text:
Do spiders learn how to build webs?
Concerning spiders, is there any research on whether web-building is an inherited behavior, or if it must be observed and learned?
e.g. Has anyone hatched spider eggs in isolation and observed whether the descendants still know how to build a web?

Spiders’ ability to weave webs is a classic example of an innate or instinctual behavior. They do not learn to make webs.
The earliest English-language scientific publication that I can find to back this claim is Porter 1906 1, which focuses on variation in the webs of Orb-weaving spiders:

The web of the Orb-weaving Spiders has long been one of the classical examples of animal instinct. It is so definite and complex, and yet so frail a structure and must be rebuilt so often under varying conditions that, a priori, we should expect it to furnish one of the best of fields for the study of the variation of instinct. If the cell of the Honey-bee varies so that, according to Prof. Wilder (73, pp. 654,655), who quotes Prof. Wyman in this connection, there may be a gain or loss of one cell in ten, then from a knowledge of the differing conditions under which the spider works, together with the frailty of the web as compared with the cell, we have as much, and even more, ground for thinking that even greater variation will be found here.

In his review of the literature, Porter directs readers to Menge's 1843 work About the way of life of the arachnids 2 for an overview of spider physiology and behavior, as well as works by Wagner 3,4 as specific references for spider instinct and its variation. Unfortunately, these works are not written in English, so I cannot verify their claims.

References

Porter, J. P. 1906. The habits, instincts, and mental powers of Spiders, Genera, Argiope and Epeira. The American Journal of Psychology, 17(3), 306–357.
Menge, A. 1843. Über die Lebensweise der Arachniden. Neuste Schr. Naturf. Gessell. IV, Danzig.
Wagner, W. 1897. L'Industrie des Araneina. Mem. de l'acad. Imp. des Sci. de St. Petersburg. Tome, XLII, No. II, pp. 269.
Wagner, W. 1900. L'arraignde aquatique (argyroneta aquatica Cl.) son
industrie et sa vie. Materia de psychologie comparde. Bull. Soc. Moscou, pp. 61-169.

Could you add a bit more detail please? For instance, does that paper have evidence that the very first web a spider makes is no worse than their last one?

@terdon It seems to me like (though I know absolutely nothing about this topic) being able to recognize issues with their web and improve upon it next time would require a lot more intelligence than just copying the way another spider makes their web, since it'd involve connecting the problem with its solution.

Spiders have been sent to the ISS to see if they can weave a web in zero gravity.  The interesting thing is that their first attempts were a mess, then after 2 days they mastered it.  It shows at least some level of learning.  But it is learning from experience, not from imitating others.

For many species the mother abandons the eggs after laying them and there is no maternal care (sometimes the mother dies after laying eggs, so really no possibility of maternal care). Paternal care is generally completely lacking as well (and sometimes the father is expected to die before hatching). And many of those species are solitary, so not learning from other unrelated spiders. So for those spiders web weaving is obviously innate.
As a bonus, this includes some species of the most dramatic web weavers, orb weaving spiders.
(Note that other spider species are fantastic mothers with a prolonged period of child-rearing, so I guess it's possible that it's learned in those species, but Occam's razor suggests that it's innate in all spiders.)

Welcome to Biology.SE! This looks like the start of a good answer, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and provides no guide to further leaning. This is a good example of how to format references. ——— You may also want to take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site.

This isn't necessarily true though. I learnt many things from my own parents, but I certainly didn't learn how solve an equation, speak French, or make armpit farts. All those came from other people. Proving that web building is innate would need not only removing the parents from the scene, but also all other spiders - and I think that's the experiment the OP is looking for.

@Graham "[M]any of those species are solitary, so not learning from other unrelated spiders."

@Graham and further, how do you rule out self-learning?  How would you prove the spiders inherently knew how to build webs rather than learned to do it on their own?

@CharlesStaats Thanks - I missed that little bit.

@RyanL You'd expect there to be a progression of complexity/competence in the designs, if they're learning. Birds' flying ability is a great example - they see their parents and practise in the nest whilst their wings develop, and chicks raised without a "role model" bird may not ever learn.

@Ryan_L Some of the spiders in question have very distinctive webs. https://en.wikipedia.org/wiki/Web_decoration So that seems to rule out learning from other species. In terms of learning from their own species, some of them tend to only live a year or less (they can live longer if the winter is mild, but the expected life cycle is that eggs survive the winter but adults do not). -- It's also possible that something is innate but still improves over time, e.g. crawling in humans. A newborn doesn't have the muscle control to crawl but will start crawling even without observing others crawling.


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How Can Homosexuality be Genetic?
I hold no strong opinions towards homosexuality one way or the other; I'll personally refrain, but don't apply my personal tastes to the rest of the world.
I remember seeing some articles a while back, and in some online debates, that there's been evidence in favour of a genetic component of homosexuality. I ignored it back then (before it became legalised), since it didn't affect me. However, after deep thinking, I started to seriously doubt those stories.
My gripe is this, based on my extremely limited understanding of Evolutionary Biology, organisms with genes which boost survivability, will tend to become more abundant. Genes that made organisms more fertile and reproduce more, will tend to become more abundant.
So, if say a particular gene, reduced effective fertility of organisms, that gene may be expected to be absent after a while. Fewer organisms with that gene would reproduce each successive new filial generation. There will be a diminishing marginal increase in the population of these gene bearers, before there eventually starts to become negative growth. I expect that population, may eventually find themselves in extinction, or on the brink of it.
In the few 100,000 years that Homo Sapiens have walked this planet, I guess there's been sufficient time for a population of genetically predisposed homosexuals to become extinct, or reach its brink. Certainly not the 5% - 10% estimated population we have today.
As such, I am unable to understand how homosexuality might be determined by genes in spite of natural selection.
My understanding of Evolutionary Biology may be severely lacking; especially as my teachers in the subject believed it was blatantly false, and were not really interested in making their students understand it. Some even going to the extent of making it seem as ridiculous as possible (I live in a country, where more than 90% of the population are genuinely religous (as in they truly believe in the existence of God) in one form or the other). I would appreciate answers to my question.
Of course, whether or not treatment of homosexuals should change, is another separate matter. It certainly does not follow from any conclusion of this inquiry; the answer to this question, is irrelevant as far as LGBT rights are concerned.

Note that there is no question in the boy of the pot. Only in the title. That makes the post arguably slightly unclear. The title would let one thing you are interested in the mechanistic mechanism by which genes can affect sexual orientation while the body of the post clearly talk about selection pressure toward those potential genes.

I guess my question would be: How can homosexuality be genetic despite natural selection?

Is this any different from How can homosexuality evolve despite natural selection?? Can you please try to clarify in what way these two questions are different?

It is possible that lack of knowledge in evolutionary biology would prevent you from understanding that these two questions are the same. Understanding Evolution by UC Berkeley is a very introductory course to evolutionary biology if you are interested.

Take the advice of @Remi.b, check out the Berkeley site. It's a mistake to assume evolution can eliminate all traits that do not appear to offer a selective advantage.

Consider that evolution works by populations, not just by individuals.  A human tribe that has a proportion of its people not attached to their own offspring seems likely to be stronger than one made up of competing male-female pairs.  To take this to an extreme, you might ask how eusocial creatures like ants, bees, and naked mole rats can be successful.

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Do women experience more bonding hormones than men after sex?
Does Oxytocin (or any other bonding hormone) increase more so for women than for men after sex?
Someone told me that it increases 4-fold for men and 12-fold for women (unconfirmed).
Is there any observable or scientific relationship between sex, Oxytocin and the desire for a monogamous relationship with a sexual partner?

Why did you delete (vandalize) your own post?

You've been told to stop vandalising your own posts already; you've been suspended on [so] for it. Stop, before a staff member has to suspend you everywhere.

Does Oxytocin increase more so for women than for men after sex?

Answer: Yes, Oxytocin level shoot up for female after sexual. It is highest at orgasm, which is the main cause women could have multiple orgasm.

Someone told me that it increases 4-fold for men and 12-fold for women
  (unconfirmed).

Answer: The level of oxytocin actually increase 5 times during sexual intercourse. Though some online article claim the male and female level as much you said, but it is not confirmed in humans.

Is there any observable or scientific relationship between sex, Oxytocin and the desire for a monogomous relationship with a sexual partner?

Answer:
Take a look at this experiment done on people to test Bonding:

Bonding is an important part of human romantic relationships, and
  research has suggested OT as a possible mediator of this effect. A
  2005 study by $Grewen\ et\ al^{4}$. found that couples who reported a greater
  amount of partner support showed higher baseline OT plasma levels.
  These couples also showed higher levels at 4, 7, and 10 min following
  warm partner contact. For women, OT levels increased sharply 7 min
  following warm partner contact, regardless of partner support, while
  male levels remained unchanged. This study demonstrates a
  relationship between supportive romantic bonding and OT, and shows
  that warm contact has a greater physiological effect on women than on
  men.[1]

A very famous study done on rats confirm that Vassopressin and Oxytocin is actually the reason behind monogamous relationship.

Almost a decade ago, Thomas Insel, Director of the Center for
  Behavioral Neuroscience at Emory University, and colleagues at the
  National Institute of Mental Health and the University of Maryland
  implicated vasopressin and oxytocin in controlling the preference for
  particular partners in both male and female prairie voles. These
  investigators found that giving a male vasopressin causes it to stay
  with its mate, whereas blocking this hormone prevents a pair-bond from
  forming. The scientists saw similar effects in female prairie voles,
  with oxytocin determining the extent of pair-bonding. In contrast, the
  administration of these substances had no influence on social
  interactions in the promiscuous montane voles. Surprisingly,
  vasopressin and oxytocin are naturally found at similar levels in both
  prairie and montane voles.[5]

Source:
[1]. The role of oxytocin in mating and pregnancy
[2]. http://en.wikibooks.org/wiki/Relationships/Hormones#Oxytocin
[3]. The role of oxytocin in relation to female sexual arousal.
[4] Grewen, K.M., Girdler, S.S., Amico, J., Light, K.C., 2005. [Effects of partner support on resting oxytocin, cortisol, norepinephrine, and blood pressure before and after warm partner contact](Effects of partner support on resting oxytocin, cortisol, norepinephrine, and blood pressure before and after warm partner contact.). Psychosom. Med. 67, 531–538.
[5] http://www.smart-publications.com/articles/oxytocin-the-real-love-hormone

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Will genetically modified food affect our health?
It's a popular public sentiment that - GM foods like tomatoes (flavr savr) will affect our health.. Is there any logical scientific explanation behind this?

I don't see a personal health question here. The question might not be very profound otherwise though.

this q. is legitimate...slightly debatable...but not at all a personal medical q....

I agree with the above comments. However, I think this question would be a better fit on skeptics.SE. By doing a simple search for "GMO" on skeptics.SE you will get several interesting hits. The question might be considered as a duplicate of other questions on skeptics.SE. I would tend to think this question should be answered following these guidelines

Would improving health count? If GMOs provide larger yields or better nutrient content with less dependence on pesticides or herbicides those would all be good things. Most of the questions I see about GMO only ask about potential negative outcomes.

It's a popular public sentiment that - GM foods like tomatoes (flavr
  savr) will affect our health.. Is there any logical scientific
  explanation behind this?

GM organisms can have different genes and gene expression than natural ones, so they can create more protein or different proteins. Proteins can be toxic, can cause allergy and can catalyze reactions which can lead to toxic products.
To create a GM plant you need dollar millions, so it is not a cheap business. The GMO food regulations are very strict (at least in the EU), so it is unlikely that you will eat a GMO which contains toxic compounds.

Whereas food safety organizations find nothing inherently unsafe in
  the process of genetic engineering, they note that new plant
  characteristics developed in the next wave of agricultural
  biotechnology could present new risks. At the same time, future
  generations of biotechnology may well provide food products with
  higher vitamin or protein content and lower allergenicity, yielding
  benefits to food consumers.

2014 - Agricultural Biotechnology: The Promise and Prospects of Genetically Modified Crops

Despite all the effort to make GMO foods safe, there are issues:

Pesticides associated to genetically modified foods (PAGMF), are
  engineered to tolerate herbicides such as glyphosate (GLYP) and
  gluphosinate (GLUF) or insecticides such as the bacterial toxin
  bacillus thuringiensis (Bt). The aim of this study was to evaluate the
  correlation between maternal and fetal exposure, and to determine
  exposure levels of GLYP and its metabolite aminomethyl phosphoric acid
  (AMPA), GLUF and its metabolite 3-methylphosphinicopropionic acid
  (3-MPPA) and Cry1Ab protein (a Bt toxin) in Eastern Townships of
  Quebec, Canada. Blood of thirty pregnant women (PW) and thirty-nine
  nonpregnant women (NPW) were studied. Serum GLYP and GLUF were
  detected in NPW and not detected in PW. Serum 3-MPPA and CryAb1 toxin
  were detected in PW, their fetuses and NPW. This is the first study to
  reveal the presence of circulating PAGMF in women with and without
  pregnancy, paving the way for a new field in reproductive toxicology
  including nutrition and utero-placental toxicities.

2011 - Maternal and fetal exposure to pesticides associated to genetically modified foods in Eastern Townships of Quebec, Canada

The study of combined effects of pesticides represents a challenge for
  toxicology. In the case of the new growing generation of genetically
  modified (GM) plants with stacked traits, glyphosate-based herbicides
  (like Roundup) residues are present in the Roundup-tolerant edible
  plants (especially corns) and mixed with modified Bt insecticidal
  toxins that are produced by the GM plants themselves. The potential
  side effects of these combined pesticides on human cells are
  investigated in this work. Here we have tested for the very first time
  Cry1Ab and Cry1Ac Bt toxins (10?ppb to 100?ppm) on the human embryonic
  kidney cell line 293, as well as their combined actions with Roundup,
  within 24?h, on three biomarkers of cell death: measurements of
  mitochondrial succinate dehydrogenase, adenylate kinase release by
  membrane alterations and caspase 3/7 inductions. Cry1Ab caused cell
  death from 100?ppm. For Cry1Ac, under such conditions, no effects were
  detected. The Roundup tested alone from 1 to 20 000?ppm is necrotic
  and apoptotic from 50?ppm, far below agricultural dilutions (50%
  lethal concentration 57.5?ppm). The only measured significant combined
  effect was that Cry1Ab and Cry1Ac reduced caspases 3/7 activations
  induced by Roundup; this could delay the activation of apoptosis.
  There was the same tendency for the other markers. In these results,
  we argue that modified Bt toxins are not inert on nontarget human
  cells, and that they can present combined side-effects with other
  residues of pesticides specific to GM plants.

2012 - Cytotoxicity on human cells of Cry1Ab and Cry1Ac Bt insecticidal toxins alone or with a glyphosate-based herbicide

Though GM crops promises to meet the world's food need and eliminate
  the world hunger and starvation, the potent harmful effects cannot be
  overlooked and these need to be taken seriously. The long term impact
  on the society cannot be overruled as it includes the health risk of
  all the people involved be it producers (farmers) or the consumers
  along with the scientists who are working in the laboratory. Hence, it
  is the need of the hour to reach and try for sustainable development
  that meets the needs of humans and the balance of nature maintained.

2013 - Cry1Ab Treatment Has No Effects on Viability of Cultured Porcine Intestinal Cells, but Triggers Hsp70 Expression

I think it is the same story as by food, pharma and plastic industry. The billion dollar profit can be more important than the consequences. Btw. if you check a regular food, which you can buy in the shop, you will find a lot of unhealthy components e.g. trans fatty acids, omega-6 fatty acids, fungicide remnants, etc... which can affect your health as well.
My conclusion is that in most of the cases it is safe, however in rare cases it might have a mild harmful effect. To filter out those cases and their causes we need further studies and better regulation.

Genetic engineering is a technology not a trait.
In general, genetic engineering and genome editing are as safe as conventional breeding and mutagenesis (introducing thousands of random mutations by radiation or chemicals to speed up the breeding process).
The safety of the resulting product depends on what has been changed or how the crops are used. You can obtain unsafe products from conventional breeding, as shows the popular example of the Lenape potato (Wikipedia), which was bred for specific traits while unintentionally increasing its solanine content to dangerous levels.
The same goes for GMOs. Glyphosate resistant crops will increase the glyphosate level in the plant and favor unsustainable farming practices like large mono-cultures and a lack of crop rotation with potential risks for the environment or even human health. On the other hand, Bt-crops have been shown to reduce pesticide use and can therefore be beneficial for health and nature.
Your tomato example is not that much related to farming. The aim was to improve shelf life, which could help to reduce food waste. Similar products are non-browning apples (Arctic Apples). Usually, they work by blocking the activity of an enzyme that normally would degrade the fruit. Of course, there are debates if the enzyme is needed for important processes in the plant and if it would have any negative effects on the healthiness of the product. But usually nothing significant is found.
Furthermore, genetic engineering can also make products healthier by introducing positive traits like increasing vitamin or healthier fatty acids.
Again, the safety of the product depends on specific changes and not on how these changes have been achieved. If we could have all these products with conventional breeding, we would do it. And we probably could, it just takes ages. So, all "negative impacts" of GMOs should really be discussed as "Do we want/need this trait and what are the effects?" and not as "Was it created by genetic engineering?".
Finally, GMOs are the best tested products on the market. While we know very well, what has been modified in these plants, we have no idea which genes have been changed in mutagenesis products. And because of strict regulations and research, approved products can generally be considered to be safe to consume. So far, there is no recorded case of someone having serious health issues from consuming GM-food, while people are dying from their self-grown zucchini (I'm not kidding).

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text:
Differential Scanning Calorimetry for bacterial membranes
I would like to study the freezing and melting of bacterial membranes and would like to use Differential Scanning Calorimetry (DSC) to obtain the glass transition temperature of the membrane. However, I am unsure where to find such protocols describing the process. Could someone please tell me how to use DSC for bacteria such as E. coli?


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What does this Barbary Macaque facial expression mean?
A girl pretended having a piece of food in her hand and pointed it to a Barbary Macaque in Gibraltar. As a response he made this facial expression to her. What does this mean?

What was the sound that it made?  Macaque vocalizations are also well studied, and it looks like it was vocalizing.

@Atl LED The macaque didn't make any sound, its lips were maybe more like this: http://upload.wikimedia.org/wikipedia/commons/e/e1/Expression_of_the_Emotions_Figure_18.png and its eyes wide open

It looks like it is trying too threat.

Source:
Individual differences in scanpaths correspond with serotonin transporter genotype and behavioral phenotype in rhesus monkeys (Macaca mulatta)

That is a threat face.  Barbary macaque threat faces often appear with a brow raise, lowered head, and an o-shaped mouth, sometimes with and sometimes without a vocalization.  Given the context you described it is not surprising the girl received a threat.  *Based on personal research experience

It would be fantastic if you provided some references.


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How to operate a microtome?

In the picture above (Source: Amazon.com, United Scientific MCT001 Hand Microtome) we can see a microtome. How is it operated?

Also, are these still used in everyday biological research? Teached for students?

Interesting picture. My guess is that this is a historic piece of equipment, but still seems to be available. The guys next door (who cut sometimes for us) use a cryomicrotome like this.

The imnstrument is shown here upside down. If it is turned around, it looks like this:

The glass disc are placed around the middle tube. The operation principle can be seen in this image:

The specimen is placed in the tube in the middle and pushed out by turning the knob at the bottom. The minimal increment for this kind of microtome is 10 micrometers. The razor knife is used to cut the slices of the specimen.
An operation manual can be found here.

Also, are these still used in everyday biological research? Teached
  for students?

It's a hand microtome allright. As Chris explained, these are used to section thin slices of plant tissue, to be examined using a transmitted light microscope. They're still availlable from several sources, for example from Euromex in The Netherlands. I still have one of those, but it's years ago I used it:

Those are hardly used anymore in research, but they are still being used by amateur biologists/botanists/microscopists.
The only uses I can imagine in research would be to use it to section a sample to see whether or not it is interesting enough to be processed and sectioned using more contemporary techniques, such as paraffin embedding followed by rotary-/sledge-/base sledge microtomy. Or perhaps in the study of life processes.
Depending on the skills of the operator (including his skills to sharpen/strop his knives!) and the nature of the sample, slices as thin as 20 µm can be sectioned, using a hand microtome.
That's often thin enough to make for a more or less acceptable botanical slide, temporary or permanent, but as kind of a norm, "regular" paraffin botanical/histological/histopathological/... sections for light microscopy are sectioned these days at any thickness between 2 - 10 µm.
That's not possible with this type of microtome.
The impossibility to section samples at a thickness thin enough to make for really clear microscopic images has burdened scientists for ages.
It wasn't untill 1883 that an American mechanic, Adam Pfeiffer, came up with a usable machine to make that happen. Pfeiffer worked further on the idea provided by two others, Cowles and Richards, who made a first prototype in 1879.
In 1886, Charles Minot, an American as well, came up with the first really usable rotary microtome.
That "Minot-microtome" is up to the present day, the workhorse in the botanical, histological and histopathological lab.
It's an interesting story, but the rotary microtome is based on a fundamentally different concept, compared to a hand microtome.
The real offspring of the hand microtome is the (base) sledge microtome, as it mimics more or less the movements of an operator using a hand microtome. But without all those impossible to controll variables.
This is a base sledge microtome, I finished restoring only a few weeks ago. It's the legendary Jung Heidelberg Tetrander II. The Tetrander was put on the market in 1910 and some of those are still in use. They're used to section large and hard samples (hard wood, bone, teeth, ...), which can't be sectioned using a rotary microtome.
At the time it appeared on the market, a popular joke amongst German histotechnicians was, that it was named "Tetrander" because it took four man to handle it... In reality it was named "Tetrander" because it was designed by four German scientists, amongst them the legendary Paul Mayer (yes, that Mayer's hemalum staining solution guy).
This one (it is operational) is capable of sectioning samples as large as about 5cm * 7cm (ca. 2in * 3in), section thickness adjustable between 1 and 50 µm.
Larger, motorized models are capable of sectioning things as hard as a concrete bloc, having the size of a modest tree. And that's no exageration...


text:
Is there biological evidence for self-awareness in animals?
I am conducting an investigation into the topic of the intelligence of
animals, in particular farm animals. I would be interested to hear a scientific and biologic perspective as to what is perceived to be self-awareness, whether it be in a human or
not. Specifically, I am interested in the high-level self-awareness that we as humans experience and that is only now, beginning to be theorised as possible in other mammals (e.g. Dolphins).
The question is framed in a robotic context, where a being (natural or artificial) is defined to be self-aware if it can approximate enough human behaviour and thought, that it becomes indistinguishable from a human. This term we could label sentience, but this is a subjective term, and so I will avoid using it for the purpose of this question. I will define a being as self-aware in the robot context, as a being capable of both conscious reflection of itself and of its own conciousness.
One of the problems I have found in my investigation, is a serious
misunderstanding about the nature of self-awareness, amongst
the general public.
It seems that many people incorrectly assume that self-awareness is a product of
a being having a soul. This is rather unfortunate for animals as orthodox
Christianity teaches that animals do not have souls, and therefore are
incapable of attaining self-awareness.
My investigation aims to bring to mainstream public attention, a new
definition of self-awareness, and to end the centuries-old misconception
that we are the only intelligent, self-aware creatures on the planet.

I don't think self-awareness and sentience means the same thing. Even a bug or plant has a response to pain and can recognize its attacker, etc... For me self-awareness means that I know that I am an individual and that I have a body. I think it is hard to talk about this topic without proper words and definitions, so I suggest you to add these definitions to your question, since in the current form it is not clear what you are asking. I assume the topic will lead you more to psychology than biology.

I appreciate your comments and I shall update my quedtion accotdingly.

You need to add the definition of 'sentience' that you are using. Standard definitions of 'sentience' often include subjective sense, perception and feeling, not involving high level intelligence or reasoning. Using these definitions, sentience in animals should be pretty uncontroversial.

The question has now been revised several times and asks a valid question which is looking for 'scientific or biologic evidence for sentience in animals'. It would be difficult to narrow it down any further without diluting the question.

@Adam893 You haven't added a definition or clarification of what you mean with sentience, just the words "high-level". Since you want comparisons and evidence for "sentience" in widely different animals, a clear definition of what kind of traits you are looking for is essential.

Many thanks for the comments, you are completely right. I have rephrased the question and removed as many subjective terms (inc. sentience) as possible.

Yes, there is a lot of evidence for self-awareness in animals. The gold standard test for self-awareness is the mirror self-recognition test (MSR)--we can tell from the behavior of an animal exposed to a mirror whether or not it can tell itself apart from other animals of the same species:

Animals that possess MSR typically progress through four stages of behavior when facing a mirror: (i) social responses, (ii) physical inspection (e.g., looking behind the mirror), (iii) repetitive mirror-testing behavior, and (iv) realization of seeing themselves. (Plotnik et al. 2006)

That quote was taken from the abstract of a paper showing self-recognition in a single African elephant, but there is evidence for self-awareness in magpies (Prior et al. 2008), dolphins (Harley 2013), chimpanzees (Povinelli et al. 2006) and orangutans (Suarez and Gallup 1981). Many of these studies use the Gallup mark test (Wikipedia):

Gallup anaesthetised the chimpanzees and then painted a red alcohol-soluble dye on the eyebrow ridge and on the top half of the opposite ear. When the dye dried, it had virtually no olfactory or tactile cues. Gallup then returned the chimpanzees to the cage (with the mirror removed) and allowed them to regain full consciousness. He then recorded the frequency which the chimpanzees spontaneously touched the marked areas of skin. After 30 minutes, the mirror was re-introduced into the room and the frequency of touching the marked areas again determined. The frequency of touching increased to 4-10 with the mirror present compared to only 1 when the mirror had been removed. The chimpanzees sometimes inspected their fingers visually or olfactorily after touching the marks.

Basically, an animal which has seen and recognized itself in a mirror recognizes the mark as being new, so it touches its own body on the marked area, which shows that the animal recognizes the image in the mirror as itself.

However, the mirror test has at least one serious flaw, in that it assumes that other creatures use vision as the primary means of identification.  If someone changed your body odor while you were sleeping, would you notice the change?

That's a definite limitation especially for animals which rely on other senses (dogs, etc.). I'm pretty sure similar studies have been attempted with other stimuli (maybe dogs and their own urine?), although I don't have a reference to back it up.


text:
Why do we sleep?
While we do know that the human body is regulated by a circadian clock that keeps humans on a sleep/wake cycle, we don’t really know why. Sleep is the time when our bodies repair tissues and perform other maintenance activities, and we spend nearly a third of our lives snoozing. Some other organisms don’t need to sleep at all, so why do we?

It seems that the notion that some animals don't sleep is the core of your question. Could you share which animals don't sleep? The definition of sleep may in fact be crucial to answer your question. An explicit definition in the question is recommended to prevent unnecessary discussions.

https://askabiologist.asu.edu/plosable/who-needs-sleep-anyway  I am not sure if this is correct or not

Possible duplicate of Why did the process of sleep evolve in many animals? What is its evolutionary advantage?

We don't actually know. But these two theories are strong candidates:

Sleep 'cleans' the brain of toxins. Metabolic waste products of neural activity are cleared out of the sleeping brain at a faster rate than during the awake state. This finding suggests a mechanistic explanation for how sleep serves a restorative function, in addition to its well-described effects on memory consolidation.
Source: Xie et al. 2013. "Sleep Drives Metabolite Clearance from the Adult Brain", Science.

Sleep helps the organism alternate between day and night. Circadian rhythms enable an organism to anticipate, rather than passively adjust to, the changes imposed by alternation between day and night. These changes relate to positive functions such as vision and negative effects such as ultraviolet light damage. They also include indirectly generated alternations such as temperature, availability of food and prevalence of predators.
Source: von Schantz & Archer. 2003. "Clocks, genes and sleep", J R Soc Med.

In regards to animals that don't sleep, the affirmation is half valid. Arthropods don't sleep, but enter a metabolic slowdown state. Dolphins put half their brains to sleep while the other half stays active. Basically, anything with a brain needs to sleep, in some way or the other.
Homeostatic regulation is an interesting clue, because it suggests that there are some conserved functions of sleep. The need to make up lost sleep must be there for a reason.
If sleeping didn't have a necessary function, it wouldn't be universal. And it most definitely has to do with the brain, because it is the organ affected the most by lack of it.

There is no actual evidence for a need to "make up" sleep. you need sleep but there is no evidence you need extra sleep after missing sleep.

There are several theories for the function of sleep (with a focus on the brain) with varying amounts of evidence (mostly through sleep deprivation's interference of these processes)...

Energy savings.
A time to open up spaces between brain cells
to flush out metabolites and toxins including beta amyloid.
Memory consolidation - move labile new memories into longer term
storage.
Create more brain space - reduce "synaptic load" gained
during the previous day's experience, so you are better able to make
new memories the next day.
Creativity - make abstract links and
problem solving.
Emotional/mood recalibration.

Why it's thought these occur in the sleep state is that it provides the right neurochemical milieu to perform these necessary tasks, which would be inefficient or even dangerous if it occurred during your conscious experience.


text:
Can a certain part of human dna can be replaced with other animals dna?
Human DNA consists of adenine, thymine, guanine and cytosine. Can thymine of other animal can be placed with humans thymine?

First: the whole base is called thymidine (consists of thymin and the ribose). There is no difference between thymidine of human or animal origin.

@Chris so that we can replace?

Where and what do you want to replace?

Thymine in all living things is identical.  It has been possible to use the chemicals from plants animals or bacteria (or organic chemistry) in human cells....

Yes. They're identical. When we eat animals or plants we digest their DNA to use to make our own DNA.

Sweet, sweet DNA...


text:
What does it mean to have different "metabolism"?
We hear talk of different body types, and that it is more difficult for certain people to lose weight than others. On the other hand, when my physician recommends that I lose weight, they say that it is really just as simple as "calories in, calories out". How can we reconcile these two?
Perhaps the "calories out" portion is different for different people? I.e. some people burn more calories than others do, doing the same activities, but their hunger level does not compensate for this?
Apologies if this is off-topic

There are differences in metabolism, and the "calories in" part is the one which differs more than the "calories out" part.
People do lose different amount of calories for the same action, but for mostly mechanical reasons. If a 50 kg person walks up a mountain at 3 km/h, and a 100 kg person walks up the same mountain at the same speed, the 100 kg person will expend more energy, because they did more work. And then there are slight differences in how we do our movement - some people's gait is more efficient than others', and uses less energy. But this is not really interesting for the explanation of having it easy/hard to lose weight.
The point is that the amount of food we intake is determined by our hunger, and our hunger is determined by hormones. Then, the amount of fat we store is also determined by hormones. If your body "thinks" you should be putting on weight, and you go on a calorie-reduced diet, it won't just start complementing the missing energy from the fat stored in your adipose tissue. Rather, it will continue diverting some of your food intake to make more fat storage, all the while rationing the energy available for other activities: making you feel tired so you don't move much, shutting down some luxurious, energy-hungry processes in the brain, mostly the ones associated with higher mental functioning, and making you feel hungry and cold so you will be more motivated to seek out food and eat. The hormones which regulate these processes are many, most of them are poorly understood, some are probably not yet discovered (orexin, one of the main hunger regulating compounds, was only discovered sometime in the last 5 years I think), and we really don't have a complete picture of everything that is involved. It is a complex mesh of finely balanced homeostatic systems which interact with each other and the environment.
The people who say that it is as simple as "calories in, calories out" are right. They are right in the sense that, if you just observe a human being and measure their energy household, you will be able to document the amounts of energy consumed, expended and stored, and the energy consumed will equal the energy consumed plus the energy stored.
But to derive from this that we are talking about a passive overflow system and, if we reduce intake, storage is also reduced, is a big leap of faith and has been proven wrong again and again. Living systems are actively reacting to any influences from outside, by mechanisms much more intricate than simple mechanic rules. Mechanics tells us that if I push you, you will fall over; experience tells us that if I push you, you will brace yourself so you don't fall over, and then try to stop me from pushing you by using words, force, or whatever else you have at your disposal. Our physiological systems are the same way. They like the situation they have chosen to be in as much as you like standing upright. If somebody comes from outside and tries to forcibly change their status quo, they do whatever they can to 1) resist and retain the status quo, and 2) stop the outside force if possible.
As for the difference in metabolism: the hormone systems of different people are differently "tuned". For example, eating pure glucose causes insulin production to spike, and excess insulin causes glucose to be removed from the bloodstream, plus a handful of other effects. But the size of the insulin spike is different in different people. Also, the extent to which cells react to elevated insulin is different. When the reaction becomes dangerously weak at even high insulin levels, we say that it's a pathological variation, and call it "metabolic syndrome". If goes really towards zero, it's called diabetes type two. And this is an example about just one of the hormones connected to metabolism and the distribution and use of energy in the body.
On a simpler level, there is no difference in metabolism where physical energy calculation is concerned. Expending one molecule of ATP will let the same number of Na+ ions to move the same distance along a nerve dendrite, across humans. But this level is not really interesting when it comes to gaining or losing weight.

Some people burn more calories than others, in the default mode.
Just sitting in a chair, I warm the seat much more than some other members of my family.  That heat has to come from somewhere.
That's a different metabolism.
But, that's not something you can order and install.  It's not a pill.  Your doctor is right to focus on what you can control, and that's intake - along with your activity level; or outgo.  (But most people are unwilling to actually do the work to change their activity level to a higher one, which is why doctors don't even try anymore - patients just lie, and then doctors have to try to catch them at it, and nobody's got time for that).
What you eat may also impact the number of calories that stick.  Not everything you eat gets digested, some passes through.  And digestion itself burns calories.  Things that are harder to digest take more energy, and leave less surplus behind.
Easy things are... easier to digest and get all the calories from.
In addition, thinner people lose weight easier.  Not fair, right?  That's life.
It may have something to do with your microfauna, but that's not well studied.  And, we're not even sure if you can permanently change those populations.

http://www.mayoclinic.org/healthy-living/weight-loss/in-depth/metabolism/art-20046508

The warming of the seat is anecdotal speculation.

So you're arguing that heat happens magically, and doesn't require caloric input? Do tell us more, I can't wait to hear about it.

And why should thinner people loose weight easier?

If I had a handy cite, I'd give it to you.  Yeah, yeah, Abraham Lincoln said don't believe everything you read on the internutz

You say "Not well studied" - It is important to cite some material that is studied in your answer.

http://www.nytimes.com/2013/09/06/health/gut-bacteria-from-thin-humans-can-slim-mice-down.html?pagewanted=1&nl=todaysheadlines&emc=edit_th_20130906&_r=2&pagewanted=all&

And what are 'those populations'?

Populations of microfauna

It is more of a comment as it stands. Earn 9 more reputation and you can comment anywhere.

Thanks for the upvote, to help me comment - oh wait.

The warming of the seat is anecdotal speculation. And why should thinner people loose weight easier? You say "Not well studied" - It is important to cite some material that is studied in your answer. And what are 'those populations'? This answer may need some work. It is more of a comment as it stands. Earn 9 more reputation and you can comment anywhere.


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What's the difference between protein and DNA behaviour during agarose gel electrophoresis?
I'm planning a science project about gel electrophoresis, and I'd like to know if there are any measurable, quantifiable (for example, things I could represent in a graph or chart) differences between the behavior of protein and DNA during agarose gel electrophoresis.
Detailed inputs and useful links are greatly appreciated.

Proteins are usually not run on agarose gels since the pores of the gel are too big to have a good separation. A 1% agarose gel has pores of around 150nm, poly acrylamide (which is usually used) have 3-6nm depending on the degree of polymerisation and gel strength. You will only use agarose gels for really high molecular weight proteins otherwise you won't see much separation of the sample. DNA samples have such a high molecular weight and can thus be separated on agarose gels.

@Chris One of the requirements of the project is to run several simultaneous experiments while changing one variable only (in this case, it's the protein/DNA). I'm separating proteins in dyes, which would explain the use of agarose.

What do you mean by "separating proteins in dyes"? Another thing: While you can't separate Proteins nicely on agarose, you can use low percentage polyacrylamide gels to separate DNA.

@chris Excuse the typo. I meant that electrophoresis will be run on food coloring dyes... you know... which are made of proteins

which food coloring dyes will you be using? Most of them are based on small molecules, not proteins.

Thats in interesting question. I think so too, that these are mostly not proteins, since most proteins are not colored.

As already mentioned, you don't use agarose for proteins, they're pretty much exclusively run on polyacrylamide gels, typically as an SDS-PAGE. I've never seen anyone run an agarose gel of a protein.

@MadScientist I'm fairly new to this (I'm only a high school freshman) and so haven't done adequate background research on the subject. I was just asking this question to see if such a project fits the required criteria and thus actually conduct a research. I'll consider polyacrylamide, though it's way more expensive and harder to find (I doubt I'll have access to the school lab or that they even have it).

I'd recommend to simply focus it on DNA and ignore proteins. You should also find out what equipment is available, you need a gel electrophoresis chamber (and they are different for agarose and PAA), power supply, the gel material itself (+ APS and TEMED for PAA), buffer, loading dye, something to stain the DNA or protein, and in the case of DNA also a UV lamp.

There are two important properties that determine how a molecule will move during gel electrophoresis:

size and shape of the molecule
charge of the molecule

You're applying an electric field, and all molecules will move according to their charge. The gel itself hinders the movement of larger molecules. This means that small molecules will move further than large molecules.
Nucleic acids like RNA and DNA have a uniform negative charge from the phosphate backbone. This means that they will generally separate according to their size and shape (plasmids can be present in different forms like supercoiled, circular or linearized).
Proteins have different charges, some have a positive charge at the pH typically used for gel electrophoresis, some have a negative charge, and some have no charge at that pH. So if you would simply run proteins on a gel, some would move backwards, some forward and some not at all.
To make the proteins separate according to their size we use the detergent SDS to denature the proteins, and to give them a uniform charge (SDS is negatively charged). Proteins are also run on polyacrylamide gels and not agarose as the size of the pores in agarose is a bad fit for the typical sized of proteins.
While I've never seen anyone using agarose for proteins, it seems that it is possible and sometimes used for larger proteins. I found one paper describing a protocol, they used very high concentrations of agarose in the range of 4-5%. I suspect that they won't handle well, but you should try that out yourself. If the proteins you're examining are a bit larger, using agarose should be possible.

Just a small addition.. Agarose pore size is huge for most proteins. However, agarose gel is used for analyzing antibody-antigen interaction. The complexes that form are huge and can be separated by AGE. See rocket immuno-electrophoresis


text:
Stay young by reinserting own DNA from years ago?
As far as I know, the DNA sequence becomes shorter every time a cell divides.
A shorter sequence results in information loss and aging characteristics.

As a countermeasure, shouldn't one stay young and healthy at least longer, if the DNA in a cell is changed with a "better" DNA (from years ago... let's say your DNA was extracted with the age of 20 and you reinsert it every 10 years or so)?

If this is true, then (as for today's technology)
- is it already possible to perfectly reproduce the DNA? (I only found articles about XNA)
- is it possible to easily replace the DNA in all human cells? (I found articles about bacteria inserting pieces of DNA into human cells)

The shortened DNA sequences are repaired by the telomerase enzyme. So, there is no actual loss of information.

I think this idea is being implemented for stem-cell therapy but not to control ageing. So, stem cells such as HSCs can be cryo-stored and used for therapy later. Umbilical cord cells can also be employed. With iPSC technique it is possible to convert a cell to any cell type. It might be theoretically possible to replace every old cell but we haven't completely understood the importance of ageing. So there is a possibility that it can have disastrous consequences (not social implications but biological ones such as cancers etc)

Lots of questions here. I recommend taking college level courses in Biochemistry, Molecular Biology, and Medical Physiology, and Geriatrics.
There are other issues than just DNA. Systemic failure is system-wide, and probably most of the issues are still yet undiscovered. Good news I guess if you want to be a researcher in this exciting field! As for DNA-ends, read up on Telomerase. As for DNA copying learn about PCR and sequencing methods. Generally speaking, reverse transcription can be dangerous. Please see many of diseases we are having a hard-time solving, which often use these pathways. Seriously avoid that one. Not everything in DNA is used by the organism at any given time, and some information is elsewhere. Moreover, what if we use DNA as DATA storage besides blueprint information? Hint: while the jury may be still out on Neurons, environmental factors may be passed as epigenetic traits by not just primary shape such as DNA methylation but by obstructing access via conformation and histone wrapping. Not even mentioning mitochondrial dna or prenatal development factors.
Instead: A good diet and exercise.

well, as I already am an engineer, taking college courses and focusing on that subject may be a little late. Because of a friend, I came across this strange idea, but it seems not to work. Thank you a lot for your explanation.

As far as I know, the DNA sequence becomes shorter every time a cell
  divides. A shorter sequence results in information loss and aging
  characteristics.

Neither telomeres nor aging are nearly that simple.

is it already possible to perfectly reproduce the DNA?

No.  Any method that would be used to replicate DNA requires using enzymes, and they always have a non zero failure rate.  You could use whole genome amplification to make a pile of DNA that was on average the right sequence, but each individual chromosome would have errors.  And forget copying over epigenetic modifications.
There are ways to get cells to incorporate new DNA, but every cell in an organ of a living organism?  And a whole mammalian genome's worth?  And to magically tell the cell that the new genome should replace the old one?
None of that is feasible.

(I found articles about bacteria inserting pieces of DNA into human
  cells)

Okay, let's get some scale here.  Most bacteria have a genome of 5-10 million bases.  Humans have a genome of 3 billion bases.  Even if a bacteria can transduce a small plasmid into a human cell, that doesn't scale up to bacteria replacing the whole genome of every cell in an organ.
And because there's always a relevant xkcd comic
http://xkcd.com/793/


text:
Is the net gain of ATP during glycolysis 2 or 8?
As I understand, 2 ATP are consumed during steps 1 and 3 (glucose -> glucose-6-phosphate and fructose-6-phosphate -> fructose-1,6-bisphosphate) and then 4 ATP are produced during steps 6 and 9 (1,3-BPGA -> 3PGA and PEP -> pyruvate)
So that's 4 ATP produced - 2 ATP used = 2 ATP gained.
However, 2 NADH are produced during step 5 (3GPA -> 1,3 BPGA), and as we know 1 NADH gives 3 ATP so these 2 NADH should yield 6 ATP.
So, if we consider the ATP produced from the NADH, the net gain is 8 ATP. Is this correct?

Possible duplicate of "Glycolysis - ATP production"? Try searching the questions tagged with cellular-respiration. I'm sure David has already written an answer elsewhere (citing Berg) that addresses this question.

Have you searched existing questions here?

@acvill i'm sorry but i dont think that answers my question.

@BryanKrause yeah i did, couldn't find any answers.

@Aditya That seems extraordinarily unlikely to me. Maybe you can link to them and explain why the questions/answers you found don't answer your question ?

@bryankrause after skimming through all the 153 questions tagged with cellular-respiration, i've found 3 q&a that are kinda related to my question this does not talk about the NADH, this does not talk about the NADH in glycolysis specifically

and this does not talk about whether the NADH should be considered during calculating the net produced during glycolysis alone

@Aditya That third link seems to cover it pretty well. How do we measure "should" in science? All that's important is to understand what happens. You can make your own "should" arguments however you'd like, as can anyone else - "should" is an opinion.

@bryankrause don't think my biology teacher likes my opinion of taking the NADH into consideration, just wanted to ask the forum on what would actually be the most "correct" opinion.

Are those reducing equivalents always converted into ATP?
When they are, is that done as part of the glycolysis pathway?

Presumably you have a text book. It most likely will have a section on glycolysis in anaerobic organisms, for example in yeast fermentation. This will include consideration of how the NAD+ needed for glycolysis is regenerated in these anaerobic conditions. There is a SE question related to this topic and my own answer. This provides an objective answer to your question of "should".

@david Just saw your answer, it was helpful. I spoke with my bio teacher again, she agreed that 8 could also be the answer along with 2. Thanks for all the help, appreciate it.

No! 8 can NOT be the answer, whether or not you have beaten down your teacher into submission. Glycolysis is a process that produces pyruvate, 2ATP and 2 NADH from glucose. It ends there. The metabolism of the pyruvate and NADH are separate processes, differing between organisms and between tissues in multicellular organisms.  Even in air-breathing organisms such as ourselves, one can demonstrate this by asking whether erythrocytes perform glycolysis, and then whether they can or do obtain ATP from the NADH. The answer is yes they do perform glyolysis, and no and no for ATP from NADH. Why?

@david thats because mature erythrocytes don't have mitochondria? so as i understand now, the ATP produced from NADH happens in a separate process independent of glycolysis (the ETS), so shouldn't be accounted for?

Indeed it does. Your course will, I imagine, deal with the Krebs tricarboxylic acid cycle and the process of oxidative phosphorylation that converts ADP to ATP. If it is a school rather than a university course it may not go into sufficient chemical detail to fully explain the process. But it would be worth waiting until you have finished covering the topic and then raise any questions you have.

And one last thing (perhaps I really should write an answer). Even changing your question to "What is that potential maximum net yield of ATP from the phosphorylation of ATP and the NADH produced in glycolysis, assuming the latter is oxidized in the mitochondria", the answer 8 is incorrect on two counts related to your statement "1 NADH gives 3 ATP". The minor quibble is that for most NADH generated in the mitochondrion it is now thought 2.5 ATP are generated. The major quibble is that cytoplasmic NADH enters the mitochondrion as FADH2 with an nominal yield of 2 ATP, now regarded as 1.5 ATP.

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


text:
Where is coagulation factor v produced?
My textbook (Physiology 9th edition, People's Medical Publishing House, Beijing) tells me that coagulation factor V is produced in endothelial cells and platelets, which is different from some other books (saying in liver). So where exactly is it produced? Or is it just not quite clear?

Why the downvote? Surely a very good question?

Not the downvoter, but I somewhat suspect the reason is that the question fails to demonstrate the basic biological knowledge to know that the liver is made of cells, including endothelial cells.

Factor V is indeed mainly produced in liver (Wikipedia), which releases it into blood plasma.
But platelets are also an important source of factor V and "may account for "~25% of the circulating factor V" (ref 1)
Platelet factor V is synthesized in megakaryocytes (ref 1), which of course are the bone marrow cells responsible for the production of platelets.
The following reference gives a much more detailed explanation of factor V
Reference (available as free pdf)
Factor V Is Complexed with Multimerin in Resting Platelet Lysates and Colocalizes
with Multimerin in Platelet α-Granules *

Catherine P.M. Hayward
Emilia Furmaniak-Kazmierczak
Anne-Marie Cieutat
Michael E. Nesheim
John G. Kelton **
Graham Côté

Journal of Biological Chemistry (1995) Vol 270, pp19217-19224

The coagulation factor 5 is primarly produced in the liver, meaning that the liver isn't the only place where this factor can be produced (F5 can possibly be produced by megakaryocytes too). After it is manufactured it circulates in an inactive form and is then converted into the active form with the help of thrombin and is able to attach to platelets. However, as far as I know, factor v is not produced in endothelial cells, there are a few factors that are, like Von Willebrand factor (VWF), factor VIII, thrombomodulin, endothelin etc., but F5 is  not one of them.


text:
What is the deepest living underground organism?
A quick search reveals Halicephalobus mephisto which was

detected in ore recovered from deep rock fracture water in several gold mines in South Africa [...] 3.6 km (2.2 mi) under the surface of the Earth.

Have any deeper living organisms ever been found?

I suspect the answer to this question is the same as to the answer as to how deep underground we've ever actually looked for living organisms.

Halicephalobus mephisto, the "devil worm" (actually a nematode) was, as of 2017, the deepest discovered species -- found living at 3.6 km below the surface! However, this species ties another deep species: Plectus aquatilis found a number of years before (~2011 I think; don't quote me). I know of no recent updates regarding multicellular organisms. Looks like acvill's answer covers fairly recent (2021) "deepest" cellular evidence

Have any deeper living organisms ever been found?

In 2021, researchers recovered microbial cells and DNA from rocks retrieved from a depth of 4,850 m below the surface.1 The New Scientist covered this finding in an article titled "Deepest land microbes ever found".

Dong and Huang say that, to the best of their knowledge, these are the deepest known microbes ever found on land. Demonstrating that the cells are living will be a challenge as microbes that live deep below the surface often operate on such a slow timescale that they show few typical signs of life such as movement or reproduction.
But there are reasons to suspect the microbes may be alive. Most importantly, they are intact rather than just cell fragments, which might hint they are carrying out basic cellular repair.

Dai X, Wang Y, Luo L, Pfiffner SM, Li G, Dong Z, Xu Z, Dong H, Huang L. Detection of the deep biosphere in metamorphic rocks from the Chinese continental scientific drilling. Geobiology. 2021 May;19(3):278-291.


text:
What nutrients are necessary for Bacillus subtilis germination?
What are the necessary conditions to germinate Bacillus subtilis spores? Under laboratory conditions, spores of B. subtilis are often heat-activated for 30 min at 70°C to increase their germination responses to nutrients. Most papers use either L-valine or L-alanine amino acids to germinate.
However, I would like to know if those are necessary nutrients for germination.
Are there other nutrients that can germinate B. subtilis?

Your own efforts to answer this question? Again.

To get you started in answering your question, here's a good paper: Analysis of the germination of spores of Bacillus subtilis with temperature sensitive spo mutations in the spoVA operon. I would recommend reading section 3.3 - Germination of spoVA mutant spores.


text:
The numbers of chromosomes during Meiosis
There is something about the numbers of chromosomes that doesn't make sense to me:
Let's take this illustration:

So a gamete has 23 chromosomes, which are haploid (have only one chromatid), is that correct?
Before meiosis it replicates, so now we have 23*2, i.e 2n as in the first left picture where it is written "Parent cell (2n)". Then I don't understand how is it formed in a tetrad. Where do the additional two come from. Also in the start we have 2n (after replication) and in the end after two divisions we have n for each gamete  of the total 4, so its total of 4n, what do I miss ?
Otherwise the first left picture is before the replication of the chromosomes, but then why are there 2n in a gamete cell, isn't it just 1n as in the end of the process ? Isn't the parent cell also a haploid with just 1n chromosomes with just one chromatid (because if it is before replication, it looks like a diploid cell).

see also: https://biology.stackexchange.com/questions/55832/what-is-the-purpose-of-two-cell-divisions-in-meiosis

I would recommend looking more closely at the image. I would suggest that it is in fact 1n. Those are two different chromosomes, not copies of the same chromosome, in the gametes.

Why do you think the parent cell is haploid?

@BryanKrause, that how it happens in humans, isn't it ? Meiosis is a cell division process, which happens from one cell to four or am I wrong ? I should be haploid isn't it ? Sex cells are haploids (gametes) in humans by definition.

@Ilya.K. Which cells in your diagram are gametes, and where do those gametes come from?

@BryanKrause, well it isn't said in the diagram itself, but meiosis is relevant only in gametes. Could it be that the parent cell isn't a gamete and the daughter cells are ?
The daughter cells are gametes for sure, the parent cell logically assuming must be too.

Getting closer :) Where do gametes come from, and what is the purpose of meiosis?

@BryanKrause that's probably the part where my knowledge is a little bit unclear. Where do they come from : I'm not sure, like they it's a differentiation thing, each cell in the body has the whole genome set (but it differentiate by the set of actual proteins generated by the appropriate rna instructions) , which means I think that each cell in the body from one hand has the whole 23 chromosomes, but in gametes as much as I understand the chromosomes are complected each from only one chromatid, and no two, because they are haploid cells and not diploid. I've probably mistake anywhere here.

@BryanKrause, the purpose is cell replication, like part of the life cycle of the cells.

@BryanKrause, are you trying to tell me that to create gametes, we need the diploid cell, which the parent cell is ? I think our lecturer didn't told us that part. Like who is the parent cell ? Cuz in the second image I've just posted, it is obviously said that from one pair of chromosomes (a pair means it is diploid and has one chromatid from male and one from female) in the parent cell we get 4 haploid gamete cells.
It's only makes sense if the parent cell is diploid. But who is it if not a gamete (and it can't be gamete) ? Like it can't be skin cell or some other tissue cell, can it ?

Yeah, I think you've just about got it. After fertilization, a typical human cell has 46 chromosomes, 2 copies of 23 chromosomes, with caveat that one of the pairs is the sex chromosomes which can be XX or XY. We call that a diploid, 2n cell, and there are 2 copies of each because one copy came from an egg gamete and the other copy came from a sperm gamete. Those 2n cells divide and divide to make all the cells of the body via mitosis. To make gametes, though, you need to make 1n cells; meiosis is how that happens.

The cells that give rise to gametes through meiosis are called germ cells; that's pretty much their job, simplifying things a bit. As far as "Like it can't be skin cell or some other tissue cell, can it ?" - as the wikipedia article describes, it depends - for animals, you're right, they're particular cells. For plants, they come from otherwise ordinary cells, a bit like making gametes from skin cells, yes, just in the right place at the right time.

@BryanKrause, thanks, that's a good point been clarified.


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Why are prokaryotic promoter sequences written 5' to 3', when transcription proceeds from 3' to 5'?
It seems that the promoter regions are written from the 5' to 3' direction. My lecture notes, for example, give the -35 and -10 promoter regions sequences like so:

Wikipedia seems to agree, on their article about promoters.
However, RNA polymerase transcribes in the 3' to 5', as in  it reads the template strand in the 3' to 5' direction. In that case, why aren't the promoter regions written also in the 3' to 5' direction?
Meaning, instead of the -10 sequence being 5'-TATAAT-3', why is it not 3'-ATATTA-5', in agreement with the direction of transcription?
My intuitive guess is that the $\sigma$ factor recognises the promoter region in a 5' to 3' directionality. But I cannot find any information to back up this guess. Additionally, if this is true, how could it have been determined (experimentally)? Furthermore, whatever the answer is, does it also apply to transcription in eukaryotes?

Possible duplicate of What direction is a sequence in databases written?

Come on. You can't have people driving on the left in one town, and driving on the right in the next. It's bad enough when us Brits go on the Continent. There's no mystery, we just read all gene features on the same strand.

@David Fair enough, I'll take it as a consequence of convention. Thanks!

DNA sequence by convention is written starting at the 5' position so the directionality is assumed without explicitly writing the 5' and 3'. As for why its not the template strand sequence. I would say that's also a convention for simplicity because you only need to write one sequence if you want to discuss genes and regulatory elements.


text:
What does it mean for the signals for transcription and translation to be "conserved"?
I was reading this article: "Overview of vector design for mammalian gene expression."  for an explanation of why mammalian cell lines are used for expressing cloned genes, and one of the reasons given is that "DNA cloned from higher eukaryotic cells is readily expressed since the signals for transcription, mRNA processing, and translation are conserved in higher eukaryotic systems." What does it mean for the signals to be "conserved," and why does this make mammalian cells a better host than other types of cells?
Follow-up question, in case the answer to that question doesn't make it clear: the article also says the machinery for protein folding and assembly are "conserved" - what does that mean (if not the same thing as in the first question) - and again, why does this make mammalian cells a superior choice of host for expressing cloned genes?

It means the signalling pathways or the mechanisms used for a particular process is the same across a number of species. The reason an eukaryotic cell was used for the expression of a gene is that the particular gene in question required a certain machinery and processes which are found in eukaryotes so for example expressing that gene in an E. coli might not have been suitable/worked. In research its always the best idea to express a gene from the species it came from to ensure its expression.

I concur with @Bez but wish to elaborate on the meaning of 'conserved'. It is generally used in the context of evolution. A conserved characteristic or gene or protein means that it has 'survived' a long time without being altered. As @Bez mentions, certain parts of the protein machinery in eukaryotes is very different from prokaryotes, the latter being considered to have arisen much earlier in evolution. For example, some post-transcriptional processes (e.g. splicing and many more differences) only occur in eukaryotes. But there are many similarities as well, such as the basic use of mRNA etc (see book section). The latter are examples of conserved mechanisms.  In the context of your question, it means that when you take eukaryotic DNA to express eukaryotic proteins it doesn't really matter which cell or host organism you take as it will be transcribed and folded correctly. For example, yeast is often used to express DNA from higher organisms as its protein synthesis is much the same across various eukaryotic species. However, expressing eukaryotic DNA in prokaryotes likely ends up in misfolded proteins without proper post-transcriptional modification and should be avoided.
As to your follow-up question: Folding of proteins happens in the endoplasmatic reticulum (ER) in eukaryotes (wiki), a cell organelle absent in prokaryotes as they lack a nucleus and associated organelles. Again, expression of eukaryotic genes in a prokaryotic expression system will end up in mis-folded proteins.
To get back to your overall question - the 'signals': DNA transcription, splicing, protein synthesis, post translational modification and folding are all regulated by signals, such as specific DNA codons to start and stop transcription, RNA codes for splicing and start translation and protein tags that are placed on specific amino acid combinations. These signals are well conserved across eukaryotic species.

I only made an edit to the post - nothing more.

auch - it's Bez thanks @Chris. Must be your name ;)

I think you agree that it's a special name :-)


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What makes heavy metals toxic?
I'm not sure all heavy metals are toxic, but most are.
Some may be present as insoluble compounds, or otherwhise hard to get into an organism, but that's a side aspect.
For example, I would count copper as toxic, even if some salts are triggering to vomit just too quickly to swallow poisonous doses.
So, in this sense, are they all toxic?
Is the toxicity based on the same mechanism?

http://en.wikipedia.org/wiki/Metal_toxicity

Heavy metal toxicity is actually due to the inhibition of the body's natural enzymes as well as the denaturing of proteins that it causes.
Here, Tchounwou et. al go into detail about the mechanics of different heavy metals and how they interact with the human body specifically. It even suggests ways that the heavy metals could be introduced.
A short summary on the damage caused by what was studied:

Arsenic inhibits DNA repair.
Cadmium toxicity isn't well known, but they think it causes single
strand DNA damage.
Chromium causes chromosomal abnormalities thought to be caused by
oxidative damage.
Lead prevents the body from interacting with Calcium which is a key
element in many biological processes. It also competes with other
metals for the active sites in different enzymes.
Mercury depletes the body's antioxidants.

So to answer your question, no, the heavy metals are not all working on the same mechanism. It all depends on what dose, how it was introduced, and the particular metal. Also, anything can be toxic in the right amount (people have died from water toxicity in drinking contests).

Water is not toxic. Excess water causes hypervolemia.

Fatal water intoxication is what I learned it was called in school.

Yeah.. Actually it is not an intoxication by water, you see. Excess water just dilutes up the electrolytes. Water is not inherently toxic.

Huh, wow I didn't know that, thanks @WYSIWYG I never actually looked into the mechanics of it.


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Chest muscle and female breast size
Do female chest size have anything to do with muscle?
I know many female athlete and their average breast size is much bigger than normal female that does not tend to play sports. Do this have any relation to chest muscle?? If so can you explain how it does.
Thanks in advance

The female breast is composed primarily of fat and connective tissue plus lobules and ducts for milk production and delivery.  The pectoralis muscles form a thin layer beneath the breast, as seen in the figure in the link. An athletic female can enlarge the size of the pectoralis muscle and the laterals muscles, just as male athletes can enlarge their "pecs" and "lats".
Exercise burns fat so athletic women often experience reduction in breast size. Of course, other factors such as diet and genetics also influence the effects of exercise on fat burning.
So, athletic females with enlarged lateralis muscles and pectoralis muscles may have a larger overall bust size but the cup size of their breasts might actually be reduced.


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Functioning of BCG vaccine
I  read (from Nature Volume507, S4–S7 (06 March 2014) :

For reasons that are poorly understood, BCG protects only infants; it
  is ineffective in older children and adults. Its efficacy also depends
  on latitude. BCG works better, and protects people at later ages,
  farther from the equator. Both effects may result from interfering
  exposure to noninfectious mycobacteria that are closely related to
  both BCG and TB. These bacteria are more abundant closer to the
  equator, and while infants are unlikely to have encountered them,
  children and adults have more exposure over time.

I am unable to understand the relation between exposure to noninfectious mycobacteria and lessening of efficacy of BCG vacccine. What exactly is the "interference" caused by the noninfectious mycobacteria ?

The exposure to environentally occurring Mycobacteria causes a immune response to these (mostly unspecific, since no real infections occur). It seems that immunizations with BCG in these individuals is causing either no, or only a very attenuated immune response
This is shown in this ("BCG-induced increase in interferon-gamma response to mycobacterial antigens and efficacy of BCG vaccination in Malawi and the UK: two randomised controlled studies.") in which individuals with a high environmental exposure to mycobycteria showed only a very small response to this vaccination. If this natural level of immunity is enough to produce immunity to tuberculosis is unknown (and can not be tested for obvious reasons).
Another possibility is that the natural occurring immunity blocks the vaccine strains so they get eliminated before they induce an immune response. See here.
This is called the masking theory,if you want to read further, have a look at this three reviews, they give a good overview over the field:

TB vaccines: progress and problems.
A novel TB vaccine; towards a strategy based on our understanding of
BCG failure.
The success and failure of BCG - implications for a novel
tuberculosis vaccine.


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What's the difference between veterinary and human snake antivenom?
Recently, out of curiosity, I looked online if snake antivenom for humans were actually sold for individuals. I found out they aren't. Not only that, but bills can get really high on countries that don't provide them in public healthcare (i.e.: USA), as in 4 digit numbers. Makes one disappointed to realize the price of production of human-use antivenom is actually really small in comparison to what they are charged for[1]:

On the other side, veterinary antivenom is sold for treating animals attacked by some venomous snake. The brand I found for sale[2] is a polyvalent antivenom: A solution of specific equine immunoglobulins, purified by enzymatic digestion and lyophilizated (freeze-dried), obtained from hyperimmunized Equidae with Crotalus ("Cascavel" aka Rattlesnake), Bothrops ("Jararaca") and Lachesis ("Surucucu" aka Bushmasters) snake venom. I included the common-names in Portuguese since these are the 3 common vipers found in Brazil, where this particular antivenom is sold. Coral snakes (Elapidae) are also found here, but I didn't find any veterinary antivenom for those (and this one I found isn't recommended for bites from them).

Some veterinary-use antivenom shows more side-effects on animals than others, specially unpurified Equine Plasma antivenom, which can cause allergic skin reactions near the application site and peripheral lymphadenopathy 48h after application[3]. The same source comments on other types of veterinary antivenom, but I'm not sure which the one I found classify on (if any, because of the targeting snakes being slightly different). The description of F(ab’)2 antivenom resembles the one provided by the brand I found: Both are purified, enzymatically cleaved/digested, lyophilized and obtained from horses.
Technically, what is the difference between the antivenom for human usage and veterinary antivenom? In an hypothetical situation that one gets bitten far from medical help, how big would be the risk of applying a veterinary antivenom? Obviously injecting drugs that are not FDA approved is not recommended, and considering the number of snake-bite related deaths is relatively low in some continents[4] it would be unwise to even give people the idea of using unapproved drugs to treat bites. I was just wondering if, after assessing a situation and realizing medical help won't come (or come in time), having one of those in hand could save a person's life after a viper bite.

UPDATES:
There's a scientific article published in the British Journal of Clinical Pharmacology, entitled "Adverse reactions to snake antivenom, and their prevention and treatment"[5], that brings light to the adverse reactions to snake antivenom. Severe systemic anaphylaxis rates can be as high as 40%, specially in places where the antivenom manufacture quality is dubious. Antihistamines and hydrocortisone didn't prove effective in controlling the antivenom acute reactions, and only adrenaline seemed like a decent prophylatic treatment to anaphylaxis. The management of antivenom acute reactions is as big of an issue as the treatment of the envenoming itself. And I'm still talking about antivenom approved for human-usage.
Speculation: Polyvalent antivenom could be more problematic than specific antivenom, because more unnecessary foreign proteins must be injected to treat the same amount of venom. Not only that, but probably the companies that manufacture veterinary antivenom are not as worried about their quality (and purification process) as ones that are more tightly regulated to produce human antivenom. For that reason, acute anaphylaxis would be more likely while using those.
Whether the risk of anaphylatic reaction is compensated by the risk of untreated envenoming is still not clear (one might say it's a question that won't have a definitive answer, or even opinion-based). I'll keep adding any new information that brings more light to the issue, but answers from people more knowledgeable in the area are very welcome!
References:
[1]: https://www.washingtonpost.com/news/wonk/wp/2015/09/09/the-crazy-reason-it-costs-14000-to-treat-a-snakebite-with-14-medicine/?noredirect=on&utm_term=.b4855c4e100c
[2]: https://www.dechra.com.br/produto-detalhe/102/master-soro-plus
[3]: https://vetgirlontherun.com/veterinary-continuing-education-update-antivenom-treatments-animals-raegan-wells-vetgirl-blog/
[4]: https://animals.mom.me/snake-bite-death-statistics-worldwide-2431.html
[5]: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4767202/pdf/BCP-81-446.pdf

You inject a horse with the venom and in return you get in its blood anti-venom antibodies. Those antibodies will be poorly tolerated in humans and shall produce an allergic reaction, even more if the individual already received horse antibodies in the past (that's how anti-(goat-IgG) antibodies are made). They will be also less efficient due to differences in the constant region of the horse antibodies, not binding well to the human Fc receptor.
One solution is to cleave the horse IgG with pepsin or papain protease to separate the F(ab’)2 or Fab fragments. But still it won't bind to Fc receptors and the renal clearance will be also faster. The good point is that such antivenom can be administered more safely to any species.
For human use the best solution is to use sequencing, plasmids, in-vitro culture, to make recombinant antibodies merging the human constant region with the variable region of horse anti-venom IgG but that's a more expensive biotechnology. And the obtained recombinant IgG will pose the same allergy problem as the whole horse IgG in other species.
It is shamely common for drugs that the manufacturers don't give enough information to tell what is what. It may very well happen that the FDA approved expensive vials are old whole IgG and that a much cheaper internet veterinary antivenom is using the recent technologies.
https://vetgirlontherun.com/veterinary-continuing-education-update-antivenom-treatments-animals-raegan-wells-vetgirl-blog/
https://www.mdpi.com/2072-6651/14/9/606/pdf


text:
Make plant experience 2 growing seasons per year by moving it across equator semiyearly
If I take a typical plant (such as e.g. a rosemary plant or an avocado sapling) across the equator from Florida to Brazil and back every year, so that the plant experiences Spring in both places, will the plant experience two growing seasons? Or is there some genetic wiring in the plant to prevent this?

Oh, can you elaborate on that? I don't live in Florida, so the question is theoretical in that regard--but the question is a practical one.

@benn I'm not sure what you mean. Are you suggesting the question would be more practical if I put in the actual state I lived in? That seems unrelated to what I'm interested in.

Thank you for the pointers @benn. The question I've asked is the one I'd like to have answered though

Hi @benn, just to repeat, this is not a theoretical question. This is a practical question that I'm concerned with. I've replaced the state that I'm in just to stay as anonymous as possible on the internet.

@dandavis Thank you for the message! I was not aware of legality issues surrounding this.

@dandavis: Plants take cues from the environment, so they might need a certain amount of cold, or other cues, before breaking dormancy.  This is something that you might expect to evolve in order to avoid the effects of an early cold snap in the fall.  In fact, many plants do require a certain number of "chill hours".  See e.g. https://ucanr.edu/blogs/blogcore/postdetail.cfm?postnum=16468

I think you'll find there's no "typical" plant.

@Armand interesting, could you elaborate?


text:
Does refrigerating (but not freezing) bread inhibit mycelium growth?
During COVID, supermarkets struggled to keep things in stock. Bread seemed to be hard to come by for a time. As a result, when I came across the brand I liked, I grabbed a couple extra loaves. I didn't want the extra to go bad, so at first I froze it, but that was harsh on the bread. However, it turned out that simply refrigerating it was amazing! It seems to last indefinitely, although it eventually hardens if left for too long (around a month?). I thought I had found a cool trick, as it takes us a while to go through a loaf of bread.
The other day I watched a YouTube video about mold growth and food safety. From 3:06 to 4:13 in the video, he explains that before bread has visible spores, there are already mycelia in the bread. In other words the bread is already moldy before mold is visible.
I began to wonder: is refrigeration actually preventing mycelium growth, or is it only preventing spores? I noticed a commenter on the video raise the same question.
In case it's relevant: Two meat thermometers sitting on the shelf where I keep my bread read 40 degrees F, as does an IR thermometer pointed at the bread bag. According to a quick Google search, that seems to be an acceptable refrigerator temperature.

Welcome calcmari. This is not simply a Q&A site, here we are expected to show the results of our own investigations into a subject here, you can [edit] to tell us what your searches found and where the sticking points are. You should also take our [tour] and refer to the [help] for guidance as to the ways of any site you post on, see our section on how to ask. There are some things you should investigate: (Cont...)

(Cont) Common bread-mould growth temperatures? What bread? What does the ingredient list say about: ascorbic acid, sulphur dioxide, sulphites, calcium/sodium propionate, ginger, garlic, clove, cinnamon? Does your jurisdiction even require these things to be disclosed on the label?  Or is is fresh from the baker's oven without preservatives? Then you can [edit] your question to include your research in attempting to answer the question and where you got stuck.


text:
Xylem vessels, lignin, wood

I learnt that lignin impregnates xylem cells, causing the cytoplasm to die due to the inability of water and nutrients to pass freely, hence creating hollow tubes adapted to transport materials. This means that in order for the cytoplasm to die and the tubes to be hollow, lignin needs always be present.. However lignin is not present in all xylem vessels... Lignin is the woody tissue that only forms the trunk of a tree. So how do these cells hollow out in other parts of the plant/tree to create empty transport vessels..??

Welcome to SE.Biology!  For details on how to use this site, please check out the tour: biology.stackexchange.com/tour and then the help pages on how to ask questions on this site: biology.stackexchange.com/help/how-to-ask. Thanks!

In particular, you have correctly deduced that what you were taught can't be completely correct.  The next step is to do some research!  A quick search for "protoxylem vessel formation plants" turned up this review: https://nph.onlinelibrary.wiley.com/doi/full/10.1111/nph.13383

I did my research... of course I dont like to wait for answers on forums.. but I didnt find what answers my question. And the info I quoted is not wrong since it is from a Cambridge University book. And why do people have these forums if members constantly assume people love asking them questions instead of "doing some reaearch"?! I obviously didnt find an answer and wanted to ask a person my question. So in case you dont like the question, dont answer it, but kindly do not patronisingly guide people to research. And if u didnt read the question, my ans is still not in the source u suggested!

Your question is much better now!  I'm sorry you felt patronized by my comments, but if you stick around (please do) you will see that many questions are posted by people who clearly haven't made even a minimal attempt at working out an answer.  Since there was no indication in your original post that you had tried to do any research I assumed that was likely to be true in your case as well.  I guess that whoever voted your question down felt the same way ...

Based on the passage you highlighted I think you are misinterpreting what is written — it does not say lignification is necessary only that it is sufficient.  I had another look at the article I suggested and from the summary "We also summarize the processes which have been shown to be instrumental during xylem maturation. This includes mechanisms of cell wall formation and cell death which collectively complete xylem cell fate." — I don't have time right now to read through the whole article, but that sounds directly relevant to your question to me ...

Just as u feel people dont do their research, the opp is true for questioners cux people constantly, instead of answering a Q, tell them to use the internet.. I or anyone might have 100's of questions while we study, we dont have the need or time to post all 100 here... but upon being unable to find a clear ans, just as we might ask a teacher/friend, we pose qs to the virtual community. So i think its only fair to give the benefit of the doubt and answer qs which is what the Q&A forum was meant for. In case one is against the institution of asking a q, lets not have these forums, is my point.

Yes but how does that death take place??? If not by lignin how does a cell lose its cytoplasm is what I dont know. PS The problem i highlighted above is what I encountered mainly on stack exchange. Nobody "assumes" things or tells u not to ask on other QnA forums like Yahoo Answers. Cux that beats the point of having a forum. Anybody, whether they have researched or not, can ask a question without community members downvoting qs they dont "approve" of for a reason like this.Thats how forums become databases for info. YA search results are mostly top of the list in frequency n content quality.

Thanks for the article.. I dont understand it clearly enough but thanks..

Please do not post text as graphics. It doesn’t index and discriminates against people with sight defects.


text:
How does bacteriorhodopsin differ from the rhodopsin present in mammalian eyes?
In my high school textbook, it is written that they are similar. So, I was just curious to know about this.
Thank you.

Welcome to Biology.SE! We recommend all posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to be a simple Q&A site, but rather a site that promotes self-learning with some expert help along the way. Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thank you for being a part of this SE!

Although they are similar in both bacteriorhodopsins  and rhodopsins being retinal-binding proteins, the similarity in their amino acid sequence is very limited.
The key difference between them is that rhodopsin is a G-protein-coupled receptor, and this is not the case with bacteriorhodopsin. A quick Google search on Bacteriorhodopsin vs Rhodopsin will send you to a Wikipedia article that says:

Bacteriorhodopsin belongs to the microbial rhodopsins. They have similarities to vertebrate rhodopsins, the pigments that sense light in the retina. Rhodopsins also contain retinal; however, the functions of rhodopsin and bacteriorhodopsin are different, and there is limited similarity in their amino acid sequences. Both rhodopsin and bacteriorhodopsin belong to the 7TM receptor family of proteins, but rhodopsin is a G protein-coupled receptor and bacteriorhodopsin is not.

A very good paper if you would like to know more about the two is by H. Gobind Khorana on the Two light-transducing membrane proteins.


text:
How does a sperm cell die?
What causes an animal sperm cell to die? Does it die somehow from being outside its original environment?
I've studied the Wikipedia page
 on sperm and I see a lot of information on what makes up a sperm cell, but can't quite figure out its lifecycle and exactly how it dies.

Seppuku; for the vast majority of cells that don't make it to the egg, upon realizing it has failed at its one and only task in life, the sperm cell takes its own life and dies in shame.

So most cells require growth factors and survival factors to stay alive in an organism. Cells which stop receiving survival factors, such as sperm, undergo a process of programmed cell death (PCD) called apoptosis. Some cells will also undergo necrosis, or autophagy, among other types of PCD. Lachaud et al. performed a study in 2004 on the contribution of apoptosis and necrosis in ejaculated sperm. They make note in the intro that from other literature that we see some hallmarks of apoptosis like externalized phosphatidylserine, fragmented DNA, etc. despite inactivated nuclei and a small cytoplasm. Their data notes that ejaculate sperm cell death mainly occurs from necrosis, however, because sperm themselves lack the ability to initiate apoptosis. However, in the testes, there's data to note that apoptosis plays a role, and the presence of apoptotic spermatozoa in the ejactulate may be result of the inititation of apoptosis by factors which still inside the body. Apoptosis of spermatozoa in the testes is currently under investigation in male infertility, and damage in cryopreservation.
Just to give you an idea of the difference, necrosis is a much messier outcome derived from physical factors, or those factors external to the cell. Apoptosis is organized, controlled, and modulated by cellular signals.


text:
Are eukaroytic promoters located in the 5' UTR region?
I was wondering if promoter sequences are located on 5'UTR region in eukaryotic organisms?

as i understand, UTR is part of mRNA (UnTranslated Region), whereas promoters are part of DNA, sequences where DNA-dependent RNA polymerase binds. So by definition, promoters can't be in UTR. More than that, since RNA Pol binds to promoter, only part of promoter sequence can be transcribed if any at all

Most promoter elements are not a part of the mRNA sequence. They are upstream (towards 5') of the transcription start site. However, a certain class of promoters called downstream promoter elements (DPE) can overlap with the geneic region. These elements have been reported to lie at 29-33bp upstream of the transcription start site and widely employed, in Drosophila [1]. Mapping of DPEs has been done for mouse human genes as well [2]. However, a detailed analysis supported by good sequencing data is yet to be done.
So, though DPEs are present in the transcript, I am not sure if they are retained in the exon. This can be confirmed by mapping the splice sites but this analysis is not presented in these papers.
You can see from the below figure [3] that most first exons in humans are big enough to harbour the DPE.

I do not think promoter sequences are on 5'UTR region. 5' end of 5'UTR is the transcriptional start site and the general transcription factor binds to immediately upstream of the 5' end on the genome (about 30 to 40bp upstream).
https://en.wikipedia.org/wiki/Promoter_(genetics)


text:
How is circadian rhythm of gastric acid secretion regulated?
Gastric acid secretion shows a circadian rhythm where acid production in the morning is minimal and it reaches a maximum towards the evening.
How is this process regulated?

I'd suggest reading wiki first.
Autonomic nervous system, the one that regulates breathing rate, heart rate and other physiological processes as a function of circadian time, regulates secretion of gastric acid. Vagus nerve, part of parasympathetic nervous system (the one responsible for "rest and digest" part of behavior, opposite to sympathetic "fight or flight") stimulates secretion of gastric acid and regulated through circadian mechanism.
See also here, Circadian variation in gastric vagal afferent mechanosensitivity:

Thus, gastric vagal mechanoreceptors display circadian rhythm, which may act to control food intake differentially at different times of the day.

This is another interesting review: Gut clock: implication of circadian rhythms in the gastrointestinal tract. It states that GI tract has its segments set their own circadian clocks, different for various segments. But all of them are operating and adjusted by main clock, regulated by, as I know, melatonin and orexin hormones.
Surprisingly, not much seems to be known about this connection. Pineal gland seems to be very important in this process, because it produces melatonin.

Thank you, I especially found the last reference interesting!