cell does not have the machinery to make purines, that machinery cannot be hijacked by the parasite to really crank out the purines.  The best they can do is hijack the salvage pathways these cells have.

From https://www.ncbi.nlm.nih.gov/pmc/articles/PMC259377/

  The apparent competition between parasites and host cells for available purines suggests that depletion of extracellular purines should be considered as an approach to treating extracellular trypanosome infections.

From https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4405406/

  Plasmodium species parasites, like many other protozoan parasites, are purine auxotrophs, unable to perform de novo purine biosynthesis. They rely on the host to provide purines

That does not explain brain cells  - unless lack of purine synthesis is a defense of brain cells against Toxoplasma, yet another eukaryotic parasite.

Nothing would please me more than for someone to poke holes in this theory. A prediction from this theory: erythryocytes in all animals should lack purine synthesis - including birds, who suffer from a form of malaria and whose erythrocytes do have nuclei.


Can anybody identify this plant? I'm from Brazil. And I have this plant at home.

Can anybody identify this plant?

It's an Epiphyllum Oxypetalum. Epi is greek for around (epi-center) and phyto is plant, epiphytes are plants that live on other plants, for example rainforest plants that grow on the canopy of tall trees.

There are lots of hybrids and lots of colors.


Molecular psychology/psychiatry literature/articles I am new biology student which is on molecular biology subject on university. I would like to know something about genetic related to neurobiology, and certainly molecular psychiatry/psychology, perhaps evolution psychology. But i dont know where to start.

Can anybody give me type to literature/articles for beginners?

For the neurobiology I'd recommend to read: Mapping the Mind and The Quest for Conscioussness , but these are kind of long books.

For shorter articles as (merely) an introduction, I'd recommend:

Manoli, D. S., Meissner, G. W., & Baker, B. S. (2006). Blueprints for behavior: genetic specification of neural circuitry for innate behaviors. Trends in Neurosciences, 29(8), 444–451. https://doi.org/10.1016/j.tins.2006.06.006

Good philosphical and historical viewpoint can also be found here:

Marler, P. (2004). Innateness and the instinct to learn. Anais Da Academia Brasileira de Ciencias, 76(2), 189–200. https://doi.org/10.1590/S0001-37652004000200002

For something more practical: The Little Black Book of Neuropsychology.

Looking forward to suggestions by others :)


Does fasting improves immunity? I have heard that fasting causes regeneration of memory cells(B- and T-lymphocytes) thereby improving immunity.Is this true? If yes, how?

Interestingly this effect seems to be true - there is one paper which claims that fasting for three days leads to the depletion of unused (and especially damaged) immune cells to save energy. When food is back at normal rates, the body starts to renew these cells which have been depleted before. This process also seems to enhance the self-renewal process of stem cells which start to replicate and further differentiate.

This works like in the figure below (from the paper below):

Although this renews a part of the immune cells, I wouldn't say that this improves the immune system. I think that here mostly naive cells (which haven't) come in contact with an antigen are shut off. If you deplete memory cells (which had this contact) this would be counterproductive, since these cells are important for a fast immune response.

Prolonged Fasting Reduces IGF-1/PKA to Promote
Hematopoietic-Stem-Cell-Based Regeneration and Reverse
Immunosuppression

There is as well an article in Science Daily, which summarizes the original paper. It can be found here.


Does destroying a virus envelope make the virus inactive? Some viruses have a lipid envelope around their protein capsid. The envelope can be dissolved with soap, but does that still leave the capsid and interior genetic material intact? If so, is the virus still active?

Enveloped RNA viruses will get inactivated quickly without a membrane. RNase is a ubiquitous enzyme that would quickly digest any exposed genetic material.
Via https://www.neb.com/tools-and-resources/usage-guidelines/avoiding-ribonuclease-contamination:

RNases are found in all cell types and organisms from prokaryotes to eukaryotes. These enzymes generally have very high specific activity, meaning tiny amounts of contamination in an RNA sample is sufficient to destroy the RNA. The major sources of RNase contamination in a typical laboratory include:

Aqueous solutions, reagents used in experiments
Environmental exposure, RNases are in the air, most surfaces and dust
Human contact with hands and skin

Without a membrane (and any associated receptor-binding proteins), the genetic material of an enveloped virus would not normally have a way to get incorporated into and infect the host cell, in any case.
Your question is about enveloped viruses, specifically, but there is an interesting exception of a kind, so-called viroids that infect plant cells. These have no capsid or protein envelope, but are still infectious.


What's the amount of blood passing through heart every second at Max Heart Rate? How many mL of blood passes through the heart every second at maximum heart rate?

Is there any formula to calculate the amount of blood flowing through the heart per sec at say for example 70% of the max heart rate?

I didn't ask
Let's assume that the person in question is a fit 23 yo Caucasian male(if there are differences for various ethnicities)

· Heart Beat Rate

  The normal heart has a rate of 72 beats per minute, but in infants the
  rate may be as high as 120 beats, and in children about 90 beats, per
  minute.

Lets say the heart beats at an average pace of 70 bpm (beats per minute)
(~100.000 times a day)

· Cardiac Output

Volume of blood pumped by the heart in a minute.

CO = HR X SV (heart rate multiplied by the stroke volume)

Cardiac output is the volume of blood being pumped by the heart in a minute. It is equal to the heart rate multiplied by the stroke volume. So if there are 70 beats per minute, and 70 ml blood is ejected with each beat of the heart, the cardiac output is 4900 ml/minute. This value is typical for an average adult at rest, although cardiac output may reach up to 30 liters/ minute during extreme exercise.

So for an average adult at rest the estimate is around 5 litres of blood per minute (~1.33 gallons)

· Cardiac Outout / second

There are 60 seconds in a minute so simply :
divide amount pumped per minute by 60

0,083̅3̅  L of blood per second
(83,33 mL of blood per second)

But this is just an average with specific variables defined... so maybe you have to take into account other factors that may vary this value.

· Factors Affecting Cardiac Output

  Factors affecting cardiac output in a healthy but untrained individual
  could be:

Increase/ decreased in heart rate
Change of posture
Sympathetic nervous system activity
Parasympathetic nervous system activity can also affect cardiac output.

  Heart rate can vary by a factor of approximately 3, between 60 and 180
  beats per minute, whilst stroke volume can vary between 70 and 120 ml,
  a factor of only 1.5.

You can read more here & here


Would short term increases in oxygen lead to beneficial effects? After some thinking, I am wondering if having a 30% atmospheric oxygen concentration (or some other concentration) for a short time would increase the regeneration of energy in a body? It seems like it does have some mental effects, but I haven't found any other positive effects on the body.

Humans are pretty well suited to a 21% oxygen atmosphere (at STP). It's what our lungs are used to dealing with, and it's what brings the appropriate amount of oxygen to our brain (in particular, most organs are more forgiving, although not a lot more).

A lower concentration grows quickly and strictly deleterious, leading in short order to hypoxia, subsequently death. A higher concentration is also deleterious, leading initially to an oxygen high (as seen with Oxygen Bars), but also causing vision problems, seizures and death.

Oxygen is also highly reactive, and increased concentrations for even short bursts could, if frequent, lead to cancers, especially lung cancer. (The primary cause of lung cancer prior to asbestos and smoking? Breathing.).

There are cases in which increased oxygen concentration can be beneficial, but they are rare and specialised.


History of ideas about the form of the genetic code In preparing a lecture on mRNA translation and the genetic code, I remembered a talk given at a symposium where they mentioned the origin of the code and how, before the code was established, various other mathematical possibilities were proposed that turned out to be incorrect.

Does anyone know about these alternative proposals?

Before it was established that there was a triplet, non-overlapping, comma-less genetic code* for what at that time were thought to be only 20† amino acids, there was uncetainty about:

The codon size (must be more than 2, but...)
Whether the codons overlapped (e.g. in a stretch ABCDEFG with triplet codons, whether ABC, BCD, CDE etc were the codons)
Whether there were ‘commas’ as demarcation betwen different codons

These and other problems were disscussed by Crick et al. in Nature (1961) 192 1227–1232. There is an introductory gloss of this on Scitable, with a link to free-view of the original paper.

Footnotes

*We now know there are variants on the standard genetic code, but all the codes have the characteristics mentioned.

†In addition to the standard 20 amino acids stop codons can be subverted in certain circumstances to encode selenocysteine and, in some bacteria, pyrrolysine.


Number of serotonergic neurons in mouse/rat DRN What is the (approximate) number of serotonergic neurons in the dorsal raphe nucleus (DRN) of mice and rats?

The mouse and rat dorsal raphe nuclei contain about 9000 and about 11.500 serotonergic neurons, respectively. It turns out the corresponding 1988 and 1982 references are widely cited - directly as well as indirectly. I could not find any newer data/evaluations.