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Terms related to megasporogenesis
Well, I am not able to understand the exact difference between megasporocyte and archesporium. Also I'm not quite able to get, how or precisely from where do these arise?
Please help.

In relation  to angiospermic megasporogenesis, archesporium cell is the precursor of Megasporocyte.

Archesporium is defined as   the cell or group of cells from which spore mother cells develops
The megasporocyte is the cell(or the tissue) which directly produces
   the megaspores.

In most angiosperm, the nucellar tissue within the ovule first differentiates into a single archesporial cell, the ancestor of the Megaspore Mother cell(MMC). In certain species, this archesporial cell may itself act as the MMC undergoing meiosis to produce the megaspores. in such cases, the archesporial cell and the megasporocyte (another name for MMC) is the same.
But in some species, the archesporial cell first undergoes a periclinic division producing two cells which further produce the parietal layer (covering of the megaspore) and a single sporogenous cell. This cell acts as the MMC, and is the megasporocyte.
Thus the archesporial cell may or may not be the same as the megasporocyte. It could be the ancestor of megasporocyte.

Thanks a lot. What I was wondering is that, as you said that archesporium can be a group of cells than would all those cells develop into a MMC or is there any type of differentiation among them so as to satisfy the requirements of any one cell which would develop into a MMC?

When archesporium is a group of cell, two things can happen. One is that most of them form the parietal layer, and a single cell matures into MMC. Or if the archesporial cell is in the male anther, most of them mature into PMC (pollen mother cell).


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What limits our ability to grow enamel rods?
From what I've understood from what I've read (which might be wrong), enamel rods extend away from the dentin in our teeth. As young people grow, the rods are thickened.
What are the technical limitations and/or problems/challenges of trying to extend/grow the rods/crystals while the teeth are in the mouth?
One issue I guess could be that the enamel is porous, and so chemicals could affect the other parts of the teeth.
But one example of trying to improve the quality of tooth enamel is Novamin, which some manufacturers have claimed creates a glass on the tooth. But I don't understand what that means.

Chandra's Textbook of Dental and Oral Histology and Embryology with MCQs p40-42 explains the complexity of enamel, and provides diagrams and images of real enamel.
What I didn't know before was that the hydroxyapatite is in the form of very small crystallites packed inside the key-like structure of the rods. The rods are packed together with a cement-like material. The rods themselves are segmented.
This small design and lack of vital parts suggest to me that bioglasses like Novamin would at least not recreate the natural enamel structure.
What isn't so easy to guess is whether crystallites from the components of the bioglass are formed on the existing crystallites, and if so, whether this can continue indefinitely, and with what qualities.

source: Stack Exchange

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classical conditioning paradigm for hippocampal learning
I wanted to know what a suitable classical conditioning experiment would be to analyze learning and memory capabilities in rodent models with respect to hippocampal long-term potentiation.
For example, I want to subject the animal to conditioning and test the behavioral readout at a certain time point after conditioning. Many , like fear conditioning experiments, are mostly attributed to amygdala processes.
I wish to know some classical conditioning task where I can understand primarily hippocampal processes.
Also is there a way to monitor hippocampal CA1-CA3 firing pattern after the training period or during the training ?
That is, I want to check if LTP will sustain after the training period or is there is any increased sustenance of LTP post training.
But if I am to do this electrophysiological experiment in hippocampal brain slices, how will I incorporate the conditioned and unconditioned aspect to this ?

First of all, your first sentence assumes something which may not be true and is still controversial in the literature. Learning and memory are thought to be related to the phenomenon of LTP but it appears you are taking this as a given.
There is a huge swath of literature on hippocampal-dependent behavioural tests like the Morris-water maze etc so I assume you are already aware of these. If you wish to monitor the HPC firing pattern:
1) during training --- you can set-up an in-vivo electrophysiology platform coupled to a virtual navigation interface and record from cells while the animals are performing a spatial navigation task.
2) after training- you can take slices from the animals as is classically done and try to induce LTP and see if your spatial learning task has influenced the amount of LTP you can get. The condidtioned and unconditioned animals will simply be the two groups which you can compare to see if the behavioural readout(spatial memory task) corresponds to changes in what is though as the cellular basis for memory(LTP)

Whitlock, J.R., Heynen, A.J., Shuler, M.G., and Bear, M.F. (2006). Learning Induces Long-Term Potentiation in the Hippocampus. Science 313, 1093–1097.
Goh, J.J., and Manahan-Vaughan, D. (2013). Synaptic depression in the CA1 region of freely behaving mice is highly dependent on afferent stimulation parameters. Front Integr Neurosci 7.
Heynen, A.J., and Bear, M.F. (2001). Long-Term Potentiation of Thalamocortical Transmission in the Adult Visual Cortex In Vivo. J. Neurosci. 21, 9801–9813.

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Largest crinoid species
On the wikipedia page of crinoids (sea lilies and feather stars), one can find the following statement in the paragraph "Morphology":

[...] and fossil species are known with 20 m (66 ft) stems, the largest recorded crinoid having a stem 40 m (130 ft) in length.

They also give some sources for this, but they also just mention the fact without specifying the fossil/species. When searching on the internet about the largest known crinoid species, one can find very often similar claims, but again without any source (probably coming from wikipedia in the end). In general, I am slightly doubting the statement about 40m of length: Statements about size of large organisms are very often exaggerated. For example, in popular science books, one can often find lengths for the giant squid (Architeuthis dux) of about 20m, while the truely largest individual every measured with scientific methods was probably "only" about 12m (see the paper here for example), which is of course still pretty impressive. In the words of S. J. Gould: "Our strong and biased predilection for focusing on extremes generates all manner of deep and stubborn errors".
Anyway, I would like to know how large/tall crinoids can get by knowing how large the largest species ever to be found was (preferably with a scientific resource supporting the claim). On my internet research, I found the species Seirocrinus subangularis (Miller, 1821) from the early Jurassic with stem lengths of about 20m, although also here the statements about size vary a lot from 15 to 25m and I am not able to find a precise, confirmed, statement.

Woah I understand your frustration. The web info on that is all confused without science references. a 40m fossil is very unlikely in one piece,  the biggest fossil ever uncovered, and if it was on a slab of rock somewhere, it would be famous among geologists and would have been in old newspapers as a local and great discovery. 1820's fossil id's are no accurate by today's standards, and if the fossil is gone, the reference is vague. I found an 18 meter claim of reference here: https://libraries.ou.edu/content/crinoid ... I am treating the wiki figure like complete nonsense.

I recommend the big guns on this... fossil forums is the biggest fossil forum full of serious, impassioned paleo academics. And Reddit is pretty specialized, too. Because this is a serious shortcoming in the web science references, and people are copying that wiki claim of 40 meters all over the web.

@bandybabboon thanks a lot! Yes, indeed, a 40m fossil is really unlikely. I will check out the fossil forum and keep this post here up to date in case I get an answer there.

Probably 40ft not 40m
Without a species name any claim like this is dubious. The wiki quote is not from a primary source but a fluff book which makes it even more questionable.
Unfortunately you are running into a issue were a lot of early paleontology work has not been digitized yet. the specimen in question is from 1906 so finding a digital copy to confirm is basically impossible. So we can only rely on the questionable sourcing to determine how accurate it is.
My best guess is this is a misquote on a real specimen.
geologypage.com has article about largest known crinoid specimens.

Taxocrinus saratogensis One of the largest fossil crinoids ever
discovered was found in the state of Indiana in the United States. The
crinoid, which belongs to the species Taxocrinus saratogensis, was
discovered in 1906 by a team of geologists led by John M. Clarke. The
specimen is estimated to be around 350 million years old and is
believed to have lived during the Devonian period. The crinoid is
incredibly large, with a stem measuring more than 40 feet in length
and a crown that measures more than 10 feet in diameter. The entire
specimen is estimated to have weighed more than 10 tons when it was
alive. This makes it one of the largest fossil crinoids ever
discovered.

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Identifying a plant in the botanical garden of Paris
I went to the botanical garden in the "Jardin des Plantes" in Paris. In a glasshouse with the name "Serre de l'histoire des plantes" on the natural history of plants (exhibiting some ancient members of plants like ferns, Cyatheales, etc.), I found the tree-like plant on the picture attached below (the one with grass-like looking "leaves"; unfortunately, I don't have a better picture because it was a bit hidden). There was no sign labelling this particular plant, or at least I was not able to spot any. Does anyone know what type of plant this is? It was rather small, roughly 2 meters in height.

It looks like a bromeliad called spanish moss, perhaps it's related to spanish moss, else it could be very different, a close up zoom of the leaves would be good.

Looks like Casuarina glauca ‘Cousin It’

@PolypipeWrangler thanks for the comment. That looks indeed very similar. But the plant on my picture has a stem, like a tree. On the first picture one can see it a bit.

@sir-thinksalot is correct. This is an Ephedra species. You can have a look at this PDF to get some spatial orientation - it should be with the Gnetales. You can look which species of Ephedra are known to be cultivated in French botanical gardens via a search on the BGCI database. I couldn't find a public database for the plants of the Jardin des Plantes, and it isn't mentioned on the accompanying MNHN website. If you are really interested, you can drop them a line and ask which species it is.

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What do alleles look like visually on linear DNA strands?
I've seen many textbook images of alleles on homologous chromosomes with the gene loci identified but how could this be visualised on linear DNA sequences with the bases written out? Is it that you would have one DNA strand with its nucleotides and then another adjacent DNA strand with nucleotides at the same locus but different in sequence? Any visual representations would be helpful
Edit:
This picture below shows how alleles can be seen on the chromosomes but it's not clear about where the change in sequence would be on the nucleotide bases. The typical diagrams show the homologous pairs but they don't usually show the change of base sequences on a small scale.

Unclear exactly what you mean. An allele is a variant. It's like having 1st edition vs. second edition of a book, where a typo was fixed on page 32. In a cell of a diploid organism, you might have 2 1st editions, 2 2nd editions, or one of each. But each of them is just a long string of characters. But there isn't a "right" way to visualize this because it's too small to see, all of these are metaphors to help us understand what's happening at the single molecule level.

An allele of a gene is a segment of DNA so its diagram will be like any DNA helix with a unique nucleotide sequence. A chromosome is a single molecule of double stranded DNA with histones. So two alleles will be two extremely similar DNA segments. Or as @MaximilianPress said two editions of a book. I guess you asked for a diagrammatic representation?

@MaximilianPress Could also be a truncated version that ends on page 100 out of 500 original pages, or arguably even one that doesn't exist at all.

I've posted an answer and I would be interested to know if it answers your question. However can I ask two things of you. 1. Please finish reading the [Tour] — we know you haven't because you don't have the badge for doing so, and it will help you learn how this site works. 2. When you ask a question related to something you have read, please post a link to it, or even a copy of a typical image in this case. And did you search for such pictures? I found the one I modified Googling for images related to Sickle Cell Allele.

Thanks for the response David, will do the tour now and see if I can attach said pictures I was referring to

I think I may understand the point of difficulty the poster is encountering, and have produced the diagram below (adapted from an internet source) in the hope that it may help.

This diagram shows the allele for the mutation in β-haemoglobin that causes sickle disease. The key points are:

There are two copies of the chromosome in diploid cells, either of which may be normal or mutated.
Each chromosome contains double-stranded DNA, so the mutation affects both of the two complementary strands. Thus the stated expectation of the poster to see “one DNA strand with its nucleotides and then another adjacent DNA strand with nucleotides at the same locus but different in sequence” is incorrect.

Now this may be a slip of the typewriter fingers on the part of the poster, but it may also be confusion because of there being two copies of the same chromosome. Anyway, the diagram seems to me to give an example of what was requested. It can be amended if necessary
Of corse the allele may extend over more base pairs if the mutation is a deletion, but let’s walk before we try to run.

This illustration could mislead some, as the left-hand part illustrates a chromosome form that is not typical in the life of a cell, but is a form that occurs during meiosis.  That special form of chromosome has two chromatids with the chromatids having different alleles.  (The normal form of chromosome has only one chromatid, and hence only one allele form.)

@mgkrebbs — Yes, that was a point of concern to me also, although I'm not an expert on chromosomes, just graphics. Is the replacement OK? The combination of 2D and 3D jars, but then, nobody is paying me for this.

Yes, that is a definite improvement, as it shows two homologous chromosomes as normally exist in a cell.

Hi David, thanks for your response - this is more what I was looking for with the visual representation as a lot of the textbook diagrams show a more zoomed out version of the chromosome which made it hard for me to visualise how the nucleotide bases looked.
Just to clarify are alleles comparing the variation of genes on the different chromosome then? As opposed to an allele being the variation of genes on one chromosome on its own?

For example is the change of sequence (on small scale terms) going to be on one antisense strand whereas the sense strand has the typical reference sequence? Or is it comparing the differences of sequences on the other homologue as opposed to a single change in sequence on one chromosome? Apologies for the long winded question. I'm just trying to visualise this for a short sequence (e.g. 10 bases) not a large scale one as usual.
Also, I think what tripped me up with the textbook diagram is that I thought the chromosomes shown only had one singular strand instead of the double stranded form.

@mydearestpotato — 1, Yes, if you take the NIH definition of allele: "An allele is one of two or more versions of DNA sequence (a single base or a segment of bases) at a given genomic location." each version, is and has to be, on a different chromosome. 2. There is no possibility of the different strands being informationally different in the double-stranded DNA of an individual chromosome in a diploid cell. This is because they have to form complementary base pairs. (Only at the point when a mutation occurs can it be on one strand, unti the DNA replicates and daughter dsDNAs are formed.)

Thank you for these explanations and the diagram, it's been really helpful


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Has anyone 'broken' an organism and then restored it to life?
Has anyone 'broken' an organism, rendering it unable to reproduce, then repaired it and observed it returned to being able to reproduce?
An example would be to restore the reproductive capacity to a cell rendered lifeless from radiation.
I've attempted, several times over many years, to find any information about this and all I've found is abiogenesis and the Miller-Urey experiment which is not the question at hand.
If there is another technical term referring to repair of life, versus creation, then I am unaware of it.
ADDENDUM: Clarified question ...limited to reproduction vs. living.

Welcome to Biology.SE! is expected that you will do some research on your own and share what you have learned when asking questions here. In addition, in a biochemical context organic refers to complex carbon containing molecules — if you got rid of those there would be very little left of an organism ...  ——— Please also take the time to take the [tour] and then the help pages starting with [Ask] questions effectively on this site. Thanks!

Ok, done. I've edited the question.

Please not that your edited-in example (which is good) does not match your first sentence: an organism that can't self-replicate anymore is still very much organic, just not alife (kind of like a virus actually).

@Nikolai So a sterile man is not a life anymore? That's kind of mean. Neuron cells are no longer alive if they don't divide?

@Cell Of course those would still be alive, I was mostly alluding to OPs example (and thinking of single celled organism for which this type of experiment might be possible). The fact that this usage of the terms oraginc/inorganic and alive/lifeless leads to wrong statements so quickly also shows, why one shouldn't use them in this context together.

Sounds to me like induced pluripotent stem cells fit your description. https://en.wikipedia.org/wiki/Induced_pluripotent_stem_cell


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What type of fish is this
I saw this fish in an aquarium in a nearby house .I am not sure which species and sex this fish belongs to.
[![enter image description here][1]][1]
[1]: https://i.sstatic.net/oOAZx.jpg

looks like a listless guppy or a platy. note the upwards pointed mouth, that is a fish that swims around most of the time and is adapted to surface feeding, they rarely stay still at the bottom. use rainwater and give them rocks and plants and they will sink less. https://www.google.com/search?q=sunset+platy&source=lnms&tbm=isch&sa=X&ved=0ahUKEwicoIK_no_kAhVJSxoKHV5yABIQ_AUIESgB&biw=1972&bih=1070#imgrc=9IXX4HlKwHCbXM:

I thought it was a gold panda molly. It looked like below [imagehttps://images.app.goo.gl/uMoAfH3o5RpF1hRk6]

Your picture is unclear. Can you please post a better image?


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Cactus plant identification
I received this cactus as a gift and I'd love to know the family/scientific name. Only one flower has bloomed since, it was between orange and yellow. At first it was perfectly spherical, but in one month it has become almost pear-shaped.

Welcome to Biology.SE! Please edit your post to include an uploaded image. ——— Links are discouraged since 1) if they break they render this post and any answers worthless, and 2) they can be used to link to malicious websites. Thanks!

Thank you tyersome, uploaded a new image!

You're welcome — that seems like an unusual shape for a cactus, but at least it's happy!  ——— You might find this website helpful for figuring out your new friend's identity ...


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What could humans do to "see" what dogs smell?
We're able to see a lot of things using computers that we can't see normally: yellow-green, UV light, X-rays, etc. What do we have that harnesses the ability to "see" what dogs smell (e.g., harnessing a dog's sense of smell to detect cancer and so forth)?

Welcome to SE Biology. Please re-read the Tour to see why your question is not appropriate here: "Focus on questions about an actual problem you have faced. Include details about what you have tried and exactly what you are trying to do. Ask about... general questions about biological concepts, questions about the biological mechanisms behind medical conditions, questions about techniques in a biological or biochemical laboratory" and "Avoid questions that are primarily opinion-based, or that are likely to generate discussion rather than answers."

@David Is it truly opinion-based? I'm asking for actual methods of being able to perceive senses that are outside of our natural abilities in the same way that we perceive sound and sight when they are outside of our immediate knowledge.

RoCo I believe your question is a valid one and fits on our site. However, please indicate what previous research you've done (e.g., Google, Google Scholar, web of science, the library, etc.) and what you've already found out (or not found). Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

In addition to my original point and that made by @theforestecologist I would have voted to close your question on two other grounds. First it was too broad, it didn’t focus on one specific problem such as odour detection of a particular disease, and second it concerns the technology of odour detection devices, rather than biology. As they say, please read the label before use.

NMR spectroscopy is a technology that is used to identify molecules. So-called "NMR spectra catalogs" document the spectra of various known compounds. Acquiring these spectra requires purified samples, expensive equipment, and time. In addition to making next-generations of this technology into something that would be practical for realtime "smelling", you'd have to match up catalog entries with what dogs actually respond to. That's going to take a fair bit of work.
There's some literature online about growing olfactory sensory neurons in a Petri dish (with difficulty). If we can learn how the signaling pathways work for "odorant detection" for specific odorants or "fragrances" that we already know dogs perceive, perhaps we could genetically engineer a cultured neuron cell to "light up" a fluorescent marker or issue some other signal that is perceptible to humans, whenever some dog-specific odor wafts in. I suspect this would be more realistic than "tabletop NMR" in our lifetime.

Warwick University's e-nose technology has been around for quite a while: https://warwick.ac.uk/fac/sci/eng/research/impact/electronicnose/
As far as I understand their technology, they sample gas, and analyse it using a solid state CMOS device to generate a signature signal for particular compounds/mixtures.  The devices have been used in a variety of industrial gas sensing applications.
There has been some progress in using e-noses in medical diagnosis, for instance this paper reports the use of e-noses to sample volatile organic compounds from urine in type 2 diabetes diagnosis: https://www.ncbi.nlm.nih.gov/pubmed/30513787
The difference from NMR is that e-noses don't generally try to identify specific molecules, but rather, to generate a signature for a particular organic compound or complex mixture, which can then be compared with other signatures from other samples using a machine-learning approach.


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How many kangaroos would you have to add to a northern climate before they could start adapting to it?
If some enterprising billionaire wanted to introduce Kangaroos to a northern climate such as the northern boreal forest by Fort McMurray in Alberta, would it be possible for the Kangaroo's to survive and adapt to that climate creating a new super kangaroo (which will henceforth be known as the polar-roo)?
How many kangaroos would have to be dumped into the boreal forest before we would have enough to reach the critical mass that some of the kangaroos would be able to adapt and mutate to this new climate and conquer the north?

Welcome to Biology.SE! While interesting your question doesn't fit the criteria for questions on this site — specifically this question is extremely speculative and consequently no definitive answer is possible.  ——— Please take the time to go through the [tour] and then the help pages starting with [Ask] questions effectively on this site. Thanks!

You seem uncertain of the plural of kangaroo. Stick with the oos — oo’s would be possessive.

Do we know that kangaroos wouldn't adapt perfectly well to a northern climate?  (Or let's say a cooler one, since Australia is in the southern hemisphere.)  It's not as though they have any chance to naturally experience such climes, or migrate to them.  There are kangaroos in Tasmania, which is about as far south as they could get without building boats.

Thanks for the suggestions! I have fixed the plurality of the kangaroos in my question.

there are (probably still) feral wallabies in the Peaks district http://www.roaches.org.uk/wallabies.html . Not boreal forest by any means, but at least northern hemisphere ...  (I definitely agree that answers to this Q are going to be opinion-based, though)


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Cannot identify this insect
Can anyone please help identify this insect. It seems to be some sort of caterpillar but I'm stumped.

Location is in Suffolk, United Kingdom
Length is around 1cm, width is perhaps 4 or 5mm.

Image opens a video clip on YouTube.

Is there a way to embed the video into the question?

There are a number of larvae that glue detritus to their backs. I'm not sure what this one is.

Welcome to Biology.SE! For identification questions please edit your post to: 1) include the location (e.g. country and region — the more specific the better), and 2) an estimate of the size of the creature. The location and size can be essential clues for identification. ——— If possible a clear, closeup photo would also be helpful. ——— Please also take the time to take the [tour] and then the help pages starting with [Ask] questions effectively on this site. Thanks!

That appears to a "bag worm", which is as you surmised a caterpillar.
This suggest that it is from the family Psychidae, but I won't even try to guess at the species.  However, if you see any adults you may be able to identify them using this website.
An example image of an North American species:

Thank you. After viewing some videos of this bag worm / case worm moth, it seems to appear, and also move in the same manner. Case closed!


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Could ions inside lungs produce hydroxyl?
I am not proficient in either biology or chemistry. However, I have a question which I can't find answer to. It seems to belong somewhere between chemistry and biology. I apologize for any errors and inconsistencies in this post.
There is a page (https://allergytech.com/sharp_plasmacluster_ion.htm) which describes a process. During this process, positive and negative ions are released to the air. They are called clusters.

The clusters seek out and surround harmful airborne substances such as
  fungi, viruses, microbes, bacteria, plant and mold spores, dust mite
  debris, etc. At this point, a chemical reaction occurs, and the
  collision of hydrogen with oxygen ions creates groups of highly
  reactive OH radicals, called hydroxyl - Nature’s form of a Detergent.

A hydroxyl radical is very unstable. To stabilize itself, it robs the
  hydrogen from any harmful airborne particles it encounters. Doing so,
  the hydroxyl radical damages the harmful micro organisms and
  deactivates them.

Below is my question.
Suppose that a human breaths in those clusters as soon as they are released to the air. Is there a possibility that inside lungs, they will encounter something that will trigger similar reaction, and in effect hydroxyl will be created, too?

I’m sorry but questions on SE Biology should be comprehensible in themselves, without the requirement to go to some third party website which may be booby-trapped or disappear tomorrow. You need to post the images at the very least.  From what you write your understanding of chemistry seems deficient. You need to sort that out too, because at the moment what you write makes no chemical sense.

Thank you. I’ve looked at the page. It seems to be an ad for snake oil.

I don't know, maybe it's an ad. The technology is described in other places like here and here. But I can't find explanation what happens to the lungs when you inhale those ions, whether they could break lung cells like they break airborne particles.


text:
What kind of moth is this? Why does it have a stinger?

Unfortunately, the moth died before I could photograph it.
The body length is approximately 2-3Inches. It was much bigger than the moths I usually see. And this is the first moth that I have seen which has a stinger. Does anyone know which moth this is?
This moth was found on Sep 16th in Bangalore, India. (Sorry, I missed this information before)

Welcome to the Biology Stack Shobana, please take a [tour] and visit the [help] for more information on this site and how it works. Please also edit your question with where you live in the world, as species present vary quite a bit depending on where you are. A large nearby city or a state, even country might be enough for us to get a good ID.

lots of things are unknown your location and the natur type is two of them.do you know for sure it is a stinger is an other unknown.

@trondhansen : I am guessing it is a stinger, I am not completely sure. It felt hard and sharp.

without knowing what country or region this is from, @shobanas it is hard to make any progress towards an ID

Without information about the origin and/or better quality photos of this moth, it reminds me of and could be a member of the subfamily Arctiinae.
What might look as a stinger, is part of its gential apparatus which is usually more or less retracted into the abdomen. Being not too familiar with moths, I guess it should be - depending on the sex - either the ovipositor or the claspers.


text:
Looking for literature that gives a systematic presentation of geometric and topological features of trees
Introduction
I am a software engineer specializing in procedural generation of 3D models, and currently I'm building a generator for 3D models of trees, founded on the theoretical work of Aristid Lindenmayer. Having successfully constructed the system framework, my next endeavor is to incorporate distinct tree species models for generation.
Challenge at Hand
Despite my proficiency in software development, I lack the comprehensive biological knowledge essential to accurately deduce tree morphologies from visual references. I feel like my unfamiliarity with botanical terminology and key morphological features of trees prevents me from "seeing" the important parts of tree morphology.
Request for Assistance
To achieve a high degree of biological accuracy in my models, I seek recommendations for literature detailing the fundamental principles governing visible tree features. This includes the distribution of branches and sub-branches, inherent regularities and anomalies of certain features, variations in tree girth across species, potential branch count and orientations specific to species, among other external features. It would be great if the resource is supplemented with illustrative diagrams. Currently, my primary interest lies in modeling Conifers, hence a dedicated section on this category would be nice.I'm not interested in chemical or developmental models. At the moment I'm just interested in the analysis geometric (quantitative) and topological (qualitative) features of trees.

Welcome to the Biology Stack. Please continue the [tour] and visit the [help] for more information on this stack and how we work. Please note the homework requirement.

I have a couple of questions about your question - 1) by "principles" do you mean how they form or just the different types of form (leaf arrangements, types etc.)? 2)What do you already know about the above (see homework...). Please also note there are roughly 73,000 tree species and about 600 different class Pinopsida species, so a general answer might not be possible, though going up a couple of divisions from species to family, might be able to generalize at that level. There will also be well studied species (timber ones) like Pinus radiata you should look into.

Not meaning to spam you at all... but a nice bit of nominative determinism in Aristrid's name - Linden is a type of tree; Tilia genus, and Meyer means "farmer" so (Linden) tree farmer.

@bob1 Thanks for the feedback sir! I added the homework tag since my question is of that kind -- it addresses a kind of basic biology concept that is trivial to professionals. Feel free to edit my question the way you see it fit. I'm new to the stack so please forgive is the question doesn't belong here.

@bob1 As for the clarifications: 1) currently I'm not interested in developmental models, so formation processes are of a lesser interest to me. References on the topic are welcome though, as I will be interested in learning about it at a future time. 2) As I mentioned, my background in biology is thin. Most of the things I know about the topic are things from computer science literature and papers. They mostly don't do a comprehensive analysis of tree features. They do a kind of pragmatical analysis that helps the models "looks good" without really diving deep into biological side of things.

@bob1 What I would like is some sort of a starting point literature for me to get familiar with the biology side of this multifaceted coin. An example of the type of "laws" I'm looking for is say how the cross section area of the branches changes at branching points. One other example would be what types of branchings are most likely to be found on tree species. By "types of branching" I mean qualitatively different types. Conifer trees usually branch away from one single main pole that doesn't change direction, while say apple tree's "main" branch changes the direction. That type of things.

@bob1 I'm aware that I can find this type of things sporadically on blogs etc., but I would like to have a comprehensive book(s) that goes through this topic in a systematic fashion, because blogs are usually focused on one topic and I have to know about the topic in the first place in order to find it. But since I'm a total beginner in learning biology and botany I don't even know the types of questions I can ask, so a list of books that I can study would be a gold mine for me. Also thanks for the bit of trivia you posted, it's always fun to find out about such unexpected connections.

Those sorts of information might be tricky to find, if they have been studied at all. I would start looking for forestry information on Pinus radiata, though there they are more interested in having a straight trunk and aren't interested in the branches so much, but cross-section of the trunk at branching might have been looked at.


text:
What are the ingredients of Pheromone Trap using for controlling Fruit flies of cucumber?

Pheromone Traps are used for fruit fly control. But I have no idea which ingredients or chemicals are used for preparing Pheromone trap

What species do you mean - is it Bactrocera cucurbitae?

I have mention about Bactrocera cucumis


text:
Do all humans experience flatus regardless of their diet?
Flatus frequency is affected by diet, so I was wondering if flatus production solely depends on the food eaten, meaning that some people never ever release flatus because they don't eat any flatus-producing food. I guess if they say they don't, they're probably in denial...

Have you read the book Gulp by Mary Roach ? Some interesting flatulence research and other researches regarding gut is brilliantly written !

Flatus is a normal product of digestion. To some extent flatus production does not depend on the types of food eaten as some of the gas is nitrogen just from air swallowed while eating. Some of the gas produced may be from bacteria in the intestinal tract. Depending on the species they may not be particularly finicky eaters, and may produce gas from any biodegradable food-item.

Eventhough food contributes the most to flatulance, it can also be caused by swallowing air when you chew gum or smoke. It can also be caused by health conditions like coeliac disease and gastroenteritis (reference). So it is indeed hard to believe when people claim that they never fart.


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Is the SRY gene the sole responsible of biological male sex?
It's very well known that the Y chromosome is what determines maleness, but more specifically this seems to happen thanks to the SRY gene located on it. Some individuals have an XX karyotype, but because of unequal crossing-over between X and Y chromosomes during meiosis in the father, one of the X chromosomes ends up containing the SRY gene, and the individual develops into a male (De La Chapelle Syndrome).
So I was wondering, is the SRY gene all that's really needed for an individual to be, unquestionably, a male? It's kinda odd how XX males have male genitalia but are classified as intersex solely because their karyotype is a typical feminine one (which should be irrelevant given how they also possess the SRY gene).

No. The SRY gene is an RNA inhibitor gene. If its target is altered to not match, you get an XY female.

To my knowledge, the SRY gene is the only gene that cause variance in sex determination in humans. Of course, many genes are then involved in sex determination cascade but none these genes have variance in humans. Because environmental variance has no impact on gene determination in humans (to my knowledge and despite a few highly criticized articles) and therefore, nothing else than the SRY gene explains the sex determination.
The genes that are involved in the cascade of sex determination are not necessarily on the sexual chromosomes. On the Y chromosome, there are some genes that are male beneficial (beneficial for the male function) but these genes are not involved in the sex determining system.
In all species, the sex is determined by the environment and/or the genes. The best way to look at it is by reaction norms. On the below picture, think of the x-axis as being the temperature. Then, if you ask the question "Does the temperature influence the probability to develop into one sex or another?" One should answer. "It depends on the range of temperature you're looking at!" If you look at only very high temperature (far right) or very low temperature (far left), only the genotype explains the sex determination. If you look at mid-range of temperature, then both the genotype and the environment determines the sex.

N. Perrin and L. Beukeboom are writing what is probably going to be a very good book that will obviously interest you. I think the book is going to be publish in 2014 only. Here is the amazon link to pre-command it.

Check out this recent article in Science (AOP).
They say that two genes- Sry and Eif2s3y are sufficient to provide the entire functionality of the Y chromosome. Alhough, there is reduced number of spermatids in these mice (Genotype :XO-Sry-Eif2s3y), the viable ones are able to give rise to healthy offsprings.

The question did not have to do with male functionalities but with sex determination system. What matters for this question are the loci which variance bring some variance in sex determination.

read the article.. it is quite interesting.. what it says is that two genes can suffice for the entire Y chromosome (in the process of sex determination and also to retain the ability to reproduce).

From what I read of the abstract, it doesn't seem that the gene Eif2s3y has some polymorphism in nature. Therefore, this gene does not influence the variance in sex determination. But when I read the OP's question again, I realize that I might have misunderstood his point. This article seem very interesting indeed and might answer to OP's question.


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Is there a good site or software to see if a primer pair spans an exon junction?
I am going to perform some RT-qPCR tests to validate an experiment.
I'm currently in the process of ordering primers, and I would like to get them from the Harvard Primer Bank since these have been validated before.
However, I would like to get primer pairs that span an exon junction (i.e., one primer on one exon, the other primer on another exon.)
Currently, I have to do a lot of steps to figure this out, since the Primer Bank only gives the positions of the primers on the CDS, and not on the entire mRNA molecule.
Does anyone have a quick way to check on which exons the primers belong?
Thank you!
Is there a good site or software to see if a primer pair spans an exon junction?

If there is a such a site, I have never encountered it. Since you say you have the genomic coordinates for each primer it seems to me like all you need is a list of the genomic coordinates of every transcribed exon in the human genome. Assuming that is correct then you are in luck because such lists do exist in the form of a GFF3 file. You should be able to obtain a comprehensive annotated GFF3 file of the human genome from the EnsEMBL website. It is possible that the UCSC browser has a similar file (except in their '.bed' format) but I  am less familiar with the contents of that site.


text:
Re-stain slice using a different secondary antibody?
I stained a free-floating ~300uM brian slice using 4 different 1º antibodies (rabbit, chick, mouse, rat).
For the mouse primary, I mistakenly used an Alexa-350 secondary, when I should have used 594.
The microscope we have in lab cannot detect the 350 fluorophore, so I'm wondering if I can re-stain the slice with the anti-mouse 594 secondary.
Thanks for your advice !
[cross-posted in reddit/labrats]

Are they the same clone? You might have blocked all the binding sites so you'll get a poor/no/noisy signal with the 594.

Thanks for your input ! They are both Alexa conjugated anti-mouse secondaries, so I'm guessing they use the same clone to make them. (?)


text:
Is there anything that is completely non-toxic to humans at any dose?
Lately I have seen a number of unrelated "scientific" debates over whether certain substances should be outlawed because they are toxic to humans. My initial, informal reaction is usually to respond that anything is toxic to humans if you give them a sufficiently large dose.
However, formally I don't know if that's really true for everything a human being could ingest in some way. I started to wonder if there were some substances that our body could handle unlimited amounts of without any negative consequences.
As this question has been (correctly) identified as a bit vague, I'll try to explain what i'm looking for. For the purposes of this question, I'm willing to ignore the limitations of actually ingesting a given substance in "the usual way". For example, if you can't physically drink enough of some liquid fast enough to kill you without your stomach filling up and vomiting, but that same liquid injected intravenously could be lethal, I could consider that toxic. I also recognize that the body can only physically contain a certain volume of stuff, after which sheer pressure would cause it to fail; I'm more interested in "biochemical toxicity" as opposed to any physical damage (I just don't know the term for what I'm looking for.)
In other words, one of my goals is to learn if, under laboratory conditions, a properly motivated researcher could always find a dose that would be toxic, regardless of the impracticality of a real person ingesting that dose under normal circumstances.
So, with that qualification, my ultimate question is:
Is there any substance we know of that is completely non-toxic to humans at arbitrarily large doses ingested over an arbitrarily short period of time?

Strictly speaking, I suppose the inert gasses (Helium, Neon, Argon, &c) wouldn't be toxic.  Likewise metals like gold & platinum that have low reactivity.  Though swallowing a bunch would probably kill you by mechanical obstruction of the digestive tract.  More interesting to me are things like vitamin A, which are necessary for health at small doses, but toxic at larger ones.

I rather think there's a lot of things that would kill you at a high enough dose, but I don't think qualify as toxic.  Like matching blood plasma clearly won't be toxic, but eventually the increased pressure would kill you.  Can you clarify your question as per this?

@MooingDuck I hope that helps. I just don't know the word that means what I want; i want "toxic because it interacts biochemically with the body, not because your kidneys rupture under the pressure."

@jamesqf: Gold actually is toxic at high doses. According to https://www.rarediseases.org/rare-disease-information/rare-diseases/byID/669/printFullReport, "Overexposure to gold (as in treatment of rheumatoid arthritis) may cause skin rashes; bone marrow depression; stomach and intestinal bleeding; headaches; vomiting; focal or generalized continuous fine vibrating muscle movements (myokymia); and yellowing of the skin, mucous membranes, and whites of the eyes (jaundice)." (The same page also mentions platinum poisoning, but gives no information about it.)

@ruakh: I think that refers to poisoning by various gold compounds, not from elemental gold.  Compounds are of course not the same as the elements of which they're composed, otherwise a few grains of salt would kill us.

@jamesqf: Hmm. But gold poisoning is a kind of heavy metal poisoning, and is susceptible to the same type of chemical therapy (namely chelation) as other kinds of heavy metal poisoning. And -- as you say -- there are "various gold compounds", and all behave the same way. So the issue is presumably gold ions? I have no idea whether dissolved gold atoms could undergo some sort of redox reaction and become ionized during the digestive process, or as they go through the bloodstream.

@jamesqf, not all inert gases are non-toxic. Xenon is used as an anaesthetic. Too much of it and you suffocate, not because it displaces oxygen, but because it inhibits breathing.

@ruakh: That's something I've always been vaguely puzzled about.  Seems to me (though I'm far from an expert) that heavy metal poisoning isn't from the metals themselves, but from various compounds/ions.  So if the metal is fairly non-reactive (like gold) you could swallow chunks of it and be unaffected.  Or for instance all the people with gold or almagam dental fillings, or other implants.

@jamesqf Yeah, heavy metals have their toxic effects in some ionized state, in which they substitute for a lighter metal that's used as a cofactor on some critical metabolic enzyme, causing it to malfunction.  If you swallow a lump of the un-ionized metal, it'll be basically a question of how much your digestive system can corrode it, which for gold = hardly at all.

Silicones are pretty inert substances but finely divided silicone (dimethicone) will have laxative action and unlimited consumption can be harmful.

@jamesqf as afar is I know Neon has never been tested but under high pressure argon and helium can both cause temporary neurological symptoms

I’ll answer this theoretically, since that’s how it has been posed. And if we’re ignoring practicalities, we may as well posit that the substance in question will be introduced directly into the bloodstream (This is, of course, simple to do in reality, but not how most people consume their non-toxic substances.) The easiest way to show that any unspecified substance can be toxic at an unlimited volume is to invoke the human body’s mechanisms for volume homeostasis.
As mentioned in this answer, the human kidneys functioning optimally can produce up to ~ 25 L/day of urine.1 This would require complete suppression of ADH (anti-diuretic hormone, a.k.a. arginine vasopressin), which would occur only if the “toxin” load were markedly hypotonic (think water).2  There is therefore a theoretical maximum volume of any substance that can be dealt with by the body, which is something less than 25 L per day. (For any substance other than water, the maximum will be lower because ADH will not be as fully suppressed by a less hypotonic load.)
A volume of any substance introduced into the bloodstream (including a product precisely mimicking the constituents of the bloodstream itself!) will overwhelm the body’s homeostatic mechanism. This will result in edema which is unpleasant and, in the case of pulmonary edema, certainly pathologic - a “toxidrome” in your scenario. In the case of hypotonic fluids, serum osmolality will also fall causing hyponatremia with all of its consequences.
Summary: No, the human body can not tolerate an unlimited volume of anything, therefore there is no substance that is non-toxic "at any dose."

1. Christopher Lote. (2012). Principles of Renal Physiology. Springer New York.

2. No, you may not drink 25 liters of water per day. For one thing, urine can not be made with a tonicity of 0 to balance this (more like 60 mOsm/kg minimum). Additionally, ADH can rarely be completely suppressed, yielding a somewhat more concentrated urine and therefore lower tolerance for hypotonic intake before serum osmolality is compromised.

"the human body can not tolerate an unlimited volume of anything" - This is basically a tautology.  It doesn't even matter how the kidneys work - no matter how the human body works, there is no way it could tolerate of unlimited volume of something.  Even a never-ending hole in the ground will overflow if you pour fast enough, no matter how big it is.

@BlueRaja-DannyPflughoeft - The question posited "an unlimited amount," not me. :-) This just seemed to me the easiest route to address a question that is otherwise difficult logically (to "prove" that no such thing exists). I went through the factors that dictate that physiologic limit for volume intake and the toxicity of exceeding it, which is why I considered it substantive enough to be an answer. You may disagree.

I know, I upvoted your answer.  I just think it's a silly question.

Not a silly question at all, though perhaps needs to be re-worded to add qualifications about amounts a person could potentially consume - as for instance water being toxic in large amounts.

This answer does get effectively what I was looking for, though I've tried to reword it to be more clear about what I meant by "arbitrarily large". Hopefully that helped?

@MichaelEdenfield The question is pretty highly upvoted, so I wouldn't worry too much. :-) Your edit did clarify your intentions. I actually think I've undermined them a bit by making it about volume rather than dose in any normal sense of the term. But if you want talk about the "most benign" sorts of infusions, my mind goes to isotonic saline or some (hypothetically non-immunogenic) whole blood product, and then the limiting factor is obviously volume. Anyway, glad it was helpful.

@Susan yes, I unaccepted your answer since I've clarified the question a bit and it doesn't really fit the clarified question. I still think this answer gets closest to what I was looking for, especially the information about the kidney's limitations on how much work they can really do, but I want to give other a chance to chime in before I re-accept it.

The kidneys don't always have to get rid of all the water a person drinks. In some circumstances a lot of water can be excreted through the skin and lungs.

@bdsl Yes, good point, I had considered mentioning these insensible losses, but the volume is relatively small in healthy individuals compared to what we're talking about here, and to my knowledge they aren't regulated (like the kidneys) in a way that allows them to participate in the dynamics of volume homeostasis (i.e. they are fixed or environmentally dependent rather than responsive to volume/solute load).

There is an applicable norwegian proverb that says; "Health in every drop, poison in every liter".

It depends largely on the method of administration. If you are atomizing the substance and delivering it via water vapor, many, many substances have no known LDLo (lowest dose required to kill a member of the tested population). Almost any substance in existence has the potential to kill you if it is diluting your bloodstream via direct intravenous injection or oral consumption; however, when it comes to inhalants, many substances cannot kill you.
Since your question was specific to intoxicants, here's a couple of examples: There is no LDLo level of Tetrahydrocannabinol (the active ingredient in marijuana) when delivered via atomization. There is also no known LD50 (a similar, albeit somewhat less reliable, metric) for lysergic acid diethylamide (commonly referred to as LSD). For psilocybin (the active ingredient in "magic mushrooms"), the LD50 is high enough that an average person would need to ingest around 6 pounds before cause for concern.
Other far more dangerous substances that can kill with vastly lower amounts include anything that speeds or slows the heart rate: most specifically, cocaine (including crack), opiates (including morphine, heroin, and various pain pills), and any amphetamine, methamphetamine or derivative substance, or other stimulant (crystal meth, ADHD medication, and even caffeine or ephedrine). Of course, the most common killer categorically from a historical perspective is alcohol.

to be honest, I was motivated by the claim that propylene glycol (what's in most e-cig liquid) was toxic. But I also know that at least one THC study claimed that THC was toxic after IV-injecting it into rats at thousands of times a normal dose, which motivated the exact wording of my question.

The absence of a known LD50 doesn't mean there isn't one.  It just means it's beyond what anyone has been exposed to.

Poor rats... :(

There is a problem with definition of toxicity — things that are dangerous in large amounts aren't usually called toxic. In spite of this, you're right: everything can be dangerous to a human in large enough amounts, or if delivered improperly.
For example, even water can be toxic if drank too much. Also, when it gets into the lungs, it may cause drowning.
On the other hand, air, while necessary in lungs, is dangerous if present as a gas in the bloodstream.
BTW, even botox (being one of the strongest poisons) is used in medicine in very small doses.

True, I knew the word toxic was being used sloppily, but that's the word I see used to describe things like IV-delivery of absurd amounts of THC, so I didn't know what other word to use.

First thing I thought of when I read this... and I remember reading about this way back when w/r Water Intoxication: http://www.cbsnews.com/news/woman-dies-after-water-drinking-contest/

The inert gasses Helium and Neon are non-toxic when administered through inhalation, so long as the patient's oxygen supply is sufficient.  They are also non-toxic when injected, so long as the injection is slow enough for them to be dissolved in the bloodstream.
You can be killed by them through various means (asphyxiation through oxygen displacement, rapid injection causing an air embolism, rapid decompression causing decompression sickness, and so on), but since the cause of death is unrelated to the chemical properties of the substance involved, it's not accurate to call this "toxicity" (unless you're XKCD).
Other inert gasses (Argon, Krypton, Xenon) may be toxic at high pressures: although I haven't found an LD50 for any of them, they can all induce nitrogen narcosis, and Xenon is usable as a general anesthetic.

Wrong.  All the "inert" gasses will kill in sufficient quantity.  It requires considerably more than you can breathe at normal atmospheric pressure but if you run the pressure high enough they turn evil.  This is what imposes the limit on scuba diving--there's no gas mixture that doesn't become toxic at a high enough pressure.

He, he :) Indeed this question smells like XKCD - arbitrarly large numbers are quite often in What if :)

@Loren Pechtel: But is it the toxic effects of the gas itself, or just that it's something saturating the blood at high pressure, then coming out when the pressure is reduced - that is, 'the bends'?  Maybe splitting hairs, but I see it as like the difference between the toxic effects of drinking too much water, and drowning.

@LorenPechtel, I've updated my answer to take into account nitrogen narcosis, since Ar, Kr, and Xe can induce it.

@Mark I doubt anyone knows the LD50 for them.  Where would the data come from?  They're going to stop using them at the depth where the symptoms become serious, nobody's going to take them to a lethal depth.  And it's not just Ar, Kr and Xe, H and He also do it.

@jamesqf No, I'm not talking about the bends, but rather what's more commonly known as nitrogen narcosis.  Everything we can breathe (except oxygen, which has it's own problems in excess) will cause it if the pressure is high enough.

@LorenPechtel, the usual way to find an LD50 is to kill off a bunch of lab rats.  For something exotic like high-pressure Argon poisoning, it's probably not worth the effort.

@Mark Yeah, you could get a LD50 for rats that way but why bother?  It's not something that's a realistic threat to a human--you'll kill yourself by accident before you get that deep.

not even AIR, because if you force too much you will explode it depends on how extreme is the "any dose" statement
water is also toxic in large Ingestible amounts
and since we go into theoretical application the answer would be dark matter
so the final answer is nothing , because the human body has evolved to exist in some equilibrium, so too much of one thing even if is harmless it itself ( like water, or proteins ) it causes an imbalance, and as a result it becomes "toxic"

Even simple water is "toxic in high amounts" as kidneys can remove 25 l per day at most. All other substances are probably even more "toxic".

Downvoter, please leave a comment.

Vitamin C won't kill you no matter how much you get into your body as long as it is enough to help prevent arterial wounds and atherosclerosis(This happens in people with scurvy or vitamin C deficiency because of how cholesterol is used to help repair the wounds and this can lead to a complete blockage of the artery and thus an infarction of all the tissue that artery supplies. So if you don't want to have an MI, one of the things you have to do is get vitamin C into your system.
Another example of this is chloride ions. While having high chloride ions might cause there to be a slower reaction time(since chloride acts as an inhibitor in neurons) it itself won't kill you. Yes it might affect the muscles by not having them contract as much as they are supposed to but this is naturally cured by urinating out more chloride and thus more sodium which can lead to a sodium deficiency which is bad because your body needs sodium in order to function. With a low amount of it it you wouldn't be able to think clearly or even have a normal heart rhythm which might lead to bradycardia from a higher pottasium concentration in the heart.

Doesn't your second paragraph just explain that chloride is in fact toxic at some dose? (The MI/high-dose vitamin C association also needs some referencing, except it's not really relevant.)

Wikipedia indicates that it is unknown if vitamin C can be toxic or not.  It cites a source (at a dead link) that apparently managed to kill rats by administering excess vitamin C, but it is uncertain whether the cause of death was chemical or mechanical.

No. The second paragraph says that while chloride is nontoxic at a high dose, high chloride results in low sodium and it is the low sodium that is toxic. as far as the association of scurvy with MIs that is actually relatively simple. When somebody has scurvy this causes them to easily get arterial wounds both external and internal. The body uses cholesterol to heal these wounds in somebody with scurvy instead of platelets. This is turn causes more cholesterol to build up in the artery causing atherosclerosis. If this happens in the heart than it can cause a heart attack or MI.

And as far as the death from excess vitamin C it was probably mechanical and not from the vitamin C itself. And even if it was from the vitamin C that does not mean that excess vitamin C in humans will cause death. In fact I have been taught that since vitamin C is water soluble and vitamin C always helps your body by strengthening your immune system and acting as an antioxidant that vitamin C toxicity does not exist, only deficiency.

high chloride results in low sodium and it is the low sodium that is toxic : you’re describing a mechanism of toxicity there, not the absence of toxicity.

This is not really a substance, but anyway.
Neutrino
Neutrinos are ghostly particles that barely interact with any matter. Therefore, no sufficient amount of neutrino (that human can ever collect) can kill you. To have a lethal dose of neutrino radiation, you must stand inside the outer layout of a giant star that creates a supernova.
Source: XKCD, Lethal Neutrinos

The source you link (and your last sentence) say there can be a lethal dose of neutrinos. The point is just that it's hard to kill anybody with neutrinos because the usual sources of lethal doses of neutrinos also produce large amounts of more lethal particles, radiation and heat and therefore a human would die from other causes long before being exposed to the lethal dose of neutrinos. Therefore, neutrinos aren't an answer to the question.

I agree. It's just that so is the top voted answer. So I take my deliberation and post this answer


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What are Antihistamines doing in a baby?
In his song Lullaby, Tim Minchin sings:

Your nappy is dry and your tummy is full
  Of enough antihistamine to chill out a bull
  Yet still all this gringing

According to Wikipedia, antihistamines are used against allergies.
So, why is there antihistamine in his baby's tummy and why is it supposed to make her sleepy?

This song most likely refers to an off-label (and usually inappropriate) use for certain antihistamines like Benadryl. They are sometimes used by parents to sedate their children, functioning through the exact physiological mechanisms @Chris describes.  Parents use it inappropriately as a means of behavioral control for active or upset children to make them more docile or sleepy, such as for airplane rides, etc.  It's not recommended by most pediatricians, because even though adverse (bad) side effects are usually rare, it is an actual medication with another primary mechanism of action having effects on many body functions, not a medication designed as a sedative.

This is not only happening in babies...
In short (I will look for some references later and edit the post) the antihistamines are effective in the whole body and block the histamines there. The antihistamines which cross the blood-brain barrier do the same in the brain and hinder the small amounts of histamines which stimulate the nerve cells there from doing so. This results in the typical sleepyness.


text:
Does body absorb nutrients less efficiently if we ingest the same amount at the same time, opposed to spreading over a larger period?
I would like to understand if ingesting a certain amount of nutrients will result in different absorption from my body, depending on whether I ingest that amount spread over time or everything at once.
For example, considering all the food I eat in one day: does my body absorb the same amount of fat and protein if I eat that same amount of food all at once, compared with eating it spread by different meals?
Similarly, could it be possible that my body absorbs less fat if I eat 4 hamburgers at the same time, compared with eating them spread along the day?

LARGE MEALS AND ABSORPTION
When consumed in usual amounts, the percent of absorbed macronutrients (carbohydrates, proteins, fats, alcohol) should not differ significantly when coming from one large or several small meals.
As an example of the composition of a single large meal, let's imagine something that fits into Acceptable Macronutrient Distribution Ranges (AMDR) in a 2,000 calorie diet: 250 g of carbohydrates, 70 g of proteins and 80 g of fats.
Most carbohydrates are digested into glucose and fructose. Glucose, when absorbed as the only carbohydrate (ingested as glucose or starch), can be absorbed at the rate 60 g/min, but the addition of fructose can increase the absorption of both together to as high as 126 g/min. When fructose is absorbed as the only carbohydrate or in the excess of glucose, it's absorption limit from one meal can be as low as 5 g or as high as 50+ grams. Certain sugar alcohols (see Table 4) (sorbitol, isomalt..) can trigger diarrhea when consumed in amounts greater than ~20 g/meal.
Virtually all ingested protein is absorbed by healthy humans (Surgery Journal). The rate of absorption depends on a type of protein: about 10 g of whey protein and 3 g of egg protein can be absorbed in one hour (JISSN).
At least 60 grams of fat consumed at once can be normally absorbed, concluding from a study in which they investigated the relationship between the amount of fat consumed and atherosclerosis.
In conclusion, the amount of macronutrients (except fructose and sugar alcohols) consumed with a single meal does not seem to significantly affect the percent of macronutrients absorbed, but it prolongs the time in which they are absorbed.
LARGE MEALS AND DIET INDUCED THERMOGENESIS
After eating one large meal, more of the consumed calories will be lost as heat than after eating several small meals:

Consuming the same meal as a single bolus eating event compared to
  multiple small meals or snacks was associated with a significantly
  higher DIT [diet induced thermogenesis]. (Nutrients, 2016)
TEF [thermic effect of food] was measured by indirect calorimetry
  for three hours following each meal and was found to increase
  systematically, in a nonlinear fashion, as meal size was increased.
  (Metabolism, 1984)


text:
Why are beavers not considered marine mammals?
They spend a lot of their lives in the water, they have fur, give live birth, have mammary glands etc...but my teacher mentioned that beavers have continually growing teeth (incisors) which supposedly excludes them from being marine mammals. The thing I'm confused about is that we also learned later that manatees & walruses (which are both considered marine mammals DO have continually growing teeth. I don't understand, any help would be appreciated :'(

It might help you to think carefully about the word "marine"...

@bob1 It might help you to think carefully about the fact that beavers sometimes brave the sea.

So do people, are we "marine"? @Araucaria

@Araucaria true, but does not make them marine any more than whales and dolphins coming into fresh water makes them aquatic.

Beavers are not Marine Mammals
According to Wikipedia, Marine is an adjective meaning of or pertaining to the sea or ocean: as Beavers can be found in a number of freshwater habitats, such as rivers, streams, lakes and ponds, they are not considered "marine".
Beavers are semiaquatic Mammals
Their wikipedia page mention that they be semiaquatic mammals (that dwell partly or entirely in bodies of water), as the European otter, the Baikal seal, the Capybara or the hippopotamus:

Beavers (genus Castor) are large, semiaquatic rodents
(...)
Other semi-aquatic mammals, such as water voles, muskrats, minks, and
otters, will shelter in beaver lodges.

Be nice to your teacher when you correct them about their answer: it's ok to be wrong sometime, even for a teacher! Hope it helps.


text:
What species are these, beetle eggs?
I posted a thread the other day and identified I have carpet beetles larvae. I have a pest control company booked to treat the place on Monday but in the meantime I’ve found these little things on the wall that keep appears and I’m wondering if these are the eggs stage of the beetles or perhaps an entirety different species? Someone on a Facebook group suggest they could just be wax or food, but how would either randomly just appear on the walls?
Size wise they are about half the size of a grain of rice or perhaps a little bigger.
Just been googling, could it be instar stage of bed bugs?
I’m based in London, UK.
enter image description here

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food (or snot-stuff) can appear to 'randomly' appear (i.e. appear unexpectantly) on walls or ceiling simply from a cough or a sneeze

These are not instars or eggs. These are debris from food or perhaps ear wax or something similar.
If they were instars you would see either a uniform larval shape - usually bilaterally symmetrical, or you would see something that indicated a body form like legs, head etc. You would also expect that they would be about the same size and shape in each case, though different age/stage larvae can have different sizes.
If they were eggs, you would generally expect them to be both the same size and both the same shape if they came from the same species. They would also be very large eggs for common insects; most butterfly eggs for example are in the 1-2 mm range, rather than 5-7 mm.


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PCR: Are primers designed to be complementary to a DNA sequence within the template DNA or to the 3' ends of the template DNA?
I was told that in order to produce primers, the DNA sequences at the 3' end of the template strand must be known, and that these primers are complementary to 3' ends of the template DNA.
However, that causes me confusion when I view the following image from my college class, which show that the primers anneal to the template DNA further down the strand:

So do the primers need to be complementary to the last 20-35 bases at the 3' ends of the template DNA or simply to any portion of 20-35 bases near the 3' end?

You seem to be confused about the template DNA having a relevant "end".  Most DNA molecules one would start with would be very long, often an entire chromosome.  The 3' ends of the two strands are essentially never near the piece one is trying to amplify with PCR.  So, no, the primers do not match these ends.
For PCR, you are trying to amplify a "region of interest" within the millions of bases you start with.  The region is necessarily bounded by two known sequences (otherwise you have nothing to prime the DNA replication).  The two known sequences define the region of interest and are the sequences one creates the two (different) primers -- the green and orange primers shown in the question's diagram. Since those two primers define the region of interest, and DNA replication will proceed in one direction (from 3' to 5'), they are exactly the two ends of the region to be replicated.  These primers of course anneal very, very far from the ends of the chromosomes.


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Modeling and Predicting Squirrel Populations
I was recommended to come here from the MathSE site. Here is the question:
I am interested in modeling the growth of the Eastern Fox squirrel population in Los Angeles, not only in terms of numbers but also in overall territory. The site iNaturalist has a wonderful database of sitings at my disposal, but I am unfamiliar with the mathematical model(s) that I'd need to use to model and predict their growth and territory.
I have taken a quick look at a paper on regular migration and this BiologySE post. Would this be what I am looking for? Or does the question I'm asking require something else? Thank you in advance for the help.
While the eastern fox squirrel is not migratory, I assume the models from the migration paper can be abstracted for my purposes. Perhaps I am wrong.
Some more information as requested by a commenter:
I am completely new to the theory of population biology. The only data I have is from the iNaturalist site, which has geotags of sitings and # of sitings. I am interested in finding out how the Eastern Fox squirrel population has grown over the past few decades, and how their territory shapes up to that of the native Western Gray squirrel. There has been commentary in Washington and NorCal about the shrinking populations of the latter, but I haven't found anything for Los Angeles. This is why I am asking here -- to see whether Eastern Fox squirrels outnumber Western Grays in a significant way (don't take 'significant' in a technical sense).

Welcome to the Biology SE. Please take the [tour] and visit the [help] for more information on this site and how it works. Lets get some things cleared up - please edit the answers into your question. How much population biology (theoretical or otherwise) do you know? How much do you know about the population as it stands now - what sort of data do you have? What do you want to find out? Also, are they migratory? if not, why do you think a paper on migration will help?

Cross-posted: https://biology.stackexchange.com/q/114138/61455, https://math.stackexchange.com/q/4866740/14578.  Please do not post the same question on multiple sites.

You might try to start with log growth, then use iNaturalist data to see if there are geographical areas of overlap in Eastern Fox and Western Gray sightings. If so, check out Lotka-Volterra to assess the competitive interactions.


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Double mutant analysis with null mutants
My professor was talking about double mutant analysis with null mutants, and how double mutant analysis won't work with hypomorphs.  I really don't understand the concept of double mutant analysis.
He was talking about pathways - if A and B are in the same pathway, then you would mutate A and he said something about the phenotype being identical.  If A and B are in different pathways, you could mutate both of them and there would be a "stronger" phenotype.
He also said it would only work with null mutants, not with hypomorphs, because with hypomorphs some of the pathway would still be active, not completely shut off.
I really don't understand any of this - what a double mutant is, the whole pathway thing, why the phenotype is "identical" or "stronger", or why you use hypomorphs.  I would really appreciate a rundown on the idea of double mutant analysis because my professor's explanation was so unclear.  Thanks in advance.

Do you mean why you DO NOT use hymomorphs ?

you may also want to see this

Basically your professor was saying some hypomorphs (weakly expressing phenotypes) do not necessarily show their phenotype since they still express some of the gene products and there are other pathways that might compensate for their lack of expression of that gene to an extent. So if you want to see a phenotypic effect then you got to have a null in those situations since that will be harder to compensate for specially in organisms that do not have that many redundancies such as Drosophila. But even nulls are not exempt to the above rule if there is another pathway compensating for them!

What is a double mutant ?

See this image.
In this mutant 1 has one mutation, mutant 2 has another mutation while the double mutant has "double"  or 2 mutations.
Key : A,B means double mutation , A means mutation in A and B means mutation in B.

Types of double mutations

a)Additive phenotype:  A, B = A + B   Implies that A and
  B function independently and on different processes.
   Eg.  A =
  short roots, B = no root hairs A, B = short roots with no root
  hairs.
  Conclusion: A and B function independently on different
  aspects of root development (A is required for normal root growth
  and B is required for root hair development.
b) Epistatic phenotype: A, B = either A or B
i) If A = B = A, B   then epistasis implies that both genes function in the same pathway and that each gene is essential to the process.   Eg. A = short roots, B = short
  roots A, B = short roots.  Both A and B are  required for
  normal growth of roots.
ii)         If A is opposite in phenotype to B, and A, B = A, then epistasis implies that  A and B are in the
  same pathway and B is a negative regulator of A.   Eg. A = long
  roots, B = short roots A, B = long roots.  A is required to
  suppress root growth and B is a negative regulator of A.
c)
  Synergistic phenotype: A, B >>> A or B.
Implies that A and B contribute independently to the same process.   Eg. A = long roots (wt = 2 cm, A = 4 cm)    B =
  long roots (B = 4 cm)  A, B = very long roots (20 cm).  A and
  B negatively control root growth independently of one another and
  are performing partially redundant functions.

When your professor was saying that if A and B are in same pathway and you mutate A and phenotype comes as if both A and B have been mutated, then he was probably referring to the epistatic phenotype.
When he was talking about having a stronger effect by mutating them both, he was talking about Synergistic phenotype.
Source : Double mutant analysis

I do not know about the hypomorph thing. Maybe someone else will help you !

Feel free to ask anything u do not understand. These things are tricky !

Hypomorphs (now commonly termed 'dominant negative') have a reduced (hypo) phenotype as compared the wildtype. Null (knockout) mutations, however, have the phenotype removed, so to say.
The reason that you would use null rather than hypomorph mutations to do double mutant analysis is because with the hypomorph, you would still see some effect of the phenotype you are trying to have eliminated.
Why do you want to eliminate a phenotype? Let's say you want to try to find the pathway for the genetic interactions between A and B. You have 2 animals you want to cross (I work with C. elegans worms, and use double mutants often). If we look at the wildtype homozygous of both animals, they will be the same. Animal 1: +;+/+;+. Animal 2: +;+/+;+. (where + denotes wildtype, and ';' means they are not linked, so the genes are independent of each other).
We will use 'a' to denote null mutation A, and 'b' to denote null mutation B.
Animal 1 will have mutation A. Animal 2 will have mutation B. So now Animal 1 will look like a;+/a;+, and Animal 2 will look like +;b/+;b. Notice that each locus is corresponding with itself - ie: in the region where Animal 1 is still +, Animal 2 is b, and vice versa (for null mutation 'a').
So then we cross Animal 1 with Animal 2 and get a;+/a;+ x +;b/+;b which will segregate in a 9:3:3:1 ratio (according to independent assortment of 2 independent genes - just draw a 4x4 punnet square to convince yourself).
We are interested in achieving the 1/16 a;b/a;b animal (also can be noted aabb, btw). And THAT is our double mutant.
Because we use a null allele, there is no chance of the wildtype phenotype "leaking" within our cross, giving us a false ratio or false assessment, as would be the case with a hypomorph (reduced, but not gone).
Now, when talking about genes in a pathway: I think this is what your professor was referring to. When we are mapping how genes interact, and in what order, we can either have the genes interacting in redundant or sequential pathways.
Redundant pathways: A -> C and B -> C. So either A or B can have an effect on C, meaning that having both is redundant, because one can do the job.
Sequential pathway: A -> B -> C  OR  B -> A -> C. So both are existing in the pathway in sequence, and both are needed.
Just as a side note, whenever you are using double mutants to find out if your pathway is redundant or sequential, you MUST compare it to a single mutant!!! Otherwise you WILL NOT be able to tell the difference between your results.
In a single mutant (A, for example), when using in a redundant pathway, you will still get phenotype C, since B is available. Just note that your C phenotype will be weaker.
When you then use a double mutant, knocking out both A and B, you will see NO expression of phenotype C. The same will apply if you knock out B instead of A.
Now, for a sequential pathway. If you use a single mutant (again, let's use A as the example) you will have no phenotype C, since A is needed to interact with B (whether upstream of downstream) in order to have an effect on C. And, if you use a double mutant (so knock out both A and B), then you will also have no expression of C, since both A and B are gone. (again, same applies if you use a B single mutant first)
So, for a redundant pathway: single mutant will have C phenotype, double mutant will not have C phenotype. There IS a change!
For a sequential pathway: single mutant will have no C phenotype, and double mutant will have no C phenotype. There is NO change!
If you would have used a hypomorph to do these experiments, then you would probably see some percentage of C expression in your double mutant experiments, making your results inconclusive.
--
I hope this helps!
[source: you can find this information in any genetics textbook (in my case, since i study worms, WormBook is a great source); I have given this information from my own experience. I have an honours degree in Genetics (Biochemistry and Medical Genetics) and am currently continuing my education in grad school (biochemistry and molecular biology).

Null mutants are not necessarily KO! they can for example be substitutions causing a premature stop codon. Hence it would be great if you made that clear in your response!


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What is meant by longitudinal splitting of chromosomes?
My textbook says that during prophase, the chromosome longitudinally splits (except at the centromere) into two sister chromatids. But what does this mean? The DNA is already duplicated in the S phase. So does this mean the uncoiling of the plectonemic coil formed by the sister chromatids? Perhaps the degradation of cohesin(I think unlikely)? I am a grade 10 student unable to find the answer(although this is not a homework question) so  please try to keep things simple.

The duplicated set of DNA in each chromosome(formed at replication in s phase ) gets separated and repacked as a new chromatids that we call as sisters, which are held together at centromere by COHESISNS & CATANANES(mechanically interlocked DNA) But the arms are seperated from each other by further condensation of the DNA, DECATANATION by TOPOISOMERASE & SELECTIVE BREAKUP OF COHESISNS at NON CENTROMERIC REGIONS (ARMS) from late S PHASE to PROPHASE & PROMETAPHASE through a CLEAVAGE INDEPENDENT PATHWAY (which is REVERSIBLE). But the complete seperation of sister chromatids at the centromere is due to the additional action of SEPARASE through CLEAVAGE DEPENDENT PATHWAY (QUICK, IRREVERSIBLE) which occurs from LATE METAPHASE TO ANAPHASE.

Your answer could be improved with additional supporting information. Please [edit] to add further details, such as citations or documentation, so that others can confirm that your answer is correct. You can find more information on how to write good answers in the help center.


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How are genetic hallmarks of aging somehow “reset” at conception?
I’m a layman and genuinely curious about this, so forgive me if I use the wrong terminology or obviously don’t know what I’m talking about. Regardless of whether parents have a child at 18 or at 40, the offspring still has the dna of a newborn at birth (in terms of dna age metrics like mutations/errors, methylation, and telomere length). Meanwhile, doesn’t conception and fertilization involve continuation and replication of genetic material from both parents? How is it, then, that information loss in the parent’s dna due to replication (which could arguably be what aging is) isn’t inherited or perpetuated across generations? How does the offspring get a "fresh" copy of dna? I assume sperm and egg cells age like any other cells in the body, right?

Welcome to SE Biology. As you say you are a layman, you will be aware from reading the [Tour] that yours is not the constituency for which this site is intended. The gist of your question is of interest, nevertheless, but the title betrays an unjustified assumption that is incorrect. There is no reset. So I would suggest it be redrafted in terms of the effect of aging and consequent mutations on DNA of the offspring. And please avoid irrelevant asides about the nature of aging. Finally, if you are unsure of an assumption you are making, please use the less didactic “Am I right in assuming…”

Hello, thank you but the assumption my question “betrays” actually had some basis in the peer-reviewed literature (see link below). Also, how is DNA methylation and telomere length “irrelevant” if these are the hallmarks of aging I’m asking about and are well accepted as associated with aging? The link to the paper that discusses rejuvenation at conception: https://www.sciencedirect.com/science/article/pii/S1471491420302173#:~:text=For%20example%2C%20on%20the%20basis,must%20be%20reset%20after%20conception.

There is no reset of the DNA itself. Any mutations in the DNA the gametes is fixed. The question of protein methylation is different and should be kept distinct. If your level of knowledge is such that you are sure something happens, I suggest that it should be easy to find for yourself, how.

Just write an answer explaining why something is wrong, in that case

NominalSystems, please keep your language civilized.

From a DNA perspective, consider that a lot of aging is stochastic. By the end of a human lifespan, it's likely that a couple of our trillions of cells have collected enough mutations to be cancerous or close to it, and that's all the whole organism needs to die of cancer eventually. A gamete is just one cell, though. "Bad" gametes that are highly damaged are unlikely to develop into a viable organism. Reproduction allows for selection of just one of the "good" cells. It isn't necessary for that selection to be "intentional" or directed, though: you just can't build a whole, functional organism with a cell that's too damaged. A skin cell, say, can do it's job just fine with a lot of damage to genes that aren't involved in the function of skin, but a whole brand new animal won't get very far.
For brain aging, part of the problem of aging is developmental. The nervous system develops through an intense choreography of guidance cues that map out the tracts that connect different brain regions and all of the sensorimotor and organ systems with the nervous system. A lot of that follows the growth of the organs and body itself; you don't grow arms first and then send neural axons down the already grown arm, the neurons that will sense and control the arm grow along with the vasculature as the arm itself grows. When a neuron dies, it's gone for good but it's not just that the information stored in the connections that neuron made are lost. There is no possible way for the longer range connections to ever be rebuilt because they depend on signalling that was only present at some moment in time. Starting from scratch will revisit all those developmental milestones.
It's also not perfect. Each gamete has maybe 20-50 mutations not found in the parent genome. Many have little effect, some might be bad, some might increase fitness. That variation drives future evolution.
(This is really just a draft: todos are to add references and discuss various ways gametes are protected from mutation like dividing early and sparsely and not doing a lot of work that accumulates oxidative stress)

But wouldn’t it be better to address the key point of what the state of the gametes is at fertilization, and emphasize that the assumption of a “reset” is incorrect. I know nothing of embryology and that sort of biology, but surely the gametes do not divide and undergo telomere shortening until fertilization, in contrast to the poster’s assumption. And isn’t there evidence that birth defects are more prevalent in the offspring of older parents? Please give us some concrete stuff rather than stochastics.

Then there is the question of methylation of chromosomal proteins and the different "imprinting" in sperm and ovum.

I realize this is only one paper, but see the highlights including “ We propose that the zygote–ground zero period is associated with rejuvenation, wherein the biological age is decreased, telomeres are extended, and molecular damage is cleared”. Link: https://www.sciencedirect.com/science/article/pii/S1471491420302173#:~:text=For%20example%2C%20on%20the%20basis,must%20be%20reset%20after%20conception.

@NominalSystems I think the telomeres are probably the most boring part of cellular aging and get way too much press for their value; telomeres are useful as a limit on unchecked replication to combat cancer. The limit is trivially reversed by telomerase. If you want to ask a more specific question about a specific paper, I'd recommend doing that directly rather than referring to it obliquely and then mentioning in a comment. I think papers like the one you reference are a bit misguided, though, and are more focused on an imaginative science of anti-aging than on understanding development.

Thanks, I only found the paper after posting the question though, but have heard this idea before. Any insights on the molecular damage portion and not just the telomeres? Also, I’m curious what you think makes the paper misguided? Is it wrong assumptions about biology? There are other papers arguing the same thing:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8232908/. What about this seems unscientific besides elucidating mechanisms of “anti aging” which get mixed in with pseudoscience sometimes in other, non peer-reviewed settings?

@NominalSystems I think it's misguided because it imagines that gametes need to anti-age (and that it's possible to do so), which I do not think accurately describes the biology. Of course you'll find a lot of papers on this, because as people get old they want to not get old so there's a lot of money and excitement around anti-aging. Note also that this is the same author of these two papers. I don't know this specific work and I'm not saying it's wrong or unscientific, but I'd urge attention towards what they define as "aging" and consider whether that's actually what aging is.

I think most people would conceptualize "aging" as involving the irreversible changes that accumulate over a biological lifetime; their measure of aging here is an easily-reversible DNA modification.

Thank you for discussing it. Seems like your overarching point is there’s a lot more to it than a few easily manipulable attributes of dna


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Atp as energy currency
I have seen that ATP and sometimes GTP is used to deliver energy to reactions in the cell. What is the reason that no other chemical is used for the purpose ? What is the charistiristics of the structure of atp( the nuclear base part , the Penrose part and the tryphosphate part) and its bonds that makes it a perfect energy currency in cells?

Maybe a dupe? https://biology.stackexchange.com/questions/81417/why-is-atp-used-as-a-source-of-energy-rather-than-glucose, probably relevant either way

Well this actually doesn't answer . It only compares atp with glucose and not focus on all parts of atp structure .

This question has already been asked and answered: Why is ATP the preferred choice for energy carriers?

This question should be closed as a duplicate, but please proof-read your questions in future. Most web browsers include spelling checkers, and if your computer is set to some language other than English, it should be possible to change it temporarily. If you have done any research on the topic you will surely have noticed that ATP is an acronym and is always capitalized. In addition, your question makes the unjustified and unjustifiable assumptions that ATP is "the perfect energy currency", and shows no evidence that you have tried to research this topic yourself.


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Electron transport chain
I am learning about electron transport chain . I have seen that complex 1 and 3 pumps H+ ions across the inner mitochondrial membrane . To do this it uses the electric work done to move electrons through the f-s clusters in the complexes . Nowhere it was shown that exactly how moving electrons in those cluster can do work on H+ ions to move them so can someone explain me that in details?


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Bug identification: Looks similar to a tiny silverfish

Found in NY outside on mailbox in a group of about 1000, it is about 1/8" long (not counting legs), with dozens of very hair-like legs. The front (?) of the bug appears to have larger leg/antennae, with the longest 2 legs pointed straight backwards.

Having posted an answer, now I'm unsure. The head seems larger on yours, but that may be a function of age and species. perhaps an expert will happen along and clear-up the matter. There are after all, loads and loads of different moth-types around in N America.

@JiminyCricket. I think it's likely to be a larval moth or butterfly, would need better photos. I don't think carpet beetle larvae tend to cluster. House centipede (Scutigera) also sprang to mind, but that definitely isn't right, it's just the lighting making the hairs look like Scutigera legs

@bob1 I agree; I was thinking Scutigera, but those have a "bend" in their legs that this doesn't have

@Xenalin If you've got any pictures from the side it might help. There are quite a few hairy caterpillars out there. Could be something like Painted Apple Moth or one of the "tent" moths. Could also try posting to iNaturalist and see what they say.

@JiminyCricket you are right! Just heard some info from the area that they are spongy moth larvae and are infesting the area. The mailman is delivering the mail to everyone's door because they are on every mailbox!

This is the larvae of the Spongy Moth (Lymantria dispar) of the Family Erebidae, it is fairly distinctive and frequent.
This species is also invasive to your area:

Lymantria dispar has been introduced to several continents and is now additionally found as an invasive species in Africa, North America and South America. The polyphagous larvae live on a variety of deciduous and coniferous trees and can cause severe damage in years of mass reproduction. Due to these features, Lymantria dispar is listed among the world's 100 worst invasive alien species. Source: https://wikipedia.org

Image ref: https://www.inaturalist.org/photos/135361551, Photo 135361551, (c) nikolettaj, some rights reserved (CC BY-NC)

Excellent ID. +1 from me.

@bob1 Haha, thanks Bob, nice to see you on another site. I think biology is the best site for me right now lol. Just found out that it existed. Time to dig through all the old incorrect species-id Q and A's