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What insect is this with furry wings?
Found this on the wall of my house in Kuching, Sarawak, MALAYSIA It is a tiny black triangular shaped insect.

Possible duplicate of What's the name of this bug from Toronto, Canada?

Very nice macro. I really like the looks of these things and hate to kill them. :-( I keep my drains free-ish of biofilm so I don't have to.

That is a Moth Fly, also known as a Drain Fly. It is in the order, Diptera, family Psychodidae. https://en.wikipedia.org/wiki/Drain_fly

Here the animal's appearance helps in a more precise identification: we're looking at a species of Clogmia Enderlein, 1937 (see here for the only New World species of the genus); this may be C. albipunctata (Williston, 1893), but southeast Asia also features native species (for the original descriptions of several New Guinea species see Pacific Insects Monograph (15), accessible here).


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How to set the phenotype in GWAS analysis?
In the GWAS analysis, my animal sample phenotype is whether an individual dies or survives. And I have every sample death time. How do I set the phenotype in GWAS analysis?

Simply, First of all, you can group samples as survived animals and dead samples and you have a binary phenotype.
In a different approach, you can use survival time (time to death) as an ordinal variable phenotype. If you want you can utilize survived sample by assign a large death time value to them.
In the third approach, you can cluster the survival time (time to death) into the desired $n$ groups by the simple procedure like $k$-means. and you have coarse grain ordinal variable you can add survived sample group at the end of The Spectrum.

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can a bacterium cell become a cancer?
I don't mean if a bacterium can be the cause of cancer inside a human. But can actually a bacterium changes in the way as normal cells change into tumor cells?
So gaining such characteristics of a tumor cell and if inside human body create a tumor mass?

related

A prerequisite for a cancer is that it is a type of cell within the human body that the immune system recognizes as it's own, and cancers are also generally multi-cellular. bacteria are unicellular and if they do reproduce wildly, then it's more of an infection than a tumor.

You ask two questions:

If a bacteria can get the same characteristics as tumor cells.
If such "bacterial tumor cells" actually can form a "tumor" within the
human body.

I assume that your question is not if bacteria can change in such a way that the can be confused with eukaryotic cells. This they cannot do. Bacteria cannot form organelles. Because they have no organelles they are solely dependent on their membrane for energy production. Because the surface area to volume ratio decreases with cell size there is a physical possible maximum size for bacteria. Here is some more in depth info on the subject.
So what characteristics can bacteria then have that tumor cells also have?
Well, according to wikipedia, a tumor is a mass of abnormal and excessively grown tissue (neoplasm) which may or may not be malignant. According to this definition bacteria could be tumor-like if the could form tissue and if this tissue could then grow abnormally or excessive.
And guess what? If you define tissue as "an ensemble of similar cells and their extracellular matrix from the same origin that together carry out a specific function." like Wikipedia does. Then you could argue that the biofilms some bacteria form are quite tissue-like since biofilms also contain an extracellular matrix, the cells within have the same origin and (in some cases) the bacteria can have differentiated functions.
However, the fact that bacteria can form biofilms does not make them tumor like. For that comparison to work mutated bacteria should be able to outgrow the rest of the biofilm. And while mutation that cause noncooperative/cheating/abnormally growing bacteria in biofilm are known, this kind of mutations cause the biofilm as a whole to grow slower. (source) In this sense comparing a biofilm to a colony of ants may be more appropriate than comparing it to tissue.
So to answer your questions:

Bacteria can form tissue-like formations, but when members of this formation do not cooperate anymore this typically leads to less growth, instead of increased growth.
Biofilms do form within humans. For example the bacterium Pseudomonas aeruginosa is assosiated with cystic fibrosis. And while cheaters exist among these bacteria, biofilms with high ratios of cheaters have a lower fitness. see this paper Therefor you would expect most biofilm within humans to be more tissue-like and less tumor-like.

No - when bacterial cells grow in an invasive manner in the body, this is termed a bacterial infection. When one’s own cells grow in an invasive and uncontrolled way, it is termed cancer.

This is exactly correct, but could do with some references, and possibly a little more about why these things are different.

Depends on how you define a "cancer".
The main hallmark of a cancer is cells with an agenda that can be summarized as "hungry, hungry, split".
Aggressive bacterial infections exhibit this behavior, digesting their host from the inside and quickly multiplying. Often, they spread quickly, which could be compared to going metastatic.
However, cancers have 2 advantages because they're technically human cells. This helps them dodge immune reactions, and makes a chemical "antibiotic" type treatment also difficult because it would be poisonous to regular human cells by definition. All of the known regular (non-personalized, non-immunotherapy) chemo treatments cause painful amounts of friendly-fire damage to regular cells.
Bacterial infections don't have this advantage - if they want to dodge immune reactions they have to figure it out on their own, and bacteria are so different from human cells that it's easy to make a chemical that selectively damages them with minimal side effects for humans.
Another cancer-like behavior that's possible in bacteria - benign to malignance. For example, suppose there's a symbiotic bacteria that mutates (or more likely, picks up a malicious plasmid) that turns it into an aggressive pathogen.

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insect paralysis in response to predator echolocation frequency
I remember a case in which some insect had evolved an adaptation in response to a predator's (bat's?) echolocation frequency. In mid-flight, it's wing muscles would become paralyzed and it would suddenly drop like a stone directly towards the ground. Does anybody know what this insect is? I thought it was a moth or a mantid.

Many different species react to bat echolocation sounds by altering their flight path or diving. This includes moths and mantids, but also other insects such as crickets, flying beetles, and likely many others as the following list (taken from this review by Miller and Surlykke (2001): How Some Insects Detect and Avoid Being Eaten by Bats: Tactics and Countertactics of Prey and Predator) is in no way exhaustive:
Crickets
"Many bush crickets can hear bats, but few seem to react to bat echolocation. However, the bush cricket, Neoconocephalus ensiger, shows an acoustic startle response during tethered flight in the laboratory (Faure and Hoy 2000). When the insects hear intense batlike sounds with frequencies from 15 kHz to at least 60 kHz, they dive."
Mantids
"Flying mantids (Parasphendale agrionina) react at distances as great as 10 m from a loudspeaker emitting batlike signals at natural intensities. They react by turning or with dives and spiral flight. The responses are all nondirectional, as would be expected from a functionally monaural system."
Flying scarab beetles
"In response to pulsed ultrasound, flying scarab beetles, Eutheola humilis, dropped or flew toward the ground, and walking beetles stopped."
Moths
"Freely flying, unidentified moths exhibit a variety of behavioral responses to bats and to synthetic batlike signals (Roeder 1967a; for recent results, refer to Acharya and Fenton 1992). Moths far from the source often turn and fly away, whereas those close to the source show zigzag and looping flight, power dives, or passive falls."
For a more recent review of the literature for the specific example of moths, I suggest reading Evolutionary escalation: the bat–moth arms race by Hofstede and Ratcliffe (2016).


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What Is This Tactic Called? (Banishing Adolescent Females)
I was watching a documentary about Meerkats the other day and one thing that stuck out to me was how the Mother of a family will banish her daughters once they reach adolescence. If the daughters try to return to the family then the mother will viciously attack said daughter, it's quite sad.
Anyway, the reason for this makes sense (in terms of evolution) because if the adolescent Meerkat were to fall pregnant, she would need more food & support from the clan, thus jeopardizing the original Mother's chance of survival.
I think this is an example of animal behavior/population control where there can only be 1 mature female in the group, like there is with bees. Am I correct in assuming this? Do all animals show this behavior for the same reasons? Also is there a general term that can be applied to this phenomenon?

The reason the dominant female doesn't want her daughter to breed is that she would prefer her own children survive, rather than her grandchildren (the children of her daughter).
I wouldn't call this population control - the dominant female isn't thinking to control the group size, rather, to monopolise the group composition.
The difference with bees is that the genetic relationship between the individuals is more complex (haplodiploid), so the female bees are more closely related to their sisters than to their own offspring!
The general term for the fact that only some animals are taking part in breeding is "reproductive skew".


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Would preserving your Eyes from Light keep them healhty?
I read about why eyesight diminishes with age.
I am aware of the fact that there are different causes that can affect the quality of image received by our eyes and that being vague would not lead to a clear answer, but I will try to make it as clear as possible.
I am wondering if worsening of the ciliary muscle is affected by how much light the eye receives or at least how much we use it.
There might be other areas affected by high light intake. Because the title of the question might not be clear enough: I basically mean the following:
Is our eyesight determined to worsen with age or does it depend on how the eyes are "used"?


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Micelles Sticking Together
I have a quick question regarding micelles. I have tried googling the answer but can't seem to find the answer. The question is, during digestion lipids are emulsified into micelles in order to increase their surface area for digestion but my question is, why don't the micelles stick together and form a clump which would decrease it's surface area?
Thank you.

Micelles have a hydrophobic core and a polar, hydrophilic surface. This surface will preferentially associate with water molecules and become solvated, rather than sticking to lipids.
Negative charge on phospholipids at the micelle surface mediate electrostatic repulsion to other micelles, keeping them from sticking together.


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When forming an enzyme-substrate complex in a spontaneous reaction, why does free energy increase?

We eat food and which is digested into proteins and carbohydrates.
Does digestion break bonds within food macro molecules and decreases free energy? Why, when looking at curve, do we see an increase in the free energy and then a decrease?

This increase is the activation energy: https://en.wikipedia.org/wiki/Activation_energy

Kinetics and thermodynamics are two separate things. The type of diagram you show is often encountered (even in textbooks) because it is thought to be a convenient hand-weaving way to convey a feeling of what is happening. However it is not correct as it mixes two different views: the microscopic molecular view (horizontal axis) and the macroscopic thermodynamic view (vertical axis).
The result is a misleading idea that the (molar?) Gibbs free energy (of what ???) can go up (event temporarily) along a spontaneous reaction. However for a spontaneous process (and "spontaneous" is key here) the Gibbs free energy of a system can never increase.
What can increase is the potential energy of a molecular system of the reacting molecules along a reaction path, which is what the vertical axis should represent. In which case the graph would represent a potential-energy profile. But defining a thermodynamic property like a molar Gibbs free energy for a single molecular entity has no meaning.
One might argue that considered as a chemical species, the transition state at the top of the curve (generally called the "activated complex") is obviously unstable and, considered collectively (i.e. macroscopically) must have a higher molar Gibbs free energy (at any specific time during the reaction). However, this is only partially true: it has a higher molar Gibbs free than the product towards which the flux of matter goes, but it necessarily has a lower molar Gibbs free energy than the reactants that are consumed (else the reactants would never form the said activated complex). Also, at the end of the reaction, when equilibrium is reached, all species have equal molar Gibbs free energy so that the Gibbs free energy of reaction is null ($\Delta_r G = 0$).
An alternative, really thermodynamic diagram is sometimes represented: the Gibbs energy diagram. In such diagram, the Gibbs energy of the successive species might appear to go up and down. But one should be careful of the impression given because such diagrams actually represent the standard Gibbs energies of the reactants, which is not their Gibbs free energy in any arbitrary state, and especially not necessarily their Gibbs free energy in the condition of the reaction considered.


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Cutting off circulation
How much force is required to cut off the blood circulation of, lets say the average human arm? I'm asking because i'm bored and want to try it on myself. I know that in just a couple of seconds with lack of blood flow you will lose complete use of your arm. I'm only going to do this for a second or two with people watching so please do not worry about safety!

If you are losing use of an arm within a couple of seconds that is because you are compressing a nerve and blocking transmission of motor signals, not because of cutting off blood circulation.

The pressure you need to apply is equal to your systolic blood pressure, about 120 mmHg. This is about 163 g/cm^2.

Thank you for the information boreora I wish you good fortune

Can you add resources to these numbers?

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


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What is the difference between a cytokine, a hormone and a protein hormone?
I'm trying to figure out the difference between hormone, cytokine and protein hormone. It's clear to me that all three are biological messengers, but there seems to some ambiguity and overlap between terms and I'm trying to understand the nuances.
In brief:

What do each of these three terms mean and how are they different?
Do any of the three terms represent a superset of the others? e.g are all cytokines, hormones? Are protein hormones just a subset of hormones?
Are the terms context specific at all? For example, cytokines are referenced in the context of immunology below, but are they actually fundamentally different from hormones?

If there is context-dependence, under which contexts should each word be used?
Are there any canonical examples of each? e.g Prolactin is given as an example of a protein hormone below, how about for cytokines and ordinary hormones?

In June 1905, Ernest Starling, a professor of physiology at University College London, UK, first used the word 'hormone' in one of four Croonian Lectures—'On the chemical correlation of the functions of the body'—delivered at the Royal College of Physicians in London. Starling defined the word, derived from the Greek meaning 'to arouse or excite', as “the chemical messengers which speeding from cell to cell along the blood stream, may coordinate the activities and growth of different parts of the body” [1]
Cytokines and chemoattractant cytokines known as chemokines are highly localized soluble signaling proteins produced by many cells of the immune system (neutrophils, monocytes, macrophages, B-cells, and T-cells) to regulate immune responses [2]
A great deal of evidence has accumulated and confirmed that hormones secreted by the neuroendocrine system play an important role in communication and regulation of the cells of the immune system. Among protein hormones, this has been most clearly documented for prolactin (PRL), growth hormone (GH), and insulin-like growth factor-1 (IGF-I), but significant influences on immunity by thyroid stimulating hormone (TSH) have also been demonstrated. [3]

References
[1]: Tata JR. One hundred years of hormones. EMBO Reports. 2005;6(6):490-496. doi:10.1038/sj.embor.7400444.
[2]: Stenken JA, Poschenrieder AJ. Bioanalytical Chemistry of Cytokines-A Review. Analytica chimica acta. 2015;853:95-115. doi:10.1016/j.aca.2014.10.009.
[3]: Kelley KW, Weigent DA, Kooijman R. Protein Hormones and Immunity. Brain, behavior, and immunity. 2007;21(4):384-392. doi:10.1016/j.bbi.2006.11.010.

Some hormones are also considered cytokines (e.g. GH and prolactin) since they target cytokine class of receptors.

Parts of the answer are in the text that you provide yourself. But I shall try to add where i can.
What do each of these three terms [hormone, cytokine and protein hormone] mean  and how are they different?
Both cytokines and hormones are a class of signalling molecules that are secreted by cells.
Cytokines are a group of small protein that  have a fundamental role in the immune system. They are typically short lived and typically have local effects and are specific cytokines are often produced by multiple cell types.
For example they cause local cells to generate heat and cause blood vessels to become wider and more permeable to blood cells. parham (2015) Some cytokines can act over longer distances, IL-6 for example cause local inflammation and regulates fever by targeting the  hypothalamus causing it to increase body temperature overall. For more information check this link.
Hormones are secreted into the blood by dedicated endocrine cells so the can regulate other cells across the body.(alberts, 2008)
Do any of the three terms represent a superset of the others?
Protein hormones are a subset of hormones. An other important subset are steroid hormones.
It can be argued that cytokines function as hormones in some situations. For example: in the case of an infection high concentrations of cytokines can regulate body temperature causing fever. IL-1α, IL-1β and IL-6 are good examples here
Are the terms context specific at all?
In some situations it can be argued that cytokines act as hormones. But the feature that groups them is that the are an actor in the immune response. This wiki discusses some differences.
Classical hormones are produced by a gland and excreted in the blood. This is not context depended.
Are cytokines actually fundamentally different from hormones?
All Cytokines are proteins and don't act fundamentally different from protein hormones. Both have to act through membrane bound receptors since proteins can not pass the cell membrane on their own. Steroid Hormones can pass the membrane and typically have intracellular receptors.
Are there any canonical examples of each?
Interferons and Interleukins are a large classes of cytokines. IFN-γ and IL-6 a well known examples.
Androgens are steroid Hormones . Testosterone is one of them.

"The difference is that cytokines act locally" - as you point out elsewhere in your answer, some cytokines act systemically rather than locally. "are produced by many cell types" - this isn't really much of a difference with hormones, since hormones are also produced by a variety of cell types.

You are right. I could have formulated that both sentence more precise. By  "are produced by many cell types" I meant that specific cytokines are typically secreted by multiple different cell types. For example: IFNγ is secreted by T helper cells , cytotoxic T cells , macrophages, mucosal epithelial cells and natural killer cells. Different hormones are indeed secreted by different cells, but most hormones are secreted  by one cell type. for example: insulin is onl secreted by Beta cells. I will rewrite my answer to be more precise tomorrow.


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Genotype -/- vs delta/delta
In https://doi.org/10.1016/j.neuron.2018.07.033, Pan et al. use the designation TMC1^delta/delta to describe a mouse strain lacking a functional TMC1 gene.  What if any is the different between the delta/delta superscript and a -/- superscript in this context?

The delta refers to a mutant allele, in this case a cysteine point mutant. The -/- refers to a homozygous null allele, in this case a knockout.


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Klenow amplification
Am I correct in thinking that in a standard probe synthesis reaction where primer/template are heated up and then cooled down for Klenow to extend, the theoretical maximum amplification is doubling of the template?
Given that there is essentially only one melting/primer hybridization step, there can't be further amplification after doubling?
I understand that there could be edge cases. IE. random hexamers are used where initial amplification product is displaced by a further upstream hexamer. But given an idea situation where we have just one specific primer and one specific dsDNA template that primers can bind to, the maximum yield will be double?

Which version of Klenow — i.e. are you asking about the fragment with or without 3'→5' exonuclease activity?

Klenow seems to lack exonuclease activity ("proof-reading"), but otherwise works like normal DNA polymerase, so I wouldn't expect anything different from PCR. On each step, as long as there is enough template and primers, you'll get doubling of current template.


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Is one Short Tandem Repeat (STR) enough for a reliable identification?
The lab simulates the analysis of just one STR in the genome. Would this analysis be sufficient for a reliable identification in real life? If not, explain what could be done using DNA to identify someone more reliably.

From the phraseology this is almost certainly a homework question. The poster is presumably long gone, but the appropriate  course of action would seem to declare it off-topic.

One STR is certainly not enough for identification because the same STR could be shared by many individuals. Combinations of many STRs, however, would be sufficient for identification. The number needed would depend on how many variants of the STR exist in the population (or species, depending on what you are identifying), and what the mutation rate is (nuclear STRs mutate relatively rapidly compared to some other genetic markers, but they are still often used because they're cheap and easy to genotype).


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Is there a reason for the lack of full RTK structures?
Bocharov et al. (2013) write that

As there are no structures of full-length RTKs [receptor tyrosine kinases], we do not fully understand how different domains function together to mediate signal transduction inside the cell.

True to the above quote, I've so far only found isolated domains of some RTKs in the PDB, but no complete structures (neither X-ray nor NMR). I am a chemist by training, so am hardly an expert in this area, but it does seem counterintuitive given the general importance of RTKs in cell signalling. Is there a fundamental reason for the lack of RTK structures?
In contrast, there are examples of full-length GPCRs, e.g. rhodopsin (Palczewski et al. 2000). As tsttst brought up in the comments, this seems to be an issue with RTKs being single-pass membrane proteins, whereas GPCRs are multi-pass. How does this affect the ability to obtain a structure?

Bocharov EV, Lesovoy DM, Goncharuk SA, Goncharuk MV, Hristova K, Arseniev AS. 2013. Structure of FGFR3 transmembrane domain dimer: implications for signaling and human pathologies. Structure 21(11):2087–2093. doi: 10.1016/j.str.2013.08.026.
Palczewski K, Kumasaka T, Hori T, Behnke CA, Motoshima H, Fox BA, Le Trong I,  Teller DC, Okada T, Stenkamp RE, et al. 2000. Crystal structure of rhodopsin: a G protein-coupled receptor. Science 289(5480):739–745. doi: 10.1126/science.289.5480.739.

In the meantime there are some structures, e.g.: Chen et al., J Mol Bio, 2015, or Opatowsky et al., PNAS, 2014 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4663128/, https://www.ncbi.nlm.nih.gov/pubmed/24449920)

Thank you, I don't know why I didn't try Google... Is there still a point in asking why full structures used to be so elusive?

One trick is to check the referring papers through google scholar, and one of them highlights the difficulty to crystallize single-pass transmembrane proteins (Valley et al. BBA, 2017, https://www.sciencedirect.com/science/article/pii/S0005273617300160#bb0475 ). Asking why single-pass transmembrane sections are difficult to crystallize compared to multi-pass might be a more general and answerable question (the answer would be described in Alberts' text book).

Large proteins are challenging for NMR: the more amino acids, the more peaks one has to assign. Peak overlap is also more likely the more amino acids you have, making assignment difficult. Some NMR strategies work well for studying dynamics of large proteins, but as far as structure determination is concerned, there definitely is a critical size past which NMR is simply not the tool for the job.
Flexible proteins are challenging for crystallography: too much flexibility can simply prevent crystallization, you can spend years only trying to get crystals, and once you do manage to grow crystals they might diffract poorly or not at all. But crystallography is often very useful to solve high-resolution structures of individual, isolated domains; this is of great help down the road to interpret a lower-resolution cryoEM map of the full-length protein.
Membrane proteins are challenging for biochemistry: purifying them and getting them to remain stable in solution is difficult.
Receptor Tyrosine Kinases (RTKs) are all of that at the same time! Large, flexible membrane proteins.
Now, with tremendous technological progress of cryo-electron microscopy (cryoEM) recently, such challenging structures become more tractable. Conformational flexibility is still an issue, but unlike with crystallography it can be dealt with to some extent (i.e. it won't prevent you from collecting initial data and getting preliminary results that can guide your next attempt).

Thank you! With regard to the issue about single-pass vs multi-pass membrane proteins that was brought up in the comments - are the former simply harder to crystallise due to greater inherent flexibility (which seems logical to me)?

I am not sure about that, but that could very well be the explanation. GPCRs have flexible loops between transmembrane helices, but these 7 helices are interacting with each other and that probably makes the whole less flexible.


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List of genes across species (or just for humans)
Wondering if there is a place that has a list/table/database of all the genes in the human genome, and/or all the known genes in all the species we've studied so far. Something that contains any of this would be great.
I found this but not sure yet if that is just for humans and just for one chromosome. But I'd like something along those lines across species, or the closest thing to that that exists.

There are a number of sites that store genetic data. The most famous of all is probably NCBI

In principle there are a LOT of these databases and depending on your specific questions you may want to look into different ones. Like already mentioned NCBI hosts basically all of the available information, however it's not always easy to find the bits you care about.
The database I personally use the most is biomart (hosted by the ensembl consortium). It doesn't just contain all known for genes for pretty much all organisms, but is also able to link this to a ot of different information sources.
I usually access the database directly via the biomaRt R package, so I can't really say how good the actual website this. However, this link should allow you to download a table of all human genes with names, (unique) identifies & descriptions (I selected these from the 'Attributes' section).


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Does mother feed information?
Does the mother feed information to the child in the fetus? If so, How is that done? IF not, How can the just born baby breath involuntarily if brain doesn't know it should generate impulses to contract and expand Diaphragm ? If information is given, What type of Information it is, And Would it be possible to feed the information of mother's choice?

You might want to look at this question https://biology.stackexchange.com/questions/31459/how-is-instinct-carried-from-one-generation-to-another

It's not like anyone can not breath for long without other access to oxygen. Pain is pretty good informant.

Why was this downvoted? It's a decent question even if somewhat dumb.
Humans don't breathe in the womb. Instead, blood with oxygen and other essentials goes in through the umbilical cord and back out through the same cord after its resources have been partially used.
"Feeding information" would require a neural connection which there isn't any evidence of. Experiments where scientists "link human brains together" generally use an electricity-based computer-mediated connection (for a good example:
https://www.cnet.com/news/scientists-connected-3-actual-human-brains-then-made-them-play-tetris/ )


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How exactly are nucleoli made of NORs?
I read that nucleoli are made of DNA, RNA, and nucleolus organizer regions. I don't quite understand how that happens with NORs. Isn't there an envelope delimiting the nucleolus from the rest of the nucleus content? Do NORs from different chromosomes come together? I mean, they are not detaching from the rest of the chromosome and aggregating freely...

No there is no membrane that separates the nucleolus from the rest of the nucleus. The nucleolus is an aggregate of all kinds of molecules involved with ribosome assembly like: precursor and mature rRNA, Small nucleolar RNAs, rRNA-processing enzymes, ribosomal proteins and partly assembled ribosomes (but no fully functional ribosomes)
Aside from all these protein and RNA there are indeed regions of the chromosome called Nucleolus organizer regions (NORs) present in the nucleolus. These NORs are located near the tips of the short p region of chromosome 13, 14, 15, 21, and 22. During interphase these regions decondensate due to proteins like nucleolin and are thus open for transcription. Many of the protein I mentioned are needed to form or present in the aggregation that is the nucleolus.


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Could one hear without his ear?
Might be a stupid question, but I'm quite curious about finding out ^^
If someone looses his ear, or for example cuts it of, just as Van Gogh did. Would he still be able to hear, since the actual organs that are responsible for hearing are on the inside of your ear canal? The ear itself more or less is just flesh, right?

Short Answer
Yes, you could hear, but it would be harder to localize sounds.
Longer Answer
The "ear" from a biological perspective includes the inner ear which is all of course necessary for hearing.
The external part of the ear is called the pinna/pinnae (plural), and yes, you can hear without pinnae; that's essentially what you do when you use in-ear headphones since they project right into the auditory canal and don't use the pinnae at all.
However, the pinnae are important both for collecting sound (therefore increasing the amplitude) and for sound localization, because they both shape the volume of sounds depending on direction (you can localize continuous sound by turning your head back and forth) and have a vital contribution to the head related transfer function that is crucial for localizing sound in elevation.
Sound localization experiments that use in-ear headphones sometimes first record the head-related transfer function with a microphone in the ear to then apply this filter to sounds that are played. This varies somewhat from individual to individual and captures the unique shape and position of the pinnae.
Note that sound localization is not only important for knowing where sounds are coming from, it can also be important to identify and pay attention to auditory objects, especially in noise, like one person talking in a cocktail party.

Algazi, V. R., Duda, R. O., Duraiswami, R., Gumerov, N. A., & Tang, Z. (2002). Approximating the head-related transfer function using simple geometric models of the head and torso. The Journal of the Acoustical Society of America, 112(5), 2053-2064.
Batteau, D. W. (1967). The role of the pinna in human localization. Proc. R. Soc. Lond. B, 168(1011), 158-180.
Brungart, D. S., & Rabinowitz, W. M. (1999). Auditory localization of nearby sources. Head-related transfer functions. The Journal of the Acoustical Society of America, 106(3), 1465-1479.
Hofman, P. M., Van Riswick, J. G., & Van Opstal, A. J. (1998). Relearning sound localization with new ears. Nature neuroscience, 1(5), 417.
Wenzel, E. M., Arruda, M., Kistler, D. J., & Wightman, F. L. (1993). Localization using nonindividualized head‐related transfer functions. The Journal of the Acoustical Society of America, 94(1), 111-123.


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Do plants experience the following feelings
I am not a student of biology,in other words I have not read biology much.
But I read that plants have life and so my question is the following:

Suppose I take two saplings of two different varieties of hibiscus(or any other tree variant) and I put them in the same pot and allow them to grow up.
  Suppose they grow up and become well grown plants after say 4-5 months.
  My question is:
Will the two saplings experience any feelings for each other,in other words will they become friends or share any relation with each other.
  Suppose one of them is attacked by insects and its growth gets shunted,will the other plant also experience some feeling for it.
If I uproot one plant will the other one feel lonely or any other kind of feeling as if its counterpart is missing.

If someone cares to answer the above questions,I would be very grateful.
Thank You

Wikipedia defines emotion as "any conscious experience characterized by intense mental activity and a certain degree of pleasure or displeasure."
Plants do not have a central nervous system and therefore no mental activity so they certainly don't have emotions in the sense that humans and animals can have emotions. However plants feel/detect being eaten and they can communicate this to other (related) plants by releasing volatile organic compounds.

But a large component of animal emotion is hormonal, e.g. the "fight or flight" effect of adrenaline.

well according to the wikipedia page on emotion an "emotion is any conscious experience characterized by intense mental activity and a certain degree of pleasure or displeasure." And while plant are aware of their surroundings I would argue that they have no mental activity, and thus no emotion. Or do you argue that animal emotion is defined differently than human emotion? But I should define emotion in my answer for clarity.

I would guess that that Wikipedia article is discussing human emotions in the context of psychology, and so is missing rather a lot.  It is perfectly possible to experience the hormonal component of emotion without any sort of intense mental activity.  A common example is the injection of adrenaline given after allergy testing: it produces the physical fight/flight symptoms without a significant mental component.  (Of course in humans it's impossible to entirely separate the physical causes/reactions of emotion from the thoughts about the reactions.)


text:
Is there a resource to query gene expression similarity? Stratified by sex?
We developed such a resource. The editors of "Bioinformatics" (at OUP) rejected the paper on the grounds that we did not run a comparison with "state-of-the-art" [similar] resources. Can someone help me find similar resources?
Link to our own resource, ExFiles.

There are some similar resources, which at the same time do not mix the ingredients in the same way as your tool. Hope that pointing out the respective differences will help your rebuttal or resubmission! e.g.:

A similar web service is part of flyrnai, where tissue-specific expression can also be compared based on sex, and genes can be queried by the similarity of their gene expression profile to other genes.
A resource which has some conceptual relatedness regarding sex-specific similarity in gene expression, and which is also based on the GTEx dataset, has recently been published in the form of tables by Gershoni et Pietrokovski, BMC Biol, 2017.
A very nice and broad resource of high-quality gene expression profiles on individual tissues, but also on response to stimuli, is EBI GXA. Though the web interface only allows to query sex-specific expression profiles, computationally minded people could readily compute (dis)similarity between samples after downloading the (well-structured) data dump of EBI GXA.
A similar tool in terms of the visualization of sex-specific expression patterns is part of gtexportal, though it seems limited to displaying a single gene.


text:
How do insects recognize their host plants?
Many insects, like butterflies have specific host plants on which they feed or lay eggs. While researching about some butterflies, I found that they lay their eggs on certain specific plants and their larvae feed on the leaves of those plants. I wonderd how do they recognize those specific plant species:

Do they use visual cues to find or recognize these plants?

Or

Do they use chemical cues, like sensing volatile compounds released by the plants? I think this might be possible as I found many species of butterflies prefer plants of the citrus family which contain essential oils. Do they just sniff around following the trails of such chemicals to find the host plant,

Or

Is it the combination of both?

Yup, insect recognize their host by the combination of both visual cues and chemical cues.

@MaqsoodAhmad- Welcome. Answers should be backed up by credible sources, preferably journal articles. Unsourced one-liners are comments and I've converted it as such.


text:
What is the name of this graph/plot?

What is the name of this graph/plot?

This is a Circos plot, often used for visualizing genomic data, but works equally well for migration and some other applications.

Circos is a software package, and is capable of producing other graphic forms, such as concentric circles.

And there are other software packages that can produce these graphs, like the R-package circlize

Ah, yes you are correct. I've only ever heard them referred to as Circos plots colloquially, regardless of the software used to produce them, but thanks for correcting me!

I think it is Chord Diagram. you can see this for more information.

"A chord diagram is a graphical method of displaying the inter-relationships between data in a matrix. The data are arranged radially around a circle with the relationships between the data points typically drawn as arcs connecting the data." based on the Wikipedia


text:
How credible is the Remenko's two-component color vision theory?
I've come across an article (in Russian), which describes a nonlinear two-component color vision theory made in 1975 by S. Remenko. The article heavily criticizes trichromatic theory as very imperfect. There's a whole page related to the criticism. Some of the citations there refer to Feynman's lectures vol. I ch. 35, where also some doubts are expressed. See e.g. the part by Feynman:

Using the three different kinds of color blindness, the three pigment response curves have finally been determined, and are shown in Fig. 35–8. Finally? Perhaps. There is a question as to whether the three-pigment idea is right, whether color blindness results from lack of one pigment, and even whether the color-mix data on color blindness are right. Different workers get different results. This field is still very much under development.

But the only English-language place I've found mentioning Remenko's two-component theory was the book "Computer Systems for Healthcare and Medicine" by Piotr Bilski and Francesca Guerriero, where the first name also looks suspiciously Russian.
So I'm somewhat skeptic about credibility of all this Remenko's theory and the criticism of the trichromatic theory. But having not much expertise in color vision theories, I thus prefer to ask the experts: is the theory by Remenko actually credible? Is it even known outside of Russian-speaking world? Has it been falsified? Is trichromatic theory really flawed in any significant way so that a replacement theory would be required (are Feynman's remarks out of date?)?

We have the physiology of colour vision nailed down pretty precisely, across a broad suite of species. There are some subtleties (there aren't, strictly, only three receptors involved in vision, and the number and properties of the receptors differ between species). But the general theory is still basically trichromatic theory. If the mechanisms in 'two-component theory' are very different, then that theory is very wrong. See https://biology.stackexchange.com/questions/39882/are-some-animals-like-dogs-and-cats-color-blind-and-how-do-we-know-that/39890

answering your sub-Q: Remenko's theory of color vision is not really shows up on Google search. So it is likely very esoteric

This is a confirmation of the theory of Remenko.
https://www.pnas.org/content/113/29/8206

It's not: Remenko's theory doesn't use any chromatic aberration to explain anything; moreover, it's two-component while the paper you link is about one-component+chromatic aberration.

That era produced a lot of very questionable science from Russia; there is no good reason to doubt the three-component color vision theory, and it's also the basis of all RGB TVs and computer monitors. However, I can't read Russian so I don't have any idea what this two-component theory is.
Typical humans have three cone cells, which is the biological origin of having three components for color vision. Colorblind individuals who lack one of the three cones have color discrimination issues consistent with the three component model. I am not aware of any credible research that questions this.
The lack of further study into the theory you refer to probably puts it into the category of "not even wrong" - based on such flawed reasoning or premises that it isn't worth disputing.

Nathans, J., Merbs, S. L., Sung, C. H., Weitz, C. J., & Wang, Y. (1992). Molecular genetics of human visual pigments. Annual review of genetics, 26(1), 403-424.

Please see the edit to the question. I've added some relevant part of the Feynman's remarks about validity of trichromatic theory.

@Ruslan Color-blindness is slightly more complicated because not everyone's color-blindness is because they are missing a particular cone. The others are because of shifts in the wavelengths the pigments are sensitive to.

It is worth mentioning hte other component of color vision which is how our brain processes color and how opponent colors work. https://en.wikipedia.org/wiki/Opponent_process

Remenko’s theory may only be dismissed (in favor of the L/M/S-cones theory) after obtaining a conclusive evidence of blue-sensitive (S) cones in humans; or at least, some primates.
How did Nathans, Merbs, Sung, Weitz & Wang (or anybody else) prove that OPN1SW is the “short wave sensitive opsin”? Has OPN1SW been extracted from a cone? IMHO various Internet “authorities” merely replicate opinion pieces. Hopefully science doesn’t work like this, where linking to Wikipedia, having the ♦ thing, 25k rep, and bashing USSR for Lysenkoism is sufficient for a heap of upvotes.

@IncnisMrsi You are free to write your own answer.


text:
How are cell death like apoptosis and entropy related?
In Perspectives on Statistical Thermodynamics, Yoshitsugu Oono, it is written that

Do not conclude, however, that since the second law is invincible,
  information thermodynamics is unimportant. It is possible for a system
  we are interested in to perform something that ordinary thermodynamics
  does not allow, and to pay the price somewhere else. For example, it
  may be possible to go beyond the limit of thermodynamics for the time
  being by shifting the average value of fluctuations, although the
  price must be paid (dearly) later. There must be such cases in
  molecular machines. It is argued that cell senescence is due to the
  accumulation of defects and wastes, but cell death could have a more
  active implication of carrying away the debt caused by utilizing
  information. Thus, entropic apoptosis and entropic altruism are
  conceivable.

but I don't understand the following two points.

Why is cell death associated with "debt caused by utilizing information"? Do cells die for increasing entropy to compensate the entropy decrease which caused by their using information (but what kind of information)?
Why can we conclude "Thus, entropic apoptosis and entropic altruism are conceivable."? Does this mean, to let other cells decrease the entropy by consuming information, some cells kill themselves to increase entropy?

Unless you have a closed system, don't bother with the second law. These sound like some poetic descriptions but they won't tell you much about biology.

It is argued that cell senescence is due to the accumulation of defects and wastes, but cell death could have a more active implication of carrying away the debt caused by utilizing information.

The first part of sentence which I italicized here is sufficient to understand the biology: cells age and die off because they accumulate defects. Organisms, whether single-celled or multi-celled, ultimately get around this by making lots of copies of themselves and expecting some to fail.
The second part of that sentence says "could" and is poetry to describe the first half, as well as the sentence that follows. It doesn't add any more science, unless you care about the existence of "entropic altruism" in the universe, which sounds to me like a religious rather than scientific approach. It's just stating that cell death (and perhaps, to an extension, death of multicellular organisms) can be useful to organisms/species rather than merely destructive. There is nothing wrong with finding beauty in physics and mathematics, but beauty in itself says nothing about how things work or how things should be.
In the context of a multicellular organism, cells kill themselves to not kill/harm the whole organism (e.g., to not develop into cancer, or as a planned event during development). The biological reason they do this is because multicellular organisms that have evolved genetic mechanisms to identify potentially harmful cells and have those cells die are more likely to reproduce and produce more multicellular organisms like themselves. If you want to interpret this as "entropic altruism" because cell death increases entropy, that's fine, but no thermodynamic argument is needed or even all that helpful in explaining the biology.
Note also that the book you cite doesn't seem to be in common use; it has no reviews on Amazon or Google books, and a previous book by the same author only has 1 review. I don't have anything against the author and they could be an excellent statistical physicist, but language like this makes me think they are not a biologist.

As far as I know, apoptosis has nothing to do with entropy, except in the degenerate and trivial case where a cell is utterly voided of energy for enough time that it stops working.
Entropy is informally defined as a low-energy state. Cells that are low on energy are typically designed to pick up more energy from the environment. A simple example: Consider a cell that metabolizes glucose into an organic acid for energy. Assume that the cell lives in an environment where glucose is readily available, organic acids are regularly cleared away, and it has transport protein channels that readily allow glucose and organic acid waste-products to cross the membrane.
As the cell uses its own glucose for energy, it gets converted into an organic acid (waste product) which builds up in the cell. Now the cell has a lower concentration of glucose than its surrounding environment - and due to the transport protein channels, glucose from the outside will tend to move into the cell down the concentration gradient. Likewise, as organic acid waste-products accumulate, they tend to exit the cell over their own protein channels because the concentration of acids in the cell is higher than its environment.
Higher-order life forms (extremely complex with billions of highly differentiated cells) implement apoptosis as a form of quality control over cells. Over time, cells accumulate damage and mutations. Exact mechanisms vary significantly by species. In humans, there are specific proteins that scan for nonrepairable damage to protein structures in cells or dangerous DNA mutations. In some cases, a cell may be programmed to stop replicating itself; extremely dangerous (oncogenic) mutations may trigger apoptosis where the cell "takes one for the team".


text:
Blood Vessels (Artery Vs Arterioles)
I just have a quick question regarding what my textbook says. I have tried searching online but I have failed to find an answer. Basically, my textbook states that arterioles are smaller in diameter compared to arteries but have a larger lumen. Isn't the diameter measured across the lumen? So how can the artery have a smaller lumen but be larger in diameter?
Thank you

Do you have the exact quote in context from the textbook? You are right, that makes no sense at all and is false, the lumen of arteries is larger than the lumen of arterioles. It's possible they are referring to the ratio of the lumen to the overall diameter, but even in that case I'd be uncertain of the statement and my intuition is that it is still false.

I have added a photo showing what the textbook states. Thank you for your reply :)

The photo shows that the book states that arterioles have a larger muscle layer and lumen. Is this correct?

The key word you are missing is "relatively": I'm not clear what they mean "relatively" to based on where you cut off the passage, but they probably mean relative to the entire diameter of the vessel; the statement is probably not true for area but you would have to choose a particular artery and arteriole to compare, and both categories have a lot of variation in size within and between organisms.
Arterioles do have a "relatively" thicker muscle layer than the great arteries because they are the place where most of the contraction takes place that regulates the resistance of different vascular beds. Because of that, though, their lumen size varies quite a bit depending on the state of the muscle. When the smooth muscle in the vessel wall is relaxed, arterioles are much larger than when contracted. Even if the book is correct that according to whatever measure of "relative" they are using, arterioles have a wider lumen, I have a hard time believing this would be true over the entire range of contraction.

I will attach entire passage

Thank you for your answer. I understand the muscle layer part but I still don't know what I should write if an exam question was to come up. Should I write that the arterioles have a smaller or larger lumen?

Arterioles have a smaller lumen than arteries. The "ioles" at the end implies they are "little arteries." If I were you I would focus on the differences in function in your studying.


text:
Can a plastic degrading bacteria science fair project be recreated in a school lab?
i am just looking for a science fair project and am fascinated by this topic. i was wondering if a project concerning the isolation of plastic degrading bacteria could be done in a school lab. I am in grade 10. Anything helps!

This mostly depends on the equipment available in the school lab & as well as time and resources available. If you can add a few more details about either the equipment present in your school, it'd be easier to say what would be possible. The other way around if you describe in more detail what you'd like to do, it's easier to say what would be needed exactly.

I am not exactly sure of the materials needed since this is just the beginning stages of finding a project. From what I've researched, the main objective would be to isolate bacteria from soils, to test these isolates for ability to degrade different types of plastic and to identify these microbes. We have until December 14 to finish experimentation and would have help from a lab technician. Do you know if this type of project would be possible and what we should inform our lab technician with in order to help us? Thanks!

You should speak with your lab technician asap - he/she will know much better what exactly can be done in the lab and will need to done. Note that 2 months is a rather short timeframe to do an experimental project, esp. since growing isolated bacterial strains is not always straightforward


text:
Is pith a ground tissue with no specialized function?
Here is a question from the book My Max Score SAT Biology E/M Subject Test (where the SAT is the exam taken by American high school students):

Ground tissue with no specialized function
  A. Xylem
  B. Phloem
  C. Cambium
  D. Bark
  E. Pith

Here, I can eliminate A, B, and D because these are dermal and vascular tissues while a ground tissue is what's between those.
As for the remaining variants, cambium is a tissue that gives rise to other tissues and is responsible for the plant's growth up and to the sides. Pith is a tissue in the very center of the plant stem and is responsible for storage of nutrients. While trying to understand the question, I even found info that it is a type of vascular tissue because it is involved in plant transport (https://www.quora.com/What-are-the-functions-of-piths-in-a-plant) although I'm not sure if it's correct (yeah, I know that Quora is not the website with absolutely credible info).
So, as I can see, both cambium and pith have their function.
Then, I decided to determine whether they are a kind of ground tissue. Pith definitely is a ground tissue, according to its definitions. However, I could not find what kind of tissue cambium was considered to be.
With all that said, I can't be sure to choose either answer. First, both tissues have their functions. Second, pith is a ground tissue, and cambium is undetermined for me.
Here is the answer, however:

E. Pith is a source of unspecialized ground tissue that adds structure
  to a stem at the very center.

I can't be sure about this answer because unspecialized means "not designed for a particular purpose." But, as I've pointed out, both pith and cambium have their purposes/functions.
Please explain why pith is written to be unspecialized. Is it because "storage" is not an "active" function like growth or transport; this tissue just exists and is able to store different substances in addition to that?
Also, is cambium a ground tissue or some other type (dermal, vascular)?

Short answer: it's not the greatest question.
Long Answer:
So there are three primary tissues in a plant: ground tissue, dermal tissue, and vascular tissue. See below for how they sort out:

However, some sources refer to the tissues of plants slightly differently, and indicate that the three basic tissue types are parenchyma, collenchyma, and schlerenchyma.

Example: "Botany: A Lab Manual" by Pfluger 2014:

The three fundemental tissues of plants are parenchyma, collenchyma, and sclerenchyma

Since these are all "ground" tissues, this approach to classifying plant tissues would suggest that all plant parts consist of some kind of ground tissue (including all the plant parts you mention in your post). In fact, this is often the case...

Again, from Pfluger 2014:

They [parenchyma] can be found in virtually any part of the plant and are the most common cell type in a plant.

Of the parts you mention, xylem is "specialized" to move water through the plant via tracheids, pits, and vessel elements; phloem moves sugars/sap through sieve tube cells which are supported by companion cells; cambium acts in secondary growth of wood and bark via the vascular and cork cambia; and bark is a water-proof protective layer.
However, "pith" is simply the central parenchyma cells in the stem, and therefore are primarily just used for storage like "all unspecialized" ground tissue.
As for cambium: from here:

Interfascicular cambium differentiates from parenchyma or collenchyma cells located between the vascular bundles (mainly in stem)


text:
Will a dog develop similar feelings with a robot as like human?
I think we are connected to the world by Biochemistry first and then physical and verbal interactions. If a robot feeds a dog regularly, pampers it and cuddles it regularly, would it develop the same feeling to the dog as it would have developed with a human?
A sci-fi robot like Ultron from Avenger movie.

Somewhat of a bad question due to being vague about the type of robot. Are you referring to modern-tech robots or sci-fi robots with human intelligence more than sufficient to ace the Turing test? Is the robot you have in mind specifically designed to look like a human?

chemistry first and then physical and verbal interactions. This is unclear. You are probably not using the terms "chemistry" and "physics" as used in science. So please define them.

the same relation is unclear. Will the dog have the same feeling of awe when thinking of the algorithm that is governing the robot's behaviour. No, it cannot understand it. Will the dog appreciate the presence of the robot. Yes, eventually. It also appreciate its bed and many other objects though.

I'm voting to close this question as off-topic because it is not about biology but about pet psychology. Also, the question is unclear and any answer would necessarily be drawn from opinion rather than evidence.

Assuming you mean a robot "designed to be human" (that means human-like behavior patterns, human-comparable intelligence, being self-aware and able to learn), then from the dog's perspective, the only significant difference is the differing smell.
There is no scientific evidence for mystical or metaphysical "connections to the world".
From the dog's perspective, the defining factors are:
Owner's behavior (petting, feeding, walking, training, rewards for good behavior or learning tricks). In this case, the robot is no different from the human.
Owner's speech (voiceprint). There's evidence that dogs understand human speech to some extent (https://www.independent.co.uk/news/science/dogs-can-understand-human-speech-scientists-say-a7216481.html). Given how adaptable organic brains are, I assume a dog would be able to adapt to even a synthetic (digitally altered) voiceprint over time or one that spoke in a conspicuously robotic manner (for example: "Temperature alert. Please fetch an external cooling fan./Your assistance above your designated specifications continues to be noted." instead of "It's getting hot in here. Grab a soda from the fridge over there?/Good dog!"
Owner's scent. The only real difference from a dog's perspective. A robot would lack the distinctive scent cues from a human, except if the robot was designed to produce those as well. Even if those aren't present, a dog should be able to adapt to a robotic owner's distinctive smell (plastic with motor oil and a hint of ozone).

Hello! This question was deemed worth of an answer, so why not upvote it? Vote early, vote often to encourage new users and keep the community alive!


text:
Michaelis Menten kinetics - Plotting to find V-max and Km
In dealing with the question above I know that if we plot 1/v against 1/[isocitrate] we can get V-max = 1/intercept and Km = slope/intercept.
However when I express the two rows of values in micromoles I get intercept = 3359, and I believe it will be in micromoles? That gives me V-max = 1/(3359*10^-6) = 297.7. However, how do I know the order of magnitude of this number? The textbook says it is pmol, but how is it picomoles/ dm3 s?

I'm voting to close this question as off-topic because this is not about Biology but numerical manipulation, and in a specific instance. There are many resources on the web for this sort of thing.

Another more general point. Do not post text as images. It discriminates against people with sight disabilities.

The order of magnitude for your intercept value depends on the axis of your graph, which in turn depends on the values / units of your input values.
As an example if your substrate concentrations are in the range of $\mu mol / l$ (which is micromolar, not mircomoles), then that is also the order of magnitue you'll get out of the calculation.
$dm^{-3}$ equals litre's ($1dm^{-3} = 1l$), it's not usually not used for concentartions, so I can't say why the textbook used it instead. Maybe they wanted to use base SI units.


text:
Control of gene expression
Eukaryotes have many genes, so how does RNA polymerase recognize a gene needed to be transcripted?

Could you please add information regarding what you know about the question and how you tried to seek information about it?

I.ve just read that RNA polymerase can  slip along the DNA molecule until it finds the gene that needs to be expressed, or this enzyme bind to the promoter after the Transcript factors bind.

Are these two ways right and enough? Is there any other mechanism?

Genes typically have promoter regions attached to them that scan for the presence of certain conditions. When a promoter's condition is met, it changes shape, encouraging RNA polymerase to bind and start making an RNA transcript of the DNA piece.
In other cases, genes can have suppressor regions where a certain condition actively blocks the attachment of RNA polymerase.
(updated for improved explanation)
Think of the (protein-coding) genome as a giant library full of books (genes). Each book tells the reader how to build 1 product (protein). In practice, a gene can code for multiple proteins via introns, but we will ignore that for simplicity here. The overall concept remains the same.
Now think of RNA polymerase enzymes as a population of simple-minded workers wandering around the library who instinctively attempt to reach for and open books on shelves that they bump into. If a worker is able to access a book and read it, the book's product will be produced. If a book happens to be excessively difficult to access or open, the worker will give up on it and resume wandering. Some workers may be more persistent than others.
Varying accessibility per book title dictates overall rate of production. The library shelves are specially designed such that books detailing construction of products in demand are "easy" to pick up (bookshelf is open and unobstructed), while products that are clearly out-of-demand are "hard" to pick up and read (book is locked down, tied to a 10-pound weight, and there's a plastic blocking piece over the front). If a book is hard to access, only the most persistent workers will read it and build the product it describes (low or completely blocked transcription). If a book is easy to access, most workers have ready to access it, causing the book's described product to proliferate.


text:
How can the leakage of mitochondrial protons generate heat?
I read the following about thermogenin:

"When thermogenin is
  inserted into the inner mitochondrial membrane, it
  accentuates mitochondrial proton leak and dissipates
  the proton motive force. Since oxidation is no
  longer coupled to phosphorylation, thermogenin is
  said to cause uncoupling. In the presence of thermogenin,
  oxidation and proton pumping continue
  at high rates but with low rates of ATP synthesis. So Thermogenin enhances
  mitochondrial proton leak so there would be heat."

Why does proton pumping without ATP synthesis generate heat?

please add a link to your source. Is it webpage or book?

Hello and welcome to Bio.SE! Take the tour to learn about the site and earn yourself your first badge.

Uncoupling ATP synthesis from the ETC (electron transfer chain; this is where oxidation takes place) by thermogenin or any other method means that the energy used to generate or uphold the proton gradient gets 'lost'.
Since physics teaches us that energy is only transferred and never truly lost, the energy consumed by the ETC must most go somewhere - heat / thermal energy is the easiest and therefore most likely option.
References

Wikipedia article on Uncoupling Proteins
Uncoupling article written in chemical terms
Short general article about brown fat and heat production

Proton pumps just like any mechanochemical process generates heat, normally much of this heat is reclaimed in the production of ATP.  Without thermogenin proton pumps produce a proton gradient, the gradient is used to power atp synthase. thermogenin is a channel protein that creates holes in the membrane preventing a gradient from building up. The pumps never stops or slows so they continuously generate higher amounts of heat, which yields a higher temperature. It is basically the reason an electric motor running full throttle generates more heat than the same one barely running.
Basically brown adipose tissue evolved a way to generate heat by running a "motor" that is not attached to anything. Its not efficient but it is better than not having a way to consistently generate heat.
source 1
source 2
source 3
source 4

This answer is not correct, the ETC/proton pumps don't slow down normally - because they ARE coupled to the ATP syntahse which 'uses up' the proton gradient, thus a stable equilibrium forms. Also the ETC/proton pumps themselves don't generate a lot of heat, that would be pretty inefficient (and  would mean that ALL eukaryotic lifeforms always generate heat, which is not the case).

Its coupled to ATP synthase in mitochondria not primarily used in thermoregulation. In brown adipose tissue which has  mitochondria focused on the production of heat it is not coupled to ATP synthase or has minimal coupling. the proton pumps are indeed the port generating the heat and it is very inefficient.

I still don't believe that the ETC (electorn transfer chain / respiratory chain / proton pump) is generating the heat itself, since that would still mean that ALL mitochondria generate heat. Also non of your sources seem to support that claim, they mostly describe that thermogenin allows thermogenesis.


text:
Chemistry of phosphodiester bond formation by DNA polymerase
As I'm teaching General Biology to my college students, I realized that I don't fully understand how a 3-P nucleotide like ATP is broken down to be incorporated into DNA during replication. How does this work??
In other words, what is the actual mechanism/reaction pathway for the following:

What I know:
I understand that ATP is typically hydrolyzed to become dephosphorylated in other contexts. I also understand that a phosphate of one nucleotide is bonded to a deoxyribose of an adjacent nucleotide via dehydration synthesis from the joining of their hydroxyl groups to form DNA.
However, I cannot seem to find a good resource (online or in any of my [admittedly simple] general bio textbooks) that demonstrate how exactly both of these reactions take place during replication...
I'm assuming that DNA polymerase is taking advantage of the released phosphates from ATP (and the appropriate forms of GTP, CTP, TTP) to become activated?
Overall, what does this whole process look like on a chemical/molecular level?
I'd love a visual (especially a video) if you could provide such a resource in addition to a thorough explanation of what's going on here.

Molecular Biology of the Gene is a good book if you have access to it.

I am unclear what you want to know. Is your question about the enzyme reaction mechanism or the thermodynamics? Your use of the word "power" in the title suggests energetically but the body of your question seems concerned with mechanistics. This and other statements about DNA polymerase "taking advantage of…" seem to indicate a basic ignorance of enzyme catalysis. Have you read the appropriate chapter in Berg et al ?

@David I want to know both and all of the above.

If you want to know all then your thirst for knowledge admirable, but your question too wide to answer on SE Biology. I would read the appropriate chapters in Berg or Lodish etc. As regards your college students, what you focus on depends on their background and the time you have. The chemical aspects require a chemical background but don’t seem particularly interesting to me, except that the dNTP substrates drive the reaction energetically and pyrophosphatase makes it irreversible. Conceptual problems — proofreading, initiation and Okazaki fragments etc.  — may be better.

@David. Thanks for the suggestions. I don't actually plan to teach them the specifics I'm asking about in this post -- these details are just for me to more fully understand the process as I explain to them a simplified version. Could you also more specifically indicate which texts you refer to? Is there a specific edition of Berg's or Lodish's texts?

This post seems helpful as a quick explanation of the reaction I'm asking about in my question: http://virtuallaboratory.colorado.edu/Biofundamentals-web/lectureNotes-Revision/Topic3-2_NucleicAcids.htm

Also relevant: https://www.biosyn.com/tew/What-is-a-Phosphodiester-bond.aspx

I have edited your title so that it is now an agnostic question, rather than one that (incorrectly) assumes a particular answer about the role DNA polymerase. I have not touched the body of the question, but after reading my answer (and that of @Nicolai) I would suggest your remove or replace the incorrect figure.

@David I've updated my image to try to better demonstrate that the arrow you've questioned is meant to be conceptual and not chemical. The image is meant to demonstrate that I'm asking about the bonding of a tri-phosphate molecule to an existing nucleic acid in such a way that a phosphodiester bond is formed and 2 phosphates are released.

theforestecologist, I found Biochemistry by  Jeremy M. Berg, John L. Tymoczko, and Lubert Stryer, to offer a great explanation of the mechanism. idk if you are still looking for reference material but its still one of my favorite all time undergrad text books

I found this paper, which goes very deep into the molecular details of the individual steps of this reaction and also discusses how this is coupled to nucleotide selectivity.
The 'basic' details about the reaction (quoted from this section, which also has a nice figure):

The polymerization reaction proceeds by a simple nucleophilic attack
  of the 3'OH of the primer on the α-phosphate of the incoming dNTP
  followed by the elimination of pyrophosphate [...] The reaction uses a
  "two metal ion" mechanism in which metal ion A activates the 3'OH as a
  metal hydroxide while both metals A and B stabilizes the developing
  negative charge on the α-phosphate in the transition state.

The metal ions are Magnesium (Mg$^{2+}$) and are properly positioned by the enzyme structure and some additional amino acid side chains also help with the activation of the reaction.

Apologia
The answer given by @Nicolai is essentially correct (and I have upvoted it). However I feel that the question embodies certain mistaken assumptions that should be challenged so that naïve readers of the question are not misled in to accepting them. (I refer to these below as ‘problems’.) I also feel that illustrations — not included in the answer provided by  @Nicolai — are needed in this respect.)
Supporting authority
I have used a 2016 paper in Science by Gao and Wang as my authority, quoting from it and reproducing part of one of its figures for those who have not library access to this journal. The authors actually propound a ‘three-metal ion’ mechanism, rather than the ‘two-metal ion’ mechanism mentioned by @Nicolai. This, however does not affect the basic points I am making, although it serves to illustrate that the details of the enzyme mechanism are of a complexity that is unsuitable for teaching at an introductory level.
Here are two key frames from Fig. 1 of that paper:

Problem 1

“I'm assuming that DNA polymerase is taking advantage of the released phosphates from ATP (and the appropriate forms of GTP, CTP, TTP) to become activated?”

An enzyme is not ‘activated’ by the products of the reaction it catalyses. The binding of the substrate may result in a conformation change that results in more favourable state for catalysis — and which might be referred to as ‘activation’‡ in a discussion of that topic; but the use of that word can only confuse at the level at which the current question is asked. This is because one of the key concepts in enzyme catalysis is ‘activation energy’ — the energy required to achieve the transition state. Activation energy refers to the activation of the reactants — not the enzyme. To quote from the paper:

Enzymes increase the rate of chemical reactions, which is thought to occur by a reduction in the activation energy required to reach the transition state (Fig. 1A)

Chemical reactions which result in a decrease in (Gibbs) Free Energy (the ‘Energy’ axis in Fig. 1A) are thermodynamically favourable. They occur slowly because they proceed through a transition state of higher energy. The role of an enzyme catalyst is to lower the energy to get to that transition state (the activation energy). As the figure shows, this reaction is thermodynamically favourable. The released pyrophosphate has no function, except to be hydrolysed by pyrophosphatases to prevent the polymerization being reversed.
Problem 2
It is unclear what the arrow at the left of the figure in the question (from the α-phosphate of the dNTP to the primer OH) is meant to represent†. Normally one would assume that this would be an electron, however here this does not make sense. As @Nicolai says

“…reaction proceeds by a simple nucleophilic attack of the 3'OH of the primer on the α-phosphate of the incoming dNTP”

i.e. the arrow should be from the oxygen electrons of the OH to the nucleophilic phosphate. This is shown in Fig. 1B (where the nascent DNA chain is on the left and the dNTP on the right). The latter figure actually shows the transition state, which allows one to see in a general way how this could be of lower energy than for the uncatalysed non-enzymic reaction. It is stabilized by the two metal ions (Mg2+), which themselves are held in the appropriate position by acidic side-chains at the active site of the enzyme.
Footnotes
‡As @user1136 points out, the expression ‘enzyme activation’ is also used to describe action of positive allosteric effectors — small molecules that increase the activity of the active site by a structural change initiated by their binding at a site distal from the active site — the allosteric site. This is a further potential cause of confusion as it has no relevance here.
†In a comment, the poster writes “The arrow in the… picture… represents conceptual movement of molecules and not ‘real-world’ chemical interactions”. If this is what was intended (I am not familiar with the source), in my opinion the authors should have used a different style of arrow (e.g. a wider one, ➡ rather than ➛, and not drawn it from the phosphate to the OH. It betrays a lack of either knowledge or concern for chemical conventions, and is particularly misleading for the student who wishes to understand biology at a chemical level. I find it inexcusable in a publisher with a reputation like that of Benjamin.

My plan is actually not to teach at as advanced level as you describe. My hope is (as a forest ecologist) to better understand the true molecular/biochemical workings of this process so that I -- being then more properly informed -- could simplify the material in such a way that I wasn't actually perpetuating/teaching pseudo-truths. Thanks for providing some clarifications.

@theforestecologist OK. I'll remove my last para.

The image that you mention under "Error 2" is from Starr et al.'s (2013) textbook "Biology: The Unity & Diversity of Life." Being an introductory biology textbook, the image is not trying to depict movement of atoms or subatomic particles. Rather, the arrow you've criticized is simply meant to be conceptual: it shows that the incoming tri-phosphate nucleotide bonds to the 3' hydroxyl group of the existing nucleic acid backbone.

I've updated the picture to be slightly clearer. There's still an arrow that you'd likely consider dubious for the same reasons mentioned in your post. The arrow in the new picture still represents conceptual movement of molecules and not "real-world" chemical interactions. However, the picture best represents my conceptual understanding of the process in question, and as such, I need to keep such a "simplified" (conceptual) image. The whole point of my question was to get a more detailed biochemical/molecular response from others like yourself more experienced in this branch of biology.

@theforestecologist — I question your arguments for retaining the illustration, but at least it allows me to address this sort of misleading content in biology texts. I have commented on it at more length in a footnote. If I had bought a copy of the text I would have pointed out the error either on the publisher's site or that of Amazon or whoever sold it. Text books are written by mortals like me. I can make mistakes, and other authors can and do. Good publishers put major texts out for critical review, but reviewers can only spot errors in areas of their own expertise.

I have edited my answer, as mentioned in other comments, but also replaced "error" by "problem". I suspect that that may have been poor psychology. (Must remember to go round the lab and replace all "poison" labels by "substance the non-toxicity of which cannot be guaranteed".)

@user1136 — I have added a footnote about the use of the term in relation to positive allosteric effectors.


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Red Blood Cell Size Vs White Blood Cell Size
I have just found out that white blood cells are larger than red blood cells and now I'm confused due to something I learnt in class. Basically, I was taught that there were spaces between the endothelial cells lining the capillary and these spaces allow white blood cells to escape and enter infected tissues to help clear out the infection. Why don't the red blood cells escape then if they are smaller than white blood cells they should fit through the spaces as well right?

there are several types of white blood cells (at least 4) and they vary greatly in size from type to type.
white blood cells are not rigid, they can squeeze through very small openings. it always buts me in mind of watching a octopus squeeze into a bottle.

So are red blood cells rigid and thats why they can't go through the small spaces between the cells? Also what happens to the white blood cells once they get to the infection? Are they broken down or do they manage to enter the capillary again?

they are more rigid, but more specifically lack the mechanism that actually squeezes the cell through, it is not a passive process, the white blood cells is physically pushing itself through the gap similar to how an amoeba moves. The last question would be a great seperate question.

I should point out that RBC precursors do need to extravasate through bone marrow endothelium to end up in the blood to begin with, but if you look at reticulocyte morphology, for example, there's a big difference compared to a terminally differentiated RBC.

Thank you for your comment CKM but I have no clue what your talking about lol. Your too clever for me :) Can you explain what you said in an easier way please? If not it is okay but I'm only in my first year of biology yet and so I don't know much other than the basics.


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White blood cells after dealing with an infection
I just have a quick question. If there was an infection of a tissue within the body, white blood cells would leave the capillaries around the tissue and enter the tissues to help cure the infection. How would these cells leave the tissue after that? Would the white blood cells be broken down or would they manage to find their way back into the capillary that they came from?

White blood cells, especially neutrophils, rapidly leave the blood and migrate in tissues toward infections (or other forms of stimulations). Many of them do die at the location of an infection, but they can also migrate back. The simplest route for this is to follow lymph flow. Lymphatic fluid is picked up by lymphatic vessels, which work in parallel to blood vessels, and from there can move back into blood. Just as an example of migration through lymphatics

Thus, we provide in vivo evidence that neutrophils, like DCs or inflammatory monocytes, migrate via afferent lymphatics to lymphoid tissue and can shuttle live microorganisms.

--Neutrophils rapidly migrate via lymphatics after Mycobacterium bovis BCG intradermal vaccination and shuttle live bacilli to the draining lymph nodes


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How does the OD correlate with the number of algae cells?
My research team and I are using a spectrometer to measure the OD of an algae sample. We are trying to answer the question "Is there a correlation between OD and the number of algae cells?"
What should we consider in our experiment? Is this an established technique?

are there any materials from your instructor that could help you? have you tried use google/web search?

No, we only have a spectrometer. Also, Google shows results for bacteria, not algae.

just to be clear: you were told: "here is spectrometer, here's some algae. Go figure how many cells is there, don't ask me anything"?

No. We are doing a research project that we chose by ourselves. We are trying to find a way to measure the amount/ quantity of algae there is. We have a spectrometer but dont know how to correlate that to the number of cells.

Hi there and welcome to Bio.SE. Although this is a weird way to count cells, I can see your line of thinking. If there is more absorbance, there are probably more algae. You'll need to control against the feed you add for the algae, get as close to uniform distribution of algae as possible, and consider that you are measuring algae per volume rather than a simple cell count that you'll presumably be doing at each OD measurement under a microscope for a tiny volume from the solution. If you could provide more details about your experimental setup and aims then you might get a better answer.

We are trying to find the effect of pH on algae growth. Along the way, we are going to measure the growth with a spectrometer. We need to find a correlation to prove that the correlation is linear, not quadratic or something else.

As with bacterial cells, number of cell and OD are correlated. I am not a specialist, but it seems that you can use microscope to visually count number of cells, then correlate it with optical density of the solution you have. This will allow you to first establish how many cell correspond to 1 unit of OD, then use OD to estimate number of cells quicker than by counting.
Just a few details: counting of cell number is done by dropping given volume of culture on a special slide with grid, then manual counting using microscope.
If we assume that 100 cells/mL (or whatever) solution gives you OD of 1, then OD of 2 will correspond to 1000cells/mL concentration. That us due to logarithmic relationship between OD and light absorption by the cell culture.

What do you mean by 1 unit of OD? Also, how would we count the amount of cells in a liquid.... take a sample?

@AProNoob added some details

Thanks so much! Wait, so the correlation is logarithmic for all cultures?!


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What bug is this? I found several in my flat and I have no idea

what kind of insect  is this? is it a moth larvea or a carpet bug?

Hello and welcome to Bio.SE! Take the tour to learn about the site and earn yourself your first badge. Also, adding the time and location where you found the insect is fundamental for its recognition!

Size as well as location are almost always needed for identification.  A clear picture would also be useful.

Location is almost never needed for insects, because insects, especially larvae, cannot be identified except to family level, and most families are cosmopolitan.

Possible duplicate of Bug Identification: Is this small tubular, black bug a bed bug?

Possible duplicate of What kind of insect can this be? This appears to be just a shell after and insect went through a metamorphosis process

Related: What kind of insect can this be?..., Can anyone help confirm this tiny insect larvae?, Bug Identification: Is this small tubular, black bug...,
How to protect my mounted insect..., What is the name of the critter..., Varied Carpet Beetle Larvae, What small insect is this?

That is the larva of a carpet or skin beetle, family Dermestidae.https://en.wikipedia.org/wiki/Dermestidae
These eat dried flesh, skin, and other dried organic matter. They are the bane of entomologists because they eat insect collections. They are used by bone-collectors to clean skeletons, and are the last insects to arrive at a corpse.


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Scientific name of a lizard's reproductive system
I need to find the scientific (latin) names of the reproductive organs of female and male lizards. So far the only result I've got is that male lizards have hemipenes inverso, but nothing on the female part.
Thanks for the help!

i'd recommend wiki and google images for that.


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What is the evolutionary advantage of getting hard nipples when being aroused? Why can they even be stimulated sexually?
I try to understand the evolutionary advantages of the body reactions of nipples and penises/vaginas. I'm confused, because I can explain the evolutionary advantage in a logical & consistent way for penises/vaginas, but not for nipples.
arousal causes stiffness
Penises are getting hard when aroused. I can make sense of that - it is evolutionary advantageous, because sperm is more likely to reach the uterus; therefore the likeliness to get pregnant is higher; therefore providing an evolutionary advantage.
But I can not make sense of nippels getting hard. I don't see any advantage that could provide. I mean, breast feeding causes stiffness through stimulation; but that is not sexual, I guess? I guess, breast feeding woman don't experience arousal because of the breast feeding?
sexual stimulation
Furthermore, why does nipple stimulation even cause arousal? I mean, why does it cause evolutionary advantages that we feel arousal when they are stimulated? Again, I can understand this part for penises/vaginas.

Are you talking about female body only, or male body as well? :)


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Can trichoptera and lepidoptera be distinguished with the naked eye?
Are there any tell-tale signs which one could use to distinguish adult trichoptera from lepidoptera? To me, trichoptera just look like moths:

One method would presumably be to touch its wings and see if scales come off, but what if we assume we don't want to catch it?

The etymology of the names will help you there: trichoptera means "hairy wings", whereas lepidoptera means "scaly wings".
If you can get a close shot (maybe with a powerful tele lens) of any possible trichoptera or lepidoptera, you can tell that it either has hairs or scales on its wings, without having to touch its wings.
Examples:

Note the hair visible above the wings. Taken from https://www.inaturalist.org/observations/18660283
Now, there are lepidoptera species that also seem to have hairy wings, such as the tussock moth:

Note the hair as well. However, the shape of the antennae would be a dead give-away: as far as I know, trichoptera shouldn't have feather-like antennae. Furthermore, the wings still have noticeable scales, besides the hair. Taken from https://www.inaturalist.org/observations/18652111
Other lepidoptera species may also seem to lack scales, such as the Syntomoides imaon:

Parts of the wings of the Syntomoides imaon are transparent. However, anywhere that has scales should exhibit some kind of iridescence. You can use your phone's flashlight and try to illuminate the insect from different angles, and you should notice some iridescence. Trichoptera wings, in contrast, should just reflect the light flatly, due to the lack of scales. Taken from https://www.inaturalist.org/observations/18652111
Also, (most) butterflies and moths have a proboscis (the "straw" that can coil up, used to suck nectar). That's usually easy to spot if you can look at the head from the side. Caddisflies don't have that. Instead, caddisflies have mandibles (used to chew through their pupal case as they emerge as adults).
I did mention using a tele lens at the beginning of this answer. Of course, that's not "naked eye" like you asked. The point is that you begin by using a tele lens. As you see more caddisflies vs moth/butterflies, you'll build up a sense of the cues to look at. And at some point you may be able to distinguish them with your naked eye (depending on how close you can get your face to the insect and how good your eyesight is).

This answer would be much stronger with a citation or link supporting your claims, as well as inclusion of a picture(s) that demonstrate the difference for the OP. Please consider revising to include a bit more detail. Thanks!


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Blood pressure in the blood vessels
Why do the capillaries have a lower blood pressure than the arteries even though the capillaries lumen is much narrower. Wouldn't the narrowness of the blood vessel increase the pressure? Also the arterioles have an even larger lumen than the arteries so shouldn't the capillaries have a larger blood pressure than them as well?

Answer: You are right that if you had one big pipe that was getting progressively narrower, the pressure in that pipe would increase. In the vascular system, you have one big pipe emptying into exponentially more small pipes. The total lumenal diameter of the small pipes is actually greater than the single big pipe.
Even though each individual capillary has a smaller lumenal diameter than each artery, the sum lumenal diameter of all of the capillaries is much greater. This is because there are way more capillaries than there are arteries.
More detail: The following image plots total cross-sectional area and pressure in the pipe against the level of the circulatory system. The sum cross-sectional area of the vessels is highest in the capillaries, simply because there are so many capillaries. You can see the pressure decreases accordingly.


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Why does M1 RNA together with C5 protein in 100mM Mg(II) fail to cleave tRNA?
Sidney Altman discovered that RNA moeity of RNAse P (M1 RNA) alone is able to perform enzymatic cleavage of ptRNA, which won him the Nobel Prize of Chemistry in 1989.
However, when I read the Nobel Lecture on Bioscience Report, Vol. 10, 1990, the figure on page 325 (the image below) confused me.

I listed the relevant parts of the figure legend as follows:
(R: M1 RNA was added, P: [C5]=2x10^(-8) M, 20P: [C5]=4x10^(-7) M)

Lane 3: R+P,   [Mg(II)]=10  mM.  ptRNA cleaved.
Lane 5: R,     [Mg(II)]=100 mM.  ptRNA cleaved.
Lane 6: R+P,   [Mg(II)]=100 mM.  ptRNA NOT cleaved.
Lane 8: R+20P, [Mg(II)]=100 mM.  ptRNA cleaved.

In Lane 3, RNAse P was formed and was able to catalyze cleavage; Lane 5 showed that M1 RNA with higher concentration of magnesium could function as enzyme.
But how did the addition of C5 protein, compared to Lane 5, inhibit the cleavage of ptRNA, as shown in Lane 6? (Or, how did raising [Mg(II)] to 100 mM compared to Lane 3 inhibit the reaction?)
And how come by increasing the concentration of C5 protein by a factor of 20 compared to Lane 6, M1 RNA was able to function again, as shown in Lane 8?
I would appreciate any kind of help, and sorry for my poor formatting.
Thanks.


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too low extention time for Taq polymerase PCR
I am currently working on my masters degree and have recieved the following question:

"you want to amplify by PCR a gene 1kb long. The Taq Polymerase you have in the lab is able to synthesize 1kb/minute. You make a mistake in programming the PCR machine and set the extension time to 30 seconds instead of 1 minute. what will happen? what do you expect to see on a gel?"

The answer I came up with was that there would be insufficient time for complete replication of the target and therefore only incomplete copies would be made. These strands would show up in a band below 1 kb because the are shorter.
This answer however, was incorrect. I browsed the web but could not find any clear answers on what would happen. anyone knows what happens?

To get amplification of a DNA fragment you need primers to anneal first so that you can extend from. The extension time is designed so that DNA is synthesized from one priming site to the other. Therefore if you have a lower extension time you will make a product that is missing the other priming site. This means that all new template strands can be amplified from one end only and you get linear amplification, not exponential. Therefore there will be too little DNA to visualize on a gel.


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Why is atropine a CNS stimulant, although it blocks the muscarinic receptors in the brain?
I know that atropine is a muscarinic  antagonist, so why does atropine have excitatory actions on the brain while it is blocking muscarinic receptors?

Short answer
Atropine inhibits an inhibitor and hence its effects are excitatory.
Background
According to the wiki page on muscarine M2 receptor:

M2 muscarinic receptors act via a Gi type receptor, which causes a
  decrease in cAMP in the cell, generally leading to inhibitory-type
  effects.

Atropine is an antimuscarinic (anticholinergic) drug.According to the wiki page on atropine:

[R]eactions to atropine include ventricular fibrillation, supraventricular or ventricular tachycardia, dizziness, nausea, blurred vision, loss of balance, dilated pupils, photophobia, dry mouth and potentially extreme confusion, deliriant hallucinations, and excitation especially among the elderly.

So atropine blocks inhibitory muscarinic receptors, and hence causes excitation.

But the brain has M1 receptors which work with all the three Gq, Gs, Gi proteins! (The question has been corrected, pardon.)


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Is this a tick?
My dog has been vomiting today and I recently found this insect/arachnid near his dog bowl. Since vomiting is one of the symptoms of a tick bite, I am concerned that this insect/arachnid is a tick. Unfortunately, since I've crushed it partially, it's hard to tell how many legs it has and what it actually is. Additionally, I'm aware that tick larvae can have 6 legs and the older ticks have 8. Below are some photos next to an Australian $2 coin, which has a 2cm diameter. P.S. This tick should be "native" to Australia.
Do you guys think this is a Tick? Could it be a flea?

This insect is squished beyond recognition for me.

No beetles are of any know threat to dogs. They eat plants and detritus.

No, neither a tick nor a flea. That is a little beetle, and would have nothing to do with your dog's symptoms.