text:
Can I use dATP instead of ATP (vice versa) for in vitro assay?
For example, polynucleotide synthesis reaction requires dATP which gives H on 3'end and synthesizes polynucleotide. For this reaction can I use ATP because I knew that ddNTPs are used so that ATP cannot be worked but I searched about it and found this,

"The unfavorable thermodynamics of the hypothetical dehydration reaction shown in Figure 4.6 leads us to ask: If polynucleotides cannot be synthesized in vivo by the direct elimination of water, how are they actually made? The answer is that their synthesis involves the energy-rich nucleoside or deoxynucleoside triphosphates. Although the process as it occurs in cells is quite complex, the basic reaction is simple. Instead of the dehydration reaction of Figure 4.6, what happens in living cells is the reaction shown in Figure 4.7. The nucleoside monophosphate being added to the growing chain is presented as a nucleoside triphosphate, like ATP or deoxy ATP (dATP), and pyrophosphate is released in the reaction. We can calculate the free energy change for this reaction by noting that it can be considered the sum of two reactions—hydrolysis of a nucleoside triphosphate and formation of a phosphodiester link by the elimination of water...
The coupled reaction is favorable because the net delta G is negative. The reaction is further favored because the hydrolysis of the pyrophosphate product to orthophosphate, or inorganic phosphate, has a delta G = -19kJ>mol. Thus, the pyrophosphate is readily removed, driving the synthesis reaction even further to the right and yielding an overall Delta G of -25 kJ>mol. Polynucleotide synthesis is an example of a principle we emphasized in Chapter 3—the use of favorable reactions to drive thermodynamically unfavorable ones."[1]

So can nucleotide synthesize can be done with ATP in vitro? If yes, how? Also what kind of ATP required reactions can be replaced with dATP?
REFERENCE:
1)[Christopher K. Mathews, Kensal E. van Holde, Dean R. Appling, Spencer J. Anthony-Cahill - Biochemistry (2012, Pearson)]

It's not clear what you are asking about. ATP is already a nucleotide. I would advise you to read the chapter in your text on enzymes and substrate specificity to discover why what you seem to be suggesting is nonsense.

@user1136 — All very interesting (although I don’t subscribe to the “great men of history” idea, especially in its “great women” revival) but we are dealing here with a chemist, who understands Gibbs Free Energy changes, but apparently has forgotten about activation energy of reactions, and hasn’t yet encountered enzymes.


text:
Do patella bones form in people born with the inability to walk?
The patella is a sesamoid bone that typically doesn't completely from and ossify until ~3-6 years of age (e.g., Source). My long-standing understanding (supported by a claim in Saladin's college A&P textbook1 sitting on my shelf) was that sesamoid bones form "in response to stress."
Well, I had a student in my anatomy class this morning ask me the titular question about people born with leg paralyses or other congenital issues preventing them from walking. To their point, if such congenitally paralyzed people never walk and therefore never place stress on the knee via the quad tendon, would they ever form a sesamoid bone (i.e., the patella) in the knee?
I've done some digging and found evidence of "nail patella syndrome" (e.g., here) which results in people not forming a complete patella. However, I was unable to quickly narrow down any sources discussing lack of patellar growth due to congenital leg paralysis.

1.  Saladin, K. S. 2015. Anatomy & Physiology: The Unity of form and function. 7th edition. McGrawHill, Education, New York, NY

In mice, patella would form, but not separate from femur.
On the development of the patella:

Previous studies have suggested a central role for mechanical load in
the initiation of sesamoid development.
Our finding that the patella initially forms as part of the femur and
is later separated by joint formation led us to revisit the issue of
mechanical contribution to patella development. To achieve this, we
studied patella development in mutant embryos devoid of contracting
muscles, as a result of the naturally occurring autosomal recessive
mutation muscular dysgenesis (mdg; Cacna1s). These mice lack
excitation-contraction coupling and, consequently, their skeletal
muscles lack contractility.
Histological analysis of sagittal sections of hindlimbs identified at
E13.5, in both mutant and control littermates, the existence of
patella progenitors, which were part of the femur. However, at E14.5,
whereas in the control we observed joint formation between the patella
and the femur, in mdg mutants this process was not detected.
Consequently, at E16.5 the mutant patella was still part of the femur.
These results suggest that, although muscle contraction does not
affect patella initiation, it plays a crucial role later during the
separation phase.

I know, you asked for human, but it is the only relevant information I found. However, while sources mention a role of physical stress in the calcification of sesamoid bones, the preceding formation of cartilage seems unaffected. Now, given the information that ossification occurs in mice without physical stress, I personally would conclude that the human patella would also calcify in paralyzed persons. Strictly, the question whether the patella forms, should be answered, if a non-detached patella counts.

Very good find! Thank you for this! +1. I will hold off accepting your answer, though, to see if anyone ever stumbles across any info regarding patella detachment, especially in humans. (I would have never thought such a topic was so difficult to research!)

source: Stack Exchange

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

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What are kinesiological factors?
I am in search of a term that describes movement, or practice of motor skills, as a factor of laterality. Would "kinesiological" be appropriate? I'll leave my two previous questions down below; hopefully it can shed more light. Thank you so much!
What type of factor is practice of motor skills?
What causes motor laterality/ side dominance?

There is no magic dictionary of "factors" that biologists use and that those writing about Biology must draw from. It seems you want to describe "practice", so use that word, "practice".

Hi @BryanKrause! Thanks for the reply; I'm writing a script for a "scicomm" video and wanted to say something to this effect: "Keep in mind, there are genetic, environmental, physical factors, et cetera, but I'll be focusing on the _________."

If you presumably plan to refer to the literature then you can use the language used in the relevant texts.

I understand. Thank you for your time and patience, @BryanKrause .

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Why can human viruses that can't infect chickens be grown in embryonic chicken cells?
Embryonic chicken cells are commonly used in vaccine production.  The viruses are grown in chicken eggs, or in embryonic cells taken from those eggs, and then inactivated or attenuated to produce the vaccine.   But why can human viruses—some of which are not known to infect adult chickens—infect immature embryonic chicken cells?
For instance, according to this WHO fact sheet (https://www.who.int/news-room/fact-sheets/detail/measles), "Measles is a human disease and is not known to occur in animals." Yet the the measles virus prepared for the MMR vaccine is grown in chicken embryonic fibroblast cells.
N.B.:  According to http://www.ogrod.uw.edu.pl/__data/assets/pdf_file/0010/2161/13a.pdf, while measles may have evolved from domestic animals, it is thought to have its origin in cattle rather than chickens: "Measles, for example, is closely related to two other morbilliviruses-canine distemper and rinderpest (a disease of cattle)" [1]
One guess is that, while a virus would normally require interaction with a species-specific surface protein to initiate membrane fusion (see https://www.frontiersin.org/articles/10.3389/fmicb.2011.00247/full [2]), and thus viral (or viral RNA) entry into the cell, the naive nature of undifferentiated chicken egg cells enables such fusion to occur without such species-specific proteins.
Another guess (in the opposite direction) is that the species-specificity of viral infection depends on species-specific cell recognition factors, and because the cells in chicken eggs are undifferentiated, or minimally differentiated, they possess a broad range of recognition factors (where the non-chicken-specific ones are lost as the cells differentiate).
It was surprisingly difficult to find information online about this.  According to the the following (https://www.jstor.org/stable/30105172?seq=1), chicken embryo cells do become more resistant to viruses as the embryo ages; but this doesn't explain the lack of species-specificity:
"Cells dispersed from young embryos were permissive to viral growth, while those from older embryos were restrictive in an age-related pattern similar to that observed in ovo. The mechanism of natural antiviral cellular resistance did not involve viral attachment or release from cells from older embryos, but apparently depended on intracellular events during viral replication. These observations suggest that increasing natural resistance is based partially on intrinsic cellular changes. Sensitivity of a given virus and responsiveness of cells to the action of interferon may be more important to antiviral resistance than the amount of interferon that the virus induces." [3]
[1] Dobson, Andrew P., and E. Robin Carper. "Infectious diseases and human population history." Bioscience 46.2 (1996): 115-126.
[2] Hashiguchi, Takao, Katsumi Maenaka, and Yusuke Yanagi. "Measles virus hemagglutinin: structural insights into cell entry and measles vaccine." Frontiers in microbiology 2 (2011): 247.
[3] Morahan, Page S., and Sidney E. Grossberg. "Age-related cellular resistance of the chicken embryo to viral infections. I. Interferon and natural resistance to myxoviruses and vesicular stomatitis virus." The Journal of Infectious Diseases (1970): 615-623.

Flu viruses are not adapted to only infect humans. In fact a lot of wild species of it show up in birds (ducks and chicken) first, before they jump to humans.

@Chris  Yes, some human viruses grown in eggs are also avian.  That's why I was careful to write, in the first paragraph, "some of which [emphasis added] may not infect adult chickens".   However the point, and the source of my question, is that eggs can be used to grow human viruses regardless of whether they can infect adult chickens or not.  For instance, eggs are used to grow the measles virus for the MMR vaccine, and measles is not known to affect animals (besides us).  [continued next comment]

[continuing....]  Thus the fact that some of the viruses grown in eggs may also happen to infect adult chickens doesn't logically affect my question, which is: What allows the eggs to be infectable, independent of whether the adult chicken is susceptible or not?

I would suggest focusing on a single viral pathogen of humans and providing references showing that that virus doesn't affect adult chickens. Alternatively, can you provide references that support your assertion that human-affecting non-influenza viruses are typically grown in eggs? I did a quick search and found two sources saying that MMR is typically produced using viruses grown in chicken embryonic fibroblast cell cultures (or human cell lines) not eggs.

@tyersome I've made it explict in my title and intro that the essence of my questions is not why viruses that can't infect the adult of the species can be grown in their eggs, but rather why they can be grown from immature, embryonic cells (irrespective of whether this is done in situ within the egg, or in such cells taken from the egg and grown in culture) . I've also given measles as an explicit example, since a WHO fact sheet (who.int/news-room/fact-sheets/detail/measles) says "Measles is a human disease and is not known to occur in animals." If I am able, I will post a primary reference.

The measles vaccine uses an attenuated virus: one that has been  modified to reduce virulence such that it is (hopefully) no longer harmful to the host but still retains the antigenic determinants to induce acquired immunity. Although in modern times rational attenuation by genetic engineering is becoming established [1], the traditional method involves simply growing the virus under conditions abnormal for it such that it must evolve to survive. This often involves culturing the virus in cell types (or possibly organisms) in which it does not typically cause infection. Due to existing variation within the viral population or novel mutations, the virus may, over time, adapt to infect these cells with some degree of efficiency. Importantly in the context of vaccine development, the genetic changes generated during this adaptation may also reduce the pathogens ability to causes disease in the host organism [2].
This effect was originally observed by Louis Pasteur in 19th century who subsequently used it to develop a vaccine against the bacterium Erysipelothrix rhusiopathiae, which infects pigs [3]. Pasteur noticed that propagating this bacterium in rabbits, in which it did not initially cause disease, increased its pathogenicity in rabbits while at the same time reduced its pathogenicity in pigs. The virus had evolved and this attenuated form was used as a vaccine in pigs.
The attenuated virus for measles vaccine was created by the same principle in the 1950s to 1960s. An isolate of the measles virus from an infected patient was successively passaged through human kidney cells, human amnion cells, fertilized hen's eggs [4] and chick embryonic cells [5]. This attenuated virus, which was now replicative in chick embryonic cells, was no longer infective in humans and was used as the basis of the measles vaccine [6].

References
[1] Bull JJ. 2015. Evolutionary reversion of live viral vaccines: Can genetic engineering subdue it? Virus Evol 1(1):vev005
[2] Badget MR, Auer A, Carmichael LE, Parrish CR, Bull JJ. 2002. Evolutionary Dynamics of Viral Attenuation. J Virol 76(20):10524–10529
[3] Bazin H. 2003. A brief history of the prevention of infectious diseases by immunisations. Comp Immunol Microbiol Infect Dis 26(5-6):293-308
[4] Milovanovic MV, Enders JF, Mitus A. 1957. Cultivation of Measles Virus in Human Amnion Cells and in Developing Chick Embryo. Exp Biol Med  95(1):120-127
[5] Katz SL, Milovanovic MV, Enders JF. 1958. Propagation of Measles Virus in Cultures of Chick Embryo Cells. Exp Biol Med 97(1):23-29
[6] Enders JF, Katz SL, Milovanovic MV, Holloway A. 1960. Studies on an Attenuated Measles-Virus Vaccine — Development and Preparation of the Vaccine: Technics for Assay of Effects of Vaccination. N Engl J Med 263:153-159

Thanks for the very informative post. I wasn't aware of the "passaging" technique in vaccine development. I'll need some time to look over the references before I reply in more detail. But my initial read of your post is that viruses grown in immature cells of species the viruses don't "natively" infect had to have been changed to enable them to grow in such cells, and that this change sufficiently attenuates the infectivity of the virus in humans to enable it to be used as a vaccine.

However, the passaging sequence you describe for measles (human kidney cells->human amnion cells->fertilized hen's eggs->chick embryonic cells) suggests that non-native infectivity is easier to achieve when you use immature cells than adult cells. I assume that's why they had to first get the virus to infect highly undifferentiated cells (fertilized egg) before it could infect slightly more mature cells (embryonic). This suggests the attenuated virus wouldn't be able to infect an adult chicken, so my question remains: Why is a virus that can't infect an adult able to infect immature cells?

A capsid is not a membrane. Viruses are acellular. Viruses are not karyotic and do not have membrane bound organelles.
If An envelope forms around the capsid, the virus buds. The envelope comes from the infected cell not the virus.

Welcome to the site. Please take a [tour] and visit the [help] for more information on what we do at this Stack site and what makes a good question and answer. In particular note that we value answers that provide (scientific) references to support the answer. I suspect that your answer should have been a comment rather than an answer as it doesn't actually address the question or any of the content in the question.

Yes it was supposed to be a comment. My apologies.


text:
Are there any real life instances of kidney organoid transplants in human?
Googling the terms "kidney organoid", "artificial kidney" etc. shows quite a huge amount of research papers regarding studies about kidney organoid synthesis from pluripotent stem cells and transplantation attempts.
But what I did not found (& my questions) are:

Are there any instances of successfully development and transplantation of kidney organoids in human beings? (yes/no)

If yes, then is it available as a therapeutic method? (yes/no)


text:
What is the species of this strange insect?
I first saw this photo long time ago, and I still can't identify the species of this insect:

any idea of the geographic region it was taken?

I didn't see the date, time, and location on this photo when I first saw it. I also typed "long-proboscis fly" on Google, but there was no photos that match the species of this insect.

it's a kind of planthopper. I can't figure out which kind. And without geography, might be impossible. See: https://inaturalist.ca/taxa/877149-Thanatodictya-tillyardi/browse_photos

Looks to be in the family Dictyopharidae, a long  nosed planthopper.
This analysis is not absolute as there are exceptions.
There are two features to put it in Dictyopharidae and Fulgoridae. The (tiny) antennae are below the eyes, not between them; and the head has a big protrusion.
The pattern and placement of spines on the legs, and the pattern of veins on the wings would help to identify it to genus level.
A helpful resource is http://hydrodictyon.eeb.uconn.edu/projects/cicada/simon_lab/peet_pages/07_Bartlett.pdf
Picture is of Rhynchomitra spp. from Wikipedia.

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


text:
Does The Sympathetic Nervous System Increase or Decrease Urination?
According to my book:

Sympathetic nervous system stimulation, leads to the release of Norepinephrine(Noradrenaline), priming the body for the "Fight or Flight" response.

It is also stated that:

The effect of sympathetic stimulation is to maintain urinary continence.

But if sympathetic stimulation results in urinary continence, why do we urinate more when afraid or nervous?

I've read this quesion, but the accepted answer states that adernaline(epinephrine) is released (not norepinephrine) and doesn't provide evidence to support why does adernaline result in more urination.

Are you sure that we urinate more when we are nervous?

I think that is what is common, you urinate when you are afraid.. @user438383


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Do all monarch caterpillars have two pairs of needle-shaped protrusions(or they can have three pairs)?
I found this here:

Is this a monarch caterpillar?
Do all monarch caterpillars have two pairs of needle-shaped protrusions?

Just a guess, but it may be species-dependent on whether they have 2 or 3 pairs of protrusions/antennae. Your first image is of Danaus chrysippus, while your lower image is of two other species.

@MattDMo Danaus chrysippus and Danaus gilippus caterpillars are very similar. Quite difficult to distinguish.


text:
How reward / penalty is comprehended?
Technically brain is composed of billions of neurons for abstract computation of the world around us. I am bit confused that how does emotions such as fear/anger gets simulated by amygdala, which is nothing more then bunch of specialized neurons but we feel it as penalty. What part of the brain senses response from amygdala and determines ok, thats fear/penalty? What exactly is penalty?
How does human comprehend reward and penalty (fear/anger/sorrow)?

you might get a better response here https://psychology.stackexchange.com/

@user438383 but I am looking for associative answer, so psychology will only provide higher lever behavioral response instead of lower level response based on synaptic aggregation

The site is Psych & Neuroscience, not just psych, but the question you are asking doesn't have great neuroscientific/biological answers. I'd situate it as part of the "hard problem" of consciousness. There are several relevant Q&As at psych & neuro.

@BryanKrause I see, i thought there might be tangible answer for example, "fear causes incoherent/abnormal synaptic actuation patterns, which is anomaly and we sense anomaly as negative" just a speculation.  Well this also makes me hypothesize that signals firing that are coherent could be sensed as positivity/reward, we associate beauty with say symmetry face so signals are quite coherent when you experience symmetric face and we associate that to positive/reward. Again just a far fetched speculation.

@gfdsal There is no reason that "abnormal" or "coherent" patterns of activity are "good" or "bad" any more than activity in a particular brain area. If your speculations were true you'd still be left with the exact same question.

@BryanKrause allright makes sense, I just made a speculation based on lie detector test, where if one lies the body responses are different from nominal in-other words "abnormal"

@gfdsal Lie detector tests are pretty poor, but they work on the principle that people are more nervous when they lie, which increases their skin conductivity as they produce sweat. Not really an abnormal response, but a completely normal one in response to stress. One of the reasons they are so poor is because indeed, answering questions in a scary environment can also make people nervous.


text:
Is new idea equivalent to forming new synaptic connection?
We get new ideas quite frequently hence I am curious that is getting new idea equvant to formation of new synaptic connections? I am aware of neural plasticity but somehow doubt that it happens quite rapid.
Since that idea was missing before one creates it makes me believe that the structure of synaptic connection was not present earlier and once the new idea was formed then the structure to simulate/produce that idea was created.
If that's the case that that's lots of neurons being connected/disconnected in few seconds which don't seem physically possible.

Not an area I have much familiarity with, but you seem to be making a lot of assumptions rather than doing some research. 1) Why do you assume "neural plasticity" isn't something that happens "rapidly" — also what do you mean by rapid? 2) Why are you assuming that conscious awareness of new idea happens the moment the associated synapses form? 3) Are synapses really binary (present or absent) or are they instead something with a strength and if the latter how would that affect your question?

1) Why do you assume "neural plasticity" isn't something that happens "rapidly" I actually couldn't get a good reference for frequency of synaptic changes (synaptic plasticity) but my assumption is based on general morphology, if new ideas get created in seconds, would it imply morphing happens. 2) Why are you assuming that conscious awareness of new idea happens the moment the associated synapses form? Because to give rise to that awareness, a pathway that leads to thought must be present, if I haven't learned about addition, I would not naturally add two number (something is missing)

3) Are synapses really binary (present or absent) or are they instead something with a strength and if the latter how would that affect your question? With what I have learned so far that they are binary winner-takes-all, All-or-None activations. So either they are active or inactive.

There is a lot of debate over what "thoughts" are in terms of consciousness, and this has been referred to as the "hard problem". However, it seems pretty clear that in some form patterns of brain activity are the "stuff" that underlies a thought/idea: if you change patterns of brain activity, you change the thought.
Therefore, I would describe a "new" idea as a "new pattern of brain activity" rather than connections. While the exact timescale of a "pattern" should be is unclear, perhaps a few hundred milliseconds is a good guess (see for example Luczak et al 2015, and the recent paper by Davis et al 2020). Brain activity is constantly shifting, of course, so really every moment experienced is a new thought of some sort.
There are too many studies to name all of them that show that some consistent pattern of brain activity is associated with some thought. The review by Harris, 2005 is a favorite of mine, but there are many levels of analysis to approach these questions. You might find some more compelling work among the studies of the biological basis of perception.
One particularly elegant paper is Liu et al, 2012. They used some molecular tricks to identify neurons in a rodent brain that are activated during a fearful context, and they cause long-term expression of a protein in those specific cells that they then use to reactivate those same cells at a later time. Reactivating those cells causes the fear behavior to return, effectively triggering the same ideas.
Connections between cells can also change pretty rapidly, but this would be better described as memory rather than an initial thought or idea. This can involve de novo creation of synapses, but more often is studied as a change in synaptic strength. Weak synapses can be strengthened with certain input patterns, and we call this long-term potentiation. The idea of connections between neurons as the stuff of memory goes back some 100 years to Ramón y Cajal.

Davis, Z. W., Muller, L., Martinez-Trujillo, J., Sejnowski, T., & Reynolds, J. H. (2020). Spontaneous travelling cortical waves gate perception in behaving primates. Nature, 1-5.
Harris, K. D. (2005). Neural signatures of cell assembly organization. Nature Reviews Neuroscience, 6(5), 399-407.
Liu, X., Ramirez, S., Pang, P. T., Puryear, C. B., Govindarajan, A., Deisseroth, K., & Tonegawa, S. (2012). Optogenetic stimulation of a hippocampal engram activates fear memory recall. Nature, 484(7394), 381-385.
Luczak, A., McNaughton, B. L., & Harris, K. D. (2015). Packet-based communication in the cortex. Nature Reviews Neuroscience, 16(12), 745-755.

This is exactly the kind of answer I was looking for. It makes so much sense to have thoughts as a pattern of various neurons firing rather then having to change a physical synaptic connection! So once again correct me if I am wrong as I want to reiterate its is highly likely that thoughts are some pattern of neurons firing instead of formation of physical connections or Neural plasticity. Right?

@metron Yes that's correct.


text:
Species that have evolved to be near identical?
Are there any species that are near identical in outward appearance but are separate species?
When I say species I mean can’t interbreed.

I don't know bro. If we cannot identify them so we cannot talk about them, can we? (This definition "Species that have evolved to be near identical" is somehow an identification itself.)

Define your criteria for being identical: outward appearance, similar ecological niches, or what?  My personal favorite are the ichthyosaurs & dolphins, and hummingbirds & hawk moths, but there are many others.

Please [edit] your post to include this information and add enough background information (ideally with references) to demonstrate that you have done the expected prior research. Comments are ephemeral and often overlooked and should not contain information needed to understand the question.  ——— You may also wish to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site since it has different standards than other SE sites (like SO). Thank you!

Differing species of nematodes can be difficult to distinguish.

Simple answer: yes, an uncounted number of them.  You need to read up on two topics: convergent evolution and mimicry.
Convergent evolution is when environmental factors cause different creatures to evolve similar appearance and lifestyle.  Perhaps the classic example of this are the dolphins and ichthyosaurs.  Despite being of different groups - mammals vs reptiles - they both evolved from land-dwelling creatures that adopted a marine lifestyle, and as a consequence a similiar appearance.
Mimicry is when one creature evolves to appear similar to another because that gives them some advantage.  Here the classic example is the viceroy butterfly, which supposedly evolved a similar appearance to the monarch because the latter tastes bad, so that birds avoid eating it.

Can the Monarch & Viceroy interbred?

@William: Not as far as I know, and I would strongly doubt it. (But I'm not an expert lepidopterist.)


text:
Are there any examples of viruses that have jumped from reptile to human?
I know that there are plenty of examples of zoonosis occurring from reptiles to humans that involve bacterial pathogens, (e.g. Salmonella) but are there any instances of viruses being transferred from reptiles to humans?
If applicable, for this question, I am only interested in reptilian viruses "jumping" from reptiles to humans, not the capacity of reptiles to serve as reservoirs for non-reptilian viruses that could potentially infect humans.

By reptiles, do you mean non-avian Reptilia?

Yes, thank you for the clarification.


text:
How to get Bacteria to attach to an Object?
I have cultured Cyanobacteria (in a media) in a beaker. I want that bacteria to attach to a cloth (e.g. Carbon). My current method is using a syringe to slowly push the bacteria to one side of a cylindric tube and exist through the other end. The cloth is placed stationary inside that tube throughout the process.
Is there a way to get more bacteria to attach to the cloth? (e.g.maybe adding something to the cloth)

Why do you want them attached to the cloth?

I am doing a study to see how long can I help the bacteria live in the cloth and I want to store as much bacteria as I can.

I wonder if you could try this membrane filter technique, but replace the membrane with a fabric of your choosing.

You might also be interested in these CDC Biofilm reactors, if your cyanobacteria are biofilm formers.

Thank you, I will read about them and see.

You're thinking in terms of making them attach to your cloth, but they want to be attached - there are more nutrients and it is safer.  Make sure they have enough light, but not too much, and their nutrients.  They may be attaching and growing, but just not as fast as you expect.
It is also possible that your strain of Cyanobacteria has lost the ability to attach.  If it has been maintained in liquid culture for many generations, any bacteria attached to the wall of the container were selected against.


text:
Can a human survive without ACE2?
I guess not, but it was discovered in 2000 so I don't know if we know enough about it. Are there people without ACE2 (angiotensin converting enzyme 2)?
It seems mice can survive, but that's not a proof on humans: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4829150/

No obviously inactivating variants are found in this gene, which provides at least negative data (humans generally seem to have at least somewhat functional ACE2). Exome sequencing across >200K humans has found a series of variants, mostly low-frequency, in the population.
Some of these variants may affect gene function, but it is not clear how, and none of them are obviously complete loss of function variants (e.g. nonsense mutations).
A more complete analysis of the data, including e.g. CNVs, might be necessary to fully address this question.


text:
If due to some reasons a small portion of our neurons die, how does our body remake them?
There are various reasons such as intake of neurotoxins, and possibly traumatic injuries, that can cause neurons to die.
After several hundreds, or thousands of our neurons die, how does our body remakes them?

Evolution set us humans up to not regenerate our neurons on the whole, which is a pity since we can regenerate our liver cells, so it's not an impossible feat. If neurons die because you drank too much, banged your head, or just because they got old, they are gone. If this death is accelerated like in Alzheimer's disease, you can literally see holes in the brain autopsy. That said, we now know that in a few exceptional areas of the brain, neurons do regenerate. It's not many cells but it's something. The two areas known to date are the dentate gyrus of the hippocampus (DG below) and the subventricular zone of the lateral ventricles (LV). See the green zones in the image below.

From Ernst & Frisen PLoS Biology 2015 (CC-by)
In those areas, like elsewhere in the body, new cells are made from stem cells, that is infant-like cells that have the potential to become many cell types. If we could only understand why some cells regenerate and others do not, we might be able to promote this. Alas, our current understanding is woefully incomplete. We'll need more research # # # before we can dream of regenerating our neurons.

It's far from treatment-ready, but successful induction of adult neurogenesis from glial cells via gene delivery or gene silencing has been achieved in rodent models, as have been other promising preliminary results.

Please suggest some ways to accelerate the regenerating process. Like some fruits/veg which can help

Hi Ravi, if there were an easy fix with food, everybody would be doing it. Sadly, there is not.

Likely one of the big reasons that certain neurons don't regenerate is that the signals necessary for them to find their distant targets are only present during a narrow window in development. There are no appropriate guidance cues for, say, a LGN cell in thalamus to find V1 in cortex in an adult brain, and providing those cues would require quite a massive evolutionary change that just doesn't have much selective pressure. Of course there are some cells that make only local connections, but you wouldn't be able to rebuild any full region of brain tissue.

Disclaimer: I'm not an expert, but my recent reading on this topic is fresh in memory, so I'm typing up something of an answer.
The body does not remake any individual cells that die. In case of cells that regenerate, their place is simply occupied by cells which are newly born, or travel from elsewhere. Every individual cell is unique, with its own copy of DNA with its own unique epigenetic information, and unique (but typically similar to other cells) exact biochemical makeup. Once a cell dies, it can not be remade.
Neurons are also pretty special among cells - their function is extremely complex, and in adulthood, new neurons are only born in some specific areas - in the brain, the main exception being the hippocampus.
Majority of learning in the human brain happens as a consequence of what neurons we have being constantly reshaped, both physically - with dendrites, spines, synaptic terminals being constantly created, pruned, their molecular makeup changed, their gene expression regulated up and down.
Unfortunately, if a neuron dies, it is gone for good, and it will not be replaced. Instead, depending on area and degree of damage, other neurons will often pick up the slack, changing function and enabling the brain to re-learn some of the function it lost. In fact, the process of neurons learning to perform different function than they originally did is common in the human brain, e.g. the size of areas processing functions of individual fingers in a musician's brain will vary based on the instrument(s) they play and their experience with it.
That said, the situation is not as grim as it looks. A few thousand neurons, in most areas of the brain... isn't much, and probably won't impair your cognition much, and neurons aren't all that fragile either - it's possible for them to starve and lose function, becoming dysfunctional, instead of outright dying, which they can in many cases recover from. People are often capable of recovering almost completely from lighter brain damage, and cases of impressive recovery from more severe damage are also not unknown.

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@tyersome I see, thank you. I will keep that in mind for the future.

Please try to add supporting references

Neuroregeneration capability is rather limited, and patients that go through the trauma that you speak of usually require life-long assistance[1]. One treatment that has come to light in the past two years uses stem cell delivery to the brain[2]. When a cell dies, if it is replaced, there are stem cells that do it (google mesenchymal or skin stem cells and you will find that system). Damage like drinking doesn't kill cells, it just hinders them (by maybe effecting their protein production), and cells can rejuvenate or heal themselves and replace those dysfunctional proteins with an autophagic process[3, 4].
Overall, I am confused about your question. The body has limited capacity to replace neurons due to the way that this very specialized cell type develops with the body (among other reasons) and it comes down to there not being a stem cell close by, ready to undergo mitosis and differentiate. So your question assumes that the human brain has the great ability to regenerate these cells. Next time there is an assumption in the question you are asking it may be helpful to provide a citation or background information with citations.

Mayo clinic. https://www.mayo.edu/research/centers-programs/center-regenerative-medicine/focus-areas/neuroregeneration
Research sheds new light on how brain stem cells are activated. https://www.sciencedaily.com/releases/2019/06/190606133822.htm
Drinking. https://www.healthline.com/health/does-alcohol-kill-brain-cells
Autophagy. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2990190/

Welcome to Biology.SE! This looks like a good answer, but answers are much more likely to receive a favorable response if you focus on primary literature and include complete references. This is a good example of how to format references. ——— I made some edits for clarity, please check that I've preserved your meaning. (Note also that some organisms do regenerate nerves.) ——— You may also want to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

I would like to add the point that only the neurons in the brain can't be replaced, if they died.
Olfaction and gustation have bipolar neurons which are replaced around 6 months ,over the lifespan of a human. Olfaction
So its not true to say that all neurons can't be replaced, some can be.


text:
Can potassium ions depolarise neuron membranes?
I am reading a journal paper about the cell adhesion molecule NCAM2 and I have come across the following statement:

To confirm the functionality of the reporters, neurons were time-lapse
recorded before and after application of 90mM K+ used to depolarize
membranes and induce Ca2+ influx via VDCCs.

I know that depolarisation is when the membrane potential of a neuron becomes more positive. I have read that the opening of channels that let positive ions flow into the cell causes depolarisation, such as the opening of channels that let Na+ into the cell.
However, the above statement in the paper seems to imply that extracellular K+ ions can also cause membrane depolarisation. I am not sure what the relationship between potassium ions and membrane depolarisation is and I have not found anything about it online. Any insights are appreciated.

Yes, this is a very basic neuroscience question, something that would probably come up in the first week of a neurophysiology class or unit.
The polarization of the membrane at rest is due to cells being primarily permeable to potassium at rest, and due to a concentration difference of potassium inside vs. outside the membrane. Inside, potassium is high, outside potassium is low.
Therefore, there is a concentration gradient such that if a cell were at 0 mV, potassium would be flowing out of the cell. There is a membrane voltage where this net flow would stop. We refer to this as the "reversal potential" or "equilibrium potential" for an ion. For potassium in a typical cell, this tends to be around -90mV. The larger the ratio of concentrations in versus out, the larger the potential. You can calculate this potential with the Nernst equation if you know the concentrations (image from Wikipedia):

From this equation you can see that the reversal potential is negative for a positive ion if [outside] is small compared to [inside]. By applying higher potassium outside than usual, the ratio of [outside]/[inside] gets closer to 1, so the reversal potential for potassium is closer to 0mV, and typical neurons that are mainly permeable to potassium at rest will depolarize.


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Identification - hornet
It has around 3cm. Does it look like a European or Asian Hornet?
The place where I found it is Central Europe/Romania but, after the wikipedia picture for Asian Hornet's head .. it looks exactly the same.
Thank you!

European hornet (Vespa crabro). In the Asian hornet, the black body bands are much wider and more uniform. For the European hornet, as in your specimen, the bands are thinner and appear as thin lines connecting triangular black dots. See this image for comparison:
https://www.sciencephoto.com/media/980933/view/asian-and-european-hornets-illustration


text:
How are cardiac cells connected by intercalated discs?
I understand that intercalated discs run transversely across the longitudinal axis of the muscle. But what I don't understand is how this same disc binds the cardiac cells together.
Are the cells joined end-to-end (in series) or side-to-side (in parallel) by the disc?

Does this answer your question: https://www.britannica.com/science/cardiac-muscle?

This helps a lot.


text:
Can Mung Bean Nuclease only digest a ssDNA 5' overhang?
Can Mung Bean Nuclease only digest a ssDNA 5' overhang, if the double-stranded region of DNA (20bp) is A-T rich at the ends?
Does this enzyme degrade 5' overhang (5bp or 30 bp) with 100% efficiency?


text:
Can we apply NGS (next generation sequencing) on DNA extracted from formalin fixed paraffin embedded tissues (FFPE)?
I'm working on the microbiome and I can only use tissues which are fixed with formalin and embedded in paraffin. Is it possible to apply NGS (next generation sequencing) on FFPE (formalin fixed paraffin embedded) tissues? I'm particularly concerned about contamination that could affect the results.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, the wording of your last sentence was very unclear — I've rewritten it and corrected many errors, but please check carefully to make sure that I have not deviated from your intended meaning. ——— We also encourage you first to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

It's a little hard to tell based on your question, but it seems that you want to do Illumina sequencing of FFPE tissue samples. This is quite routine, Illumina sells kits for it.
I do not know how the FFPE process affects microbial cells, but people have published recently on doing metagenomic analysis of FFPE tissue samples. This suggests to me that it is possible.
If "any contamination" is a problem, then maybe there are additional roadblocks; low-level contamination is a routine problem in metagenomics, which is exacerbated by complicated, old, or low-input sample types. I would suggest treating it the way you would treat any other metagenomic sample, and try to exclude the possibility of contamination through methods and account for it in data analysis.

Thank you very much , yes i have fears about paraffin and its remove could cause any artificial mutations in the DNA , it  can be a real problem for the sequencing process.

People have been doing FFPE sequencing on Illumina instruments for years. Literally a decade, I believe.

@swbarnes2 oh yes, it is quite routine as i said. I think that the only question is how viable/mature it is for metagenomic sequencing.


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What is the function of human Trypsin Inhibitor if trypsin is secreted in the inactive form of Trypsinogen?
I was reading about pancreatic digestive enzymes in a Textbook of Medical Physiology and I came across Trypsin Inhibitor. The text stated that:

It is important that the proteolytic enzymes of the pancreatic juice not become activated until after they have been secreted into the
intestine because the trypsin and the other enzymes would digest the
pancreas itself....  ....substance called trypsin inhibitor. This
substance is formed in the cytoplasm of the glandular cells, and it
prevents activation of trypsin both inside the secretory cells and in
the acini and ducts of the pancreas.

It also states that:

When first synthesized in the pancreatic cells, the proteolytic
digestive enzymes are in the inactive forms trypsinogen,
chymotrypsinogen, and procarboxypolypeptidase, which are all inactive
enzymatically. They become activated only after they are secreted into
the intestinal tract.

My question is, why is Trypsin Inhibitor secreted if trypsin is already secreted as trypsinogen which can only be activated in the intestine?

I think this is a pertinent question, which deserves more attention. My own brief survey suggests that there is no simple answer. If nobody else answers I'll summarize what I can find when I have a moment.

@David As you say, it is not an easy answer. It's a matter of time.

@Chris I’m not blaming anyone. Just trying to draw attention and let the poster know that he might have to wait for a proper answer.

I’m voting to close this question because it is cross-posted with an answer at: https://medicalsciences.stackexchange.com/questions/24834/why-is-trypsin-inhibitor-present-if-trypsin-is-already-secreted-in-form-of-tryps Please see https://meta.stackexchange.com/questions/64068/is-cross-posting-a-question-on-multiple-stack-exchange-sites-permitted-if-the-qu

@BryanKrause — Thanks for noticing that, and saving me spending my time duplicating someone else’s work. Which is one good reason why cross-posting is anti-social.


text:
DNA extraction kit for microbial mats, rocks, and soil in a remote area
I am hoping to perform a metagenomics study of samples from a lava tube. It will be in a remote area (with no large scientific equipment) and I would need to bring all scientific equipment myself. For the sequencing, I plan to use either the Field Sequencing Kit or the Rapid PCR Barcoding Kit from Oxford MinION. However, I am unsure how to extract DNA before using the Oxford Minion kits (and in a manner, of course, that complements it).
Are there DNA extraction kits that can followed up Oxford MinION kits and can be performed without heavy equipment for the following sample types?
a) microbial mat
b) soil
c) lava rock
Thank you for sharing your advice!

Those are some pretty tough samples to get high-quality DNA from, even in a lab. Your best option is probably to place samples in a nucleic acid preservation buffer and carry them out for extraction later.
That said, there are some potential solutions. Akonni has some kits that don't use any centrifugation and they claim they'll work on soil and stool, so they might be good enough for your applications. They kind of seem like they're based on the same principle as this kit-free protocol (this protocol is for Plasmid DNA, but I'm sure it could be adapted for Genomic DNA with a little R&D on your part). In either case you'd probably want to look into a portable bead-beater to disrupt/lyse your samples. This will shorten your DNA fragments through shearing, but it's probably necessary to get good extractions from any of these materials.
A few companies also make portable centrifuges that run on 12V car plug adapters, assuming you'll have a vehicle somewhere within walking distance. That could open your options up to using a Powersoil kit or even something like a phenol-chloroform extraction, which you might not need a bead-beater for. (Note: you absolutely would need a properly fit-tested, full-face respirator with the appropriate chemical filters to do phenol-chloroform work without a proper fume hood, plus a way to haul out your waste).
If it were me, I'd still probably use a preservation buffer and do the extractions and analysis back at the lab.


text:
How to identify an unknown species from its genome sequence
I am currently using ILLUMINA PE DNA sequence data, which I trimmed (Trimmomatic), corrected (Rcorrector) and assembled (SPAdes). I am now interested in using the genetic sequences from my contigs to identify the original organism (I know it is a bacterium).
I have tried using ncbi's BLASTn on one of my contigs with default parameters, on nucleotide collection database. The contig length is about 360 000 bases long. I let the query run for 30 minutes before stopping, nothing came of it. I am assuming 360 kbp is too long.
I was thinking of maybe using a ribosomal subunit sequence (which are used in phylogenetics) to identify the species, or at the very least find the taxonomic family. Is this approach feasible? How can I identify ribosonal subunit sequence from my total sequence?
If not, what would be the best way to approach this question?

Did you use web interface BLASTn or local instalation? What was the library against which you run your query? How long was the contig? 30 minutes seems long.

Crossposted here https://bioinformatics.stackexchange.com/questions/14487/how-to-identify-an-unknow-species-from-a-fasta-containing-genetic-sequences

I’m voting to close this question because it has been crossposted to another (more appropriate) SE site. It also seems to fit this sites criteria for "homework".

@tyersome Definitely Not homework. This is my first time using a StackExchange platform (other than StackOverflow), did not know of the "no cross-posting" rule. Thank you for letting me know.

One of the reasons for the "no-cross posting" rule is that members of one list may spend time and effort answering a question unaware that the question has already been answered on another list.

So how did you solve it? Blasting pieces of your contigs should give good guesses and https://blast.ncbi.nlm.nih.gov/Blast.cgi should work fine with a 360kb contig (restrict to bacteria).

I would suggest using a tool designed for this purpose such as GTDB-tk (slow but informative), mash (very fast but very reference-dependent), or something similar.


text:
Relation/difference between metabolism and cellular organisation

In the highlighted paragraph from NCERT textbook, they mention that cellular organisation is the defining property of life forms while metabolism without exception is also the defining property of life forms. My doubt is whether the term 'metabolism' also includes the metabolism reaction in vitro condition too or metabolism only means all the chemical reactions occuring in the cell excluding in vitro condition. If what I mean is true, does cellular organisation and metabolism both mean the same thing? But then again if both are the same thing, metabolism also should be the defining property of life forms, but it is not the case as mentioned by my textbook. So that means both metabolism and cellular organisation are different things. Is this right?

This paragraph appears to draw a distinction between "the sum total of all reactions in cells" and "some isolated reactions that occur in cells". The former is "metabolism" and one defining trait of life; the latter are "metabolic reactions" and can occur in a test tube, and if so they do not fit tidily in a living/nonliving distinction (the paragraph talks about "not living things" but "surely living reactions", which is one way of illustrating the confusion I guess).
As to whether "metabolism" and "cellular structure" are the same thing, I think it's not so much that they're literally the same thing but they're not really separable, are they. The cellular structure is made by "all the chemical reactions in the cell", and "all the chemical reactions in the cell" are mediated by the cellular structure. It's a bit like trying to separate out "a race" from "the people running in the race". You can have one or two metabolic reactions happening in vitro, but if you had all of them in your test tube, happening the same way they do in the cell, you'd have a cell.
The reality of course is that there isn't a single all-encompassing definition of "life", so don't try and nitpick things too much. Metabolism is important because it's what allows living things to do what living things do, thermodynamically speaking. Cellular structure is important because it happens to be the way all living things implement their metabolism, and arguably it is a necessary requirement for metabolism to occur (there are arguments for why you need a small space enclosed by a membrane for example). Other things are also important like reproduction (and other near-universal feature of life that is a basic thing living things do, and allows Darwinian evolution), being subject to Darwinian evolution (because that is the process that leads life to being optimized in the way it is, and able to do the things it does to begin with), sensing and reacting to its environment (all this stuff about "what life does", well, those are universal things life does)... That means you can have arguable examples like viruses, which I would expect your textbook to call "nonliving" because they do not have metabolism or a cellular structure, but some others might call "living" because they have genetic information, replicate, are subject to Darwinian evolution and share a common ancestor with all other known life. The labels are less important than the features one is discussing at any one time. I expect your textbook probably says something like this at some point.

thank you so much!


text:
Turning off the IP3 cascade
After PIP2 has been converted into IP3 and DAG by phospholipase C (PLC), some of the IP3 opens calcium channels in the endoplasmic reticulum and calcium ions can enter the cytoplasm. However, it is unclear to me how this IP3 cascade is terminated. Is IP3 somehow degraded, do high calium concentrations result in closure of the calcium channels or is there some other mechanism?

IP3 is indeed degraded, this is done by a specific phosphatase which is called "Phosphoinositide 5-phosphatase (INPP5A)". It catalyzes the reaction in the following way:
1-phosphatidyl-1D-myo-inositol 4,5-bisphosphate + H2O $⇌$ 1-phosphatidyl-1D-myo-inositol 4-phosphate + phosphate
The enzyme cuts of the 5'-Phosphate group and leaves 1,4-Inositolphosphate, which is subsequently recycled. The schematics looks like this in the left side (figure 1 from the reference):

Reference:
Inositol trisphosphate 3-kinases: focus on immune and neuronal signaling

The IP3-DAG Pathway is triggered by an external stimulus that causes the conversion of PIP2 to IP3. When the stimulus is absent, the pathway does not function.
For example, TRH (Thyroptin Releasing Hormone) causes the IP3-DAG Pathway to occur in the cells in the Anterior Pituitary causing them to secrete TSH (Thyroid Stimulating Hormone) to the Thyroid Gland. When the Hypothalamus stops sending TRH, then the IP3-DAG Pathway in the TSH-secreting cells stops so TSH is not secreted.
Note: I am in high school right now so I may not have adequate experience in Cytology to answer this question. However, I tried my best!
Hope this helps :))

This does not answer the question asked. The question is wondering what happens to the IP3 after is is free to bind it's receptors.

Good  try and stay inquisitive.


text:
Harbor Seal behavior and personality
I'm doing some research on Harbor seal behavior, but I haven't been able to find much on general behavior such as personality,  quirks, ect. Does anyone have anyone have any firsthand experience with harbor seals that could tell me what their general demeanor is? Are they playful? Curious? Shy? What are some behavioral actions that you see them do often? How do they react with their social groups? Do they have obvious hierarchies or do they mostly ignore each other? Any information is helpful, thanks!

Was this that question on Worldbuilding where they said people in the Biology SE could help?

Welcome to SE.biology! This paper looks like it might be useful

@DanPar yes it is

@user438383 Thank you this is perfect!

I think that the first to do is an ethogram about the behaviors of the Harbor seal...
Do you search for previous publications about Harbor seal behavior? See:
de Vere, Amber J., "Do Pinnipeds Have Personality? Coding Harbor Seal (Phoca vitulina) and California Sea Lion (Zalophus californianus) Behavior Across Contexts" (2017). Master's Theses. 273.
https://aquila.usm.edu/masters_theses/273


text:
Extracting DNA from a kiwi
I have two questions regarding this experiment.

Online instructions say to use 5g washing up liquid, 2g salt and 100ml tap water mixed together with a mashed up kiwi. Do I use a full kiwi ?

Instructions say to use coffee filter paper or a fine sieve. Would laboratory filter paper work or would it be too fine ?

Also, how can I improve on this method to get maximum yield etc ? All advice and suggestions welcome.

Yes, a full kiwi. The method is rather crude and the yield you get is not so high, because you will not break up all cells and also loose some of the DNA which is bound to the cell debris.

Lab filter paper of course works as well, as would a fine cloth (cheese cloth for example). The receipe is designed to work with stuff that people have usually in their kitchen, which is true for coffee filters, but usually not for laboratory filter paper ;-)

Great , and how would I increase the yield ?

With household chemicals? I don't think this will bring much. This is a demonstration and for this purpose it works pretty well. We have done this with bananas.

While it wouldn't increase the yield, I used isopropyl alcohol to precipitate (and thereby increase visibility) of extracted strawberry DNA.  Admittedly this was in a group setting (~10) so the total yield was higher, but I was could still scoop up small globs of visibly white DNA clumps in pill bottles without magnification or undue effort


text:
Which is the best model organism to implement an evolutionary study for P.falciparum?
I have to study and implement some evolutionary statistics for P.falciparum. In your opinion and by your experience, which organism should I consider in order to take the orthologs to implement this study?In general, If I wanted to extend this study to P.knowlesi, P.vivax and in general to all the parasites evolutionary related to the asian monkey plasmodia, which organism you suggest me to consider as a template? I thought about P.berghei but, since I have to consider also the Vinckeia parasites (mouse plasmodia) is there a good organism, out of the plasmodium genus, that could come in handy serving as a reference point for all these species?
Obliged

Is there a reason to not do all of them, if you are only doing computational analysis ("evolutionary statistics")? The meaningfulness of the work will increase significantly with each additional organism included.

Yes the analysis is set to take in consideration the whole set of the organisms. I have only to find a good protozoan to take the orthologs. In human M. musculus is good enough, but for plasmodia?I though about some haemosporidia. What can you suggest  me?

i would suggest taking orthologs from as many species as possible (ideally 10+ minimum) and using their phylogeny to combine information. estimates will only get better with more information.

Thank you for your precious suggestion


text:
Identify this extremely tiny white bug please!
I have noticed these extremely small, hard to notice with naked eye bug for about 3 nights now. Twice on my body in the kitchen and once on my thumb in my living room. I managed to catch one last night from my living room which has an area rug near a mattress, coffee table and couch. I managed to put it in a small 2 inch box with white lid. Today it seems little brownish and inspected it under a microscope.
First  picture is of the box size to put some real world perspective on the actual size.

Second pic is of the bug lying on the white lid, doesn't seem to be even 1.5 mm.

Third and fourth pic is from the microscope(150x), I had to move the bug so I might have squished it a bit.

We are getting bite marks and are almost convinced that this bug is the reason as we never had a bug problem ever. The only other thing we noticed is a silverfish in our living room but not sure if that can cause these bite marks.

Do you have birds or rodents in the home? Do you have birds nesting or spending a lot of time on any structure on the outside of your house?

Yes, we did have 2 bird nests in front of the main door on the roof, which we let since we didn't want to hurt the birds. But the birds left last week and we washed the nest afterwards on Monday10/5.

It appears to be a seed tick (tick larva). Have you visited a natural area or grassy area recently? As @theforestecologist seems to suggest, they could be from the birds that nested by your door.

Thanks @perfectionist. We have not been to any grassy area recently. We did however have 2 bird nest on the adjoining wall (with a window) under the roof which we let it be as we were not aware of consequences :)

@theforestecologist - I know you linked the thread which talks about Ornithonyssus. Just wanted to check if you think this is the same specie I am dealing with. This is to see if we can eliminate Red Mite /Dermanyssus Gallinae from the equation) and considering we are in USA, its highly likely we don't have Ornithonyssus Bursa (tropical fowl mite) so we might be able to zero in on Ornithonyssus sylviarum(northern fowl mite). We are infested for for about 4 months now and I am not sure how to devise an eradication plan since each type requires some specialized steps as I found in my research.

@Anx sorry to hear :/. You'll need to include better pictures if you want anyone online to help determine your species. If you've narrowed down to a few species as possibilities, see if you can find a resource or 2 that tell you what to pay attention to in order to differentiate them -- Using that info, take really clear zoomed-in pictures of body regions that are important for telling species apart. If you update your post asking to differentiate these species specifically, include a few more detailed photos and link to some useful info you found already, I'll reopen your post as unique.

Also, you might also consider contacting a local exterminator for help. If you're concerned about price, some will help ID a species before providing a quote... ...

@theforestecologist Appreciate you responding so quickly on this. We did reach out to a number of pest control operators (total 62 so far), but Orkin was the only one who came back with Bird Mite identification however they were not aware of specie level information. Also, we no longer have any visible mites in our environment, we were lucky to catch that first one. We have already gotten the pest control spray done 11 times by now, but these mites are so hard to beat :(  My last resort is to try fumigation but I am worried about the unhatched eggs..(as people reported) resulting it useless.


text:
Is water movement across cell membrane purely diffusive or it always requires channels?
If we see nephrons, in the descending part of Loop of Henle (LoH), water movement is allowed but solute movement is not. On the contrary, in ascending LoH, solute movement is allowed but not water. What exactly restricts this movement?
I am particularly interested in understanding the movement of water across cell membranes and then answering the above query.

Water across cell membranes occurs due to osmosis( which is based on a concentration gradient). so water diffuses through the cell membrane. sometimes water channels called aquaporins can be found.
https://www.anaesthesiamcq.com/FluidBook/fl1_2.php
https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/aquaporin
In the loop of Henle, the water, and Na+ & Cl- exchange occurs due to the counter-current principle takes place. the interstitial fluid has a certain sodium chloride concentration. the filtrate that is entering the descending limb of the loop of Henle, has a particularly low NaCl concentration.so because of that water moves from the loop of Henle to the interstitial fluid.simultaneously, at the ascending limb of the loop of Henle just adjacent to that particular point, water concentration is high in the interstitial fluid. so because of that NaCl moves to the interstitial fluid (Na+ actively, and for ion balance, Cl- passively.) this happens along the length of the loop of Henle. what restricts water movement from the ascending limb of the loop of Henle is that that limb has no aquaporins and the descending limb has numerous (with relative to other places in the nephron). anyway, here's a link for you.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3468499/

Actually osmosis is based on a chemical potential difference, which is not quite the same as a concentration gradient.

So it means water movement is very minimal through physical diffusion. It requires an Aquaporin for transport across cell membrane. (Inspite of the fact that water is a tiny molecule)

yes. "The cell membranes of a variety of different bacteria, fungi, animal and plant cells contain aquaporins through which water can flow more rapidly into and out of the cell than by diffusing through the phospholipid bilayer". I got this from Wikipedia https://en.wikipedia.org/wiki/Aquaporin

As @Roshelle Perera points out, the textbook reason for differential solute and water movement in different parts of the LoH is osmolarity, which is nicely explained in this wikipedia article.

Coming to an interesting point, about the movement of water across cell membranes through aquaporins, this is helpful:{1}

The discovery of aquaporin membrane water channels by Agre and co-workers (6, 7, 191, 192) answered a long-standing biophysical question of how water crosses biological membranes specifically, and provided insight, at the molecular level, into the fundamental physiology of water balance and the pathophysiology of water balance disorders. Out of at least 10 aquaporin isoforms, at least 7 are known to be present in the kidney at distinct sites along the nephron and collecting duct.
Aquaporin-1 (AQP1) is extremely abundant in the proximal tubule and descending thin limb where it appears to be the main site for proximal nephron water reabsorption. It is also present in the descending vasa recta. AQP2 is abundant in the collecting duct principal cells and is the chief target for the regulation of collecting duct water reabsorption by vasopressin.

The journal further elaborates on these APQ's and their function in detail, do read it if you are interested, but the following diagram sums it up pretty well, so I am just going to expand on this:

A: schematic representation of the structural organization of aquaporin-1 (AQP1) monomers in the membrane (top and bottom).

Aquaporins have six membrane-spanning regions, both intracellular NH2 and COOH termini, and internal tandem repeats that, presumably, are due to an ancient gene duplication (top). The topology is consistent with an obverse symmetry for the two similar NH2- and COOH-terminal halves (bottom).

The tandem repeat structure with two asparagine-proline-alanine (NPA) sequences has been proposed to form tight turn structures that interact in the membrane to form the pathway for translocation of water across the plasma membrane.

Of the five loops in AQP1, the B and E loops dip into the lipid bilayer, and it has been proposed that they form “hemichannels” that connect between the leaflets to form a single aqueous pathway within a symmetric structure that resembles an “hourglass.”

B: AQP1 is a multisubunit oligomer that is organized as a tetrameric assembly of four identical polypeptide subunits with a large glycan attached to only one.

The direcrion of flow of water, again, depends on osmolarity.

...Only inward water flow (swelling) was examined, but it was predicted that the direction of water flow through AQP1 is determined by the orientation of the osmotic gradient. Consistent with this, it was later demonstrated that AQP1-expressing oocytes swell in hyposmolar buffers but shrink in hyperosmolar buffers.

Please note that the linked journal is brilliantly detailed, so there are several points that I have skimmed over. I recommend reading it if you have time.
{1}-https://journals.physiology.org/doi/full/10.1152/physrev.00024.2001#:~:text=Aquaporin%2D1%20(AQP1)%20is,for%20proximal%20nephron%20water%20reabsorption.&text=AQP2%20is%20abundant%20in%20the,duct%20water%20reabsorption%20by%20vasopressin.


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Are there ontologies for the description of the look of plants?
Are there existing ontologies for the description of the look of plants?
I am looking for something formally defined giving me at least or better more information like in descriptions:

They are mainly deciduous shrubs and trees, often with brush-like foliage, often spiny to deter grazing, and masses of small, pea-like yellow blooms which are sometimes fragrant.

which I took from https://en.wikipedia.org/wiki/Genista .
The use case is to be able to procedurally generate 3D models of them, which are not too far away from the reality as far as an ordinary person would notice.

To transform an object in an ontology to an image of that object?  Sounds unlikely, I doubt that any botanical ontology is that developed and detailed.  It would be great if it worked.  Could be used to check the ontology.  The website https://www.ebi.ac.uk/ols/ontologies lists 251 biological ontologies.  There are several on specific plants or groups of plants (brassica, beet, oats) and several that might be more relevant to you: Plant Ontology, Plant Phenology Ontology, and Plant Trait Ontology,

Not a complete solution, but a lot of what I think you want can be done with L-systems.  See for instance "The Algorithmic Beauty of Plants" (Downloadable here: http://algorithmicbotany.org/papers/#abop ) See also various things to be found under the heading of Algorithmic Botany.


text:
Could be misleading using some terms to describe certain phenomena?
I am implementing a series of comparative analyses related to Low Complexity Regions in some organisms. Given that these regions show a wide range of length (measured in amino acids) and different characteristics, writing my report I would like to use "mosaicism" to describe this interspersion. Given that the term mosaicism is used to describe when someone have two or more genetically different cells inside his or her organism, I am in doubt if using this word could be misleading or, given that the term per-se indicates a set of gussets that compose a picture, to consider it somewhat elegant given that is clear enough what I am talking about.
Obliged

Please [edit] your question and give some more background (or provide helpful links) regarding what "Low Complexity Regions" are and explain their characteristics. Based on what you did say, I'm not sure "mosaic" is the best way of describing the phenomenon.

Regardless of what term you choose, define at the beginning how you'll be using it for the purposes of your analyses.  Clarity is probably more important the precise word you settle on

Do you know what a mosaic is? Do you really understand why the term mosaicism is employed. I am not clear what the phenomenon is you are describing. You use the word interspersion. What is wrong with that? Can you draw a diagram in which this phenomenon is compared to a non-interspersed reference so we can see whether the word fits or another may be better, or indeed whether an additional adjective will remove any ambiguity.


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Can anyone identify this chrysalis?
What kind of chrysalis or pupa is this? It’s about an inch and 3/4 long and is hanging off the brick siding of a house in Piedmont North Carolina. It wiggles when it is touched. It has been hanging there for at least two or three weeks.


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Why is the food we consume right from birth not immunogenic to elicit an immune response?
Excluding the hypersensitive reactions which are individual specific, how is  food we consume considered safe by the immune system?

Actually for few food items we do develop some sort of immunity. Let me give an example—
Suppose in an individual's RBC membrane, there's a specific ABO antigen (let's say the subject has "A" blood group).
Now in that individual, how do you think anti B antibodies will be formed?
It will essentially be due to some food intake and subsequent exposure to 'B Antigen'. Hence we usually tend to say that 'blood group—A' has anti-B antibody.
This article might be helpful (See the section: Basic Biochemistry$>$ABO Phenotype--4th paragraph)

https://www.ncbi.nlm.nih.gov/books/NBK2267/

Can you link to some literature that shows we are exposed to ABO antigens through food?

Yes, sure. I have added  an article.

That's interesting, I never knew that before. Or, if I was taught it once I forgot :)


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

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

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

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


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Determine similarity in percentages between species A and B, A and C, and B and C

The chart above is a graphic that shows the amino acid sequence differences between different organisms for a protein keratin.
The question I am required to answer begins as, "Keratin is made up of about 450 amino acids. Determine the similarity in percentages between species A and B, A and C, and B and C. Explain how amino acid sequences can be used in determining how closely related two species are."
My initial solution to finding the percentages is dividing the respective differences in the chart above by 450. Then, subtract that number by 100, and hence, find the similarity percentage. For example, for species A and B, I would divide 4 by 450, resulting in 0.89%. I would next subtract this percentage from 100%, resulting in 99.11% similarity. Is this the correct procedure?
My initial solution to explaining how amino acid sequences can be used to determine how closely related two species are is as follows: The larger the difference in amino acid sequences between two species, the less closely related two species are. Is this explanation correct as well?

Step number one is correct, but note that there are several similarity (or alternatively distance) measures. What you choose is the simplest and most intuitive one and it a good one without any other assumption or explanation given.
Step number two is also correct, if the similarity is a good proxy for when the last common ancestor between two species is in time, which in this case should be.


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What is more dangerous, exotoxins or endotoxins?
Since gram- negative bacteria tends to cause disease to human and they mostly produce endotoxins. Does this mean that endotoxin is more dangerous than exotoxin? and if that so why?

No. Exotoxins are more dangerous than endotoxins. endotoxins are made up of lipopolysaccharides, but exotoxins are made up of proteins, of which most are enzymes. due to the catalytic nature of enzymes, even a small amount of exotoxins can be dangerous (even micrograms of exotoxins can be dangerous).
[differences between exotoxins and endotoxins]1


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Shannon diversity index: Pi relates to all found species, or number of species by site?
I am trying to dig into Shannon's species diversity index to compare the species diversity between different sites. For this, I need to calculate the 'relative abundance of species within the community'[details here][1]. What I do not understand is if this relative abundance relates to all species in a sample, or all found species?
In my example, I have in site1 6 species: a, b, c, d, e, f and in site2 two species: g, h. Should I calculate the proportion by species by site relative to 6 and 2, or to 8 (6+2, as species do not overlap between the sites? This is dummy example, likely species will reoccur).

If calculated by total number of species (8): Shannon H = 1.11 and 0.820,
if calculated by total number of species by site (6 & 2): Shannon H = 1.29 and 1.26.

I wonder which one is correct? The general trend is the same (site1 is more diverse then site2) but differences between indices seems quite large.
Dummy example to calculate Shannon's H step by step with dplyr. The commented out mutate allows to change if distinct number of species and their sum will by calculated by site or by total.
# Create dataframe with two sites and 6 and 2 different species. Area indicate abundance of species.
d<- data.frame(site = c(rep("s1",6),  rep("s2", 4)),
               species = c(letters[1:6], letters[5:8]),
               area = c(59,12,11,10,5,3,
                        10,5,21,20))

# Calculate sum of the area
# calculate distinct number of species, vary if the distinct area calculates by sum or by total??
d %>%
  mutate(species_n   = n_distinct(species)) %>%   # !! should 'mutate' by placed before the grouping variable or after?
  mutate(species_sum = sum(area)) %>%
  group_by(site) %>%
 #mutate(species_n   = n_distinct(species)) %>%
 #mutate(species_sum = sum(area)) %>%
  mutate(spec_pi     = area/species_sum) %>%
  mutate(pi_ln       = abs(log(spec_pi))) %>%
  mutate(sp_shannon  = spec_pi*pi_ln ) %>%
  mutate(shannon_comun = sum(sp_shannon))

I am trying to dig into Shannon's species diversity index to compare the species diversity between different sites

Shannon's diversity index is a measure of alpha diversity, or diversity within a community. If you are considering each site a different community (which is sounds like you are), then you would calculate Shannon diversity for each site separately, without consideration of the other sites.

What I do not understand is if this relative abundance relates to all species in a sample, or all found species?

Relative abundance is not a function of the number of species found, but the total number of observations collected (similar to sampling effort) at a given site. So, if you made 100 total observations at a site and 10 of those belonged to Species X, the relative (proportional) abundance of Species X is (10 / 100) or 0.1, regardless of the total number of different species present, and regardless of any observations from other sites.
I can't comment on your code, because I don't do tidy-verse. I guess I'm (apparently) old school and still use Vegan and LabDSV for community analysis (I may be biased since I learned community ecology from the author of the LabDSV package). But in general, for any measure of alpha-diversity, each community gets it's own value, and you would not consider any observations from other sites in that calculation, regardless of whether there is species overlap between communities.
For a more direct comparison of diversity between sites, you would use a beta-diversity index like Bray-Curtis dissimilarity, which compares each community to every other community in your analysis.


text:
What is the mechanism of aspirin as an anticoagulant?
I understand that aspirin prevents blood clots from forming by interfering with the clotting action. I want to know at which stage aspirin interferes with clot forming and what really happens in the process. I've used google to understand this but did not find a satisfactory answer.
For example, here I found:

How can aspirin prevent a heart attack?
Aspirin interferes with your blood's clotting action. When you bleed, your blood's clotting cells, called platelets, build up at the site of your wound. The platelets help form a plug that seals the opening in your blood vessel to stop bleeding.

But this clotting can also happen within the vessels that supply your heart with blood. If your blood vessels are already narrowed from atherosclerosis — the buildup of fatty deposits in your arteries — a fatty deposit in your vessel lining can burst.

Then, a blood clot can quickly form and block the artery. This prevents blood flow to the heart and causes a heart attack. Aspirin therapy reduces the clumping action of platelets — possibly preventing a heart attack.

Every site I visited had descriptions like this (mostly concentrated on the medicinal side). I want to know what aspirin does that prevents blood clotting at the chemical level, which I haven't been able to find.

I found another question and answer here that already seems to answer your question, so I've marked it as a duplicate. There's no penalty for a duplicate question, it will help people who see your question first in search find the answer they want and helps us keep things orderly.

thank you very much. stay safe


text:
Unknown plant, please help me identify it
Years ago I was into keeping tropical fruit trees/bushes indoors. One of them didn't do well under my care so I planted it outside to enjoy the final year before European winter gets it. It somehow survived, barely. Each year it did better though so 5-6 years later it's full of edible fruit. I don't know what it is. Can somebody identify it?

is it this: https://www.youtube.com/watch?v=KTYMG7mziRw ?

The fruit looks a lot like something from the Syzygium genus. Can you show us a cross section (lengthwise) of the fruit?

@JimN I think you may be correct.

crush one fruit, see if it has flesh crunchy like apple - if so probably Syzygium

It worries me a bit that you don’t know the species, yet you know the fruits are edible. I hope you simply remember it’s supposed to be edible when you first got the plant?

JimN, yes that was it. Jujube (Chinese Date). Some variant of it

It appears to be a cultivar of Jujube (Ziziphus zizyphus) also known as Chinese date - https://en.wikipedia.org/wiki/Jujube
This is based on JimN's correct observation. I looked at a few dozen images of Ziziphus Zizyphus - both fruit and leaves. They appear to be identical. The fruit tastes as described. The fruiting progression matches the description in Wikipedia.

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

I understand where you are coming from but what you are suggesting is an online form of politics and bureaucracy (time-wasting). I will edit my answer to oblige


text:
Need help identifying what looks to be a skull
  ( BOTTOM VIEW )I was given this skull(?) by someone a few years ago, it was found washed up on a beach in Panama. I collect bones so usually I’m really good at IDing skulls and I’ve spent some time trying to just generally research skulls that look the same. I’ve looked at snake, fish, mammal, and bird skulls but none of them seem to match, it’s just a very odd shape. I researched on animals that live in the water in Panama but none of them matched up. I could just not be looking hard enough or looking at the wrong things. It doesn’t have a lower jaw and the eye sockets or at least I think they are, are very deep inside the skull. It does seem to have a base for vertebrae. Which is why I assume it’s a skull along with the general structure. The top part of the piece is completely flat with a small incline.
This is my first question so please tell me if I’m missing anything.

I don’t know if it’s just my view of the app, but I don’t see a photo of the specimen, which would be helpful. Could you upload one? Thanks!

I apologize I forgot to add the images I’m so sorry

Im having a problem with my post, It won’t let me paste the pictures I wanted to add. I’m sorry for any inconvenience I thought they were part of the post.

@Jacob You might try from desktop if you are using a phone. Or if a phone is the only option, at least use the browser version and not an app.

thank you! using the desktop version worked.

Welcome to Biology.SE! Please [edit] your post to include the size and if possible pictures from other angles. Thanks!

Probably not a skull. It's probably part of a bird's synsacrum


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Reason for partially double-stranded DNA of Hepatitis B virus
According to my school biology textbook and also Wikipedia, hepatitis B is the only Hepatitis virus to possess partially double-stranded DNA.
I found an image from here
What is the reason for the partially double-stranded DNA?
(It seems that it can be triple-stranded as well.)
I found this information in this research about duck hepatitis B virus

Similar to classical retroviruses, viral assembly begins with the formation of intracellular nucleocapsid particles that specifically package the pgRNA. However, all hepadnaviruses undergo a maturation phase during their morphogenesis that is characterized by the reverse transcription of the pgRNA prior to membrane envelopment and secretion as extracellular virions, rather than subsequent to entry into new target cells, as is the case for classical retroviruses (for a review, see reference 20). Thus, secreted hepadnaviral virions contain only the “mature” ds DNA, whereas intracellular pools of nucleocapsids contain nucleic acid species from all the intermediate stages of reverse transcription ranging from only pgRNA to single (minus)-stranded (ss) DNA as well as ds DNA, a fundamental observation made by Summers and Mason 2 decades ago (22)

What is the special advantage of having such a genome?

are there any other organisms with partially double stranded DNA or partially double stranded RNA as well?

I've edited your question slightly. "Reason for" is the way to express your question. ("What's the use of" is a vernacular expression implying that something has no function.)

I would recommend removing the second question. Hepatitis viruses with different genome structures are not closely related so there is no reason to expect that they would have similar structures.


text:
What is "KK1 enzyme"?
In the book "The Kaizen Way" by Robert Maurer, I've read the following:

When we’re sitting, our muscles go into a form of hibernation, causing
our bodies to shut down the enzyme (called KK1) that breaks down some
of the fat in the blood.

However, when I tried to google "KK1 enzyme", I got nothing about any enzyme. I mean, I got this website and this article, but they don't contain the name "KK1" at all.
What was meant by that? Is it scientifically accurate?

KK1 is a putative potassium channel blocker in the venom of the Manchurian scorpion, but I couldn't find any evidence for a mammalian KK1 protein of any function, let alone fat metabolism.

Sounds as if he has no idea what he is talking about. I'd trash the book immediately.


text:
What is this insect? Possible assassin bug? or kissing bug?
I saw this bug (around 2 cm) in the front of the balcony door inside the room.

I googled and found two same insects- Assassin bug and Kissing bug. Could they hide their eggs inside the room? Should I be worried?
I live in Vienna, Austria
Thanks in advance
Update: I found this bug here https://www.massaudubon.org/learn/nature-wildlife/insects-arachnids/western-conifer-seed-bugs
The bug that I saw looks like a Western Conifer Seed Bugs! Do you agree?

I found this bug here https://www.massaudubon.org/learn/nature-wildlife/insects-arachnids/western-conifer-seed-bugs

Kissing bug that carries Chagas disease is in the Americas.

Yes, it does seem to be a Western Conifer Seed Bug (Leptoglossus occidentalis). Not a hazard to people.
Photos from Italian language wikipedia.

This ref below suggests it may be looking for somewhere indoors to wait out the winter. It lays eggs on conifer leaves.
http://www.zin.ru/animalia/coleoptera/pdf/steyrer_perny_2008_new_insect_species_in_austria.pdf
"Two New Insect Species in Austria: One Established, the Other One Not (Yet)" by
Gottfried Steyrer and Berhard Perny,
Forstschutz Aktuell, num 44, 2008

Thank so much for your help. Now I can calm myself down. It sounds harmless. Blaming myself for killing a harmless creature.


text:
Is synthesizing DNA in-house feasible?
I've been reading up about DNA writing, and it seems there are machines available around the five-figure US dollar mark for DNA synthesis, and I'm considering picking one up for my lab.
We normally order our DNA/oligos from IDT and similar companies, and for cutting down cycle time from a few days with next-day shipping to a few hours with in-house printing, as well as potentially saving on cost with enough scale (how much is enough scale?), this seems really promising for our lab.
Is this a reasonable thing to do?

Have you looked at how much reagents cost?

@Cell Is that the concern?

I'm not sure. My ex-supervisor purchased a DNA sequencer and the consumables were so pricey it was actually cheaper to send samples to a dedicated facility. The only reason we would use it was if we wanted results in a few days and not weeks. I would look into it if I were you.

it would be helpful to know more about the scale of oligos, etc. Definitely look at the consumables price. I know that for the opposite approach, DNA sequencing, the technology advances so quickly that it really doesn't make sense for independent (small-medium) groups to buy their own sequencing instruments, as they're pretty finicky, so most people just send their libraries to a dedicated provider like genewiz or a university core facility.

So far as I'm aware, the big distinction right now is whether you want dsDNA or oligos.
If you often want lots of oligos, then getting your own synthesizer likely makes sense. Run the numbers and see what the time for return on investment will be and you'll see if it works for you financially.
If you want gene-scale dsDNA, you're currently generally better off getting a specialist company involved (or a foundry, if you've got one that you can access). Not only do they have economies of scale, but they have a lot of experience figuring out how to handle difficult sequences and assemblies.  If you take it all in house you might appear to save money but actually end up losing significant money and time when you count in the time and frustration that your lab ends up spending to go from oligos to genes.
If you've got particular expertise or highly specialized needs, it's a whole different story, but that doesn't sound like the case based on your question.
Note that there are a number of desktop synthesis companies that are working to make this answer obsolete right now, and it may well change quickly in the future.