text:
How is the flicker fusion rate interpreted as an on-off rate?
In our experiment we use a fly to determine the flicker fusion frequency, i.e., that frequency where the fly starts perceiving a pulsating light as a constant light source. The human eye also has a flicker fusion frequency. For example, most people cannot see the flickering of a fluorescent tube, which equals the main frequency (60 Hz in Europe & USA).
Our experimental light source needs two input durations, namely how long the light is ON and how long it is OFF for. The input is provided in ms. From what I found out so far is that the unit Hz equals the frame rate, namely pictures per second. So a frame rate of 50 Hz is 50 pictures during 1 second.
But in my experiment it is about flashes of light, namely a light phase and a dark phase. Does the dark phase then count as a picture? So what I mean is whether 50 Hz represents 50 times lights ON + 50 lights OFF, or does it mean 25 times lights ON and 25 OFF?
Also, how long is then each light pulse?
My assumption is:
50 Hz are 25 lights on and 25 lights off within 1 second.
50 pictures in 1000 ms
1 picture per 20 ms
20 ms / 2 = 10 ms lights ON, 10 ms lights OFF

Besides the fly, I don't think the main question has anything to do with biology. I'm voting to close as off topic

@theforestecologist - I think questions like this are not Bio per se, but frequencies and cycle times are so fundamentally important in the visual and acoustical sciences that I strongly argue to keep this post alive. Biologists often don't receive training in signal processing, although it's an essential part of some pretty big disciplines. I have attempted to make the question biologically more interesting too, adding the key term 'flicker fusion' in there + a link

@AliceD I agree that they are important, and I can see why the OP asked this question here. However, unless the OP edits in a way to make the question more biologically relevant, I think it's off topic. This is more for their sake b/c they could likely get good answers if asked elsewhere. However, I just saw that you provided a perfectly viable and useful answer (+1), so that seems moot at this point :p. But even your answer does not mention anything biological. This whole Q&A would still probably be more appropriate on Physics.SE in my opinion.

If questions about chromatography get closed, I can't imagine how this one would be on-topic.

@canadianer I think everyone here is biased toward their own interests. The question here is so fundamentally linked to my areas of research I find it on topic. Others outside this field think differently. That's OK.

@AliceD I disagree, it's not okay. If this or any other question is about biology then it shouldn't be closed because some people don't realize the connection. I'm not sure what can be done about this, though.

@canadianer - it's not that black and white I'm afraid. I've added substantial biological context in the question when 2 votes were in, and despite these efforts  it still got closed.

@AliceD That suggests to me that we have a problem with the way we close questions. I would re-iterate my point that if a question is about biology it should be on-topic on this site.

Also, mains frequency in North America is 60 Hz.

Short answer
A light flashing at 50 Hz means there are 50 flashes of light per second. The unit hertz means cycles per second. 1 cycle is the time it takes for the light to be ON and OFF. 50 Hz cycle time means a cycle time of 20 ms. If light ON and OFF times are equal, then the ON and OFF times are both 10 ms each.
Background
The unit hertz (Hz) is a frequency unit in the International System of Units (SI) and is defined as

one cycle per second

A textbook example where the unit Hz finds its use is a sine wave (Fig. 1). 1 cycle per second would be 1 Hz. A cycle, as can be seen in the figure, is a complete wave consisting of a positive phase followed by a negative phase.
In the right panel of figure 1, a square wave is shown. Again, a cycle time is the time it takes for one complete square wave to develop, i.e. a positive phase and a negative one.

Fig. 1. Sine wave (left) and square wave (right) sources: Simon Fraser University, Integrated Publishing
Now, in your example, you can depict the lights ON as the positive block in the square wave in Fig. 1 above, and the lights OFF as the negative phase. Together (light ON + OFF phases) they form one cycle. So a light pulsing at 50 Hz means it flashes ON and OFF 50 times.
The cycle time then is 1 second/50 = 20 ms. If we assume that the ON and OFF times are equal, which they obviously do not have to be, then light ON is 10 ms, lights OFF is 10 ms.
On the wikipedia page on the hertz unit, a flashing light example is actually illustrated and explained.


text:
How much do arteries expand during pulse?
Arteries expand during a pulse. The amount of expansion may differ from artery to artery. How much do arteries expand? I understand it might be a range. Inform the same. Even values specific to some arteries will be fine.

I assume you're asking about humans -- is this true, or are you asking more broadly? Also, please indicate some of your own research for this question. (See How do I ask a good question for some tips for writing good questions on Bio.SE).

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
How do AC magnetic fields affect tissues?
AC magnetic field refers to an oscillating magnetic field. How do AC magnetic fields affect human tissues in vivo?

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
How many animals inhabit the United States?
How many animals inhabit the United States and its waters? Not the number of species, but the number of individual animals. And since animals are diverse, maybe we can limit the estimate to just vertebrates - domesticated and wild. I totally get that nobody knows the answer to this, but I'm wondering if anyone has made an estimate, or if there are sources from which I could piecemeal an estimate.
Thank you!

Perhaps you could try here to start calculating a rough estimate.

Related post: How many organisms have ever lived on Earth?

If you are interested in the number of pets, this can be found here: http://www.aspca.org/animal-homelessness/shelter-intake-and-surrender/pet-statistics (e.g.:It's estimated that 70-80 million dogs and 74-96 million cats are owned in the United States.)

Do humans count?


text:
Motile egg cells
According to the Wikipedia article on anisogamy, some types of this form of sexual reproduction involve motile egg cells, i.e. they're capable of movement under their own power, just like sperm cells.
Is the "egg cells can be motile" part true? If so, what examples of anisogamous species exhibit this? Because this could have tremendous implications on how to define "male" and "female"; having motile egg cells means that you could have a hypothetical species in which it's the female that "inseminates" the male with her gamete(s), with the sexes being assigned based on which gamete absorbs the other as in oogamous reproduction.

Eggs of Laminaria angustata are flagellated.

No other examples?

This article mentions that rabbit eggs can move quite far: https://academic.oup.com/biolinnean/article/120/1/1/2864987


text:
Can the characteristics of an offspring depend on the locality of its conception also?
Transfer of characteristics from a parent to its offspring is explained in biology. When an adult male and female (of humans) who are displaced from their local environment to another (say, a different continent)for a considerable period of time, conceive and give birth to a baby, the newborn also shows some traits related to the people of the new locality . How is this explained?

Do you have a reference of this actually happening ? Which traits are we talking about here ?

Kindly add little more specifics into the question, such as

What do you mean by considerable period of time?
What kind of organism are you referring to?

Off-springs are defined by the genes of their parents. Not the country they live in. Your claim (unless you can show a very good reference for it) is primarily opinion based.

Are those human offspring and parents ? Can you give examples of traits that a child of Asian parents would get from being conceived in Africa ?

maternal effects do exist (where offspring characteristics are partly determined by the phenotype of the mother, which in turn might be affected by the environment during pregnancy), but that doesn't sound like what you have in mind ...

I meant visible traits like skin and hair colour, their texture, even facial features (the bone structure) to an extent. This is just a personal observation, no references.

@beena benny if you observe a child who has traits of a local as well as the parents, keep in mind that marriage is a legal concept, not a biological one.

@beenabenny In that case it seems like the first question ought to be "DOES a child's traits depend on where they were conceived", and you ought to know that as far as current knowledge in biology and genetics go, for traits such as hair colour, texture and bone structure the answer is "they don't". If you have more details on your personal observations that could be useful; maybe we could find out how the conclusions you drew from those observations are wrong, or they could point us to a phenomenon we hadn't thought about or weren't aware of and thus help answer the question better.

Nurture vs. Nature

Genetic makeup can not vary with the place of conception, but certainly the way genes are expressed can change with change in place of conception. Such changes are called epigenetical changes. Epigenetic change is switching on or off of genes which can be achieved by various method:-
1)  DNA methylation
2)  Histone modification and
3) RNA associated gene silencing
In theory, change in place of conception, can result in silencing or activation of differential genes in foetus. In fact there is this nice article which discusses how maternal nutrition switches on or off six genes in foetus 1 and [2]. Even stress can cause such epigenetic changes [3]. These environment triggered changes may also result in change of phenotype. For example in mice, the agouti viable yellow (Avy) gene which is a retrotransposon and is found in upstream of the agouti gene. The Avy elements are generally methylated and hence are shut off but in Agouti mouse, they are unmethylated and therefore switched on, which leads to a yellow coat.Though this methylation or unmethylation in agouti mice has not been proved to be a result of environmental factor, but in a strict theoretical sense this can happen (with some or other phenotypic trait)

1] Painter R.C., Roseboom T.J., Bleker O.P. Prenatal exposure to the Dutch famine and disease in later life: an overview. Reproductive Toxicology 20, 345-52 (2005).
2] Maternal nutrition at conception modulate DNA methylation of human metastatic epialleles(NCBI)
3] Exposure to stress even before conception cause genetic changes to offspring(science daily)

Your answer is a good one, but keep in mind OP's clarification in comments - they're talking about "visible traits like skin and hair colour, their texture, even facial features (the bone structure) to an extent." Do epigenetic modifications typically lead to changes in that kind of trait ?

I probably missed out the comment section while answering the question. I will edit my question to include the aspect of visible traits.


text:
Terminology regarding sensory receptors
I was recently asked the following question:

Compare the following pairs of receptors in the same
  sensory system. Include in your discussion:

The distribution in the
  sensory epithelium;
What kind of stimulus is effective in activating
  them;
Their physiological response properties, function and central
  connections.

Rods and cones
Pacinian corpuscles and free nerve endings

In particular, I was not sure what the sensory epithelium is. Is it getting at the fact that Pacinian corpsucles are subcutaneous, while free nerve endings are cutaneous and that cones are centralized at the fovea?
Alos, I am not sure what their "physiological response properties" refers to. Since they are receptors, would their responses just be the output (i.e. peripheral/foveal vision and vibration/pain sense)?

The distribution in the sensory epithelium indeed refers to the location of the different receptors. And indeed, you are also right that cones are concentrated in the fovea, and rods are mostly found more eccentrically in the retina (Kolb, 2012. I would say the free nerve endings are situated just below the epidermis, and the PCs in deeper layers of the dermis (Fig. 1). But check your notes on what your prof. wishes to hear about this.

Fig. 1. Skin receptors. source: Neupsy Key
The physiological response properties of receptors is not their output per se. It is the way they respond to stimuli, that includes their output, but also includes the sensation of physical stimuli through second messenger systems or otherwise, and eventually the output. Kolb (2012 goes into detail on the physiology of photoreceptors in quite some detail and for the physiology of touch receptors I would refer to Dougherty in Neuroscience online.
References
- Dougherty, Somatosensory Systems. in: Neuroscience online. University of Texas
- Kolb, Photoreceptors. In: Webvision. The Organization of the Retina and Visual System (2012)


text:
correction of read counts for spikes
I have 4 RNA-seq samples (1st is control and the other 3 are treatments) and 5 spikes. I used different concentrations for 5 spikes but over different samples, I used similar concentration. for example I used similar concentration for spike1 in 4 samples. and this is the case for the rest of spikes. I am trying to normalize the read counts for the spike. do you guys know how to do that?
this is what I have done so far:
I counted the spikes in different samples and and got the ration of them (treatments compared to the control for all spikes). the ratio is as expected (looking at the concentration of spikes).
one thing that I can do to correct the read counts for spikes is to multiply by the ratio between samples. but I am not sure if that is the right way.

The most common and simplest normalization method for spikes is the Total Count Normalization. It's actually what you're doing here, so what you're doing here is correct. TCM is a useful algorithm for normalizing sequencing depth, that includes your spike amounts.

https://academic.oup.com/bib/article-lookup/doi/10.1093/bib/bbs046

has reference on the TCM normalization.

Gene counts are divided by the total number of mapped reads (or library size) associated with their lane and multiplied by the mean total count across all the samples of the dataset.

The paper doesn't talk about spike-in controls, but the idea is the same. We'd use the spike-in controls for estimating the difference in sequence depth (instead of the whole data set).


text:
Where does new blood comes from when penis get erected?
In Humans, During sexual arousal in males, his penis will get erected with blood.
Where does this new blood coming to fill his penis which is required for erection ?

There are areas in our body which act as reservoir for blood , so when a body part needs excess of it can be diverted to it. ex: lungs.

see this : http://biology.stackexchange.com/questions/20174/where-does-extra-blood-come-from-to-fill-your-muscles-during-exercise?noredirect=1&lq=1


text:
Are mosquitos attracted to farts?
According to wikipedia, female mosquitos (the ones that bite) use the protein in our blood to provide nutrition for their eggs.
I was lying in bed the other day with mosquito's bothering me, and had one coming. So I thought, this will teach these no-good insects to be bothering me! But then it struck me that they might actually like it because of the protein.
Since they're after the protein in our blood, and I'd imagine that a fart is a very creamy soup of proteins indeed, maybe it won't chase them away.
So I held it in. Did I do the right thing?

Lol farts are not a creamy soup of protein. http://www.oddee.com/item_98612.aspx

"I'd imagine that a fart is a very creamy soup of proteins" you sure you're talking about fart here? ;)

I'm voting to close this question as off-topic because we are trying to maintain a scientific stack. Far fetched trivial questions on gaseous (or other rearward O.o) output do not belong here imo.

It is scientific. Just because it is an often humorized subject does NOT invalidate its scientific significance. Why the downvote?

This is a biology forum - It's only natural that such subjects will occur now and then. And what's the point of using unfamiliar terms like 'flatulence' which nobody uses or understands anyways? @AliceD

@MarcoPrins do you mean, in a way, why do we call brain as 'encephalon' even if no layman uses or understands it anyways? Anyways, I downvoted because the base of your question "I'd imagine that a fart is a very creamy soup of proteins" is wrong.

If you rewrote the question with a ton more maturity AND demonstrated that you've done some previous  research of your own (i.e., determining that farts aren't creamy protein soups),  then i  would  consider this  question  on topic. See here  for tips on  writing  good questions on our site.

I confess. I didn't really hold it in.

Apart for the fact that your question is deeply strange, I will try to reply to you.
Mosquitoes are attracted by several factors that make them able to recognize their prey; two of these are: Warm bodies and CO2.
CO2 is the product of your mitochondrial respiration, when you breath out from your lungs you expel liters of this gas.  This is how mosquitoes understand that you are alive. You are warm and you breath !
One of the devices used to kill mosquitoes is in fact a giant vacum  cleaner that warms up till 37°C and emits CO2, by burning gas.
Going forward with your question: Let's speak about farts.
Farts are not "a soup of proteins". Farts are gasses (mostly methane) and CO2 produced by bacterias during the decomposition of the food that you ingest. That is also why your excrements smells more when you don't poop for a long time. They fermented more :P.
So, since it is true that part of a fart is composed by CO2 and they produce a warm cloud around you, I would say YES, they do attract female mosquitoes. But so do you. So release your gasses, or stop to breath at all.
Hope I've replied to all your doubts.
Cheers
I didn't know we were peer-reviewed.
Here my references.
https://en.wikipedia.org/wiki/Flatulence .
https://www.amazon.com/Lehninger-Principles-Biochemistry-Fourth-Nelson/dp/0716743396   .
http://labs.russell.wisc.edu/mosquitosite/preventing-mosquito-bites/carbon-dioxide-baited-mosquito-traps/ .
A biologist.

Please add some references to your answer.


text:
How can we move our lips even though they don't have any bones?
How can we move our lips even though they don't have any bones?
We can move everything if it is attached to the bones. Example: Legs & Arms.
otherwise we can't move it.

Have you heard the term 'muscles'?

Yes. I heard it. How does it answer this question?

Muscles don't need to be attached to bones to function. Look at slugs.

@user47532 Tongue, eyelids, eyeballs, nostrils: do you have an idea about how we move them? Heart also "moves"! Please do some basic reading before asking a question.

@JM97 they are not bones. I was trying to get a point across that bones are not necessary for movement. It has already been said by others too. Muscles need to be attached to something to exert force but that need not be a bone.

Because of the Orbicularis oris muscle, it's a complex of muscles in the lips that encircles the mouth, It forms the greater part of the substance of the lips, lying between the skin and the mucus membrane, and extending from the edge of each lip to its root.


text:
Database for drug-target relation
I'm writing a thesis on bioinformatics and looking for drug-target databases. I'm implementing a open-source application for a tool called Cytoscape and so far I've used a open-source database called DrugBank to retrieve drug-target data, but I've read a paper on a database called Drug2Gene that combines multiple open databases into a unified format. The paper is from 2014, but all websites are down and I was wondering if someone here knows of any other databases/resources that does this and is maybe up-to-date? I want to utilize as much open-source data on drug to target relation as possible to provide a simple way of accessing all these resources. Drugbank is regularly updated and a good source, but with so many different databases with a decreasing overlap of data I was happy to stumble across Drug2Gene database only to realize I can't get it and it's probably not up-to-date.
I will be very thankful for any tips as I'm purely a Informatician and feeling helpless in finding thing related to biology.
Source: Drug2Gene paper

There are quite a lot drug databases. I think DGIbd is a good place to start (see below). Further there are a lot of databases which describe drugs and their targets, take a look at these (and the links at the bottom) hopefully you can use several of these in your implementation.
SIDER

SIDER contains information on marketed medicines and their recorded
  adverse drug reactions. The information is extracted from public
  documents and package inserts. The available information include side
  effect frequency, drug and side effect classifications as well as
  links to further information, for example drug–target relations.

DrugCentral

DrugCentral provides information on active ingredients chemical
  entities, pharmaceutical products, drug mode of action, indications,
  pharmacologic action. We monitor FDA, EMA, and PMDA for new drug
  approval on regular basis to ensure currency of the resource. Limited
  information on discontinued and drugs approved outside US is also
  available however regulatory approval information can't be verified.

Therapeutic Target Database

Therapeutic Target Database (TTD) is a database to provide information
  about the known and explored therapeutic protein and nucleic acid
  targets, the targeted disease, pathway information and the
  corresponding drugs directed at each of these targets. Also included
  in this database are links to relevant databases containing
  information about target function, sequence, 3D structure, ligand
  binding properties, enzyme nomenclature and drug structure,
  therapeutic class, clinical development status. All information
  provided are fully referenced.

Potential drug target database (PDTD)
NOTE: I think this one is coupled to DrugBank however you can take a look here

PDTD is a dual function database that associates an informatics
  database to a structural database of known and potential drug targets.
  PDTD is a comprehensive, web-accessible database of drug targets, and
  focuses on those drug targets with known 3D-structures.

PharmGKB

The PharmGKB is a pharmacogenomics knowledge resource that encompasses
  clinical information including dosing guidelines and drug labels,
  potentially clinically actionable gene-drug associations and
  genotype-phenotype relationships. PharmGKB collects, curates and
  disseminates knowledge about the impact of human genetic variation on
  drug responses through the following activities: Annotate genetic
  variants and gene-drug-disease relationships via literature reviews
  Summarize important pharmacogenomic genes, associations between
  genetic variants and drugs, and drug pathways Curate FDA drug labels
  containing pharmacogenomic information Enable consortia examining
  important questions in pharmacogenomics Curate and participate in
  writing pharmacogenomic-based drug dosing guidelines Contribute to
  clinical implementation projects for pharmacogenomics through
  collaborations Publish pharmacogenomic-based drug dosing guidelines,
  very important pharmacogene summaries and drug-centered pathways
  Display all information on the website and provide comprehensive
  downloads

STITCH

To facilitate access to this data, STITCH (‘search tool for
  interactions of chemicals’) integrates information about interactions
  from metabolic pathways, crystal structures, binding experiments and
  drug–target relationships. Inferred information from phenotypic
  effects, text mining and chemical structure similarity is used to
  predict relations between chemicals. STITCH further allows exploring
  the network of chemical relations, also in the context of associated
  binding proteins. Each proposed interaction can be traced back to the
  original data sources. Our database contains interaction information
  for over 68 000 different chemicals, including 2200 drugs, and
  connects them to 1.5 million genes across 373 genomes and their
  interactions contained in the STRING database.

SuperTarget and Metador

An easy-to-use query interface enables the user to pose complex
  queries, for example to find drugs that target a certain pathway,
  interacting drugs that are metabolized by the same cytochrome P450 or
  drugs that target the same protein but are metabolized by different
  enzymes. Furthermore, we provide tools for 2D drug screening and
  sequence comparison of the targets. The database contains more than
  2500 target proteins, which are annotated with about 7300 relations to
  1500 drugs; the vast majority of entries have pointers to the
  respective literature source. A subset of these drugs has been
  annotated with additional binding information and indirect
  interactions and is available as a separate resource called Matador.

Pharos

Pharos is the user interface to the Knowledge Management Center (KMC)
  for the Illuminating the Druggable Genome (IDG) program funded by the
  National Institutes of Health (NIH) Common Fund. (Grant No.
  5U54CA189205-02). The goal of KMC is to develop a comprehensive,
  integrated knowledge-base for the Druggable Genome (DG) to illuminate
  the uncharacterized and/or poorly annotated portion of the DG,
  focusing on four of the most commonly drug-targeted protein families:
   G-protein-coupled receptors (GPCRs); nuclear receptors (NRs); ion
  channels (ICs); and kinases. For more information on opportunities in
  the druggable human genome see this poster

KEGG drug

KEGG DRUG is a comprehensive drug information resource for approved
  drugs in Japan, USA, and Europe unified based on the chemical
  structures and/or the chemical components, and associated with target,
  metabolizing enzyme, and other molecular interaction network
  information. All the marketed drugs in Japan, not only the
  prescription drugs but also the OTC drugs, are fully represented in
  KEGG DRUG and integrated with the package insert information (labels
  information). These include crude drugs and TCM (Tradictional Chinese
  Medicine) drugs.

The IUPHAR/BPS Guide to PHARMACOLOGY (database)

The information in the database is presented at two levels: the
  initial view or landing pages for each target family provide
  expert-curated overviews of the key properties and selective ligands
  and tool compounds available. For selected targets more detailed
  introductory chapters for each family are available along with curated
  information on the pharmacological, physiological, structural, genetic
  and pathophysiogical properties of each target. The database is
  enhanced with hyperlinks to additional information in other databases
  including Ensembl, UniProt, PubChem, ChEMBL and DrugBank, as well as
  curated chemical information and literature citations in PubMed.

DGIbd

The druggable genome can be defined as the genes or gene products that
  are known or predicted to interact with drugs, ideally with a
  therapeutic benefit to the patient. Such genes are of particular
  interest to large-scale cancer profiling efforts such as TCGA, ICGC
  and others that identify lists of potential cancer driver genes from
  high-throughput sequence and other genome-wide data. In cancer
  therapy, the increasing number of targeted drugs--those designed to
  inactivate proteins carrying activating amino acid changes as
  determined by mutational analyses--make more compelling the need for a
  searchable database of drug-gene interactions, available here.

There are a lot more databases, maybe these links will help you:

Drug to Target/Gene/Protein Interaction Databases
Question: Database Of Drugs Targeting Genes
Drug Databases


text:
Why is pith of Cucurbits hollow when mature?
What is the evolutionary significance of pith in cucurbits? Does it serve a function by being hollow? Or is it an evolutionary vestige? What function would it have had in its ancestors?

Pith autolysis is a phenomenon due to which in some dicotyledonous plants like cucurbits, the pith gets hollowed.
Background: We all know that plants get their Carbon from atmosphere in the form of Carbon-dioxide, and fixes it by photosynthesis. During rapid growth Carbon requirement may not be in pace with rate of carbon fixed by photosynthesis alone, So some plants adopted pith autolysis.
This is useful for a  plant when it is in scarcity of carbon, Scarcity here implies that the plant is not able to get enough carbon for its growth with just photosyntgesis. So the plant autolyses it's pith to get required carbon to maintain its growth.Thereafter this carbon resulting from autolysis ,is transported to growing regions of plant.
Source:https://doi.org/10.1006/anbo.1995.1063

Could you explain this a bit further in your answer? As it is,  your answer is a bit vague. Thanks


text:
Is there really a clear distinction between dinosaurs and birds?
Traditionally, birds are classified as a class of dinosaurs and the term non-avian dinosaurs is introduced to refer to the rest.
As recent discoveries suggest that some dinosaurs may have been warm-blooded and that some dinosaurs had feathers, the distinction between birds and dinosaurs seems blurred.
I have often heard statements like "Birds are the only dinosaurs that survived the Cretaceous–Paleogene extinction event.". With recent discoveries, isn't this how the clade of birds is defined rather than a fact about the extinction?
// not sure if this question belongs in biology, sorry

Related: If dinosaurs could have feathers, would they still be reptiles?

The question relies entirely on a definition. There is no right or wrong when dealing with definitions. Anyone is free to define birds and dinosaurs as (s)he likes. The question of weather the definition is accurate or very arbitrary with loads of limit cases would be of interest though. Of course a lot of dinosaurs lineages went extinct. One lineage did not, they became bird.

Related: Why do the ancestors of birds still exist?

Dr. Thomas Holtz wrote a full chapter on it in "Dinosaurs: The most complete and up-to-date encyclopedia", Random House, 2007.

The placement of the bird clade within the dinosaur clade is based on much more than just "having feathers and being warm-blooded"; paleontologists have discovered many, many ancient bird and theropod fossils, and as a result their understanding of what the theropod clade was like overall and how the bird clade developed within it is precise enough that discovering another group of dinosaurs was warm-blooded or even had feathers won't result in the conclusion "wow that dinosaur was closer to birds than we thought", but "wow feathers were a much more common feature among dinosaurs than we thought".
If you look at the Wikipedia page you can see there are many "bird-related" clade names that cover different levels of similarity to modern birds. From "Neornithes", which is defined as the clade containing all modern birds, to "Paraves", defined as the group containing all organisms closer to modern birds than to Oviraptors, which are all within Maniraptorans, which is itself pretty deeply nested within the Theropod clade...
So basically what I am trying to say is, our understanding of where birds fit within Dinosauria is precise enough at this point that no discovery about a single trait is going to "blur the distinction between bird and dinosaur"; it might change our idea of dinosaurs in general to be more bird-like, meaning that traits we thought were bird innovations might have been standard-issue in dinosaurs for a long time before, but it will not necessarily change our whole understanding of how birds and dinosaurs are related.
As for this :

With recent discoveries, isn't this the definition of what a bird is rather than a fact about the extinction?

It isn't; the paleontological definition of what a bird is is not at this point an ad-hoc definition related to "whatever survived the K/Pg extinction". Even Neornithes, the crown group of all living birds, originates to before the K/Pg extinction. For example, the splits between ostriches and other birds and within that latter group, of ducks and geese from other birds are thought to have happened during the Cretaceous. And there are some researchers who argue that a few fossils indicate that some non-avian dinosaurs survived the extinction; the consensus view is that those fossils are dated wrong, but that this position exists shows that "non-avian dinosaurs went extinct at the K/Pg boundary" is a fact-based question, not a definitional one.

Also note that several major groups of "birds", like the enantiornithines and hesperornithiforms, didn't survive the K-T extinction.

Right; these aren't in the crown group of modern birds, and enantiornithines in particular are way upstream of modern birds, but they're definitely animals that if you saw them you would think they were birds (in fact the first fossils of these animals were misidentified as belonging to modern bird groups). They are one reason why "bird" can refer to many different paleontological groups; the crown group of modern birds, a higher-order group like Avialae to include those archaic forms, etc. Which further illustrates that the definition of "bird" doesn't hinge on feathers or the K/Pg boundary.

Yes.  I think the problem is mostly linguistic, in the distinction between "are" and "evolved from".  I mean we all evolved from fish, but if someone said you are a fish (or expected you to breathe under water :-)), you'd look at them somewhat askance, no?

@jamesqf not quite; there is a linguistic issue but also a substantive one. People would look at you askance if you said you were a fish, but nobody would disagree if you said you were a mammal. The relationship between evolution and the nested hierarchy that life by and large falls into is that the nested hierarchy is the result of evolution - groups diversify, spawning subgroups etc, so all descendants of one group are still more like each other than they are like descendants of other groups, meaning that "is descended from" and "belongs to this group (based on overall similarity)" coincide.

Exactly my point.  Saying that humans are mammals conveys one set of information; saying that humans are synapsids conveys a different (and generally not very useful) set, which is less confusingly conveyed by saying that humans are mammals, and mammals evolved from synapsids.  Likewise saying that birds are dinosaurs conveys different information from saying that birds evolved from dinosaurs.  (And at least two very different groups of dinosaurs, and other creatures like pterosaurs & dimetrodon that people think are dinosaurs.)

@jamesqf well for one thing that's a strange point you're making, because "synapsid" isn't a vernacular term it's a technical one, a technical field where clades are accepted as a salient concept, and cladistically "humans are synapsids" and "humans evolved from synapsids" are exact synonyms that convey the exact same information. More to the point, the fact that "are" and "are evolved from" mean the same thing in certain contexts is itself a very important set of information (about how evolution works and how today's life results from it) that gets conveyed when one uses them as synonyms.

One modern definition of birds, due to Gauthier, is the smallest clade containing all extant dinosaurs. However, this is not equivalent to the dinosaurs that survived the Cretaceous-Paleogene event, as these are not a clade. The bird clade dates back about 150 million years, and the Cretaceous-Paleogene event was also a mass extinction for birds, although after that they became much more diverse.


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Why is it possible to calculate the equilibrium potential of an ion using the Nernst equation from empirical measurements in the cell at rest?
In trying to understand the Nernst and GHK equations, I've hit upon a snag somewhere deep in my understanding of the subject matter.
Scenario 1: when calculating the membrane potential of a living cell at rest we use the Goldman equation. This requires us to measure both the concentrations of the ions and the membrane's permeability to said ions, at rest (at least for the concentrations).
Scenario 2: given two cells separated by a membrane (as in Figure 3 here), with a different concentration of KCl in each cell, and having the membrane permeable only to K ions, we can compute the equilibrium membrane potential using the concentrations of the K ions - after the system has reached equilibrium.
So far so good. Here's my question:
Given a living cell at rest with all its ion concentrations, the Nernst equation is used to compute the equilibrium potential of a single ion, using the concentrations at rest. Why is this allowed? As I understand it, the concentrations as measured are what the cell "decides" them to be - it can change the permeabilities of the channels, or create more pumps, etc. - and then we'll measure different ion concentrations at rest. And these concentrations will change if a cell decides to open or close some channels (which is what happens to create the action potential). But the concentrations that are used as input for Nernst's equations should be measured at the actual, not just the steady state, equilibrium (right?).
So, why can we use the steady state measurements to derive the equilibrium potentials?

Excellent question! The answer is actually a really cool and crucially important detail about membrane potentials and the movement of ions. Basically, the electric force is very strong. You don't actually need to move many ions for the membrane potential to fluctuate dramatically. The number of ions that "move" to establish equilibrium is tiny compared to the actual concentrations. That's why the Nernst and GHK equations are so powerful: what really matters is the relative permeability of different ions and the gross concentration differences, not the changes in their concentration that occur when, for example, voltage-gated channels open during an action potential.
You can calculate just how many ions have to move, which depends on the size of the cell. Here is a nice example from the reference I have linked below:

For a typical cell, 1 microcoulomb of charge (6 × 10^12 monovalent ions) per square centimeter of membrane, transferred from one side of the membrane to the other, changes the membrane potential by roughly 1 V. This means, for example, that in a spherical cell of diameter 10 μm, the number of K+ ions that have to flow out to alter the membrane potential by 100 mV is only about 1/100,000 of the total number of K+ ions in the cytosol.

Therefore to answer your question: why is it allowed to use the resting concentrations? Because the concentrations of the ions don't change by more than 1/100,000 fold with a 100mV swing in potential, and there isn't much impact on the GHK/Nernst equation from a change this small. For example, as the voltage goes from ~-70mV when a fairly typical neuron is at rest (and the membrane is most permeable to K+), up to maybe +30mV at the peak of an action potential (and the membrane is most permeable to Na+), only a "few" sodium ions actually cross the membrane, so maybe the internal sodium concentration changes from 10mM to 10.0001mM. The thing that changes most during an action potential is not the actual concentrations, only the permeability to different ions.
Maybe an additional misconception you have is about the cell "deciding" what the concentrations are. Indeed, if the concentrations of particular ions changed dramatically, it would be necessary to recompute equilibrium potentials. The key concept is that those concentrations don't change much during normal functioning of the cell, and they don't have to change much to observe big changes in membrane potential. An excitable cell uses those swings in membrane potential as the signal, rather than the concentrations of the ions. One exception is calcium, see the note at the end.
Reference:
Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K., & Walter, P. (2002). Ion channels and the electrical properties of membranes.
(as a side note, movement of ions does matter over a longer time scale, which is why it is necessary for the Na+/K+ pump to constantly operate to keep the membrane potential steady, and some ions like Ca2+ are at such low concentrations normally that the influx of calcium can be substantial relative to the resting concentration, which is partly why calcium is so powerful as a second messenger and why calcium chelating components of the cell are important)

Thank you for your prompt response, but unfortunately I don't understand how this relates to the question. Can you elaborate more, please?

@VladimirGritsenko I made an edit to try to connect it more explicitly to your original question. Does this make sense? If not, perhaps I am misunderstanding your question, can you clarify?

I think I understand now - since the factor that most affects membrane potential are permeabilities, not concentrations, (and thus concentrations change very little during an AP), we can treat the steady state as a very close approximation to equilibrium?

@VladimirGritsenko Mostly right - steady state and equilibrium are the same thing, but you are probably thinking about "rest" or a cell in the absence of external input. There is a new steady state/equilibrium voltage any time something happens to change the permeabilities. Ions will flow until that new equilibrium is reached, but it doesn't take the movement of very many ions and it isn't enough to appreciably change the concentrations.


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Do pyrosomes reproduce by ways other than cloning?
I know that Pyrosomes are large colonies of floating tube-like animals that live in the sea, particularly in the tropics. They are just like any type of free floaters
I know  that pyrosomes can reproduce by cloning, but are there any other ways that they can reproduce?

What research have you done before asking it here?

Please provide a link reference in your question where I have inserted [reference required]. "I know for a fact" is not appropriate here, because it does not provide the means for readers (such as myself) to check the background to a question.

Yes. sexual reproduction. From a <1min google search: "Pyrosomes make both eggs and sperm... alternating asexual and sexual reproduction results in giant swarms of pyrosome colonies." We ask that you do your own research before asking questions on Bio.SE. Please update your question with some indication you've done prior research to avoid having it downvoted/closed. See here for tips on writing good questions. Thanks.

Indeed pyrosomes use a very interesting form of reproduction. They actually use both sexual and asexual form of reproduction each time they reproduce. Pyrosomes, which are colonial tunicates, produce both egg and sperm. In each pyrosome of a colony, a single egg is fertilized and develops into a 4-staged animal. This form leaves the parent body and starts forming its own colony. It does so using the process called budding, which rapidly develops a new colony of pyrosomes. You can see here, here or here for more information.
source (in french though ;)


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Where and how is information about pathogen immunity stored in a cell?
If all of the DNA is being used, then how would the cell be able to store new information about pathogens in DNA? It's like a full hard drive that can't hold any more. So does the cell just compress the information about the pathogens and then just adjust the existing information about pathogens?

All the body does is produce a ton of cells that can recognize single antigens. Each time you encounter pathogens, some of these naïve cells contact antigen that can activate them. The activated clone replicates itself, forming effector cells that can deal with pathogens.
As the infection is cleared and the population of effector cells begins to contract (i.e. many die off or become anergic), some of them undergo changes which alter their migratory pattern and longevity. Some can stay in the tissue that was originally infected as tissue-resident memory cells. Some home back to the lymph node and hang there as central memory cells. The lineage is affected largely by chemical signals being produced by the tissue and other immune cells in the vicinity.
Upon re-encounter of the same pathogen, if it has some of the same antigenic determinants as the original infection, these memory cells are already known to be specific to them. Encountering the same antigen will cause these memory cells to undergo another round of clonal expansion, producing more effector cells and additional memory cells so the process can repeat. These events can be limited by telomere length or inhibitory molecules, as a caveat.
The key understanding is that the immunologic memory is actually stored in the repertoire of long-lived memory cells, and in part results from recombination events at the T or B-cell receptor locus during their maturation before they're released as naïve cells.
See: Abbas (2014). Cellular and Molecular Immunology, 8th ED., many different chapters.

There is also 'intrinsic' and 'innate' immunity. Immune cells can recognize common patterns on pathogens, such as lipopolysaccharides, double stranded RNA and flagella and respond to these shared patterns. These common responses are more ancient. 'Adaptive' immunity is relatively new.

That makes a lot of sense. Like I said to the other person, I'm just taking AP Biology at school, so I'm not very knowledgable of this field. So if you get an infection on your foot, and your lymph node with those memory cells is around your neck, will it send those memory cells to the foot, or does the lymph node just protect its immediate surroundings? Also, you mentioned the textbook. Do you recommend that book for further research at my level of knowledge, or should I start out with less advanced material?

There are pathogen sensing cells called Antigen Presenting Cells which nibble on bacteria and proteins in different environments, these cells then migrate back to lymph nodes where memory cells are 'present' the antigens they picked up. If there's a match then you initiate the so called 'adaptive immune response'.

So in that case, would the Antigen Presenting Cells only make it to the local lymph nodes? In that case, memory cells in the neck would not be helpful to an infection in the foot.

Central memory T cells are considered a circulating subset. They home to lymph nodes temporally (time-dependent) through the expression of the receptors CD62L and CCR7. There's actually a neat paper in immunity about how T cells circulate on a circadian clock of sorts, and so they come out of the lymph nodes and circulate every now and then. This basically means your central memory T cells aren't always in the neck, and it's how a DC in the draining lymph node in the foot can find a naïve or memory cell to prime.

Also note that while im quoting T cells, many things are the same for B cells in terms of trafficking, just not for function/activation.

You're asking for a course in immunology, which is far too long to include here.You have several misconceptions. Short and oversimplified answer, the information is not stored in one cell, but in trillions, each with a single piece of pathogen information. Within each cell, the information is stored in DNA, which in these particular cell types can be modified. Your hard drive analogy, like most such analogies, is completely misleading and you should abandon it. There are several introductions to adaptive immunity online; you might find one (such as here, here, or here) helpful.

Sorry, I'm just taking AP Biology, and it was a topic that we're learning about. I definitely want to get more into it, so I'll probably try to find some resources to learn more. Do you have any recommendations aside from waiting until college?

The IMGT writeup is probably a good starting point -- I think if you're taking AP Bio you should be able to follow it pretty well.  You might jump to the "Mounting an Immune Response" section for a quick overview. The Wikipedia article on the Adaptive immune system goes into more detail; you might want to follow some of the links in the introduction.


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Is there any alternative to x-gal white/blue screening for the monitoring of pseudomonas aeruginosa beta-galactosidase activity on agar plate?
I want to screen a pseudomonas aeruginosa mutant library carrying a lacZ transcriptional fusion for dysregulating mutations. I tried to do it on xgal plates but the accumulation of the blue color makes the screening difficult. I saw that people are using macconkey or endo agar media for two-hybrid beta-gal screening in E. coli for instance. I wonder if it would be something to try even with pseudomonas (which would only possess the lacZ gene, so no permease etc...) and if someone here ever tried it ? Or if other beta-gal substrates could be used for this application ?
thanks
Julian

I think your problem will be even worse when you'd use MacConkey or Endo plates. You can see differences between different kinds of bacteria / expression of certain enzymes on those plates, but the coloring / decoloring is based on soluble compounds that easily diffuse.
Hydrolysis of xgal creates an insoluble product that's staying more or less at your colony. Of course it's not perfect and after a while you have a completely blue plate, but this would happen much faster with a soluble compound.
Try adjusting your conditions so you can look at the plate before it's completely blue. Things you could try: look earlier, plate them a little bit more dilute so colonies are further apart, use less xgal so your final coloring is less intense, look for some papers that use xgal for screening and steal their tricks.


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What makes cows stop being able to produce milk?
I'm writing a paper about cows and want to discuss why they stop producing milk. Is there a disease that causes them to stop producing milk?

OP noted that they had difficulty logging in - namely that it still treated them as a guest even though they were logged in.


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Organic battery?
Similar to the Matrix movie where humans were used as a source of electricity but different by using electric eels. Farmed like tuna what would be the electricity exchange to the food they eat?

I don't have the math at hand for the actually energy efficiency, but let's just start from the storage capacity.
Basically, an electric eel wouldn't make a very good battery. They could be a decent, albeit fairly inefficient capacitor, but they actually store little energy. Using data from Wikipedia on Electric Eels it works out to something less than 2 joules (less than 1kilowatt over 2 ms), whereas an AA battery is around 12000 joules.
You're going to need a very, very big tank to store any appreciable amount of energy, before you even worry about how much food it will take you, let alone the animal welfare concerns with forcefully discharging a tank of eels at your whim.

What if they where grown like farmed tuna?

(side note: this could make an excellent question for Randall Munroe at XKCD's What If if you phrased it in the form of "how much would I have to feed a tank of electric eels sufficient to power the world's energy grid")

@Muze How you farm them doesn't change the basic math that you will need 6000 of them to equal a single AA battery. (and by the way, tuna is probably not the best example for farming - it is quite difficult to farm tuna and only recently achieved) I think it's off-topic to discuss here the sustainability of AA battery production but I am confident I can get one from the local supermarket for less cost than you will ever be able to feed and house 6000 fish.


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A strand of my hair has a grey section in the middle, how is this possible? And why does it happen?
My hair is usually brown and black, I haven't dyed my hair for two years and if I had this would be strange. A strand of hair went from black(roots) grey (middle) then light brown(bottom).
How does hair change color along its length? And why does this happen?

I am curious about this too! I am naturally blonde, and on some of the strands of my hair I have random sections of red, then it goes back to blonde.

Your hair gets its color from a compound known as melanin, produced by special cells called melanocytes. There are two versions of melanin - one that produces dark pigmentation and the other that produces light pigmentation. If your natural hair color is brown/black, then it normally has a specific amount of dark vs light pigment. The middle section of this hair is grey because there was an absence of melanin production when the hair was still growing. There could be multiple factors (including stress , as described on the library of congress site), but it's nothing to worry about. Your melanocytes started to normally produce melanin again, which is why the newest hair growth (closest to the roots) is dark in color (dark brown/black).

Hi, @Kate. This is a good answer, thanks. I've often heard about the stress link with grey hair. Could you provide a citation to it? Could you provide a citation about the temporary lack of melanin production. I know some people produce a grey hair once in a while, but I thought the whole hair would be grey, not a section. Generally, on this site citations are useful for good answers.

Sorry - new here, didn't know! Here's a useful link:
https://www.loc.gov/rr/scitech/mysteries/grayhair.html

Welcome to Bio.SE :). I added the link into your answer. I have a feeling that this question will be closed though since it might be medical related.

It has recently been found that hair greying can be reversible in humans.
https://elifesciences.org/articles/67437

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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What is the relationship between complexity and organization in biology?
Is there any relationship between what we can call complexity and what we can call organization in biology? And if there is, what is it? Can we define these terms independently of each other or would the definition of one of them always inescapably include the other and vice versa? If the second is the case, what can such a relationship tell (or, at least suggest) us about life?

I would like to draw a parallel between my question and another question here on SE pertaining to the same notion-that of complexity in biology, to show how we can shape a question in a much clearer and precise style and get more information about the same issue. Here it is- http://biology.stackexchange.com/questions/13853/why-and-how-does-complexity-usually-tend-to-increase-through-time/57005#57005 I'm trying to show how the topic discussed there can be presented in clearer and more exact style if we concentrate on a particular issue instead of trying to cover everything in 1 question

I think if one starts out a question with a clause that includes "depending on the definition of the terms you use" one must be prepared to provide such definitions, otherwise it isn't possible for anyone to answer without using their own definitions and therefore making the question opinion-based.

Hi, @YordanYordanov. Complexity & organisation have specific meanings depending on context. For example, I work with sequences in terms of simple and complex depending on their linguistic entropy. Some people would call a protein structure complex if it was very disordered due to estimations of chemical entropy. Some people would call one cell more complex than another if there were more external forces interacting with it, others if the structures were more varied. Because of the vagueness of the term "complexity" in this question, I'm voting to close as off-topic.

I have edited my question. Are you happy now, @Bryan Krause ? In this form is it still "opinion-based" according to you?

Hey, how can you put it on hold? I just edited it! What is the problem now?

I and the others voted to put the question on-hold before your edits (I think @James gives a good argument for why, in addition to my own answer). I will review your edits - questions put "on hold" can always be returned to an open status after edits.

I will wait then and if you reopen it I will delete my comment and this comment, too.

Unfortunately I don't think the edits resolved the issues. Your question really contains a dozen different questions all going in different directions. "Can we define these terms independent of each other" - this is really just an opinion question. Sure, someone could do so if they wanted to, because they are choosing the definitions. I could define complexity as "number of photons emitted" if I wanted to. I don't think your question is uninteresting, but it is not suited to the question-answer format of this site - as written, it is more of a discussion question.

What about now? I managed to shape it into a question pertaining only to whether there is any relationship between the definition of complexity and organization in biology. The point is is it possible to define complexity  in biology without including organization in the definition of it and the vice versa? Are they interrelated in codefinitional circle we can't escape and if they are-why? How is this not an interesting topic for discussion in a biology Q&A? Don't you see implications if the 2 terms are mutually dependant on each other for their definitions?

The whole point is that questions for discussion are not questions for this site - questions should have a correct answer (within the bounds of existing knowledge, of course), not based on opinion, or they don't belong. I don't want to hijack your question, but consider something like the following, which I still feel is not ideal but it is not a question I would vote to close: "Are there any academic works that distinguish between complexity and organization in biology such that they need not be correlated with one another?"

Then do you suggest I make 2 new questions-1 is there relationship between the definition of complexity in biology in terms of the organization of the organisms and 2-is there relationship between the definition of organization in biology in terms of complexity? Would that be more "fit" for you?

I still am amazed how quickly you put this question on hold while other questions pertaining to the same field and also having many unclear questions mentioned in them like this one-http://biology.stackexchange.com/questions/13853/why-and-how-does-complexity-usually-tend-to-increase-through-time/57005#57005 are still standing active even after years have passed? What is so "unclear" here that is "clear" there to put my on hold so quickly?

@YordanYordanov the other question was asked during our beta. The community was a lot less clear on what constitutes "answerable". Now it's resurfaced I'll initiate a close vote. People may be hesitant to follow since it has 7 upvotes (people like the question) and an accepted answer that seems at least superficially satisfying. If in the future you have an issue with a question, it'll be best to raise it on that question rather than a different question. This site is vast.

@James , the issue I have is where is the place for Q&A about complexity in biology on that site. Should I use questions like the one I show you (which I personally-you're free to disagree-think is quite vague and broad)q should I make my own questions and use the tag complexity or may be something else, What do you think will be the best question for regarding the issue of complexity here on this site? What should be asked-what it is, how to measure it, problems regarding different definitions and/or measurements of complexity,its significance for evolution, ect.How to ask questions about it?

I'm ready to delete this entire question if you can provide me with better ways to ask about the problems associated with the discussion of complexity in biology. What do you consider would be appropriate question about complexity in biology on this site? If you manage to provide better question I'm ready to delete this one in its favour.

@YordanYordanov I agree the other question is vague and have opened a close vote on it. I see questions on complexity being more along the lines of "How can I quantify the complexity of system/thing X in a biologically relevant way?" This question is on hold and will be closed sooner or later unless it is successfully reopened.

I want to delete my question in favor of this one-http://biology.stackexchange.com/questions/57178/what-is-the-meaning-of-complexity-in-biology but the systems just will not allow me. I feel this one is better and if somebody wants to put it on hold it because it is a duplicate of this one I should delete this one, not my second question. What should I do?

Here's food for thought. Entropy is always considered to flow naturally in a direction of order, to disorder. That is, the higher entropy a system has, the greater degree of disorder it has, and the less amount of work it can perform.
Now, look at a cell. It is a biological system of organic molecules that are able to organise themselves in a way that outweighs the forces of entropy. To "fight" the natural tendency of the universe that moves toward a state of disorder requires a highly complex system. And, in the process of going against entropically favorable mechanisms, a cell is also able to produce its own energy (stored as potential energy, or ATP if you will).
I guess you could say, a more complex system is able to organise itself in a greater number of ways for the purpose (and I use this word very loosely, as nothing really has a purpose) of yielding entropic energy to do work.

I think you are on very right track here. The question, however remains can we define organization as the state which forces the system to go against the entropy gradient and if we can, then what is really complexity then? Does the increase in organization drives the increase in complexity or is it the vice versa? Or may be some even more intricate and "complex" relationship?

Another thing to consider is that complexity can sometimes be more apparent than real, because an underlying simple mechanism that is not understood by the observer can give rise to complex results.  For instance, consider how the growth of plants &c can be modeled by L-systems (https://en.wikipedia.org/wiki/L-system ), or how the widely different forms of mollusc shells conform to a few mathematical rules.  Or indeed, how a couple of simple principles produces evolution.

"Does the increase in organization drives the increase in complexity or is it the vice versa?" seems a lot like the question, "did the chicken or the egg come first?". I do understand why people voted to put this question on hold - because there isn't really any way to answer it. I honestly do not know because it is too abstract. I think I have somewhat of an idea about how it works, but I have no idea how it came to be.


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Is there any liquid in the bone medullary cavity
I am looking at the effect of intramedullary nails on tibial bones and can't seem to find anything on fluids present within the medullar cavity/canal. Since this is where blood cells are formed I would expect there to be at least a bit of blood in the cavity. I also read somewhere about something called 'liquid bone marrow'. Can someone please confirm whether there is blood in the cavity and whether there are any other fluids present. Thanks in advance.

Bone marrow is almost a liquid.

@JM97 so there is a liquid and a solid component (spongy tissue). but what is the liquid composed of then?


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Can plant fruit and seeds be albino like animals?
There are numerous examples of albino animals, including snakes, birds, fish, mammals---humans too. Apparently this comes from some a genetic defect that results in lack of pigment.
What about plants? Obviously a lack of chloraphyl would be fatal for a plant, so I'm imagining the seed or fruit being white. Does this exist in nature?
Edit: I'm thinking of fruit/seeds that are not normally white.
Note the wiki page I cited has only 2 paragraphs on this:

In plants, albinism is characterised by partial or complete loss of chlorophyll pigments and incomplete differentiation of chloroplast membranes. Albinism in plants interferes with photosynthesis, which can reduce survivability.[4] Some plant variations may have white flowers or other parts. However, these plants are not totally devoid of chlorophyll. Terms associated with this phenomenon are "hypochromia" and "albiflora".[5]

That last part seems what I'm interested in, but the cite is a dead link.
Later in the article:

The primary function of pigments in plants is photosynthesis, which uses the green pigment chlorophyll along with several red and yellow pigments including porphyrins, carotenoids, anthocyanins and betalains.

No cite there and not much info anyway.
So are white seeds or fruit found in nature?
If you're curious, I originally thought of this as an alternative way of getting white chocolate from an albino cocoa bean, and maybe even a white coffee bean too.

Coffee beans are green before they are roasted; the brown color comes from the Maillard reaction (and possibly some caramelization), same thing that makes bread brown on the crust, and chocolate as well. Coffee or chocolate without the color wouldn't taste anything like normal. And white chocolate isn't really chocolate, it's a candy made with only the "butter" from cocoa beans which is really just a vegetable oil.

@BryanKrause Right that is why I wanted a "real" white chocolate, tho ofc who knows what it would taste like. I didn't know about the green coffee beans tho. Interesting.

White seeds: rice? White fruit: banana (not the peel of course)?

Great place for me to plug the super interesting story about  albino redwoods

@WYSIWYG Was thinking more like seeds/fruit that are not normally white but have suffered an albino gene.

@DrZ214 What about the classic finding of transposition in maize kernels by Barbara McClintock? That is, of course, within the same organism. There are variegated leaves too. Some vegetables also show variegation. There are white eggplant varieties. Do any of these examples fit your query?

@WYSIWYG I supposed it's a question of what exactly is considered an albino gene as opposed to a "normal" gene responsible for white or yellowish-white that we would not consider defective. Corn, maybe, but yellow and white could be kinda a gray area. I have never heard of white eggplant so I think yes there, but OTOH squash is yellow and eggplant and squash are very similar. Interesting, tho, that all those examples are vegetables and not fruit.

@DrZ214 Eggplant is a fruit.

@WYSIWYG Is it really? Yikes, it is. And it's a berry too? I'm sorry but what a terrible thing to classify as a berry IMO. It's a good thing we have genetics to use instead of tastes.

Do flowers count? There are some species where part of the population is white, e.g. Frittellaria meleagris

@RHA As far as I can tell, yes those count.

Don't know whether it counts as albinism, but there are quite a few white fruits out there.  Off the top of my head, there are white pumpkins, white corn, white peaches, white carrots,..

When thinking of albinism in fruits, the only thing I could think of is strawberries. Yes, there can be albinism in strawberries! They are nearly always assocoated with excess nitrogen and are usually tasteless. According to a research by Lieten et al, their mineral composition also differes. Albino strawberries contain higher N:Ca and K:Ca ratio than normal fruits. Another study by Sharma et al shows that albino strawberries show less lipoxygenase activity. Also, Hwang et al and team found that presence of more than normal silicon also causes, among many other things, albinism.

You can get more information here, here, here and here. Obviously, there could be numerous other examples, but albino strawberries is all I could remember.
PS the exact genetic cause and mechanism of albinism in strawberries is not known yet. When searching online, I only found a study by Plante et al which suggests presence of mixoploid cells over a critical number which might have an effect on it.

That's neat! Can they be safely eaten? Do they taste bad? If it's only a nutrient problem that causes it, and not a gene, then there must be some technical definition that I don't know that might exclude them.

Most probably the exact cause is not known and must be genetic. Also, they are mostly tasteless, but not harmful.

Interesting, so it could be a genetic defect that causes them to take up too much wrong nutrients. BTW you should get +1 just for that new link to acadamia. I've never seen a in-html paged document that loads so fast plus word searchable with CTRL+F like normal. Everyone else does pdf.

Albinism is very rare in plants, because most plants can't survive long without photosynthesis. A notable exception is Sequoia sempervirens, an American tree that seems to be able to survive as albino through parasitism. Source

In some plant species with coloured flowers, some specimens are white. A good example is Fritillaria meleagris, for a photo of the white flowers see the Dutch wikipedia page.

Another example of white flowers is Corydalis cava.

However, this is not true albinism, because green parts of the plant are not affected.

Good answer, +1! I've added photos and corrected links, feel free to roll back :)


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DNA mutations in CHO-KI mammalian cells
The mammalian cell line CHO-K1 has 24,383 genes. After 70 doublings (from a starting number of cells, 1) a
total of ~4,000 mutations have occurred in the overall population of cells (i.e. not all in one cell), due to incorrect DNA breakage repairs (non-homologous end joining), with the mutations randomly distributed throughout the genome. Assuming that 2% of CHO genome consists of crucial genetic information (1.5% coding and 0.5% regulatory). What number of genes will be affected by these mutations?
My attempt:
I was thinking that the mutations should be spread randomly and so 24383*70/4000 genes may be affected but doesn't that assume the mutations are one per gene and the affected areas are actually important to protein expression?

70 doublings from starting number of cells = ?

starting number of cells = 1

I suspect this question is a lot easier than it makes itself out to be, though I may not be thinking straight. It doesn't matter how many cells you start with or how many doublings there are. Nor, for that matter, does it matter how many genes each cell has. There's a 2% chance that a random mutation will affect "crucial genetic information"; I must assume that that refers to genes. So $0.02*4000=80$ mutations would be expected to affect genes.

Just to be picky: the concept of gene is always a bit fuzzy and many regulatory regions being so far from the coding regions that many would not consider most regulatory sequences as being part of genes. However, introns which are in the other 98% category would quite definitely be considered part of a gene.

@Remi.b Agreed, though in that case there doesn't seem to be enough information to answer the question. Or perhaps they are expected to just use the 1.5% value for CDS.

Some definitions of a gene: https://en.wikipedia.org/wiki/Gene, but it would be better to follow convention: http://www.ensembl.org/info/website/glossary.html, or if that does not engage sufficiently then perhaps some video tutorials? https://www.vectorbase.org/tutorials/other-bioinformatic-resources-tutorials/galaxy


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For Penicillin Binding Proteins, why is the enzyme-peptide complex less stable than the enzyme-β-lactam complex?
I'm trying to figure this out. I cannot find any publications that go into good detail about the chemistry of PBP inhibition by β-lactam antibiotics.
PBPs cross-link adjacent pentapeptides to form peptidoglycan. My understanding is that, in most bacteria, this pentapeptide has a terminal D-Ala-D-Ala dipeptide. The enzyme removes the terminal D-Ala and forms a D-Ala-Enzyme complex, where the enzyme is linked to the rest of the peptide via ester bond to the D-Ala.
However, when PBPs bind to β-lactams, they also form a β-lactam-ester-enzyme complex. However, this complex is more stable so the β-lactam remains in the active site. Why?
Any good publications are also very welcome.
I would also like to ask, is there any reason the "β-lactamoyl-enzyme" complex can't be hydrolysed?

According to Foyes Principle of Medicinal Chemistry, the significant difference is the crowding of the active site by the cycle next to the lactam ring, which prevent attack on the ester and release of the drug from the PBP.

Reversing the reaction to the beta-lactam is unfavorable given the resulting ring strain.
I would personally expect the ester to be hydrolysable (water being much smaller), but not very rapidly given the active site somewhat shields the complex from water. Foyes disagrees on that. ("Water is also an insufficiently effective nucleophile and cannot hydrolyze the complex either.")

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Where occurs diamine oxidase in kidneys - in cells or in extracellular space?
I would be interested in where the enzyme diamine oxidase in kidneys of human/animals mainly occurs? In cells or in extracellular space? A literature reference if available would be great. Thanks!


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Degradation of PMSF in protein extract while dialysing - safe for feeding to animals?
I would like to use the protease inhibitor PMSF in enzyme isolation. The obtained enzyme diamine oxidase (or better the protein extract) is tested oral on dogs.
According to Wikipedia, PMSF has a lethal dose less than 500 mg/kg, but also degrades rapid in water, which would meet my application. (The half-life is short in aqueous solutions, 110 min at pH 7, 55 min at pH 7.5)
After roughly isolating the enzyme, I dialyse the protein extract for about 12 hours. Is this time sufficient, so that there are no or only small amounts of PMSF in the extract anymore?

Be careful with the toxic dose - it is not disclosed for which species this is valid. I would assume this is for humans and might be drastically different for dogs. So we can most like not give you an advice on a safe dose.

How much PMSF would you feed the dog if you used the initial prep? And do you want to use PMSF to be sure, or do you actually need a protease inhibitor?

@VonBeche How much PMSF would you feed the dog if you used the initial prep? -> Nothing, I want it to degrade in water while 12 hour dialysis. And do you want to use PMSF to be sure, or do you actually need a protease inhibitor? -> I am relatively sure that in the protein extract are proteases and I want to get the maximum yield of enzymes.

Please do / show some back of the envelope calculations to see how much would end up in the dog. Dialysis will approximate dilution for a small molecule like PMSF.


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Why do we have more sweat glands in our palms?
Why is it that we have more sweat glands in areas such as the palms of our hands and the soles of our feet? I just learned that there are more there but I am curious as to why that is.

That increases sensitivity of receptors

You sweat much stronger in the palms of your hand and the soles of your feet, because they contain a much higher density of eccrine sweat glands. According to Sato et al., (see reference 1) there are something like 64 glands per cm² on your back, 108/cm² on your forearm and 600-700/cm² on the palms of your hands.
This is thought to have different reasons: First, sweating is an important way to control the body temperature.
Sweat works as a defense by anti-microbial peptide dermcidin, it is also seen as am important way to maintain the conditioning of the skin and as well as a lubricant for contact surfaces. (references 2-4)
Sweating is controlled by the sympathetic (autonomic) nervous system, and can be triggered by acetylcholine and adrenaline. This explains why you get wet palms when coming into stress.
References:

Biology of sweat glands and their disorders. I. Normal sweat gland
function
Systematic review focusing on the excretion and protection roles of
sweat in the skin.
Dermcidin: a novel human antibiotic peptide secreted by sweat
glands.
The human eccrine sweat gland: Structure, function and disorders

Good answer, +1! But I just wanna say that you added very little about the exact point the OP asks 'why?'. Please try to elaborate that point :)

@another'Homosapien' No problems, editing is fast, I have not much time not to look up more references. BTW: A number of references also state that sweating on the hands is important for thermal regulation, which is the most important role of the eccrine glands.

@Chris gave a nice answer, but I thought it would be better to include an answer to the 'why' part of the question. To start with, let me first say that the eccrine sweat glands on palms and soles respond to emotional stress, rather than increased body temperature 1. With that being said, the answer to the 'why' part becomes likely to get changed.
As one might know, its pretty difficult to answer the 'why did this happen during evolution?' question; there can be only theories with (usually) no conclusive proof. So, in this case too, the 'why' part remains without conclusive answer, and just theories prevail. According to the most prevailing theory, the emotional sweating causes sweaty palms that can help control the humidity of the outer layer of the skin. This could improve the friction on the skin thereby helping when you begin to sense you will be hunting an animal, fighting enemies, or about to climb a cliff (just to add, ever thought why your fingers get wrinkly after a long bath?). The generalized sweating that results from your hypothalamus then helps cool the body when these intense physical activities are happening. It also produces an odor that sends out pheromone signals to those same enemies/animals. The pheromones also could help signal potential mates that you are natural selection’s answer to their mating needs2. Again, this is just a theory and likely to have flaws, while the definitie answer is still not known. You can also have a look at the answers to this question for some more details.
References:

Sokolov, VE; Shabadash, SA; Zelikina, TI (1980). "Innervation of eccrine sweat glands". Biology Bulletin of the Academy of Sciences of the USSR. 7 (5): 331–46.
Wilke, K., Martin, A., Terstegen, L. and Biel, S. S. (2007), A short history of sweat gland biology. International Journal of Cosmetic Science, 29: 169–179. doi:10.1111/j.1467-2494.2007.00387.x


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Why do doctors use a new thread for each stitch?
Why do doctors use a new thread of the same kind for each stitch instead of using a single thread for the entire stitch?

Using a single thread for a suture also known as continuous stitching has a major con that it has higher risk of failing if the suture is cut in just one place. So it is generally avoided eventhough it is very easy to do.
On the other hand interrupted stitching ( one thread for each stitch) is favoured because of lesser risk of failing, eventhough it is time consuming than continuous stitch.
Source:https://en.m.wikipedia.org/wiki/Surgical_suture

If they used a single thread, then a single break in that thread would cause the entire thread to fall out of place. Using multiple threads means that if a break were to occur, the rest of the stitches would still be able to hold their place.
One time I had 5 stitches in my hand while I was snowboarding. Sometime during the day I fell down and one of the stitches came out; there was a lot of blood, but it was probably nothing compared to how much blood there would've been if it was a continuous thread and the whole wound opened.


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How does bone marrow acts like a valve?
Wikipedia says:

Furthermore, bone marrow performs a valve-like function to prevent the backflow of lymphatic fluid in the lymphatic system.

How can bone marrow act like a valve eventhough they neither have lymphvesseles nor contracting property?

Could you explain why you think bone marrow should not have a lymphatic system?

@anongoodnurse I really didn't understand how is your question related to my question. My question is how does bone marrow acts like a valve to prevent back flow of lymph even though it does not have any lymph vessels, I know muscles can act like a valve by contracting , but not about bone marrow which neither has ability to contract nor have any lymph vessels. Hope you understand my question, Thanks.

I think your question is predicated on at least one false statement. What if marrow does have a lymphatic system?

Okay then also how can it act like a valve?

Hey, you didn't even react to the preceding comment. Do some reading! Show where you're hung up.

My top priority was to know the mechanism behind it, If we even consider that bone marrow has lymphatics then also it doesn't mean that it can prevent back flow in lymphatics since they don't have any contractile property. Also many sites say that bone marrow doesn't have lymphatics, What I have learned is that bone marrow produces lymphocytes which enter into circulation by diapedesis into sinusoids. So, in this sense it makes bone marrow a lymphoid organ but I still don't understand how direcly(or indirectly ) does it prevent back flow of lymph. Thanks, hope you understand my query.

First of all, though bone marrow is not considered a part of lymphatic system because it is not connected to lymph vessels, yet it is the site of production of both B- and T-lymphocytes and is thus considered as primary lymphoid organ1. So, it is closely related to lymphatic system.
On doing some research, I can conclude that bone marrow itself actually does not perform the role of a valve. It is the lymph vessels itself which perform the valve-like function. See this2:

As lymph capillaries carry lymph away from the tissue spaces, they merge to form larger and larger vessels. These larger lymph vessels resemble veins, but their walls are thinner and they have more one-way valves to prevent lymph from flowing backward. Whereas the cardiovascular system has a pump (the heart) to move fluid (blood) through the system, the lymphatic system does not. It relies on the contraction of muscles to move lymph throughout the body. The larger lymph vessels have a layer of smooth muscle in their walls that contracts rhythmically to "pump" lymph along. The contraction of skeletal muscles, brought about by simple body movement, and the mechanics of breathing also help to move lymph on its way.

So, I'd consider that paragraph as one of the few places where Wikipedia has given incorrect fact.

I highly doubt that it could be wrong fact, anyway thanks for efforts.

As long as they mean bone marrow there, and there are no back ups, and counterexamples already present, I would consider it as incorrect.


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Development threshold of a blowfly species differ depending on situation?
Within a species, does the lower development temperature threshold remain the same in all situations (also known as the development zero temperature)? For example, would the temperature threshold be the same for larvae grown on small carcasses compared to large carcasses? e.g. mouse carcass compared to human/pig carcass.

Are you talking about minimum developmental time when you write "lower development threshold"? To me, it is unclear what the threshold is referring to.

@fileunderwater I am referring to the lower development threshold, t, expressed in the equation D(T-t) = k, and also known as the development zero temperature.


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ECG wave names origin
Why do electrocardiogram waves go  P, Q, R, S, T and not like A, B, C, D? Is there any specific reason behind this?

Interesting question! I searched briefly and came up with an answer from this short paper.
I won't repeat all the details of the paper, but to be not a completely link-only answer I will give a brief summary:
The technology used at the time was a lot different than modern ECG leads: it used a Lippman capillary electrometer that used moving mercury to detect brief current changes.
With this relatively primitive device, there were 4 apparent features in the trace, which were named A B C D (earlier, a different physiologist saw only two ventricular features that he logically named V1 and V2).
However, it was known that this primitive measurement was not showing the actual electrical signal, but rather a filtered version due to the physics of the mercury in the tube, which was subject to inertia and friction. When a physiologist used mathematics to essentially "deconvolve" the filtered signal to get the original signal back, he plotted both curves next to each other: one labeled A B C D, the other labeled P Q R S T (note that in this deconvolved version of the trace, there were 5 components rather than 4).
As for the choice of P Q R S T, the source I reference notes that these were the letters commonly used by Descartes, and since then have been commonly used to refer to series of variables when one needs to distinguish between ABCD, XYZ, etc.
Later measurements that directly displayed the 5-component PQRST wave continued to use that terminology.

Original: Einthoven W. Ueber die Form des menschlichen electrocardiogramms. Arch Gesamte Physiol.. 1895;60:101–123.
Reproduced in: Hurst, 1998

References:
Hurst, J. W. (1998). Naming of the waves in the ECG, with a brief account of their genesis. Circulation, 98(18), 1937-1942.

According to this site: http://www.ecglibrary.com/ecghist.html
Originally the waves were designated as A,B,C& D but after correction they were termed as P,QRS,  T.

Why PQRST and not ABCDE? The four deflections prior to the correction formula were labelled ABCD and the 5 derived deflections were labelled PQRST. The choice of P is a mathematical convention dating from Descartes (as used also by Du Bois-Reymond in his galvanometer's 'disturbance curve' 50 years previously) by using letters from the second half of the alphabet. N has other meanings in mathematics and O is used for the origin of the Cartesian coordinates. In fact Einthoven used O ..... X to mark the timeline on his diagrams. P is simply the next letter. A lot of work had been undertaken to reveal the true electrical waveform of the ECG by eliminating the damping effect of the moving parts in the amplifiers and using correction formulae. If you look at the diagram in Einthoven's 1895 paper you will see how close it is to the string galvanometer recordings and the electrocardiograms we see today. The image of the PQRST diagram may have been striking enough to have been adopted by the researchers as a true representation of the underlying form. It would have then been logical to continue the same naming convention when the more advanced string galvanometer started creating electrocardiograms a few years later. (For more on Descartes see Henson JR. Descartes and the ECG lettering series. J Hist Med Allied Sci. April 1971;181–186)


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What's the difference between proliferation and diffusion when talking about changes in tumor density?
Cell proliferation and cell diffusion seem to be important quantities to estimate when trying to understand or measure tumor growth, but I don't really understand a) the difference between them or b) their relationship to tumor growth.
Cell proliferation refers to cellular subdivision. This doesn't necessarily mean tumor growth because something can subdivide but still have the same net mass, right?
Cell diffusion on the other hand, refers to changes in cell density. Supposing cell proliferation is constant and we have positive diffusion, that would mean that cells are 'spreading out' (ie the mass is less dense but bigger). Is this correct? Would positive diffusion be equivalent to tumor growth?
This question came up when reading this paper. It talks about estimating diffusion and proliferation parameters in order to solve the reaction-diffusion equation which is, in turn, used to model tumor growth.

I would also like to see a reference to these terms if you have one.

A tumor by definition is an abnormal proliferation of cells but I don't think diffusion has anything to do with cells actually diffusing. Rather, the carrying capacity of a tumor depends on such parameters as nutrients or oxygen, which must diffuse further inwards until they cannot reach cells. Hence, the core of large solid tumors tends to be necrotic. It's also my understanding that there is a natural pressure that forces older cells inwards to the core of the tumor, as the outside layers continue to divide and grow outwards, increasing the diameter of the tumor.


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Number of Bacteria
I am creating a mathematical model for the growth of Synechocystis. sp PCC 6803 and Methanosarcina barkeri Fusaro in photobioreactors and anaerobic membrane bioreactors respectively. I have a couple of questions regarding this:

When you buy these strains, or bacteria in general, from a supplier, how many bacteria will you receive? (I need this for the initial number of bacteria)
How do you find/calculate the half-saturation constant? (Used in Monod's equation)
How do you find/calculate the growth limiting substrate? (Used in Monod's equation)

Any help would be appreciated!

What are your thoughts on questions 2 and 3? We can't really help you if you haven't even tried to answer these questions by yourself...

When you buy these strains, or bacteria in general, from a supplier, how many bacteria will you receive? (I need this for the initial number of bacteria)

You don't know how many cells you'll get. Depending on the strain and on how it was preserved (frozen, freeze-dried, liquid culture), the percentage of viable cells in the sample you get can vary a lot. Anyway, it is not like this that you will find the initial number of bacteria for your model. Before inoculating your bioreactors, pre-cultures have to be prepared. You won't be directly using the supplier's sample as inoculum.
As for how to determine the cell count in your pre-culture, it really depends on what kind of equipment you have access to. If you have access to a flow cytometer, then you can get the cell count directly. Otherwise, you can use more "traditional" microbiological techniques (Optical density, Petri dishes, Dry weight ...).
You might even consider using another variable than cell number for your growth model. It is often the optical density or the dry wheight that is modelled, rather than the number of cells.


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

I am looking at an old study on soil symbiotes that used lentils on agar, their method is described as {Surface-sterilized (1 min in 70% ethanol and 3–5 min in 3% NaOCl) and pregerminated (48 h on 1% water agar)} if that helps.

It sounds like your first issue is with seed germination. I am assuming you are doing a seed sterilization. You may want to try allowing them to imbibe water for about an hour after the sterilization process, and then wrapping them with aluminum foil and placing them in a fridge for a day or two. I've done this with Medicago, which is another legume. However, not sure if it works for your lentils.
The root may also have trouble developing given the micro-nutrients in the media. I am curious what recipe for media you are using, as the amount of agar may also affect the ability for these roots to penetrate the media. I have had trouble germinating legume seeds when there were 100+ seeds in a plate as they inhibit each others growth.
It's hard to give a clear answer, but try optimizing your seed sterilization protocol and media recipe and best of luck!


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Rosetta - What score does RosettaDock use for I_sc?
I want to get a score using Rosetta for how well a protein binds to a ligand. I understand RosettaDock has a score called I_sc which will give me a number to indicate that.
I found documentation in https://www.rosettacommons.org/demos/latest/tutorials/scoring/scoring about how Rosetta scores structures, but not sure what scoring function RosettaDock uses and whether it is the talaris2014 score.
So the question is what scoring function is used in RosettaDock for calculating I_sc.
Cheers

Unless you (a) ran some absolutely ancient version of Rosetta or (b) explicitly specified a different score function, your protocol should have used the current default ref2015. This will be the default until a few years when the next major update is released.
You can verify this by checking your log file, which should have a line like
core.scoring.ScoreFunctionFactory:  SCOREFUNCTION: ref2015


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What is meant by "catalytic amount of a hormone"?
This textbook says:

In the classic definition, hormones are secretory products of the ductless glands, which are released in catalytic amounts into the blood stream and transported to specific target cells (or organs), where they elicit physiologic, morphologic and biochemical responses.

What is meant by catalytic amount? Does it mean that amount required for catalysis? I know only renin which is catalytic and act as an enzyme, and many other hormones are non enzymatic so why the term catalytic is used in general sense?

In my opinion it isn't a very good phrase for a textbook because it doesn't have much meaning, but I believe what they are trying to convey is that they are released in small quantities, like is typical of enzymes - you don't need a lot because they work over and over again. By contrast, there are a lot of proteins in the blood that are expressed in fairly high quantities, like those involved in coagulation, to the point that they make up a non-negligible component of the blood.

@BryanKrause - I think they mean simply enough hormone to get the desired response. It can be alot or a little.

@anongoodnurse Perhaps, I guess that's why it really isn't clear. When a recipe for a chemical reaction says "catalytic amount" of something they usually mean a very small amount compared to the actual amount of reactants...like a "catalytic amount of platinum" - it just seems really strange to apply that terminology to hormones. This looks like one of the English textbooks written by a non-native speaker that we see a lot of questions about - sometimes the answer is just that a non-native speaker used a phrase they learned in a different context in a flawed way.

@BryanKrause - I too think it odd phrasing and unclear. I think of a catalyst as something that facilitates a chemical reaction. A "catalytic amount" of insulin depends on how many glucose molecules are in the bloodstream...

The writer obviously means “small amount”, and has chosen his words badly as hormones do not themselves catalyse reactions.
The idea he is probably trying to convey is that a few molecules of hormone binding to their receptor can cause changes to many molecules within the target cell. This often (generally?) involves catalysis within the cell produced by the receptor activating an enzyme, so one can understand the line of thought leading to the misuse of this term.