text:
Tissue fluid water potential
just a quick question. Is the tissue fluid the same water potential as the cells it surrounds? I am a bit confused because if it was lower it would cause water to leave the cell and if it was higher water would enter the cell and both aren't really good for the cell. I believe tissue fluid is isotonic, am I correct?

Yes, cell membranes are highly permeable for water. While diffusion through the membrane is possible (description, and some science), it is most effective through water channel proteins (aquaporins). The different expression levels of aquaporins in different cell types result in differences in the permeability.
And yes, the tissue fluid has to be isotonic to the cell interior. The water balance in the body is therefore highly regulated. If not enough water is available, the blood osmolarity (ratio between solubles and water) increases. This is sensed in the hypothalamus (an area in the brain which is a major player in hormone regulation) and results in production of the hormone vasopressin. This will not only increase your thirst (and therefore add more water to the system) but also regulate aquaporin expression, improving reabsorbtion of water in the kidney (nicely shown here, actual science here). Urine production is of course also important in the response to drinking too much, which can be harmful as well..
If tonicity is deregulated, this has serious consequences for the body (some more science). For example, mutations in vasopressin or kindney aquaporins can result in very similar phenotypes, characterized by dehydration because water levels cannot be properly regulated (even more science).
edited for more explanation, because people complain when I give short answers to short questions ;)

Can you elaborate? It's (again) a 2-liner - such posts are often recognized by the bot as low-quality and face deletion. Please explain why membranes are permeable to water (they are hydrophobic! - aquaporines) and what the dangers are of tonicity dereg. Note that the first answer is not great, so it's great you are trying to add a better answer.

Hi, thank you Alice for saying exactly what I was about to. Why are the cell membranes permeable to water? Aren't they hydrophobic? Unless the water can only move in and out through aquaporins?

I have already added more explanations and resources after Alice' comment. Membranes are highly permeable because of aquaporins. Water can nevertheless also cross the lipid bilayer by itself. I am not a physicist and won't be able to explain the atomic forces, but there is a lot of water compared to lipids and the cell has a very large surface. That's why the chance of this interaction is high. https://youtu.be/ePGqRaQiBfc

Not necessarily-
cells are surrounded by a plasma membrane that creates a waterproof seal from their surroundings. This membrane contains embedded proteins, called transporters and channels, that enable the selective passage of water, ions, and solutes to maintain a membrane potential, or concentration difference between inside and outside. This enables cells to maintain homeostasis, despite changing external conditions.
You can learn more about these processes here:
https://en.wikipedia.org/wiki/Membrane_potential

But the membrane doesn't prevent water from moving through it right? So if the water potential was higher or lower water would still leave the cells right?

Yes that's true, most animal cells passively conduct water. Notable exceptions would be some epithelia- for instance cells in the kidney are able to concentrate urine. This means they must be able to establish osmotic gradients.

Sorry, this is wrong. The cell membrane is highly permeable for water. The membrane potential you are talking about is the electrical potential from the distribution of charged ions.


text:
What insect is this with 'horn' at the side?
Found this interesting insect hiding behind the thin branch of flower (the diameter of the branch is 3-4mm) in my garden in Kuching, Sarawak, Malaysia

@Karl Kjer It's most likely a Leptocentrus taurus, even though the perspective in the photo doesn't allow to observe the prominent dorsal thorn.
https://www.flickr.com/photos/some_soul/15316794326
https://indiabiodiversity.org/observation/list?count=0&hasMore=true&max=10&offset=0&sort=lastrevised&taxon=72846&view=list
Ants are always trying to come in contact with these mimic treehoppers for collecting the sweet juices secreted by them. Maybe the OP can confirm that.

That is a treehopper. Order Hemptera, family Membracidae. I looked on a site for membracids of Malaysia, and could not bring it to species-level. But I am confident that it is a membracid. This family is characterized by sometimes bizarre protrusions of the pronotum.
https://en.wikipedia.org/wiki/Treehopper

source: Stack Exchange

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

sort: votes


text:
What does 'virus prototype strain' mean?
Does the term 'prototype virus strain' mean the first virus isolated and without mutations?

A prototype virus may or may not be the first isolated virus of a group. It's essentially the same as a "reference" virus -- in fact, the International Committee on Taxonomy of Viruses
(ICTV) uses the terms interchangeably, as in the  Hepeviridae Study Group which has a column entitled "Prototype/Reference Strain".
In many cases the reference virus is the first isolate, but it isn't necessarily the case. The ICTV is the official body that determines reference strains, and they may choose a different virus as the reference/prototype. For example the first isolate may turn out to be unusual or an outlier in same way, so that a more typical strain may be chosen as a reference or prototype (I don't know offhand of examples of this though).
"Prototype" is often used in a broader sense as well, where a group of viruses can act as prototypes for a still broader group.  For example, "The genomic structure of Pencillium chrysogenum virus (PcV), the prototype of the genus Chrysovirus ... " (pdf link) uses "prototype" to refer to all the viruses in the Pencillium chrysogenum group, as compared to the broader genus.

virus strain:

Different lines or isolates of the same virus (e.g., from different geographical location or patients)

prototype:

the first example of something, such as a machine or other industrial product, from which all later forms are developed

I think prototype of virus strain is first isolated virus of that strain.
Refferences

Principles of Molecular Virology fourth edition; Alan J. Cann; page 64.
https://en.wikipedia.org/wiki/Strain_(biology)
https://dictionary.cambridge.org/dictionary/english/prototype

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


text:
Does turbidometeric method count cell number or cell mass?

Here it says that scattering is inversely proportional to cell number but also says that we can observe greater absorbance as cell number increases.
So does turbidometeric method work on cell mass or number ?

Your text says that scattering is proportional to cell number, which is correct. It is not inversely proportional, as you stated.

But if counts it under measurement of cell mass and not number ?

The spec measures the amount of light scattered by a sample, so increasing the number or size of the cells will increase measured absorbance.

Imagine a room full of flying insects. One could estimate the number of insects in the room by shining a flashlight at one end and observing its brightness at the other end. If the room is densely packed with tiny flies, the flashlight will appear darker from the other side of the room because the flies block the light. A smaller number of butterflies, which make a larger shadow, would block the same amount of light and give the same absorbance. Both the number and size of the insects affect the amount of light transmitted through the room.


text:
Insect identification request - Is this a bed bug?
I live in Spain and today I found several of these in my son's jacket. I am afraid they are bed bugs nymphs because last year we had a bedbug epidemic in some neighborhood houses.
The insect in the photo is about 1mm and has green spots in his body. Maybe they are just aphids that have been brought from the park.

Green spots? Probably not a bedbug, then. Bedbugs feed exclusively on blood meals, which means that any coloring you spot in the nymph would be brown or red.

As the answer suggests, I do not think that bed bugs would have green spots.

I got curious and after some image search I got two candidates:

Plagiognathus repetitus

Mullein Bug

Great that you answered your own question! Can you add links to e.g. Wikipedia pages or other sources about these insects?


text:
I'm trying to identify this salamander-looking creature I found in my house today in Coos Bay, Oregon. It is about 2" long. What is it?

This is about 2" long. It is white on its underside and looks like a small salamander, except for it being white underneath. It is about 1/8th inch wide.

Search for  Larch Mountain salamander Plethodon larselli images; some I found look similar but this is very rare endangered species and Coos Bay is a bit south of the reported range (Columbia river gorge and north) and it's mainly a mountain species.  Size is right, color approximately right.

The body form looks more like a skink than a salamander. Close to a 5-lined skink (https://www.wildlifedepartment.com/wildlifemgmt/swg/t35p1/WMA/E_fasciatus_AT.shtml) but those aren't native to OR>

@kmm I think you may be correct, looks like there are scales which aren't present in a salamander (and apparently salamanders usually have 4 front digits).  Searching for images of lizards/skinks for CA/OR/WA doesn't turn anything up, and each state has high quality web sites for herps.  Maybe it's a juvenile form that is not well documented?

That is definitely a lizard, not a salamander. Salamanders don't have scales. It is a Northern Alligator lizard, Elgaria coerulea, in the family Anguidae.
https://www.inaturalist.org/check_lists/9307-Reptiles-of-Oregon
https://en.wikipedia.org/wiki/Northern_alligator_lizard

Is that typical coloration for the juvenile form?


text:
Red neurons - Acute neuronal injury

“Red neurons” are evident by about 12 to 24 hours after an irreversible hypoxic/ ischemic insult. The morphologic features consist of shrinkage of the cell body, pyknosis of the nucleus, disappearance of the nucleolus, and loss of Nissl substance, with intense eosinophilia of the cytoplasm.  -Robbins textbook of pathology

Taken from Robbins pathologic basis of disease, 9e, pg.no1265, fig: 28-13B

Why in case of neurons there is shrinkage instead of swelling as in other cells?

There is not some simple dichotomy of "neurons shrink and other cells swell" in response to hypoxia/ischemia.
Neuronal death can be necrotic or apoptotic or both, and at different stages different morphology is observed: generally swelling earlier, shrinkage later, though both are observed together early as well. Eosinophilia/"red neurons" tends to occur later as mentioned in this passage (after 6 hours, consistent with 12-24 hours) so that's probably why the author is referring mostly to shrinkage. Cells can also have swelling of some organelles, like mitochondria, despite shrinking overall.
Without further context of the passage you provided it's hard to say much more.

Garcia, J. H., Yoshida, Y., Chen, H., Li, Y., Zhang, Z. G., Lian, J. I. N. Y. I. N. G., ... & Chopp, M. (1993). Progression from ischemic injury to infarct following middle cerebral artery occlusion in the rat. The American journal of pathology, 142(2), 623.
Jenkins, L. W., Povlishock, J. T., Lewelt, W., Miller, J. D., & Becker, D. P. (1981). The role of postischemic recirculation in the development of ischemic neuronal injury following complete cerebral ischemia. Acta neuropathologica, 55(3), 205-220.
Portera‐Cailliau, C., Price, D. L., & Martin, L. J. (1997). Excitotoxic neuronal death in the immature brain is an apoptosis‐necrosis morphological continuum. Journal of Comparative Neurology, 378(1), 10-87.

Not much infiltration of phagocytes is seen in above figure. Shouldn't apoptotic cell need more phagocytes in close vicinity to immediately clear of the bits of cytoplasm which are shed off?

@JM97 Sorry I'm not sure what the answer to that question is for sure from the perspective of histopathology, just conceptually though I don't see any reason that absence of phagocytes demonstrates lack of apoptosis. Certainly microglia would be present to clean up at some point of healing but apoptosis itself can be initiated intrinsically.

There has to be something special as coagulative necrosis, a usual feature of ishcemia is not seen in CNS as given in chapter 2 of Robbins.

Search for Exicitotoxic programed cell death. Acute Neuronal injury occur by this pathway. This is like Necroptosis. Cell shrinkage is seen due to Glutamate.  I have added some screenshots of my search,, rest you can search yourself.

Read more at
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4398818/

@JM97, please do reply if this was helpful.

thanks for your efforts. I will certainly read excitotoxic cell death now. again thanks.


text:
Could a human become infected with rabies in such a way that even prior vaccination wouldn't stop the infection?
Given the highly persistent nature of rabies after entering the brain, I was wondering whether certain ways of exposure to this virus could be risky even for a previously vaccinated individual. I understand that no vaccine is 100% effective, but would the risk of infection be particularly increased in case of exposure at some particular site on the body? Which mechanisms of the rabies infection would play role in this situation?

It would be helpful to further explain the reasons for the downvote so that I could improve my question or avoid asking unsuitable questions in the future (and possibly delete this one). While I welcome constructive criticism, downvote without any explanation doesn't really help anything.

There is one down vote and one close vote. I expect they're from the same user. The close vote reason is "primarily opinion based", which is probably because your question comes from a work of fiction. On Biology.SE, when you frame your question with, "I was watching this TV show... could this really happen?", you prime readers to expect your question to require speculation.  There is a real and answerable question here, though. I considered editing it to take out the TV show frame for you, but I'll let you decide if you want to do that or not :)

I don't want to put words into your mouth here, but as it stands the title text doesn't quite ask the same question as the body text - could you edit one or the other? I'd suggest keeping the question in the body.

Reframing your question as:

Are rabies exposures at specific sites on the body riskier than other sites, even for a vaccinated individual?

Possibly for post exposure prophylaxis, but probably not for pre exposure vaccination.
Rabies transmitted by a bite or scratch (almost all cases) involves a period of slow replication in muscle tissue at the site of the bite or scratch (see Murray Medical Microbiology Ch. 60 for a general discussion). This is called the incubation phase, and it is highly variable. The incubation phase is followed by a prodrome phase (virus binds receptors of sensory neurons at the site of exposure, and travels to the CNS) and neurological phase (infection of the brain).
An effective immune response is believed to be the result of both an antibody response and cell mediated immunity during the prodrome phase. Post exposure vaccination is effective because the incubation period provides enough time for a naive immune system to mount a protective response (same reference). Regardless, rabies post exposure prophylaxis (PEP) includes both active and passive immunization, i.e., vaccine and human rabies immune globulin.
Both post and pre-exposure prophylaxis failures have been reported. As discussed here cases with pre-exposure vaccination failure involve immunocompromised individuals. Cases with post-exposure prophylaxis tend to involve failure to fully follow guidelines (some are summarized here), but there is a recent case where guidelines were followed. These cases tend to involve bites or scratches to the head and face, which tend to involve a more rapid progression from incubation through prodrome to the neurological phase.
So, since reports of post exposure prophylaxis failure tend to involve specific locations of exposure (head and face), it's reasonable to assume that an exposure there has a higher risk. There is no data supporting this risk for cases with pre-exposure vaccination.

What a vaccine does is simply providing the body an attenuated (avirulent) form of the pathogen, in this case Rabies. What our immune system does is recognise the particular foreign substance and produce immune cells against it, of which some cells remain as memory cells which would trigger an immune response much faster if the same pathogen enters the host again (assuming that the vaccination was successfully performed).
However, as you know that many virus mutate very quickly and if the extent of mutation leads to production of new rabies virus which is highly distinct from the form that was used as vaccine then the host will not be able to identify the new virus as rabies.
In that way the infection may take place


text:
What do phagocytes secrete?
What do phagocytes release after interacting with a pathogen? I know that this is a broad topic but I only need a general and concise answer.

Hi and welcome to Bio.SE! What type of phagocytes? I'm not an expert, but immunology responses like these are incredibly complex. What would also be helpful to a potential answerer would be your own attempts at an finding answer, and why those attempts didn't answer your question.

Wiki has lots of information about the interaction. They are secreted as purrulent flow. it sounds like a homework question which has been mixed up?

I think it would be hard to delineate what secretions are specifically because of phagocytosis, because in that sort of environment you have multiple types of cells secreting things, and multiple signals through such pathways as toll-like receptors (TLRs). So, I looked at papers involving activated professional phagocytes such as macrophages and neutrophils. The secretome of the activated cells follows a somewhat typical pattern for innate immune cells: IL-1ß, TNF family, interferons, IL-6, IL-8, and a host of other chemokines and cytokines (1, 2, 3). Mast cells of course secrete things such as histamine in response to Fc-receptor stimulation and TLR signaling.
Non-professional phagocytes like epithelial cells lack receptors to make phagocytosis efficient, but I'm far less certain about the body of data on non-professional phagocytosis. We know that activated epithelium and endothelium secrete inflammatory signals to attract immune cells, for example, like IP-10 which attracts CXCR3-expressing cells.

Phagocytes eat the pathogen cells by process of phagocytosis. They engulf the cell debris and pathogens by forming pseudopodia around them. However there are other cells which perform secretion. For example mast cells secrets histamine, serotonin etc. and fibroblasts secrets the blood matrix


text:
How does transition of osmoregulation occur in fishes when they migrate from sea to rivers and vice-versa
From my high school level knowledge I can recollect that there are two types of migration in fishes-

From marine to fresh water
(like in Hilsa which grows in the marine water but migrates to the fresh water only for reproduction and then the young return back to the marine water)
From fresh water to marine
(like in eels that live in the fresh water but migrate to the marine water to reproduce)

The only mechanism I had read about osmoregulation in aquatic organisms was via the ionocyte cells in the gills of the fish.
So my question is:
How do they change their osmoregulatory mechanism during this migration?
Just a follow-up:
Are there any other mechanisms by which they osmoregulate

I found a publication related to the osmoregulation in salmon that might be interesting to you. I'm copying the abstract because it basically answer your question.

Smoltification, also called parr-smolt transformation, is a complex developmental process that consists of a number of independent, but coordinated changes, in the biochemistry, physiology, morphology and behavior of juvenile salmon in their transition from freshwater to seawater life. A key component of smoltification is represented by the physiological adaptations that enable smolts to thrive in hyperosmotic environments. Instrumental to this process is the ability of smolt gills to gradually become capable of actively secreting salt through specialized cells known as mitochondria-rich (MR) cells, ionocytes or chloride cells. NaCl secretion by teleost gills is therefore accomplished via the secondary active transport of Cl - and the passive transport of Na + . The driving force for active transport is provided by Na + /K + ATPase, which maintains low intracellular Na + and high intracellular K + concentrations. However, this NaCl secretion mechanism needs at least two different ion channels: A CFTR type chloride channel for the passive exit of Cl - and a potassium channel to recycle extracellular K + , which is a thermodynamic prerequisite to work under conditions imposed by high extracellular salinity in seawater. The characteristics of K + channels required for NaCl secretion from MR cells into seawater are still unknown for Salmo salar and only recently have begun to be studied in other teleosts.

You can find the complete paper here.

thanks for the reply.But how does the reverse happen...I mean can you throw some light  on how the adult Hilsa or Salmon transform it's osmoregulatory mechanism during its migration from the marine to fresh water?

I don't know. Maybe is easier to move from salt water to fresh water, since you'll only need to shut down the regulatory mechanisms?. @user33690

Possible, infact I thought that too at first. But in fresh water fishes the ionocyte cells (chloride cells) act to drive the reverse reaction...that is, they take up $Cl^-$ from the surrounding water. So that kept me wondering...what was actually happening- some sort of transitions or simply stopping the entire process


text:
Primer design for PRP24-TAPtag
I have a problem with my proteomics homework. I was asked to design primers used to create a homologous recombination box to create PRP24-TAPtag yeast. I know that homologous regions should be 40-50nt and that my primer should include overhangs. I was told to base off of this publication:
https://www.ncbi.nlm.nih.gov/pubmed/11403571
I have designed primers before, but this time I have encountered really big problems. I have found both my plasmid, pBS1479, TAPtag and PRP24 protein sequences, but I have no idea how should I join them to create primers and how to include the TAPtag. This is my first time using this method. Are there any tools I can use for this task?
Should I add tag sequence to C end of my protein, then use plasmid seqence to create overhangs?


text:
Can a plastic degrading bacteria project be recreated in a school lab environment?
I am looking for a science fair project and am wondering if this could be a good idea. I am in the 10th grade. I am not exactly sure of the materials needed since this is just the beginning stages of finding a project. From what I've researched, the main objective would be to isolate bacteria from soils, to test these isolates for ability to degrade different types of plastic and to identify these microbes. We have until December 14 to finish experimentation and would have help from a lab technician. Do you know if this type of project would be possible and what we should inform our lab technician with in order to help us? Please reply asap as we don't have much time left to find a project. Anything helps. Thanks!


text:
Why is the mechanism of inheritance for this disease autosomal dominant?

An unrelated couple has a daughter and a son with the same rare condition. Neither parent has any obvious signs of the condition, but the father's mother (paternal grandmother) and her brother have the same condition. Select the most likely mode of inheritance:

A. X-Linked
B. Autosomal recessive
C. Autosomal dominant
D. Multifactorial
E. Mitochondria

The correct answer is C. But I'm confused why it would be autosomal dominant when neither parent has the phenotype. I thought it might be autosomal recessive, even though this mode usually does not have a family history, just because of the fact that the paternal grandmother and her brother both had the disease, and this is consistent with the horizontal pattern associated with autosomal recessive inheritance. For it to be autosomal dominant, the disease would have to be incompletely penetrant, which seems like a less likely scenario than it being autosomal recessive.
Can someone explain why it is dominant, not recessive?
Thanks!

Why does incomplete penetrance seem less likely than autosomal recessive?

I think this question is not possible to answer without knowing the frequency of the deleterious alleles in the population.  There's no way to assess whether incomplete penetrance is more or less likely than an undetected mutation in the mother's side.  Since the question doesn't mention the mother's family at all, and only the father's, that suggests to me that the question writers don't want you to think that anything is wrong in the mother's side.  That would make it dominant with incomplete penetrance.

Yes. I'd add in addition to using the magical key word "rare", they've specified the couple is unrelated. You have to read between the lines a bit, but whenever you see "rare condition" in a test question, be suspicious of any answer that would require two unrelated individuals to be carriers.

Thank you! And thank you for the tips on how to read between the lines for these types of problems. Many of these problems are very poorly/unclearly worded, so half the battle is just trying to decipher the wording.

Possible answers

A. X-Linked

It is possible. However, it is unlikely. The condition is claimed to be rare and as the daughter carries it, it means that the mother must have been a carrier. As the paternal grandmother also express the condition, it means both of her parents must have been carrying it. It is therefore a little unlikely. We would mainly see the condition in men but much fewer cases in women.

B. Autosomal recessive

It is indeed possible. As A, it is unlikely though. As the condition is rare, it is unlikely that both the parents of the paternal grandmother were both carrying the mutant allele and also the mother of the two kids is carrying the mutant allele. I would tend to think it is therefore unlikely. If we had more information (such as the frequency of the disease and/or how many siblings bother the paternal grandmother has), then we could have a better opinion about the likelihood of "B." being the good answer.

C. Autosomal dominant

No, it can't be as none of the parents don't express the condition

D. Multifactorial

The term "multifactorial" is a little unclear to me. It might mean that there is environmental variance and/or it might mean that there are several loci that affect the inheritance of this condition (with eventually some epistasis). All of these are definitely possible and likely (see below).

E. Mitochondria

It is unlikely as 1) the disease is rare and 2) the father's mother expressed the disease. The father did not transmit the mtDNA (as mtDNA is inherited from the mother only).
What I would answer
For the vast majority of phenotypic conditions we consider, the inheritance is controlled by several SNPs and there is some non-zero environmental variance (that is, heritability is different from 1; see this post).
In my opinion, the question is hard to answer, not because it is a hard question but because it lacks information (and clarity). If I really had to answer, I would probably answer "multifactorial".

Sons are more likely to exhibit X-linked conditions, not less.

Autosomal Dominant with incomplete penetrance can be fairly common, for example
SPASTIC PARAPLEGIA 3, AUTOSOMAL DOMINANT; SPG3A
HYPOPHOSPHATEMIC RICKETS, AUTOSOMAL DOMINANT; ADHR
There's also the chance of mosaicism in the father. Check OMIM for incomplete penetrance and autosomal dominant to get an idea.


text:
How does peanut pollination work?
I got curious about peanuts and when I found some photos on the internet, I could see they have flowers. However peanut fruit is underground.
How does pollination of peanut flowers affect the fruit underground? Or are there two kinds of fruit, one from flower and one from the underground?

https://en.wikipedia.org/wiki/Peanut

@John Where exactly is the explanation? Do you really think I didn't check wikipedia before asking?

Under the heading botany, it explains the entire process.


text:
How are sound waves amplified while traveling within the cochlea?
How are sound waves amplified while traveling from the basal membrane to apical membrane within the cochlea? Are they amplified by the movement of the stapes?

Short answer
Sound waves are, technically, not amplified in the cochlea. The answer to your question, however, is that outer hair cells amplify the acoustic signal in the cochlea.
Background
To answer your question what mechanisms exist that amplify sound within the cochlea - none.
What is amplified within the cochlea is the traveling wave that moves across the basilar membrane. The cochlear amplifier is mediated by the outer hair cells. These outer hair cells are thought to be able to contract and extend when the basilar membrane moves and thereby amplifying the traveling wave (Fig. 1).
The middle ear ossicles as you say do amplify the acoustic sound, but they are situated in the middle ear, as is the tympanic membrane, which also amplifies sound by funneling a large contact surface onto the small stapes footplate.This is not the answer to your question, as they are all middle ear structures.

Fig. 1. Inner ear structures (Fettiplace et al., 2001)
Reference
- Fettiplace et al., 24, Trends Neurosci (2001); 3: 169-75


text:
Why does a lightsource postpone the time it takes for the leaves falling from a birch tree?
It is autumn and the leaves have already left their trees on all birch and other trees that has leaves, except one. This birch has a spotlight pointed to the tree and it is on 24/7. I have recognized that this birch have lost almost no leaves. And if we take a closer look at this birch, the back side of the birch, which is faced away from the spotlight have lost a noticeable amount more leaves than the front side which is directly hit by the light from the spotlight.
My conclusion is that having a lightsource pointing to a leafy tree will postpone the time from when it loses its leaves, relative to trees that does not have a lightsource pointerd at them.
 But I have no idea why this is happening. I do not know anything about trees, leaves, chloryphyll or the reason why trees drops their leaves in the autumn.
If any one is a expert in this field and might know why this is happening, or just have a hypothesis of why this is happening please provide it since I find this really interesting and I can't find anything on Google about this phenomenon.
You can make your anwer as complicated as you wish, I will understand it even if I might need to Google some of the things in the answer :).
Thanks!

Hi, first of all i higly recomment you to take a tour in our help center. Belive me, this provide you with lots of information about this site including valueble price.  About your question if i understod it right you would like know if light source can post pone the deatf of leaves on tree. I higly doubt it. First off all the light source is very dangerous and tricky energy source. So i think it rather be vice versa.

Yes, you have understood my question right. The thing is that I have had  this spotlight pointed at many different trees under many years, and I always get the exact same result. So I have started to see a pattern. Lets say you have 2 trees, X and Y. If i point the lightsource at X, that tree will lose its leaves much later than other trees of the same species, while Y will lose its leaves same time as all the others trees. If I then switch the lightsource to Y another year, Y will lose its leaves much later than the other trees and X will lose its leaves the same time as the other trees,

Don't really have time to write out a proper answer, but the basics is: tree's (as well as many other organisms/animals) are able to measure length of a day using light sensitive proteins combined with circadian/rhythmically expressed regulators. This allows trees (etc) to properly regulate physiological functions - like losing leaves -  according to the seasons. Since tree/plants are immobile targeting with a big spotlight will confuse their light sensors and disrupt this system (more than for animals which can/will move away at some point).

The leaves drop because of the sharp drop in temp.
your 'keeping a spot[heat]light on them 24/7'' ,isn't allowing the tree to 'feel' the drop in temp. Therefore keeping it's leaves longer[postponing falltime] .Trees appear to be sensitive to temp.change.
I dont believe trees are 'Photosensitive' that applies to cannabis.

It's to do with the chemistry taking place in the system, and then in turn the balance of energy resources.
Leaves contain chlorophyll, a molecule that traps light energy. It is large molecule containing a long carbon chain and a magnesium atom surrounded by 4 nitrogen atoms. In terms of a plants energy resources it is an 'expensive' molecule, but it is worth it as it is important to the plant.
The conversion of light energy by plants, using chlorophyll, is called photosynthesis. The chemistry of photosynthesis using chlorophyll is complex, but essentially Carbon Dioxide (CO2) from the air is combined with Water (H2O) from the roots to produce sugar and oxygen. Excess sugar is transported to the roots and stored as starch, and some sugar is used to keep the living cells throughout the plant alive. They need energy and this gained through respiration. Again, the actual chemistry is quite complex, but simply put the cells take in Oxygen from the air and 'burn' the sugar to release energy, this gives off Carbon Dioxide and Water. (There is plenty of resources and explanation on the actual mechanism - search for "ATP and ADP in plants")
Notice that it starts with carbon dioxide and water and ends with carbon dioxide and water, the energy is held within the chemical bonds.
When there is plenty of light (and water) the rate of photosynthesis, and therefore the rate of energy production, is high. The plant is producing excess energy, and the leaves are 'worth' the energy needed to keep them alive and functioning. Note that temperature also has an influence. The warmer the temperature (to a point) the greater the rate of photosynthesis.
So, in temperate climates with markedly different day lengths and temperatures between the summer and winter seasons some plants have evolved to be deciduous and shed their leaves in the autumn. The point at which this will start to happen will be when the day length shortens, and the temperature drops, and so when the amount of energy that the leaves are able to produce starts to balance the amount of energy being used to maintain the leaf.
If a plant has an artificial light source then the leaves will continue to be able to produce more energy than they use and so will be retained for longer.


text:
Does drying meat in the sun make digesting it easier?
I was looking into the relationships between man, fire, brain size, evolution, etc. and I learned about other methods of food preparation that eased digestion, but did not use fire. Then, this question popped into my head. Specifically, I am wondering how much easier is sun-dried meat to digest; how much of a benefit is gained in the amount of energy needed for the digestive process?

I doubt it's easier to digest, the point of drying to make it harder for bacteria to digest which should make it harder for humans but our sheer mass means we can power through. You might find a better answer on the culinary stack. We also expect you research it yourself before asking it here.

Various food processing methods, such as cooking, can make meat easier, that is faster, to digest. The purpose of drying meat is to extend its shelf life, not to make it more digestible. Drying removes water from the meat and somewhat physically (but not really chemically) change it.
The amount of calories used for digestion is not that high; probably less than 100 Calories per day, so meat prepared in different ways does not likely significantly affect the amount of calories burnt.

Depends on how you define digestion.
If you consider chewing to be part of digestion, then this actually makes it more difficult as dried meat ("jerky") is harder to chew (into small pieces that are easier to digest) and harder for liquid (including saliva) to permeate.
Otherwise, ease of digestion is best defined at the molecular level. Tough fibers tend to be difficult to digest; pure protein can generally be hydrolyzed except in specific cases of structures specifically designed to withstand digestion. No idea if sunlight causes significant enough structural changes to change how digestable the meat is - that would depend on if the sunlight causes chemical reactions that "tenderize" the meat.


text:
How are chromosomes counted at the end of mitosis in a plant cell?
Page 89 of the Study Guide for Campbell Biology, 11th Edition has the following question:

A plant cell has 12 chromosomes at the end of mitosis. How many chromosomes would it have in the G2 phase of its next cell cycle?
a. 6
b. 12
c. 24
d. 48

Page 449 states that the answer is b.
As far as I understand, the number of chromosomes a cell has in G2 phase is double the number of chromosomes as it has after mitosis (which would imply the answer is c).
For (b) to be true, the plant cell must have had 6 chromosomes at the end of mitosis, but the question states it had 12. The only way I can imagine this to be true is that the question assumes that "a plant cell [...] at the end of mitosis" represents both daughter plant cells before the cell plate & cell wall has fully split the two daughter cells up, but doesn't "the end of mitosis" imply that the cell wall has completely formed and there are two cells (each with 12 chromosomes)?

I think I know what is confusing you.
A chromosome can have one or two chromatids. If you have two chromatids, you don't necessarily have two chromosomes. This is what happens during S-phase, during replication. Before the S-phase each chromosome had one chromatid, after the replication, it has two. So the number of chromosomes stays the same.
In the karyogram (the picture with all chromosomes), each object is one chromosome. Usually those will be double-chromatid chromosomes, and you will see a nick (like here). After these chromosomes divide, you get two separate objects → two identical chromosomes.


text:
What is the difference between transport proteins and effector proteins in gram-negative bacteria?
When considering pathogenic gram-negative bacteria, is there any difference between the function of  transport proteins and effector proteins? Or are they of the same functionality? Any reference would be very helpful.

Any difference with what? Gram positive, non-pathogenic strains? Please  expand your question to make it more clear.

This is a pretty clear question. It's asking for the difference between two types of proteins involved in bacterial pathogenesis. They are often not well described in microbiology classes.

Is there any difference between the function of transport proteins and effector proteins?

Yes. In this context, the term "effector proteins" refers to proteins that are inserted into a host cell on infection to modulate host cell processes. Effector proteins are inserted into a host cell using a secretion system. The proteins involved in the secretion system are transport proteins, but the effector proteins themselves have a wide variety of functions. They include enzymes, transcription factors, and protein-protein interaction partners, and they have been shown to regulate many host cellular processes, from metabolism, to vesicular trafficking, cell adhesion, and apoptosis.
You can read more about this here.  This review has an interesting perspective, and the Wikipedia page on Bacterial effector proteins isn't bad either.


text:
When in the cell cycle is the number of chromosomes normally reduced?
Page 96 of the Study Guide for Campbell Biology, 11th Edition has the following question:

A reduction in the number of chromosomes per cell occurs
a. During meiosis I
b. During meiosis II
c. During mitosis
d. During the S phase of interphase

Page 451 states that the answer is a.
I thought that the number of chromosomes at the end of meiosis I per cell equals the number of chromosomes in the parent cell (although sister chromatids remain attached), whereas the number of chromosomes at the end of meiosis II per cell equals half the number of chromosomes of the parent cell. If so, isn't the answer b?

It is the other way around. Meiosis I (or reductional division) splits chromosome pairs so each cell gets half of the chromosomes of the parent. Meiosis II (or equational division) splits double-chromatid chromosomes (making two single-chromatid chromosomes), so cells retain the number of chromosomes, like in mitosis.

If more clarification needed:

before the S phase: 23 pairs of chromosomes, 46 single-chromatid
chromosomes
before the meiosis I: 23 pairs of chromosomes, 46
double-chromatid chromosomes
before the meiosis II: 23
double-chromatid chromosomes without their homologous other
after the
meiosis II: 23 single-chromatid chromosomes without their homologous
other
after fertilization = before the S phase

(I'm talking about humans here.)

You could use C and .5C or something like that for the chromosomes and put the human values in parentheses.


text:
quadrupedalism in human
Recently I saw a BBC documentary on a family from a remote village in turkey where one couple has 18 children and out of which 5 are walking on four legs. These children are 28-34 yr old & have been like this since the birth. Is that story true ? if yes, then what is the explanation behind this in terms of biological evolution ?

@Ruchid Dalwadi Hi welcome to Biology SE. Feel free to take a tour, and take your first badge ! :)  You will find out there how to ask in your SE.  And now about your question. I think you can give us a few refference such a neme of documentary. Last but not least you should do some research on your topic before you post it. Please prevent your question from beeing unanswer. :) Good luck with your biology knowladge seeking :)

this would be a better fit for the skeptic stack

@L.Diago I am grateful for the piece of advice to the new comer here :)

@John with all due respect I did not realize that this question does not fit here as I am asking for a biological explanation as well.

Its fine that you did not realize, I am saying you will have a better chance of getting an answer on the skeptic stack. IS the claim true is outside the biology stack wheelhouse.  It would be important to establish if the claim is true before asking the rest of the question. https://skeptics.stackexchange.com/

@John makes sense :)

peice of advice the first thing they will want is the source of your claim, so finding out which documentary will be helpful.

I'm voting to close this question as off-topic because 1) the source is missing and 2) the question is hardly a fit for Biology.SE and should rather be asked on Skeptics.SE

It sounds like this might have been the BBC2 documentary "The Family That Walks on All Fours", in which case the Wikipedia page about it (linked) may contain all the answers you need.
In short: yes it's real; this is the Ulas family in rural Turkey. This is thought to be the result of a an inherited recessive genetic mutation resulting in cerebellar ataxia that impairs balance, meaning that they cannot balance well enough to walk confidently on two legs. From the Wikipedia page on the documentary:

Not being able to manage the balance needed for bipedal walking, they
  perfected in its place their initial bear-crawl into an adult
  quadruped gait. The family's walking likely has nothing to do with
  genes involved in the human evolution of upright walk.

(a "bear crawl") is a four-legged walk which uses your hind feet, rather than your knees)
It does not tell us much about evolution, but it does tell us something about how plastic motor development is. However, several of the experts interviewed in the documentary became interested in the case because they wondered if it might in fact offer insights into the genetic basis of bipedalism, so it's not a ridiculous assumption.

Interested in knowing what motivated the downvoter - don't be shy, I'm not strongly emotionally invested in this one :)

Id say that this is the result of continuous inbreding, which can result in a deletion of the gene that codes for "learning how to walk".

There is no such gene.

This is pure guess work. Also, it make little sense; why would inbreeding lead to gene deletion anyway?! Finally, I don't think either that such gene exist (to double kmm's comment)


text:
At what rate does C-BSE occur spontaneously?
BSE is back in the news here in the UK thanks to a new detection in Scotland. I haven't looked into transmissible spongiform encephalopathies much for a decade or so, but as I understand it the general model for TSEs is that an initial spontaneous misfolding of the protein PrP catalyses the misfolding of other PrP proteins until (over a fairly long incubation period) spongiform structural changes, amyloid plaque formation and other pathological changes cause CNS disease typically manifesting as behavioural changes. Ingesting a dose of misfolded protein can infect new hosts of the same species, and thus farming practices which include feeding animal byproducts to the same species can inadvertently amplify transmission, which resulted in the BSE epidemic in the UK back in the 1990s. Rarely, this transmission process can cross the species barrier.
I can find references to spontaneous scrapie in sheep and spontaneous CJD in humans, but very little on classical BSE in cattle. I do remember that there was a theory that BSE orginated when cattle were fed meat-and-bone-meal (MBM) from scrapie-afflicted sheep. I have found one peer-reviewed article suggesting that at least one type of atypical BSE (H-BSE) can occur spontaneously. I have also found one popular-science article that sounds like it describes spontaneous BSE, but it's unclear whether this is C-BSE or the H-BSE finding above (it's behind a paywall) and it's over ten years old, so I don't know what further developments there have been in this area.
Can classical BSE (C-BSE) arise spontaneously in cattle populations, and if so at what rate?

This paper suggests it was still be an unanswered question in 2006: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3291375/


text:
Anyone know what emerged from these cocoons?
Found a little universe in the back of a ceramic decoration I put up outside in summer...the concave back was full of grainy soil and several exited cucoons...anyone know what critter this is/was?!

Could you please add the size of these cocoons and your geographical location?


text:
What spider is that?

It was scared because my cat was playing with it. I saw it tonight (22 October) in Slobozia, Romania. I never saw something like it. The back is white with no points or marks or lines.

need a better picture from the top to help identify.

This is the only picture I have. It was big and I was kind of afraid

@Cataleya could you estimate the size?

okay I am not expert but I think the title is low and bad ,d oyou think

It's pretty clearly an Araneid of some kind, based on the large, globular abdomen, the eye arrangement at the front of the 'head', and the characteristic defensive posture when out of the orbweb.  All known orbweavers are completely harmless to both cats and humans, so nothing to worry about!
Unfortunately, I'm not familiar enough with central European spiders to tell you exactly what it might be, but I can assure you that it is not the only problem biter in your area - one of the Black Widows.  I include a photo I found of a common orbweaver in Europe (the Cross Spider) which was also caught out of its web, and in a similar position (although clearly not having been attacked by a cat..).  Whether yours is normally a plain white species, or yours is a leucistic (all-white or partially-white) variation of a normally darker and patterned species, I have no idea.  As I say, I'm not familiar enough with European spiders to be confident about something like that.


text:
Can you please help me identify this insect?

I have been trying to get rid of this bug and need help to identify it.
I found this in my bedroom first.
I don't think this is a bed bug as I saw it fly. It is black with some white spots on it.
Any suggestions on what it could be are greatly appreciated.
Thank you!

Can you please edit your question and add where you found this insect?

That is a bean weevil, family Chrysomelidae, subfamily Bruchinae. If you have dried beans at home, check for an infestation. Throw out the contaminated beans, and put your others in sealed plastic containers, or in the fridge. https://bugguide.net/node/view/13857

Thanks Karl, I checked my beans one kind of them was indeed infested with them, no rice or other grains were infested. But I still have one question how come they spread that much? Because there is a huge no of those in my house

They must have found another food source, or were attracted by the original infestation.


text:
What insect is this? (England)

Found this in my room and haven't seen anything like it before. It was about 4-5cm long and has wings. Flew away before I could get a better picture.
Photo taken from the Midlands, UK

The angle is a bit hard to see, but did it look like any of these? https://biology.stackexchange.com/questions/41682/identification-of-an-insect-from-midwest-us https://biology.stackexchange.com/questions/73638/what-type-of-insect-in-this?noredirect=1&lq=1 https://biology.stackexchange.com/questions/69158/help-identify-the-insects-i-keep-finding-at-my-house-auburn-wa?noredirect=1&lq=1

It looked a bit more narrow but it's head reminded me a little bit of a stink bugs. I don't think it was that though :/ Hard to tell since it flew off!

Okay; those have only recently shown up in the UK so maybe a long shot anyways, but I think you will have trouble getting a good ID without a more clear picture unfortunately.

i think i have a answer. But it might be schocking :)

I think i have an answer it is this nice guy.

Latin name is Leptoglossus occidentalis.
Short description of Leptoglossus occidentalis:

Western Conifer Seed Bug
  The Western Conifer Seed Bug Leptoglossus occidentalis is a large and conspicuous squashbug, reaching a length of 20mm when adult. It is easily distinguished from all other GB coreids by its reddish-brown body, transverse white zigzag line across the centre of its wings and characteristic leaf-like expansions on the hind tibiae.

Still i think i am right only with genus.

It looks absolutely adorable and looks more or less like what I saw. My measurement may have been a bit off at 4-5cm.

Maybe it is some species from that genus with bigger body. Still i saw it in my home town too, so i ll try to dig more information today.

I'm reasonably sure you're correct at the family level, less so further down ... the OP photo doesn't seem to show expanded hind tibiae.


text:
For how long would a flu-contaminated parcel be an effective disease vector?
A parcel has been delivered and contaminated by a person who has the flu.
For how long would the parcel be an effective disease vector?

Is spraying it with a 10% solution of bleach, letting that sit for 10 minutes really not an option?

Are we talking about actual influenza here? Most people, when they say “I have the flu” mean “I have a moderately serious cold”. The symptoms are somewhat similar but the pathogens causing it, as well as the severity of the disease, are completely different.

@swbarnes2 Rubbing alcohol or hydrogen peroxide also make good disinfectants, if bleach is not readily available.

@KonradRudolph true, and to a certain extent, both of those things ("I have the flu" means I have a respiratory virus, and most non influenza respiratory viruses are less severe) cancel out. In a community where confirmed influenza cases have spiked, the sensitivity of "complains of flu like symptoms" is high (which is what you want), and the specificity is higher than you'd think.

Worth noting, you can avoid this kind of concern in the future by getting your flu shot.

@Maxander you should avoid people with flu-like symptoms and practice good hygiene regardless. The flu shot is beneficial in a number of ways, but does not replace these measures.

To the close voters, this is not a "personal medical question", as defined and used here. It could be edited to depersonalize, but unlike personal medical questions, you need no personal clinical information to answer this one. When I was in clinical practice I would much rather someone find this answer on a website than bother my nurses with "how long should I wait before handling a package". The correct answer here is is not "go see your doctor"

OP, I've edited your question to make it more clearly on topic here and keep it focused on your question of interest, which is about the package itself. I disagree with the close votes you were getting, but your most recent edit included more text about your personal exposure history.  Please roll back or tweak the edit if you'd like. Be aware, though, that the more the question is "am I personally at risk for the flu" and less it is "what is the biology of flu transmission via fomites", the more likely it is this question will be closed.

Thing to note: postal packages might also have been contaminated several times due to being handled by infected or contamintated postal workers, or by being in contact with other infected packages, etc... And not only by flu, but other infections too. Actually, chances that any package you receive is sterile is practically nonexistent. So just practice good hygiene always (wash your hands, do not put them in mouth/nose/eyes etc)

@DeNovo I've simplified the question. What do you think of it?

@Wilson personally, I think it's less fun now, but my preference for fun questions might be a minority preference :)

How long should I wait before handling the parcel to avoid contracting the virus?

If you use gloves, or don't touch your face and just wash your hands after opening, you don't have to wait at all.  If you don't use gloves or want to pick your nose, rub your eyes, or fiddle with your beard while opening the package, wait 24 hours if the package is nonporous, and 2 hours if it is not. Generally, whether contaminated or not, don't lick, eat, inhale, or rub your eyes with the package :)
Influenza and similar respiratory viruses are transmitted by large droplets, aerosols, and fomites. Your package is a fomite, an object that can be contaminated and transmit disease. There is some debate about what mode of transmission is most significant for influenza, but fomites definitely do transmit influenza and similar viruses. In a study of homes and daycare centers with children who had an active influenza infection, 59% of home objects that were tested were positive for influenza. It's reasonably likely that your package was, at least at some point, contaminated.
@LDiago's answer is useful here, but deserves some clarification. The UK National Health Services information cited in that answer comes from this seminal study. I'm not entirely happy with the wording on the NHS website, though. Virus survives on nonporous surfaces for 24-48 hours. Virus is transferred from nonporous surfaces to hands in detectable amounts for 24 hours. If your package is paper, the relevant test is transfer from cloth or paper. Virus survives for 8-12 hours, and is measurably transferred to hands after 15 minutes to 2 hours. In any case, virus transferred to hands from a fomite survives for only 5 minutes.
Infection from fomites, however, requires virus to be transferred from the fomite to (typically) the hand, and then from the hand to respiratory tract epithelium. Inoculation of nasal passageways is sufficient for infection in laboratory conditions. Conjunctival and oral inoculation may also play a role. You can read more about this in Cecil Medicine Ch. 372 and Murray Medical Microbiology Ch 59.

i am sorry. I agree with you. I didnt checked the relevence of this study.... So thank you for your answer :)

+1 for the excellent advice of not inhaling mail order parcels!

"wait 24 hours if the package is nonporous, and 2 hours if it is not." - dang, that double negative is really tripping me up. So, you mean, "wait 2 hours if the package is porous, and 24 hours if it is not"?

@cell0 I rolled this back because the appropriate usage here is "Virus survives", not "the virus", and "the relevant test is transfer", not "transferred". The test isn't transferred, the test is transfer (of virus). I appreciate your editing efforts. Please try to evaluate whether you've changed the meaning of a phrase by editing it, though.

From the UK National Health Service:

Flu viruses capable of being transferred to hands and causing an infection can survive on hard surfaces for 24 hours. Infectious flu viruses can survive on tissues for only 15 minutes.
Like cold viruses, infectious flu viruses survive for much shorter periods on the hands. After 5 minutes the amount of flu virus on hands falls to low levels.
Flu viruses can also survive as droplets in the air for several hours; low temperatures increase their survival in the air.
Parainfluenza virus, which causes croup in children, can survive for up to 10 hours on hard surfaces and up to 4 hours on soft surfaces.

Any idea why the virus can survive 24 hours on hard surfaces, but only 15 minutes on a tissue?

How does the tissue kill the virus in 15 minutes?  It doesn't have anything that can break down the virus afaik.

@Nelson, dehydration.  Most viruses (and bacteria) are quite susceptible to being dried out.


text:
Linkage between chromosomal loci and the Hardy-Weinberg principle
Referring to the Hardy-Weinberg principle, which is always stated with respect to a particular locus on the chromosome, if we observe that two different loci are either always together in Hardy-Weinberg equilibrium, or never together in Hardy-Weinberg equilibrium, can this give us any information about the linkage between the two loci?

Linkage is a physical reality
Linkage refers to the physical presence of several loci on the same chromosome. Two loci that are said to be in close linkage mean that they are locataed relatively close to each other on the same chromosome.
Linkage disequilibrium is a statistical reality
If two alleles at two different loci are found on the same haplotype than expected by chance (that is more often than the product of the respective frequencies), then there is an statistical association between these two loci. We refer to this statistical association as linkage disequilibrium (abbreviated LD). If there is absence of statistical association, then the two loci are independent and we talk about linkage equilibrium.
Let's consider two bi-allelic loci. We will call the two loci A and B and the two alleles A0, A1 and B0, B1 at loci A and B, respectively. Let $p_{AB}$ be the frequency of the haplotypes that contains both A1 and B1. Let $p_A$ and $p_B$ be the frequencies of the alleles A1 and B1, respectively. Then LD between the loci A and B (called $D_{AB}$) is defined as
$$D_{AB} = p_{AB} - p_Ap_B$$
There are other related mathematical definitions of LD than $D_{AB}$, such as $D'_{AB} = \frac{D_{AB}}{D_{max,AB}}$ and the correlation of coefficient among the two loci $r_{AB}$.
Linkage disequilibrium and Hardy-Weinberg equilibrium
You will note that, knowing whether or not each of the two loci are in H-W equilibrium (or respecting the assumptions of H-W equilibrium; see this post) tells you nothing about LD among these two loci. For example, two loci can both be at H-W equilibrium but be in LD (or in linkage equilibrium). Similarly, two loci can both be at H-W non-equilibrium but be in LD (or in linkage equilibrium).
Linkage and linkage disequilibrium
Various things can affect LD. In theory, there is no need for linkage to have linkage disequilibrium. A strong epistatic interaction for early life survival between two loci (whether or not they are in the same chromosome) can eventually cause  LD. However, most of the cases of known LD probably concern pairs of loci found in tight linkage. There is a diversity of processes that lead to LD and reviewing them would be outside the scope of this answer.


text:
How to find idea for essay
I'm studying microbiology in Iran
The university that I'm studying in doesn't provide that much help in research areas and we don't get to research or write essays that much ,while I'm trying to write an ISI essay and communicate with universities abroad in order to get admission for my masters degree and be able to study abroad
But the problem is , I don't know how to start and find ideas for writing papers and research
Like, what is the first step you take as a scientist when you want to start research?

This question would be better suited to the academia stack exchange.

You might want to start by browsing the research papers (think of them as "essays") at https://www.plos.org/ to find the areas you are most interested in.  They have thousands of peer-reviewed articles which you can read for ideas for your essay and research ideas.   You might then consider contacting the authors of those papers to inquire about education or work at their institutions.


text:
Why does eating saturated fat increase blood cholesterol?
I am interested in the biochemistry of diet and the way we have been advised to eat for the past forty years.
In researching an explanation for the relationship between dietary fat and blood cholesterol I came across the following: "It is clear that eating too much saturated fat increases the levels of cholesterol in the blood, especially our "bad" cholesterol which doctors refer to as LDL". This is from heartuk.org.uk.
"It is clear ..." - really?
I am mystified! I understand that dietary fat, other than very short chain fatty acids, does not immediately enter the blood stream but is transported via the lymphatic system as triglycerides packaged in protein assemblies called chylomicrons, finally entering the blood via lymph nodes under the armpits. Once in the blood the triglycerides are hydrolysed into fatty acids and transported to appropriate cells in albumin complexes.
Where does LDL feature in this transportation? And, by the way, why just saturated fats? Surely the small intestine doesn't differentiate between saturated and unsaturated fats, or does it?

Focus of your question seems twofold:
a. there is a missing link between chylomicrones/saturated fat going straight to adipose tissue on one side and liver producing bad cholesterol/LDL(VLDLP) on the other side - causality?
b. there is no reason to differentiate saturated from unsaturated fat: either unsaturated fats share the same fate or they pass over to the liver directly, and why should they not induce production of bad cholesterol/LDL(VLDL)

"Surely the small intestine doesn't differentiate between saturated and unsaturated fats, or does it?" - To formulate in another question: fate of saturated and unsatured fats in instestine/enterocytes?

In short: It may not be saturated fat by itself but high saturated/unsaturated fat ratio and high animal/plant fat ratio in the diet that increases the risk of heart disease.
A systematic review of the effect of dietary saturated and polyunsaturated fat on heart disease (NMCD Journal, 2017)

Reducing saturated fat and replacing it with carbohydrate will not
  lower cardiovascular events or CVD mortality although it will reduce
  total mortality. Replacing saturated fat with mono- or
  poly-unsaturated fats or high-quality carbohydrate [from whole-grain
  food] will lower cardiovascular events.

Saturated Fatty Acids and Cardiovascular Disease: Replacements for Saturated Fat to Reduce Cardiovascular Risk (PubMed, 2017)

Replacing dairy fat with carbohydrates from refined starches and added
  sugar was not associated with increased or decreased risk of coronary
  heart disease (CHD), stroke or total cardiovascular disease (CVD).
  However, replacing dairy fat with carbohydrate from whole grains
  reduced the risk of CVD, CHD and stroke. Relative to other animal
  fats, dairy was found to have less impact on CVD. When 5% of energy
  from dairy fat was replaced with animal fat from non-dairy sources,
  risk of CHD increased by 6%. However, when 5% of energy from dairy fat
  was replaced with an isocaloric amount of polyunsaturated fats, risk
  of CHD was reduced by 26% and CVD risk was reduced by 24% [41].

A basic explanation of the underlying mechanisms:
The liver produces low-density lipoproteins (LDL) and high-density lipoproteins (HDL). Lipoproteins are composed of triglycerids, phospholipids, cholesterol and proteins.
LDL caries cholesterol from the liver to the peripherial tissue, including arterial walls, where it can accumulate and cause atherosclerosis. This is why LDL is called "bad cholesterol" (even if LDL is only a carrier for cholesterol). HDL clears excessive cholesterol from the blood and carries it to the liver for disposal, so it is called "good cholesterol. (Heart.org.uk)"
High LDL levels are associated with an increased risk of coronary heart disease (Bentham Open).
One possible mechanism by which saturated fats increase (LDL) cholesterol (PLOS):

Saturated fat is thought to increase LDL-C primarily through
  down-regulation of hepatic LDL receptor activity, leading to reduced
  clearance of LDL particles [from the blood].

Why is it saturated and trans fats are bad and unsaturated cis fats are good? The only difference between the two isomers is shape: saturated and trans fats are essentially linear whereas cis fats are bent. If indeed there is a causal link between linear fats and vascular disease then surely it can only be due to their conformation?

In medicine and nutrition, it may be enough to know what is the net result of high consumption of a certain nutrient without knowing the mechanisms. I'm sure, the exact effect of various types of fatty acids on LDL production is described in detail somewhere, but this is too much for this site, at least for me. They could know more on https://chemistry.stackexchange.com/ . The metabolism of LDL occurs in the liver, so you do not need to concentrate on what happens in the intestine and how fats come to the liver.

@adlibber Trans-fat are quite stable because the molecules are tightly packed due to trans structure. And saturated fats do not have a double bond (which makes the molecule reactive) , so they too are stable.

Interesting point user237650. So does stability = ‘bad’? And if so why so?

Fair criticism Jan but you could also say that all these questions relate to physics as well. This is a human physiological question and I felt that ‘biology’ was a more appropriate cover than ‘chemistry’. I’m not a biologist nor am I a biochemist so imagine the difficulty I’m having with this subject! i’m in fact an old retired systems engineer interested in all the noise about nutrition!

@adlibber, It can help tremendously if you say what is the exact goal of your research? Do saturated fats increase LDL? Do they increase the risk of heart disease? Or you are strictly interested in how all this happens on biochemistry level? I had a feeling that you are trying to find a direct connection between the structure of fatty acids and LDL synthesis. While this can make sense, it can be misleading, because you need to see the whole picture: the sum of effects of all fatty acids on LDL...

@jan, my goal is to find out whether eating a high fat low carb diet with lots of dairy etcetera is going to kill me. I am confident enough with my research thus far to have stopped taking statins after ten years of medication for high cholesterol. The subject is also of great importance in terms of the current obesity and associated diabetes epidemics. Getting into the available science helps to clarify the fog.

I edited my answer and the essence of it is in its first sentence. The risk of heart disease seems to increase with high sat/unsat fat and high animal/plant fat ratio. So, it's about what comes in and what comes out. Merely concentrating on the isolated effects of various fats and other nutrients on LDL alone can be grossly misleading.

@adlibber I can't say for sure but I think it will be hard to metabolize them. Also read this, but again I can't say if the claims are entirely true.

@user237650 many thanks for the link. Is Kendrick correct is the big question of course! If he is then he is in agreement with my understanding obtained elsewhere and hence my original question. The BMJ came out with this a few months ago illustrating the abject confusion on the subject. My gut (excuse the pun) tells me Kendrick is right!

re last quote. (PLOS): It's an empirical study, isn' it. However, in "Discussion" at the end of the paper there is some  theory on reasons for LDL being bad which I haven't  understood.

They asked about why increased saturated fat intake increases blood cholesterol levels, they did not ask about heart disease risks

"Why does eating saturated fat increase blood cholesterol?"
From your explanatory text I understand: ... as it is transported by chylomicrones and not by LDL which is commonly known as "bad" cholesterol.
I'm paraphrasing even more: How could eating saturated fat which is not transported by LDL (termed "bad cholesterol"), and for this reason should not lead to more LDL in the blood, be held responsible for "bad cholesterol"?
There are two common misunderstandings I think your question brings up (educating, to me):

Chylomicrones are not the only transporters of (saturated) fatty acids. There are the VLDL as well doing that job. The difference is termed "dietary fat" versus "endogenous fat". The liver is the body's biggest producer of (saturated) fatty acids (interestingly, the liver produces but saturated fatty acids!). This fat is transported from the liver to tissues  by VLDL (Very Low Density Lipoproteins). It is no trivial knowledge that LDL is not produced by the liver "as is", only the VLDL are. However, VLDL become "bad" LDL in the bloodstream.

Lipoproteins and Chylomicrones per se, as transporter molecules, incorporate cholesterol, in different amounts and percentages of total weight. From textbooks it may be easy to tell whether   cholesterol is a "part" of the transporter or being transported as  "package". Cp.Dr. Malcom Mkendrick (paragraph"re-cap")

What might appear as   some   "breaking news" AD Cooper · 1997 "Chylomicrons are formed in the intestine and transport dietary triglyceride to  peripheral tissues and cholesterol to the liver." Still another one: Enterocytes not only produce chylomicrones but VLDL, too.

Both Chylomicrones/chylomicrones-remnants and VLDL/"VLDL"(called LDL) resemble each other in their "later life" termed "remnant". What remains of VLDL after unloading fatty acid is termed LDL, and  packed cholesterol may  look like a building block of the lipoprotein (as the LDL receptor of tissue cell takes up LDL as is - no unloading).  Hint: my misunderstanding taken for typical learner's was to think of LDL being sent off by the liver - not correct: it's VLDL off from the liver, and "remnancy" after unloading fatty acid at the veins' walls. So VLDL become LDL in the blood stream. There is a special page in Wikipedia not easy to find:Remnant cholesterol
These preliminary remarks  are  practical hints, as you may search for "why does eating saturated fat increase VLDL (very low density lipoproteins) and get some clues and discussion via google -instead of searching for "saturated fat and LDL
Why is LDL held responsible for "bad cholesterol"? Among the lipoproteins it has the highest load of cholesterol; and  as a "remnant" transporter of cholesterol it does seem to unload cholesterol  at arterial walls just as that same transporter (named VLDL at that point)= does with fatty acids -  if tissue cells not in need of cholesterol do not express the LDL receptor (Nobel prize winners Brown and Goldstein's research on familial hypercholesteraemia).
That said, why then should reduction of dietary saturated food reduce VLDL and/or LDL (your question translated to that formula) as the only "clear" effect of saturated food is a higher production of chylomicrones which are very low in cholesterol?
Did you read my latest news up above?  I think it is no common knowledge that chylomicrons are  involved in cholesterol transport from the intestine to the liver.  Simple inference from that: more cholesterol input (combined to saturated fat) causes more cholesterol output (combined to fat, VLDL which becomes LDL "on deliverance").
However, searching  through literature, your question turns out  to be valid - nothing is "clear" and undebated, and that goes for the   following simple reasoning as well, recurring to basic knowledge (before I knew about chylomicrones delivering cholesterol to liver):
Effect of dietary saturated fat is that the liver will be able to synthetize and deliver to tissue cells more of  so called endogenous fat as it receives  more of fatty acids FROM tissues the more those tissues receive fatty adics from chylomicrones (see below about pathway from tissue TO Liver-Hint: it is not irrelevant in respect of your question that short fatty acids do not need chylomicrones for uptake from intestine, and it seems that in early scientific discussion the high amount of any kind of fat, saturated or not, was subject of debate).
Any surplus of fat the liver produces is transported to tissues (Stryer/Berg, Biochemistry)  by
VLDL, the Very Low Density Lipoproteins.
The important crossroad of those pathways is at  the arterial wall where VLDL unload endogenous fat from and made by the liver. VLDLs thus become "ILDL - Intermediate-Density Lipoproteins", half of which is returned to the liver for turnover, half of which,  however,  become LDL (how? By "unloading more fatty acids", cp. Berg/Stryer, Biochemistry).
So, this presumed mechanism is in favour of the quote cited: more saturated fat deliverd by chylomicrones will lead to more saturated fat in VLDL  which, after unloading fatty acids, become "bad" LDL transporting cholesterol (only). More saturated fat input is seen here as a "commodity" the liver replenishes its production of endogenous fat with.
Let me give you some quote describing the pathways, to see how the liver receives (saturated) fatty acids taken in by chylomicrones that have delivered to storage fat tissues (not to liver!). VLDL are only needed for transportation FROM the liver, not to the liver. How might liver input of fatty acids, leading to bad LDL, be heightened by chylomicrone input?
From:
[K.R. Feingold, Introduction to Lipids and Lipoproteins][1]

"...The exogenous lipoprotein pathway starts with the incorporation of dietary lipids into chylomicrons in the intestine. In the circulation, the triglycerides carried in chylomicrons are metabolized in muscle and adipose tissue by lipoprotein lipase releasing free fatty acids, which are subsequently metabolized by muscle and adipose tissue, and chylomicron remnants are formed (...) then taken up by the liver. The endogenous lipoprotein pathway begins in the liver with the formation of VLDL."
In Berg/Stryer,10ed., Fig. 26.16 depicts Fig 36.1 of Goodman/Gilman: The liver receives free fatty acids released into the blood by "adipose tissue", i.e.  tissue cells that have received saturated fats from chylomicrones.
So, if (saturated) fat input is transported to STORAGE tissue by chylomicrones high input of fat may lead to excess,  surplus storage of fat in adipose tissue, then to  free fatty acids input of   the liver which metabolizes to endogenous triglycerides(!) "re"-transported to storage and/or catabolic tissue. It may be a question of debate whether LDL from VLDL being turned to ILDL is a metabolic switch the aim of which is to "store as much as possible" - where, at the end of the line  fat broken down in liver and re-metabolized to cholesterol by the liver (via acetyl-CoA) can be stored as  cholesterol by any cell that is able to store away cholesterol,then not using cholesterol as building block of its membrane.
This point alludes to the second part of my answer that differentiates between animal and plant tissue: animal cells much more than plant cells might be able to STORE cholesterol which might explain why animal fatty tissue contains roughly 100 times more cholesterol thatn plant fatty tissue, see down below.
Quote continued:
"The triglycerides carried in VLDL (annot. see quote above: triglycerides made by the liver)  are metabolized in muscle and adipose tissue by lipoprotein lipase releasing free fatty acids and IDL are formed. The IDL are further metabolized to LDL, which are taken up by the LDL receptor in numerous tissues including the liver, the predominant site of uptake."
Surpringly, the liver emits LDL, but does have LDL-receptor.
These LDL-receptor of the liver are said to take receive "chylomicron remnant", see, for instance, Dr. Malcom Kendrick
Assuming those LDL-receptor of the liver also take up LDL that has been refused by tissue cells however,  seems coherent to some basic principle of "store ("can"..) as much as you can": fat non used or stored in tissue being receivevd by the liver (free short fatty acids in blood!), liver handing its surplus back to tissue on VLDL; surplus fatty acid in liver metabolized to cholesterol, delivered to cells, cholesterol not taken up by cells  returned to the liver.
Thus, deposition of bad cholesterol in veins can be seen as some last resort of storage activity, in case the liver does restrict LDL-receptors as presumably tissue cells have done before.
Thus, excess (saturated, but, as you suggest: same should apply to unsaturated) fat in food might lead to excess storage activity by bad LDL.
Refering to the distinction between saturated and unsaturated fat your question seems to focus on  see, for instance,  Palm Oil Consumption Increases LDL Cholesterol Compared with Vegetable Oils Low in Saturated Fat in a Meta-Analysis of Clinical Trials
Ye Sun et al.,  This digest of empirical studies speaks in favour of saturated fat in contrast to unsaturated fat increasing "bad" (LDL) blood cholesterol. Doing quick research I did not find any explanatory theory. Here is  hint: Among unsaturated fatty acids there are some that are "essential" (as vitamins are). That is mentioned here:  [bmj.com] 5https://www.bmj.com/content/361/bmj.k2139 Maybe metabolism of essential unsaturated fatty acid signals a situation where there seems to be less need to turn fatty acids into cholesterol and send it to tissue cells (because those are signalled to be able to synthesize enough on their own). That's one idea.
Even if there is somehow "clear" causality in
dietary fat - chylomicrones - liver production of endogenous fat - VLDL - VLDL remnants - LDL
it seems to be debated on if there is a  difference between saturated and unsaturated fat in that respect. "You're right."
In the following, I would like to show that the statement "less fat, less cholesterol" your question refers to  might still be correct, in its statement of a rule of thumb, in its empirical result, especially in what regards differentiating unsaturated and saturated fat.
Content of cholesterol in food may be considered as   proportional to content of saturated fatty acids.
If you exclude saturated fatty acids from your diet according to the rule quoted in question you end up with zero input of cholesterol, and you end up as a vegetarian.
This is because

food from plants does not contain saturated fats - with a few exceptions: coconut and palmoil, nuts..., and

food from plants does not contain cholesterol in form and relevant quantity as animal food does.

"While cholesterol averages perhaps 50mg/kg total lipid in plants, it can be as high as 5 g/ kg(or more) in animal."
This is a factor of 100!
Quote is from a paper advocating the opposite point of view (no bias):
Journal of Chemical Education  J. Behrman* and V. Gopalan, Cholesterol in plants
However,
"There is a widespread belief among the public and even among chemists that plants do not contain cholesterol. This error is the result (in part) of the fact that plants generally contain only small quantities of cholesterol and that analytical methods for the detection of cholesterol in this range were not well developed until recently (1). Another reason has todo with the legalities of food labeling that allow small quan-tities of cholesterol in foods to be called zero (...). The fact is that cholesterol is widespread in the plant kingdom although other related sterols, such as β-sitosterol (henceforth referred to as sitosterol), generally occur in larger quantities. No current biochemistry text that we have examined provides an accurate account of cholesterol in plants.  Here is a suggested paragraph for the next generation of biochemistry texts: More than 250 steroids have been described in plants (3).Of these, perhaps sitosterol, which differs ..."
I think it's legitimate to inversely defere from this quote that food derived from plants, at least, does not contain cholesterol in  amounts relevant to nutrition.
See also Athel Cornish-Bowden
From  Wikipedia:
"Plants make cholesterol in very small amounts.[...] In larger quantities they produce phytosterols, chemically similar substances which can compete with cholesterol for reabsorption in the intestinal tract, thus potentially reducing cholesterol reabsorption." Wikipedia, Cholsterol
From Biology online
"Because of cholesterol that provides cell membrane structural integrity and fluidity, animal cells need not to have cell walls such as that in bacterial and plant cells."
Refering to point 2 of reasoning above:
"Most animal fats are saturated. The fats of plants and fish are generally unsaturated."
Wikipedia, Unsaturated Fat
Thus, avoiding saturated fat means avoiding animal fat, thus avoiding cholesterol.
Again, this reasoning is not what the quote  cited in your question seems to refer to or be based on. As an empirical rule it might be correct for the reasons stated.
To sum up: Even if it must be admitted that there are relevant amounts of saturated fat in plants, reducing saturated fat in diet in any case reduces cholesterol input (even if that'd mean the exclusion of coconut, palm oil and peanuts, from the diet - in that way you'd sure still end up a veggie).

No references are cited to support this answer.

@Bryan Krause I added some reference and am sure to be able to add many more references. However, I have become some suspicious mind with you - personally! - and I am begging you to either withdraw comment or downvote, explain what's wrong, or - best - delete this anwer that moreover I guess is not politically correct. Can user delete answer on his own? thanks.

Yes, users can delete their own answers. The references you've included do not seem to support the main conclusions in this answer. The first includes a quote but the citation is not sufficient for a reader to find the source of the quote, and therefore invalid. The second is also insufficient for a reader to find the source of the quote.

Hi, Bryan Hi,  Thank you for your criticism, I tried to amend accordingly, and very much expanded my answer according to what the question seems to focus on.  Let me know if you want me to delete the answer. There will be others.

I gave you an upvote for trying so well to support your answer. (I didn't read the sources, so I won't comment on their appropriateness.) I can't remove downvotes; only the downvoters can do that. To notify Bryan, you need to "ping" him by using the @ character before his name (he didn't get notification of your comment.) I'll do that for you: @BryanKrause - Is this answer improved enough for you to remove your downvote? Thanks.

Upvoted your answer for the amazing effort. It is definitely educative to me. Please don't delete it. The SE community behaves too protective. I have always felt with most SE sites that curiosity is not welcomed by the SE community. There is sadly always an attitude of "you should know better" or "how can you ask such a foolish question" or "how can you write such an amateurish answer". I have always faced unnecessary and unexplained mass down-voting.

I think you are right to question this "wisdom". In my opinion the statement from the web site that you linked is simply wrong. The idea that eating fat would make you fat dates back to the 1960s and was originally published by an MD just as offhand speculation, not any kind of science. Since then many others have just mindlessly repeated this incorrect idea.
First of all, it is physically impossible more or less for fats to be transported through the intestinal wall (see http://www.vivo.colostate.edu/hbooks/pathphys/digestion/smallgut/absorb_lipids.html or Heinemann, T & Axtmann, G & von Bergmann, Klaus. (1994). Comparison of intestinal absorption of cholesterol with different plant sterol in man. European journal of clinical investigation. 23. 827-31.) Dietary cholesterol has to digested into more basic lipids and then transported through the intestinal wall by special molecules to be absorped by the body. So, the idea that eating eggs or whatever would give you "high cholesterol" is just an irrational idea.
Note that you will find papers with statements like 30% of dietary cholesterol is absorbed or 50% of dietary cholesterol is absorbed by the body and so forth, but these papers are either just observational papers that have no real controlled science behind them, or they are misleading. For example, it is true that 50% of dietary cholesterol gets DIGESTED and absorbed, but what gets absorbed is not cholesterol but monoglycerides and other small lipids that are the product of digestion. There are a lot of nutritional papers out there that just gloss over this and falsely imply that because cholesterol is being digested, that it is being absorbed whole, which is not true.
Virtually all serum cholesterol is synthesized by the body in the liver. The liver synthesizes cholesterol from fructose, a simple sugar that can be derived from complex sugars like cane sugar or from carbohydrates, such as wheat. Carbohydrates are first broken down into starch, then the starch is converted into sugars and the fructose component is circulated to the liver where it is converted into cholesterol or other things, such as triglycerides.
Concerning transportation of LDL: LDL is insoluble in water and cannot be transported across epithelial membranes. It must be digested into small lipids like monoglycerides with a watersoluble shell and then be transported by micelles. In the blood, triglycerides or LDL cholesterol manufactured by the liver can be transported for storage by special molecules called lipoproteins which emulsify the LDL and allow it to be transported in an aquaeous medium (the blood). In this form the LDL cannot cross any bodily membranes, but can only be placed in storage areas with direct blood contact. To be utilized as food for cells, LDL and triglycerides have to be circulated back to the liver where they are further broken down into COA, glucose and other types of molecules that cells can use as food.

Please add some (simple textbook) reference to "LDL is insoluble in water..." - that can't be true, as the function of the Lipoproteins is to make water insoluble fat soluble in blood, in water for transportation purposes. Please add some reference for tissue taking up cholesterol by "micelles", not by LDL-receptor (not to mention Nobel prize winners Goldstein/Brown). Did I get you wrong?

@PeterBernhard All lipids are insoluble in water. Very first sentence in this book: https://www.ncbi.nlm.nih.gov/books/NBK305896/. LDLs are not and cannot be transported across the intestinal wall for various reasons including their size. "Cholesterol is only minimally soluble in an aqueous environment and thus must be partitioned into bile salt micelles prior to absorption." direct quote from this book: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2692399/. I am aware there are papers claiming dietary cholesterol can be transported across the intestinal wall whole (continued)....

The intestinal wall has a paracellular pore size of about 10nm and only hydrophilic molecules smaller than this can traverse it. Micelles fit these restrictions. LDL, triglycerids and other large lipids are at least this large and are NOT hydrophilic, so they have no way to pass through the intestinal wall, unless they have been digested to smaller molecules and then attached to or enveloped by hydrophylic carriers such as micelles.

My first impression of your answer was that it might be a comment to my answer, rightly questioning the premise of its second part, ie.e. more cholesterol in food  means more bad cholesterol transport to cell.  Actually, the question here - there are several others on Stackexchange - focuses on "more fatty acids", and even more: on saturated fatty acids input.  - More fat does not mean more VDHL? Didn't you mention fat being stored away before it gets to the liver? Then "insuline" might be a worthy word.

Highly enlightening I find "The intestinal wall". Bluntly: LDL has got anything to do with the intestinal wall, as you mentin LDL in that context. I'd be interested in your textbook or even internet reference for LDL not soluble in water or blood.  How could LDL be a transporter of fatty acids? The word "acid" has it: any acid is hydrophilic. Can it be? The fat renders the LDL soluble? That is amazing and should clearly be emphasized in any textbook. Are you sure?

@PeterBernhard Did you not read my comment? "All lipids are insoluble in water. Very first sentence in this book: ncbi.nlm.nih.gov/books/NBK305896." Maybe read my entire comment before making snarky remarks? Do I have to link this book a third time?

I'm no good at snarkiness, please apologize. You want me to delete my comment, that'd be ok with me. Your reference is useful to anyone, however, it does not cover "LDL". These Lipoproteins are proteins, after all, so to say, and should be soluble. Snarkily: "...LDL, triglycerids and other large lipids" not soluble - not correct! Please falsify me. Is it okay for me to read and "digest" my lengthy comments into some list or so, to shorten what might be considered small talk by webmater and peer?

Let us continue this discussion in chat.

Again, your answer focuses on uptake in intestine, and that is 50 percent maybe of what the question is about. No "snarkeyin'": please explain more what your understanding of LDL is.

"Low Density Protein" is a protein, thus soluble in blood and water
Nowhere it's written that LDL gets closer to the intestine wall (pun: it's written on any wall of textbooks that LDL gets close to the arterial walls). You seem to state that LDL is a transporter from the intestine. That's not correct.

From Wikipedia: "Chylomicrons transport lipids absorbed from the intestine to adipose,  ... and  ... muscle tissue, where their triglyceride components are hydrolyzed by the ... lipoprotein lipase, allowing ... free fatty acids to be absorbed .... When a large portion ... s been hydrolyzed, chylomicron remnants are formed and are taken up by the liver, thereby also transferring dietary fat to the liver."
I'd be interested in knowing if "pancreas lipase"    breaks down unsaturated, not saturated fat, within intestine for "easy uptake", similarly: enterocytes, in stead of muscle/adipose cells.

From 2nd paper : "major lipoproteins secreted by the intestine are VLDL and chylomicrons." Surprising to all I bet. Enterocytes and liver cells so similar.   However:  LDL not mentioned in text.   LDL, in evolution, might have started as you appear to wrongly assume: as an uptake instrument. It wouldn't be surprising if you'd be right assuming enterocytes shedding LDL into the intestine... what for? For uptake of triglycerides - it's just the inverse of VLDL converted to LDL by un-loading. In evolution LDL might once have up-loaded. Please accept moving to chat except you want me to stop "it".


text:
What type of wildflower is this?
I live in Utah and I'm wanting to plant some Utah native plants in my backyard. There is this wildflower everywhere in the mountains of Utah and I really want to know the name. It looks like some sort of Paintbrush (Indian, Wyoming) but I've searched for those and they don't look the same.

As picture doesn't have different close up looks, by its color and looks I think, this is definitely a species of Castilleja ,commonly known as Indian Paintbrush or prairie-fire :

Castilleja, commonly known as Indian paintbrush or prairie-fire, is a genus of about 200 species of annual and perennial herbaceous plants native to the west of the Americas from Alaska south to the Andes, northern Asia, and one species as far east as the Kola Peninsula in northwestern Russia. These plants are classified in the family Orobanchaceae (following major rearrangements of the order Lamiales starting around 2001; sources which do not follow these reclassifications may place them in the Scrophulariaceae). They are hemiparasitic on the roots of grasses and forbs. The generic name honors Spanish botanist Domingo Castillejo.

It is more likely to be a species of Castilleja called Castilleja rhexifolia.
Common names : Alpine paintbrush , Rose(y)  paintbrush.
Family : Orobanchaceae (Broomrape Family)
From reference : Comparison between Castilleja haydenii and Castilleja rhexiifolia ;

Castilleja Rhexiifolia bract colours are most often hot rose-pink, but they range from subtle magentas to flaming rose to hot iridescent pink.

And on the left and right sides of the question picture have comparatively lower/light pink colour or iridescent pink color and the central flowers are comparatively darker or more magenta when compared to side ones.
Side ones :

Central flowers /focused flowers :

Welcome to Biology.SE. You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion, which is not appropriate for answers on this site. ——— Thank you for taking the the [tour], but please also consult the [help] pages for additional advice on [Answer] effectively on this site.

@tyersome Thanks a lot for the guidance! I have updated my answer.


text:
Why is peripheral vision not bleached by daylight?
In daylight, rods are known to be bleached: we have to wait some time after going into darkness before scotopic vision becomes effective. But, as I understand, peripheral vision is also mostly due to rods, since away from the fovea, cone density rapidly declines.
But I wonder then: if rods normally saturate in bright light, why does peripheral vision still work in daylight?

Short answer
In photopic lighting, peripheral vision is mediated by cones.
Background
The rods are indeed saturated at daylight, and even at twilight (source: Nature). However, the cones are active and although their density in the periphery is low, they are still present (Fig. 1). Hence, peripheral vision in photopic lighting conditions is mediated by cones. Because of their low density in the periphery, however, visual acuity is low (Kolb, 2012).

Fig. 1. Rod & cone densities in the retina. (Kolb, 2012)
Reference
- Kolb, Photoreceptors, In: Webvision: The Organization of the Retina and Visual System. Utah University

This seems to contradict this answer, which doesn't appear to rely on scotopic vision to explain its point. Is it wrong?

@Ruslan For primates, AliceD's answer here is better. See also Stabell, U., & Stabell, B. (1976). Absence of rod activity from peripheral vision. Vision research, 16(12), 1433-1437. and Stabell, U., & Stabell, B. (1982). Color vision in the peripheral retina under photopic conditions. Vision research, 22(7), 839-844.


text:
Identify plant from genus *Solanum*
This spring we have recieved from a local Botanical garden in Southern Germany a pack of seeds with the label "surprise". We could grow one plant from the seeds, the seeds looked like "pepper" = Paprika Capsicum annuum seeds. The plant got about 50 cm high and bore one fruit of 5 cm length including the trunk. The leaf in the picture has 10 cm total length. It has a very rough backside but not really hairy one. Also the upper side feels rough but there are no hairs. Also some yellow flower can be seen.
Initially I thought it is some capsicum so I cut it but was surprised when I saw the thick pulp. The skin is also quite strong and like very soft leather. It has a nice sweetish taste and some remembrance of lemon in taste but also some exotic "veggie" note. What could that plant be?
After searching the web my idea was that it could be Solanum sessiliflorum DUNAL, that is Amazonian tomato or "cocona". But I am not sure at all. Any hints appreciated!

If I were you I would probably ask the garden :)

Yes, I had already that thought as well ;-)