text:
How would a plant sprout and grow in a zero gravity environment?
Have any experiments been carried out involving sprouting and growing plants in a zero gravity environment? If so, what was the outcome? How did the plants sprout out of the soil without gravity? Did they grow outward or toward light sources?

There have been several experiments in growing plants in microgravity (strictly speaking, we do not achieve "zero-g" since astronauts remain in orbit about the Earth).
Changes in plant growth due to the influence of a gravity field is sometimes called gravimorphogenesis. More specifically, gravitropism is a differential growth response of plant organs to gravity. For example, roots grow downwards (positive gravitropism) and shoots grow upwards (negative gravitropism) on Earth.
Studies (e.g. 1) suggest that in micro-g, there is no preferred direction; roots may grow "up" and shoots "down".
It is thought that this growth response is due to the relative distribution of auxin in the plant. On Earth, auxin will preferentially move down into the root-tips due to the location of amyloplasts in the root-cap cells. In micro-g, amyloplasts do not settle at the "bottom" of the plant, therefore there is a more generalized distribution of auxin, and therefore there will be no preferred growth direction.
In addition, changes in plant gene expression as a response to micro-g environments are also being investigated (2) and suggest that auxin transport inhibitors may block the activation of the auxin responsive promoters in Nicotiana spp. (tabacco).
(1) Mechanisms in the Early Phases of plant Gravitropism CRC Crit Rev Plant Sci. 2000 ;19 (6):551-73  11806421  Cit:65
(2) Transcription Profiling of the Early Gravitropic Response in Arabidopsis Using High-Density Oligonucleotide Probe Microarrays, Plant Physiol. 2002 October; 130(2): 720–728.
doi:  10.1104/pp.009688

I find over 100 articles returned by a PubMed query for "Arabidopsis microgravity." Arabidopsis was taken aboard at least one if not more Space Shuttle missions to answer this and other similar questions. A couple recent papers from this search are:
Spaceflight transcriptomes: unique responses to a novel environment.
Paul AL, Zupanska AK, Ostrow DT, Zhang Y, Sun Y, Li JL, Shanker S, Farmerie WG, Amalfitano CE, Ferl RJ.
Astrobiology. 2012 Jan;12(1):40-56.
PMID: 22221117
An endogenous growth pattern of roots is revealed in seedlings grown in microgravity.
Millar KD, Johnson CM, Edelmann RE, Kiss JZ.
Astrobiology. 2011 Oct;11(8):787-97. doi: 10.1089/ast.2011.0699.
PMID: 21970704
Parabolic flight induces changes in gene expression patterns in Arabidopsis thaliana.
Paul AL, Manak MS, Mayfield JD, Reyes MF, Gurley WB, Ferl RJ.
Astrobiology. 2011 Oct;11(8):743-58. doi: 10.1089/ast.2011.0659.
PMID: 21970703
Gene expression changes in Arabidopsis seedlings during short- to long-term exposure to 3-D clinorotation.
Soh H, Auh C, Soh WY, Han K, Kim D, Lee S, Rhee Y.
Planta. 2011 Aug;234(2):255-70.
PMID: 21416242
A novel phototropic response to red light is revealed in microgravity.
Millar KD, Kumar P, Correll MJ, Mullen JL, Hangarter RP, Edelmann RE, Kiss JZ.
New Phytol. 2010 May;186(3):648-56.
PMID: 20298479

It might be helpful to include clickable links to your answers =) n.b. I realise that your rep might be prohibitive in doing this for the time being =D

Agreed, links are helpful, but someone may wish to refine or rerun my query, rendering links less useful. There's enough info in my response to be helpful to this audience and I think that is the main point.


text:
How to tell petiole apart from stem?
How to tell petiole apart from stem? Is it by the rule that there is usually a pair of stipules at the base of a petiole?

Petioles typically have the presence of one or more of the following:

Stipule at base of the stalk
Axillary bud between the stalk base and attached stem
Leaf scar when removed

Source: Miami University

Source: Wikipedia
None of these characteristics would be present if the stalk you were looking at is a stem.

However, they are not always each visible on every species...
From: Oregon State University Dept of Horticulture:

It is not always easy to find the bud at the base of a petiole, it may not be visible early in the growing seaon and sometimes a mature bud is “hidden”, such as being enclosed by the petiole base.

From Wikipedia:

although in many species the stipules are inconspicuous or entirely absent (and the leaf is then termed exstipulate)

Leaves are usually borne from petioles and rarely from the stem itself -- so presence of a leaf (or compound leaf parts) is usually indicative of a petiole as well. However, sometimes plant leaves lack a petiole altogether, as in the case of sessile leaves.
In other instances, specifically those of compound leaves, the stalk of compound leaves (i.e., the rachis) will lack the properties previously described for a petiole, but following the compound leaf to the nearest stem typically will result in locating the petiole with one or more of the above mentioned characteristics at its base connecting the compound leaf to the stem.

source: Stack Exchange

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Does preservation in ethanol alter leaf litter mass?
I have benthic samples that were collected with an Ekman dredge from some small ponds.  The samples contain quite a bit of coarse particulate organic matter (CPOM, basically dead leaves).  I would like to quantify the amount of CPOM in the samples but they were preserved with 70% ethanol in the field.
Is there any evidence that ethanol preservation alters benthic CPOM mass?

How do you plan to separate the POM from the rest of the sample?

We run the samples through a 1 mm sieve to separate CPOM from the remaining sample.  The coarse fraction is then dried at 50 dC and ashed at 550 dC to determine LOI and % OM.

This sounds like something that would be straightforward to test empirically. As a bonus, any effect of EtOH on your samples (bias) could (possibly) be quantified and accounted for, especially if the effect is small. The questions you are asking will inform how best to do this. But I do suspect EtOH might dissolve some hydrophobic compounds in the coarse fraction. Maybe try evaporating it first and adding water. Not ideal, but likely more informative than throwing samples out!

This paper implies the EtOH extractable fraction in willow leaf litter is small ~2% http://download.springer.com/static/pdf/61/art%253A10.1007%252FBF00337374.pdf?auth66=1384973693_83a38241ac58aaa903579eadfcf550a8&ext=.pdf but this will vary by species (eg pine tar). Again, this effect can be measured on samples similar to yours.

@Abe Thanks for the paper, I look forward to reading it.  We are actually testing this now.  The initial tests with fairly old OM showed no effect but we are planning some tests with fresher OM to see if that makes a difference.

It's very likely that you should have at least minor changes in mass.

The reason is because ethanol can extract a number of substances from leaves (e.g. tannins, pigments, etc.).

However, you could still easily double check on your own.
You could still figure out the mass of the CPOM even without knowing the answer to this answer directly.

Drain and collect the EtOH.
Determine mass of separated CPOM.
Determine the excess mass present due to any leaching/dissolving from the CPOM by using density = mass / volume (or ρ=M/V) with your collected volume of ethanol.

EtOH has a density of 0.789 g/mL  at 20°C. 70% EtOH has a density of 0.885 g/ml at 20°C.
Determine the volume of the collected EtOH.
Determine the mass you'd expect of "pure" 70% EtOH given your volume (m = ρV )
Determine the mass of the collected EtOH
Subtract the expected mass from your calculated measured mass. The difference (if any) would represent mass leached/dissolved from the CPOM.

But consider that EtOH evaporates quite rapidly which could give you a false reading. Why not try with some leaves of a not-that-important-sample? Weight them before, put them in alcohol for some weeks and weight after (let the alcohol attached to the leaf litter evaporate before weighting).

Evaporation shouldn't matter  because  you  would  measure  densities.  Any CPOM mass  would remain in  the  fluid.  In fact,   with evaporation,  the concentration of remnant cpom would  increase  per ml,  and so would likely make  subtle density discrepencies  even more apparent

Ok, thanks for clarifying, I wasn't aware of that.

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What is the scientific and common name of this bug?
Captured this under my stereo microscope. Much more beautiful than appearing on my camera sensor.
Can someone help me identify it and explore more?
Also is it having a compound eye ?
Location: New Delhi.

I'm pretty sure it's a hemiptera, looks like a stink bug, though I don't recognize the color. And yeah, those are compound eyes.

Pentatomidae(http://en.wikipedia.org/wiki/Pentatomidae).
Great pic! can you tell us the geographic location this found?

@DevashishDas New Delhi, I found it near my table lamp on first floor in evening, where I have kept some plants. Then I took a leafe, and gently placed it on it, and photographed under my microscope.   I found that it became stable as soon as it came in contact with the leaf, otherwise it was moving here and there and jumping a lot. And thanks for the link.

@DevashishDas Post your comment as an answer so that it can be accepted by the OP and the question can be closed.

@TheLastWord That's not the answer though, the question asks for species, and pentatomidae is the family name.

Definitely appears to be Pentatomidae (as others have pointed out) due to shield-like, broad bodies. With over 4500 species and larval stages demonstrating significant variability even within species, ID can be difficult without knowing specific fauna, size, habitat, etc.
The OP doesn't list a size, but because OP is viewing under a scope, I assumed this is a fairly tiny species.
I came across this similar-looking unknown species (simply labeled "PK03") of the genus Eysarcoris

 Credit: CBG Photography Group, Centre for Biodiversity Genomics
The Eysarcoris genus is present in India (e.g., see indiabiodiversity.org with example of "two-spotted sesame bug")
A similar species well known throughout Europe is Stagonomus venustissimus (previously classified as Eysarcoris):

 Credit: Jose Manuel Sesma (2016); appears to be originally posted here
I cannot say if either of these species is correct (doubtful), but I think they are closer than the other provided answer.
I'll update if I find anything specific.

To answer your other question about the eye:
Yes, shield bugs (Pentatomidae), like most insects, have compound eyes.

Buschbeck and Friedrich (2008)1 discuss this highly conserved trait found in most arthropods.

Also, the red dot medial and nearby the eye? That's an ocellus, a simple eye.

 Oregon Department of Agriculture

1: Buschbeck, E.K. and Friedrich, M., 2008. Evolution of insect eyes: tales of ancient heritage, deconstruction, reconstruction, remodeling, and recycling. Evolution: Education and Outreach, 1(4), pp.448-462.

It belongs to Pentatomidae family. More on the Wiki page

That's correct, but pentatomidae is the family name, and the question asks for species.

The answer will be more useful for future reference if you add some rationale for your determination.

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Can spider silk be synthesized to be used for 3D printing?
With the recent rise in 3D printing, I keep hearing about more novel ways to use the technology: cell 3D printing, liquid aluminum or plastic 3D printing. For example,   this Ted talk deals with printing a human kidney. What interests me is if the current technology can be adapted to print with spider silk. The silk has some amazing properties, and apparently there are multiple types of silk that spiders use.
I found this project: Spiderbot 3D printer.  Can spider silk actually be synthesized in large enough amounts to enable 3D printing?

Just a note, the spiderbot printer you linked to is a multimaterial, but it does not print in spider silk =)

The "...in large enough amounts to enable 3D printing?" part of your question is, I think, still unknown, but spider silk has been being synthesized in transgenic goat milk for quite a long time already, and I suspect that it's now just a matter of time before the answer to your question is an unqualified "yes."
See Macromolecules, 2011, 44 (5), pp 1166–1176, doi:10.1021/ma102291m

No, but there is research towards it
there are two methods to look at.
Replicating spider spinnerets and the correct glands is very difficult but not impossible. It is currently a focus of research becasue it would both produce and shape the silk.
The other method is using vat grown silk and pulling it through a printing process, Not yet possible but will probably happen before the first since it involves fewer new processes, possibly. Spider silk can already be added to printer media and printed, but this only makes up a portion of the material. It cannot be printed by itself yet, which is what everyone wants.

Synthesizing spider silk seems to be developing quickly, but for 3D printing we need not just synthetic spider silk, but a liquid form that can solidify once printed. I would imagine it is going to be two or more liquids mixing together at the printhead and then bonding and solidifying with the adjacent layers, like spider silk epoxy.

There are commercial spider silk projects:
In May 2017 Kraiglabs delivered spider silk samples to a US military contractor:

“We are pleased to report that we have delivered the first samples of Dragon Silk to our US Army sponsor for independent performance confirmation,” said the Company’s COO Jon Rice.  “These samples mark the starting point for what we hope will be a long lasting and profound impact on protective equipment for those dedicated to protecting us.  The speed that our Indiana facility was able to ramp up to meet this request helps to confirm, that we have the ability to promptly deliver a top quality, cost effective, fiber to the Army and future commercial customers.”

Bolt Threads presented it's first Spider Silk product at SXSW:

Bolt Threads, a San Francisco-based start-up working on the next generation of advanced materials, is unveiling a limited edition knit necktie, made of its 100% Boltspun spider silk.
  [...]
  More specifically his team of dozens of scientists, engineers, technicians and designers, have developed a way to closely mimic silk created in nature by producing a fiber from corn syrup that was fed to a yeast fermentation, which secretes a 80kDa Major Ampullate (dragline) spidroin protein. Once the protein is harvested and purified into a powder, it is wet spun into fibres, twisted into yarns and knitted into the tie.

Last year Spiber announced a spider silk parka for the Japanese market:

The $1,000 "Moon parka," selling only in Japan, is a gold-colored jacket that uses the same design as typical North Face parkas. However, the item is made from a synthetic spider silk developed by Spiber, according to Bloomberg.

Producing a large amount of the silk doesn't seem to be a key problem. On the other hand, it's not clear that the current companies offer a product that you can use with a 3D printer.

spiders silk can't be synthesized very accurately. Carbon is much easier to integrate into 3D prints, it's very commercialized, and only 1-2 3D printers using carbon is available. Silk is much more complex:
They still don't understand the structure and lacing of the proteins very well. milestones of research demonstrate the technical difficulty of the task:
"Solid-State C-13 Nmr of Nephila-Clavipes Dragline Silk Establishes Structure and Identity of Crystalline Regions" 1994
"The molecular structure of spider dragline silk: Folding and orientation of the protein backbone"2002
"Molecular orientation and two-component nature of the crystalline fraction of spider dragline silk"1996
"Stretching of supercontracted fibers: a link between spinning and the variability of spider silk"2005
Spider silk is immensely complex, and contains multiop;e proteins woven together in specific patterns to achieve different elasticity and strength, and the spiders typically have mutliple glands for different types of silk, which use very specific pH gradients and complex chemistry and physics, which we can't match at all.
this page gives some info on recent industrial advances:
https://www.sciencedaily.com/releases/2017/01/170109124957.htm
it sais that you need 1000 protein fibers wound together to make a single spider's silk thread.
this page gives recent advance.
http://cen.acs.org/articles/92/i9/Spider-Silk-Poised-Commercial-Entry.html
For the moment, spider's silk is not commercially available for textiles or fibers, except for stuff taken out of a spider. A spider isn't heavy you can't print much from a spider :)
for the recent spider silk news, see here:
it's all research news as of summer 2017, not sales and business news. so... spiders silk can't be synthesized with volume and accuracy to compete in any commercial fields. Making some of the proteins found in the silk is only the smallest and easiest part of the puzzle.


text:
What's food mode?
I've been watching a The Crocodile Hunter episode about Komodo dragons, and Steve Irwin kept speaking about the animals being in "food mode", in which they apparently change their behavior to one of a killing machine. He said if bark falls of a tree when they're in food mode, they'll snap it.
Is it for real? I googled "food mode" but nothing interesting came up. Which animals have a food mode like this? Is it restricted to reptiles? Does it have a scientific name? Can I read about it somewhere?

I suspect he just meant "when they are hungry" and likely was playing it up for TV.
According to the San Diego Zoo, they only manage to eat about once a month, and spend a few days digesting their prey.

Adults spend an average of 26 days searching for prey. 10-20 minutes eating. (A 50 kg female was observed to swallow a 31 kg boar in 17 minutes). 3-6 days is spent in digestive pause.
Ingestion rate may be as much as 2.5 kg/min - higher than any other predator except large snakes.
High digestive efficiency (70-90%) Time is dependent upon temperature (about 26 hours at normal body temperature) Cool nights can delay to almost 5 days. Stress can slow or even stop digestion (defecation of partially digested prey may occur)

http://library.sandiegozoo.org/factsheets/komodo_dragon/komodo.htm


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Do animals get sick from eating dirty food or eating off the floor?
Humans have very strict tradition of hygiene, such as washing hands before eating, using utensils, and in general keeping as much distance between food and dirt as possible.
At the same time, most animals would eat off the floor or eat food with foreign particles stuck to it ( after being dropped on the floor). Many animals, like cats groom themselves, practically licking off (and swallowing?) dirt off their coats.
Do animals suffer adverse effects, such as indigestion or disease from consuming food that is dirty by human standards?
Or is it something about the human digestive system that cannot handle the same kinds of dirt that animals can?

Hygiene is very much cultural, compare fastidious Americans that use Clorox wipes on everything to indigenous cultures that have very few taboos against dirt.

There's a parallel to be drawn here with carnivorous animals eating raw meat, too. I naively expect that they just get more parasites (ie. that our admittedly cultural components of cooking do in fact also help protect against infection), but I'd be interested to hear if there's more to the answer.

I'm sure it varies wildly based on the animal and what they're eating.  In general, if in the course of an animal's natural feeding process it picks up a little dirt, it has evolved to cope with that.  Animal's behaviors and guts have evolved to fit their food source and lifestyle.  For a behavioral example, seals will eat rough rocks to help breakdown bones (and barf them up when they get too smooth).  Guts have evolved symbiotic relationships with microbes that are specifically adapted to the food source, termites have microbes to help them break down wood, whereas we don't have the microbe population to pull that off.  Interesting side note: it was found that one of the gut microbes in some Japanese people has gotten a horizontally transferred gene from a bacteria that lives on seaweed, probably helping them break down seaweed.
There could be a problem when the body is challenged with dirt that contains uncommon substances that the body isn't adapted to.  I'm sure if a cat rolled around in soil contaminated with a lot of arsenic it probably wouldn't be doing very well after licking off all the dirt.
This does bring up an interesting current medical hypothesis called the Hygiene Hypothesis.  Basically, these things you are talking about, utensils, antibacterial soap, etc. are all very very recent developments in human evolution.  As a result, proponents of this hypothesis think that our bodies are adapted to challenges by microbes and parasites, and depriving our bodies of that exposure when we are young totally screws up the development of our immune systems.  This would explain why we see a huge increase in allergies and autoimmune diseases in the developed world, our immune systems are totally miscalibrated, and freak out over harmless things like pollen (allergies), or worse, attack self-antigens (anti-insulin antibodies in type I diabetes).  Human children are animals, and baby animals should play in the dirt!

Horizontally transferred seaweed-eating gene? Wow!

One of my all-time favorites :)

Animals certainly occasionally get sick from eating contaminated food, just as humans used to before our standards of sanitation improved.  There are various adaptations/considerations for this. Apologies for not being able to find scholarly references. Here are some anecdotes, some of which are speculation/urban legend:

Predators eat fresh meat, which is less likely to be spoiled
Vultures lack feathers on their heads and bathe frequently to minimize exposure
Dogs supposedly eat grass to induce vomiting when they've eating something bad (fairly disputed)
Rats and other scavengers have excellent senses of smell, and can likely detect common contamination or over-spoilage
Some scavengers may have more aggressive digestive systems to reduce infections

Only 100 years ago, humans weren't so well off ourselves. While food hygiene is only part of it, our increased sanitation has reduced mortality from infectious diseases substantially.  From the CDC:

In 1900, the three leading causes of death were pneumonia,
  tuberculosis (TB), and diarrhea and enteritis, which (together with
  diphtheria) caused one third of all deaths (Figure 2). Of these
  deaths, 40% were among children aged less than 5 years (1). In 1997,
  heart disease and cancers accounted for 54.7% of all deaths, with 4.5%
  attributable to pneumonia, influenza, and human immunodeficiency virus
  (HIV) infection (2).

It would be interesting to find a break down of the improvement from agriculture/cooking, water/sewage, medicine, etc.


text:
Does the Valsalva maneuver require a completely closed airway? How do the effects compare to exhalation against partial resistance?
The Valsalva maneuver is defined as "attempted exhalation against a closed airway", "The effort to breathe out forcibly while the mouth and nose are firmly closed or the vocal cords pressed together", or, colloquially, straining as if you were trying to poop. It can "pop" the eustachian tubes open, stimulate the vagus nerve, and briefly spike blood pressure, occasionally leading to people dying from a burst aneurysm on the toilet.
Some breathing practices involve pushing air out against resistance, such as ujjayi breath in yoga. This can be done by partly closing the glottis while exhaling, or by firmly exhaling through the mouth with lips slightly open, as if one were whistling. It can also happen while forcefully exhaling through a congested nose.
This seems like it should raise eustachian and thoracic pressure in the same way as the "full" Valsalva maneuver, though to a lesser extent. Are the effects of these other breathing practices similar to the Valsalva maneuver, or are there any unique effects of the Valsalva maneuver that only occur with a fully closed airway?
As a second question, would you expect any unique effects exhaling against resistance? It seems different in that the practitioner is still breathing, and that they can continue the practice indefinitely, as opposed to a breath-holding Valsalva.

Since commercial divers that wear diving helmets cannot pinch their nose shut with their fingers, a retractable 'nose clearing device' is provided in the helmet, or similarly a block that the nose can be pressed against. The device generally does not completely occlude the nose, but enough that if the exhaled flow rate is high enough, the middle ear can be equalized.

The eustachian tubes exit into the nasal cavity superior to the glottis.  Thus restricting the glottis while exhaling cannot increase pressure in the nasal cavity / eustachians.  Only by closing the nostrils can that be achieved, and only while exhaling.  Even a technique like circular breathing cannot maintain pressure in the nasal cavity since that's necessarily the entry point for every new breath, be it mouth or nose.

Please add some references to your answer.


text:
When is an anatomic entity named "laterale" vs. "lateralis"?
I'm trying to learn the latin names of anatomical entities and I have a hard time remembering whether it's "Os cuneiforme laterale" or "Os cuneiforme lateralis".
In that case it's "laterale". But in a case like "Nervus cutaneus antebrachii lateralis" it's "lateralis". What's the logic here? How do I remember the right one?

Though I answer the "whats the logic here" part of the question in my answer, I don't really mention how to remember the right one. The simple (but awful) answer is to memorize a ton of Latin (and Greek) grammar and inflection rules and memorize a bunch of declensions ;p.

This is actually much more of a lesson in Latin linguistics/grammar.
The root, Lateral, comes ultimately from latus meaning “side" or "flank” in Latin. [Source].

By adding one of these suffixes we instead create an adjective meaning "of the side."

However, the suffixes differ in their inflection (specifically their gender):
Laterale has the neutral, singular suffix of the nominative 3rd declension.
Lateralis has the masculine, singular suffix of the nominative 3rd declension.

 Source: Wiktionary

The difference between the gender-assignment of these suffixes is due to Agreement.

[Agreement] happens when a word changes form depending on the other words to which it relates. It is an instance of inflection, and usually involves making the value of some grammatical category (such as gender or person) "agree" between varied words or parts of the sentence.

More specifically, adjectives must agree with the nouns they modify in case, number, and gender.

Let's break down each of these anatomical structures to understand the agreement-induced inflections [Source]:
os cuneiforme laterale - each of these words is neutral/singular:

os = noun, declension 3, nominative, neutral, singular
cuneiforme = adjective, declension 3, neutral, singular
laterale = adjective, declension 3, nominative, neutral, singular

nervus cutaneus antebrachii lateralis - the 2 adjectives match the  masculine/singular noun they describe:

nervus = noun, declension 2, nominative, masculine, singular
cutaneus = adjective, declension 2, nominative, masculine, singular
antebrachii = noun, declension 2, genitive, singular
lateralis = adjective, declension 3, nominative, masculine, singular

 Note: you see a shift to the genitive case for antebrachii because in this instance this phrase means "Lateral cutaneous nerve of the forearm."

Latin Linguistics  For Dummies:

Declension = category of nouns in Latin and Greek with broadly similar case formation (i.e., they are inflected/conjugated similarly).

Inflection = the modification of a word to express different grammatical categories such as tense, case, voice, aspect, person, number, gender, and mood.

Nominative = The case used to indicate the subject of a finite verb.

Genitive = The case used to express some relationship such as possession or origin. It corresponds roughly to the English preposition "of."


text:
What's the difference between the terms "muscle" and "muscle organ"?
Foundational Model of Anatomy distinguishes between Muscle organ and Muscle. What's the difference between the two?

Your links do not work. If there is relevant info at either link, please quote it as necessary in your post. Also, please clarify what you are referring to regarding "Foundational Model of Anatomy". If this is a book, please include a more complete citation (i.e., include authors, year, edition, publisher). Thanks

The word "muscle" is applied to both the organ and to the tissue.

There are 3 types of muscle tissue: skeletal, smooth, and cardiac.

Below is a decent quote from SEER explaining this (my emphasis added):

A whole skeletal muscle is considered an organ of the muscular system. Each organ or muscle consists of skeletal muscle tissue, connective tissue, nerve tissue, and blood or vascular tissue

If the word "muscle" is used on its own (i.e., without specifying "muscle tissue" or "skeletal muscle"), it is typically referring to the whole skeletal muscle organ.

Examples: chest muscles (pectoralis muscles), thigh muscles (quadriceps and hamstrings), etc.

Note: the word "bone" is used in a very similar manner.

"Bone" can refer to the entire organ (e.g., femur) or to one of the two recognized bone tissue types (compact bone and spongy bone).

In the context you state, seemingly nothing. "Muscle" is listed as a homonym of "Muscle organ". So it seems, for the sake of the website you like to, there is no difference (unless they are using homonym differently).


text:
What is Saccus in Embryology?
The word seems to be of German origin.
I have it here

Saccus lymphaticus inguinalis,
  Saccus lymphaticus jugularis,
  Saccus lymphaticus posterior,
  Saccus lymphaticus retroperitonaealis.

I would like to use the word "sinus" instead.
However, Google search does not give good results for it.
What is the meaning of the word "saccus" here?

From the Latin saccus, bag, which is in turn from the Ancient Greek sakkos, sack or bag.

Saccus simply means sac or bag and is is closed cavity. The lymph nodes develop from the structures, see this image:

Superior cardinal vein (jugular vein)
Jugular lymphatic sacs
Right subclavian vein
Axillary lymphatic sacs
Left brachiocephalic vein
Thoracic duct (bilateral)
Lumbar lymphatic sacs
Iliac lymphatic sacs

The image is taken from this webpage, which should be interesting for you.


text:
Why do these earthworms stay between the road lines?
This article shows pictures of earthworms during floods in Texas. The worms ball up, supposedly in order to survive the floods.

Photo Credit: Texas Parks And Wildlife Department
Can anyone explain the phenomenon a little? I can't seem to find anything about this online. I know that earthworms surface when it rains for oxygen, but it seems weird that they meet in the middle of the street.

Interesting...It is almost as if earthworm herds perform gradient descent (or ascent in this case) like an intelligent robot to find the driest place in the surrounding area and moves to that location - but I wonder if the earthworms were moved in between the yellow lines intentionally to induce some journalistic shock value

Agree, we know they've been poked with a stick.
Perhaps the reason is not biological but hydrological. Roads are crowned to improve drainage, so in a flood the center is most likely to be exposed as the water recedes.  There's also something dark in the mass that  I can't make out but it doesn't look like worm; maybe it's important.

The first question: what the worms do on the ground during the flood? One of the answers to this question is -
"It gives them an opportunity to move greater distances across the soil surface than they could do through soil," said Dr. Lowe. "They cannot do this when it is dry because of their moisture requirements."
The second question: why they form ball after moving to the ground. There are two answers to this question:
First, as a part of surviving mechanism to prevent drying. As you can see, they cannot come back to the soil across the asphalt, thus they form balls and wait the weather to improve.
Second reason to form the balls - communication:
"The earthworms use touch to communicate and influence each other's behaviour, according to research published in the journal Ethology.
By doing so the worms collectively decide to travel in the same direction as part of a single herd."

I think another aspect to this has actually nothing to do with worm biology and instead relates to the roads and cars:

Roads are typically graded so that water runoff moves off the roads -- this usually means that the center line(s) are a high point in the road.

See here for example
As a result, the worms would experience the least amount of water and runoff force if they congregated in the middle.

Two "forces" could prevent formation of balls in the middle of either lane.

Water runoff might be stronger there preventing a stable "footing" for the worms to remain.
Even if balls formed in the lanes, car traffic would almost certainly destroy them leaving little evidence of them behind (especially if rain was washing them away).

I'm sure the other answers play a part in this phenomenon aswell, but I was taught that worms do this because the worms dont have eyes, yet they still can sense light from dark, because staying out in the sun too long would dry them out,
So they are between 2 yellow lines (to them they think that must be light) and the middle line is dark (the asphalt itself) so ultimately the worms are very confused and think they are somewhere safe and dark (like underground)
They pass the first line trying to get through the light in search of darkness, and get stuck in the middle because they think the next line is more light. They sadly believe they have found a safe haven.

Thank you for your answer but it would be great if you could cite some authoritative references. References are important so that one can verify the information and can learn the details of the topic. Good references include peer-reviewed articles, books and websites of reputed academic/scientific organizations. Wikipedia is also good if it in turn is properly referenced.


text:
Is there any reason the common housefly continues to return to an area?
This might come off as a really silly question. But I'm wondering (especially in the case of food) if there is any reason a fly would continue to try and sit on top of a piece of food even after swatting it away. I assume (it could be misconception) that it is instinctive that animals and insects would leave an area if it is harmful / dangerous to their existence after having close encounters more than once. Is this not the same for the fly?
I have this question mainly because I recall waving a fly away several times while eating lunch, and I couldn't understand why the fly wouldn't just find another place where there is food or somewhere safer.

I don't think it's a silly question, but it is a common error to anthropomorphise animals.
Insects respond to cues which they have evolved to respond to, and this is how they 'make decisions'. They do not have free will or any more complex decision-making process like common sense. This is evident is lots of insect behaviour: flying repeatedly at a closed window; landing on brightly coloured clothes instead of flowers; and returning to a food source when they are in real danger of being swatted!
When a fly senses the food (often by olfactory receptors), they are 'programmed' to fly towards it in response to some chemical they sense depending on the species and food. They may not have adapted a response to swatting, or perhaps the food cue overrides others. In nature swatting is not so much of a threat to a fly. Some animals may brush them away, but since they are not really doing any harm in feeding from another animal's food, they are mostly ignored.
CO2 traps are used to entice and kill mosquitoes. The mosquitoes are attracted to CO2 (as it is dispelled from the animals from which they blood feed), they will only evolve to avoid the traps if there is another cue which they could eventually associate with a negative effect.
Another thing to remember when thinking about insect behaviour is that their life strategy is very different to ours. Insects are more r-selected than humans, meaning that each individual life has not had so much energy put into it as a more K-selected animal (such as humans), and to compensate for this, many more young are produced. This often results in more risks being taken by individuals since there will still be a viable population even after many deaths.
Chapter 4 of 'The Insects' by Gullan & Cranston gives a good introduction to the sensory responses of insect behaviour. There are other books on the subject, 'Introduction to insect behaviour' by Atkins looks like a good starting point, but I have not read it yet.


text:
(How) does coppicing fundamentally alter tree growth?
I am interested in adding the ability to model coppice tree production to a model of perennial crops (Miguez et al 2008)..
Implementing the biomass pools and allocation parameters required for tree growth is relatively straight-forward.
However, it is not clear to me if it will be necessary to account for any changes in growth form and physiology (e.g. allocation, allometry) associated with coppice management.
Are there any models that explicitly model coppice regrowth? Are there any particular issues that I should consider?

Fernando E. Miguez , Xinguang Zhu, Stephen Humphries, German A. Bollero, and Stephen P. Long. GCB Bioenergy . 2009 . Volume 1 Issue 4, Pages 282 - 296 (link)

According to Deckmyn et al (2004), the primary effect of coppice management is that the fraction of total biomass in roots is relatively higher after coppicing, and that a substantial fraction of carbon in roots (~20% of root mass) is reallocated aboveground to support shoot growth in the spring following coppicing.
Because of this large re-allocation, coppiced plants are able to grow more rapidly (and reach canopy closure sooner), than seedlings (Ceulemans et al 1996) it is important to consider that canopy closure (maximum leaf area index) occurrs more rapidly after coppicing

Deckman et al, 2004 Poplar growth and yield in short rotation coppice: model simulations using the process model SECRETS. Biomass and Bioenergy doi:10.1016/S0961-9534(03)00121-1
Ceulemans et al, 1996. A comparison among eucalypt, poplar and willow characteristics with particular reference to a coppice, growth-modelling approach Original Research Article
Biomass and Bioenergy, Volume 11, Issues 2–3, Pages 215-231 doi:10.1016/0961-9534(96)00035-9


text:
Is there a standard format for plant community composition data?
FIA has a nice database of forest Inventory data, this would be great except that it does not seem capable of handling data from non-tree species (e.g., grasslands, wetlands).
Is there a standard database or flat-file format for collecting plant community data (e.g., biomass, cover, dbh as appropriate)?

There does not appear to be a current standard, but Veg-X is a standard that has been developed to facilitate exchange of plot-based vegetation data, and may provide the closest to what you are looking for.
Veg-X is described in Wiser et al 2011 and the project home page is http://wiki.tdwg.org/Vegetation/
From the abstract:

The exchange standard for plot-based vegetation data (Veg-X) allows
  for observations of vegetation at both individual plant and aggregated
  observation levels. It ensures that observations are ﬁxed to physical
  sample plots at speciﬁc points in space and time, and makes a
  distinction between the entity of interest (e.g. an individual tree)
  and the observational act (i.e. a measurement). The standard supports
  repeated measurements of both individual organisms and plots, allows
  observations of entities to be grouped following predeﬁned or
  user-deﬁned criteria, and ensures that the connection between the
  entity observed and taxonomic concept associated with that observation
  are maintained.

Wiser, S.K., N. Spencer, M. De Caceres, M. Kleikamp, B. Boyle, & R.K. Peet. 2011. Veg-X -- An international exchange standard for plot-based vegetation data. Journal of Vegetation Science 22:598-609.


text:
What soft tissue separates bones of toes?
I need to know a little about the "knuckles" of toes; specifically the 4 areas that separate the 5 proximal/metatarsal joins.
I'd like to know the terms for areas that might be damaged if the width of the foot were to be repeatedly compressed there. Is there even a name for just the general "knuckle area"?
Thanks

This question might have a better fit in Biology.SE.

Could you add a picture pointing to the joint(s) you are talking about? It's hard to tell if you are describing the joints between tarsals and metatarsals or between metatarsals and proximal phalanges.


text:
How does the colinearity of the HOX genes determine the body plan of an organism?
I was recently reading about colinearity in the HOX genes that give an organism its high-level body plan (where the order of the HOX genes on the chromosome follow the head-to-tail order of body segments, such that the head gene comes before the thorax gene, comes before the abdomen gene, etc).
I'm really just a layman  interested in this stuff (only completed A & P I), but I was under the impression that the location of genes on a chromosome has no bearing on the expression of those genes or phenotype of the organism -- in other words, that genes can be anywhere on any chromosome.
Do we understand how the order of the HOX genes ends up being expressed as the order of the body segments? Do we know why the positioning of these genes matters when the order of other genes don't?

Have you read Sean Carroll's "Endless forms Most Beautiful" ?I think you will get a complete answer in that book.

By the way, the order of the other genes is also important .  If it were not so, translocations of bits of chromosomes won't be harmful. Have to confirm this though.....

@biogirl maybe you could provide a short synposis of Carroll's book in an answer?

To tell you the truth, I have not read it completely. So, it's really difficult for me to answer this.

I'm a Biologist, the book @biogirl is talking about is one of the greatest works to read. The HOX Genes is an extensive topic. You'd better read some articles.

@John It might help if you could provide a reference for your claim.

@Remi.b Take a look at the Wikipedia page: http://en.wikipedia.org/wiki/Hox_gene#Colinearity_of_Hox_genes

This reply is very late, but for the benefit of biogirl, chromosomal translocations can indeed be harmless, so long as they are gene-dose balanced, and their break-points don't disrupt genes or important regulatory regions.
For example, many people live normally with balanced translocations and only find out when they have some trouble conceiving children and receive genetic counselling. Many translocations have occurred in evolutionary time between chimps and humans. The strict collinearity of Hox genes really is something special in animals, I think.

Gene dosage is often extremely important and so unbalanced translocations that affect gene dose often lead to a disease phenotype.

I have suggested that the colinear arrangement of Hox genes is instrumental in a “segment counter” - a mechanism allowing cells in the embryonic mesoderm to determine in which segment a cell is located and to activate the genes according to the location along the body axis.1 I have also posted an animation explaining the process. ## Reference: ##
1: Kudlicki, A. (2019). Why a Constant Number of Vertebrae? Digital Control of Segmental Identity during Vertebrate Development. BioEssays.

You might be interested in this book
When writing Hox Gene collinearity (or colinearity as it is often misspelled as explain in wiki!) on Google scholar or WebOfKnowledge you will get many results on the subject. It is still today an ongoing debate.
Below are some sentences I pick up from these articles. It is certainly hard to understand as I hardly understood what I wrote! The best for you is to go through this review. It is not easy (at least for me but it is not at all my field) but I think it is the best source of information you can find on the subject.
This and this might also help you to understand the debate on the subject.

There are several types of collinearity:
Spatial collinearity is the sequential 3' to 5' expression of Hox Genes along a body axis. Spatial collinearity can be associated with time dependence where the most 3' is expressed first. This is defined as temporal collinearity.
There are two main models to explain the mechanisms hidden behind this ordering.

1) Collinearity is based on transcriptional regulation and specifically that is limited by the progressive 3' to 5' opening of Hox cluster chromatin and/or mediated by global control regions
2) Collinearity depends on interactions between the Hox genes themselves. These interactions include 'posterior prevalence', a negative interaction among Hox proteins that clearly relates to functional collinearity in Drosophila.

Evolution:
It is suggested that collinearity evolved by repeated tandem duplication of an ancestral ur-Hox Gene

Great, this is what I was looking for! It says I can award the bounty in 3 hours. You'll receive it as soon as SE lets me.

Quoting from some parts of Sean Carroll's book - Endless forms most beautiful, I have tried to provide you with an answer but, remember that this can never suffice for the reading of this great book.
Yes, we do understand how the hox genes' expression is regulated.
From page 126-127

......The establishment of these Hox zones and their subsequent action
  in sculpting the different forms of repeated parts is the fundamental
  genetic logic upon which the modular forms of large,biletarian animals
  is built.
The genetic logic relies on genetic switches at two levels. One set of
  switches belongs to the Hox genes themselves. these switches activate
  each Hox gene in different zones that will become different modules of
  the animal. Another set of switches contain signature sequences that
  are recognized by Hox proteins and that control how other genes are
  expressed in different modules.
In both arthropods and vertebrates, the Hox genes are developed in
  zones along the main body axis. The distinct zones of each Hox gene's
  expression domain are governed by genetic switches, and seperate
  switches control Hox gene patterns in different tissues such as the
  ...... Because of the logic of the genetic switches, the cells that
  belong to one module express different Hox proteins or combinations of
  Hox proteins than those in adjacent modules....

Let us take an example of Ubx gene which leads to formation of wings in the 2nd and 3rd thoracic segments of  drosophila. This gene is turned off in the first thoracic segment  but in the second and third segments, it is turned on. This regulation can be achieved because of the genetic switches which in turn can be switched on or off by activators and repressors. These activators and repressors are unevenly distributed in the embryo and so regulation of switches in different parts of the embryo is possible.

The question is complex and it is nice that you looked up to your book to find this out. But does it answer to "why the order of the HOX genes correspond to the order of the body parts?" ?

@Remi.b is right. While this is a well-researched answer, it doesn't address specifically the colinearity that I was inquiring about--why the order of these genes on the chromosome matter.

@John Well, I just answered the first part of the your question. " Do we understand how the order of the HOX genes ends up being expressed as the order of the body segments? ".

@Remi.b answers the second part in an excellent way !

I have suggested that collinearity of Hox genes is a mechanism to maximise physical segregation between active and inactive Hox genes within the Hox gene cluster. This is to minimise interference between Hox genes in these two states.  See 'The significance of Hox gene collinearity' in Int. J. Dev. Biol. 2015 Vol 59, pp 159-170. Or download from https://www.researchgate.net/profile/Stephen_Gaunt

Thx for your contribution, but your answer does not answer the question "HOW does the order of genes in a DNA string determine the body plan".


text:
Manifestations of open foramen ovale in adults
I read that foramen ovale opens in 30% of adults.
I do not know how much of these openings can then close again.
Probably, none.
It is not pathogenic if no symptoms.
It allows blood to enter from right atrium to left atrium (fetal), but from left atrium to right atrium in adults.
Assume that 50% of blood is doing so in adults.
This means that 50% of blood is not oxygenated.
Heart has to pump stronger to get some level of oxygenated blood as before.
Some thoughts about manifestations of open foramen ovale

hypertension
ischemic hypoxia
Clubbing
possible organ failures
higher risk for infections, SIRS and sepsis

Therefore, I think open foramen ovale can be a risk factor for myocardial infarction.
What are the manifestations of an open foramen ovale in adults?

As I recall the 30% of patients are only probe patent and therefore of little significance in terms of blood mixing under normal conditions where right sided pressure is lower than left sided (therefore RA will NOT flow into LA).  They are at higher risk of stroke from paradoxical embolism (which does cross through the PFO).  I'm not convinced by any of those bullet points as your original premise is off - a PFO will not cause a 50% shunt right to left.

I think what you may be thinking of is Eisenmenger's Syndrome though you should also read through the Cyanotic Heart Defects section.  Can you also clarify what you mean by "COPD-hypoxic-nails"?

@RoryM COPD-hypoxic-nail like curved nails caused due to hypoxia in peripheral system.

Clubbing?

A fully patent foramen ovale (pfo) is rare however a partial or small pfo is present in about 30% of the population.
Now the manifestations you described are partially correct. A pfo causes a left to right shunt in the adult whilst a right to left shunt in the fetus. In the fetus this is normal. In the adult, it is left to right because the left atrium is at higher pressure than the right. Due to this some of your manifestations are the wrong way round but still correct.
For example you mentioned hypertension, but presumably you meant systemic hypertension. It is more common at least in the early stages to get pulmonary hypertension. The pressures in the left atrium cause the pressures in the right atrium to increase when there is shunting. This is frequently seen when pressures in the left are increased due to factors like systemic hypertension. Coronary artery disease can also worsen the shunt and increase pressures in the right atrium and pulmonary pressures because the left ventricle can be stiffer.
Despite all this the more common presentation of a clinically significant pfo is right heart failure. Volume overloaded,the right heart dilates and fails. This will cause the usual presentation of right heart failure i.e. peripheral oedema, ascites and hepatomegaly.
Of course increased pulmonary pressures also causes strain to the right heart and can also cause right heart failure.
They then may go on to develop congestive cardiac failure and the exertional dyspnoea that comes with it. The inadequacy of the right heart can lead to excess strain to the left heart through a number of mechanisms that leads to it also failing. Dilation of the right heart can also lead to atrial fibrillation which in turn leads to stroke all being other possible presentations.
Cyanosis usually doesn't occur at least early in the disease as there isn't a shift from right to left (unoxygenated to oxygenated) but the other way round.
The severity of the pfo will lead to the severity of the clinical manifestation and how early it is picked up. Most people have routine checks of their heart (the murmur is usually pretty loud) so it is frequently corrected before any clinical disease manifests. In patients with small pfos they may never notice unless they become hypertensive or put strain on their heart during pregnancy. Yes they have a slight disadvantage as they lose some oxygenated blood but not anything noticeable.
If anything is unclear or you have more questions, please ask.

Thank you very much for your clear answer! I corrected the mistake in my question body. I am digesting your answer and will ask when I get new thoughts which I cannot solve myself.


text:
What is this insect? (Location: Hong Kong; size: 8 mm long, 4 mm wide, 2 mm thick; color: black with some brown at center on the top)
What is this insect? (Location: Hong Kong; size: 8 mm long, 4 mm wide, 2 mm thick; color: black with some brown at center on the top)

The insect in the picture was slightly damaged after an altercation with a human.

This is a cockroach.
Although about 30 species typically associate with humans and human habitats [source], the only ones that I know that have strong parallel dark lines running in the rostral/caudal direction are the Asian cockroach (Blattella asahinai) and the German cockroach (Blattella germanica).
According to Wikipedia, these 2 species appear very similar. At the adult level, it's actually more behavior (B. asahinai is a better flyer and tends to fly toward light) and habitat (B. asahinai prefers living outdoors while B. germanica prefers living indoors) that "best" differentiates these two species.
Your specimen is not an adult, however, as is made very clear by the extension of the dorsal parallel stripes extending beyond the pronotom, by the relatively small size of your specimen (<10 mm long), and by the absence of clearly-developed wings [see here for descriptions].
This wingless and long-striped specimen is an immature nymph. Although UFL indicates that late instar roaches of these two species can be identified by the presence of white spots on the dorsal abdomen of the Asian roach, your specimen appears to be an earlier instar and does not yet have this spotted pattern.
As in the adult stage, the early instars of B. asahinai and B. germanica also appear quite similar:

 German (left) and Asian (right) early instar nymphs. Photograph by Dina L. Richman (University of Florida); [source].
German nymphs are slightly smaller than Asian roach nymphs, but again they are quite hard to tell apart (often times being less distinct that the above picture).
I've been told that the most useful way for differentiating is simply by location: if found indoors it's more likely German and if found outdoors it's more likely Asian.
Regardless, if it was found inside, you need to act quickly to prevent an infestation...


text:
How do susceptible organisms prevent parasites from overcoming resistance?
Bt corn is genetically modified to kill borers, but "regulations require farmers to plant conventional varieties as well, which is intended to stop the borers becoming resistant."
-Source
How do susceptible organisms prevent parasites from overcoming host resistance?

In an environment where all plants are resistant to certain parasites, a rare breed which has a mechanism against this resistance has free play - lots of food and no competition. However, in plants which do not have the resistance, this rare parasite breed may be at a disadvantage compared to parasites who do not have the mechanism against that resistance (even if only because they do not waste energy on a defensive mechanism they don't need).
By mixing resistant and unresistant plants, it is probably possible to maintain high enough a competition of parasites without that defensive mechanism to prevent the ones with the mechanism from developing. It's natural selection at work :)


text:
How fast is water transported from roots to leaves?
I understand basically how water transport from roots to leaves through the xylem works, but I have no idea of the timescales involved.
How long does it take for water to get from root tips to leaves? How does this speed change in different parts of the plant? How does it differ between different plant types? How is it affected by plant size?
Also, I guess it changes from relatively fast in the middle of the day to almost zero at night, but how does it change during a normal sunny day (e.g. sinusoidal? More like a square wave?)

Could someone please tag this "water" and "xylem" and then delete this comment?

You can retain this when you edit your question.

We usually use more general tags and not down to a very fine characterisation of the question. So plant-physiology is fine here.

If you assume the plant has a constant total supply of water, then uptake must equal output. If you could measure total water vapor escaping from a plant, you'd know the rate water must flow through the plant.

@user137: True. But I don't know where to get that data for a whole single plant (of any size)

related: http://biology.stackexchange.com/questions/1096/how-does-water-move-throughout-plants http://biology.stackexchange.com/questions/11044/how-do-trees-lift-water-higher-than-10-meters

@user137: Wrong. There is part of the water not evaporating but going down in phloem sap,  https://www.boundless.com/biology/textbooks/boundless-biology-textbook/plant-form-and-physiology-30/transport-of-water-and-solutes-in-plants-183/transportation-of-photosynthates-in-the-phloem-699-11924/images/fig-ch30_05_07/

@Joce It was a good first order approximation. Maybe if you had a potted plant and covered the dirt to prevent evaporation from anything except the plant, then put the whole thing on a sensitive scale. The change in weight might tell you the mass of water escaping the plant. That could give NET flow up the plant.

@user137: Do you have data showing that it is a good approximation? It seems to me that water efficiency would imply an evaporation much smaller than sap flux. This wouldn't contradict pore-pressure driven sap flow, although of course there is always some unavoidable evaporation for this process.

Yeah, net water evaporation is going to be much less than xylem flow rates. I'm interested in xylem flow rates. In particular, I'm interested in the (distribution of) time it takes for a parcel of water to get from the roots to the leaves. Approximations are fine though (e.g. for a Sequoia -  Minutes? Hours? Days?).

You can find some answers for your questions in this paper (it is only for Ricinus communis, but you may follow the cited by from google and find for other plants):
http://onlinelibrary.wiley.com/doi/10.1046/j.1365-3040.2001.00704.x/full
velocity in the phloem (0·250 ± 0·004 mm s−1)
xylem in the light (0·401 ± 0·004 mm s−1), in the dark (0·255 ± 0·003 mm s−1)

Graphs on daily change are on the paper.

Great, thanks! That's about 1.5m/h in the light, and Castor plants get to a few meters, so I guess it might take a few hours to get from root tips to stomata.


text:
Is Pork more prone to carrying higher loads of parasites than Beef?
My friend told me that pork is dangerous due to containing worms.
I told her that beef contains worms too and that's why we cook it.
We went to steak restaurant and ordered "medium" beef.
And that makes me think a lot. Why I can order medium beef? It's still rare inside.
I have never heard people ordering medium pork.
Is pork more prone to worm investation than beef/cows?
What sort of worm we have anyway?

Depending where you are , Brucellosis  ( undulant fever ) is more likely a problem with beef ( and milk ).  Not deadly but debilitating ; my mother lived with it for 40 years,  If treated "soon" antibiotics will cure it , but if it becomes chronic ,there is no cure.

Cooking pork to rare or medium rare depends on where you live ; A friend , native of Scotland said he never saw pork roasted past medium rare until he came to the US. I usually cook pork roast to medium rare in the US.

@jamesqf Yes, there is an actual historical basis for some food restrictions, including not eating pork or shellfish - the lack of refrigeration or other safe methods of preservation.

Trichenellosis from pork occurs in about about 5 people per year since the 1980's in the US. it has a 0.2% mortality rate there. We can say that 1 American/ 1 European dies from pig meat every 20 years. That's a fair concession. Worldwide the death rate is in the 100ds per year from pork, compared to 3 million who die from the fat in beef and chicken and lamb and excess sugars, and 1.35 million attributed to cars.
The other pork parasites are less dangerous and have less than a 90 cases per year in the USA, mostly people coming from epidemic areas. https://www.oie.int/doc/ged/d9157.pdf
Beef can transmit tuberculosis, E-Coli, BSE/CJD and sarcosystosis. E-Coli from unsanitized beef kills many times more people than pork born diseases, i.e. 100 times more people in the US die from E coli from beef, it is one of the main vectors and a lot more difficult to control than via pork. E-Coli is uncommon from pork. Worldwide many thousands of people die of E-Coli from beef every year.
There were an estimated 147 000 new cases of zoonotic tuberculosis and some 12 500 people died of the disease in 2016. Beef are the main causal agent. All animals have tape worms and other worms.
Beef, Lamb, Pork, chicken, and milk all increase the risk of heart attacks and strokes because animal fat can increase cholesterol dramatically, and eating beef from one region can make you more susceptible to heart attacks than pork from another region, because the fat content can vary a lot. Far more people die of heart attacks than animal parasites these days, about 1 million times more rich people die from animal fat and sugar related disease than from pork parasites.

No pork parasites are counted on this list of parasite deaths, globally it's perhaps 50-350 per year.

About 99.999 percent of people that die from meat, die from the fat and other high sugar diets, and it doesn't matter if it's pork or beef. (source WHO)... 5 million people die every year from tobacco, and 2.5 million die every year from Alcohol, especially in very poor countries.
The income levels of people that die from parasites and alcohol are very low, something like 99.9% of parasite deaths are poor people and 90% of alcohol deaths.
So you can concede that alcohol kills many poor people, but that animal parasites from pigs kill 10,000 times less people than alcohol. Pork kills a million times less people in the west than cars or fatty foods.
Details:
There are three important parasites found in pigs which pose
a risk to humans who ingest raw or undercooked pork
products. These parasites are Trichinella spiralis, a nematode
or roundworm, Taenia solium, a tapeworm, and Toxoplasma
gondii,

You're basically saying that tapeworm is a problem for pork however they won't kill you anyway because you're rich. Okay. Is pork more susceptible to worms than beef

It's a very good answer. However, the main question, to response to that religious dogma, is if pork more likely to have worm than beef?

Oh, yes, you are right. I added paragraph 3 and 4. It appears that bovine tuberculosis and E Coli kill at least 20,000 people every year. and that pork doesn't harbour them... A trivia thing: The Chinese have banned imports of beef from Brazil that tested positive for covid 19, although that's probably more of cause of deforestation than a human risk.

is pork more likely to have worm than beef?

Case study I (Chungcheongnam-do, Korea)
From November 2009 to April 2010, a total of 241 fecal samples of pigs and beef cattle (136 and 105, respectively) were examined by direct smear and centrifugal sedimentation methods. The overall positive rates of intestinal parasites among pigs and beef cattle were 73.5% and 4.8%, respectively, and the double-infection rate was 10.3% in pigs. Of 136 specimens from pigs, Balantidium coli, Ascaris suum, and Entamoeba spp. infections were found in 88 (64.7%), 24 (17.6%), and 5 cases (3.7%), respectively. Of 105 beef cattle, Entamoeba spp. infections were detected in 5 cases (4.8%). From these results, it is shown that pigs raised on rural farms in Chungcheongnam-do had a high B. coli infection rate and a moderate A. suum infection rate than cows.
Case study II (Poland)
Sera of 3111 pigs and 2411 cattle from 16 regions of Poland were examined for the presence of anti-T. gondii IgG using the direct agglutination test (DAT). Pepsin-digested samples of diaphragm and heart of seropositive animals were examined for the presence of T. gondii DNA (B1 gene) by nested PCR and real-time PCR, while non-digested samples were only examined by nested PCR. The B1 gene DNA samples were genotyped at 11 genetic markers using multilocus nested PCR-RFLP (Mn-PCR-RFLP) and sequencing.
Seropositive DAT results were found in 11.9% of pigs and 13.0% of cattle. The highest seroprevalence was found in pigs from Podkarpackie (32.6%) and in cattle from Mazowieckie (44.6%). Data analysis showed that cattle > 5–10 years-old, as well as cattle and pigs from small farms, and pigs from farms with open production systems, had higher odds of testing seropositive (P < 0.05). Among the examined tissue samples, positive PCR results were found in samples from 12.2% and 10.2% of seropositive pigs and cattle, respectively. Among the samples successfully genotyped by Mn-PCR-RFLP and sequenced, four samples were identified as T. gondii type II and one sample as type I.
Case Study III (US)
The prevalence of viable Toxoplasma gondii was determined in 6,282 samples (2,094 each of beef, chicken, and pork) obtained from 698 retail meat stores from 28 major geographic areas of the United States. Each sample consisted of a minimum of 1 kg of meat purchased from the retail meat case. To detect viable T. gondii, meat samples were fed to T. gondii-free cats and feces of cats were examined for oocyst shedding. Initially, 100 g of meat from 6 individual samples of a given species were pooled (total, 600 g), fed to a cat over a period of 3 days, and feces were examined for oocysts for 14 days; the remaining meat samples were stored at 4 C for 14 days (until results of the initial cat fecal examination were known).
When a cat fed pooled samples had shed oocysts, 6 individual meat samples from each pool were bioassayed for T. gondii in cats and mice. Toxoplasma gondii isolates were then genetically characterized using the SAG2 locus and 5 hypervariable microsatellite loci. In all, 7 cats fed pooled pork samples shed oocysts. Toxoplasma gondii oocysts were detected microscopically in the feces of 2 of the cats; 1 isolate was Type II and the second was Type III. Analyzed individually, T. gondii was detected by bioassay in 3 of the 12 associated samples with genetic data indicating T. gondii isolates present in 2. The remaining 5 pooled pork samples had so few oocysts that they were not initially detected by microscopic examination, but rather by mouse bioassay of cat feces. Two were Type I, 1 was Type II, and 2 were Type III. None of the cats fed chicken or beef samples shed oocysts. Overall, the prevalence of viable T. gondii in retail meat was very low.
Conclusion
Beef and chicken have negligible amounts of the parasite, while pork has low levels that are effectively eliminated by proper cooking. Also, death from pork consumption is way less and uncommon than other means of dying.
References:

Ismail HA, Jeon HK, Yu YM, Do C, Lee YH. Intestinal parasite infections in pigs and beef cattle in rural areas of Chungcheongnam-do, Korea. Korean J Parasitol. 2010;48(4):347-349. doi:10.3347/kjp.2010.48.4.347
Sroka, J., Karamon, J., Wójcik-Fatla, A. et al. Toxoplasma gondii infection in slaughtered pigs and cattle in Poland: seroprevalence, molecular detection and characterization of parasites in meat. Parasites Vectors 13, 223 (2020). doi: 10.1186/s13071-020-04106-1
Dubey et. al. "PREVALENCE OF VIABLE TOXOPLASMA GONDII IN BEEF, CHICKEN, AND PORK FROM RETAIL MEAT STORES IN THE UNITED STATES: RISK ASSESSMENT TO CONSUMERS," Journal of Parasitology 91(5), 1082-1093, 2005, doi: 10.1645/GE-683.1


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Why is the prefrontal cortex called such?
Pre means before. Frontal means front.
What does cortex means? Brain?
Is it the front most part of the brain? Is it located at the most frontal part of the brain and that's why it's called prefrontal cortex?
Is morality processed at ventro medial pre frontal cortex or at anterior singular cortex?
My background: I am a programmer. I just want to understand humans brain the way a programmer understand computer. It seems that we don't have CPU. We have huge analog based memory. And we got registers instead of tons of abstract variables. Understanding why certain part of the brain is named under certain things will help me a lot in remembering where exactly that thing is and why. It's something very useful in my ways of learning math and programming.
Basically there are 2 theories.

Prefrontal cortex is named as such because it's before (or in front
of) prefrontal lobe.
It's because it's behind prefrontal bone (the
way other brain lobes are named)

Some people told me to just look that up on wikipedia. If you can show me something in wikipedia explaining the exact answer I am looking for I will be very happy.

It seems your question can largely be answered by reading the wikipedia article

I have read wikipedia article. Most contain info such as occipital lobe is named such because it's behind occipital bone. I got to dig a lot before I found what ob caput mean.

From the Wikipedia article: The term "prefrontal" as describing a part of the brain appears to have been introduced by Richard Owen in 1868.[6] For him, the prefrontal area was restricted to the anterior-most part of the frontal lobe (approximately corresponding to the frontal pole). It has been hypothesized that his choice of the term was based on the prefrontal bone present in most amphibians and reptiles.[6]

I think in general "cortex" means "outer layer", and it's used for many things besides the brain: https://en.wikipedia.org/wiki/Cortex_(anatomy)

Okay I didn't found it when I look for it. People got to read the whole article. Do you think this kind of question is appropriate? I am not a doctor. I just want to learn a lot because it fascinate me. I am a programmer.

You don't have to read the whole article. The contents directs you to a section called Etymology.

The prefrontal cortex (PFC) is a part of the frontal lobe (Fig. 1).
Lobe means

[A part] demarcated from the rest of the organ by a fissure (crack), sulcus (groove), connective tissue or simply by its shape. For example, there are the frontal, parietal, temporal, and occipital lobes of the brain.

Cortex means

The outer or superficial part of an organ or bodily structure (such as the kidney, adrenal gland, or cerebellum or a bone); especially: cerebral cortex

The frontal lobe is called as such, because... it's in the front of the brain.
The prefrontal cortex is called that way because it forms the frontmost part of the frontal cortex. Prefrontal means

anterior to or involving the anterior part of a frontal structure

Anterior meaning

situated before or toward the front

Indeed Siddiqui et al (2008) mention:

The anterior part of the frontal lobe referred in the literature as ‘pre’-frontal lobe has been simultaneously referred to as ‘frontal granular cortex’ and ‘frontal association cortex.’ The anterior most portion of the frontal lobe is occupied by the PFC...

Reference
- Siddiqui et al., Indian J Psychiatry (2008); 50(3): 202–8

Fig. 1. The frontal lobe includes the prefrontal cortex (PFC). source: Socratic

I think the term pre-frontal does not mean anatomically in the front of the frontal lobe of the brain. This is regarded to the history of discovered area , that the choice of the term was based on the prefrontal bone present in most amphibians and reptiles.you can find this in etymology part ▶enter link description here

Interesting. There is no prefrontal bone in humans.

Are you sure? got sources?

@J.Chang not in the human ,the prefrontal bone which is present in most amphibians and reptiles and this has been hypothesized for the choice of the term .


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How quickly do estrogens break down in the environment?
Of all the synthetic hormones we use, estrogens are probably the most common.  They are used for birth control as well as hormone replacement therapy.  This researcher also shows that there is plenty of it in milk because dairy cows are often pregnant while they are being milked.
Estrogen is a sturdy compound, very much like cholesterol.  I was wondering if anyone had any idea how long it would survive in the environment, given that some people are concerned about it interrupting animals life cycles.  How fast does it break down in the wild?

As in, in the air..?

estrogens have negligible concentration in the air. they would tend to be in the ground or in water taken in by plants an animals.

Months to years - although the actual duration in a specific environment depends on the nature of that environment and is tied to oxygen level. Higher oxygen, faster degradation. Less oxygen, the estrogen molecules interconvert among various closely related molecules which hampers both their detection and their degradation.
For more info, please see: Environmental science: The hidden costs of flexible fertility (Nature 485, 441 (24 May 2012))  and this Science Daily article.

Thanks for telling me about doi links and doing it for me in this case.


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Why is blood removed from meat?
Blood is removed from meat before it is consumed. Below is, for example, how chickens are processed from Wikipedia.

Removed from transport cages
Hung by the legs on a shackle, mounted on a conveyor chain.
Stunned using an electrically charged water bath
Killed by cutting the blood vessels in the neck
Bled so that most blood has left the carcass
Scalded to soften the attachment of the feathers
Plucked to remove the feathers
Head removed
Hock cutting to remove the feet
Rehung in the evisceration room
Gutted or eviscerated to remove the internal organs
Washed to remove blood and soiling from the carcass
Chilled to prevent bacterial spoiling

Why is the blood removed? Does it just simply taste bad? This might be a stupid question but being vegetarian, I may not know.

we find in the Bible a command not to eat blood and to drain it before eating flesh. This practice may have its roots there.

Just a guess: blood may contain active immunological modulators and endocrine molecules. But this may be just a general practice because blood is consumed as food.

I'm voting to close this question as off-topic because it is about processing of food. Changing the pitch of the question may help.

Blood finds use in many different dishes as well as biotechnological applications. Research-grade BSA (bovine serum albumin) is derived from cow's blood, there are not special facilities, same cows go for steaks and car seats. So part answer is economical: blood can be processed further. Also it is just easier not trying to preserve liquid inside vessel already opened by slitting the throat. It also seems that blood can rot faster than other tissues, maybe, because in dead animal immune responses are deteriorated and every infection in blood will activate.

Can you add some references, especially for your last sentence?

I will try to add some reference, but my guess is that bacteria can travel faster in liquid, rather then in tissue through extracellular matrix.

Right, it's your guess, which is why I asked for references.

I wouldn't have thought it was to do with rotting, but clotting.

I found a forensic article that states the following:

Because the protective agencies of the body are absent, the bacteria spread through the blood vessels using the proteins and carbohydrates of the blood as culture media.

I was unable to find anything more on this with my limited searching skill, though I plied it to the best.
There was an interesting study on the relation between decompostion of animal meat and the bacterial load though. It was a good read!

Please cite the reason for downvote, so that I can improve the answer.


text:
Possible to Gain More Weight than the Food You Eat
I was wondering if it's possible to gain more weight than the mass of the food you eat. At a first look, this is impossible because of the principle of mass conservation, but are there other things to take into consideration?
For example, fat contains carbon. Does the body use the carbon we breathe to produce the fat necessary to store any energy we don't use? And a relevant question: how efficient is human fat at storing energy, compared to what humans normally eat?

I don't know if you consider water as food, but you can easily gain weight by just drinking water. You might want to look into what can be absorbed through your skin as well.

No it is not possible.  Humans are heterotrophic organisms, which means that we use organic molecules (i.e., food) as a source of nutrients and energy.  We use the nutrients to add mass to our bodies.  These nutrients are the familiar carbohydrates, proteins, lipids (fats), etc...  During digestion food is broken down into simpler organic nutrient molecules that are then used to make our body tissues.
So even if we only used food for nutrients we could not gain more weight than the food we consume but note that the food is also used for energy. This means that some of the mass of the food that we eat is not used to add mass to the body but is "burned" as metabolic fuel.  The mass of the food used for energy is expelled from the body as waste in the $CO_2$ that we exhale and in the metabolic waste in the urine.
The carbon in the air is mainly $CO_2$, which is an inorganic molecule.  Only autotrophic organisms like plants can use inorganic molecules as a source of nutrients.  Since inorganic molecules usually contain less potential energy than organic molecules autotrophic organisms need a different source of energy.  Plants use sunlight.
Finally, fat contains about 9 Calories per gram whereas a Big Mac has about 2.4 Calories per gram so fat has almost 4 times the energy of a Big Mac.
(Calories are the amount of heat that is released if all of the energy in the organic molecules is released so it is an estimate of how much energy the body can get from food)

I think this is a good answer to a good question, and I've registered those feelings:  Nevertheless, I'm wondering when (if ever) a living human's body did not contain some autotrophic life, perhaps most commonly in the form of bacteria (which, at least in the time--decades ago--when I studied biology systematically, had or have usually been considered as microscopic relatives of plants).  As their activity would affect our state of mind, etc., I've usually considered us to be living partly in symbiosis with such forms of life (that might, consequently, not be easily distinguished from us).

One thing that might be worth mentioning here is that there is drink as well, which contain large amount of calories. Particularly alcohol surprisingly. Just mentioning it because it might be overlooked.


text:
What is a "pure odorant"?
This article about testing for Alzheimer's, via changes in the ability to smell, said:

She thought of peanut butter because, she said, it is a “pure odorant”
  that is only detected by the olfactory nerve and is easy to access.

I'm not clear on what that means. Assuming a person had their mouth closed, then wouldn't any odor be detected only by the olfactory nerve? Wouldn't a lemon, say, work exactly the same?

good question. you might have to ask the original researcher. This might be her? http://oge.med.ufl.edu/Students/Current/Stamps-Jennifer.htm

To answer this question, you need some background info first.
There are three "systems" used for the sense of smell. The first is the olfactory system. This system allows us to recognize what a smell is. You can tell the difference between gardenias and grass because of your olfactory system. The second system is the trigeminal system. This system tells you whether an odor is irritating or pleasing. It gets its name from the trigeminal nerve--the nerve that gives feeling to your entire face. Your sense of smell is all tangled up with the trigeminal nerve, meaning that some odors are painful to smell and some are not. When you smell ammonia and it stings your nose, that is the trigeminal system at work. The third is the vomeronasal system. It's thought to be use for detecting pheromones. However, it isn't important to this explanation.
So. What is meant by a "pure" odorant? It means that it only smells. It doesn't create a reaction in the trigeminal system. It only activates the olfactory system. Those who have lost their sense of smell are still able to distinguish many smells because of the reaction by the trigeminal system. One study I've read tested 47 different smells for people who have lost function in their olfactory system. Out of those 47, 45 of them were identified by the people with no sense of smell. The two that were not identified (decanoic acid and vanillin) didn't stimulate the trigeminal system and are thus considered to be "pure" odorants. In other words, pure odorants are odors that only smell and don't feel like anything. There are very few "pure" odorants, and peanut butter is one of them.
So, when someone says Alzheimer's changes the ability to smell, they have to make sure they're only testing smell and not touch too. That's why they need to use a "pure" odorant. Otherwise, the Alzheimer's patient might still be able to identify the scent and the test would be useless.

Can you add a reference/review to the description of the three "smell systems", and the reference to the "One study I've read..." section?

One of the downsides to asking questions on this site, (unlike tech-sites), I'm not really qualified to decide if an answer is correct. :) But looking at it, it does answer the issue of "pure-ness" in an odorant, so giving a checkmark.

I could not find a concrete definition after searching several sources, but after reading a few papers I think the term Pure Odorant refers to its Olfactory Bulb profile. Peanut Butter will stimulate specific Olfactory nerves, and only that set of nerves, whereas impure Odorants may stimulate part of the profile and also other parts of the Bulb depending upon the impurity.
Basically, Peanut Butter has a unique smell that you can't replicate, and thus cannot mistake in either flavor or scent when compared to similar compounds. You may  not even be able to tell it was Peanut Butter at all if not for the scent.
A Lemon would not work the same way, as the major Odorant in a Lemon is Limonene - which is present in all citrus fruits. You would activate the same neuronal pathways for Lemons that you would with Oranges, Limes, and Grapefruits.
That's my best assessment.

So you're saying that peanut butter stimulates only a small section (of the Bulb, whatever that is), whereas other scents will trigger multiple nerve sections, and so can be faked with a different set of odorants?

@JohnC - More or less. Peanut Butter has a unique scent and is readily available. Using purified Limonene would work, as I'm sure there's a nerve profile for Limonene - but the purified product isn't readily available. The benefit of Peanut Butter is specificity. It's a known scent (to people in countries that like peanut butter), and a unique scent that's instantly identifiable. You could confuse oranges with limes or lemons by scent, but a healthy person will always recognize peanut butter as peanut butter. It tests sense of smell and cognitive function simultaneously.

Not sure I really understand why a "pure odorant" was needed for the test, then. All they were doing, was measuring the distance at which the odor could be detected, not what it was. While I can see that peanut butter is useful, for non-odor reasons (sticks to a spoon, etc), I still don't see why a lemon (or lemon juice on a Q-tip) wouldn't have worked just as well. Possibly that line was just intended to sound more scientific than, "it sticks to the spoon." :)

@JohnC - There may not have been a very good reason. They wanted something with a unique smell that was cheap, and Peanut Butter was probably a convenient option. More important than the smell is the caveat that the lack of smelling abilities found in the study can be attributed to more than just Alzheimer's. It's a quick and dirty early signal, but it also has a pretty high false-positive rate.


text:
Can someone identify this bird?
We recently found a nest in the back garden and a little bird inside. Can you help us identify it? The nest is quite small like the bird so we are wondering whether this is the parent or a baby chick. Is there anything we can do to help it or are we better off leaving it alone?
Update: I'm from the UK, currently in Oxfordshire to be more precise.

Took me a ridiculous amount of time to locate the bird in the picture :L

Looks like a Carolina wren. They are common small brown birds.  The call is a loud three syllable call that sounds sorta like cheeseburger cheeseburger cheeseburger.  Regardless it is certainly better off if you leave it alone.

Well it's not a Carolina Wren, then...

@RoryM still can't find it. Now I'm afraid to keep looking at the picture, lest it be a joke with a monster who pops up screaming. I mean, I know it surely isn't the case, but still...

It looks like a passerine bird, but I can't really tell the species without seeing the whole body. As for what to do with it, your best course of action is to leave it alone. Trust me. Once placed tissue paper over a pigeon's eggs to keep them warm, and the mother crushed them when she landed on the nest because she didn't see the eggs.
If there are eggs in the nest, try noting down what color they are. Passerines have colored eggs.

The bird needs to be left alone; that's the best help you can give it.  Anything more than watching it is liable to lead to nesting failure (e.g. abandonment of the nest).  The bird looks attentive and quiet, and so is most likely an adult keeping the eggs or chicks warm.  The bill suggests a seed-eating bird, but there are large numbers of those (e.g. finches, sparrows, grosbeaks, ...) and I can say little more from the evidence.

This is not really an answer.

@WYSIWYG, it responds directly to the last sentence of the post, to wit: " Is there anything we can do to help it or are we better off leaving it alone?"  It also gives addresses the other question ("Can you help us identify it?") by giving more information than the accepted answer, i.e. by naming three specific possible subgroups of the passerine birds.