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Maternal immunity without prenatal vaccination?
It is recognized that antibodies from the mother provide a level of protection to infants. This is why mothers are often advised to get vaccinated when they're pregnant. However, does the vaccine have to be given during pregnancy or would a vaccine taken as a child-teenager, if still effective as an adult, function the same way?
I'll try to give an example to clarify. Suppose a person is fully vaccinated against Whooping Cough, at least based on the current schedule, but does not receive a pre-natal vaccination. Is it reasonable to suppose that if the vaccine is still effective and is causing the body to produce antibodies, that these maternal antibodies would be passed on such that the infant would still receive some protection that it would not receive had the mother not received the childhood vaccinations?
Further Detail
I am interested in this question because it could influence studies which look at rates of infection/cases in infants, in order to measure the effectiveness of cocooning. These studies assume that because these children are too young to be vaccinated, the vaccine cannot be influencing their susceptibility, except through cocooning. But if childhood vaccination results in a high enough IgG levels, that might not be the case, and so this result should be considered in such studies as this one.

Pre-conception and prenatal immunizations are recommended for several reasons, protection of the mother (during a higher risk period), fetus, and newborn. Pertussis is a very particular case. Can you clarify whether you're asking for your own family, or as a matter of general interest?

This is an immunological question. To what degree, if any, does vaccination of a person when she's young, increase the odds of maternally derived immunity against the pathogen?

got it. let me know if there's anything i didn't answer for you!

tl;dr

If a woman was vaccinated when she was a child, will she be able to provide passive immunity to her children?

It depends on the vaccine. Generally, if the mother still has high levels of protective IgG  during the third trimester (especially if it's type 1 or 4), those antibodies will cross the placenta and provide passive immunity to the newborn. In whooping cough, though, good levels of newborn IgG require vaccination in the third trimester.
Maternal immunizations
Immunizations are given to adult women prior to conception, while pregnant, and after delivery to protect the mother from infection, protect the fetus from infection, protect the fetus from congenital anomalies associated with maternal infection, and to protect the newborn from infection through passive immunity and through decreased exposure to infected contacts. The exact recommendations differ for different vaccines and different levels of maternal risk. From the same recommendation, you can see that some vaccines are recommended only if maternal antibody titers are negative and some are recommended regardless of maternal antibody titers or prior immunization.
Passive immunity of the newborn
IgG undergoes active transport from the maternal circulation to the fetal circulation across the placenta.

The reference linked above is an excellent review of transplacental antibody transfer and the science that underpins maternal immunization recommendations for passive immunization of the newborn (especially in the case of whooping cough). Key points here include:

Newborn IgG levels correlate with maternal IgG levels (i.e., the active transport mechanism isn't saturated in most cases). This suggests that low IgG for a particular antigen in the mother will result in low IgG for that same antigen in the newborn.

Antibody transport begins as early as week 14, but both the total transport and the rate of transport increases over the length of the pregnancy. This suggests an hypothetical optimum time for an intervention that would temporarily boost the level of any antibody.

Pertussis example
Whooping Cough, or pertussis, the illness caused by Bordetella pertussis, an encapsulated bacteria, is quite dangerous in the newborn. A few years ago recommendations for vaccination against pertussis were updated to immunization in the third trimester, regardless of the mothers prior immunization status. This recommendation is based, in part, on the understanding of transplacental transfer of IgG described in the article I linked in the earlier section, and in part on data on the association between timing of maternal immunization and fetal, all in the context of increased pertussis case rates.
Shortly after these recommendations were updated, additional, more thorough data confirmed this recommendation, though it suggested a slightly narrower window for the ideal time of Tdap administration (from 27-36 weeks to 27-30 weeks).
An aside re: the relationship between passive immunity of the newborn and childhood immunizations
Passive immunity from antibodies transferred to the fetus during pregnancy declines pretty sharply after birth. By 8 months the maternal IgG contribution is effectively gone. This is passive immunity because only the products of B-cells (the antibodies) are transferred. Immunization of the child, on the other hand, provides active immunity, because they develop the capacity to produce their own antibodies. I'd refer you to the allergy and immunology chapter of Bernstein and Shelov's Pediatrics for Medical Students, a surprisingly good general reference.
How should we interpret the linked article in the OP
This article is a comment on a very interesting study in baboons. It doesn't present any new data, but does comment on epidemiological data from a natural Swedish cohort between the discontinuation of whole-cellular pertussis vaccine 1979 and introduction of acellular pertussis in 1996. They reference this data through a misinterpretation of yet another study that analyzed infection rates between 1986 and 2007. The misinterpretation is as follows:

The (1996) drop was pronounced in infants too young to be vaccinated (Fig. 1A), itself a clear indication of herd immunity.

This is incorrect. That figure represents the decrease in infection rates for infants under 1 year of age at the point when vaccine was re-introduced. This included infants who were vaccinated (at 3 and 5 months).
The data before the re-introduction of vaccine, e.g., in 1995, though, does provide a good natural experiment for the epidemiology of pertussis in a non-immunized and immunization remote population. It had been 16 years since the use of whole-cell pertussis and you can clearly see the waning immunity in the population incidence as a whole. If you are really interested in digging into these questions, this cohort is a good place to start. Sweden is very good at collecting important data, so it may be out there.

Hello Dan, this is a good amount of information. However, while I agree that prenatal vaccination offers the best protection, the question I asked is if it is reasonable to conclude that childhood vaccination would result in high enough IgG levels to result in ANY maternally derived immunity.

Thinking about it, based on evidence that even after five years after the vaccination, there are still significant IgG levels and we've concluded that Pertussis antibodies can be transferred, it seems reasonable that, while maybe not enough to provide full protection, childhood vaccination could influence infant susceptibility to Pertussis infections.

@DanielGoldman both remote maternal immunization and maternal infection are considerations. Your question is very interesting. I'm not fully able to answer it, but there are probably data out there that could help. I've edited my question to address the article you linked, but I don't think that's going to be completely satisfactory :)

That's fine. The information that you've provided has been helpful. Maybe the lack of a complete answer is a suggestion that research should be doe on the topic. Shame I don't run a lab. I'd get right on it.

Is it reasonable to suppose that if the vaccine is still effective and
  is causing the body to produce antibodies,

Vaccines do not cause anyone to make antibodies their whole life.  Eventually, the antigen in the vaccine is cleared away, and the immune system stops reacting.  But memory cells have been created, which are ready to quickly re-active the immune system if the antigen is encountered again.
Think about it.  Can you name any childhood diseases that are known to usually skip a generation?  People lived for thousands and thousands of years with no vaccines, and everyone got every disease their mother got as a girl.

Vaccines do cause people to make antibodies their entire life. Long lived B-cells continue to secrete antibody at a low level. There is a not inconsequential circulating level of antibody present long after exposure to some antigens. Certainly the passive immunity from this circulating level of antibody is not the same thing as the robust response from an expanding clone of memory cells, but it is there, and is the basis for, among other therapies, IVIG infusions for primary immunodeficiencies. If you want to edit this answer, I'd be happy to upvote it.


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Is it possible to directly uploaded controlled imagery into a person's conscience?
I was wondering, is it possible to use electrical charges and/or EM waves to induce imagery directly into a person's mind?
I got this idea because since almost everybody dreams, and dreams are images created by the brain, i wondered if it was possible for an outside source to forcibly make someone see a different image without harming them.

In principle there's no reason why we shouldn't be able to do so. In practice, we do not seem to be anywhere near able to do so.
We are barely able to decode natural images from fMRI information, and before you can hope to induce imagery you should usually first be able to decode it.

This answer isn't all that different from answering a question like "Is it possible to travel faster than the speed of light?" with "In principle there's no reason why we shouldn't be able to do so" ...when physics kind of gets in the way it gets quite messy.

Except we already know that brains can be stimulated in the right ways so why would it not be possible by stimulating the appropriate regions directly?

I just think you are underselling the distance between current capabilities and what is necessary.

source: Stack Exchange

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

sort: votes


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What exactly does Curare do to the peripheral nervous system?
so, I was told:

If you give them the right dosage it'll wear off within an hour or two.
  It was used for veterinary stuff until they tried it on a human and realized it only paralyzed you and didn't block the pain. I don't know the exact dosage but if you go over the limit it'll start to relax the lungs
  So the exact dosage will be exactly enough to paralyze them without injury.

SO, naturally, I was wondering, what exactly does Curare do to the peripheral nervous system?

Curare is a plant alkaloid originally used as a poison on darts and arrows used in hunting. It is a competitive antagonist for the nicotinic acetylcholine receptor, which is found in the neuromuscular junction and autonomic ganglia.  We know a lot about this receptor and it's blockade by curare, so most good basic pharmacology textbooks devote a fair amount of space to it and you'll find mention in many physiology and neuroscience textbooks. I'd refer you to Goodman and Gilman Chapter 11 for a general reference.
The basics are as follows:
Curare is a quaternary amine. This means it has a charge on it and cannot cross the blood brain barrier. This was confirmed in 1947 by Scott Smith (pubmed link), an anesthesiologist, who administered very high doses of d-tubocurarine to himself (while under mechanical ventilation), resulting in complete paralysis but no central CNS effects. It's an interesting read if you get the chance, and records very carefully details of the minute by minute response for 4 hours of a series of administrations and reversals (with an acetylcholinesterase inhibitor).
What you get, as reported by Smith and confirmed by others, is blockade of motor outflow with skeletal muscle paralysis (including respiratory muscles) and also probably some ganglionic blockade (this is supported with further research since 1947). There are no changes in sensory inflow or any central effects. The blockade of the nicotinic acetylcholine receptors is reversed with an acetylcholinesterase inhibitor by increasing the amount of acetylcholine in the cleft to the point where it overcomes the competitive inhibition by curare.

+1 Were the reversals self-administered as well? ;-)

@uhoh that would be a real trick, wouldn't it.

The paper can be downloaded from the journals website. And since I am at home right now, there should be no paywall.

@Chris thanks for the non-paywall link. I added it to the answer.

Nice finding btw.

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


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Is it possible to re-align of SAM/BAM files?
I am carrying out some metagenomic comparison using whole genome sequencing approach. I would like to filter out reads from my files in a sequential manner, thus I would like to align to a first reference genome, then use the generated SAM/BAM file to extract the mapped reads with samtols view -F4, re-generate fastq files and align those to another reference genome. This decreases the size of the input and speeds the procedure.
Using BWA, though, I get an error of file synchronization when doing the second alignment:
[mem_sam_pe] paired reads have different names:
"HISEQ:90:C3UNJACXX:1:1107:16388:61141",
"HISEQ:90:C3UNJACXX:3:1303:2008:58095"
[mem_sam_pe] [mem_sam_pe] paired reads have different names:
"HWI-ST1437:64:C3UM1ACXX:4:1214:3833:62731",
"HWI-ST1437:64:C3UM1ACXX:4:1202:18519:45906"

This is weird since the fastq files were generated by the filtered BAM file, samtools should have known how to keep the synchronization of the files.
My question is: is it possible to realign a BAM file? maybe not with BWA, at least with another tool?
Thank you.
The procedure I carried out is:
# align
bwa mem -R <read_group1> <ref.fa> <file1_1.fq> <file1_2.fq> -o <file_aln.sam>
# convert
samtools view -Sb <file_aln.sam> > <file_aln.bam> # sort samtools sort <file_aln.bam> -o <file_alnSRT.bam>
# select mapped
samtools view -h -F 4 <file_alnSRT.bam> -o <file_alnMAP.bam>
# convert to fastq
samtools fastq -1 <filemap_1.fq.gz> -2 <filemap_1.fq.gz> <file_alnMAP.bam>
# re-align
bwa mem -R <read_group> <ref2.fa> <filemap_1.fq.gz> <filemap_1.fq.gz> | samtools sort -o <file_realign.bam>

Looks like I solved it by using PICARD: extracting the aligned reads but without sorting, I used
java -jar picard.jar SamToFastq I=<file_alnMAP.bam> FASTQ=<filemap_1.fq> SECOND_END_FASTQ=<filemap_2.fq>
bwa mem -R <read_group> <ref2.fa> <filemap_1.fq> <filemap_1.fq>

From samtools flagstat the output looks fine.


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Palaeontology and Palaeobotany
Could someone please clarify the roles and differences between palaeontology and palaeobotany. My textbook says the palaeobotanists study plant and animal fossils, but other sources say that this is incorrect.
Thanks

Paleontology is the main scientific branch, which study fossils and prehistoric times.

Paleozoology studies the fossils and biology of prehistoric animals.
Paleobotany studies fossils and biology of prehistoric plants.
Paleobiology studies the biology of prehistoric organisms.
Paleoecology studies the prehistoric ecological systems and ecology.

In fact, putting the prefix "paleo-" turns every scientific branch of biology to a branch concentrating on this subject but in prehistoric times.

For the most part a Paleontologist will be willing to study whatever their fossil site produces. Which is why many scientists who are really "paleozoologists" just call themselves paleontologists.


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Caterpillar resembling a snake
I found a very interesting caterpillar. It's 5 cm long and  looks like a snake. I discoved it in a greenhouse on a vine in the Czech Republic.

I found two types: a green one and a brown one, both with same length.

What species is it?

Looks like the larvae of an elephant hawk moth (Deilephila elpenor).

 Green Variant. ©2005 Henk Wallays  (CC BY-NC 3.0)

In the Sphingidae family (like the snake-mimic caterpillar in this post).

Description: typically brown-gray color with black dots along length of body. Young larvae are yellowish-white or green, but some mature larvae also can be green colored. Fully-grown caterpillars reach 7.62 cm in length.

Have a backward curving spine or "horn" on the final abdominal segment.

 D. elpenor color variation. Source: A.R. Pittaway & I.J. Kitching
Range: Most common in central Europe and is distributed throughout the palearctic region.
Habitat: variety: including rough grassland, heathland, sand dunes, hedgerows, woodland, open countryside, and even urban gardens.
Source: Wikipedia


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Is this a leafhopper? (Italy)
I'm located in Bologna, Italy, in the city center. I found this insect on by bean plants, I think it's feeding on their leaves.

What is it? The answer to this question suggests that it is a leafhopper, but I can't find the exact species. When approached, they seem to jump away.

 Altough related to the question I linked, I don't think it's a crosspost, because in that question I want to know primarily what's the solution to the problem of white spots on bean leaves, while here I ask for the exact species in the photo.


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Gene flow analysis with a single mitochondrial marker
I am currently studying a mud snail genus called Ecrobia. Several species of this genus occur in both the Mediterranean and Black seas. Therefore, I would like to investigate whether there is:

Intraspecifc gene flow between the Mediterranean and Black sea populations
Interspecific gene flow between the Ecrobia spp. occurring in the same water body

Therefore, I have a couple of questions:

Is it possible to perform a gene flow analysis with a single mitochondrial marker (COI)? If so, which program could I use to run the analysis?
Ideally, how many individuals per population are required? If I don’t have enough individuals, is there a rigorous way of clustering populations?


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Identify a lone bone (jaw including teeth) found on a beach at Trouville-sur-Mer (France) in 2018
Found this on the beach at Trouville-sur-Mer in France, on 11 May 2018. It was laying in the sand, close to a trash can. Considering the strong smell of sand within the skeleton, it must have been near the sea for a very long time.

What species is this from?
Also posted on other identification websites and fora:

https://www.inaturalist.org/observations/14323892
https://observation.org/waarneming/view/160056539
https://forum.waarneming.nl/smf/index.php?topic=431852.0
http://www.nhm.ac.uk/natureplus/message/115302/

The length of the bone (the piece remaining) is under 12 centimeter.
The height of the only easily removable tooth (the smallest remaining one) is under 25 milimeter.

Old pictures in sunlight (all in low resolution & without measure bar):
Click the images for enlargement.

Update of 22 July 2018 (most in higher resolution & with measure bar):
This new set of pictures is archived at Wikimedia Commons.

Jaw with teeth (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, length smaller than 12cm, side A, photographed on 22 July 2018 - Image 1 of 3

See Wikimedia Commons for a higher resolution.

Jaw with teeth (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, length smaller than 12cm, side A, photographed on 22 July 2018 - Image 2 of 3

See Wikimedia Commons for a higher resolution.

Jaw with teeth (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, length smaller than 12cm, side A, photographed on 22 July 2018 - Image 3 of 3

See Wikimedia Commons for a higher resolution.

Jaw with teeth (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, length smaller than 12cm, side B, photographed on 22 July 2018 - Image 1 of 2

See Wikimedia Commons for a higher resolution.

Jaw with teeth (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, length smaller than 12cm, side B, photographed on 22 July 2018 - Image 2 of 2

See Wikimedia Commons for a higher resolution.

Jaw with teeth (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, length smaller than 12cm, top side, photographed on 22 July 2018 - Image 1 of 3

See Wikimedia Commons for a higher resolution.

Jaw with teeth (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, length smaller than 12cm, top side, photographed on 22 July 2018 - Image 2 of 3

See Wikimedia Commons for a higher resolution.

Jaw with teeth (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, length smaller than 12cm, top side, photographed on 22 July 2018 - Image 3 of 3

See Wikimedia Commons for a higher resolution.

Smallest remaining tooth from jaw (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, height smaller than 25mm, side B, photographed on 22 July 2018 - Image 1 of 2

See Wikimedia Commons for a higher resolution.

Smallest remaining tooth from jaw (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, height smaller than 25mm, side B, photographed on 22 July 2018 - Image 2 of 2

See Wikimedia Commons for a higher resolution.

Can you do a close up shot of the teeth from above, so we can see the crown layout, that is one of the main ways to identify mammal material.

Sasquatch for sure :p.

@John I have now added new pictures, including the teeth from above.

It would be great to have a scale bar in the photo, so that the size would be easier to determine. However, by the shape of the teeth, I will propose that it is the back half of the jaw of a pig. Here is an image from the National Maritime Museum:

This one is from Vanuatu and has a rather elaborate mesial portion of the jaw, but the teeth look very similar. It's virtually impossible to know the bone's age or species, however.

Thank you for your answer. Yes, posting these images on Identification apps/websites/fora, I also became aware of the usefulness of a scale bar. Within a couple of weeks, I can take high-resolution pictures with a scale bar. --- Do you think any conservation archive, museum or researcher could be interested in analysing or conserving the specimen? How would I be able to find such an interested party easily?

without knowing what rock it came out of there is not a lot that can be done scientifically with what you have. Although someone might be interested in trying to figure out where i eroded out from. Contact the nearest natural history museum.

I agree with @John. Without additional provenance information, it's not much use scientifically. However that does not mean that a local museum would not be interested in it for display.

@kmm I have added new pictures, which show the bone with teeth from above and also feature a scale bar. Please update your answer if appropriate.


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How do plants absorb CO2?
I see many repeated claims that plants absorb $CO_2$ from the air.
$CO_2$ goes into the stomata, while $H_2O$ evaporates and leaves those same stomata. The $CO_2$ dissolves in the water in the plant sap, and then goes to wherever it's needed.
It occurred to me that in loose moist topsoil, there is a tremendous surface area for $CO_2$ to leave air and get into the water. And that water does get absorbed by plant roots. Meanwhile there is plentiful O2 that soil bacteria can use to oxidize organic matter in the soil and convert it to $CO_2$. In my imagination, this looks like a far more efficient way to collect $CO_2$. Instead of wait for the $CO_2$ from decaying organic matter to diffuse out of the soil into the air above and then enter stomata and dissolve in water there, cut out the diffusion step. The rising sap would carry $CO_2$ to wherever it will be used.
It seems to me this would be easy to test. Grow plants in sealed containers with their stems sticking through small holes in an impervious barrier. Introduce $CO_2$ containing $C_{14}$ either into the air above with the leaves, or into the air below with the soil the roots are in. Observe which way gets more $CO_2$ incorporated into the plants.
Have experiments like this been done? My quick search did not find experiments like that. It found only the many-times-repeated claim that plants absorb $CO_2$ through their stomata.

Carrying CO2 "in the sap" is not that easy of a step, especially compared to simple diffusion: as plants do not significantly decrease the local CO2 level, diffusion is basically a free pump insuring constant CO2 concentration. Furthermore, while CO2 does dissolve into the water, its concentration is rather low naturally. (Natural fluids that transport CO2 in large quantities, such as blood, have enzyme like carbonic anhydridase to create bicarbonate for mass transport; which soil water won't have.). Also, it maybe possible to disprove this theory by just cutting a leave and using the c14.

You see many repeated statements (not claims) that plants absorb CO2 from the air through the stomata of their leaves. For example, you can read an account of this in Lodish et al., Molecualr Cell Biology. This is because the phenomena has been studied by numerous professional scientists for over 50 years. Your question shows a lack of the research required before posting on this list. If you had done that you might have discovered that typical experiments use (rootless) leaves and manipulate the CO2 concentration. I have voted to close.

Thank you for the link. This link shows that plants absorb CO2 in the mesophyll, from the air space. Water from the xylem evaporates into this space and leaves through stomata; this drives the movement of water from the roots. O2 created by plants also leaves through stomata. It does not show that the CO2 comes only through stomata and not with the water. Using rootless leaves would prevent roots from collecting CO2, though. Still, normal photosynthesis with no root and only normal CO2 air levels would plausibly say that CO2 from air is enough.

Eliane B, thank you for responding. I think that since CO2 level in soil air can reach as high as 8% during wheat cultivation, it seems plausible to me that plants might find a way to sequester that resource rather than just let it diffuse into the outer air and then concentrate it again from there. And that probably happens. https://www.nature.com/articles/415451a

For most terrestrial plants, assimilation of soil inorganic carbon seems to be quite low. This may be because RuBisCO, the carbon assimilating enzyme, is generally more of a limiting factor than CO2 diffusion.
Ford et al. (2007) found that "soil DIC [dissolved inorganic carbon] contributed ~0.8% to whole-plant C gain, and ~1.6% to belowground C gain" in seedlings of Pinus taeda exposed to 13C-labeled soil DIC. Ubierna et al. (2009) observed no contamination in leaf CO2 efflux by 13C-enriched soil watering of large conifers, despite showing that the water was taken up by the trees. However, Bloemen et al. (2012) did observe assimilation of labeled carbon directly infused into the stems of poplar trees.
Some aquatic plants in certain habitats may be adapted to assimilate much more carbon via their roots.
Plant physiology is a rich and mature field, and isotope analyses are a primary tool with a long history. Additionally, CO2 and other gas exchange can be directly measured across leaf surfaces.
The carbon flux between the soil and the rhizosphere is complex and bi-directional, but overall, more carbon is generally lost through the roots than absorbed.
There are also dozens, or probably hundreds, of studies labeling leaves or above-ground material in various ways and tracking the fate of those elements, of which this is just one.

Thank you! I'm an amateur at this and my quick lit searches didn't find this.

Thanks to David's comment above, I learned enough vocabulary to do a better lit search.
Yes, $CO_2$ supplied to roots is absorbed and distributed by the xylem to places where it is photosynthesized. This is not in doubt.
The remaining question is how much of the $CO_2$ used by plants comes through stomata from the outside air (where it is present in concentration around 0.04%), and how much of it comes to roots from subsurface air (where it is present in concentration that varies widely, up to 8%).

The water in the plant absorbs Co2 from the air, Co2 dissolved in water equals H2CO3 carbonic acid, but carbonic acid is an extremely weak acid since it does not ionize sufficiently to produce a very high hydrogen-ion concentration. Glucose production from Co2 & pure H2O requires an electron to be in two places at the same time, absorbing light energy by this electron, de-crystalizes some of the electron working-mass that is responsible for rearranging Co2 & H2O into the crystaline C6H12O6-glucose molecule. The process of photosynthesis is one of "particle-flow" within a plant molecule and molecular bulk-flow within that same plant is a process of respiration. Respiration must also have a working-mass as well, H2O is one of the primary open-loop vehicles and light is the other primary open-loop vehicle that drives the closed-looped function of a plant. Being the difference between the interference of particle-flow in an inertial frame of reference, and the interference of the acceleration & de-acceleration of bulk-flow in a non-inertial frame of reference. Photosynthesis has similar characteristics as a alternating current transformer, they both are frequency dependent and use electrons to drive the machinery that absorbs & transforms Co2 with other molecules.

Welcome to Biology.SE. Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. ——— Answers should directly and clearly address the original question — yours is very hard to follow (try adding some formatting and make sure you read the entire question). Answers are also much more likely to receive a favorable response when they include supporting references (primary literature is best). Without that support, answers are indistinguishable from opinion and thus are inappropriate for this site.

@user62753, one way the CO2 diffuses into stomata and inside the leaf the exposed water dissolves CO2 which is then converted to something else that's easier stored. The other way, CO2 would diffuse into water adsorbed onto soil particles and then be taken in by roots where it would be converted into the same transport molecules. It makes sense to me it would happen both ways. The CO2 concentration in the upper air is 0.04%, while the CO2 concentration in the air near roots can reach 8%. My claim is testable, it has been tested, and it is true.


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Polar renal scarring in pyelonephritis?
Why does infection and scarring occurs at poles in Vesicoureteric reflux but not in Obstructive pyelonephritis?

It is said in Robbins that, it is due to polar papillae being flattened or concave unlike convex lateral papillae, but why is it not the case in obstructive pyelonephritis?
Also why polar papillae are not convex?

It's more an issue of the extent of reflux than anything else. If you look at the data on scarring, you'll see that grade III and IV VUR present with lateral scarring as well. So, any pyelonephritis that is associated with gross dilation of the ureter and collecting system will give diffuse scarring. Mild dilation, you'll get scarring where the reverse flow goes first. I can't answer the question about why the reverse flow goes to the poles first. The authors of the paper I linked have their own speculation. Robbins has another. Neither have evidence on the mechanism.


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Does adenylate cyclase stimulate or inhibit acid secretion in the stomach?
I am confused about my teacher's notes.
"Acid secretion is stimulated by ACh, gastrin and histamine.
Histamine stimulates adenylate cyclase which increases cAMP production."
When I looked this up apparently gastrin decreases AC (adenylate cyclase) production. If histamine and gastrin both stimulate acid secretion why does one increase and the other decrease AC?
Also in her notes the acid secretion inhibitors are acid, protein, fat as they cause the secretion of CCK and secretin and these stimulate AC. But I thought AC stimulated acid secretion not inhibited it?
Thank you.

Can you share your reference for your reading about gastrin decreasing adenylate cyclase? In parietal cells, gastrin acts through a separate second messenger system, $IP_3$ and $Ca^{++}$, where histamine acts through cAMP.

That makes more sense. Does the CCK only use AC to stimulate acid secretion then? I think CCKb receptor is used to stimulate acid secretion and inhibit it by the CCKa receptor? It says this in my teachers notes: "CCK and secretin both act to stimulate adenylate cyclase (pro-secretory): hence, actions on acid secretion are indirect." but why are CCK and secretin in the inhibitory section of gastric secretion.


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Spermatogenesis question
I found this diagram in my textbook regarding the process of spermatogenesis. But, I doubt if the labelling done is correct or not. Especially, I can't figure out any difference between the cells labelled as spermatids and those as spermatozoa. Also, I doubt the labelling of Sertoli cells.
Please help me clarify my doubt.

As per my textbook,

The spermatids are transformed into spermatozoa (sperms) by the process called spermiogenesis. After spermiogenesis, sperm heads become embedded in the Sertoli cells, and are finally released from the seminiferous tubules by the process called spermiation.

I edited your question to convert the image of text to actual searchable text.

Notice the cell labeled "spermatid" is still attached to the Sertoli cell. Once released from the Sertoli cell, spermatids are called spermatozoa.
This process (release of the spermatid to form a spermatazoon) is called spermiation
EDIT
The text you added is still correct, but not well explained. Spermiogenesis is the development of the spermatid, the haploid 1N gamete produced by the second meiotic division, into a cell with a long flagella with a small amount of cytoplasm. Spermiation is the release from the sertoli cell. Both spermiogenesis and spermiation are involved in the development of a spermatid to a spermatozoon, but the specific point where we stop calling them spermatids and start calling them spermatozoa is release by the Sertoli cell, or spermiation, a substantial process in its own right. Both spermiogenesis and spermiation are important steps in the conversion of the haploid 1N gamete to a motile, free spermatozoon.

Your answer does not match at all to the theory in my book. Please see my edited question again and help me out. Thanks.

@DJKoustav your text is still correct, but not well explained.

@DJKoustav If my answer doesn't fully answer your question now, let me know. Otherwise, please mark it the answer by checking the gray checkmark next to it. See someone answers. Thanks!


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Succulent weed identification
There is a succulent-looking weed growing in a crack in my driveway. What is it?

Conditions: Dry, full sun, asphalt & gravel, no competition.
Date: 2018-07-16
Location: Toronto, Ontario, Canada
Size: 40cm x 40cm x 2cm

I am not familair with the flora of the New World, but this looks like Common purslane, Portulaca oleracea

@RHA is correct, it is Portulaca oleracea (RHA you should put this as an answer).  This is purslane in one of its favorite and classic environments, a driveway crack!  If this specimen has not been sprayed, you might taste a few leaves -- people put it in salads. And if don't want it around, pull it now, it is about to bloom and the seeds will be abundant.

This is Common purslane, Portulaca oleracea. It is used in salads, although it contains oxalic acid and there are poisenous plants resembling Purslane, see comment below.
https://en.m.wikipedia.org/wiki/Portulaca_oleracea

An acquaintance advised me of this: 1) Make sure you can distinguish it from hairy-stemmed spurge (which is poisonous) 2) Purslane contains oxalic acid, so those at risk of kidney stones should not eat too much! More info here: https://jstookey.com/node/214


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Does pouring water on your skin affect the evaporation process and heat loss?
Recently I've been playing football in the sun pretty hot temperatures. During the water breaks I tend to pour a lot of water over my head to cool me down, now this has an instant effect on cooling me down but in the long run would this have any affect on my body temperature? We know that the body cools itself by using heat to evaporate sweat on skin, would drenching  my head and face in cool water affect this process or not?

Drenching your head and face with cool water will both directly cool your skin (because cool water is colder than you) and contribute to evaporative cooling. Your skin doesn't care if the water that evaporates comes from sweat you made, the pool, a water bottle or a hose.
The Khan Academy video is a good review of the principle.


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Black oyster of sweet water
I have seen recently a documentary starting with introducing of the spectacular black oyster of sweet waters which imitate exactly like a prey fish in order to convey its eggs to predator fish's gills, while it had no eyes to see the form of prey fish favored by the predator fish.
The amazingness of what this creature do provokes me to ask some questions about this strange creature and know more about this odd phenomena and theories represented for evolving of such marvelous creature.
How the black oyster detect completely kind of prey fish which is favourite food of target predator fish ,and make a very detailed simillar image of it in order to deceive the target fish while it has no eyes to see?

I believe you're talking of the members of the families Unionidae and Margaritiferidae, which have a larval stage called glochidium. From the Wikipedia page linked here:

This larva form has hooks, which enable it to attach itself to fish (for example to the gills of a fish host species) for a period before it detaches and falls to the substrate and takes on the typical form of a juvenile mussel. Since a fish is active and free-swimming, this process helps distribute the mussel species to potential areas of habitat that it could not reach any other way.

This interesting study about phylogeny of these species shows that lures mimics mainly fish, but also different prey species such as insect larvae. Some species display an aspecific lure, while others show fine mimicking in order to attract a precise set of host fish species.
As to how luring evolved:

What drives the evolution of luring? Very little is known about what drives the evolution and diversification of luring, which has evolved independently multiple times. In Lampsilini mussels, luring appears to have arisen early, and the complexity of the lure has increased through the lineage. It is likely that diverse selection pressures govern the evolution of luring. One hypothesis is that luring increases the rate of prey encounter without incurring the metabolic costs associated with active search and pursuit. Alternatively, luring may present predators with an opportunity to exert control over a prey’s movement, reducing the risk of injury when hunting. Luring systems present a unique opportunity to understand signal design and evolution.

Do oysters need to see in order to evolve the lure?
No. Evolution of a body part does not require sight or will. From this blog post:

Note that [...] the mussel can’t see the fish it’s parasitizing.  In this case natural selection is literally blind. Those mutations in the mussel that make its brood pouch look more fishlike will give it a reproductive advantage over its confrères, even if it can’t see the fish it’s deceiving. Note as well that selection has “acted” (I’m anthropomorphizing here: selection doesn’t really “act”, for it’s not an external force but a process of gene sorting) not just on the appearance of the mussel, but on its behavior.  It has genes that make it wiggle its brood pouch in a fishlike manner.

The mechanism is all here:

1st step: mutations that modify the coupling of fish bites and glochidia release/mantle shape/the movement of the mantle arise.
2nd step: The bearers of favourable mutations will have more progeny and the population will have more and more bearers as generations pass.

No need of being conscious about anything. :)


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White resin or powder on conifer needles
I often notice that certain conifers often have a whitish powder on what seems to be their youngest needles, giving them a blue green tint. Does anyone know what this is? Is it something excreted by the trees themselves, is it a yeast or some other endophytic microorganism? Very curious and unfortunately I don't have a microscope.

I believe this is actually crystallized sap which formed on and around the bud as the bud opened up and new leafs emerged.
Note that some coniferous trees have a powdery coating as part of the leaf itself, continuing on throughout the life of the leaf. Blue spruce is a good example of this, as its dark green needles appear blue/gray due to a waxy coating the needles. This wax can be easily scraped off the leaf.

Thanks for your answer! In the case of blue spruce, does the powder diminish overtime, for example on shaded needles that receive less sunlight?

Great question @DezmondGoff. I can confirm that conifers with powdery or waxy needles will have patches with significantly more or less coating, but I don't know what the causes of that are (whether it's time, sunlight, types of leaf).


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What values to be taken for x-axis and y-axis?
I did a lab on form and function in photosynthesis and I recorded the values of absorption spectrum in spinach chlorophyll extract. I have the following data and I need to draw a graph. I didn't understand what I should take for x-axis and for y-axis. Can anyone please explain this.

Are you trying to plot the slope, or are you also trying to do linear regression as well? The answer and sources that I give you depend on this.

@NabeehaChowdhury I need to draw a graph which describes, how many peaks does the absorption spectrum contain? and at what wavelength is the photosynthesis greatest? How does the color of an angiosperm leaf relate to the absorption spectrum you have generated?

It doesn't matter really, but for aesthetics sake, you'd plot the wavelength on x and the absorbance on y. We tend to visualize such data as spectral or absorbance as "peaks" on the range of interest. There's a fairly good example here. It has something to do with convention: traditionally
 the independent variable on x and the dependent variable on y. There's a good answer on cross-validated on the matter, too.


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Can toilet or sewage aerosol transfer eggs of human parasites?
Flushing a toilet produces hundreds of thousands of tiny droplets containing viruses and bacteria (source).
Additionally vomit and feces of infected people sometimes contain extremely high concentrations of viruses or bacteria.
Similarly, sewage water produces droplets and was proposed as the transmission mode in the SARS outbreak in Hong Kong in 2003.

Apart from viruses and bacteria being transferred through toilet and sewage aerosol, can human parasite eggs be transferred as well given the droplet size?
I'm interested in the aerosol, not the relatively large droplets that land on the toilet itself.

Common small protozoa that are present in infective loads in stool have not been documented in toilet aerosols. The size of the organism is going to be an issue here. As you can see from this table from the CDC, intestinal parasites (and ova) of concern to human health are larger than most droplets. Compare, E. coli and Shigella (0.5 - ~2 $\mu m$). Salmonella tends to be a litter larger (up to 5$\mu m$), but I expect those 5 $\mu m$ specimens are not the ones transmitted through aerosols. Cryptosporidium would probably be the most likely candidate, and that's one shown in the first linked study to not be present in aerosols. I wouldn't say it's impossible, but certainly transmission through aerosolized particles is less likely than for the smaller viral and bacterial organisms.


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What diurnal red & black moth is this?

Seen today on a hot summer day in Stockholm, Sweden. Length around 25 mm.

Looks like a six-spot burnet (Zygaena filipendulae)

Diurnal moth of the Zygaenidae family.

Description:

has a wingspan of 30–40 mm (1.2–1.6 in)...The fore wings are dark metallic green with six vivid red spots (sometimes the spots are merged causing possible confusion with other species such as the five-spot burnet). Occasionally, the spots are yellow or even black. The hind wings are red with a blackish fringe. The larva is plump and hairy with variable markings, usually pale green with rows of black spots.

Habitat:
meadows, woodland clearings, sea-cliffs and rich, grassy/flowery areas.
Range:
common throughout Europe, June - August.
Sources:
wikipedia


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Why is exercise good?
The fact that exercise is healthy is a bit counter intuitive to me. If we have any machine, a car for example, the less we use it the longer it lasts. Then how is it that using our body to do sports, to a reasonable amount, lead to longer or healthier life?
My guess is that lack of activity might resemble starvation no matter how much food we consume. Then the body instead of repairing itself tries to save energy as much as it can. Are there any other ideas to explain why exercise is good?

Re "the less we use it the longer it lasts", this is simply not true.  Machines do degrade from not being used: lubricants harden up, corrosion takes place, &c.  See e.g. "ramp rot" in airplanes, or "barn find" in cars.  OTOH, a well-maintained machine lasts longer than a neglected one: I personally fly a plane built in 1966, and drive a 1988 truck.

This question, as formulated, doesn't have a good scientific answer.

There is a similar question and answer here: https://health.stackexchange.com/questions/16786/how-does-exercise-improve-health

You may want to look into Hormesis. However, the idea that exercise works via (mitochondrial) hormesis seems controversial.

As jamesqf points out in comment, "the less we use it the longer it lasts" isn't always true even of machines. Sometimes if a machine isn't used, the moving parts start sticking together through rust or other decay processes, which does not happen when the machine is used and the moving parts move regularly against each other.
Another example that comes immediately to mind is a hybrid car, which needs to be driven regularly or the battery runs out. Granted this doesn't affect the car's longevity (I think?), but it is another example where use maintains functionality better than disuse does.
This is even more true when we actively maintain machines, fixing them as they break, replacing parts, oiling, etc.
The key point here is that decay is inevitable. It is a law of thermodynamics, and it doesn't care whether something is in use or not. Granted, things will sometimes decay faster if they're used, but not always, and they'll always decay either way. The only way to forestall decay is active maintenance. This isn't contradictory with decay being inevitable, because you can actively maintain something only for so long (it takes work and energy).
This is relevant to biological system because that is how our body works: it is constantly self-repairing and self-maintaining, for the length of the person's life. One reason we die is that it stops doing so as efficiently as one ages. But as long as we are living, these processes mean our bodies aren't a static object: they are a dynamic system that is constantly reacting to outside and inside stimuli. And that system, including the self-repair mechanisms, are set up such that they work best within a certain range of motion and activities. It so happens that range doesn't include "no motion or activities". Likely because we evolved as an active species, so being able to function efficiently when active is useful, and some of the things that make us able to function efficiently when active can cause some harm when we aren't. For example, we store fat in order to use it when food isn't available and as fuel for effort, but if too much of it accumulates it has effects on hormones and inflammation that our bodies don't deal with well. Another example is how our muscles waste away when we don't use them; this is useful for an active species that needs the muscles it uses and shouldn't waste energy and protein on those it doesn't, but an inactive species might be better off conserving its muscles through periods of inactivity, so that they would still be capable of moving well those rare times they do need or want to.
Having said that, look at high-level athletes getting injured, getting early arthritis, etc... It is possible to exercise more than the body's self-reparation abilities can handle, and that also leads to health problems down the road.

Do you have a particular source that maintenance activity is (roughly) an inverted U-shape with respect to stress?

@qeschaton: I'm not sure I made a claim that precise; indeed I don't think I said anything more precise than that a lack of activity/exercise is not very healthy, some amount of exercise/activity is healthier, and a sufficiently-high amount of exercise/activity can be harmful. Is that what you want a source on?

I'm interested in a source for "And that system, including the self-repair mechanisms, are set up such that they work best within a certain range of motion and activities." The more quantitative the better.

I don't have a source for that, I was working from the general principle that systems that work, have certain circumstances under which they work more or less well, and the most basic distribution of those circumstances is a bell curve, and that happens to fit the overall picture here. For quantitative sources of how that applies to the human body, any quantitative source will involve a very specific subset of the question, like the relationship between some specific form of exercise with a specific health outcome. But I can look and see if I find anything.


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Why did we evolve to be able to see this specific set of wavelengths only?
It is understandable that life didn't evolve the capability to sense all wavelengths of light, it simply didn't need it. My question is, why did it evolve the set of wavelengths it has, for example, the human visible range is 390-700nm, so why couldn't it be a different set of wavelengths, like, (say) 300-620nm? Is there a reason for it?

I also think this is a duplicate of above linked question

Well humans actually have a reduced spectrum compared to non-mammals. Reptiles and birds have 4 color sensitive cell types (cones), mammals lost two of these as modern mammals are descended from early mammals who were nocturnal. Primates evolved a third cone, (a mutant variant of one of the two they had before) Primates did this because many a frugivores and color is excellent for determining when fruit is ripe.

Can you add your sources?


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Can you identify the species?
Sighted today. Its feathery tail was moving.

Please see https://biology.stackexchange.com/tags/species-identification/info and edit your question.

Using your link and a basic Google search using your descriptive words "moth with feathery tail", similar images were found.  It appears to be a female moth of the genus Diaphania.  There appears to be many species in this moth genus, and several look similar. Assuming you live in North America, it is probably Diaphania hyalinata. It is most commonly called "melonworm moth" and looks exactly like your linked image. Apparently they can do garden damage and can be considered a garden pest. That was good coffee.
https://en.wikipedia.org/wiki/Diaphania
https://bugguide.net/node/view/237001/bgimage
https://bugguide.net/node/view/7924/bgpage
http://www.growingproduce.com/vegetables/pest-of-the-month-melonworm-2/


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Mechanism by which hypokalemia reduces insulin secretion
Is there any known mechanism by which hypokalemia reduces insulin secretion?

This video explains a mechanism, but its inherently wrong because ATP dependent K+ channels will allow movement of K+ from inside of cell to outside.

tl;dr
Hypokalemia hyperpolarizes membranes by increasing the $K^+$ gradient, making $\mathcal{E}_K$ and consequently $\mathcal{E}_m$ more negative. This makes any signaling event controlled by depolarization less responsive.
It's complicated, but we can understand the effect by looking at $K^+$ alone
Good catch. Yes, the video (and diagram) are incorrect. The electrophysiology of pancreatic $\beta$-cells is still an area of active research. Your textbooks (e.g., Costanzo Chapter 9, under Regulation of Insulin Secretion) will tell you that an increase in the $\frac{[ATP]}{[ADP]}$ ratio closes ATP-sensitive $K^+$ channels, which depolarizes the membrane. This is, in large part, correct, but not thoroughly understood, and not only by decreasing the $K^+$ conductance of the membrane. Further work in the years since that linked article supports the importance of a $Cl^-$ gradient and anion current, but $K^+$ conductance is still involved, and probably still underlies the mechanism through which hypokalemia reduces insulin secretion.
Membrane potential is determined by the concentration gradients and permeabilities of ions
The membrane potential of the pancreatic $\beta$-cell, as with the neuron, is determined by both concentration gradients and permeabilities of the membrane to ions. I'm sure the OP understands this, but for the general reader, you can read about this basic principle in any neuroscience or physiology textbook. You can calculate the membrane potential using the Goldman equation or chord conductance equation. Both are representations of the same principle, but I think the chord conductance equation is more intuitive. We'll simplify for our purposes to.
$\mathcal{E}_m  = \frac{g_{i}}{g_T} \mathcal{E}_i + \frac{g_{j}}{g_T} \mathcal{E}_j + \frac{g_{k}}{g_T} \mathcal{E}_k + ... $
Here, for ions i, j, k, ..., the membrane potential is equal to the sum of a series of terms for each ion, with each ion term being a product of the equilibrium potential of that ion ($\mathcal{E}_i$) and the portion of the total conductance across the membrane that the conductance of that ion represents. Conductance can roughly be understood as permeability. More open ion channels means a greater permeability/conductance to that ion.
Short term changes in membrane potential used in signaling are accomplished by changing the conductance of the membrane to specific ions. If the $\frac{g_i}{g_T}$ increases for ion i, the membrane potential moves closer to the equilibrium potential for ion i.
The concentration gradient determines the equilbrium potential
Each ion has an equilibrium potential, a membrane potential at which the net current of an ion across the membrane is 0. From the Nernst equation, we can say:
$\mathcal{E}_i \propto log_{10}\frac{[I]_{out}}{[I]_{in}}$.
Here $[I]_{out}$ is the concentration of the ion outside the cell, and $[I]_{in}$
is the concentration inside the cell. We've eliminated the proportionality constant because, in physiological conditions, it's constant, it's different for pancreatic $\beta$-cells (vs. neurons), and it's not relevant to our discussion (since we're not going to make any calculations with real numbers. If you are very careful, you'll notice the log term has outside concentration on the top, inside concentration on the bottom. You may find the Nernst equation written with a negative proportionality constant and with the inside concentration on top. These are equivalent because of how logs work.
Changing conductance, or permeability, changes the membrane potential
When you increase the conductance of a membrane to a particular ion, the membrane potential moves closer to the equilibrium potential for that ion. This is why in the neuron, for example, increasing the conductance of the axon membrane to $Na^+$ causes depolarization. The equilibrium potential $\mathcal{E}_{Na}$, is positive. The resting membrane potential is negative. Higher permeability to $Na^+$ moves the membrane potential closer to $\mathcal{E}_Na$.  Similarly, increasing the conductance of the axon membrane to $K^+$ (after the membrane has depolarized) repolarizes and then hyperpolarizes the membrane. $\mathcal{E}_K$ is negative (more negative than resting membrane potential). Higher permeability to $K^+$ moves the membrane potential closer to that large negative $\mathcal{E}_K$.
Increasing the permeability of pancreatic $\beta$-cells to $K^+$ hyperpolarizes the membrane
I'm using examples of the neuron because this is typically where these concepts are most thoroughly taught, but lets try to apply our understanding to the pancreatic $\beta$-cell. Concentrations, permeabilities, and membrane potentials are a little different, but not that much. Resting membrane potential for a $\beta$-cell is about -60mV. Threshold potential for $Ca^{++}$ release (which leads to insulin secretion) is between -50 and -40 mV. (Refer to my earlier linked articles). I don't have an exact number for $\mathcal{E}_K$, the equilibrium potential of $K^+$ in $\beta$-cells, but it is more negative than the resting membrane potential of that cell. We know this because (as is demonstrated in the linked studies), the OP is correct, increasing the conductance of the membrane to $K^+$ causes a net $K^+$ current out of the cell, rather than in, moving the membrane potential to a more negative state (hyperpolarizing the membrane), similar to what we see in neurons.
Decreasing the permeability of pancreatic $\beta$-cells to $K^+$ DEPOLARIZES the membrane
As discussed in Constanzo Chapter 9, ATP-sensitive $K^+$ channels close (not open) in response to an increase in the $\frac{[ATP]}{[ADP]}$ ratio. This decreases the $K^+$ conductance of the membrane, allowing the membrane potential to move closer to other equilbrium potentials (e.g., $\mathcal{E}_{Na}$, which is positive). With $\mathcal{E}_K$, which is more negative than the prior membrane potential, contributing less, the membrane potential becomes less negative, or depolarizes.
You can use a less mathematical reasoning to work out what happens when the $K^+$ conductance decreases as well. Close a $K^+$ channel and positive ions that would have moved out of the cell stay inside the cell, making membrane potential less negative, depolarizing the membrane. This is effectively the same as bringing positive ions inside the cell.
When the membrane depolarizes, $Ca^{++}$ is released, which causes secretion of insulin.
Hypokalemia
In hypokalemia, outside concentrations of $K^+$ decrease. This has an effect on the equilibrium potential, $\mathcal{E}_K$. From the Nernst equation above, we can look at the log term to see how $\mathcal{E}_K$ changes when $[K^+]_{out}$ decreases. The fraction $\frac{[K^+]_{out}}{[K^+]_{in}}$ is less than 1 in all human cells (there is more $K^+$ inside the cell than out), so the log term is going to be log(some number between 0 and 1). You can work this out using a calculator, but in this domain (0-1), the log is negative. It is larger and negative the closer you get to 0, smaller (but still negative), the closer you get to 1. If this behavior is unfamiliar to you, I encourage you to explore it with a calculator.
If you decrease the numerator in the log term ($log_{10} \frac{out}{in}$), as we do in hypokalemia, you get a larger negative number. This doesn't change the net direction of flow, or current for $K^+$ at levels that occur in the cell. It's still net out. $\mathcal{E}_K$ is more negative than it would otherwise be, so why doesn't decreasing conductance/permeability by closing the ATP sensitive $K^+$ channels do the same thing and depolarize the membrane?
Closing ATP sensitive $K^+$ channels in the setting of hypokalemia does cause depolarization, but not enough. You have to go back to the chord conductance or Goldman equation and consider the effect of $\mathcal{E}_K$ on the membrane potential before the ATP sensitive $K^+$ channels are closed. With a more negative $\mathcal{E}_K$, the chord conductance term $\frac{g_{K}}{g_T} \mathcal{E}_K$ is more negative, and the overall $\mathcal{E}_m$ is more negative. Global hypokalemia effectively hyperpolarizes the membrane, not just in the pancreatic $\beta$-cell, but everywhere. This is an important principle for understanding the consequences of hypokalemia, not just in insulin secretion, but in all settings. As a rule, excitable membranes are sluggish in hypokalemia (except Purkinje fibers). This is why, for example, it causes muscle weakness.


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What waste products do cells secrete in culture, and at what rate?
I am designing microfluidic chips for mammalian cell culture. One aspect I am interested in modeling is the rate at which I must renew media to ensure that:

Cells receive enough nutrients
Cytotoxic waste products are removed before they reach concentrations that would be detrimental to the cells.

Number 1 is fairly easy. Numbers for glucose uptake rate, for example, are available for many cell types. Number 2 is proving more challenging. I cannot find articles that detail secreted metabolites, including their secretion rate and the relationship between their concentration in media and toxic (or other) effects on cells.
Are there any resources out there on quantitative assessment of secreted metabolic waste?


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Bite Force of Triceratops
Estimations (or measurements) of bite force is usually conducted for toothy predators like sharks, theropod dinosaurs and crocodiles. For example: Tyrannosaurus had a bite force of about 57 kN (about 5.7 tonne-force) while a 5.2 meters long Saltwater Crocodile (Crocodylus porosus) recorded a 16,700 Newton bite (by Gregory M. Erickson). See my earlier question Reference for the bite force for Nile Crocodile for reference.
However, although paleontologists agree herbivore ceratopsian dinosaur Triceratops had quite a strong bite due to large jaw muscles anchored to (part of) the frill, and sharp hard beak. However, as far as I am aware, no one ever tried to quantify how strong is Triceratops bite. But maybe there are some estimations in paleontological literature and scientific research. So to sum-up my question:

What is the bite force of a fully-grown bull Triceratops?

Size for reference: Triceratops length was 8-9 meters and weighed 6-12 metric tonnes.

these may be helpful https://www.jstor.org/stable/2406631?seq=1#page_scan_tab_contents and https://pdfs.semanticscholar.org/744f/48001115d764d2ff4ad9a47de599900bf531.pdf

A Nile Crocodile bite force was measured to be 5000 lbf (22.24 kN) by Dr. Brady Barr. The bite force of T. rex is about 3 times higher.


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Why is the hippocampus considered to be a cortical structure but not the amygdala?
I'm having some trouble understanding the anatomical differences that classify the hippocampus as a cortical structure but not the amygdala. I have included the screenshot of a diagram from Gray's Clinical Neuroanatomy.

Medial aspect of the left cerebral hemisphere demonstrating some limbic structures (yellow). The anterior nuclear group of the thalamus is coloured orange, and the rest of the thalamus is magenta. The approximate position of the brain stem is outlined in a heavy interrupted line.

I have suggested an edit to your question that corrects the link to the figure. However, I am not sure that the figure adds anything to the question. If anything, it shows that the hippocampus and the amygdala are both areas of the limbic system. You may want to have a look at the Wikipedia page on allocortex and if that does not satisfy your curiosity, maybe read the Cortex: Statistics and Geometry of Neuronal Connectivity.

You can't distinguish cortical from deep structures from a picture like the one you reference in Gray's Clinical Neuroanatomy. The hippocampus is a cortical structure because its cell bodies are in the outer layers of the cerebrum. The amygdala is a deep structure because its cell bodies are in nuclei. I'm not sure if your textbook has stained sections, but if it does, that should help clarify the difference between the two structures.
In this sagittal section you can see both. Notice the hippocampus (at both ends) follows the bumps and grooves of the cortex where the amygdala is a circular/almond shaped cluster of cells.


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Advantages of Monogamy over Polygamy and Vice Versa In Nature?
Some animals take on a single partner, possibly for life, while others have multiple partners over their lifetime, possibly even at the same time. What are the advantages to each approach, and how much is conscious choice verses instinct?

Only Polygamy or the more generic polyamory?

This question seems really broad.  What, in specific, are you trying to figure out.  The advantages and disadvantages depend strongly on the type of creature and how advanced it is, and the question about choice vs instinct applies a human-centric view of animals which doesn't really make a lot of sense.

Have you researched the available sources of information?

It's all about genetic diversity which increases the chances of long-term of a species. More partners leads to more genetic combinations.What puts a brake on open mating all around is parents, usually, males wanting offspring with their genes to survive. Evolution will tend to favour both trends. What we see is what it gives.

This doesn't look too broad to me as an old student of the life sciences.   I might just offer an answer too.

Why are you asking this on Worldbuilding? It looks more like a biology question.

Polygamy spreads genetics further, but usually you trade that spread for care of the offspring.
Monogamy means less genetic diversity, but the offspring usually get more attention and care, meaning they're more likely to survive.
So it's more babies where more will die, or less babies that take more energy to grow and nurture but more likely to survive.

This sums it up. Monogamy encourages the father to stick around and help the mother care for the offspring, since they aren't looking for other mates (unless the mother dies). There is an incentive for males to cheat, though, since (if successful) they can get somebody else to look after their own child. Polygamy is a broad term here. If you mean a harem, only a relative handful of males will spread their genes (good for selecting the best, not so good for genetic diversity). If you simply mean mating and moving on, it allows lots of gene spread but with lower survival rates for children.


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Why a cell contains all DNA when it only needs a few genes?
Is that what they called junk? Why does a simple cell have the DNA code for everything else when it just needs a few codes to function? Wouldn't that be a wasteful?

Why does a cell contain all DNA when it only needs a few genes ?

I interpret this question to mean "why does every cell contain the whole human genome even though it doesn't use it all, i.e. why does a liver cell contain the genes for eye color?"
If that is what you meant, then we can easily answer the first question in your actual text:

Is that what they called junk?

No, that is not what is called "junk DNA". "Junk DNA" can refer to many concepts, but generally it refers to parts of DNA that serve no function in the body: they are not transcribed into proteins, they don't serve to regulate other genes, and if you remove them or change their sequence this will have no effect on the overall organism. This means it refers to parts of DNA that are used nowhere in the body, not parts that are used in one place but not in others.
How much DNA is "junk", how useless it actually is, and why we have it are complex questions that don't all have known answers, but it is completely different from your headline question.
I don't have the time to look up a detailed answer to your first question so I will leave that to others, but here are some elements that might help:
1) I think cells use more genes than you realize. I don't know the proportion of genes that are used for the cell to live as a cell vs those that are used for the specific tasks this cell needs to do beyond maintaining itself and reproducing, but I'm pretty certain there is no cell in the body that "only needs a few genes". I would even guess all cells in the body use most of the genes they contain.
2) not all cells contain an unmodified copy of the whole genome. Some cells lose their nucleus, i.e. their DNA entirely (red blood cells); others multiply some genes that they use a lot.
3) having said all that, I would guess that liver cells indeed don't need the genes for eye color, yet they might have them. Consider that cells reproduce by copying themselves, and copying their whole genome. Is it more of a waste to keep the copy as it is, or to go around before or after the copying cutting out all the bits this specific cell won't use? Do I go around editing the code of my text editor and recompiling it to get rid of all the functionalities I don't use? I might save some space on my hard drive but it is very obviously not worth my time to do that either. If the extra DNA doesn't do enough harm, there is no reason it would be taken out; indeed the wasteful thing would be to do so.

Whether there is junk DNA

The common view of a gene is a sequence of DNA which, upon transcription, which I assume in your understanding is a process by which DNA is read by a RNA polymerase to produce mRNA, and upon translation, produces a functional protein to regulate cellular metabolism (sum of all chemical reactions in a cell). It is not until the discipline of epigenetics emerged that we discover that most of other non-protein-coding sequences have important regulatory functions on the protein-coding sequences. Without them, the cell simply has no clue as to when it should produce more of a protein and when it should produce less, or whether the protein should be produced at all. And of course, DNA also encodes information about rRNA, which is an integral component of ribosome, which you know, is imperative for protein synthesis. Thus, the ‘functions’ of the DNA cannot be limited to protein synthesis, and after extension of the concept of functions, the parts of DNA we can dispense with are incredibly small.
Then let it be argued that those small parts of DNA which really serve no functions are the junk DNA. In fact, even this view is untenable because the ‘functionless’ DNA may be situated between the important sequences that can subtly affect the chemical properties of the protein interactions during an important biochemical process. Specifically, consider NtrC, a bacterial transcription regulator that activates transcription by directly contacting the RNA polymerase. Note that the regulatory sequence (the part of DNA the protein binds to) is very distant from the promoter of the gene(the part of the gene that RNA polymerase binds to). To directly contact it, DNA looping must occur. It is a phenomenon in which an otherwise linear DNA macromolecule is looped out(imagine bending a wire so that two extreme end of the wire touches each other) to allow for the contacts between molecules. Since the protein has such biochemical properties that allow it to contact another protein at a distance, we do not know what will happen if the ‘junk DNA’ the DNA spacing the promoter and the regulatory sequence is deleted. It is well possible that the two proteins will not make contacts anymore. And DNA looping is also ubiquitously found in transcription regulation of eukaryotes.

Why a cell needs to contain all the DNA when it only needs a few genes to function

Once the notion of junk DNA is found to be elusive. This question’s premises no longer hold. But let’s assume there are really genes that when deleted have no observable effects on the phenotypes of the cells or their health, why does not nature delete them during differentiation of stem cells? To explain it in evolutionary terms, there are two main mechanisms nature can design to keep the ‘functionless’ genes at bay during differentiation of stem cells. One is to silence them by wrapping them in a compacted nucleosomal structure, or to delete them once and for all. We do not know if nature has once experimented with deletion, if it has then this design must have endowed less fitness then the wrapping model. What reasons then can we speculate about the failure of the deletion model? To delete the useless sequences, there is a widespread effects on the length of the DNA, the resultant secondary structure (topology of the chromatin). And a protein must be designed to specifically recognise what genes to delete, together with the cooperation of nucleases. This is analogous to writing a computer code that contains information that specifies some of the codes to be deleted while not influencing the instructions of the code that follow, all while being consistent in the process. This is logically possible, and we can never say this design is entirely prohibited. But computationally this is not as elegant a solution than just genes in the DNA that code for a repressor protein for the ‘useless’ code when the right time has come, or by just using proteins to wrap around the sequences to render them unreadable.

Whether ‘non-functional ‘ DNA constitutes a waste

Not at all.

I expect you were downvoted because it's not the consensus that little to no DNA has no function. It isn't just about how non-coding DNA might have other functions; for example, looking at which parts of the genome show evidence of selection and which don't can serve as a proxy for them having a function or not, and by that metric most human DNA is indeed "junk". I also don't think it has been shown that most non-coding DNA has a regulatory function. Some yes, most no. Highest number I find is 40% here, and even that's a hypothetical. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3431477/


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What is an "Alternative Sensation"?
As far as I know, alternative sensation it's a sensation to distract people from the original stimuli, for example when you have to get an injection, the nurse will pinch you in the other arms so your brain is distracted and will not focus on the original pain in the arms that's got the injection.
But I also read here, alternative sensation refers to the brains that can process stimuli from multiple senses, for example when the eyesight is bad, the ears will take up and boost the visual system to help and stimulate the visual system (Visual + Auditory) .
Which one is exactly an 'alternative sensation'? Also, what is Time-Frequency in alternative sensation ? I would appreciate any references too.

My goodness, neither one of you gave an upvote to the other! Question was taken seriously, nice answer written, and then accepted, and yet both currently sit at zero upvotes, zero downvotes! I'm tempted to down vote you both ;-) (just kidding on the last part)

"Alternative sensation" is not specific terminology in neuroscience - it is just the noun "sensation" with a descriptive adjective "alternative." It just means that it is referring to a different sensation than whatever the "primary" one is.
Knowing what this term means in a given context depends entirely on that context, and may not have any relationship to other contexts.
Time-frequency refers to how something varies in time and frequency. In the context of stimuli, for example, an auditory stimulus can have different "tones" or "notes": those are different sound frequencies, and those frequencies can happen in sequence. To describe a sound visually, one will often present a 'heat map' showing when (time) and at what frequency that sound has energy. Touch stimuli can also have a time-frequency representation, where the frequency indicates the vibration speed of the touch.

My goodness, neither one of you gave an upvote to the other! Question was taken seriously, nice answer written, and then accepted, and yet both currently sit at zero upvotes, zero downvotes! I'm tempted to down vote you both ;-) (just kidding on the last part)


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What is these mushrooms in my indoor pot?
I am living in Japan and in summer, it's very hot and humid even inside my room.
Today, I've found two mushrooms in the pot of a plant.
What is this species? It's very surprising than within one day they grew like this.

Looks like Lepiota sp.

@RHA Please don't answer in comments.

@kmm It's not an answer but a suggestion.

Suggestion: If you leave them and the cap turns to black slime .they are comatus coprinis, shaggy mane.  Good to eat ( the next crop).

Note: regardless of the expertise of anyone here, do NOT try to eat anything you have identified by someone on the internet.

Thanks! Yes, I'm not gonna eat anything. It's maybe edible in the wood but inside in a pot I've put some unknown fertilizers.. don't wanna try haha

They do look a lot like a common mushroom called "shaggy mane" mushroom (Coprinus comatus). This may not be a correct identification though, so do not eat them.  They are widespread around the world, but usually grow outside.
Yes it is amazing how rapidly the fruiting body of many fungi can grow. I am providing an interesting Wikipedia link with more information. You can also search to find other images using Google images online.
https://en.wikipedia.org/wiki/Coprinus_comatus


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Does all cells in individual has same mitochondrial DNA?
I read that genetic code is universal except for mitochondrial DNA.
However, I want to clarify (generally speaking, regarding humans especially):

does all mitochondria in the same cell have almost the same mitochondrial  DNA?
does all cells in a single individual have almost the same mitochondrial  DNA overall?
does all the siblings in one family have almost the same mitochondrial DNA overall?

Thanks :)

Are you asking about mtDNA in humans or in general?

@qeschaton humans :)

In a homoplasmic individual, all mitochondria is the same. Therefor will be the same amongst cells and between siblings/mother. Unless some mutation occurs. A homoplastic individual either has all mutated mitochondria or all functional mitochondria of the same type.
A Heteroplasmic individial (more than one type of mitochondria) mitochondria occur when a mitochondria has accumulated sufficient mutations. When a hetroplasmic mother has children, the siblings have varying ratios to each other and the mother.
When you produce oocytes, a selected number of mitochondria are transferred into each. During maturation, there is a rapid replication of mt-DNA, which can lead to a random shift in mutated DNA between the offspring and the mother. This is the mitochondrial bottle neck. Bottlenecks enforce mechanisms that omit cells or individuals, in this context mitochondria, ideally such that only the healthiest mitochondria are transmitted.

In a heteroplastic individual, different cells or populations can have varying amounts of of the mutant mitochondria (including complete homoplasmy).


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What is the effect of non-vaccinated people on vaccinated people?
Many times have I heard that anti-vaccine people are dangerous even to the vaccinated population. Is that true? If so, how can it be? People say that germs will attack them, and soon they would eventually grow and spread even toward general population which actually got its vaccines.
I mean it's so counter-intuitive: if I'm vaccinated even when disease will spread I shouldn't be in danger.

I'm upvoting because this is an important question. There are problems with the assumptions (if i'm vaccinated even when disease will spread I shouldn't be in danger), but that's exactly what makes it important.

The only way to prevent a species to evolve is by extinguish (eradicate) it. If some people continue to carry a disease, those germs can evolve into a new, more resistant, more pestilent form that could attack even the immunized individuals.

1st point: I feel that we should rather put the blame on the inefficiency of the vaccine, instead of the people who refused the vaccine. The vaccine is like a shield or a firewall - it does matter how strong the attack is, but if the shield fails to prevent the disease, the developers of the vaccine should't claim 'hey, you were surrounded by too many unvaccinated people', but instead improve the vaccine. 2nd point: not all diseases are transmitted only from one human to another. Plague was transmitted by rats. Should we blame the rats for refusing the vaccine?

@AliceD I'm not sure what the guidelines are for moving a discussion to chat, but the recent comments here don't seem to be directed at improving the question or explaining a vote.

@Newtonfan01 What characteristics of a germ corresponds to "the strength of attack"?   Is it just the quantity of organisms?

Putting aside people who do get vaccines, there are some people who can't get some vaccines and rely on everyone who can getting the vaccine and ideally eradicating the disease altogether, or, second-best case, not contracting it themselves so they can't give it to anyone who can't get the vaccine

Would you like us to disregard the ideas which anti-vaxxers spread?  Ideas spread far more virulently than any disease.  The battle over the idea of vaccination vs the idea of avoiding vaccinations is a much more brutal one than the mere biology of disease.

the more it can spread the larger chance it can mutate and become dangerous to those who are vaccinated for the first unmutated version.

Vaccines do not protect 100% from the disease. When enough people are vaccinated the disease outbreaks die out quickly. The problem is that when not enough people are vaccinated, the diseases do not die out, but linger in population. So, you keep bumping into sick people, and eventually get sick too. That's the simplest explanation I could come up with. If you're not satisfied, I'm afraid some differential equations will be in order.

Biology is rarely black or white, all or nothing. Protective immunity is generally not an on/off switch, where from the moment you're vaccinated you're infinitely resistant for the rest of your life. You shouldn't expect that, having received a smallpox vaccine, you could have billions of smallpox viruses squirted directly into your lungs and shrug it off without noticing.
Given that (fairly obvious) fact, you should immediately think of scenarios where vaccinated people are still at risk of disease following exposure to unvaccinated people. What about older people who were vaccinated 20 years ago, 50 years ago? What about people whose immune systems are slightly weakened through lack of sleep or obesity or stress? Any of these vaccinated people might well be protected against a brief encounter, but not against, say, being in an airplane seat for 18 hours beside an infected child shedding huge amounts of virus, or caring for their sick child.
It's all sliders, not switches. You can have a slight loss of immunity (4 hours sleep last night) and be protected against everything except a large exposure (your baby got infected and won't rest unless you hold him for 8 hours). You can have a moderate loss of immunity (you were vaccinated twenty years ago) and be protected against most exposures, but you're sitting next to someone on the subway for an hour. You may have a significant loss of immunity (you're a frail 80-year-old) and still be protected against a moderate exposure, but your grandchild is visiting for a week.

Good answer. See my answer for some data.

I think one point you can add to this is that unvaccinated people who host a virus allow it to propagate and evolve, which can undermine the efficacy of the vaccination.

You could add that, depending on the disease, some percentage of the vaccinated may show a low immune response and will never develop immunity, although vaccinated.

to restate Blackthorn, unvaccinated people also provide a place for the disease to reproduce and potentially mutate into a new strain that the vaccine does not help with. This happens constantly with the flu.

I like this answer, except for the "(fairly obvious)" part.  It sounds condescending, and it is not something that is obvious to everyone.

I think it's also worth mentioning that there exist groups of people that can't be vaccinated for legitimate reasons (allergies, immune deficiencies, etc.). For them even 1 unvaccinated ill person can be deadly.

@Beska It's not obvious that a vaccine is not a perfect defense against a disease? Sorry, but I think the typical person off the street would say "never say never."

@corsiKa I disagree, as I suspect that many people think that's how vaccines tend to work...but as I have no evidence either way to support/refute it, I'll just leave it at that.

@BlackThorn viral escape mutants are rarely observed in an effective vaccine, and generally are not the public health challenge they seem to be in fiction. They are an issue during vaccine development. Influenza variation (and subsequent vaccine failure) is due to recombination in non-human hosts. The unvaccinated certainly cause harm to the vaccinated, but this is not a significant mechanism for that harm.

@de-novo Influenza variation (and subsequent vaccine failure) is due to recombination in non-human hosts This part is not correct; you've confused the antigenic drift with shift. It's not clear how much influenza vaccines contribute to antigenic drift in humans, but it's probably not a major factor . In general I agree with your comment, but influenza is a complicated story in many ways (too complicated to deal with in a comment).

@iayork certainly both shift and drift both lead to viral escape. I was trying to emphasize the fact that the virus has non-human reservoirs and the decreased effect human vaccination has on that virus because of the non-human reservoir. Your right. to complicated for a comment :)

Shift has happened 4 times in the past century, drift happens every year.  It's simply wrong to say that "Influenza variation (and subsequent vaccine failure) is due to recombination in non-human hosts".

I think that herd immunity should be mentioned... as it impacts the number who are infected and standing next to you.

Since 2000, in the United States alone, there were 16 reports of outbreaks or groups of outbreaks where the outbreak started with an initial case in an unvaccinated individual and resulted in disease in previously vaccinated individuals. The epidemiology of pertussis is a little different, and transmission happens in many cases apart from a clear outbreak, but there are several documented pertussis outbreaks that led to disease in vaccinated individuals as well. This JAMA report provides a good summary.
Herd immunity is important, especially in highly contagious diseases with no significant non-human reservoir, e.g., measles and pertussis. @iayork's answer is correct that vaccination is not an on/off switch. About 15% of measles cases in the US involve vaccinated individuals, and these have all been the result of transmission that started with an initial unvaccinated case (see previous reference).
These are bad diseases. They can cause serious illness. Half of infants who get pertussis need care in the hospital. For measles, 25% of all cases involve hospitalization. For both, life long disability (deafness, brain damage) and death are real possibilities. 1 in 100 infants with pertussis die, 1-2 in 1000 measles cases die. The harm intentionally unvaccinated people cause to vaccinated people and people who can't get vaccinated (because of their age or other health problems) is real and well documented.
Edit:
In light of another answer and some comments, I'm adding a couple paragraphs putting vaccination in context with other strategies for prevention of infectious disease.
Relevant to this question, as is clear from the epidemiological data discussed above, vaccines are not 100% effective. Some vaccines are more effective than others. Measles vaccine, for example, is in the mid to high 90s. Flu vaccine effectiveness, depending on the population and year, can range from the 40s to the 80s. You can read about vaccine effectiveness in the CDC pink book, Epidemiology and Prevention of Vaccine-Preventable Diseases.
Other strategies for preventing infectious diseases depend on the great diversity of host/pathogen interactions. A few things are generally useful, and often effective. Wash your hands, wear a condom, and stay home when you have a fever. There is no good data on the general advice to stay home when you have a fever, but quarantine is effective for specific illnesses, especially in concert with vaccination and other preventative measures (see the CDC pink book). Limiting the isolation and sedentary behavior associated with staying home to cases where there is a fever has biological plausibility and minimizes the negative immune and other health effects of those behaviors (see Cecil Medicine, Chapter 288).
Along with vaccines, each of the strategies mentioned in the previous paragraph helps protect the individual who uses them as well as other people. So they are good for you and the people around you. You can practice all of them. I'm confused, but not surprised, when the effectiveness of some other strategy is used as an argument against the use of any of the others. You can compare the measured preventative efficacy and effectiveness of each strategy, and come to the conclusion that vaccines generally give the best results (both on an individual and population level), but I'm not sure why, for example, you would decide not to wash your hands because you got a particular vaccine, or not to get vaccinated because you washed your hands.

Can you expand on people who can't be vaccinated? You mention them in the last paragraph and I don't want to just add another very similar answer. Though the amounts of people who can't get vaccinated for medical reasons isn't great (roughly a 1000 children a year in the US states I checked) that's still some and probably doesn't cover children who just have delayed vaccinations for health reasons which can also be a problem.

@DRF that's a reasonable answer in itself. Feel free to add it. You start by looking at the JAMA article I linked (it's on PMC, so no paywall). Table 1 includes numbers on non-medical exemptions. If you subtract unvaccinated cases from unvaccinated with non-medical exemptions, you'll get the number of cases in individuals who couldn't get vaccinated (prior to getting measles). It wouldn't be a bad idea to include a little bit on what level of vaccination coverage is required to have herd immunity.

@DRF sorry, CAN start, or COULD start. You're free to answer however you like; I just wanted to give you some helpful data :)

I DID start but it's a longish article.:) Thanks for the pointer.Actually I suppose it's not all the longish but still I need to read and digest it first.

I'm afraid I don't understand "For measles, that number is 25%, but for all cases." which seems self-contradictory. Could you clarify?

@DennisWilliamson it's a different denominator. For pertussis, infants get severe illness much more frequently. Half of all infants with pertussis need to be hospitalized, but very few otherwise healthy adults. For measles, 25% of everyone (all cases) ends up needing hospitalization.

+1 for mentioning herd immunity

The toughest part about "herd immunity" (a favorite talking point of an anti-vacc aquaintance of ours who's in the healthcare field and therefore really ought to know better) is knowing that their kids are wandering around unvaccinated, are therefore at higher risk of infection and death in the event of an outbreak, in which case if they died we'd have to go to the funeral/memorial/whatever, and knowing full well I can't say, "Sorry you counted on herd immunity. Next time COUNT BETTER!".

@BobJarvis herd immunity is relevant for both the vaccinated and unvaccinated populations. When vaccination coverage is above the predicted threshold for herd immunity, we don't get outbreaks with disease in vaccinated individuals. When it's below the threshold, you get outbreaks (and often disease in both groups).

Something which may help is a model.  There is a standard model based on a key number called R₀, the basic reproductive number.  This is a highly boiled up number which indicates how many uninfected people will be infected by a single infected individual.  Trivially, if R₀>1, the disease will spread through society, and if R₀<1, it will vanish because each infected generation infect fewer new people each generation.  R₀ is basically derived from the number of contacts a person can make before showing enough symptoms to sequester them at home, times the chance of any interaction transmitting the infection.  The longer the incubation period and the more infectious the disease, the higher R₀ is.
It's a massively massively boiled up model.  You can look to science for more accurate models which account for all sorts of features.  However, it is a good enough model to demonstrate a concept called herd immunity.  Herd immunity decreases the odds of a contact with an infected person spreading the disease.  After all, a vaccinated individual is far more likely to go unaffected.  This is typically modeled with an extra factor S, such that the reproductive rate of the disease is R₀S.  If q is the vaccinated portion of the society, then (1-q) is the number of succeptable people, so the reproductive rate is R₀(1-q).
Now remember, if the reproducitve rate is greater than 1, the disease flourishes.  If it's less than 1, it dies off.  Having a strong vaccinated base has been shown to be a very effective way of keeping that reproductive rate down.
Consider, as an example, Measles.  Measles is considered to be an excellent disease for demonstrating herd immunity.  Its R₀ is somewhere between 12-18, meaning each infected person is likely to infect 12-18 people before getting quarantined.  If a populus is 95% vaccinated, then the reproductive rate drops to R₀*(1-.95), which is somewhere between .6 and .9.  This means the disease will die out if the population is that vaccinated.
Again, modeling based on the basic reproductive number is considered to be a gross tool, but it is effective at demonstrating the risks associated with insufficient vaccinations.  If there is a large enough unvaccinated pool to let the disease flourish, everyone is exposed to the disease every day as it runs rampant in the society.  Vaccines are awesome, but they are not magic bullets.  You can still get diseases after being vaccinated, it's just much more rare (the term to look up is Vaccine Efficacy).  The more you're around a disease, the more likely it is that you just get unlucky.  Even a vaccinated person benefits from a reproductive rate less than 1, so that the disease never flourishes in the first place.  The less effective a vaccine is, the more one is dependent on a high rate of immunization to drive the reproductive rate down below 1.
Also, another strong argument for vaccination is the presence of immunocompromized individuals.  Many individuals cannot receive vaccinations for one medical reason or another.  For instance, immunizing someone with HIV is a tricky business which I would refer one to a doctor for more information.  Those on transplant lists may be advised against receiving vaccinations.  These individuals are entirely dependent on the so-called herd immunity effect to insulate them from these diseases.  As the reproductive rate for a disease gets closer or above one, it becomes hard to protect these individuals.

Think of every human being as being a walking petri-dish, full of growth medium. When you grow a large colony of micro-organisms, you are allowing that population to experience a larger number of mutations. Every mutation is one more potentional strain that can beat the defenses of our immune systems, even those provided by vaccines. So, if you don't get vaccinated, you are potentially providing safe harbor to the micro-biological parent of the next vaccine-resistant/anti-biotic-resistant super-flu.
This same principle is why large super farms are so dangerous: huge numbers of animals provide more opportunities for micro-organisms to experience mutations that allow them to infect more resistant hosts. The fewer hosts that a micro-organism  can infect, the lower the number of opportunities for mutation.
This is one facet of the issue, among those others have mentioned.

authors: Bob Jarvis - Слава Україні


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Is it possible to guide animals to a new breeding ground?
(This is a question for a book I'm working on.)
One of the threats to some animal species is the disappearance of breeding grounds (because of the spreading human population, or for example because of ship routes).
Hypothetically: would it be possible to encourage a species to breed on another place? Has that ever been tried? What do animals do naturally - do they seek another location, or rather keep trying?

Hello and welcome to Biology.SE! I suggest you to take the tour to learn about this site and earn yourself your first badge. Also, can you provide a practical example of "breeding ground"?

"Breeding ground" - I'm sorry English is not my native language and I'm by no means a scientist. I mean the place where animals go to mate / spawn (f.ex. certain eels in the Sargasso Sea, if I'm not mistaken).

One example where it has been tried is with whooping cranes: http://operationmigration.org/

The problem that you mention deals primarily with habitat fragmentation, which has a great impact on species conservation. A fragmented habitat will impair migration and can result in inbreeding depression. This has been dealt with wildlife crossing in various sites in the world.