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Is there any disease in common between human and insects?
I am not asking about disease transferred by insects.
I am wondering is there any disease that commonly make both human and insects sick?

Welcome to Biology.SE! Many human pathogens are transmitted by insect vectors and these pathogens often also have deleterious effects on the insects — are those kind of examples of interest to you? (If so, please [edit] your first line to make this clearer.) Thanks!

@tyersome, Many thanks. I mean only the common pathogens that are very serious on both human and insects eg. making their life paralized, disrupted or cause death.

What research have you done to answer this question yourself?  You can search for insect viruses for starters. A better approach would be to educate yourself on the general features of virus diseases — what determines their host specificity and how they spread. The major differences in this regard between humans and insects should lead you to the most likely answer to your question.  Learn to save your own life.

@David, I searched google and the websites talk about everything but not the thing I want. Do you have any answer to this question? BTW, I am not a biologist but an engineer.

Patience. We have some virus experts here, who I would have expected to answer you. They may be busy saving the world from the coronavirus at the moment, as you can imagine. I’m busy too, but will get back if nobody answers. Why do you ask, anyway?

@David, asking mostly for fun. But, I am curious to know if a human virus from a sick human can kill insects too? Also, I am curious about the similarity of human body and insects when affected by a common virus/bacteria.

Been very, very busy, and had difficulty finding the sources I hoped for, but finally found time to honour my promise.

It is always difficult to prove that something does not happen, so I will restrict myself to saying that I know of no examples and think it unlikely that there will be a common viral or bacterial disease of human and insects.
Viruses are not limited to a single host, but the typical host range of mammalian viruses would not appear to extend to insects, as far as one can tell from the literature — see e.g. the Wikipedia entry on Virus.

Viruses are by far the most abundant biological entities on Earth and they outnumber all the others put together.[134] They infect all types of cellular life including animals, plants, bacteria and fungi.[3] Different types of viruses can infect only a limited range of hosts and many are species-specific. Some, such as smallpox virus for example, can infect only one species—in this case humans,[135] and are said to have a narrow host range. Other viruses, such as rabies virus, can infect different species of mammals and are said to have a broad range.[136] The viruses that infect plants are harmless to animals, and most viruses that infect other animals are harmless to humans.[137]

Likewise for the host range of bacterial pathogens, judging from articles such as an article by Baümler and Fang in the Cold Spring Harbor Perspective on Medicine.
One general molecular reason for expecting a limited host range that would exclude insect/human pathogens relates to the means by which the pathogens enter the host cells. Quoting, for example, from the abstract of an article by JM Casasnova:

To initiate the infective cycle, the viral genome must therefore translocate from the viral particle to the cytoplasm. Via distinct proteins or motifs in their outermost shell, the particles attach initially to specific molecules on the host cell surface. These virus receptors thus mediate penetration of the viral genome inside the cell, where the intracellular infective cycle starts. The presence of these receptors on the cell surface is a principal determinant of virus host tropism.

The membrane proteins that act as receptors generally differ between related members of a species, but mutations can allow the viruses to cross species barriers. However the extreme difference in cellular structure and biochemistry between insects and humans make it unlikely that this could happen, even if the cell type and protein still exist in common. Consider, for example viruses such as Hepatitis A, B and C which infect the human liver. My own favourite insect — Drosophila melanogaster — does not have a liver as such, its functions being served by the insect fat body.
I am less familiar with other aspects of the viral life cycle that relate to physiology (my background is chemical) but these clearly differ and would affect modes of transmission, for example respiratory and sexual.
These latter considerations will also apply to pathogenic bacteria. As an anecdotal conclusion to an imperfect answer, I would mention the bacterial diseases of silkworms that affected the French silk industry in the 18th century. There are several accounts of Louis Pasteur being called in to eradicate the disease but these contain no suggestion that the workers breeding the worms contacted the disease.

Tribute to Pasteur for ‘saving’ the silk industry at Ales, nr. Nîmes, France

Flaviviruses are an important group of virus, including yellow fever, dengue, zika, west nile, japanese encephalitis, tick-borne encephalitis. These viruses spread through the human population via arthropod vectors. The vectors have separate tubes for pulling blood in and injecting saliva; so in order to infect a vertebrate, the virus has to get from the blood meal in the arthropod vector's gut to its salivary glands where it can be injected into the next vertebrate host. This can only be done by infecting and reproducing in the tissues of the 'vector'. They can perhaps be more accurately thought of as a class of arthropod viruses which use a vertebrate vector in some cases:

the wide diversity of flavi-like viruses found in invertebrates, as well as their deep phylogenetic positions, suggests that they may represent the ancestral forms from which the vertebrate-infecting viruses evolved.

from  https://jvi.asm.org/content/90/2/659
For west nile and Japanese encephalitis, humans are a dead-end host, that is, an infected human doesn't produce enough virus for a mosquito to get infected from feeding on them.
As for how sick the arthropods themselves get from these infections, I wasn't able to find much information. West nile gets into the brains of infected mosquitoes, so I would expect significant pathology. However, if the mosquito is incapacitated it cannot bite a second host so there is evolutionary pressure for milder disease.

Few bacteria infect both humans and insects - though not many people care about keeping insects healthy.
Yersinia pestis causes plague in humans (and some other mammals) and in the Oriental rat flea can block the foregut. I don't know how bad that is for the flea, or whether this counts as a disease of insects.
There are some similar genera (groups) of bacteria living in and on both hosts; Clostridium, Lactobacillus, Enterococcus, Staphylococcus, Pseudomonas. The last has species on plants as well.

Though quite a lot of people care about making insects sick, as for instance biological pest controls such as Bacillus thuringiensis: https://en.wikipedia.org/wiki/Bacillus_thuringiensis


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What is meant by translational repression by an upstream open reading frame?
The NCBI report on the human huntingtin gene contains the following statement:

“This gene contains an upstream open reading frame in the 5' UTR that
  inhibits expression of the huntingtin gene product through
  translational repression.”

But no specific reference it given. Can anyone explain what this means.

What I understood is that the promoter of the gene can only bind to repressors and inhibits translation. Am I right?

No. Please cite the source of your quotation. You say there are many mechanisms to achieve this, but do you know what “this” is? Do you know what translation is and what in a general sense repression would mean? (And how translation differs from transcription? Your talk of promotors suggests not.  Or is it this particular example? In which case, as stated, give us your source.

@David  https://www.ncbi.nlm.nih.gov/gene/3064  The last line of the Huntington gene summary is the source of the quotation. The reason why I say there are many mechanism for "this" is http://www.jbc.org/content/285/37/28506.full    https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1007059   etc. I know the basic difference between transcription and translation. And repression, as I know, is the process of inhibitors binding to the promoter hence repressing transcription and translation.

No. Repression is a general English word meaning to subdue or put down, and a general molecular bioscience word to diminish or inhibit, which can be applied to many systems, and implies no mechanism and certainly does not require promoters, which are in no way involved in translation (at least in eukaryotes). I’ll look at the paper later.

@David oh..okay. Thanks!

Summary
The statement refers to the small but significant translation of short open reading frames (ORFs) of huntingtin mRNA, 5′ to the main open reading frame that encodes the large (3144 amino acid) functional product of the mRNA (and gene). It has been reported that the translation of these short ORFs decreases (i.e. inhibits) the translation from the main ORF. It is implied that this is a mechanism for regulating the expression of the gene, and, as it occurs on the mRNA in the cytoplasm, it is an example of ‘translational regulation’ — specifically inhibition. The precise mechanism of this regulation — although not unique to this mRNA — is apparently unknown.
Translation of ORFs in eukaryotic mRNA
Most eukaryotic mRNAs are functionally monocistronic — i.e. they encode only a single protein — unlike bacterial mRNAs. Initiation of protein synthesis involves selection of an initiation codon (usually AUG) by a complex of initiator-tRNA and the small ribosome subunit, but, in contrast to prokaryotes, the mechanism in eukaryotes involves scanning along the mRNA from the 5′ end. In the majority of cases the initiation codon of the protein product is the first AUG, but the significant number of exceptions suggest an effect of sequence context or mRNA secondary structure.
In recent years evidence has accumulated that in cases where the first AUG is not that of the main protein product, a small amount of translation from such 5′ upstream ORFs does often occur.

Diagrammatical representation of mRNA with upstream ORF (blue with initiation codon represented as an open triangle) and main ORF (black with initiation codon as closed triangle.)
Regulatory role of upstream ORFs
Johnstone et al. (2016) have reviewed a large body of evidence that indicates that upstream ORFs are translational repressors in eukaryotes. This has generally been established by measuring the extent of translation of the main ORF after manipulation or removal of the upstream ORFs. Much less is known about the actually mechanism of such regulation, which may vary from case to case, and certainly the paper on huntingtin only offered speculative possibilities. These include:

Binding of small peptide products of the upstream ORFs to the AUG of the main ORF
Pausing of ribosomal initiation complex at upstream ORFs impeding the progress of other to the AUG of the main ORF
Change of mRNA secondary structure by the binding of the ribosomal initiation complex at upstream ORFs increasing the difficulty of the initiation step in which the 5′ end is ’melted‘.

It also appears that the extent of the translation of upstream ORFs — and hence the extent of the repression — can itself be regulated by mechanisms such as the phosphorylation of initiation factor eIF2.

Seems odd that translation occurs in the so called untranslated region.

@canadianer — History. I didn't want to go into it in any more depth, but the initial assumption back in the 70s and 80s was that because mRNA was monocistronic (e.g. beta-globin) there was only one translated reading frame. It is obviously necessary to be able to name features of something one is discussing, and the regions of the mRNA 5' and 3' of the region coding for the protein were of interest — e.g. did they have any function regions, describing where the initiation complex started etc. At the time "untranslated region" (UTR) seemed appropriate. Knowledge changes, names stick.

Of course; just seemed amusing.

@David Thank you very much for your insight. I am new to the subject and have no background so this was really helpful.

source: Stack Exchange

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Inhibitory functional connectivity
Functional connectivity may be defined as

»the temporal correlation between spatially remote neurophysiological events, expressed as deviation from statistical independence across these events in distributed neuronal groups and areas«

or alternatively as

»the presence of statistical dependencies between two sets of neurophysiological data«.

Images of large-scale brain networks typically show highlighted regions of interest that - in my humble understanding - are supposed to be functionally connected. But being highlighted means being active (at least more active than other regions), and thus functional connectivity seems to be mainly excitatory (even though only virtually).
But what about inhibitory functional connectivity? Can it be found by equal statistical means as excitatory functional connectivity - and how would it be "highlighted" in brain images?

On Neuroimaging Analysis

But being highlighted means being active (at least more active than other regions)

This is not the case in functional connectivity analysis, or indeed not necessarily the case in any sort of functional neuroimaging analysis. The colormap highlighting in such images as you referred to (see the primary reference for that particular image) reflect statistic scores, commonly z- or t-statistics. Correlation simply means that time-courses behave similarly over time, and the color coding tells you how strongly they correlate with the “common profile” of the cluster. This makes no direct statement regarding the total “activation level“ over time, as represented by e.g. the area under the curve of the timecourse. In fact, such a metric would be meaningless, since fMRI signals are de-meaned so that they fluctuate around zero (as seen e.g. in the timecourses depicted here). Functional connectivity networks thus do not imply in whatever fashion a higher level of activity in highlighted networks. For further visual clarification you can consult Figure 1. of this article showing that functional connectivity networks can be and often are active at the same amplitudes and have similar levels of “total activity“ as visually inferred from the integral of the power spectra. This integral analysis is not presented, however, as it is meaningless.
On Inhibitory Functional Networks
Whether functional connectivity networks are implied to be excitatory depends on the exact mode of analysis. If the analysis is truly based only on detecting large correlation scores, identified networks will not resolve inhibitory projections, as such connections would cause anticorrelation rather than correlation. It could still be that a functional connectivity network is based on multiple areas receiving strong inhibitory input from an upstream node, yet that node would not be part of the network. Consequently, proficient functional connectivity analysis will identify networks via methods such as independent component analysis (ICA), which are able to group both strong correlation and anticorrelation together, as seen here.
TL;DR
Yes it can, it often is, and it's generally highlighted in blue.

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Are there "old" neuron types in the neocortex?
"Old" may mean a neuron type that appeared early in the tree of life, and it may mean – going together – that it comes early in the lineage tree of neuronal cells, rooted in the fertilized ovum:
[This is only for Schmidtea mediterranea. Could someone give me a link to a comparingly nice lineage tree for human neurons, please?]
My question is twofold:

Are there neuron types in the adult healthy brain co-present with some of their differentiated descendants?
Are there "old" neuron types in the neocortex, that either appeared early in the tree of life or come early in the lineage tree?


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Do cats ingest everything that they lick off themselves during grooming?
Cats are well-known for licking themselves clean, but what happens to all the loose hair and sand and mud and wet substances that they lick off themselves? Do they ingest everything? Do they cough up and vomit out a furball later with all of this? How is a cat's digestive system suited to handle all the inedible environmental substances?
I have a pet cat and I've never understood where all that she licks off herself is going.

It’s your cat. Watch it and tell us what you observe. Note that in English one preposition is enough — “off of” is too much.

My cat's a feral but friendly cat. She visits me by herself, a couple of times a day and several times a week; meows, eats the food I provide, shows me a great deal of affection (sometimes even brings me mice), sits by my side and grooms herself to no end, even takes small naps. But when all is done, she just gets up and leaves. She's not a home cat, and I don't have a chance to watch her full habitual routine.

Their digestive system breaks down all the substances it can break down and the rest is vomited or expelled within faeces

Cat licking is partially to clean themselves (including of odors that might attract predators) but is also used as a cooling mechanism (they sweat little and so use evaporation of saliva as a cooling mechanism), socialization, and to help spread oils. Most hair in short haired cats passes through the digestive tract with no issue. Source The hair that is unable to pass through the cat will accumulate in the stomach and be coughed up as a hairball (generally every 1-2 weeks) source.
For more on a cat's digestive tract see here. Note also that the human digestive tract can manage all manner of weird things to and just allow it to 'pass through' and this is the 'default' behavior for many digestive tracts.


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Understanding ancestry testing mathematically
Forgive me if this question has been asked here before, because it is something which should be very easy to find, but I can't seem to find an answer no matter where I search.
The question is simply where to learn the mathematics that goes into things like popular ancestry tests, and also more academic things like determining ancestry components of historical groups (e.g. usage of the terms Ancient North Eurasian, Eastern European Hunter-Gatherers and all that).
It is clear that if someone gets an ancestry test saying say 32% Scandinavian, then of course that doesn't mean 32% of their base pairs have a convenient "Scandinavian" label attached to them, rather there is some statistical inference going on behind these percentages, and I would like to understand that.
Suppose I have the raw data of my own fully sequenced genome, and also a database of the genomes of many individuals from various populations (of course grouping them into populations is already something that involves some assumptions that I would like to learn more about). Where would I learn how to analyze that myself to produce something like the results of an ancestry test? Is there a textbook someone could recommend that gets into the actual algorithms used?

I'll give here a simple, non-technical answer because I'm assuming you don't need to actually perform an analysis of ancestry.
So, detecting ancestry is a non-trivial task. Given your genome sequence, you would need to compare some "informative" regions of the genome with the homologous sequences of some population (say, of a database with other genomes). These informative regions are usually some parts of the genome that vary across individuals (variation is used because differences are informative: some populations vary on particular sites, distinct from other populations). At the core, this is a question on how to compare "character strings" (DNA is composed of 4 characters, namely, A, T, C, and G). But these strings exist in a complicated structure: a human genome is partitioned in 23 pairs of chromosomes, within each individual. However, the question of ancestry is not about individual sequences really, but about population-level changes in DNA composition. So, in fact, you need to consider population-level factors: size of the populations to consider, the rates of recombination (DNA exchange across chromosomic pairs), mutation rates, and even population structure (people move geographically!).
Given these (and, many other) factors, people build models of "coalescence": given a sequence of interest, how likely is that it shares some ancestor with another query sequence? So, the models try to relate these two sequences (say, the one you are interested), with a query (say, a "consensus" Scandinavian sequence), and then make a model of a 3rd sequence (the ancestor!). This process is repeated to test many hypothesis, so you end up with many probabilities. On top of this, you can estimate the ancestry for any given part of your genome, and this is what most companies do (say, 23 and me).
In summary, you are correct that a "% Scandinavian" does not mean sequence similarity per se. It implies an estimation of common ancestry. This estimation comes from models of shared ancestry. If you're unsatisfied with this simple answer, and want a more technical answer, I recommend reading this paper. An intermediate-level explanation is found here.

What is ancestry?
I think some of the confusion in ancestry proportions stems from the fact that 'ancestry' can really mean several different things in different contexts. I would really encourage people to read this short piece, as it does a good job of clarifying what the different terms mean https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1008624
What something like 23andme is trying to do is to infer how much of your genome most closely matches the genome of a particular pre-specified reference population. This is relatively easy to interpret if one parent if from Nigeria and the other is from Norway, since it will roughly be 50% Norwegian and 50% Nigeria, but becomes more complex to interpret when someone is 70% Norwegian, 20% Danish and 10% Swedish, for example.
Summary of the 23andme process
Since you specifically asked about 23andme, I will try and give you a relatively simple explanation of how they end with the numbers that you might have got on the report.
What 23andme are trying to achieve is essentially a 'classification' problem - they have a genome from an individual of unknown ancestry (call this the target individual), and they would like to describe it in terms of some pre-defined set of different ancestries (like 'Norwegian' or 'Nigerian'). To achieve this, they first need to assemble some kind of reference dataset of individuals of whom they know in advance to be of a certain country. For this, they will choose individuals who they know have e.g. all of their grandparents and great grandparents from Norway - so they genomes of these individuals will be reflective of general Norwegian ancestry.
They use something called Support vector machine Learning, which is just a fancy computational method, to 'learn' what segments of Norwegian ancestry look like. This is analagous to the AI algorithms which are able to tell the difference between an image of a cat and a dog. If you 'train' the AI with enough labelled examples, it can accurately classify new images. In the same way, if you train the SVM algorithm with enough examples of what Norwegian or Nigerian DNA segments look like, it can classify the probability that a new segment comes from a particular reference population.
They then take the genome of target individuals and split it up into chunks along the genome (something like 100 chunks per chromosomes). They then apply the SVM algorithm to calculate the probability that a particular chunk comes from a particular reference population. So for example, there might be a certain chunk of the genome which has a 70% chance of coming from the Norwegian reference population and a 30% chance from come from a Danish reference population. If the individual is admixed, the the next window may have a 90% chance of coming from the Nigerian reference population and a 10% chance of coming from the Cameroonian reference population.
They will then go across the genome and look for windows of 'high-confidence', where the probability of the window coming from a particular reference population may be higher than say 90%. If you add up the high confidence windows across the genome for each reference population, you will end up with your overall ancestry proportion for that population.
Other ways of inferring ancestry
There are many, many other ways of inferring ancestry proportions/components. For example, Principle Component Analysis, ADMIXTURE analysis, clustering methods, all of which have different strengths and weaknesses.


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Did any warm blooded animals evolve back into cold blooded?
Pretty much as title says - wondering if evolution can go from mammal back to reptile - either in theory or practice.

The terms "warm-blooded" and "cold-blooded" are very undefined.Please have a look at this post or this post for the correct terms and concepts. I suppose that you meant "endothermy" and "exothermy" instead of "warm-blooded" and "cold-blooded" but I am not 100% sure.

I think your question will be improved by doing some reading on thermoregulation and then incorporating that knowledge to create a better defined question. For example you could start with this wikipedia article and the associated articles.  ——— You also seem to be confusing taxonomic groupings (e.g. mammals) with types of thermoregulation (e.g. "warm bloodedness), which is likely to get a negative response ...

Secondary ectothermy has been suggested in living crocodylians by Seymour et al. (2004). Their rationale is based on:

Presence of a 4 chambered heart (otherwise only found in endotherms)
Post-cardiac shunting via the foramen of Panizza and "cog-tooth" valve, which develop secondarily in crocodylians
Lung structure and ventilation during locomotion

Thus ectothermy in extant crocodylians is associated with being aquatic or semiaquatic. These authors suggest that endothermy may have been ancestral for dinosaurs as well.
Seymour RS, Bennett-Stamper CL, Johnston SD, Carrier DR, Grigg GC. 2004. Evidence for endothermic ancestors of crocodiles at the stem of archosaur evolution. Physiol Biochem Zool 77:1051–1067.

There is no evolutionary "ratchet" that prevents a life form from evolving "backwards".  However, it is statistically unlikely because it would pretty much require all of the environmental factors that changed during the transition from "cold blooded" to "warm-blooded" to change back in the reverse order, because all of those factors contributed to the selection pressures that caused the "forward" evolution.
It would be analogous to getting a set of moving billiard ball to reverse direction and re-form an earlier pattern: reversing any one ball's velocity would be fairly easy, but getting all of the balls to cooperate to re-form a static pattern that ends up shooting out the queue ball is so unlikely as to be effectively impossible.
That said, for a modern form (B) to evolve into another form (C) that resembles an archaic form (A) without actually being that archaic form would "only" require a sequence of environmental changes that leads to the evolution of (B) from (A).  It just wouldn't actually be the archaic form.  It would be a process analogous to convergent evolution.


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What does microglia process length tell us?
I'm reading a study investigating traumatic brain injury and alcohol consumption and the researchers measured microglia process length as an indicator of brain damage. I was wondering what that would indicate and how does it an imply brain damage?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular it would helpful to define all abbreviations (I did that for you) and to include reference information and a link for the study you refer to. ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

Part of this question is due to the function of microglia in the healthy brain (as we currently understand it).  The general idea is that microglia in a healthy brain are in "surveillance mode," and have long, thin processes that extend of the cell body to monitor the environment.  It would be like beat cops splitting up and walking the streets when no crime is reported, they're just monitoring one large area by spreading everyone out.  However, when some insult occurs and microglia are activated (which just means they get into a mode responsive to some insult or injury), which results in them having shorter processes and enlarged cell bodies to focus on the damage done in their immediate vicinity.  This would be like one of the beat cops seeing a crime, then calling for back-up.  Now the focus is on the scene of the crime or site of damage.  Therefore, if your microglia have long, thin processes, everything is pretty much normal because these microglia are not activated.  However, having a lot of microglia with short, thick processes indicates that they are activated in response to some injury or insult.  This is why a common practice is to use microglial process length as an indicator of microglial activation and, in turn, some form of damage to the brain.
In shorter terms:

Long, thin processes = lack of microglial activation and little to no brain injury
Short, thick processes = microglial activation, indicative of brain injury

My source is just my experience in neuroscience and reading these types of papers, but there's more information on microglial activation here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5431479/ which includes some discussion of process length and morphology.

This answer is almost certainly correct. Probably the only better reference would be if OP had shared a citation of the paper they are reading, which almost certainly explains this in brief as well.


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Species identification: what kind of fungus is this?
Found in a cave
Location: Israel
The white tentacles appear to be sticky. When they touch something, they stick to it and detach from the main body

Welcome to Biology.SE! Please [edit] your post to include the size of these structures, where they were located in the cave (e.g. on the walls near the entrance), and why you concluded they were fungi. ——— If possible clear, closeup photos of the structures from multiple angles would also be helpful. Thanks!

I think these are parasitized insects.
Fungi of various types can infect insects.  The end stage produces these fruiting bodies.  Here is an example I found on the excellent site WhatsThatBug.

Here is another example.

http://www.anura.it/the-parasites-parasite-everyone-has-a-bad-day/clasp04/
The second site notes

Entomopathogenic fungus (Clavicipitaceae sp.) killed a troglophile
  moth, Veins cave (Grotta delle Vene), Italy

I would guess something similar for what you found.
I must say your images are incredible.  The long fungal tendrils on the second image are the most amazing example of this I have ever seen.


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How to analyze phosphorylation shift by western blot?
I want to see the phosphorylation shift in my protein of interest.
I have created a point mutation in my protein. so that it will not able to go for the phosphorylation compare to my control. i want to check by western analysis.
i can see a very small shift. is it possible to get a better shift?
Another important thing is my protein size is ~150 kDa.
can you please share any suggestions on this

Are you dealing with phosphorylation of tyrosine, threonine, or serine? 2) What is the difference between the control vs. WT? 3) Why do you want to do this — there may be alternative techniques that could be more reliable ...

Exactly serine to alanine. Fine, actually one allele is knocked out, another allele is mutated. Wt is a parental cell line. control is a single knockout without a mutation. I know there are other methods available but i wanted to verify by western analysis

Why is there an apparent size difference between the WT and control?

Did you do SDS-Page or a native gel?

Why is there an apparent size difference between the WT and control? For this Wt i used a different tag (smaller size). Control and my experiment i used the same tag (bigger in size)                                                                                Did you do SDS-Page or a native gel?     SDS- Page

Please [edit] your post to include all the relevant information from these comments. Comments are ephemeral and thus should not contain material essential for understanding the question. Thanks!

The run length of bands in an SDS-PAGE (which your western is probably based on) depends - at least in theory - only on the size of the protein: SDS binds to proteins with a fixed size ratio and thereby provides a negative charge based only on size. Unless you have reason to believe that your protein is an exception from the usual (which might be indicated by things like not running at the expected size) you will very likely not be able to see a band shift (change in run length) based on presence or absence of phosphorylation in a standard western blot.
Things you could try to detect the phosphorylation:

Use phospho-specific antibodies. These are often expensive, tricky to use or just not available, but this is the only ting I can think of working with a standard western blot setup
run a native-PAGE, that way your run length depends on shape, size & charge of the protein. I still wouldn't expect a single phosphorylation to be cause a visible shift for a 150kDa protein, but you can try. This might require using longer run-time of the gel to get really high resolution for the size you are looking for

I agree that observing a shift for a 150 kDa protein may be difficult, but shifts due to phosphorylation can be seen for some proteins on SDS-PAGE gels. See for example this paper.

@tyersome I guess it is possible in some cases even though it normally shouldn't happen - I edited the answer. Also note that the authors of that paper were "using a modified acrylamide/bisacrylamide ratio" for the gels to get a visible separation of the two bands.

Yeah, it will take 15 to 20 hrs to complete the run. sometimes the gel gets a small break. i


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How does a virus stick to a non-biological surface?
Recent events has triggered an renewed interest in understanding how a virus is able to stay on a surface.
For sake of argument, let's assume we are dealing with a Corona-type virus. One can then speculate that a virus sticks to a (non organic) surface due to a London-force (a Van der Waals force) interaction between the surface and the virus Spike S protein. But I really have no idea and it's just a wild guess.
I'm looking for research and experiments on this topic but I can't find any, most likely because I am not asking Google the right question or using the correct biology language.
How does a virus stay attached to a non-biological surface?
(Are there any "stickiness" measures for this?)
PS. When I say non-biological, I mean glass, metal and plastic.

It might be useful to look into studies that have been done into colocalization of viruses and bacteria on (organic) biofilms (e.g., https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4993353/).

The virus never appears isolated. When it is distributed by droplets or feces that is the transportation medium. And those are sticky by them selfes.

@aggsol do aerosol droplets last days attached to surfaces even when said surface appears dry? Is it microscopic?


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What is this unusual structure inside this banana?
I was eating a banana, and I found this strange biological structure inside of it.

It was a bit tougher than the banana, and ran inside of the body through most of the length. To be clear, I peeled back banana with my fingers to reveal it; it was enveloped inside. It was accompanied by a small void.
No idea what this is, never seen anything like it. It didn't taste good. I'm thinking it might be a mutation. Anyone know what this is?

"didn't taste good"? Are you insane?

@A.I.Breveleri thought it might give me powers.

@A.I.Breveleri I would assume that's how OP found out something was wrong with their banana. :-)

@John yep :√)

It looks like some species of Nigrospora genus took over the inside of that banana. According to Wikipedia, N. sphaerica was first isolated from bananas. The other species that you will find referenced online is N. oryzae. In the articles I
cite below the colonies are grown in potato dextrose, though.
Here is a picture of the red fungus inside a banana (from the Canadian Food Inspection Agency):

Googling 'Nigrosporia banana' also returns lots of similar pictures.
To get a better answer, a sample could be taken from the banana and then cross-check what you see under the microscope with the oryzae morphology images seen in the researchgate article.

Well I won’t be eating bananas again.

That's freaky, I don't like that.

@Phoenix Just get revenge on their (distant) family, by consuming copious amounts of mushrooms.  It's just like the mafia... only eating food.

Wikipedia says it has antiviral properties. Maybe you should eat it?

@CJDennis It has some side-effects too, so I wouldn't recommend it. Although apparently they've successfully used it against MRSA cultures, so perhaps it has potential in derivative form. But I suspect this is one of those cases where the cure is worse than the original ailment.


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Can anyone identify this mite?
I live in a flat in the UK and have caught such mites a few times on my skin. I think they are responsible for my bites. On one occasion one mite had one dark spot in the middle instead of two.
Does anyone know what it is?
Regards

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Why would it be beneficial for cortisol and corticosterone to exhibit pronounced anti-inflammatory activity?
These questions are always a little silly (as we will never truly know), but it always struck me as odd that corticosterone and cortisol exhibit pronounced anti-inflammatory activity.
Because these compounds are released during fight-or-flight episodes, it seems almost counter-intuitive for an organism to promote "anti-inflammatory activity" during an event that is most likely coincident with injury (i.e. wounds from fighting / escaping).
Anti-inflammatory activity, I believe, is fairly synonymous with anti-coagulation activity. If wounds are most likely to occur during periods of fight-or-flight (which is a reasonable intuition), why would organisms select for a glucocorticoid that has additional effects such as reducing acute clotting capacity?
The only thing that I can think of is there is an energetic cost to initiating the coagulation cascade, which would siphon energy away from skeletal muscle. Any thoughts / hypotheses?
Cheers~

Interesting question. It's easy to imagine why you would want to suppress inflammation in a fight-or-flight situation. Inflammation can cause painful swelling, fever, and it can dull mental acuity, all of which might hurt your chances of a win or escape.
After a little PubMed search, it looks like sympathetic adrenal responses (like cortisol) can actually induce a net hypercoagulability of the blood (1). So, even though inflammation does induce coagulation, it looks like the sympathetic anti-inflammatory response is not necessarily synonymous with anti-coagulation. This also makes sense in the context of Cushing's Syndrome, where hypercoagulation is associate with elevate cortisol levels, among other factors (2).


text:
Is it safe to work with HeLa cells?
Hela cells are infected with HPV. So is it safe to work with them? What are the safety precautions?

Most guidelines for HeLa (and most cells of human origin) say they should be kept at a BSL2 level. For example, from a 2007 publication in Applied Biosafety:

Work with cell cultures from human or primate origin should generally be performed under BSL2 conditions. Containment level 1 may be considered if all manipulations occur in a Type II biosafety cabinet ...

--Animal Cell Cultures: Risk Assessment and Biosafety Recommendations
ATCC general guidelines recommend BSL2 containment for the broad category covering HeLa:

Biosafety Level 2

Cell lines that harbor mycoplasma or any other BSL 2 agent (See: NOTE)
Cell lines exposed to or transformed by a primate oncogenic virus
Primate cell lines that contain viruses
Cell lines carrying a part of certain viral genomes, even if whole virus is not released from the cell

--ATCC® ANIMAL CELL CULTURE GUIDE: tips and techniques for continuous cell lines
Their specific page for HeLa also recommends BSL2, with the note "[Cells contain human papilloma virus]".
That said, HeLa cells have been very widely used, including for decades before modern lab safety practices were agreed on, and I'm not aware of any actual problem ever arising (including such amazing practices as injecting live HeLa cells into convict "volunteers" to see if cancers would appear - They did not).
So the answer to the question is that it is safe to work with HeLa cells, but that proper BSL2 lab practices should be followed.


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Why do guard cells open stomata when they are swelling?
As the concentration of potassium inside guard cells increases, water enters the cell by osmosis.
But why does the swollen causes the stoma to open?
Does it relate to the thickness of the cell wall?
If so, how?

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@tyersome, thank you for telling me that. However I have tried to do some research on it and I know how the concentration of potassium ions affects the cell's water potential which makes them swell or shrink.But my question is how swollen change the shape of cells and therefore open the stomata---why don't cells come more closely when swelling as they have larger volumes? ( and unfortunately I can't find the answers on the internet.)

Sorry I should have looked at that page closer, you are correct it doesn't actually answer your question. This site seems to have a reasonably clear explanation, though it doesn't address all types of stomata. Does that help?

The link that @tyersome mentioned in the comment does a great job of answering your question. In the event that you read it and still have some confusion, here is a metaphor: imagine guard cells as two modeling balloons (the long kind that clowns use to make figurines) that are slightly inflated and attached together at both ends. Since they are only slightly inflated, they are able to sit flush next to each other. Now let's say you inflate the balloons. Since they are still attached to each other at both ends inflating them will cause them to bow outward and away from each other. The expansion will cause there to be space between the two balloons.
This is not a perfect analogy since guard cells have a varied amount of rigidity in their cell walls contributing to the shape when water enters. But maybe this can help you visualize the concepts introduced in the link above intuitively.


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What kinds of fish tend to have a rapid death after being caught?
I am asking this question because I am trying to make my diet less cruelty-oriented, for this reason this question can be related to trolley problem since I am coping with an ethical problem trying to minimize the the core aspect i.e. suffering.
On the contrary I would like to know what kinds of fish suffer the least after being caught. I know that shrimps/prawns die very quickly since they cannot breathe out of the water, for instance here I have read that prawns die after  just a couple of minutes out of water. But for medium/small size fish is different, especially for those which are mass-caught. Not to mention the explosion of bowels caused by rapid pressure variation.

https://philosophy.stackexchange.com/

@JohnHadish I think technical knowledge about pain is required in order to answer


text:
How to estimate mRNA counts from Relative Promoter Units (RPU) or RNAP per second (PoPS) in E. coli?
I need a rough estimate on how to translate RPU or Polymerases Per Second (PoPS) to mRNA count (or even better protein count) in E. coli.
I understand that any number we come up with will be a very rough estimate of it, but for now, I need a placeholder value to do some modeling on genetic circuits in E. coli until a more verifiable number comes about.

Can please you explain (or provide a link to) what you mean by these terms as they are not very common? In general, mRNA count is easier to estimate than calculating the speed of polymerase. So you are better off counting mRNAs directly instead of extrapolating from these parameters. Protein count is even more difficult to estimate using these parameters. You can't have a good estimate of protein counts unless you know about translation initiation and elongation rates and protein degradation rates.

Yes, of course, I added the links just now. I know it would be much better to have mRNA numbers and then simply estimate protein numbers using an average ratio for E. coli. However, there is a study I am basing of my work and we only are going to have RPU or PoPS to base of, so was wondering if anyone had any references or rough estimates as to how to translate these into mRNA numbers for E. coli

I could not find any paper that discusses these issues. So this answer is just based on my guess.
From the this page:

Transcription rate is generally a parameter associated with a
  particular transcript and has units of transcripts per unit time. In
  contrast, PoPS is essentially transcription rate at a particular
  location on the DNA. The value of PoPS just downstream of a coding
  region should be equal to the coding region's transcription rate.
  However, there are certain positions at which a transcription rate
  doesn't necessarily make sense yet PoPS does. For instance, as
  biological engineers, we care about the rate at which RNA polymerase
  moves through a terminator (or the PoPS downstream of a terminator)
  but yet most people don't talk about the transcription rate of a
  terminator.

What we want is the transcription rate for every gene. You can estimate it using PoPS corresponding to that terminator.
Now, at steady state the mRNA concentration would be the rate of formation divided by the rate of degradation (removal): rf / rd.
Since the study that you are referring to, calculates PoPs, I would guess that it is based on some standard BioBricks parts. You are likely to have have mRNA degradation rates associated with these transcripts (even protein formation and degradation rates, possibly). If you don't have the mRNA degradation rate then at least for long lived mRNAs, you can assume the rate of removal to be same as the dilution rate (loge2 / doubling time). Substitute this in the equation for steady state and you should get mRNA concentration.
Steady state protein counts would be: mRNA counts × protein formation rate / protein removal rate.


text:
Why is there disagreement on the number of surfaces of the human heart?
I am finding that some state that there are 5 and some that say that there are 3.
For example, "Cardiology: An Integrated Approach" that was published in 2018 states that

There are 3 surfaces of the heart: anterior, inferior, and posterior

Radiopedia, Teach Me Anatomy, and others state that there are 5.
Why is there this difference? What exactly is a surface?

Hmm. Curious what answers you get. Anecdotally, I've studied cardiac (and especially coronary) anatomy extensively and have never seen these "surfaces" described. Seems silly to me and not related to the actually relevant anatomy.

Heart surfaces are not clearly anatomically defined but arbitrary determined in the context of the heart orientation, that is the relation of the heart to other organs. Different sources mention 3 or 5 heart surfaces and there seems to be no "official" agreement about this.
Most sources (Dartmouth College, Gray's Anatomy for Students 2004...) agree about at least 3 surfaces:

Anterior (or sternocostal)
Inferior (or diaphragmatic)
Left pulmonary

Many sources (TeachMeAnatomy, KenHub...) mention additional 2 surfaces:

Posterior (or base)
Right pulmonary

The reasons for disagreement:

The heart base may not be considered a distinct surface (as in the picture).
The right pulmonary and anterior (sternocostal) surface are often considered one surface.

Picture: Heart surfaces (source: Echo Class 101)


text:
Why are eyes more sensitive to flicker in periphery — contradictory answers
In terms of the perception of flickering by CRT monitors, This answer suggests that peripheral vision has faster response and is thus more sensitive to flicker due to being provided by rod cells.
But in another answer it's said that rods are saturated at daylight and even at twilight. These two answers are in contradiction, since the light from CRT mentioned in the question pointed to by the first link above is quite above the photopic threshold.
So, how to reconcile these two answers?

It's not entirely clear what you mean by "why".  Do you mean the mechanism by which the sensitivity is accomplished, or the evolutionary reasons why such sensitivity might increase survival.  (That is, something moving fast at the edge of your visual field might want to eat you :-))

@jamesqf I'm interested in the mechanism.

I think the most likely explanation is that ambient lighting conditions in the room where OP was sitting, as described in the original question, might not have been bright enough to saturate the rods. Under mesopic conditions, both rods and cones are active. Hence your statement that

...since the light from CRT mentioned in the question pointed to by the first link above is quite above the photopic threshold.

may not hold. Since rods indeed have quicker responses, the periphery may be more sensitive to the flickering of a CRT or light bulb.
Note, however, that cones have flicker fusion frequencies of up to 90 Hz (reviewed by Perz, 2010), and CRT screens and light bulbs flicker at frequencies following the mains (50 or 60 Hz). Hence, cones may still be able to pick up the flickering. Since OP reports on an anecdote, experimental conditions may have been suboptimal and their report might have been unreliable. So we cannot exclude OP was using photopic vision, regardless their report.
Reference
- Perz, Master's thesis, Eindhoven University

"Hence your statement <...> may not hold" — how can this happen? Typical monitors have brightness on the order of hundreds of cd/m² (sRGB standard mandates 80 cd/m²). This is far above the photopic threshold of 5 cd/m² given in BIPM Rapport (Principles Governing Photometry. 2nd Edition. 2019, section 4.5).

It depends on the distance you are from it and the angle you are looking at it.

Brightness is distance-invariant. But OK, I don't know what angle of view typical CRTs have...

@AliceD In units of luminance, it shouldn't depend on distance.  FWIW, I much more clearly perceive 120 Hz flickering in LED lamps through my peripheral vision, even for very intense lighting thousands of times more than the photopic threshold, so I suspect that the answer is more complex. Cones in the perhery are sparse and physically larger, so their sensitivity to flicker/saccades may be different.  That would make some sense, since peripheral vision is there to alert you to something you need to look at with foveal vision.

@user1850479, that is interesting. Thanks for that


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From a hosts point of view, which comes first, effect of toxins on pathways or identification of toxins by immune system?
From a pure biology perspective, when a pathogen (gram-negative bacteria) affects a host by secreting toxins, what comes first, the effect of the toxin on the pathways or identification of the toxin by the immune system? A generalized overview would be very helpful.

That really depends on the toxin: Some of them are toxic in so low doses that they are never recognised by the immune system (like Tetanus toxin). So it would be good if you could clarify the question towards a specific toxin.

@Chris I have edited the question. Does that help?


text:
Peptides neither produced by the ribosome or the non-ribosomal peptide synthase complexes
I read in Wikipedia:

While there exist a wide range of peptides that are not synthesized by
  ribosomes, the term nonribosomal peptide typically refers to a very
  specific set of these as discussed in this article.

I was wondering what peptides are being referred to. I can only think of synthetically produced peptides. I can not find any source for other peptides not produced either by the ribosome or by the non-ribosomal peptide synthases described.

One peptide that comes to mind is the metabolically important reducing tripeptide glutathione — γ-L-Glutamyl-L-cysteinylglycine:

This is synthesized from cysteine, glutamate and glycine by reactions catalysed by glutamate cysteine ligase and glutathione synthase:

Synthesis of glutathione (GSH) — two subunits of glutamate cysteine ligase (GCL) are shown
Other examples may involve amino acids not specified by the genetic code which have particular roles in metabolism. For example, taurine, which has a sulphonic — rather than a carboxylic — acid group, can be metabolized to the dipeptide γ-Glutamyltaurine which may have a role in the brain.
These two examples relate to L-amino acids, albeit with a peptide bond between the side-chain glutamyl carboxyl group rather than the α-carboxyl group. However a D-amino acid dipeptide, D-alanyl-D-alanine, synthesized in the reaction catalysed by D-alanine-D-alanine ligase, is a precursor of bacterial peptidoglycan synthesis.
All the examples given have in common the fact that the peptides are very short (di- or tri-peptides) and can be synthesized in reactions requiring one or two specialized enzymes. Bacterial antibiotics synthesized by the non-ribosomal peptide complex tend to be appreciably larger, requiring repeated formation of peptide bonds.


text:
Does anyone know any statistics about the rate of cell division of malignant cells?
I've tried to look online to find some statistical data about the rate of growth of any type of cancerous cells, but haven't been able to find any. Would anyone know an appropriate time period for a single cancer cell to divide? Obviously, this hugely varies with the stage of cancer and type etc., but I am looking for any acceptable figure correct to an order of magnitude.

Have a look at this post for some related information. Meanwhile, please also narrow down your question to a specific kind of cancerous cell so that the question is not broad. I don't know what is an order of magnitude in your case but the doubling time can vary from a few hours to more than a day.

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text:
Swing bucket for PCR
I see a swing bucket rotor for PCR trips and don't know what step is using? What difference if I use fixed - angle? In addition, Which step I can use swing bucket instead fix - angle in molecular biology (Example: extraction, purification,..) to improve centrifugation efficiency?

For a PCR preparation, swing bucket or fixed angle does not make any differences. The only thing you want is that everything is soluble, in the same volume, and homogeneously mixed.
The main difference between swing bucket and fixed angle is how the pellet will be formed in the tube. Depending on the type of extraction or purification you are doing it would be advantageous to have a large pellet on the side (fixed angle) or at the bottom (swing bucket).
This article explains it in much more details if you are interested: https://handling-solutions.eppendorf.com/sample-handling/centrifugation/this-and-that/detailview/news/when-to-use-a-fixed-angle-rotor-or-a-swing-bucket-rotor/


text:
How does chest wall compliance affect functional residual capacity (FRC)?
The functional residual capacity is made up of expiratory reserve volume (ERV) plus the residual volume (RV) - i.e. the volume of air remaining in the lungs after passive expiration.
Compliance of the lungs is said to affect FRC. For example, if compliance of the lung increases (e.g. in emphysema), there is less elastic recoil and less air is passively expired, resulting in increased FRC. Could one explain this as increased compliance (where compliance = ∆V/∆P) meaning that the same intrapleural pressure at end of passive expiration results in a greater lung volume (FRC) at that time? This seems to explain instantaneous volumes rather than the actual expiration of less air.
How does this translate to compliance of the chest wall? As recoil of the chest wall tends to be outwards, would reduced compliance mean that there is greater tendency to recoil outwards, making intrapleural pressure more negative and reducing expiration of air, leaving greater FRC?

How is recoil of the chest outwards?  Doesn't the chest tend to recoil inwards?  Expiration is passive due to recoil of the chest inwards.

Recoil of the lungs (alveoli) is inwards, but chest outwards, I thought? As this is what sets up an equilibrium that allows the intrapleural pressure to be negative relative to atmosphere?

As far as lung is concerned both inspiration and expiration are passive. Lung just responds to intrathoracic pressure by accommodating more air during inspiration and expelling air during expiration. The active processes in the lung as far as air flow is concerned are limited to the bronchial tree smooth muscles which can increase or decrease the resistance to air flow. The compliance of the lung parenchyma is a function of its anatomical composition.
During inspiration the thoracic volume is actively increased by:

Outward expansion of ribs by the intercostal muscles
Downward expansion of diaphragm

This increase in thoracic volume is refected in all intra thoracic organs:

Venous return increases due to the negative pull
Negative pleural pressure causes air to be pulled into the lungs

Normal expiration on the other hand is passive due to relaxation of the above mentioned muscles. Relaxation will cause a decrease in the thoracic volume which will push the excess air and blood out.
An increase in the compliance of the thoracic cavity would mean weakening of the fascia and bones of the thoracic cage. In other words, the structures that the muscles attach to will become weak. This will cause muscle action to cause excessive expansion of the thoracic cage during inspiration and during expiration due to weaker pull by the attached structures, even residual tone of the muscle may cause distortion of anatomy preventing adequate reduction in the thoracic volume causing increased residual volume. Thusb reducing the volume of the air expired.


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IU Unit in Virology
In a paper recently I saw "Cell are infected with 50,000 IU of virus per 100ul well". I can not seem to find a defintion of this unit? Is it a functional unit or just a count? If someone is familiar with this definition please let me know.
It is a retrovirus. The thesis is here (page 18):
https://tspace.library.utoronto.ca/bitstream/1807/98170/3/Mazzanti_Andrew_D_201911_MSc_thesis.pdf

IU usually stands for "International Units". It can be functional of just a count. You'd have to search specifically for the meaning of IU for viruses to know what number of viruses per 100ul tat specifies.


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True anatomical/physiological explanation for "metaphysis" etymology
The anatomy textbook1 I use for my students states that the prefix meta- means "between:"

The metaphyses (me-TAF-i-sez; meta = between; singular is metaphysis) are the regions between the diaphysis and the epiphysis.   [my emphasis added]

This sounds reasonable given the explanation. However, I have never seen meta- applied in this manner; more generally, the suffix meta- usually seems to refer to "after."
In fact, Dr. Toby Arnold's Glossary of Anatomy provides the following etymology of the word metaphysis:

metaphysis: Greek meta = after, and physis = growth; hence, the end of the shaft of a bone alongside the epiphysial or growth cartilage  [again, my emphasis added]

The latter explanation is somewhat underwhelming, but the etymological usage fits more with my prior experience with meta-.
So, which is it?
Can someone find a reputable source definitively indicating a clear anatomical/physiological explanation for why meta- was used in the case of "metaphysis"?

A webpage on EnglishLearner.com reports that our earliest usage of the term "metaphysis" came from an obstetrician named William Dorland (1864–1956) in the early 20th century. I couldn;t find additional info.

1. Tortora, G. J. and B. Derrickson. 2014. Principles of Anatomy & Physiology, 14th edition. John Wiley & Sons, Inc., USA.

meta-:

word-forming element of Greek origin meaning 1. "after, behind; among,
  between," 2. "changed, altered," 3. "higher, beyond;" from Greek meta (prep.) "in the midst of; in common with; by means of;
  between; in pursuit or quest of; after, next after, behind," in
  compounds most often meaning "change" of place, condition, etc. This
  is from PIE *me- "in the middle" (source also of German mit, Gothic
  miþ, Old English mið "with, together with, among"). Notion of
  "changing places with" probably led to senses "change of place, order,
  or nature," which was a principal meaning of the Greek word when used
  as a prefix (but also denoting "community, participation; in common
  with; pursuing"). (Etymonline)

physis:

The growth plate, or physis, is the translucent, cartilaginous disc
  separating the epiphysis from the metaphysis and is responsible for
  longitudinal growth of long bones. (The Royal's Children Hospital Melbourne)

Anatomically and physiologically, meta- in metaphysis means next after physis (growth plate or epiphyseal plate) and refers to the changing (growing) part, which is in between the non-growing parts of a long bone (diaphysis and epiphysis):

The metaphysis is the wider portion of a long bone adjacent to the
  epiphyseal plate. It is this part of the bone that grows during
  childhood; as it grows, it ossifies near the diaphysis and the
  epiphyses. (Orthopaedicsone)

Picture: Parts of the bone (Radiopedia, Creative Commons license)

Thanks for the answer, @Jan. I was surprised to see meta referring to "between", but I now know it's not unprecedented. A comment on your last point though... So -physis is actually the part of the word referring to "growing" (changing), but you got me to thinking: the epiphyseal plate (associated with the metaphysis) is all about growing the bone's length (i.e., "beyond"), so I wonder if this is the physiological explanation for the etymology??

Again, I appreciate you finding the linguistic source, but could your try to provide a source that supports your last paragraph directly? Makes sense to me too, but I'm curious to see a reputable indication of Dorland's reasoning  (or modern physiological interpretation thereof)

consider metaphase, between-phase.

@theforestecologist, I made it simpler: anatomically and physiologically, meta- in metaphysis means "next after" physis and "between" diaphysis and epiphysis.

@John duhhh. Wow, you just made me realize I've explored this very question before but focused on metaphase previously. Of course, meta is between in that context! Oy I knew that! (I need more sleep before I post questions :p). Thanks, Jan, for the updates!

Bones grow for a long time.(teenage? adolescence?)
what does the suffix "-physis" mean? "Growth", so bone is longer and longer. We know the vital part of bone is metaphysis, but let's suppose that we are ingorant, simply observing that the bone shaft growing after the LINE between the bone shaft and "骺".
(both ends of bones are called “骺” in Chinese)
Bone's length is the diaphysis itself, growing INSIDE it.
Bone's length is following the metaphysis, growing AFTER it.
Bone's length is not influenced epiphysis (both ends of bones are called “骺” in Chinese), growing BELOW it, and “骺” is OVER the shaft.
This is why we use prefixes "dia-" "meta-" and "epi-", because this is how the components relate to the length.


text:
What is holding the immune system back to not attack human body cells?
There are plenty of loose proteins or other macromolecules free floating everywhere. Why wouldn't they be seized and presented to T cell to trigger an immune response? Does each of these molecules have a signature portion? Or do the presenter cells have some sort of friendly molecule database? Would a normal person's immune system ever possibly generate something like Tocilizumab, i.e. an antibody targeting a normal receptor in most cells?

What research have you done to try to find the answer to this question yourself? You are expected to do this before posting here. Have you searched for "self-tolerance" or similar terms or phrases?

The immune system of human body can keep human health from disease, but for many people, the immune system is the cause of disease. When the autoimmune system is in disorder, healthy cells and tissues will be killed as viruses, which will lead to a variety of immune system diseases.
Recently, scientists in the United States have discovered the genome that causes the disorder of the human immune system, which is equivalent to the "middle manager" of the immune system. This discovery is likely to bring new hope to the treatment of human immune system diseases, which has been published in the latest issue of nature.
Self defense system out of control immune cells "killing each other"
In the human immune system, a kind of immune cell named T cell is responsible for directly contacting and resisting the invading pathogen. Whether these cells can function normally is controlled by "regulatory T cells". Simply put, "regulatory T cells" are like a "double-edged sword", which can not only prevent T cells from attacking human body's own healthy cells indiscriminately, but when its regulation fails, it will cause immune cells to "kill each other" to normal cells, and its consequences usually include inducing type I diabetes, multiple sclerosis, lupus erythematosus and other immune system diseases.
Scientists have previously found that whether "regulatory T cells" can work normally is related to a major regulatory gene called Foxp3. If Foxp3 is dysfunctional, the human body will lack the active "regulatory T cells". But scientists don't know how Foxp3 controls "regulatory T cells.".
Richard young, a biologist at Whitehead Biomedical Research Institute of Massachusetts Institute of technology and Alexander Marson, a doctor of medicine, and other researchers recently discovered 30 genes directly regulated by Foxp3. It is by combining with these specific genes and regulating their activities that Foxp3 can complete the control of "regulatory T cells". If Foxp3 is the "boss" of the immune system, the 30 genes found in this study belong to the "middle manager".
Immune system diseases are related to the damage of "regulating T cells"
Researchers point out that ten years ago, it was found that the "regulatory T cells" in the human body are responsible for directing the immune system to resist foreign invasion, and the question is why the immune system that should protect health attacks its own cells. Now it has been found that there are gene defects in "regulating T cells" in the body with autoimmune disorder.
When "regulating T cells" cannot guarantee the normal operation of the immune system, the immune system begins to attack cells that should not be attacked. When the "regulatory T cells" were destroyed, several organs of mice developed serious immune system diseases. In some common human immune system diseases, such as multiple sclerosis, there is not no such "regulatory T cells", but there will be some dysfunction. In other words, "regulating T cells" failed to play its due role.
What is the problem of "regulating T cells"? "Studies have shown that when the immune system is disrupted, the activity of these genes is lower than normal. It is this reason that makes the activity of "regulatory T cells" decline, leading to its failure to work properly. Three years ago, scientists have found the main gene controlling "regulatory T cells", which is called Foxp3.
The researchers used DNA biochip technology to scan the complete genome of T cells and map the genes regulated by Foxp3. In the process, the researchers identified 702 Foxp3 binding sites. Until the discovery, the researchers admitted, they had no idea how Foxp3, the main regulator, dictated "regulating T cells.".
Anti rejection treatment for organ transplantation
The latest research shows that the "middle managers" of these 30 immune systems are not working properly. Because "regulatory T cells" are controlled by these specific genes, it can be said that most of the immune system diseases such as type I diabetes, lupus erythematosus, multiple sclerosis, rheumatoid arthritis and so on are determined by these genes.
The next step, the researchers say, is to determine how the 30 specific genes "dictate.". It has been found that these genes are closely related to each other and usually work together to control T cells, but the specific mechanism is still unknown. On the other hand, we should look for chemicals that can simulate the regulation function of Foxp3, the main regulator gene, in order to achieve effective therapeutic immunity.
In addition to the treatment of autoimmune diseases, this finding can also be used for anti rejection treatment in organ transplantation. When performing organ transplantation, once the patient's body rejects the transplanted organ, the operation will fail. Therefore, doctors usually use anti rejection drugs to temporarily inhibit or shut down the immune system.
At present, cyclosporine is mainly used to inhibit the immune system. It can inhibit a protein called activated T-cell nuclear factor (NFAT), which can also be controlled by Foxp3. If necessary, the researchers said, the 30 genes can also be used to "target the target", and the effect of inhibiting the immune system is more obvious.


text:
Does the human eye see things at twice the distance in a mirror?
If I'm standing 3ft away from a mirror and looking at something in it that is behind me but 5ft away from the mirror, do my eyes see that object as 3ft? Or 8?

8 feet. You can do ray tracing for a plane mirror and see that the image will "appear" at an equivalent distance behind the mirror. The light hits your eyes at the same angle as if the object really were that far away.

As a side note, this is why nearsighted people will have trouble seeing distant objects in mirrors, even if they put their eyes close to the mirror.

@user137 don't answer questions in the comments. With the link attached and a little more elaboation on the answer it's a good answer imo

I'm voting to close this question as off-topic because it appears to be primarily about optics rather than biology.


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Does the body use radio frequencies in the range of frequencies used in mobile phone networks?
I read something related to the biological effects of "mobile phone radiation". It was not as far from reality as one might expect with this topic. The context was about the acceptable distance of mobile phones to the human body. Mobile network operators specify minimal distances of some cm.
I was surprised to read that the human body actively uses electromagnetic waves in or near the frequencies used by mobile phone networks.
Is that true?
Or partially true?
Or at least plausible?

German source: https://www.diagnose-funk.org/themen/mobilfunk-anwendungen/mobiltelefone/smartphone-nicht-in-koerpernaehe-benutzen
Relevant section translated (paragraph above the image):

Human body cells also communicate via electromagnetic vibrations, such currents are measured, for example, in the case of a cardiac ECG or brain EEG. The mobile radio signals are in the frequency range of the body's own vibrations. It is therefore not surprising that electromagnetic radiation can disrupt brain waves, heartbeat and other body functions. The health risks posed by high-frequency electromagnetic fields (EMF) have been sufficiently researched and documented. Diagnosis: Radio documents this on the website www.mobilfunkstudien.org

The body doesn’t use electromagnetic radiation (other than sunlight) as far as I am aware, but the reference in your original question didn’t say that, it said it could affect cells and cause them to become cancerous, like other radiation — e.g. ionizing radiation — that the body doesn’t use. Why did you remove the reference?

@David I added my original reference

Sorry about that. Must be confusing your post with another. Anyway, I was going to make some general observations but I’ll have a glance at the original first. I can read German.

Following the trail I ended up with an English-language paper by Yu et al. in a Elsevier journal I had not previously encountered, Science of the Total Environment. This claimed to show an effect of 4G radiofrequency radiation on rat testis and rat fertility. I can find nothing in the paper corresponding to the section you translate, or on the Diagnose: Funk report page you provide a link for. The only electromagnetic radiation that the human body uses to communicate as far as I am aware is electric currents.

The claims in the quote seem pretty vague to me. "Human body cells also communicate via electromagnetic vibrations" isn't really accurate, and if you wanted to stretch it to be accurate you'd have frequencies that are nowhere near the ballpark of those used in cellular communications. The conclusion "The health risks posed by high-frequency electromagnetic fields (EMF) have been sufficiently researched and documented" is laughably false, and I think a good cue to distrust the whole source.


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Does cartilage connect to other cartilage?
In the definition of a Ligament in Oxford states:

A short band of tough, flexible fibrous connective tissue which
  connects two bones or cartilages or holds together a joint.

the wording of "two" prior to bones or cartilages sounds like it could be bone to bone, cartilage to cartilage, and bone to cartilage.
Are all of these combinations correct? If so, is there a good example where each one can be seen for reference?

A ligament can connect two bones:

Picture 1: Knee joint ligaments (source: Wikipedia, Creative Commons license)
A ligament can connect two cartilages or a bone and a cartilage:

Picture 2: Larynx ligaments (source: Wikipedia, Creative Commons license)
Ligaments can also connect internal organs:

Picture 3: Ligaments connecting abdominal organs (source: Wikipedia, Creative Commons license)


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I want to replicate an experiment in cell biology, and I have a question about centrifuge RPM vs. x g
https://med.stanford.edu/news/all-news/2019/10/cytoplasm-of-scrambled-frog-eggs-organizes-into-cell-like-struct.html  This is the experiment which I want to replicate.  In the article describing the experiment, they said that they used a centrifuge capable of 12000 x g for 15 minutes.  I was wondering if I could possibly use a centrifuge with lower x g for a longer time interval and get the same result?  Like...possibly 6900 x g?

The new article you linked doesn't actually describe the methods used in that experiment, which are important here. While centrifugation time can in some cases make up for a lower speed it doesn't always work: some(/smaller) particles will not not sediment at all at lower speeds, independent on how long you run  the centrifuge.

@Nicolai The methods are in the supplemental data. They use microcentrifuges for their centrifugation step, which should be standard lab equiment. jeffrey Do you have a small centrifuge for 1,5ml tubes available in your lab?

Yes, I do have a small centrifuge capable of 10000 RPM.  It produces 6900 x g.

It's the question if they used 12.000 rpm because it is needed to seperate the mixture or because they simply put it on max. speed. I wouldn't be surprised if the answer is the later. You can of course have a try and see, if you can get a good separation with your centrifuge.


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Can anyone identify what is the name of this plant?
I found this plant on the side of the street in Melbourne, Australia. Looked like someone just removed it and threw it from their garden. So I took it home and planted it.
The plant had damaged leaves which I removed. (https://i.stack.imgur.com/htnbK.jpg)

Welcome to Biology.SE! If possible clearer, closeup photos (or a description) of the leaves and the stem from multiple angles might be helpful. In particular, I wonder whether the leaves thick (fleshy) and waxy like a succulent or are they relatively thin? ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

There are so very many succulents in the world (and you now have one in your garden!) Wait until the roots have established themselves well, then cut the stalks back to about two inches. You'll be able to post a better identifiable picture when it starts to grow back.


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Transmitted electrons in TEM
When some electrons of the electron beam pass through the specimen, what exactly happens after that in order to produce the black white image? What I understand is that electrons transmitted collide with a film and make that part of it black on the image, and those that don't collide make their part white. But why is it said that electrons that pass readily make the area brighter or more electron lucent and vice versa for scattered electrons?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular I'm not sure this is the appropriate for this question since it appears to be a physics (or maybe engineering question) rather than anything directly related to biology. Thanks!

Thanks for being curious about a biological subject on a site about biology. As a contributor here, I deeply apologize that your curiosity is being stomped upon.

I apologize for asking here but I didn't really focus on the site to ask in since I'm studying it from a histological source.

I'm voting to close this question as off-topic because it is about the physics of TEM rather than biology.

The pixels in a TEM image are whiter or blacker based on the dose of electrons that impact that pixel in the whatever detector is being used to form the image, be that photographic film, a scintillation screen, or a direct detector camera.
As for how the image that reaches the detector is formed by the specimen being imaged, there are two different mechanisms.
Amplitude Contrast is relatively simple - denser parts of the specimen scatter electrons strongly enough that some electrons do not make it to the detector at all, so pixels below these parts of the specimen will receive a lower dose than pixels below less dense parts of the specimen.
Phase Contrast is more complex, and is responsible for most of the contrast in high-resolution cryo-TEM. Briefly, the specimen is illuminated by a parallel beam of electrons and every "pixel" of the specimen scatters some electrons but lets most of them pass straight through without interaction. The scattered electrons go off in a different direction than the main beam but are focused back by the lenses to the same point on the detector as the unscattered electrons. Because the scattered beam took a different path from the unscattered beam, and because electrons are waves as well as particles, there is a phase difference between the two beams which causes them to interfere. Typically, areas of the specimen that scatter electrons more will cause destructive interference, so darker pixels. If there is no scattering, then there is no interference, so brighter pixels. There are many resources explaining the technical details of this mechanism (1, 2, 3), but these tend to focus on crystalline specimens.


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Is the "first pass effect" diminished more by some foods than others?
This effect and its considerations are fairly well known but it's never been clear to me whether it's a greater consideration with some types of food than others.

This completely depends on drug in question.

@Jan I don't see how. My question doesn't ask the extent to which it happens; merely whether or not it happens at all. If any drug that experiences a first pass effect has that effect diminished more by some foods than others then the answer to my question is "yes."


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Do scars generally continue to undergo beneficial changes after maturation?
I understand that succumbing wound healing, a modulated scar would go through a process of scar healing which I understand to be remodulation and maturation.
Do scars generally continue to evolve in beneficial ways throughout the life of a human?
That is to ask; might it be that a scar's evolution could be comprised of two major stages "primary" and "secondary" and that the primary stage is consisted of remodulation and maturation and the secondary is comprised of "post maturation" evolution which could last during all life of a human?
In general, scars do get changed after being "healed", at least by general bodily changes from aging effecting all tissues in general (including the scar tissue), but there might also be a "post maturation evolution" as well.

I'm a bit confused. I think you're asking if scar remodeling continues indefinitely? No, it does not, but there is a two stage remodeling, the first short, the second over as long as a few years.

I think my terminology is similar but enough different: I know there are only "remodeling" and "maturation" (which corresponds to the "second remodeling") you mentioned ; any of the way --- yes, I ask if there is healing beyond maturation or secondremodeling.

I had a serious burn on my arm 2” by 1” and it has shrunk over time - some 40 years...

Please [edit] your question to make it clearer — it is being considered for closure. —–– Some suggestions: 1) Based on the answer you accepted, "healing" doesn't seem to have been the correct choice of words — you could reword your questions to something like 'Is scar tissue altered after maturation?'. 2) Also "succumbing" doesn't seem to make sense in this context — did you mean something else?

@tyersome hello to you ; I have did a similar change; I think it's good.

I agree that looks better, but I'm going to make some edits of your grammar and to make your title more concise. ——— However, succumb means "fail to resist some negative force", so as far as I can tell "succumbing wound healing" doesn't really mean anything. Did you by any chance mean "secondary to"? Also, what do you mean by a "modulated scar"? If that has a specific meaning please provide a link. (Note: It is important to use generally accepted terminology to avoid confusion, so it would be great if you were to read up on this subject a bit and make sure you are using the correct words!)

The collagen that holds together scar tissue is continuously degraded and replaced. (Plastic and Reconstructive Surgery, 1976) If collagen synthesis slows down, due to scurvy for example, old wounds can in theory reopen. Historic records of sea voyages contain descriptions of long-healed wounds opening back up in scurvy victims, and these cases are cited authoritatively in some papers (e.g. Annals NYAS 1961), but it is difficult to test experimentally.
I would describe this more as 'maintenance' of the scar, rather than as 'continuous healing', but it may be of interest to you.


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WHO Essential Medicines vs Essential Medicines for Children
Per the WHO (World Health Organization), there are a list of "Essential Medicines" such as those listed on their Wikipedia page.

Is there a database link for this directly other than Wikipedia?
What is the difference between the "Children" list and the regular list. Is one a complete superset of the other? I noticed the "Children's" list is much larger.

I would like to make an open JSON database of some sort regarding a more easily accessible and organized way of accessing this data in a Postgres database or something. What do you know like this that exists?
https://en.wikipedia.org/wiki/WHO_Model_List_of_Essential_Medicines
https://en.wikipedia.org/wiki/WHO_Model_List_of_Essential_Medicines_for_Children

Wikipedia links to ressources: this is the first references of your linked article: https://www.who.int/medicines/services/essmedicines_def/en/ - it should contain all information that is needed, though arguably not in an easily parseable format

Neither list is a superset of the other.  The children's list is longer but notably lacks medicines for reproductive health and perinatal care.


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small airborne microorganisms, are in many instances attached to bigger particulate substances?
From https://biology.stackexchange.com/a/90193/56476

very small airborne microorganisms, are in many instances attached to bigger particulate substances in the air, whether liquid micro droplets or solid particles. ... but this may be reason for higher risk of respiratory infectious diseases when PM2.5 air pollution gets high.

Can someone confirm this great logic?
I think it is true, but just need a confirm from the public! :)
Many thanks.

You should surely address your concern about this to the person whose answer you are quoting, asking for evidence to support the statement, rather posting a separate question. If you really must post a separate question, you need to show that you’ve tried to find the answer yourself.

I don't know about air, but that's totally true for water: turbidity is a measure of water particulates, and micro-organisms naturally attach to particulates and feed from them.


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Chromosome position mismatch for SNPs in dna tests
TL;DR: why is the position reported by DNA testing companies for an SNP on a particular chromosome different than the one in dbSNP/SNPedia databases?
I'm analyzing the raw DNA exports for the same person from 2 different companies.
There is, as expected, a small number of discrepancies on the genotype reported.
Strangely, there is also a (smaller) number of discrepancies on the chromosome and position reported for the same SNP (about 0.02% of the rs-ids that are common to both exports).
Trying to find out who is right, I looked at SNPedia and dbSNP. To my surprise, while SNPedia and dbSNP (logically) agree on the positions, they never seem to match the positions reported in the raw DNA exports.
While the two companies that I used agree on the position in the vast majority of SNPs, they are apparently always different from dbSNP. In 75% of the 101 differences between the two companies, the position number only differs by 1.
I'm surprised by this and I feel that I'm missing some underlying piece of information.
What can explain these differences?
Does the "position" in the DNA exports from 23andme and MyHeritage represent some other biological property than the position reported by dbSNP/SNPedia? Or is there a conversion formula? Or is the information from the exports unreliable?

Welcome to Biology.SE! Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular, this question seems like it might be a better fit for the Bioinformatics site. ——— The different companies might be using different versions of the human genome than those online databases — your best bet may be to contact the companies and ask why their numbers are different. Thanks!

Most or all consumer DNA companies doing autosomal SNP tests deliver their raw data (at least by default) based on human reference genome build 37 (GRCh37).  This is effectively the standard for this arena because it is compatible with existing files and other companies, allowing matching and other processing.  dbSNP and SNPedia have changed to use the next major genome update, build 38 (GRCh38).  The major genome builds can be expected to have different position numbers for most all comparable places in the genomes, including of course all SNPs which are defined in both builds (most of them).
So the differences in positions shown in your raw data files and dbSNP/SNPedia are due to this difference in the reference builds they are based on.  I don't know a way of getting build 37 positions on SNPedia, but on dpSNP one way of seeing the build 37 position is to scroll down to "Genomic regions, transcripts, and products", "Choose placement" of GRCh37, and then hover over the blue highlighted SNP name, which will show a drop-down list with the (build 37) position, among other things.


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Is there term for thermophilic-halophilic plants and if so, what is it?
I know that in botany there is a wide classification for plants that can survive in hot deserts (semi-arid or arid) and harsh climates such as 4-season countries with a tendency to droughts each year (such as Palestine).
This classification, as I understand it, is thermophilic plants (hot loving).
But there is also the classification thermophilic plants which are also halophilic (salt loving), i.e. can survive and even flourish in extremely low and salty ground? Examples of such plants are found in the Ein Feshkha reserve near the Dead Sea in Israel and other similar Thypa and other plants reserves near the Dead Sea (current) shorelines in Israel, Palestine and Jordan.
Is there term for thermophilic-halophilic plants and if so, what is it?

Well, at least in other biological contexts, such organisms are often simply referred to as being thermohalophiles (or as being thermohalophilic).
Examples of the use of these words:
Bacteria:

Mavromatis, K., Ivanova, N., Anderson, I., Lykidis, A., Hooper, S.D., Sun, H., Kunin, V., Lapidus, A., Hugenholtz, P., Patel, B. and Kyrpides, N.C., 2009. Genome analysis of the anaerobic thermohalophilic bacterium Halothermothrix orenii. PLoS One, 4(1).

Denger, K., Warthmann, R., Ludwig, W. and Schink, B., 2002. Anaerophaga thermohalophila gen. nov., sp. nov., a moderately thermohalophilic, strictly anaerobic fermentative bacterium. International journal of systematic and evolutionary microbiology, 52(1), pp.173-178.

Pereira, M.M., Antunes, A.M., Nunes, O.C., da Costa, M.S. and Teixeira, M., 1994. A membrane‐bound HIPIP type center in the thermohalophile Rhodothermus marinus. FEBS letters, 352(3), pp.327-330.

Biochemistry:

Amoozegar, M.A., Salehghamari, E., Khajeh, K., Kabiri, M. and Naddaf, S., 2008. Production of an extracellular thermohalophilic lipase from a moderately halophilic bacterium, Salinivibrio sp. strain SA‐2. Journal of basic microbiology, 48(3), pp.160-167.

I'll note that I haven't found evidence of plants being referred to in this specific manner, but read the example papers below for use of the related phrases "thermohalophyte vegetation" and "thermohalophytes", respectively:

Accogli, R., Nutricati, E., Famà, L., Medagli, P., Manno, D., De Bellis, L., Marchiori, S. and Colasante, M., 2008. Iris revoluta Colas., natural hybrid origin species: characterization and preservation problems. Plant Biosystems, 142(1), pp.162-165.

Vekhov, N.V., 1996. Thermal and freshwater springs of the Chukchi Peninsula: Unique subarctic ecosystems. Part ii. flora. Polar Geography, 20(3), pp.209-220.

Is this word-blending approach the best or most appropriate? I Couldn't say; but there is certainly prior  precedence for combining the habit adjectives into "thermohalo-".


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What are the upper and lower sets of teeth are called?
I'd like to know the correct term for the a group of teeth in the skull and jax (mandible) Not the specific types of teeth i.e molars, incisors, carnassials, canines etc but what a set of teeth get referred to. the upper teeth.

Upper teeth: maxillary teeth
Lower teeth: mandibular teeth

The term, "maxillary", is given to teeth in the upper jaw and "mandibular" to those in the lower jaw.

If you search these terms you will find many references.
You can start with wikipedia which has many cross references.


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What is this spider found in day time?
.
South India
Arm to arm about 3 inch in length. Day time. was hiding inside a cardboard storage box.

It's definitely a species of Huntsman spider maybe of the genus "heteropoda" or "olios". Sorry I couldn't be more help.

Welcome to Biology.SE! You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. ——— Please also take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


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Has anyone attempted to add extra senses to a creature through a BCI/Neural interface?
Basic BCI's (Brain computer interfaces) have been available for quite a while now and allow users to preform rudimentary tasks such as moving prosthetic limbs with force-feedback or moving a mouse on a screen through only neural impulses.
I'm interested if anyone has performed experiments in the direction of adding non-native extra senses to a creature using a neural interface/BCI. For example, feeding a magnetometer's sensor reading or clock data into a BCI and using that to give the person/creature a "sense" of magnetic fields or exact time.

Short answer
Yes
Background
This subject touches upon a related technologie, namely sensory substitution, where a lost sense is replaced by a still functional sense, for instance:

The BrainPort developed by Wicab that lets blind people taste light (Fig. 1) (Stronks et al., 2016).
The, now discontinued, yet still highly popular Optacon device developed by Telesensory Systems that allows blind folks to scan a normal printed book page with a camera and read it back through braille input via this device (Stronks et al 2016).

However, you are specifically asking for devices that add novel sensory information, referred to as sensory augmentation, or sensory enhancement. The technique of sensory substitution can,quite obviously, be easily extended to add novel sensory perceptions, simply by using a sensor capable of sensing stimuli that the human sensory systems cannot, for example magnetism, infrared light and what not, for instance:

Mapping the magnetic North on the human body through auditory or tactile actuators (Schumann & O'Reagan, 2017).
Electrically stimulation of the brain in response to otherwise invisible infrared light (Thomson et al., 2013).

References
- Schumann & O'Reagan, Sci Rep (2017); 7: 42197
- Stronks et al., Brain Res (2015); 1624: 140–52
- Stronks et al.., Exp Rev Med Dev (2016); 13(10): 919–31
- Thomson et al., Nature Communications (2013); 4: 1482

Fig. 1. BrainPort V100 vision substitution device. source: Plaid Zebra