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Zygosity and Strands
I am not a biology expert but I have done some homework on understanding alleles, chromosomes, dna in the human genome. Still baffled by a question though:
As I understand it at a particular locus for e.g. if a human has a A on one chromosome and a G on another that individual is considered Heterozygous at that locus because of the difference in the nucleotides (A/G in this case).
However, my question is. What about an individual that has an A on the 3' -> 5' strand (and hence a complement T on the 5'-> 3' strand) on one chromosome but T on the 3'-> 5' (and its complement on the other strand) on the other chromosome. Is this individual considered heterozygos or homozygous?
Basically my question boils down to does the "directionality" of the A-T pairing matter on both chromosomes?
I was thinking it should as only one strand can code for genes which the other doesn't so it should matter whether the A is on the (3'-5') or on the other strand..
Any advice would be great!

As @Nicolai's answer suggests, when you are thinking about coding genes, you should really just think about one strand at a time. Also note that zygosity is normally considered at the gene/allele level, as far as I know, people rarely talk about "zygosity" for a particular base pair, especially because single base changes don't always have an impact on the protein produced. (someone who does more genetics might disagree with me)

Thanks Bryan. I did accept @Nicolai's answer. However, I am not sure I understand what you mean by "Zygosity at a gene/allele level". Per my understanding a gene is just a certain sequence of nucloetides on a strand and allele's are just different "versions" of the same gene present on different chromosomes. So, I thought zygosity has to do with variances in nucleotides on different chromosomes.

crossposted on biostars.org: https://www.biostars.org/p/264076

@Shanbhag Yes, it does, I'm just saying that "allele" and zygosity has whole-gene connotations. If you are talking about alleles for just a single base pair, you are implying that there is no variation in any of the other base pairs. Also, alleles that are actually different at the base pair level but produce no phenotype in any combination might be grouped all as "wild type" alleles. It's just a different level of analysis in most contexts.

@BryanKrause When talking about SNPs zygosity or at least the terms homozygous/heterozygous are usually also used. I guess depending on ones background the connotation of zygosity with genes might differ

The directionality of the strands matters, because genes can be encoded on both strands of a chromosome (each strand can be read in 3'-5' direction by RNA polymerase). Therefore someone with the A-T case you described is also heterozygous.


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Clinical Microbiology Books
I am looking for a good book about Clinical Microbiology, particularly good in Bacteriology and Bacteria Diagnosis (medium, plates, type of colonies...). With good photos. What are the bests in your opinion?
Thank you.

Manual of Clinical Microbiology.
My version is old, but it is an excellent reference considered gold standard in the clinical science industry and by educators.   It has been used by clinical microbiologists for many years and is still coming out with updated revisions. It comes as a two volume set due to comprehensive content. Published by the American Society for Microbiology.
http://www.asmscience.org/content/book/10.1128/9781555817381

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How much DNA do humans have?
A normal human body has approximately 3 billion base pairs. Given that humans have 10 trillion cells, how is that the number of base pairs of DNA is less than the number of cells? It can happen only if most of these cells don't have DNA, or have I misunderstand the topic?
Can you give an account of why the number of cells exceeds the number of DNA base pairs significantly? Isn't it logical to have more DNA base pairs than the number of cells?

What research did you do before posting this question? Your conclusion was clearly absurd, so an attempt to identify the flaw in your argument was called for. I am voting to close this question as extremely low quality.

No, number of base pairs is not at all related to number of cells. The correct statement should be 'a normal human body has approximatrly 3 billion base pairs of DNA in every cell'. I suggest you keep studying.

1 base would code for one cell? That would make for either very simple cells, or very information dense DNA.

Answer to the question
How much DNA is there in our cell nuclei?
In humans, there are about 6 billion base pairs in the nucleus of each cell. Why 6 billions and not 3? There are 3 billions base pairs per haploid genome (see ploidy) and therefore 6 billions base pairs for the whole genome. This number may actually further double during specific phases of the cell cycle. Each single cell contains a copy of the whole genome (with a few exception such as red blood cells for example).
So the total number of base pairs in a 10 trillion cells individuals is about $6\cdot 10^9 \cdot 10^{13} = 6\cdot 10^{22}$ base pairs.
Further information for fun
How much DNA in our cells outside of nuclei
Now, in cells there is DNA outside of nuclei. In animals (incl. humans), we have DNA in mitochondria as well. there is of the order of 104104 base pairs per mitochondria (16,569 sites to be accurate) and there are of the order of 104104 mitochondria per cell, that is 108108 base pairs total per cell which is only one order of magnitude below the number of base pairs in the nucleus per cell.
There is therefore an extra $3\cdot 10^8 \cdot 10^{13} = 3\cdot 10^{21}$ base pairs in cells outside the nucleus.
How much DNA in bacteria living in the human body?
Note that by "in the human body", I also include "in the gut" even though the inside of the guts are typically considered as being the outside our body.
There are about 100 trillions of bacteria in every one of us (this number is a vague approximation; see wiki > Human microbiota). Yes, most of the cells living in us are not our cells but are bacterial cells!
Bacterial genome vary widely but as a gross and almost insulting approximation, let's consider that the average bacterial genome from our microbiome has a genome size of $10^6$ base pairs (note bacteria don't have nuclei or mitochondria).
That means that in our body we have to add to the above numbers $10^6 \cdot 10^{14} = 10^{20}$ base pairs (which is only a hundredth of $10^{22}$).
How much DNA in the viruses in our body?
Let's not forget our virome. Unfortunately, I could not find estimates of the number of viruses (and viroids) in our body.
How much DNA is outside cells and viruses in our body?
Of course, there's plenty of DNA in our body. There's DNA in everything we eat and this DNA end up in our blood stream and in our cells. I failed to find an estimate of how much DNA does that represent.

The addition of mitochondrial base pairs would not even show up on that measurement anyway, mitochondria only have a few genes.

@John Actually, there is of the order of $10^4$ base pairs per mitochondria (16,569 sites to be accurate) and there are of the order of $10^4$ mitochondria per cell, that is $10^8$ base pairs total per cell which is almost of the same order of magnitude than the number of base pairs in the nucleus. So... it may show up on these calculations. It would show up for sur if we consider an extra significant digit.

Right I forgot about multiple mitochondria per cell, my bad.

Add the mito calculation as a footnote to the answer ? Makes the answer even better.

3 billion is the size of the haploid genome. Somatic cells have 6 billion bp.

@canadianer It can go to 12 billions bp depending on the stage of the cell cycle.

@RoniSaiba Following your advice, I wrote a few more far fetched calculations.

@Remi.b: Want to do another far-fetched calculation?  Suppose you liquified a human body, and forced it through a filter that extracts DNA: how much would you have?

@jamesqf I have it at around 65 grams.

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How is yellow elastic cartilage a true cartilage?
My book has only mentioned the fact but no reason is given so I would like to know the reason for it. I would like to know what more to add in the body but the question just doesn't get posted.

What research have you done , have tried googling it atleast? Question which doesn't show attempt are likely to be deleted.

Yes i have already googled it even asked the same question but it always open wikipedia which donot provide me my answers

Could you cite the book?

A TEXT BOOK OF BIOLOGY

author name pls

Wikipedia cartilage defines it as being composed of specialized cells called chondrocytes that produce a large amount of collagenous extracellular matrix, abundant ground substance that is rich in proteoglycan and elastin fibers. , then states that: Cartilage is classified in three types, elastic cartilage, hyaline cartilage and fibrocartilage, which differ in relative amounts of collagen and proteoglycan. The term elastic cartilage links to a separate page describing elastic or yellow cartilage. What other information do you need?

Maybe he wants the reason why its called "true"

https://books.google.co.in/books?id=uIWU4x4Rq0cC&pg=PA32&lpg=PA32&dq=%22true+cartilage%22&source=bl&ots=GNYGWHvaR4&sig=O__pwHVGQjZEerZvASTSTbUDwOk&hl=en&sa=X&ved=0ahUKEwjT87G7tJ7VAhUmTY8KHQOICyMQ6AEIQDAI#v=onepage&q=%22true%20cartilage%22&f=false

jm97 it the book i mentioned is by...Dr.Rameshwar p.singh,Dr.Shree krishna subedi,Mukti ram aryal and Dinesh chandra adhikari....and i what i want to know is mentioned in title

True cartilage is something of a simplification or a misnomer, they are saying that it truly a form of cartilage and not another elastic tissue type. in fact
"true cartilage" is a term coined by your book. They could have also said it's part of the cartilage family of cell/tissue types.
It's similar to cartilage under a microscope, structurally and has similar consituents, although yellow cartilage also contains elastin. If you were to dissect humans, you would probably find that there are a lot of variations of cartilage of different elasticity, midway in between both forms.
this page is full of info and pics:
It's a good idea to check wikipedia and 2-3 pages to find results to that kind of query, you will find fabulous resources, whereas on stack it is really for studies that take more than 20 minutes via google.


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Role of auxin and cytokinins in vascular cambium or callus formation
Usually, auxins promote cell growth and cytokinins promote cell division. But, I got an information from my teacher that, in case of vascular cambium or callus formation, auxins promote cell division and cytokinins promote cell growth. Is this 'information' true? If true, why?


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What is this worm like creature?
Recently while cleaning my garden, I saw this worm like creature which resembles a leech but is humongous in size if I compare that with commonly found leeches in my area, Kolkata, West Bengal, India. I did not see something like this before so, I captured a snap of this creature and posting it here to know more about it if someone can give me a hint.

Possible duplicate of Identifying a thin, black, worm-like creature with a hammer-shaped head

This question already has an answer here

This is obviously not a duplicate. The specimen here is clearly different from Bipalium kewense, as I explain in my answer.

This is probably a land planarian, a flatworm (Plathyhelminthes) from the Subfamily Bipaliinae, called "hammerhead worm". This Subfamily is native to the Indian subcontinent, which matchs your description.
According to Wikipedia,

The subfamily Bipaliinae is characterized by having a semilunar head that gives them the common name "hammerhead worms". The head has peripheral sensory pits on the ventral side and small peripheral eyes on the dorsal side.

You can see this semilunar head on the animal's anterior end (right hand side in your photo).
This subfamily contains the largest flatworms known. The larger one is Bipalium kewense, which can grow up to 40 cm.
However, the individual in your photo doesn't seem like B. kewense, which is a quite narrow worm and has a large head, with a different colour and stripes pattern:

Source: https://niceworms.wikispaces.com/Bipalium+kewense?responseToken=05b65f9b09b41aa5da58c3026c7f3ce8e
The one in your photo seems more like B. adventitium, which is a bit wider and has a smaller head:

Source: https://www.inaturalist.org/taxa/82290-Bipalium-adventitium
The problem is that B. adventitious adults are only 10 cm long, and that is hardly humongous.
So, I'd just say "it is a Bipaliinae flatworm", without narrowing it down to the species.
PS: It's not a leech (Annelida) because, among other clues, it clearly lacks metamerism.


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Can pheromones be received other than by odor?
I'm trying to understand how deodorants affect pheromones in humans.
Wiki states:
Axilla

In humans, the formation of body odor happens mostly in the axillary
  region. These odorant substances serve as pheromones which play a role
  related to mating.

Deodorant

A deodorant is a substance applied to the body to prevent body odor caused by the bacterial breakdown of perspiration in armpits, feet, and other areas of the body.

Can the opposite sex receive pheromones if a person uses crystal deodorant (doesn't have a fragrance; doesn't block sweating; prevents body odor by creating an invisible, protective barrier against odor-causing bacteria)?

Despite the Wikipedia page you link to, the existence of human pheromones is still a matter of debate. For the most part human body odor comes from the breakdown products of sweat and skin by bacteria. These smells may play a role in sexual attraction, but they aren't strictly pheromones since the odorants aren't actually secreted by humans, but by bacteria that live on our skin.

We have only 5 senses, a 6th sense has been controversial, and some 6th senses are sometimes reported in new research in newspapers, but none have been conclusively been added to the clearly known 5. There is a second olfactory organ that deals with social signals in other animals, that we possess, the vomeronasal organ.
Pheromones are only olfactory molecules, so you can't get them other than by catching molecules and analysing them, i.e. smelling.
Humans react very strongly by attraction to some perfumes other than pheremones, and you arent supposed to block all your smells, only make them containable, a bit is probably a good thing.
Scientists did publish a study claiming that people can tell if they make a good immune response / metabolic genetic combo with a partner from smelling a potential partner's t-shirt.

"We have only 5 senses, a 6th sense has been controversial" - This is meaningless. There are well over 5 senses. The 5 senses thing is a biology myth taught to children.

Are the pheromones in the bad scent after sweating? As I said, take for example, deodorants that don't block sweat but "disable" bacteria. Can opposite sex catch these molecules or deodorants block them?

Meaningless? It's BioPhysics categorization, and current affairs, news headlines, So, No, Actually it is a Bio-Physics subject. And Artmal is not a doctor, no one even understands the question very scientifically, If you know a kinder reply to him, give it. Energy is transmitted in 5 major groups into the human mind: Chemical scent of the air, and chemical scent of taste, Soundwaves, Photons, Kinetic Energy.


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The human brain in numbers II: synaptic connections
The overall number of synapses in the human brain is roughly 1,000 trillion, i.e. 10,000 synapses per neuron.
My question here is three-fold:

I assume that each structural type of neuron (basket, pyramidal, ...) has a somehow characteristic average number of in-coming and out-going synaptic connections, i.e. not every type of neuron will have about 10,000 in-coming and 10,000 out-going synaptic connections. I am looking for a thorough overview of these characteristic numbers by structural type.
I assume that for some functional groups of neurons (see The human brain in numbers I: neurons) there are characteristic average numbers of in-coming and out-going synaptic connections per neuron. I am looking for a thorough overview of these characteristic numbers by functional group.
Finally, for some functional groups there are presumably characteristic ratios of inner and outer synaptic connections: "x % of the in-coming synaptic connections of a neuron in group X come from other neurons in this group, the rest comes from the outside. y % of the out-going synaptic connections of a neuron in group X go to other neurons in this group, the rest goes to the outside".  I am looking for a thorough overview of these characteristic ratios by functional group.

Woah, that's just too broad a question! Divide it into (at least) three questions, lest even a bounty of +500 points is not very likely to get you a complete answer for such a big question...

Yes, incredibly incredibly too broad. You might look into projects like the Blue Brain Project in Europe and the BRAIN initiative in the US.

I'd like to, but these are real huge projects with vast web sites. And I am not sure if I would find thorough and concise overviews of the kind I'm looking for. So if anyone knows...

@hansstricker honestly, if you ain't sure you'd get all that you want even on such vast websites, how do you expect somebody here to pack all of it in a little answer?

The little answer might be a link that would be hard to find.


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Why will happen if plant phloem does not contain sieve plates?
What are the primary functions of the sieve plates that make them so crucial? I've done a bit of reading online and found
"Sieve plates are perforated end walls separating the component cells (sieve elements) that make up the phloem sieve tubes in vascular plants. The perforations permit the flow of water and dissolved organic solutes along the tube and are lined with callose."
However, wouldn't the flow of water or organic diluted be faster without the extra sieve plates obstructing the flow? Or is there some other functions of the sieve tubes?

First of all, phloem sieve cells (opposing to xylem vessels) are live cells. In the phloem, a transport occurs not like in water pipes (with free movement of liquids) but through cells transport structures, particularly through plasmodesmata. As live cells, sieve elements need all standard structures, including cell wall, to sustain functionality.
Moreover, the phloem transport is (at least partially) an active process. I.e. to transport something you have to spend some energy. Today the most supported hypothesis of phloem transport is Pressure Flow Hypothesis . According to Wikipedia:

While movement of water and minerals through the xylem is driven by
  negative pressures (tension) most of the time, movement through the
  phloem is driven by positive hydrostatic pressure. This process is
  termed translocation, and is accomplished by a process called phloem
  loading and unloading. Cells in a sugar source "load" a sieve-tube
  element by actively transporting solute molecules into it. This causes
  water to move into the sieve-tube element by osmosis, creating
  pressure that pushes the sap down the tube. In sugar sinks, cells
  actively transport solutes out of the sieve-tube elements, producing
  the exactly opposite effect. The gradient of sugar from source to sink
  causes pressure flow through the sieve tube toward the sink.

So, a plant needs live cells to support such mechanism.
Here we come to sieve plates. In plants, live cells interacts by means of plasmodesmata. In simple words, they are extensions of endoplasmatic reticulum which connect the cytoplasm of two cells and act as transport channels. And sive plates are simply places of highly hypertrophied plasmodesmata region.
So in conclusion:

Phloem transport is a partially active transport which occurs with
an involvement of cells transport structures like plasmodesmata.
The region of hyper-developed plasmodesmata on sieve elements wall
appears as sieve plate.
That is why an absence of such structure will not provide any gains in conductivity.

UPD. In response to Jim Young comment.
Damage protection is not a major role of sieve plates. Again, sieve plates are areas where plasmodesmata penetrate cell wall. Plasmodesmata act as the main vector of intercellular transport. So, the transport is the main purpose (or a reason) of sieve plates.  The damage protection is an additional property and not an aim of these structures. As to tyloses, yes it is a common mechanism of vertical transport prevention in xylem. But xylem vessels consist of dead cells. They are literally pipes. Therefore it is possible to cork up xylem vessels by simply inserting packs of fibre. BTW, that is why cavitation in vessels can cause embolization.  In contrast, phloem cells are live cells (with cytoplasm and EPR). They conduct water and sugars not by free flaw but with an involvement of intercellular mechanisms. That is why mechanical embolization is not a case for phloem cells.

My understanding is a bit limited and highly simplistic. As I understand, the purpose of sieve plates is damage control. The sieve plates are crossed by long p-protein molecules that assist in translocation across the plates. When damage occurs, these proteins become detached and clog the pores of the sieve plate, sealing the tube. Without the sieve plates, compartmentalization of damage would need to be accomplished in a different way. Ray cells project tyloses into xylem lumens - presumably some analogous self-sacrifice by companion cells could seal phloem tubes, but it isn't - why not?


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What is "multiple" myeloma?

Multiple myeloma, commonly referred to as myeloma, is a cancer of the plasma cells found in the bone marrow.(source)

Is there any significance in calling myeloma as "MULTIPLE" myeloma?

Any reason for downvote? what sort of attempt should I show in this question if I am unable to it by googling?

You often claim to have googled something but found nothing. Yet, it's that very attempt to find an answer that would make your questions more on topic. You claim, how can I include my research if I found nothing? Well, then, tell us what terms you used when you googled. Not my downvote (I never stopped to wonder so it was interesting), but yes, my closevote.

Wikipedia, first result in Google by the way, second paragraph: "When only one mass is present, it is known as a plasmacytoma while more than one is known as multiple myeloma". Did you actually google "multiple myeloma"? You just asked "what sort of attempt should I show in this question if I am unable to it by googling?" in your comment above... well, I believe that googling "multiple myeloma" is what one expects.

@GerardoFurtado I google etymology of multiple myeloma and myeloma vs multiple myeloma.

Next time just google "multiple myeloma".

J. Von Rustizky, a Russian pathologist working in the laboratory of Friedrich von Recklinghausen (1833–1910) in Strassburg in 1873, introduced the term “multiple myeloma.” At autopsy, a 47-year-old patient examined had eight separate tumors of bone marrow, which Von Rustizky called “multiple myelomas,” and he noted that the nucleus of the tumor cells was located in the periphery of the cell membrane — a morphology highly suggestive of plasma cells.

source: Kyle, RA, Steensma, DP (2011) History of multiple myeloma. Recent Results Cancer Res., 183: 3-23
From the same item:

The most commonly recognized [first documented] case is that of Thomas Alexander McBean, a highly respectable tradesman from London in 1850. Mr. McBean excreted a large amount of protein that was described by Henry Bence Jones in the middle of the 19th century. Jones was a well-known physician and made many contributions to medicine.

The Bence Jones protein is in fact an immunoglobulin light chain. Purified Bence Jones protein were sequenced by FW Putnam, and
variations between patients were some of the first clues to the existence of the variable regions of immunoglobulin molecules.

Hmm, in addition to the information I get from your answer, today I learned a new googling skill, which is to get etymology we should also try History of _________. Thanks.

Another good strategy would be searching databases like PubMed for "review" articles. These will almost always have "history" sections in the beginning, and even if they're very short, they'll usually have citations to other papers that you should look up—perhaps even the original, as in this case. @JM97


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How do animals identify their offspring?
Recently I was watching a documentary about penguins and how a mother penguin lost its chick. Then it went looking for it, and among a horde of penguins it was able to find its chick and take it back.
What really intrigued me is that the penguins looked exactly the same. Animals don't have as many
distinctive features as we humans do, such as significally different hair color, skin color, they don't really look very different. Rather animals of the same species look very similar.
Just consider the following image:

How can one even differentiate between all these penguin chicks? Even the parents look very similar to me.
So how can parents spot their offspring among all of these penguins that look almost identical?

It varies a lot from species to species. The question How do animals know who their child is? is too broad, you probably want to ask How do penguins know who their child is? instead.

@Remi.b its not only for penguins, but for animals in general

Well the I am voting to close as the question is too broad as mechanisms vary a lot from species to species. Some would use facial recognition (e.g. sheep), others would use smell, others would not need to recognize as only their offspring stays in the neibourhood, others don't recognize their youngs, most species use some mixture of those cues, etc...

All the penguins appear (and would smell) similar to you. But not to the penguins.

nature gives them variance so that they recognize very easily what is important to recognize. to know the difference, many tests have been done, using sound proofing, visual screens, and they can probably recognize them by sight or sound, although sound is probably the main recourse because birds have very good ears and variable voices, and it's a 2 way thing, the parents call and the baby replies, it's not random sounds.

Many mammals recognize their offspring by smell, some by cry, etc. In my flock of goats, at kidding time the mothers always smelled the anuses of the infant offspring (after they had fed at least once) before allowing them to nurse. Their particular milk and the way it is digested by the offspring had a unique smell. If it was right, they nursed. If not, they were rejected. This is not unique to goats, but there are other ways as well. This is a broad subject.

@anongoodnurse You are a molecular biologist, a physician, a fan of Shakespeare, probably a parent given your activity on Parenting.SE (or maybe just a pediatrician?) and you're raising a flock of (anus smelling) goats! You sound like an interesting person to be around!

@Remi.b - Thanks for saying that; it's quite kind. Many people just think I'm crazy. ;)

You don't have to close it. I mean you can. I know its broad but its just something I wanted the answer too, and I think @anongoodnurse and the rest have given me really good answers. even remi has, thanks alot everybody

It's only a partial answer given that it's a fairly broad question, but I discussed the specific mechanism for this in sheep here: https://biology.stackexchange.com/questions/46306/why-would-a-mother-reject-her-offspring-if-it-has-been-interfered-with-by-huma/46388#46388

Penguins (and many birds) recognize their offspring and mate thanks to vocalizations.
It's called individual vocal recognition, it's like when you recognize your friend voice among a group of chatting people.
Scientific article references for penguins:
Jouventin P., Aubin, T., Lengagne, T. 1999. Finding a parent in a king penguin colony: the acoustic system of individual recognition. Animal Behaviour 57(6):1175-1183.
http://www.sciencedirect.com/science/article/pii/S0003347299910862
Aubin T., Jouventin P. and Hildebrand C. 2000. Penguins use the two–voice system to recognize each other. Proc. R. Soc. Lond. B. 267:1081–1087.
http://rspb.royalsocietypublishing.org/content/267/1448/1081.short

Animals used several ways to tell who their child is, some use sounds, yes, some use spatial cues and THEN sounds to zoom in the individual they want to find, and sometimes they even need to confirm by smell!
Here is a good reference that describes this process and the different sensory cues used in a pinniped species:
Kaja Wierucka, Benjamin J. Pitcher, Robert Harcourt, Isabelle Charrier. (2018). Multimodal mother–offspring recognition: the relative importance of sensory cues in a colonial mammal. Animal Behaviour 146: 135-142
https://www.sciencedirect.com/science/article/pii/S0003347218303208
For more information specifically on what kinds of information animals can glean or transmit use of acoustic cues, this book is really informative!
Coding Strategies in Vertebrate Acoustic Communication (Animal Signals and Communication 7) 2020 Editors Thierry Aubin and Nicolas Mathevon
https://link.springer.com/content/pdf/10.1007/978-3-030-39200-0.pdf

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Placebo effect and why they work
I'm just wondering how the placebo effect works on people. If a patient is given fake drugs , how does that make him better? So what if they feel more "assured", how would that help the body immunity (t cells, phagocytes, etc) fight the infection better? How does phycological emotions affect the physical aspects of our immunity? Also I've read an interesting article online showing us that placebo effect works even when you know you are given fake drugs? This really complicates my understanding. How would such a approach even work?
http://www.health.harvard.edu/blog/placebo-can-work-even-know-placebo-201607079926

well for a start it helps if your remember emotions are chemical reactions occurring in the body, psychological and physical are not separate.

The paper isn't about immunity, and the answer is in the paper you cite: Kaptchuk says placebos... can work for conditions that are defined by “self-observation” symptoms like pain, nausea, or fatigue. “People can still get a placebo response, even though they know they are on a placebo,” he adds. “You don’t need deception or concealment for many conditions to get a significant and meaningful placebo effect. Placebos don't work on serious illnesses (they don't fight infections or cancer); they work on perception of illness and on the mind-body connection in illness, which is too broad.


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Effects on body without fitting routine to external time (non 24 hour Circadian clock)
Often I find myself trying to fit my daily routines to factors such as those of the external time, e.g. to light levels outside, and those that others around me live by.
However this often seems inconvenient- often having to round up or round down time spent on certain activities to fit them into my day. Sometimes I find myself tired which affects the quality of my work, but I 'know' it is not necessarily time to sleep due to the outside light levels and the timezone given to me, so I must carry on until some 'reasonable' time is reached.
I was wondering, is there a significant (negative) effect to the following process:
Assuming I need to do nothing which involves direct involvement of others, I attempt a task (inside, controlled temperature with lighting if needed) which I want to attempt until either it is complete, where I then move to the next task, or feel like I must postpone to perform a bodily function (eat, sleep etc.) until these themselves have been satisfied.
Repeat this indefinitely, irrelevant of outside time conditions/ factors, which we assume to be reasonably 'normal'.
(I have an infinite supply of food, water etc. )
Assume work can only be completed with at most minimal tiredness.
I would expect that maybe on average, the times at which humans are to proceed through the tasks match up with the 'normal timings', but I would argue that for myself, this would be caused by quite large fluctuations either side that cancel each other out. (Perhaps at some point I would wake up in the afternoon, another day go to sleep in afternoon).
I would like to know how much of our regular routines is psychologically influenced by others around us compared to how much this is intrinsically in our genetics.
These 'normal' routines seem to make sense for many primates- time of day effects ability to see surroundings, perhaps what food sources are present. But one could argue whether this is as relevant for humans with technology to overcome many of these factors.
I am aware of the Circadian clock, and that it has its own genes, and that it is maintained through certain light stimuli, but I do not know what precise functions it maintains in the body.
So
What would be the physiological/psychological consequences of ignoring the factors of time when completing tasks?
How much of the common human routine is psychological (from being influenced/ made to by others) compared to intrinsic instinct?
Are there any sources/studies conducted on this before?


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What's the name of this Heteroptera bug from Toronto, Canada?
My friend already identified it as belonging to the Heteroptera order, but I was wondering if anyone knows the name of the species.
Found in Toronto, Ontario, Canada, on July 21 2017, in a residential bathroom.

@BernardoRamos Yes, thank you, I forgot to add it, here it is.

This is, indeed, a Heteroptera bug.
Luckily, this is not a kissing bug (which could be infected with Trypanosoma), but just an assassin bug, from the Species Reduvius personatus. Its common name is masked hunter.
Here is an image of the same bug, also in Ontario, from the Canada Pest Control website:

Source: http://pestcontrolcanada.com/5723-2/
And in this photo you can see the long rostrum, just like in your second photo:

Source: https://www.youtube.com/watch?v=9fIBT7IJHn8
Finally, to see an assassin bug in action (a different species, though), have a look at this video from the Smithsonian Channel: https://youtu.be/hXFRAmWiaa4


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Feffects of frequent & sudden variation in room/surrounding tempratues
If out door temprature is like 40°c with 100% humidity and indoors temperature is around 35°c. Whereas an air conditioned room in the house has  a temperature maintained at 20°c with very less humidity.
A person doing household chores moves in & out of all three temperature zones very frequently, like 3 to 5 times every ten minutes, for a total duration of say half hour.
In such a situation, what could be the physical effects on ones body?
Can it cause dizziness, sleep onset, fatigue, headache & muscular cramps, palpitations, breathing problems etc?

We cannot give medical advice or diagnoses on stack exchange. There are legal repercussions for such advice.

Rehan, you might ask this (after depersonalizing it) on Health.SE. Personal health is exactly that: personal. I'm an old lady. My dogs thrive on activity, so I go outside and chuck balls in awful heat for a few minutes, then come in to cool off, then go out again, etc., and I feel nothing untoward. That doesn't mean someone who has, say, an autonomic nervous system problem wouldn't suffer from doing that.

@John - Medical advice on Stack Exchange does not constitute a professional (doctor-patient) relationship, therefore does not constitute a legal problem. It is not technically different than the advice given on Law.se or a cooking site (if a bad answer ruins your dinner party, can you sue? I doubt it.) The problem is ethical.


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Voluntary actions of Autonomic Nervous System

Somatic motor activity is always voluntary, while ANS motor activity is usually involuntary. pgno:762

This indicates the possibility of voluntary activity by ANS.
So, what are the voluntary actions by ANS?

My Attempt:
Wikipidea says:

Most autonomous functions are involuntary but they can often work in conjunction with the somatic nervous system which provides voluntary control.

So, is right to say that Flight or Fight response is the voluntary activity of ANS?

I have no idea what the author has in mind, but their statement is wrong from the beginning: somatic motor activity is not always voluntary. Reflexes are a good and obvious example.
"Fight or flight" response is basically half of the entire ANS (the sympathetic part), so that's incredibly broad. Parts of that response are definitely involuntary.
I think it's more likely that Wikipedia is thinking of things like breathing, which is normally under ANS but you can also manually control your breathing. They may also be thinking of things you can do to directly influence your autonomic responses, for example, if you start running, you are voluntarily moving your muscles, but the autonomic nervous system will also participate (for example, by increasing your heart and breathing rates).

So is it still correct to say ANS is not always involuntary?

@JM97 I think it makes most sense to just think of the ANS as involuntary, because that's really the whole point of differentiating the ANS from the somatic nervous system, while remembering two things: 1) The ANS does not exist in a vacuum, it shares a body with the rest of the nervous system, and as such is not immune to influence, and 2) Absolutes are always risky in biology - someone will come around with a particularly clever example or a way of narrowing a definition to disprove an absolute statement.


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When a muscle contracts, does it store potential energy like a spring that is released upon relaxation?
A colleague of mine who mainly focuses on clinical chiropractic work claimed recently in a book he wrote that muscles in the pelvic floor have "elastic recoil."
What he means by this is that a muscle behaves like a spring and, upon relaxation, releases potential energy somehow.
I am highly skeptical of this and want to verify if this is true or not.
When a muscle contracts, does it store potential energy like a spring that is released upon relaxation?


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Should you perform an ordination (such as PCA) of abiotic variables before a Redundancy analysis (RDA)?
I have a dataset of viral 'OTUs' across various sample points from different sites/times.
I also have meta-data collected at these same sample points, for things like temperature and the concentration of key chemical compounds.
My goal is to identify if these (or some of these) abiotic variables correlate with the variation in the OTU community diversity- for now I am planning to do an RDA.
What I am wondering is whether or not it makes sense to conduct ordination on the abiotic variables before doing the RDA? I have done a PCA on these abiotic variables and it is clear that these variables alone clearly do not cluster in any sort of recognisable pattern (for example if you colour them by 'season' there is no clear clustering at all).
So I was thinking that perhaps doing an RDA would not be valid, because if the abiotic variables don't cluster logically in an ordination of them alone then surely it doesn't make sense to plug this data into an RDA?

I really don't know much about RDA (so correct me if I am wrong), but to me RDA is a method of ordination as well, so the sentence makes sense to conduct ordination on the abiotic variables before doing the RDA makes little sense. When you state your goal, it seems like you would like to perform some hypothesis testing which is, I think not what an RDA does. Am I wrong? Why don't you just have OTU community diversity as response and your abiotic variables as explanatory variables in a simple GLM? You don't even seem to need a MANOVA (which would require ordination + regression).


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Use numbers or algebra when introducing an evolutionary biology concept?
I'm working on an (approximately 20 pg) evolutionary biology paper for submission to a journal.  The paper introduces a couple of strategies (I use "strategies" loosely; they can be carried out by unconscious individuals).  I have described the strategies verbally.  However, I have also tried to offer additional clarity by putting the strategies into some numerical form.  I would imagine that there are many possible models that could be used to test these strategies.  I am using one model, with so many simplifying assumptions that even if I were to carry through an algebraic treatment under this model, it would be of little use in giving a general representation of when the strategies can be selected. My goal is to go through an example under the model in order to show how the strategies are supposed to work, not the conditions under which they can be selected.
Is it easier to follow an example with numbers or with algebra in place of those numbers?

It is easier if you use numbers and avoid symbolic calculation however, it is much more powerful if you can do symbolic calculations.

If you want to learn more about mathematical modelling in evolutionary biology, I recommend A Biologist's Guide to Mathematical Modeling in Ecology and Evolution by Otto an Day

I'm not asking whether it's easier to do.  I'm asking whether it's easier to follow.  Re powerful:  I am using one model, with so many simplifying assumptions that even if I were to carry through an algebraic treatment under this model, it would be of little use in giving a general representation of when the strategies can be selected.

to follow for the reader? IMO, symbolism always carry more intuition to the reader esp. if the number of variables is greater than say 3. You can always replace the symbols by realistic numbers in your end result to ensure the reader understands. ...I am not sure I'm answering your question though...

Yes, to follow for the reader.  What do you mean by symbolism?

Oh I just mean using letters instead of numbers. I guess I took that term from symbolic computation but it may not be the right term.


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What type of fish is this and why is it so big?

This is a screenshot from a youtube video that you can watch here:
https://www.youtube.com/watch?v=zcdJNPYkIE0

Some sort of grouper?

I think it's the pacific goliath grouper

Yeah but its a whale. this is a "fish" from the title so I didnt assume it to be huge

White Shark? Whale Shark? Tuna? There are lots of large fish species...

I'm simply going off the name of it. When someone mentions "fish" you don't really imagine the really big ones. Fish you usually imagine small. Whereas if someone mentions "shark or whale", then obviously you have a different idea on size.

Whales are mammals, not fishes - calling a large fish a whale is just wrong (and of course the confusingly named whale shark is not a whale at all). Sharks are fishes, but they are a separate category of fishes from the rest. There are both large and small sharks. The smallest ones are only ~20cm, which probably makes them smaller than what you typically think of when you think of "fish".

Why is it so big? Because it’s parents were. It’s called heredity.

@KSplitX have a look at the mola mola, tuna, sturgeon, catfish, and the largest fish species in the world, Rhincodon typus for examples of BIG fish!

That is a Queensland Grouper (common name).

to be a proper answer you need to include how you determined this.

Welcome to Stack Exchange! When you reach 50 reputation points you can leave comments on other people's posts. There's a fairly high bar for posting answers, and as the other comment mentions, adding supporting sources is always a good idea and almost always necessary here. Don't worry about the negative voting so much, but if you can explain what it is that leads you to this conclusion, that would be better.

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


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What are those brown scars in the eyes?
I have recently realised that one of my friends had brown scars or marks inside his eyes. He says that he doesn't know what they are and has been there since young. What could this possibly be ? Are those parasites ?

Do you mean the lines in the white part of the eye ? Because that are blood vessels

Yeah, but why are they brown

The photo quality is bad but they are actually not how one would expect blood vessels to look like. Or it it just natural?

The photo is not of sufficient quality to allow for even an educated guess. Sorry. It's interesting, though. I'm a doc and I've never seen anything quite like it. If you could get a really good picture, I'll do some research.

@JM97 - That's the iris! You can't even see the pupil in that photograph. Are you sure you don't want to update your profile?

humans do make mistake.

one can see two lines from iris rim into sclera.

The image is not clear, but it is possible to have essentially "freckles" on the sclera. Just like on the skin, these can be harmless or not, but judging here gets into personal medical questions which we do not allow.

@BryanKrause - Those aren't typical pigment deposition. I'm very interested in what they might be.

@anongoodnurse  I have found a clearer picture.


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What is this worm or larva I found in my walls
We were recently doing some major remodeling in our 1920s era home and found what looks like a nest of small meal worms. I am wondering if anybody can identify them! Here are some photos:

Our home is in Denver CO. I didn't see any living examples so it is possible they have been there for nearly 100 years.

You are correct!, those are definitely mealworms. If you're not already aware, mealworms prefer to live in dark places (so under/in woodwork is expected) and typically eat decaying material, but are also partial to consuming new plant growth.

During the larval stage of a mealworm (of which will eventually grow into a Darkling Beetle), a mealworm will undergo 10-15 molts before pupating. That being said, the collection of carapaces that are shown in your picture is probably the work of just a few beetles.
I cannot attest as to how long it takes for a mealworm carapace to deteriorate, but sure, those remains could very well have been there for decades. If the location in which you found these remains has a dirt floor, you could possibly try identifying trails that were left by the developed beetles. Their trails looks like this:


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Electrogenic ion transporter

At the molecular level, electrical current across cell membranes ﬂows through three unique classes of integral membrane proteins (see Chapter 2): ion channels, electrogenic ion transporters, and electrogenic ion pumps.1

later it is said:

One class of electrogenic transporters includes the adenosine triphosphate (ATP)–dependent ion pumps.2

Is there any fundamental difference between "electrogenic" ion transporter and "electrogenic" ion pump, considering the fact that denosine triphosphate (ATP)–dependent ion pumps are also included in the former?

My attempt:
From this site ,Secondary active transporters are electrogenic, so if I consider those as electrogenic ion transporters , then also iam still confused why sodium potassium pump is in the category of ion transporter but not in ion pump.

Pump and transporter are synonymous: they refer to proteins that, unlike channels, use a form of active transport to move ions or molecules against their concentration gradient, although "pump" is most often used in the context of primary pumps, that is, those that directly use ATP, whereas "transporter" is more often used to describe the whole category or secondary pumps that use existing gradients.

then also iam still confused why sodium potassium pump is in the category of ion transporter but not in ion pump

I have no idea where you are getting this statement from, clearly the sodium potassium pump is a pump.
Gadsby, D. C. (2009). Ion channels versus ion pumps: the principal difference, in principle. Nature reviews. Molecular cell biology, 10(5), 344.

It's from the second source, textbook by boron

The author is differentiating them as two different entities as in 1st source.

I don't think so, I think the author is acknowledging that there are proteins commonly known as pumps and those commonly known as transporters (partly by the primary/secondary tendencies of naming, which I mentioned), and intending to be fully comprehensive by listing both terms. It does not imply they are actually separate categories. The only other explanation is that the author is wrong.

For example, searching google for "humans, mammals, and" returns a paper titled like this: Influenza type A in humans, mammals and birds: determinants of virus virulence, host-range and interspecies transmission.: that author certainly isn't making the case that humans are not mammals.

3 unique classes of integral membrane proteins.....

I think that's just flowerly prose. Ignore it. They are the same. Textbooks are rarely perfect.


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Name this insect
This is the monsoon season and some black insects are flying in my house. They have a very bad smell. Does anyone know what is the name of that insect, including English and Hindi name?

Your photo is not exactly the best one for species identification. However, since you said that it has a "very bad smell", it seems to me that it is a bug (Hemiptera) from the Family Pentatomidae, which includes the stink bugs.
Quoting the Wikipedia page linked above:

The stink bug derives its name from an unpleasant scent from a glandular substance released from pores in the thorax when disturbed. The chemicals involved include aldehydes, making the smell similar to that of coriander. In some species, the liquid contains cyanide compounds and a rancid almond scent, used to protect themselves and discourage predators.

I have never been to India, but in South America I've encountered some stink bugs which produced a very disgusting smell, some of them unbearable (for a couple of seconds only).
Here is a close view of a stink bug (this one is not from Asia and, therefore, probably not your species):

Finally, to narrow it down to the species, you have to check the Pentatomidae species in India.

I think it is the earth boring dung beetle from the family Geotrupidae.

The photo is not a stinkbug, and it doesn't look like any dung beetle I'm familiar with.  I agree with MB_7 that this is a member of the Cydnidae, which are noted for their foul smells.

It is a bit old but since I ended up here while searching for the same insect, here is what I believe is the insect in question (I also have an experience with it in our little garden).
Its name is: "burrowing bug" or sometime referred as "Cydnidae" (scientific name).

Also, check out this video (if it still remains) :
https://www.youtube.com/watch?v=FABjzwRTeR4
Best regards,

That's the earth boring dung beetle. It has a very bad smell and it belongs to the family Geotrupidae. You can learn more about it here https://www.britannica.com/animal/dung-beetle

Is there any way to get rid of them? As Their smell is very burst that if I flies on body and get rubbed. These insects are flying around my house as this is the rainy season.

@SagarGupta well you can check their source around your house and how they come into your house


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Is perception contrast based?
If I understand it correctly, humans can discriminate shades and colours based on their inherent contrast, as in we can see colors because there are different colors. Same for shades and for acoustic phenomens, because to differentiate two sounds they have to differ in some quality of sound: pitch, loudness, duration.
So the question is whether all perception is contrast based. One I would presume not to be contrast based is spatial perception, because it simply is there and always works in a standard manner.

I think contrast is incredibly important to perception to the extent that I would answer "Yes" or at least "Mostly yes", but I also think a proper answer to this question would be just far too in depth, which makes the question rather too broad. Note that spatial perception is also based on contrasts, but on contrasts in space rather than other stimulus features. That said, there are some examples of absolute perception, "perfect pitch" is one, and some types of perception are probably more akin to threshold phenomena.

Sure.

I think this question is fundamentally really good. However, as othwe users indicate, it is too broad. Limiting it to a single fundamental concept in one modality would greatly increase the potential of this post, e.g., is intensity perception (luminance perception) in the visual system relative or absolute?


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Flower/Plant Identification
Could anyone please identify this flower/plant found on the semi-shaded banks of a river in East Ireland? It was located near Japanese Knotweed and looks quite similar to this.

That is Himalayan balsam (Impatiens glandulifera).

Tall, stems often reddish. Lvs opposite or in threes, with small red teeth. Fls large, pale to dark pink-purple, with short bent spur; July-Oct. Bare places, especially by streams.

The Wild Flowers of Britain and Northern Europe. Fitter, Fitter, Blamey. 1974. Collins, London.

We have a species of impatiens in the US called Jewelweed. Those seedpods when ripe are fun for kids: they pop suddenly on handling, scattering their seeds. :) The sap is a nice topical anti-itch field remedy for mosquito bites, poison ivy, etc.

Yes, jewelweed is mentioned as an alternative name on the WP page. It is considered to be an invasive weed in the U.K. because it can take over riverside land.

Yes, definitely invasive on this certain riverside.


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Light signals in the courtship and mating
I am investigating on the emission of signals in the courtship and mating in the animals.
I know that the fireflies emit light signals as a courtship ritual.
Are there other animals that use this phenomenon of luminescence?

Many Ostracods (esp. the Cyprididae) use bioluminescence to attract mates. The Bermuda fireworm (a polychete worm) also uses bioluminescence to attract mates.
If you have not yet, you should definitely have a look at wikipedia > Bioluminescence


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Gene networks in insects
I am working on gene networks and I currently have the honey bee gene network to work with. What I am missing is a gene network that I could compare it with. Could you please guide me to a database/website that I could use to download a gene network and use for my study. I am looking for gene networks from closely related species (hopefully another honey bee gene species (other than Apis mellifera or a hymenopteron. I am open to all flying insect species really. Kindly advice.

I am not sure what a gene network is (in so far as it is hypothetical concept) but the kind of data you have for honeybee must exist for the insect to end all genetic insects. Have you looked?

Not closely related but Drosophila is well-annotated: http://www.droidb.org/DBdescription.jsp. Unfortunately interaction networks are most likely to be found in model species, of which there are not many. Some work on wasps seems to have been done by Amy Toth (https://scholar.google.com/citations?user=kzt2orQAAAAJ&hl=en) and by others (https://bmcbiol.biomedcentral.com/articles/10.1186/s12915-016-0285-y) but they are not clear well annotated networks. I got that just by googling I am sure you could find something.


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Why do fully grown organisms need protein intake?
If proteins are building blocks of an organism then it makes sense why a growing organism would need an intake of them, but why would a fully grown organism need proteins (aside from those lost by shedding skin, growing hair etc.) and not recycle other proteins back into amino acids.
I understand that protein can be broken down to generate energy when needed or when there's too much of it in the body, but given enough energy from other sources (like glucose), it seems that proteins wouldn't need to be used for these processes.
Is there perhaps a net loss of amino acids during protein biosynthesis?
My question was inspired after reading this study of a man who was fasting for 382 days and was given only water and mineral supplements:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2495396/pdf/postmedj00315-0056.pdf

I've checked both of these and they still don't answer my question. Protein degradation explains that proteins can be broken down into amino acids, which I am aware of, hence the question: If the body can do this, then why the need for external amino acids? Just supply energy for analysis and new synthesis.

Please note that the man was using/losing protein as well as using fat as evidenced by the continual excretion of creatinine (which comes from muscle protein breakdown.) This is not ideal and were he not morbidly obese and on a medically supervised fast, he most likely would have died.

I see you have edited your question to clarify that the question is one of why not all the amino acids used for breakdown are not available for reuse. I'll remove my close vote and delete my comment.

@David The question hasn't been edited (unless it was deleted and reposted and I missed that) - it was always about why recycling doesn't provide enough amino acids.

@David I have not edited the question.

Ok. Can't have read it properly.

One reason is hair, skin, and certain excretions also contain protein which is lost. Hair contains little else in fact.

@anongoodnurse: And for an opposite extreme, consider the stereotypical 98 pound weakling who takes up bodybuilding :-)  Or even me, as I shift from my winter skiing muscles to summer hiking/biking/horse riding ones and back again.

If we can trust medlineplus, urine accounts for only around 80mg of the required 40-65g daily protein intake: https://medlineplus.gov/ency/article/003580.htm

Take it from the man: "This process of recapture is not completely efficient, and some amino acids are lost by oxidative catabolism. Metabolic products of amino acids (urea, creatinine, uric acid, and other nitrogenous products) are excreted in the urine; nitrogen is also lost in feces, sweat, and other body secretions and in sloughed skin, hair, and nails." https://www.ncbi.nlm.nih.gov/books/NBK234922/ ("Recommended dietary allowances 10th ed.")

"why would a fully grown organism need proteins (aside from those lost by shedding skin, growing hair etc.) and not recycle other proteins back into amino acids." --- proteins are recycled, but not 100% of the time. Also, there are billions upon trillions upon trillions of proteins in our body, and some of them are always going to be in need of replacement. Our bodies aren't perfect, by any means. Anything beyond this and you're fine picking and looking for a specific detail in an answer. It's as simple as that.

Protein is polymerized amino acids.
Humans do not require protein intake, but certain essential amino acids are required.  These essential amino acids are usually obtained through protein intake, but intake of the free amino acids themselves would suffice.
Amino acids, in free or protein form, are lost from the body due to urination (see Diverse characteristics of the urinary excretion of amino acids in humans and the use of amino acid supplementation to reduce fatigue and sub-health in adults), perspiration, menstruation, ejaculation, tear drops (see Amino Acid profiles in human tear fluids ), skin exfoliation, hair and nail growth, nasal mucus (see Identification of human nasal mucous proteins using proteomics), and vaginal mucus (see Proteins of Cervical Mucus).  Additional loses can occur due to additional bleeding, lactation, child birth, spitting (and other activities causing loss of saliva), and coughing up mucus.
Synthesis of new proteins from amino acids is constantly required by the body (see NUTRITION AND PROTEIN TURNOVER IN MAN). Though there are chemical pathways to reuse amino acids, it is necessary for the concentration of each amino acid to be non-zero, and therefore some fraction is necessarily lost through excretion.
Beyond just direct excretion of amino acids and proteins, there is excretion of nitrogen-containing metabolites such as urea, uric acid, creatinine, ammonium salts and bilirubin.

Just as a note, the first study you cited reports an average excretion of 5.1 mmol amino acids per L of urine. The average weight of an amino acid is somewhere around 110 g/mol (Histidine is at 155 and Glycine at 75, so the two most prevalent amino acids nicely balance each other out to the average of 115 as well). That makes 0.0051 * 110 = 0.56 g of amino acid per L of urine. Daily urine excretion is between 800mL and 2L, so that's perfectly in line with medline's 80mg excreted per day. (Healthy) urination is therefore unable to account for any significant fraction of amino acid loss.

Which basically leaves us with losing about 50g of protein through the other things you mentioned. If you consider how much we sweat (10-14 L PER DAY), lose skin and hair, and how much enzyme juice we secrete into our food to digest it...

@Armatus 50 grams lost per day is only if you eat more than you need.  24 grams per day is enough to supply all the needed nitrogen for the body.  https://books.google.com/books?id=bUEfAwAAQBAJ&pg=PA129&dq=minimum+protein+per+day&hl=en&sa=X&ved=0ahUKEwiI_cKNq6rVAhUFOD4KHWP1DiEQ6AEIUDAI#v=onepage&q=minimum%20protein%20per%20day&f=false Only 6.3 grams per day of essential amino acids are required according to table 12.7 of that reference.

@Armatus if protein is the only nitrogen source, some will go to  porphyrin synthesis https://en.wikipedia.org/wiki/Porphyrin#Synthesis which is excreted as bilirubin in feces and urine https://en.wikipedia.org/wiki/Bilirubin and related molecules.  So there are indirect ways of excreting protein, beyond just directly excreting amino acids or protein.

@Armatus I don't think an average human sweats 10-14 L per day (possibly excluding extreme heat and such), because that means you would need to drink probably well over 16 L of water to account for this loss plus urine and water loss due to breathing. From what I understand most of the excess proteins end up as an additional fuel for the body.

@Armatus Urea excretion through urine is something like ~25 grams per day. That would be the primary method of excretion of amino acid metabolites.

@BryanKrause only when protein/nitrogen consumption is high is urea the main route of nitrogen excretion.  When nitrogen intake is 1.6 grams/day, only 20% of nitrogen in urine is in the form of urea.  https://books.google.com/books?id=nUMrAAAAYAAJ&pg=PA93&dq=12+g+of+urea+each+day&hl=en&sa=X&ved=0ahUKEwj9keHvvazVAhVHjz4KHTIXBLQQ6AEIPDAE#v=onepage&q=12%20g%20of%20urea%20each%20day&f=false For the OP situation with no food intake, the urea fraction would be very low.

@DavePhD Yes indeed, I was trying to reconcile with Armatus' statement that 50 grams of protein are being lost (if that much is eaten) and implying that has to be lost in things like sweat, skin, and hair. It doesn't: when 50 grams of protein are lost per day, a large fraction of that would be excreted as urea.

Makes perfect sense. Imo you should modify your answer to reflect that the primary reason for protein intake is then to supply nitrogen or to save the body some work converting other metabolites into amino acids. (Yeah the sweat thing was a bit ridiculous... I've never felt like needing a bucket to collect my sweat)

Some amino acids are also consumed by metabolic activities that transform them into other molecules, like hormones, that can't be turned back into amino acids.

@John yes, like tryptophan in the serotonin and kynureinine pathways

A fully grown organism is subject to senescence and on a narrow perspective one of the signs of aging is the accumulation of large amount of lipofuschin.

In unstressed situations protein homeostasis is balanced by folding and stabilization of proteins by chaperones of the Hsp family [1] and the controlled degradation of proteins by the proteasomal system.[source1]
[see also]

However,

One of the highlights of postmitotic aging is the intracellular accumulation of highly oxidized and cross-linked proteins, known as lipofuscin. Lipofuscin is insoluble and not degradable by lysosomal enzymes or the proteasomal system, which is responsible for the recognition and degradation of misfolded and oxidatively damaged proteins. These aggregates have been found in various cell types, including heart, liver, kidney, neuronal tissue, and dermal tissue, and are associated with the life span of a single postmitotic cell and, consequently, of the whole organism. Lipofuscin formation appears to depend on the rate of oxidative damage to proteins, the functionality of mitochondrial repair systems, the proteasomal system, and the functionality and effectiveness of the lysosomes. This review highlights the current knowledge of the formation, distribution, and effects of lipofuscin in mammalian cells.[source]

Lipofuschin is known to contain oxidised proteins,lipids and glycosides as follows:

This accumulation of aggregates is the final fate of protein damage under stress conditions. Under such circumstances oxidized proteins may not undergo appropriate proteolytic digestion but instead, cross-link with one another or form extensive hydrophobic bonds. It is believed that the cross-linked proteins react further with other cellular components, forming a fluorescent material referred to as lipofuscin (Fig. 1F). Lipofuscin is accepted to consist of oxidized proteins (30–70%) as well as lipids (20–50%) [23] and from the fifth decade of life, bound sugar residues were also detected in human lipofuscin. [source]

The lipofuschins are present in residual bodies of lysosomes ,the centre of protein recycling.
Lipofuschins render the non digestibility of the oxidised proteins as follows:

According to this model, an intralysosomal accumulation of lipofuscin can be considered as the long-term result of a decreased degradation of oxidized proteins and an increase in intracellular free radical formation. Metals, including Fe, Cu, Zn, Al, Mn, and Ca, comprise up to 2% of lipofuscin [26] and especially catalytic iron seems to be an important factor in further oxidation reactions of the initial protein aggregate. In mammalian cells iron is the most abundant cellular transition metal and a fundamental player in the above mentioned mitochondrial–lysosomal axis theory of aging [source]
Another major characteristic of lipofuscin is its ability to inhibit the degradation of oxidized proteins by competitively binding to proteolytic enzymes including the 20S proteasome as mentioned above as well as lysosomal proteases. How exactly the proteasomal substrate recognition functions is still under investigation, but one of the recognition motifs might be exposed hydrophobic patches from oxidatively damaged and partially unfolded proteins [5,28]. It seems likely that the proteasome also binds to such exposed hydrophobic oligopeptides on the lipofuscin surface but is then unable to completely degrade or to release these peptides, resulting in proteasomal inhibition [source]

The lipofuschins being the undigested remains,it can be said that the lysosome fails to recycle the entire endosomal protein specifically with aging (when it becomes very prominent).
Thus, some of the loss of amino acid may be attributed to its lack of recycling.

Can you try to add some scale of reference to how much waste protein really ends up as lipofuschin? Given how long it takes such material to build up, and given that it seems like most sources focus on the lipid, rather than protein content, I am doubtful that it consists of any substantial fraction of the day-to-day amino acid needs. A different answer here says that about 6 grams are needed daily; if this was all accumulated as irrecoverable wastes in cells, we'd be growing over 2kg of body weight annually just in those granules - that makes no sense.

@Bryan Krause senescence takes years! OP asked:" but why would a fully grown organism need proteins (aside from those lost by shedding skin, growing hair etc.) and not recycle other proteins back into amino acids."aside from these phenomenon ( already discussed in the 1st answer)the only one i could find was senescence...i think i stated there will be some loss of amino acid during recycling not all...and speaking of accumulation...gaining weight? i think there will be age related degeneration of the cells rather than weight gain...apoptosis too.

@Bryan Krause as for "scale of reference"try the aging link already in the answer

What I mean by scale is: of the daily requirement for protein (that is, the inherent waste or use in the system), what percentage belongs to the mechanisms you are describing? I think that percentage is very low; I don't see in your references where that information is given, just a note that it accumulates with age.


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Wasn't extinction of dinosaurs necessary?
Beginning from the triassic era, dinosaurs crawled for millions of years. So my basic idea is, that had the dinosaurs not been wiped out, they would have eaten all the flora on the planet then. Because :
1)They (herbivore giants like brachiosaurus, triceratops etc) didn't have any predator. So population growth.
2)they must have had a great requirement of food for one day. (think of an elephant who has to eat a tenth of its way)
Doesn't All of this sum up to speak that nature found a way to save the biosphere (then) by extincting them?

That's not really how anything works in nature.

Speaking in the language of nature, if dinosaurs are fit enough for their environment, they deserve to live as long as they get sufficient food. And if plants and trees can't protect themselves from dinosaurs, they deserve to be eaten up.

Basic misunderstand about how one can make sense of nature
Nature is not a conscient being (or at least not falsifiable conscient being) trying to optimize the amount of flora or whatever you would like to optimize. There is no conscious will in the processes of evolution, in the course of a meteorite or in the decay rate of some radioactive material. Things just happen through causality (and eventually pure randomness when you go to quantum physics), not because there is a wish for this thing to happen.
So, in short no, dinosaurs did not get extinct because someone thought it would be better this way.
This discussion is not a matter of science but of philosophy of science and philosophy of knowledge. You can further this discussion on Philosophy.SE, they will be much better than me at addressing this misunderstanding.
Dinosaurs did not really get extinct
By the way, dinosaurs did not really get extinct as birds are dinosaurs. The number of dinosaurs lineages just suddenly (sudden in terms of geological time at least) decreased.
Loosely related to that, you might want to have a look at the post If dinosaurs could have feathers, would they still be reptiles?
For how long were dinosaurs there?
Dinosaurs (excluding aves, that is the lineage giving rise to modern birds) have roamed the earth from 226 millions years ago to 65 millions years ago (period called the Mesozoic). There is much more time separating the Plateosaurus (late Triassic; ~210 millions years ago) to the Triceratops (late Creaticious; ~68 millions years ago) than between the Triceratops and the first Homo sapiens (~250 thousands years ago). Dinosaurs have been around for long enough so that we can consider that they were not just eating all the plants!
As you assumed that predator population would just grow indefinitely in absence of preys, you might want to have a look at What prevents predator overpopulation?.

@SiddhantShekhar I just want to bring your attention to an edit in the section For how long were dinosaurs there? to try to help you getting a sense of how long was the so-called "age of dinosaurs".


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Why do I see so many kinetochores?
I am analysing RPE-1 cells from humans and I do not understand why I see so many kinetochores by immunofluorescence (more than 100 in many cells). They are in prometaphase.

Are you sure that they are RPE-1? Not a cell culture expert but other common cell lines are highly aneuploid (e.g. https://www.researchgate.net/post/How_many_Chromosomes_are_there_in_this_picture), and cell line contamination is very common.


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What are chromosome dimers and how do they relate to recombination?
I am reading the book Molecular Genetics of Bacteria 4th ed. and I don't fully understand the concept/visual representation of dimer chromosomes. Consider the following quote (pg 35):

an odd number of crossovers occurring between any 2 sequences on the 2 daughter DNAs in the dimer will resolve the dimer, but an even number of crossovers will recreate a dimer.

In panel 2, did another recombination event occur to yield 2 daughter chromosomes with the same sequences? The colors made me think they each might not have had their original complete sequence.
Thank you for the answer to my crossover occurrence question and their relation to dimer formation and resolution.

Welcome to Biology.SE. I wanted to improve the format of your post but I was not exactly sure what you were asking. I've made an edit feel free to roll back if you don't like it. Also, if you accept the edit, you should definitely edit the <insert something> elements. +1 btw

The quote is not so specific to bacterial genetics as much as to genetic recombination in general. Have a look at this answer to understand why the question of whether an even or an odd number of recombination events occur between two loci matter.

Your question is rather broad. It would be better to ask about something specific that is confusing you about chromosome dimers.

Is your question why an even number of crossovers will recreate the dimer during resolution? That can be answered, though it would help if you explained why this doesn't make sense to you.


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What sections of the brain can be removed without causing instant death?
Years ago I've read about a young man you had lost a large section of his brain (frontal lobe) in an accident but surprisingly he survived it and continued his normal life. You may have read about that.
Now let's break down the question into 3 steps. Which parts of the brain can we remove without:

Affecting the normal life. This means, still being able to see, talk, understand, and more. Just like a normal person.
Losing conscious. This includes just being able to maintain conscious, being able to think and understand.
Dying. Which means only having the crucial organs such as heart and lungs running.

UPDATE
I'm neither looking for a list of every part of brain's million sections, nor it's possible to cover them all in a single answer. I'm merely looking for a list of widely-known largely-scaled sectioned, such as the below image.

Image credits goes to Mid Brain Power.

this reminds me of https://en.wikipedia.org/wiki/Phineas_Gage

Thank you for the link. This is a similar accident, didn't know about it :)

This question is too broad. For example, what do you consider to be a part of the brain?  Glial cells can be removed without any consequences. Neurons are constantly dying in your brain too, apparently without consequences. Perhaps you are aiming at which anatomical structures can be removed in totality? Perhaps you can define in the question at what scale you are thinking, and if you are talking bilateral transection, or unilateral only etc.

If you have examples of where my comments are not useful let me know. In general I am just trying to improve questions. The best posts are specific, clear questions and those typically receive the best answers as well.

I think you just don't recognize how broad this field is. I am in the field of studying consciousness, and it is clearly not understood within the field what structures are necessary for consciousness or even if it makes any sense to think about it in terms of particular structures at all. This thread is just going to produce speculation, and so far the only answer is horribly misleading. I agree with @AliceD that this is far too broad.

Many areas of the cerebral cortex aren't essential to life/consciousness, damaging/removing them will only destroy the function associated with that area, e.g. visual cortex in the occipital lobe, auditory cortex in the temporal lobe etc. The Corpus Callosum can sometimes be bissected without any major detrimental effects to the "patient/victim".
Edit: The point here is that what appears to be a major link between the hemispheres of the cerebral cortex can be destroyed without necessarily killing the patient. Whether it falls under the same surgical category as a frontal lobotomy or not, I don't know.
Generally the "lower" portions of the brain, midbrain and brainstem are more important as regulatory centres. However these are each made up of multiple smaller regions, each involved in multiple functions, e.g. the Pons, medulla, thalamus. Removing any of these could have wide-ranging consequences, e.g. the thalamus is important for integrating multisensory information.
So, broadly speaking, cortex damage is OK, midbrain/brainstem, probably not unless you only removed very small regions (e.g. removing the cochlear nuclei from the Pons would probably only affect hearing).
If you use the added image, you can predict what removing each brain area would affect, removing the brainstem would remove respiratory centres, certain death. Removing visual areas would lead to blindness, but probably not death.
Fully answering your question would probably require an entire book to list all of the known brain regions and the implications of removing them.

No no no - the corpus callosum cannot be bisected without major and detrimental effects. It can be bisected without causing death but that is fully different. It can be bisected and result in a higher quality of life for someone having debilitating seizures otherwise but that is fully different. The thalamus isn't important just for "integrating multisensory information" - removing the thalamus would completely destroy someone's ability to experience external stimuli.


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Name this green giant insect hanging on the wall
This Insect was found on the wall of the Party Hall, Where I went to my Girlfriend's birthday party. This insect looks very greeny. I am in India.

You simply found Parasanaa donovani, Which is the large bush-cricket found in India and various countries in Southeast Asia.

"Simply"? I'd be very excited to see one of those!


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What is the volume of menstrual flow in non human hominidae?
I'm looking for reliable data related to menstruation in animals, with especial focus on apes. I have found that some articles and cientific studies point that only chimpanzees have copious menstruations, but there is not refrence to the volume of menstrual flow at all, and what is more intriguing this alleged copious menses are not consistent with two important observations, first that in a studied carried on some captive female chimpanzees only a keeper reported an observation of menstrual flow in a female on one single day (and the researchers didn't agree it was actual menstruation), and the second one that field researchers reported of a period of adolescent infertility in young female chimpanzees, about two years in which they have intercourses but not pregnancies, and yet they didn't notice a sign of menstruation.

I'm trying to get to a more deep understanding of the evolutive process of menstruation. I'm familiar with the study of Emera and Romero about the evolution of menstruation and think it has left this important matter outside the box. Also I want that the wikipedia article about menstruation in mammals, which is rather ambigous, get to this point in a clear manner.


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What is the scientific name of this lovely orange black flying beetle?
Found on Rangoon creeper (Combretum indicum)

@GerardoFurtado Thanks captured with my phone in my terrace garden

For the beard of Zeus, was this photo taken with a phone? Incredible.

This is a blister beetle from the species Mylabris pustulata.
Here is another photo for comparison:

Source: http://www.knowyourinsects.org/Coleoptera1.html
And, just for fun, the specimen in my link and yours, side by side:

It's worth mentioning that Mylabris has been confused with the Genus Hycleus, and the synonymy is complex.


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Are these images of carpenter ants?

When I searched carpenter ant in Google, this looks kind of like some of the images. Some other images show reddish or winged ants and I have not seen any of those.
I've seen 3 or 4 of these big black ants in the last month we've been in our new house, wondering if I should be concerned.

Which country is this one from?

@Nakx - this is in the United States, Minnesota.

There are probably a few similar species that are hard to distinguish, but Camponotus pennsylvanicus is a common black Camponotus in the USA.

Correct color? Yes
Proper antenna shape? Yes
Thorax shape? difficult to assess
Pinched waist? Yes
Heart-shaped head? Yes

Generally speaking, carpenter ants are black/brown in color, have bent antennas, a pinched waist, a round thorax, and a heart-shaped head.
And to address your confusion from seeing winged ants when searching on Google.. winged carpenter ants appear a few years after a nest/colony has been formed, so if you're not seeing any wings, it may be a relatively new colony.
One last thing.. carpenter ants (should) have hair on their abdomen. From your pictures I'm not seeing any hairs.
Conclusion: I'm 90ish% confident that's a carpenter ant.

i think the rings might actually be made of fine hairs... sucks to see these things in a home we just bought

That explanation is pretty close -- the more reflective rings on the abdomen are more or less hairless, the less reflective rings with enough fine hairs to scatter the light.

Hmm, the picture that you shared has ants with a striped abdomen, a characteristic feature of Carpenter ants.

(source: doyourownpestcontrol.com)
Wikipedia seems to confirm the same thing.
Carpenter ant
So I would say yes, this is a carpenter ant.

It is a Camponotus, but other genus also have striped abdomen (Formica for example).


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What is the best way to calculate the biological diversity of samples from bacterial/viral OTU tables?
I have a few large OTU tables of bacterial and viral datasets. The samples are across different sites and times.
I would like to visualise the community 'diversity' across the times for which I have data. For example it would be interesting to see if community diversity peaks in the summer months and falls in the winter months- in a repeating pattern.
I have not come across much advice or literature which looks at looking at diversity for large OTU datasets. Considering the OTUs are essentially arbitrary and that there are thousands of them, what is the best way to calculate and visualise the each samples diversity?
With the vegan package on R it is quite easy to calculate the Shannon/Simpsons diversity index for an OTU table. Can you simply use this on a 'raw' table of OTUs?

There are no best way I think. Those indices are different definitions of diversity. I don't think there has been much argument of whether one is of greater of interest for, say conservation purposes or whatever. I think you'll just have to pick one you like! The fact that OTU is a rather arbitrary grouping concept won't change much to the discussion. Note that there are many other indices of diversity (have a look at this answer for a list of measures of diversity)

I don't know much though on this topic and it might be worth having a look at the book Measuring Biological Diversity from Magurran

I mostly concur with @Nathan's answer, and in particular with the references he provided.
As Shannon & Simpson indices can be hard to interpret and can be non-intuitive, I prefer using Hill diversities as suggested by Nathan (the Jost 2006 and 2007 refs are great to read up on this). The main argument is that Hill diversities give effective number of species that are comparable between samples and follow the duplication principle.
Hill diversities rely on a unified formula (see this wikipedia article) with one parameter, q. Increasing values for q correspond to increasing weighting of taxa abundances in the diversity calculation:

D with q=0 does not account for taxon abundance, so is just the number of taxa, or richness
D with q=1 is not defined, but asymptotically approximated by e^H where H is the Shannon entropy. D_q1 is the effective number of species with abundance weights.
D with q=2 corresponds to the Inverse Simpson index (1/D_Simpson). D_q2 weighs more abundant taxa even more strongly.

One can choose any value for q (with q=1 with the limit e^H), and comparing diversity estimates for varying q can give you an idea of sample evenness. Setting q=∞ gives the Berger-Parker index (the fraction of individuals in the sample belonging to the most abundant species).
Importantly, for alpha div analyses on (16S/18S-based) OTUs, I would always generate rarefaction curves first, and then generate diversity estimates at a common, rarefied number of reads per sample.
You can do most of this using the R package vegan. The phyloseq package provides various alpha div estimates in one command, but no Hill diversities. I've written a few simple functions to perform rarefaction and calculate (rarefied or non-rarefied) Hill diversities from an OTU count table matrix:
function.rarefaction.R
function.alpha_diversity.R

The vegan package is suitable for your needs, but you may find you need to use others or code your own functions.
Due to sequencing biases, you shouldn't trust the 'raw' counts of your OTUs (unless you have a good reason to do so—I'm not sure how your OTUs were obtained). Rather, you may consider relativizing your site-by-species matrix. You can do so using the decostand() function.
Then, you can use the diversity() functions to analyze diversity; but you may also consider looking into other approaches to assess local diversity, such as rarefaction and sampling-based approaches, species equivalents and Hill numbers (Hill 1973, Gotelli and Colwell 2001, Jost 2006, 2007). The books by Magurran and McGill (2011) and Legendre and Legendre (2012) are extremely helpful.


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What is gene,alleles and traits?
Gene is present on chromosomes so the alleles should be same as gene but what is difference between them and what is traits?

The "traits" part of your question (which is really a separate question) is probably answered here: https://biology.stackexchange.com/questions/48692/how-to-define-a-trait-objectively

An allele is a variant of a gene. To understand what that means, the easiest is to consider a simplified example...
Simplified example
There is a gene for eye color. Eye color is a trait (aka. phenotypic trait). In the human population, there are different variants at the gene for eye color. These variants are called alleles. There is the allele 'blue eyes', the allele 'green eyes', the allele 'brown eyes', etc...
Locus
Above I wrote An allele is a variant of a gene. It would actually be more correct to say An allele is a variant at a locus but I did not want to introduce one extra word too early. A locus is a region of arbitrary size on a chromosome.
Genetic variation and phenotypic variation
If there are more than one allele at a given locus, then there is genetic variation in the population at this locus. This genetic variation can cause variation in various phenotypic traits.
Considering again the example of the gene for eye color, the fact that there are different alleles at the gene for eye color causes that there is variation in eye color in the population.
Although it may be too advanced for you, you can learn more about these concepts and how it related to heritability in this post.
Source of information
You can also have a look at the wikipedia articles

Allele
Gene
locus
Phenotypic trait

Or have a look at an intro course such as these ones at Khan Academy.


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How greater magnitude implies greater frequency of action potential?

Greater the magnitude of receptor potential, greater is the rate of discharge of action potentials in the nerve fibre.1

Now consider a case where stimulus ( strength ) is large , so there is more accumulation of positive charges near the spike generator region, this would then form action potential , this action potential should then travel in both directions just like at initial segment , where SD spike clears the existing EPSPs, so if I apply same logic here then antidromic Action potential should clear those generator potentials. If I am right then how is more stimulus causing more frequent action potentials?
Case2: If we take the scenario where there is no antidromic conduction of action potential ( for some unknown reasons) then more and more generator potentials are coming at spike generator region(1st node of ranvier) then also how it is causing more frequent action potential generation , if we consider that fact refractory period is constant for all action potentials( in a particular neuron)?

There are several important points to answering your question, each somewhat independent of the others. First, lets think about this problem from the perspective of the axon hillock, where action potentials are thought to be generated.
Conduction of action potentials requires voltage-gated sodium channels
When you talk about antidromic action potentials, you mean when they start at the "end" of an axon and return towards the cell body. You can also get backpropagating action potentials into the cell body and dendrites, but these are impaired by two things: 1) fewer voltage-gated sodium channels, so the action potential is weaker or not really an action potential at all, and 2) impedance mismatch. The axon is very narrow; the soma is very big in comparison (this is less of a factor in the context of peripheral sensory receptors where the soma is located far from the site of action potential initiation, but it is still true for the neurites there). A few sodium ions coming in around the axon hillock is enough to depolarize that membrane enough to start an action potential, but when those ions diffuse passively into the rest of the soma, they have a lot more membrane area to cover, and they don't cause as much depolarization.
What all of this means is that the "strength" of a backpropagating action potential isn't less than that of an action potential in the axon.
Frequency is relative
When people talk about frequency coding of intensity, they are talking about a gradual increase in frequency, not going immediately to refractory period. For example, a cell may fire at 1 Hz, then fire at 4 Hz, then fire at 16 Hz, then fire at 64 Hz. If the cell has a refractory period of 5 ms, even at 64 Hz it is nowhere near it's theoretical maximum firing rate.
Related to that point...moving ions takes time and cells are not isopotential
Threshold isn't reached immediately in the axon hillock when a "refractory period" ends: that's the difference between an absolute and a relative refractory period. Ion concentrations and ion permeabilities set an equilibrium potential, but, it takes time for the potential to actually reach that equilibrium, and both the present voltage and equilibrium potential can be different in different parts of the cell: this leads to current flow, which takes time.
After an action potential, the axon hillock typically hyperpolarizes for a bit, sometimes followed by a brief depolarization. During that time, if there are other parts of the cell (such as dendrites) that are still relatively depolarized from a receptor potential, ions will be flowing from those areas into the axon hillock. This depolarizes the axon hillock, but again, this takes time (I'm purposely repeating that to convey a feeling of this all being a dynamic, moving process, with ions moving through each step). The amount of time it takes will depend on the voltage difference, so a bigger depolarization in the dendrites will bring the axon hillock back to threshold sooner.
Not that many ions flow during an action potential
This has been a recurring theme here, see this answer: Why is it possible to calculate the equilibrium potential of an ion using the Nernst equation from empirical measurements in the cell at rest?
The change in membrane potential isn't just because ions flow: it's because permeabilities change, briefly creating a new equilibrium potential. If you have in your mind massive quantities of sodium and potassium ions flowing, completely upsetting the ionic balance in the cell and drowning out all other electrical activity, you have it wrong.
Stimuli are often long-lasting
Especially if you are talking about a mechanical stimulus, most will last a lot longer than an individual spike, which is only ~1ms long. So although one transient stimulus can cause several action potentials, often what actually happens is that those receptor potentials are quite long lasting. Effectively, they set a new "resting potential" for the cell which is above the cells' firing threshold.
In summary:
Receptor potentials depolarize the cell, bringing them to or beyond firing threshold. An action potential starts in the axon hillock and propagates down the axon, but only has a minor impact on the rest of the cell. Importantly, the action potential is really brief, not many ions move, and there is current flow in both directions, so the depolarized parts of the cell are still depolarized somewhat even after a spike. As the initial axon segment recovers from post-action potential hyperpolarization and sodium channels leave their inactivated state, current from the receptor potential is flowing in, depolarizing the cell to threshold and causing another spike. Repeat.

"So although one transient stimulus can cause several action potentials, often what actually happens is that those receptor potentials are quite long lasting. Effectively, they set a new "resting potential" for the cell which is above the cells' firing threshold." --> Would this mean that it then takes less for cell to fire next (as the new resting potential is above the initial resting potential)? I am asking because that would be not consistent with adaptation (which I assume would increase the threshold)

@Pugl Both are possible, on different time scales. When held at a depolarized potentials, cells can somewhat paradoxically become less excitable: this is because of voltage-gated sodium channel inactivation. The more VG Na channels are inactivated, the fewer are available to open, so more depolarization is required to reach the positive feedback underlying an AP (it's possible to depolarize a cell enough that it can never spike, called "depolarization block"). Adaptation can also occur at multiple stages. I can't say much more about a general case.


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Bicarbonate concentration in saliva

From the picture it can be seen that Bicarbonate is secreted into lumen of duct of salivary glands by exchanging Cl- ions.
So if flow rate of saliva is increased then its obvious that less Cl- is taken in the cells and less bicarbonate is secreted out.

At high flow rates, there is less time for reabsorption and secretion, and therefore the saliva is most like the initial secretion by the acinar cells. Thus, with the increase in flow rate the concentration of ions changes2

But it is also said that when flow rate increases the bicarbonate concentration also increases and when flow rate decreases bicarbonate concentration also decreases.
Doesn't this contradict the former fact?

The introduction to this paper clearly states that bicarbonate concentration increases with flow rate.

When did I denied that? My question is if bicarbonate is exchanged with Cl- as in the figure then higher flow rate should decrease the bicarbonate concentration as per diagram, but its quite opposite. Why so?

Also if flow rate is slow then bicarbonate concentration n must be higher , since more time for its secretion , bur the final result is opposite again.

I don't understand why you assert that high flow rate would have that effect. In fact since it is clearly an incorrect inference I think that you need to explain your logic. 'I think this thing but it is wrong, why is it wrong?' Isn't a very good question.

Let me explain, primary saliva formed isotonic to plasma, then in the duct much of Cl- is taken in and HCO3- excreted out, so this implies that as long as the saliva is in ducts, its concentration of HCO3- should increase and Cl- decrease. if I am correct till here then slow flow rate means higher HCO3-, but the textbook says quite opposite.

If flow rate is high then less time for Cl- to be taken up and HCO3- secreted so in effect the HCO3- will be less compared to normal flow rate, but the text says quite opposite again.

But all of this assumes that the rate of bicarbonate movement is constant.

Isn't it depended on Cl-? If yes then why there is not a concomitant change in Cl-?

According to this:

Yet another significant finding was the discovery of HCO3− absorbing mechanisms like NHE3 and NBC3 (NBCn1-A) at the luminal membrane of the ducts, which suggested the ducts absorb and scavenge HCO3− in the resting state.

So, initially saliva is isotonic to plasma, it is both reabsorbed and secreted, if its flow is slow, more of bicarbonate is reabsorbed, if the flow is high less bicarbonate is reabsorbed. Therefore when flow rate increases bicarbonate concentration increases.

Source of image:

At low salivary flow rates, HCO3- is reabsorbed by the striated duct cells and so very little reaches the mouth. At high flow rates, the striated ducts can't keep up and so HCO3- reaches the mouth at high concentration (<25mM)).
This makes perfect sense, from a physiological point of view. HCO3- is valuable to the body and not something to throw into the gut for no reason. The main purpose of unstimulated saliva is to keep the mouth lubricated, help you to talk and so on. Unless you are feeding the plaque bacteria, there is no great amount of acid to neutralise and therefore no need for a high HCO3- saliva. When you feed yourelf, and also your plaque bacteria, you stimulate salivary flow and produce a high HCO3- saliva, with a high buffering capacity, just when you need it.(Source)