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Why don't all male animals kill a rejecting female?
If a male animal is sure that the female animal will not reproduce with it, wouldn't it be mathematically optimal for the male to kill the female? (To ensure that no alleles of the "overreact-to-rejection" gene in other males can make use of the female as a reproductive resource)
I might be missing something very obvious here, but I can't seem to see why a gene for "kill-rejecting-potential-mate" wouldn't spread through the gene-pool.

I think you are missing many possible explanations. For example, females fight back - combat is risky and would be just as likely to prevent success with future potential mates. Additionally, in many species females are on average stronger or larger than males. It also seems to me that reducing the number of potential mates, even after a rejection, is a poor strategy. While a male is busy battling with the rejecting females, the other males are busy mating with all the others. I also don't know what you mean by "overreact-to-rejection" gene...

Evolution isn't just about an individual passing its genes on, it's about a population surviving and adapting through time. Limiting your numbers does not appear a good survival strategy on the population level. You are possibly eliminating alleles that are, or would be in the future, of selective advantage.

Why do you think all females don't kill males they reject?

Combat is risk. Rejecting female may kill rejected male.. thereby removing gene for male who over react to rejection. Females may move in groups, so injuring one female member may result in all females in herd to reject said male. Combat take time. While rejected male is spending time killing rejecting female. Other males are mating with non rejecting females. Males do produce daughters. Murderous rejected male, may produce murderous rejecting daughters.

I asked moderators to delete this question, but:
1: Everyone seem to assume that I am misogynist. I'm not. In fact, I am glad to see the "outrage" against apparent misogyny 2: @swbarnes2: because male animals often give very little contribution to reproduction. 3: @ bpedit: a gene that result in the death of a whole population would still spread through the gene pool, even if only in the local gene pool before the latter's destruction.

@bedit: This is in fact wrong. Selection does neither work on populations (it works on individual phenotypes and maybe ... maybe on groups with close kin - that is at least debatable) nor does it generally favour survival (and by no means survival of a population), unless survival is necessary for reproduction. It actually is about individuals passing on genes that lead to selected phenotypes.

A "kill-rejecting-potential-mate" gene??? This quite frankly is utterly absurd! I mean come on, please acquaint yourself with the concept of a gene first before broadcasting such theories.

The simple answer is most animals females can fight back. Its similar to the reason male to male fighting often evolves to become more and more ritualized. Fighting is risky, and the closer in size and capabilities the fighters are, the riskier it becomes. Behavior that tends to get you injured for little to no benefit tend not to get passed on. and there is little to no benefit in killing females for a male. Plus a female who is alive can change her mind later, so there is a direct benefit to the male for not harming her.
Now there are animals where a female will be bullied into mating to the point of risking injury or death. Those animals are very rare and have high dimorphism, they have males that are MUCH larger and more dangerous than the females, to the point the female is incapable of being a significant threat to the male. It is most common in animals that express harem polygyny. It also tends to carry the risk of inbreeding.
One horrifying example is hamadryas baboons. Males maintain a harem and threaten any female that even strays too far from the male. They even bite disobedient females.

There's natural selection for males that do what ever they can to stop a female mate they already have from having an affair because if she has an affair, she might produce an offspring that's not his own so they can't get as much food to rear as many of his own offspring. Although killing her makes her unable to have an affair, it's not selected for because she can't produce a kid that is his own either if she's killed. If she deserts him in addition to rejecting him, there's no evolutionary advantage in him killing her because she won't stop him from finding another mate that will produce a kid with him. It would however be an evolutionary advantage for a male to reduce his options and do something to make it so that he will be unable to not kill his mate if she rejects him. Females who did not reject males that reduced their options in that way would be selected for and then in response to that change, males that reduce their options in that way would be selected for. If after that, a mutant male that could make it look like they reduced their options when they didn't arose, it would outcompete the males who actually reduced their options and then females who rejected a male would stop being selected against and maybe it some cases be selected for.

You need to reread the question more carefully.  It is about killing non-receptive females not killing promiscuous ones.


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What do spiders do all day?
I found a question about ants sleeping - Do ants or other insects sleep, and if so why?, but I don't think it really answers my question.
For the question, I'm mostly referring to web-making spiders, say orb webs.

So a spider set up shop inside my house late last year. It built a web high up in the corner and started catching moths and stuff. I know it's been there and it's the same spider because I've watched it grow.
But when the spider isn't catching something, eating or building a web - what is it doing? Just waiting for web vibration?
I imagine if it was outside it would be hiding or trying not to be prey. I also imagine it might be looking for a mate. What I can't figure out is what this spider does all day.
Why would it build a web where no other spiders are and then stay there for months doing nothing?

It is meditating. But the one outside my back door is plotting just when and how to scare me to death by jumping on my head. I can tell by looking deeply into the largest of its four pairs of eyes. Where is @Roland when we need them?

Why don't you think it could be hiding or trying not to be prey indoors? I doubt the spider is quite aware of the barriers your house provides to entry of certain predators, or that it has chosen a place that is less likely to be frequented by its conspecifics. I think what you are describing: building a web and waiting, is essentially the activity of "hunting" for a spider.

@BryanKrause - Indeed, house spiders are just that: house spiders.

@anongoodnurse I thought house spiders didn't have a long enough lifespan for the amount of time it has been here.

They can live about two years if they have food. And they can survive on really tiny things, like drain flies.

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Plasticity between excitatory and inhibitory neurons?
All that I've learned about synaptic plasticity only concern the synapses between excitatory neurons. For example, all pyramidal neurons (excitatory) in the cortex have plastic synapses between them, but as far as I know there are no plastic synapses between pyramidal neurons and their inhibitory interneurons.
So I am curious, are there any plastic synapses between inhibitory and excitatory neurons?

Various forms of plasticity has been reported for inhibitory-excitatory synapses as well. See below figure from [Woodlin et al. 2003].

Holmgren CD, Zilberter Y (2001) Coincident spiking activity induces long-term changes in inhibition of neocortical pyramidal cells. J Neurosci 21: 8270–7
Woodin MA, Ganguly K, Poo MM (2003) Coincident pre- and postsynaptic activity modifies GABAergic synapses by postsynaptic changes in Cl- transporter activity. Neuron 39: 807–20

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Cortical projections from layers 2/3 back to 4?
As all excititory neurons in layer 4 are stellate - they have no apical dendrites that could project to layers 2/3. However, I have seen some diagrams showing axonal projections from layers 2/3 back to 4, but then I see other diagrams that don't show it.
Is there enough evidence to show axon projections from 2/3 to 4? If so why do so many diagrams leave them out?

I've upvoted both Q&A but referencing your question would greatly improve both Q&A

Excitatory neurons in layer 4 are not all stellate in all cortical areas, for example see Smith and Populin, 2001 who show clearly that in auditory cortex most excitatory cells in layer 4 are pyramidal. There are also many cortical areas that have no clear "layer 4" and also do not contain spiny stellate cells.
In general, intracortical circuitry is not fully understood. Although your question shows understanding of this next point, let me highlight it anyways because it is a point that is often forgotten: neither axons nor dendrites are constrained to the layers containing soma. Therefore, it is possible for a cell of "layer A" to contact a cell of "layer B" even if the "layer A" cell has no axons in "layer B" and the cell of "layer B" has no dendrites in "layer A": they could have axons and dendrites in "layer C", for example.
One approach has been taken by some such as Binzegger et al., 2004 is to estimate intralaminar cortical connectivity based on co-occurrence within a given layer of axons and dendrites. This approach is an approximation, of course, because there is no guarantee that axons contact dendrites randomly within a given layer. For example, axons could preferentially contact the dendrites of inhibitory rather than excitatory cells, and this would fundamentally influence the circuit dynamics.
The result from Binzegger et al (their Figure 1 is a fairly clear summary figure, if you want to start there) is that, although there are some predominant patterns of connectivity, there is no pure feed-forward circuit: all of the connections are at least partially reciprocal. For the example you gave, layer 2/3 to layer 4, the number of connections from layer 2/3 to layer 4 is estimated to be about half as many as the number of connections from layer 4 to layer 2/3.

Figure from Binzegger et al, 2004; Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported License
However, it is also possible that these connections preferentially target inhibitory cells rather than excitatory cells in layer 4: see Thomson et al., 2002.
It is likely that the variety in sources/diagrams you are familiar with is simply because people take different approaches to complex systems (and different approaches may be warranted in different situations). Some people choose to highlight the most salient features, perhaps the strongest layer-to-layer connections, in the hope that this produces an understandable, though simplified, model. Other people choose to highlight the vast complexity, emphasizing all of the smaller details that may actually be important.
For an analogy, a chef is likely to just deal with olive oil. They don't care that olive oil is actually a collection of several fatty acids: it's just olive oil to them, and the importance to them is that olive oil is distinct from another vegetable oil. A biochemist, however, might be interested in the specific fatty acids and might point out that those specific fatty acids are found in all sorts of other oils. Neither one is likely to convince the other that they have the better answer for all purposes.
Neither approach is strictly incorrect or better than the other, until better understanding makes one of the approaches obsolete.

References:
Binzegger, T., Douglas, R. J., & Martin, K. A. (2004). A quantitative map of the circuit of cat primary visual cortex. Journal of Neuroscience, 24(39), 8441-8453.
Smith, P. H., & Populin, L. C. (2001). Fundamental differences between the thalamocortical recipient layers of the cat auditory and visual cortices. Journal of Comparative Neurology, 436(4), 508-519.
Thomson, A. M., West, D. C., Wang, Y., & Bannister, A. P. (2002). Synaptic connections and small circuits involving excitatory and inhibitory neurons in layers 2–5 of adult rat and cat neocortex: triple intracellular recordings and biocytin labelling in vitro. Cerebral cortex, 12(9), 936-953.

I really would like to see more diligent users as you here. +1. I hope my bounty has helped in your sustained release of awesome posts :-)


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How does stimulus reach neural threshold?
I understand that when the stimulus into a neuron is greater than the threshold it triggers the action potential. Do all the contributing stimulus have to occur at the same time, or can they occur over time?
If neurons A and B connect to C, and C needs both A & B to activate to reach the threshold; can A fire first, then B - or do they both need to fire simultaneously?
If they can contribute towards the threshold over time then is there a decay that eventually returns the neuron to resting potential?

There is temporal summation of the stimuli. This is modeled in the Hodgkin and Huxley model .
To imagine the whole process, you should know that in the dendrites of the neuron, electric impulses are propagating passively ( the strength of the stimuli is decreasing over distance and time), in the axon the electric impulse is active ( in the form of action potential(AP) ).
Let me explain your second question with the help of mathematics:
Let's assume that T is the threshold value.
Func(x, t) is a function of the stimuli, where the depolarizing effect is decreasing with time and distance:
Func(A, t) > Func(A, t+1)
So after your assumption:
Func(A, 0) + Func(B, 0) = T
If we don't take into account temporal summation, in other words, if we are looking at only just one phase of the time, and A and B stimuli are not simultaneous, and in t=0, then there will be no AP.
Func(A, t1) + Func(B, t2) < T , where t1 != t2
But with temporal summation we can add previous stimuli into the equation. For example:
From the previous asyncronous stimuli, we got our two decreasing depolarizing factors, and over time we got one more stimulus from A, then with temporal summation they CAN produce an AP.
Func(A, t1) + Func(B, t2) + Func(A, 0) >= T,
if Func(A, t1) + Func(B, t2) >= Func(B, 0)
So after a depolarizing effect, the neuron enters into a hyperpolarized state and most of the sodium channels are inactive. This is called the refractory period. This is when, even A and B is applied simultaneously there will be no AP. And after the membrane potential gets back to his resting potential, then the whole process (including the temporospatial summation) starts from the beginning.


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Evolution & Celluar Chemistry
I'm new to this site but had a question on evolution, apologies if some of these questions seem basic but they are from a book i am reading challenging the role of chance in evolution.
Taking the example of Polar bears in the Arctic, how does evolution determine that it was white fur that was a beneficial trait rather than any other colour of fur? Is this a random change in cellular chemistry?
The book argues that there should be more evidence of polar bears of all shapes and sizes but with no evidence, asking "why should the creative factors provide only single options in the polar habitat and let natural selection sit idly by?"

Your question seems to be based on a profound misunderstanding of evolution, and from your quote you seem to be reading a creationist book that is deliberately misleading you; however, your actual question is unclear. Could you rephrase so we know what you're actually asking?

First and most important of all: Evolution neither knows nor determines anything. It happens. And if it is not negatively selected, it will occur.

@Chris I'd hold that last sentence, or clarify what "it" is.

Welcome to Biology.SE. You said The book argues. What book are you talking about?

The book is called "Revelation, Rationality, Knowledge & Truth", it is from a creationist point of view which is why i wanted to get some clarity on some issues. If my question is unclear i apologise and will attempt to ask again. It will probably help if i just quote the passage in question which i am having trouble understanding -

@ZainChawdry You won't learn much about evolution from a creationist. However, you might be interested in debunking creationist fake arguments. I would strongly recommend that you start by reading a science book and then when you know what evolution is you can get back to a creationist book if you want to see if what they say about evolution make any sense.

The reason you're having trouble understanding the passage is that the author is deliberately lying and trying to obfuscate his argument.  He's pretending that his description of evolution is related to the real understanding; it's not. It's as if someone said "Cars have square wheels, which is why they don't perform well on grass-covered interstate highways".  It's impossible to debunk the claim because it's not reality-based; there's nowhere to start.

You raise a good point, and are right to be confused by the book. "why should the creative factors provide only single options in the polar habitat and let natural selection sit idly by?" I literally don't know where to begin to answer this statement. A comparable question is If you squeeze play-doh through a square hole, why aren't there lots of different shapes and sizes of play-doh? Silly, idle physics.

The question is quite unclear but I'll try to say a few words that may help you.
You seem to be considering evolution as an individual that decides what is good and what is not. You seem to be considering the evolution as determing at any time point what will be good for a given species. That sounds very wrong.
Evolution is much more than Natural Selection (NS) but for the purpose of this answer I will talk only about NS. NS is a differential of fitness. Fitness is a function of both the expected reproductive success and expected survival of an individual. The environment is part of what determines the fitness of an individual.
So the question, you might be willing to ask is why is having white fur advantageous for a polar bear. The answer is on this post. In short, polar bear live in a very cold climate and their white fur is actually made of clear tubule which let the sun get through and reach their black skin. If it is unclear for you why dark matter warms up faster than lighter matter, you might want to follow a short physics lecture on light.
I would recommend that you have a look at a very introductory class to evolutionary biology such as Understanding Evolution by UC Berkeley for example. It is pretty short (much shorter than reading the book you're reading and you will learn so much more about evolution).
EDIT
I will not be able to explain you the basics of evolution theory entirely as it would not fit in a single post. So, I am reacting to your first comment but for the follow-up questions, please just have a look at an introductory source of information first and we will all gain lots of time. (No aggressivity here, I just want to avoid spending my day on this single post). Once you've finished an introductory course you are very welcome to ask further questions. Btw, evolutionary biology is a very big field. There are a large number of researchers (me and other users on this website included) who work during their whole to further our understanding of evolutionary processes.

Natural selection must wait for these painstakingly slow changes to provide a large variety of options for it to choose from

This is wrong for two reasons. 1) NS tends to be a relatively fast process for rising the frequency of beneficial mutations. 2) NS does not give options to chose from. It is even the opposite NS remove options to keep only some of them. Mutations create options. In more correct terms, mutation increase the genetic variance while NS (and genetic drift that I haven't talked about yet) remove variation.
A1 allele is a very simple software for students in evolutionary biology that help the to simulate the action of NS and genetic drift on an already polymorphic locus. You might not understand what is meant by "polymorphic locus" but this just mean you need to have a look at an introductory course to evolutionary biology.

if random changes in the cellular chemistry can suddenly alter the colour of hair from black to white, why cannot they change the colour of the hair from black to blue or red or crimson or violet or green, how did cellular chemistry know that what was needed in the arctic climate was only white?

Well, again the hairs aren't really white!
Mutation are random (although this statement can be misleading because there is variation in mutation rate). A mutation is just a "mistake" done during the replication of DNA. An organism does not make mutations to achieve a particular goal. It just make mutations. This is why the vast majority of mutations are deleterious (=decrease the fitness of the individual carrying it).
Now, some mutational effect (in terms of phenotype and not fitness) are more likely than others. For example, a polar bear may already produce a number of pigments that it could "easily" use for colouring its hairs. For example, a polar bear already produces dark pigments (such as melanin) and it is reltaively likely for that a single mutation could darken the fur of the polar bear. If having darker fur was beneficial then this mutation would increase in frequency in the population(assuming no genetic drift which is wrong but this is a story for another time). On the other hand, a polar bear does not produce violet pigments (to my knowledge). As a consequence, it would take a much larger number of mutation (each of which aren't necessarily beneficial) for a population of polar to have a light violet fur (and we would need to assume that having a light violet fur is beneficial).

Many thanks for your answer,what do you think of this passage in a creationist book I'm reading-"Natural selection must wait for these painstakingly slow changes to provide a large variety of options for it to choose from. For instance, if random changes in the cellular chemistry can suddenly alter the colour of hair from black to white, why cannot they change the colour of the hair from black to blue or red or crimson or violet or green, how did cellular chemistry know that what was needed in the arctic climate was only white?"

As said in the answer, its actually not white. And, as said by many others, evolution doesn't know anything; its just a matter of chance. Fur color would have also converted to blue/crimson/brown, but since white was more advantageous, so it flourished and took over other colors. Here by colors, I mean the species with that color.

@ZainChawdry If this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered.


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If crocodiles are k-selected, why do they supposedly "not age," as in avoid senescence?
I recently saw a few sources stating that Crocodiles do not biologically age, implying negligible senescence. Basically, a 70 year old crocodile is in the same physical/health condition as a 7 year old crocodile. However, crocodiles are K-selected, meaning that populations are generally close to their carrying capacity. If they do not exhibit natural senescence, isn't that evolutionarily disadvantageous, because the younger crocodiles with more slightly more fit genes will not necessarily replace the older generations, meaning that crocodile populations would adapt to environmental changes significantly slowly. Can someone please explain to me how this lack of senescence can apply for this type of species?

Your premise is almost certainly wrong.  As a rule of thumb, virtually every popular account that claims certain animals don't age is bullshit. Unless you have a peer-reviewed paper that explicitly states the animals doesn't undergo senescence, assume that it does. In this case this paper offers an unconfirmed claim that old crocodiles are senescent.

Comments
You seem to use the term evolutionary advantageous vs disadvantageous for the species rather than for individuals. It is a very common misconception from the general public. You might want to follow an introductory course to evolutionary biology such as Understanding Evolution (UC Berkeley) for example.

younger crocodiles with more slightly more fit genes

"fit genes" does not mean much. Again an introductory course to evolutionary biology should help you there.
Answer
You'd right though that absence of senescence causes longer generation time and therefore lower response to selection pressure (such as those caused by an environmental change). But populations don't evolve in order to maximize the probability of the survival of this population (related to first comment above).
Those that live longer, leave more offspring and therefore long-lived individuals are expected to dominate the population in the long run. The evolution of senescence is not exactly that easy though otherwise no species would show any sign of senescence (see Why does evolution not make our life longer?).

Sorry, I'm a bit confused on two things. Firstly, for the younger generation being fitter, doesn't that generally apply in times of selective pressure? In this case, the slightly more fit individuals will reproduce a bit more and thus, more offspring will carry on those genes.    And also, during selective pressure, more fit individuals will reproduce, so generally the alleles for the more advantageous genes will appear in higher frequencies, causing the population to adapt to environmental stresses.

Yes, you are right, the expected the change in population mean fitness is increasing by the value of the additive genetic variance in the previous generation. Of course, it is only the expectation from a distribution. I removed this small piece of sentence.

The main point is that you seem to think that what is increases the probability of a population to survive should be selected for while this is not what natural selection does.

So as of crocodiles, they have been able to maintain the negligible senescence due to a lack of selective pressures? Otherwise, crocodilian populations would have lower responses to environmental stresses.

It is possible that an eventual quasi-absence of external causes of mortality (such as predation and parasitism) would remove the interaction between age and reproductive success resulting in more efficient elimination of old-age deleterious mutations. I realize I might use concepts you could be unaware of here. I would strongly recommend that you read Why does evolution not make our life longer?, you will like this post!


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Which fish did modern tetrapods descend from?
Did modern tetrapods descend from Tiktaalik or Ichthyostega? While I understand that in terms of all tetrapods, the lineages of Tiktaalik and Ichthyostega both would be included, but I want to know if their lineages have continued to the modern day. Since they also have 10 million years between them, it's possible that both of their lineages have not continued to the modern day. It's also possible that neither of them have continued to the modern day and it was a later fish species altogether whose lineage has continued to this day in the form of currently living tetrapods even though Tiktaalik and Ichthyostega were the first vertebrates on land. I'm especially interested in knowing which fish species have humans descended from. I'd be grateful if anyone is able to shed any sorta light on this.

Your question cannot be answered.
One of the effects of how incomplete the fossil record is, is that it is impossible to say if a species was a member of a direct line or a side branch. we just do not have the resolution in the vast majority of the fossil record to tell. The answer could be both, neither or one or the other and we would not be able to tell. All we can say is it is likely they were closely related to or part of our ancestral line. But the working assumption is always that you have a related sister species and not the ancestor unless you can show extremely good evidence otherwise, (which is so rare you can assume it is impossible in extinct vertebrates).
Tiktaalik and Ichthyostega only give us a rough idea of what our ancestors would have been like. It is impossible to say with any certainty if either was a direct ancestor or merely a sister species to them. This is part of the reason cladograms are constructed the way they are, so that no fossil is ever put on the direct line.
Source.
Source 2
Note: Tiktaalik probably did not live on land, more likely it was a shallow water air breather.
Also whatever species was the ancestor of tetrapods, all living tetrapods would be its descendants. One aspect of population genetics is for a specific individual in an ancestral population, past a certain point in a linage  either every descendant is your descendant or you have no descendants.

You can study the reeources under "stem tetrapod tree" and tetrapod limbs. you can see the relationship in the list of the second image.
The trees suggest that tiktaalik and ichtiostega are not direct ancestors, they are close ones, so modern tetrapods descended from their common ancestors, not from their species.
vertebra:

lower jaw:

front limbs:

Technically they descended both from the tiktaalik and Ichthyostega because Ichthyostega was later, but in the same family and evolutionary line as tiktaalik.

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Of all the tetrapods to have ever lived, some would be descendants of Tiktaalik and some of Ichthyostega, yes. This makes sense. However, I'm especially interested in conclusive works that posit both the lineages having continued to this day. I am not sure if there's any work of that sort, I certainly couldn't find any on my own level, hence, posted this question here. I'm also interested in knowing which of the two happen to be ancestral to human beings. I'll edit the question to reflect these.

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What's the definition of 'natural prey' and 'natural predator'?
I am sure we all see both of these phrases used commonly, but is there a reason as to why the terms 'natural predator' and 'natural prey' are used as opposed to just 'predator' and 'prey'?
Below are two examples of each amongst numerous others from Wikipedia.
The Wikipedia article on Wolverine says

Wolves are thought to be the wolverine's most important natural predator, with the arrival of wolves to a wolverine's territory presumably leading the latter to abandon the area.

The Wikipedia article on Leopard seal says

The only natural predator of leopard seals is the killer whale.

The Wikipedia article on Leopard says

The leopard is primarily threatened by habitat fragmentation and conversion of forest to agriculturally used land, which lead to a declining natural prey base, human–wildlife conflict with livestock herders and high leopard mortality rates.

The Wikipedia article on Reptile says

Snake farming has been troubling for conservation in the past as it can lead to overexploitation of wild snakes and their natural prey to supply the farms.

Are there preys that wouldn't be natural preys to their predatory animal? Are there predators that wouldn't be natural predators to their prey?

Can you cite an example?

@BryanKrause, I have managed to attach a few to the body of the question itself.

whenever you have a question about definition in biology the answer is "it depends." Which is why we need context for the question.

Natural world be used in situations like these for 1 of 2 possible reasons (and potentially both simultaneously):

to indicate ecologies that exist due to the organisms evolving together in that area (vs interactions with non-native species)

to indicate non-human interactions.

Humans have strongly altered the ecologies of many organisms, including through the impacts of introducing non-natives. As our species grew and spread across the globe in the last couple hundred years, we ourselves have acted as the non-native species -- entering ecological communities in which we did not evolve with the local species.
The above context has traditionally been viewed as "non-natural" because it was mediated by human decision-making and technology vs. "nature" undergoing evolution.

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What plant is this? I can't identify

Please help me identify this plant. This was shot in the assam-meghalaya region of india.


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What species of spider is this? Could anyone help

This image was taken in assam, India. The size was around 1cm. Could anyone help identify?

can you add an estimated size? 5 mm? 5 cm?

This is a male Carrhotus sannio (the females are brown/grey). The white dorsal stripe on the cephalothorax is right beneath the outside eye; the upside-down v-marks on the back of the abdomen point to two white lines (sometimes broken) which run parallel to the length.
Gallery of males:
https://inaturalist.ca/taxa/334660-Carrhotus-sannio/browse_photos?quality_grade=any&term_id=9&term_value_id=11

It looks like Adanson House Spider, Hasarius adansoni. From the eyes, it's definitely a salticid, and the reported 8mm size for females is close to the 1cm you estimated for yours. Here's an image from spiderid.com with similar markings:

Pattern of white strips and dots is different in both images. It is definitely Jumping Spider (salticid), but not Hasarius adansoni.


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Stochastic parameters in population growth equations
I'm more of a mathematician than a biologist, so I had a question about an application of the population growth equation to real-life models, and thus would like to ask biologists for their insights. The equation I'm looking at is the following (in reality, I have n-species but it's just an extension of this two dimensional problem):
$$ \frac{dx_1}{dt} =x_1\Big(b_1-a_{11}x_1-a_{12}x_2 \Big) $$
$$ \frac{dx_2}{dt} =x_2\Big(b_2-a_{21}x_1-a_{22}x_2 \Big) $$
where the $b$ are growth parameters, and the $a$'s are all parameters describing interactions among the species (and carrying capacity). The papers I've looked at for stochastic perturbations with these equations have primarily dealt with stochastically perturbing either the $b$ parameters while holding the others constant, or perturbing the $a$ parameters while holding $b$'s constant. However, these papers are written by mathematicians with no biological experience, so the decision on which sets of parameters to perturb are somewhat arbitrarily decided without any biological basis.
For the biologists, can someone suggest some cases for where it would be more biologically reasonable to perturb the growth parameters and some cases were it would make more biological sense to perturb the interacting parameters? I ask because I'm a part of some interdisciplinary neuroscience project which is using equations of this form to study interacting neuron clusters, but since I'm a math person and not a biologist, I am trying to understand reasonable explanations for what stochastic perturbations mean biologically for these parameters.

This is somewhat similar to the https://en.wikipedia.org/wiki/Lotka%E2%80%93Volterra_equations You can probably find related articles here: https://www.google.com/search?q=Lotka+Volterra+equations+perturb , https://scholar.google.com/scholar?q=Lotka%E2%80%93Volterra+equations+perturb Note: I don't know what "perturb" means in this context.

Since you are asking for the biological interpretations about these parameters, it is important to realize that the model you are presenting is a non-dimensionalized version of this model:
$$ \frac{dx_1}{dt} =b_1x_1\Big(1- \Big(\frac{x_1 + \beta_{12}x_2}{K_1} \Big)\Big) $$
$$ \frac{dx_2}{dt} =b_2x_2\Big(1- \Big(\frac{x_2 + \beta_{21}x_1}{K_2} \Big)\Big), $$
which can also be written as:
$$ \frac{dx_1}{dt} =b_1x_1\Big(1- \frac{x_1}{K_1} - \beta_{12}\frac{x_2}{K_1}\Big) $$
$$ \frac{dx_2}{dt} =b_2x_2\Big(1- \frac{x_2}{K_2} - \beta_{21}\frac{x_1}{K_2}\Big). $$
This clearly shows how this competition model is merely the logistic Verhulst model, with an extra term attached. This extra term is simply describing to what extent each individual in "species" 2 is using up the resources of "species" 1 ($K_1$), where $\beta_{12}$ describes this relationship (~proportion of species 2 that is counted as species 1). The parameters in the model formulations above are also more easily interpreted in ecological/biological terms than the $a_{ij}$s in your model.
To go from this latter formulation to yours you substitute:
$$a_{11} = b_1/K_1$$
$$a_{12} = \frac{b_1\beta_{12}}{K_1}$$
$$a_{22} = b_2/K_2$$
$$a_{21} = \frac{b_2\beta_{21}}{K_2}$$
As you can see, this means that the $a_{ij}$s are composites of other parameters, and perturbing $a_{ij}$s could correspond to either $b_i$, $K_i$ or $\beta_{ij}$ being perturbed. It also means that perturbing e.g. $b_1$ in your model while holding $a_{11}$ fixed means that you are actually also perturbing $K_1$ to offset the change in $b_1$ (since $a_{11} = b_1/K_1$), which will introduce a positive temporal correlation between $K_1$ and $b_1$. This is a strong assumption to make. This also means that $a_{ij}$s are not strictly "interaction parameters" as you call them, but they include other aspects as well.
Since realistic cases and scenarios for perturbations may often be expressed in terms of the parametrization I give above (e.g. random fluctuations in population growth rate or carrying capacity), these relationships are essential to keep in mind.

You just have 6 parameters in this model and you can easily perturb each of them individually while holding the others constant. This will let you know the individual effect of different parameters.
To assess the global sensitivity of the system to "environmental" perturbations, what you can do is to a random multivariate sampling of parameters. You will get different combinations of parameter values. Then you can plot the distribution of any metric that you intend to study.
However, if you intend to perturb a single parameter or a few parameters in combination, the choice of which ones to perturb depends on what you intend to study. System can, in general be insensitive to certain parameters. Local sensitivity analysis can be done to study the effect of parameter on the steady state. This you can do by taking a derivative of the expression for steady state with respect to the parameter. For a simple model such as:
$$\frac{dx}{dt}=x(b-ax)$$
local sensitivity of the steady state $x^*=b/a\ $ to $a$ would be $$\frac{dx^*}{da}=-\frac{b}{a^2}$$.
From here you can see that the effect of perturbation of $a$ on $x^*$ would be higher than that of $b$.
However local sensitivity analysis does not tell anything about dynamics and for complicated systems it may be difficult to guess which parameter would have the strongest effect.
For such cases you may do a random sampling and then run a classification/regression algorithm to determine which parameter had the strongest effect on your metric.
Another approach is to guess which parameters are likely to get perturbed in the natural course of events. This, you would know from prior knowledge of the system. If we assume steady environment, then the carrying capacity is not likely to change much. However, for a population of great phenotypic diversity, the growth rate may vary a lot.


text:
Population dynamics ODE with Allee Effects
From reading about Allee effects, it appears that there is a modification of the one-dimensional logistic equation to account for an allee effect given by:
$$\frac{dN(t)}{dt} = rN\left(1-\frac{N}{K} \right)\left(\frac{N}{A}-1\right)$$
Here, $r$ is the species growth rate, $K$ is the carrying capacity, and $A$ is the threshold for the population to not go extinct $(0<A<K)$.
A few questions about this model:
1) What is it in this equation that determines whether or not the allee effect is strong or weak? It seems like the parameter $A$ would determine where the threshold is but not whether or not the effect is strong/weak.
2) I'm interested in an extension to a system of $n$ interacting species. Suppose I have $n$ competing species where each one is subjected to its own allee effect. Is this a suitable modification of the above ODE for $n$ species?
$$\frac{dN_i(t)}{dt} = r_iN_i\left(1-\frac{\sum_{j=1}^n\alpha_{ij}N_j}{K_i} \right)\left(\frac{N_i}{A_i}-1\right)$$
where $1 \leq i \leq n$. In that regard, the first two terms are the usual Competitive Lotka-Volterra model, and the last term accounts for the Allee effect.

First, Allee effects (also positive density dependence) can be modelled in several different ways, and the equation you give is one example. The terms weak and strong Allee effects are in my experience used in a couple of different ways. Most often, strong density dependence is used to denote Allee effects where the per capita population growth rate can become negative, which means that there is a critical point in population size, below which the population will tend towards extinction. Weak Allee effects are then used to describe cases where the population growth rate is negatively affected by low population sizes, but where the per capita population growth rate cannot go below zero (so populations will grow at low population sizes). Remember that in the classic logistic model, per capita population growth rate is maximized when population size is low (limit towards N=0), while it is maximized between N=0 and N=K in models with an Allee effects (in the model includes a concept of carrying capacity).
Using this definition of weak vs strong,  your model has a strong Allee effect, since per capita population growth rate will go below zero at the threshold A (see below). However, sometimes strong/weak is used to denote some sense of relative influence of the Allee effect on population dynamics, for instance if per capita population growth rate at low population sizes is decreased a lot or a little compared to the logistic model, even if both cases would correspond to a weak Allee effect in the first sense.
For comparison, here are two examples of how an Allee effect can be modelled, that shows how the per capita growth rate is affected with an weak Allee effect (see e.g. Boukal & Berec 2002 and Ferreira et al 2012) or a strong Allee effect (your model):
$$\frac{dN(t)}{dt} = \frac{r}{K}N^2\left(1-\frac{N}{K} \right) \tag{weak}\label{}$$
$$\frac{dN(t)}{dt} = rN\left(1-\frac{N}{K} \right)\left(\frac{N}{A}-1\right) \tag{strong}\label{}$$
If per capita population growth rate (dN/dtN) is plotted against population size for these two models, as well as for the standard logistic model, this is what you get:

In these examples, r=0.7, K=100 and A=20. As you can see, there is a big difference between the weak and strong case. The population growth rate (dN/dt) at different N is shown below:

As you can see, if populations using the strong Allee effect are started below A (in this case 20) the populations will decline towards extinction (since dN/dt is negative below A).
The multi-species extension including species interactions that you propose looks ok to me, for that particular formulation of the Allee effect.
Also, for a flexible way to study the Allee effect, you might be interested in this formulation (see Boukal & Berec 2002), which can produce both a strong and a weak behaviour:
$$\frac{dN(t)}{dt} = rN\left(1-\frac{N}{K} \right)\left(\frac{N}{K}-\frac{A}{K} \right)\tag{flex}\label{}$$
This function will produce a weak Allee effect if $A \leq 0$ (very weak if A is far below 0) and a strong effect is $A>0$. The weak model I give above is a special case of this formulation with $A = 0$. Per capita growth of this model is given below, for two values of A (with r = 0.5 for the logistic model and r = 0.38 for the flex models)

As a sidenote, I've also seen cases where negative density dependence at low population sizes is described as an Allee effect (so that Allee effect can be used to denote both positive and negative density dependence at low population sizes), but this is not very common. For a particular species, negative density dependence at low population sizes (in excess of what is found in the standard logistic model) could e.g. be found in situation where predators have a switching behaviour, so that they stop eating the prey when it becomes rare.

This was an absolutely wonderful answer and very well-explained for someone like me who is a math guy with little biology experience. Thank you VERY much!

@Brenton I'm glad you found it useful!


text:
On stochastic Lotka-Volterra predator-prey model
I am currently working (as a mathematician) on some estimations involving an stochastic predator-prey type model in which some of the coefficients have been perturbed by a Brownian Motion yielding to a system of stochastic differential equations.
The basic formulation of this problem can be found for instance in this article.
We have the following model
\begin{equation}\label{0}
    \begin{cases}
    dX(t)=X(t)\left(a-bX(t)-\frac{sY(t)}{\beta+Y(t)}\right)dt\\
    X(0)=x>0,\\
    dY(t)=Y(t)\left(\frac{h X(t)}{\beta+Y(t)}-c-fY(t)\right)dt\\
    Y(0)=y>0.
\end{cases}
\end{equation}
where we use Holling II response function.
In the literature (mostly mathematics literature) the authors propose to perturb the birth rate of the preys $a\mapsto a+\dot{B}_1(t)$ and the mortality rate of predators $c\mapsto c+\dot{B}_2(t)$.
This yields to the following (stochastic) system
\begin{equation}\label{1}
    \begin{cases}
    dX(t)=X(t)\left(a-bX(t)-\frac{sY(t)}{\beta+Y(t)}\right)dt+\sigma_1 X(t)dB_1(t),\\
    X(0)=x>0,\\
    dY(t)=Y(t)\left(\frac{h X(t)}{\beta+Y(t)}-c-fY(t)\right)dt+\sigma_2 Y(t)dB_2(t),\\
    Y(0)=y>0
\end{cases}
\end{equation}
I know nothing about biology but I am concerned about a couple of things regarding this particular formulation:

If we assume that the Brownian motions are perturbing the birth/mortality rates, how can I interpret the fact that this new "perturbed" rates can become negative (due to the effect of the BM). Does it have any sense (in the framework of this particular model) to talk about "negative birth rate" or "negative mortality rate"?
What if the "perturbed" mortality rate goes beyond $100 \%$? Mathematically nothing "wrong" will happen, but what about the interpretation?

Notice that the "noise"  and the model as a whole can be interpreted differently (ignoring the fact that we are actually modelling the dynamics of two species) but my main issue is that if I(together with many authors) am stating that we perturb a certain parameter I believe that we must respect the basic assumptions of the model!
I hope everything's clear and I thank you all in advance, any opinion or suggestion will be welcome!

Have you considered to change how the noise scales with the population sizes? If done properly, this avoids negative population sizes and other unrealistic results and may be more realistic anyway. More specifically, if the noise is bounded by the square root of the abundance (for small abundances), everything should be fine. A typical example for a model that does this is the minimal market model.

To interpret $a$ and $c$ as a birth and mortality rates is somewhat inaccurate, as $a$ and $c$, as written are density-independent rates that grow or shrink populations exponentially. If $a$ were negative, the prey population would shrink and most people would find a problem like that unexciting unless it was, say, a sink population maintained by immigration from another population. This is true of $c$ being negative, where the predator population would grow independent of the prey population. More accurately, $a$ can be interpreted as the difference between birth, $b$, and deaths, $\delta$; i.e., $a = b - \delta$. In this case, depending on the kinds of stochasticity being added to the model, negative $a$ is not just normal, but expected. The same is true for $c$. Ultimately, a perturbations like the white noise in this equation is simultaneously perturbing the difference between birth and death rates, which explains the negative difference.
The value of the rates seem to have the same interpretation if they are constant or are perturbed to an arbitrary magnitude.

I hope this helps!

thank you very much, now it's clear that my understanding about the true meaning of the parameters was actually wrong.  In case you care I leave you the link to the preprint of the article I mentioned in the question https://arxiv.org/abs/2009.14516

You're welcome. It seems to be inconsequential to your work and tends to be prevalent in the mathematical literature, so it's not a big deal. The work looks interesting and I will study it later. Since you are working in 2D, I also wanted to pass along a method that is of growing interest to find the quasi-potential of the system to study stability and first-passage time: Nolting and Abbott 2015. (The supplemental material is where all the math is hidden.)

Ey Chris thanks for the reference, the approach seems very interesting and uses some techniques that I've never seen! I'll be reading it in detail since my idea was that of further studying the two dimensional case!


text:
What insect is this? I spotted it on a wall in a bedroom

This is the closest distance & the best photo resolution I could get from my handphone.
I discovered it on a wall in my bedroom.

Could anyone identify what insect is it?
Why the insect is in the bedroom?
How do I prevent this insect from staying in the house?

Thank you

Welcome to Biology.SE. Identifications questions should include: 1) one or more clear closeup photos of the organism (photos from multiple angles if possible); 2) the location (e.g. country and region — the more specific the better) where you observed this organism; and 3) an estimate of the size of the organism. Please [edit] your post to include this essential information after checking to see whether a similar question has already been answered. ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site.

"Why [is] the insect... in the bedroom?" sounds a lot like "Why did the chicken cross the road?"


text:
Why are eggs "egg" shaped?
Is there a reason as to why chickens lay "egg" shaped eggs, as opposed to spherically shaped eggs (or a random shape)?
For extra points:

why do plant seeds often come in this same "egg" shape (e.g. avocado
seeds), as opposed to a sphere?  Is it a coincidence that avocado
seeds and eggs are the same shape?

There is variance in egg shape; sea-birds often use a more pear or conical shaped egg to prevent it from rolling off the cliff (where they nest) if it is disturbed. Some reptiles lay very spherical eggs (some turtles) whereas some reptiles lay very elongated ones (see black pine snake eggs).
I imagine that we don't see square eggs because they would be difficult to shape and difficult to lay. Shape may also influence strength.
Google your question (like I did after writing the above) and it will come up with this article which pretty much says what I just did. Here are some of the author's key points...

"If eggs were rectangular little boxes, they would be very strong on the corners, but very weak in the middle of the straight walls."
"The strongest shape of all is a ball, or sphere. But if you were to push or gently nudge a spherical egg, it would roll away downhill, never to be seen again."
"So one reason that eggs have an asymmetric tapered oval shape is that if you nudge them, they'll come back to you. They'll sweep out a circle around the pointed end, and come to a stop with the pointed end facing uphill. In fact, the eggs of birds that have their nests on cliffs are more oval than the eggs of birds that nest on the ground. This means the 'more-oval' eggs of these cliff-nesting birds will roll in a very tight little circle, and be less likely to roll out of the nest — and off the cliff."
"Another reason for eggs to be egg-shaped is that they fit together quite snugly in the nest, with only small air spaces between them. "
"Yet another reason that eggs are tapered is so that they can get pushed out of the hen."

An interesting study on egg shape: http://vis.sciencemag.org/eggs/

Wasn’t it Ken Dodd who said the ohh-argh bird laid square eggs?? :)


text:
Metrics or operations on genome sequences in human genomic research?
Edit distance may be an important metric for measuring the similarity of two genome sequences.  For example, if A = GCAATT and B= CGAATA, then the edit distance of A and B is 3. Such a metric is intuitive and may be useful in comparing the similarity of two sequences.
I wonder is there any more complex or advanced metrics used in human genomic research?

The question of how similar two DNA or protein sequences are, is one of the most important problems in bioinformatics. While there is no definitive answer Bayseian statistics are often used to group sequences. There is a good explanation of the theory on this wikipedia page.
Alternatively one of the most commonly used programs to find similar sequences is BLAST. It is getting a little bit dated but you can find an overview on the statistics used by this program on this page
But there are many other methods out there.


text:
Are any species of life now increasing besides humans?
I see how many species are growing extinct, but what species (excluding humans) are increasing in number?

Chickens. Dogs probably. Lots of others. Even some populations of Tigers are increasing in number thanks to conservation efforts. The question is too big to answer completely. If you have a species in mind then I'd as about that instead.

Yes, many are, especially ones associated with humans and human-generated structures and conditions (e.g., trash, global warming, water nitrification). Some hitchike on subjects of human commerce (e.g., potted plants, tires) and we tend to call them called "invasive species."
Some prominent examples in North America are the European starling, rock dove, house sparrow, domesticated cat, wild horse (mustang), tumbleweed, kudzu, many eucalyptus species, purple loosestrife, garlic mustard, zebra mussel, Argentine ant, fire ant, Japanese beetle, Asian long-horn beetle, Phytophora infestans, etc. One of my favorite examples, and a rather odd one, is the nine-banded armadillo.

(source: sfsu.edu)
Some of these species are increasing in abundance at the cost of other species, increasing the pace of extinction.
http://www.nature.nps.gov/biology/invasivespecies/

You might want to find a slightly more updated graphic, seeing as the 1982 territories are projected. Try Wikipedia.

Sure, but I will not find one this beautiful. Also, the projections held very well.


text:
Is DNA sequencing coverage a function of sample purity?
How is coverage affected by the purity of a sample? And can coverage for a sample be affected by other things, like the library preparation or manner in which the sample was stored?

Coverage is basically affected because of concentration of the strands in the library. It can be affected at any of the several steps of DNA isolation, library preparation and sequencing.

So factors which go into coverage in short-read sequencing (and Sanger sequencing).

Depth is the obvious one. All else being equal you get a bang-on Poisson distribution of coverage over a genome, which is why more sequencing = more coverage.
The human genome and transcriptome is not all equal. Illumina sequencing is ultimately (most protocols) dependent on PCR amplification which means that any factors which influence PCR-amplification ability will also effect sequencing depth. The two obvious ones in this respect are: 1) Regions of extreme GC content and 2) Regions containing secondary structures (RNA mainly).
Alignment is the next major source of error for regions being 'dropped off' depending on how your aligner deals with multi-mapping reads. Some genomes have very young transposable elements which are highly similar to one another and very abundant. For most aligners that means that you can get either huge coverage or really small coverage depending on how the genome is assembled.
For low-input sequencing techniques you get major sources of DNA/RNA contamination from the enzymes, reagents and preparation of the samples. This can largely be minimized by having 'clean' samples and using large amounts of input DNA/RNA.

Depending on the sequences you're studying read-depth can be the only factor you consider or if you have difficult regions or specific questions you can deal with a whole swath of problems.
So in answer to your question: yes DNA quality will directly effect coverage. Sometimes you can 'just sequence more' to get over this problem, sometimes you need to go back to the drawing board.

The largest contributor to sequencing coverage (on a Hiseq, I assume) is how many reads you get, which mostly depends on what percentage of a flow cell you give it.  Obviously the rest that you mentioned contributes, and purity might be a big issue if you are looking for a subset of cells you were trying to isolate out of a larger pool, but the easiest way to get more coverage is to hog more real estate on the flow cell.

I don't understand what you mean by flow cell percentage - would you please briefly elaborate?

If you are not talking about short read technology, then it's more applicable.  Obviously, the most direct thing contributing to coverage is how many reads you have.  More reads, more coverage.


text:
Link between hypoglycemic events in Type 1 diabetics and clinical anxiety?
I recognize that the scientific community is aware that the chemical stress pathway is mediated by glucocorticoids. The pathway response initializes as a result of some sort of stress (potentially chemical, such as low glucose) and the hypothalamus secretes corticotropin-releasing hormone which binds to targets on the pituitary gland. This causes the release of adrenocorticotropin-releasing hormone, which binds to targets on the adrenal cortex and promotes the production of cortisol.
In the event of hypoglycemic stress, cortisol concentrations rise everywhere in the body as a result of this stress signaling. For Type 1 diabetics specifically, hypoglycemia is a common side-effect of treatment.
I also recognize that the anxiety response is largely mediated by amygdalae activity, and the amygdalae are known to have receptors for cortisol (they are the ‘fear’ center, after all). From my research, the morphology of dendrites in this brain structure as well as other centers for mood/emotion are shifted into less functional patterns as a consequence of chronic exposure to glucocorticoids such as cortisol (Krugers 2010). Additionally, glucocorticoids cause serotoninergic receptors to become less sensitive to activation (van Riel 2003).
So my questions are:
if hypofunctioning of serotonergic receptors in the Raphe Nucleus leads to excess firing of hippocampal and amygdalae neurons, which is believed to be one of the primary mechanism through which anxiety manifests itself, why hasn't chronically high levels of cortisol, as a result of hypoglycemia, been implicated more in anxiety disorders in Type 1 diabetics? Is there a link to clinical depression from here?
SSRIs are consistently used to treat anxiety in the short term, but for diabetics, the crux of the issue seems to be the chronic exposure to high levels of cortisol. Has anyone studied or seen this in their practices/research?
Sources:
Krugers 2010
http://www.ncbi.nlm.nih.gov/pubmed/20820185
van Riel 2003
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059694/


text:
What is the scientific opinion on plus lens therapy?
Plus lens therapy is the theory that most myopia is environmentally triggered and that conventional corrective minus lenses increase nearsightedness over time. Thus the hypothesis that applying plus lenses for nearsightedness will invert the environmental pressures and halt or reverse existing myopia.
What is the scientific majority and minority opinion on plus lens therapy?

Are there any sources on this theory that are non-commercial?

@Chris I've found a variety of sources of differing levels of empirical induction on plus-lens but as yet no clear conclusions from scientists; as least in the limited places I've looked (I'm not a biologist). Since the therapy only requires $10 plus lens, commercial incentives are limited.

Personal anecdotal evidence: After a year of +1 diopter lens, my permanent eyesight has improved somewhat (was only mild myopia to begin with) in a 8 - 12 hour x 7 day a week computer environment; where I've worn lenses about half the time. As plus lens are only a partial replication of natural long distance, I suspect you could run the risk of strabismus if you undercorrect too much at short distances relative to your level of myopia. Hasn't happened to me, but then I no longer get a decent blur point at +1 and will probably need to increase to +1.5 to progress closer to 20:20 or higher.

Plus lens therapy can indeed reverse myopia, but it does take time. Your eyes did not develop myopia in a few days.
The eye represents its environment. Fitting chicks, monkeys etc. with minus lenses always INCREASED the amount of myopia, while plus lenses always reduced myopia and resulted in hyperopia (lens compensation).
Putting monkeys in a confined environment showed a myopic shift. Monkeys in an open
environment showed a refractive state about +1.00 diopters.
IMPORTANT: As I have said: Unfortunately, it does take time! Do not expect results after 1 week of plus lens therapy. That is why so many people give up and think that myopia is irreversible. You also do not build muscles after 1 week.
Kind regards.
EDIT:
Optical defocus and effects in HUMANS: http://www.ncbi.nlm.nih.gov/pubmed/20592235
Defocus on chicks: http://www.iovs.org/content/44/7/2818.full
Monkeys in a confined environment: http://www.iovs.org/content/2/6/571.short

Welcome to Bio SE. It is recommended to provide some references- specially for some of the statements in your answer. For example, could you cite the research done in monkeys? Or any other research supporting that plus lens reverse myopia?

The human eye is dynamic and always represents its visual environment. Thus, why was myopia so rare in early mankind, but now so present?
It can not be only caused by genetics. The worst thing you could do is wearing your full minus lens prescription while doing near work. When you think of how your myopia initially started (a lot of near work) and then you wear your minus (unfortunately, often over-prescribed), you are in your "initial" state again. And the cycle repeats itself - over and over again.
By reversing myopia, you must also consider prevention. When you do a lot of near work (long-term), wear plus lens to protect your eyes. It makes your eyes as if they are looking in the distance and thus relaxing your eyes effectively.
Try the following: Measure your Snellen score, then do near work for 3 hours or so and then check your Snellen again. You will see your sight will get worse (in this case temporarily). If you continue, your eyes will adapt and become myopic.
Unfortunately, plus lens therapy is not mainstream. Often people say "it does not help" or "it causes cataracts" and so forth. But therapy needs to be applied over a long-timeframe. Consider it as a "long-term diet".

Can you support your assertions with any decent studies?

Welcome to biology stack exchange. We usually ask for answers to provide some citation to support their conclusions, and I can't find the references you say you added in your first sentence. I would also suggest you change the style of the answer, the capitol letters and bold text makes the answer appear confrontational and the overall tone of the answer appears very opinion based.


text:
Why are compost worms sensitive to light?
I read that compost worms dislike light. But I'd say they don't have eyes and I couldn't imagine their skin is sensitive to light in general, is it? And if so, then why?

Making a quick guess I would say that Sunlight would dry them out fairly quickly as they do not have the dead layer of keratinized cells on their surface that protects them as mammals do. Also UV light will damage their DNA pretty rapidly, again for similar reasons, so keeping in the dark and having a photosensitive response to sunlight would likely have been an evolutionarily advantageous strategy for the niche they inhabit.

And yes, cells, even unicellular organism, can be sensitive to light and can move as a result of those sensations. Aquatic Microorganisms will often adjust the depth they are at in water as a result of the presence or absence of light. Remember that a photon will impart its energy on electrons in the cell and excited electrons can cause chemical reactions to take place and these reactions can stimulate the organism to move.

It will sounds counter-intuitive you but earthworms do sense light with their skin. They don't have eyes but they have specialized nerve ending equipped with photoreceptor cells. They are all over skin but concentrated towards first segment of worm. Prostomiun are main light sensing organ in worms. Following image shows their position in first segment of earthworm. (Image source: cronodon.com).

Closer look of above image taken from same website,

Structure of photoreceptors
Earthworm have microvillar photoreceptors like insects (Rohlich et al 1970). Detailed structure is discovered long back.

There is not much information about phototrasnduction in worms but it is well characterized in it's close relative C. elegans (Ward et al 2007).
Now coming to why part, you might wonder if they are spending most of time buried why do they need photoreceptors ? @AMR has guessed it correctly. They use this as protective system. Photoreceptors helps them providing information about how near they are to surface because UV radiation will harm them or probably kill. If there is higher light sensing, they go back to darker regions. You can find similar information from UMICH press release.


text:
A plant in my aquarium seems to be growing small plants under its leaves, what's going on?
In my aquarium I have this plant. I think it's a kind of swordplant. I've loosely attached it to a large piece of driftwood in the hope that it will grow itself on there, I saw that they had done the same in the petstore.
Now recently other plants have started to grow from under its leaves. I've tried to take a picture of it, these are the biggest ones but there are smaller ones on other leaves:
The plant seems to be doing pretty well, I added some iron and fertiliser to the water. The aquarium is positioned so that it catches a bit of direct sunlight late in the day and tons of indirect sunlight almost all day. It also houses shrimps and two apple snails.
My question: What are these small leaves? Is the plant procreating or does are these some kind of parasitical plants of another species?

From what I see ,it does look like some kind of Echinodorus ( Amazon sword). They do propagate by stems with new plants. They prefer to have roots in substrate.

Yeah I agree it looks like some sort of Amazon Sword, but I also know that grows stems with plants and that's not what I see here, so I'm still wondering what these are.

Java fern has new little plants that start from the leaves but  the photo does not show enough for identification. I have a bunch of java fern and it does not need substrate.

I looked up some more pictures of Java Fern propagating, that is for sure what this is, thanks! Crazy, I never knew this. Will try to get them to grow into mature plants:)


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What happens when the brain is no longer capable of co-ordinating or regulating the heart and breathing rates?
Does the heart no longer function? Does it go into ventricular fibrillation?
What happens?

It's considered a requisite on biology.se that at least some of your reading is presented with your question. [What caused the heart to beat? Why would the heart fibrillate? Etc.] Otherwise it will be closed as homework. The site tour and the help center  provide guidance on how to use this site. Please take a few minutes to read about the kind of questions which are on topic here.

I think this answer needs specification. Total collapse of vital functions by, eg, destruction of the brainstem centers controlling breathing will lead to death. Suppression of these centers by opiates may lead to reduced cardiac and pulmonary function, but not death.  Please specify your question.

@ChrisStronks I'm sorry but I don't see what to specify?

A specific medical condition, or theoretical situation would help, but @CRags has answered already.

Damage to the brainstem - the part of the brain responsible for controlling breathing and the heart - has different effects on the heart and the lungs.
Every heartbeat is not directed by the brain. Instead, the brain has a "throttle" to the heart, by which it can regulate the heart rate up and down, but the actual heartbeat is initiated by special cells in the heart, called pacemaker cells. In the absence of signals from the brainstem, the heart will continue pumping; this is (one of the reasons) why people who need ventilators to breath for them do not also need their heart pumped for them.
Breathing, however, is directly controlled by the brain. Without signals from the brain, breathing will stop completely (the technical term is "respiratory arrest", but that literally just means "breathing-stuff stopped-ness"). Survival time without breathing depends on a number of factors, but at room temperature, without medical intervention (ie. rescue breaths or a ventilator) and barring any special circumstances, is only a few minutes. Permanent brain damage sets in a few minutes later, even if the person can be resuscitated.
Of course, without any breathing, the heart will stop beating due to a lack of oxygen before long. The general progression will be from sinus ("normal") rhythm, to ventricular tachycardia, to ventricular fibrillation, to asystole ("flatlining").

The heart beats are initiated by the pacemaker cells which are located in the heart itself. So absence of neural input will not affect heart function by much. Though heart can function without neural input, it will not be able to respond to stimuli. The human heart rate is regulated beat by beat through the vagus nerve. This would be lost. The sympathetic system would be able to influence heart rate through the adrenal gland. But even this is delayed. Plus till the levels of noradrenaline falls to normal heart rate will be high.
The contractility control also will be lost pretty much.
The respiratory centers are located in the medulla and in the absence  of brain stem outflow the person will be under respiratory arrest which is a medical emergency.

Is neural input not necessary? And "heat" should be "heart"  +1

Neural input to the heart is only regulatory→ it increases/decreases rate, contractility, etc... I will edit answer to give more info, thanks for pointing out the typo @ChrisStronks

This answer fits in well with the other +1


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What are the advantages of blood's redness?
Although this page (http://evolution.berkeley.edu/evosite/evo101/IIIE5aNotadaptation.shtml) denounces the idea that blood's redness is not an adaptation, I remain inquisitive on the matter since no scientific research has been performed in studying its possible advantages.
Does anyone have any ideas on the advantages of having red blood?
Thank you for your time and effort

I don't think there is an advantage in blood being red. It is a byproduct of the heme being coordinated in the middle of the heme as the active center. Hemolymph has a copper atom there and is more blue/green due to this fact.

I think your article explained it quite well. Blood is an adaptation. The color of blood is not; it's a coincidence.

@Chris Thank you for your detailed reply, your chemical background has proved useful here.

@anongoodnurse So what should I do with this question? Delete it?

Totally up to you. If you want a better answer, you can leave it and see what comes up?

I can make this into an answer if you want. It would be a rather short one, though.

@Chris I would be extremely grateful if you could do so please.

The reason why blood is red is rather simple: It is the iron atom in the middle of the heme, which plays the central part in binding oxygen. Depending on the oxidation state the blood looks either dark or light red. The structure is the following (taken from here):

That the color only depends on the coordinated metal atom is shown by another related molecule, the hemocyanin, which is the oxygen carrying molecule in the hemolymph of insects. It contains copper which is colorless in one oxidation state and blue-green in the other. The function is the same, the color is different.

Thank you for your answer but I'm a little confused - weren't there four Fe molecules?

This is true for the hemoglobin. This consists of four subunits. Each of these carries one heme with one iron atom. Together you have four hemes in the hemoglobin molecule.

Ah, I see - so your picture shows one heme and one iron atom

Yes, this is clearer this way.

@Chris did you mean blood is red rather than heart is red? I am changing it. Please revert if you feel it is wrong.

@CRags You are absolutely right. Thanks for finding this error.


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If we change our breathing rate so easily, then what is the point of measuring it?
When we are self-conscious of our own breathing, its rate changes very easily. Therefore, if it changes so easily, what is the point in measuring it?
Thank you for your time and effort

We may be able to voluntarily control our respiratory rate, but only for a short while. The buildup or depletion of CO2 will force us, against our will, to either speed up our respiration or slow it down. So, you can't effectively "fake" your respiratory rate for long, nor, to an astute observer, convincingly.
Normal breathing patterns are "normal" for a reason. Aberrations from normal do occur in pathological states, but they are compensatory mechanisms driven by a number of factors your blood chemistries: the pH and the intimately linked CO2/H-CO3 concentrations, etc. You can pretend any way you like: you won't be able to keep it up comfortably. Also, normal breathing isn't simply "breathe in/breathe out". It is a more complex thing characterized by an inspiratory phase of certain duration, an expiratory phase of a different relative duration, and a normal, periodic deeper breath (close to a sigh), all done physiologically and unconsciously.
With certain illnesses come certain breathing patterns. You might be able to fool one person's quick assessment, but not more than that. If the faked breathing pattern (largely unsustainable anyway) doesn't appear physiological, you will be quickly found out.
For that reason, a sustained increased or decrease in respiratory rate is indicative of particular pathologies, whereas a normal respiratory rate is a helpful sign.

Thank you. Excellent and fast answer. This is what Stackexchange truly is.

But what about doing slightly deeper or shallower breaths instead?

@imallett - See the edit.

authors: Ольга Ганеева


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How do centrioles auto-locate to opposite sides of cell during mitosis?
I realize that centrioles are made of 9 triplets of microtubulin wound together with a hollow core, and that they are responsible for the configuration of the spindle during mitosis. The spindle fibers attach to the kinetochores of the sister chromatids and pull, ultimately separating them in preparation for cytokinesis.
How do the centrioles recognize where to go in the cell, such that they are oppositely positioned with one another? Is the mechanism similar to how neurons "find their way" during development to forge the correct connections that give us sight, etc, but on a subcellular scale?

relevant paper http://www.nature.com/ncb/journal/v6/n7/full/ncb0704-581.html

During cell-division centrioles move towards opposite 'poles' and finally get attached to cell-membrane. Different factors influence & drives this process, most still not discovered. So this mechanism is largely unknown. From the scientific literatures published on this  matter till recently we can say that this process should include:

A structure along which the centrioles can migrate,
Molecules associated with the movement of centrioles,
Signal molecules triggering this process,
Signal molecules determining the direction of migration.

To answer 1., Microtubules form a intra & inter-cellular network along which subcellular structures can move. Actin & Myosin are also involved in some cells. For reference read Ganong's review of Medical Physiology. (the example you stated in your question about neurons is a substantially different process. But neurotransmitters are carried with the help of Microtubules. Chromosomal structures also are arranged with the help of them.)
For points 2,3 & 4 read this paper, these parts are very clearly described there.
Thank you.


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taqman probes to measure telomere length
Has anyone previously used the TaqMan probe 5'-FAM-AGGGTTAGGGTTAGGGTTA-MGB-NFQ-3' (or something similar in terms of targeting TTAGGG), which targets the telomere repeat sequence (TTAGGG), to estimate telomere length through RT-PCR?

Please carefully re-read the [Tour] for this site which makes it clear that it is a Question and Answer site about specific biological problems, NOT a chat site. "Has anyone used…?" is an attempt to start a conversation, not a biological question. It might be possible to convert this into a question (albeit starting the title with a capital letter) of the type "Can this probe be used to do such and such?", although evidence of your own attempt to answer the question by an internet search would need to be included.

I’m voting to close this question because it is an attempt to start a conversation, not a question in terms of SE Biology.

David, this is a specific and genuine question, and definitely not an attempt to start a conversation. If you believe it can be reworded more appropriately feel free to do so. Thanks.

As I wrote, even after reformulating you ned to show evidence of having tried to answer it yourself. I cannot do that for you. And while you are about it you should edit your title with a capital letter. As for conversation, a question that starts "Has anyone previously used…" strikes me as soliciting a reply from specific people in the community. If your meaning was "Are there any reports in the literature…" you should have written that, but, to repeat myself, you need to do the literature search to find out.

Ending up here suggests the literature search and colleague search has been exhausted. But hey, if you are so determined to shut this question and its exploration down then who am I (or reason for that matter) to stop you.  It's this type of nonsense that is slowly killing these sites whilst ensuring more and more people flock to AI regurgitation.

We expect new users to find out the procedures on this site and to follow them. The site aspires to providing something more than AI, or conventional dialogue sites, and that is why SE sites are different. They are different in encouraging improvement of questions (and answers) — through direct editing for typos/language/grammar, and by suggestions in comments. There are specific recommendations on research in Asking a Good Question for good reasons. Tell us what you have found about methods normally used to measure telomere length.


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What is a polar plot of relative neural firing
I am taking my PhD qualifying exams on monday, and there is a seemingly simple practice problem that I can't seem to figure out, and I was hoping someone here would have some knowledge, or at least be able to point me in the right direction. My background is in electrical engineering, so apologies for my ignorance.
The question is:
Cell A is strongly phase-locked to spindle oscillations (12 Hz) at 180 degrees, and cell B has monosynaptic excitatory connection to cell A. Assume the synaptic delay is 3ms.
1- Draw the polar plot of cell A’s firing relative to spindle oscillations.
2- What is the relationship of cell B to spindle oscillations? If it is also phase locked to spindle oscillations what would be the degree of locking? Draw the polar plot. If the independently calculated polar plot of cell B does not show significant phase locking with spindle oscillations, what is a possible explanation?
I can't find a single resource that tells me how to draw these polar plots. Can anyone help me out?
EDIT:
12 Hz --> 83.33 ms period
Cell A fires at 83.33 ms * (180deg/360deg) = 41.66 ms
Cell B fires at 41.66 ms +3 ms = 44.66 ms
Phase of Cell B firing is (44.66 ms/83.33 ms) * 360 deg = ~192 deg
Is that right?

Can you explain what you understand and don't understand? Surely you've encountered polar coordinates in engineering, no? have you tried Googling something like "polar plot" + "spindle oscillation"

If you map every spike of a neuron to the phase of an oscillatory process (in your case a 12 Hz sine wave) then you can plot an histogram of that phases. It's usual to plot the histogram in polar coordinates as in the figure below.
For cell B, you will need to map the synaptic time delay in to phase delay using the oscillation period. This is assuming that a synaptic event from cell A induce cell B to spike and there's no other synapses or intrinsic properties of Cell B that perturb the entertainment.

Mansouri, Farrokh, et al. Frontiers in neuroscience 12 (2018): 877.

thank you so much! I couldn't figure out how to add images to this comment, so I added the polar plots to the original post. Does that seem right? I just dont want to misunderstand.
Thanks again


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Are there adaptations in tropical fish to compensate for less oxygen in water?
Warmer water means that the amount of gases- especially oxygen- dissolved in it reduces, since solubility of gases in a solution in most cases decrease with an increase in temperature.
I'm interested in knowing if tropical fish have any adaptations to account for this reduced oxygen compared to fish in colder waters. Any modification of the gills maybe?
Referencing the below articles, I have come to the conclusion that tropical fish end up migrating to shallower waters or cooler habitats due to the oxygen depletion, showing that this decrease in oxygen is serious enough to affect them. However, this may be due to excessive heating of oceans due to global warming. I'm curious about whether fish in tropical regions have any adaptations for living in ocean water that is heated purely by natural means, not anthropogenic ones.

References:
https://www.usgs.gov/media/images/temperature-affects-dissolved-oxygen-concentrations
https://www.pca.state.mn.us/sites/default/files/wq-iw3-24.pdf
https://www.sciencedaily.com/releases/2015/06/150604162455.htm
https://www.nationalgeographic.com/science/article/150313-oceans-marine-life-climate-change-acidification-oxygen-fish

How having access to less oxygen would be accounted for by swimming faster?

I'm not sure, that was just me speculating that a higher rate of respiration would mean more oxygen could be inspired in less time.

Welcome to Biology.SE! While dissolved gasses do tend to decrease with increasing water temperature there are many other factors that contribute to the actual concentrations (e.g.s: rate of use, rate of mixing with the atmosphere). Please [edit] your post to include evidence that dissolved O₂ is actually lower in tropical waters, by how much, and whether this difference is biologically significant. Without that background research (which is expected) your question is based on speculation and is thus off-topic for this site. Thanks!

Thank you; I've edited my question for the same. I wasn't able to find how much in magnitude this oxygen depletion was, and most articles I checked were about how global warming is decreasing the (especially tropical water) oxygen levels. I understood that a faster metabolism ('swimming faster' @Exocytosis) does not allow for adaptations to less oxygen.

Fish that live in cold water for most of the year actually have particularly strong hypoxia-tolerance adaptations, i.e. from summer heatwaves and algal blooms, compared to fish that are better oxygenated by waves and flowing rivers.
Goldfish and other fish are able to rapidly change the surface area of their gills in less than a day.
Carp, killifish, goldfish and oscars have 2/3 times as much glycogen in their bodies than river fish i.e. rainbow trout.
There's a lot of research into the biochemistry of fish's oxygen response, i.e. gene expression changes, things like decreased expression of genes involved in the citric acid cycle.
Probably you will find most of the information on the wiki page, there are also summaries of current advances in the field.
On coral reefs, oxygen is a limiting currency for all the fish and zooplankton. The reading suggests to me that hypoxia adaptations depend mostly on heatwave events and low current waters vs rivers and coastal waves than by tropical vs pelagic and temperate regions.

Thanks for the answer, this is what I was looking for. These adaptations are only viable to a certain extent and not seen in all fish, correct? –

Many can breath air directly ; examples - bettas, gouramis, paradise , some catfish . No doubt others that do not come to mind .

Thanks.This is an adaptation seen only in tropical fish (Labyrinth fish are endemic to fresh waters of Asia and Africa), while @aliential 's excellent answer was more to do with fish that live in cold water.


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Calling Alterations in Exome Data
What are the main technical differences between accurately calling somatic point mutations vs copy number variation (CNV) in exome data? Side note: would you need other -omic data to accurately infer CNV (exome data isn't enough)?

Exome data can be used to determine both somatic point mutations and copy number variations.  The limiting element for the power of detection for both is read count (how many reads per gene).
Exome data:  Exome data uses a reference (for a trio, that would be parents; for cancer, that would be a paired normal sample from blood or non-invasive tissue) in order to determine if a certain point is mutated or not.  Next-generation sequencing is prone to sequencing errors, so having a high enough read count is essential to properly calling a somatic mutation.  Even so, issues with highly repetitive sites can make this difficult.
Using exome data for copy number is happening a lot nowadays.  The number of reads is used as a proxy for how many copies exist, and the balance of alleles at any given gene tells you whether there has been loss of heterozygosity.  Of course, with exome data, you aren't getting truly genomic data.  But there is enough coverage using the exome to pick up the big events.
CNV data: Copy number analysis is now conventionally done using a high density SNP (single nucleotide polymorphism) array.  These are designed to be biallelic, and come in two types.  First are the copy number SNPs, which are designed to give the best information about copy number.  Then there are the genotyping SNPs, which give information about loss of heterozygosity.  Often, SNP array data is higher quality, but this is determined by your platform.  Newer platforms have extremely high coverage of the genome and can allow you to really pick out focal changes.
These arrays, based on manufacturer's recommendations, are not meant to be used for somatic mutation calling.

As far as bioinformatic pipelines, you can use similar tools for each.  For example, the Aroma package in R has pipelines for both Exome & SNP array data.  GISTIC 2.0 from Broad can be used to find focal copy number changes.
A word of caution: It is always best to validate what you find in one platform with another.  I recently worked on a paper that used both Exome sequencing and SNP array data to determine copy number.  Using GISTIC, there were no focal peaks that matched.  The broad chromosomal trends were the same, and that's what the group reported.

Thank you, really nicely worded and clear. As a follow up, would RNA seq data help clear up some of the confusion associated with highly repetitive exomic data, potentially by comparing matched normal and tumor transcriptomic data? Would using DNA microarray data help you infer copy number variation also?

Expression data only tells you about expression (transcription) levels, not necessarily inherent copy number.  However, there is a relationship.  It depends on the scientific question.  RNA data is VERY useful additional data, because it allows you to connect gains or losses with transcription level changes (which may arguably be more biologically interesting)!

My understanding is that DNA microarrays (such as those used in CGH) give copy number information but not LOH information, and therefore don't give a full picture of what's going on.  For example, you can have 2 copies, but have lost one parental allele (and thus duplicated the other parental allele).  This wouldn't show up in CGH, but does using SNP array data.

Right - it sounds like you would need to combine the DNA microarray data with whole exome or genome data to get that connection. 2) Thank you so much!! Would you mind upvoting?


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How do drugs enter synapses?
Many psychopharmaceutical drugs change synapse chemistry or directly agonize neuroreceptors in the brain. For example, cabergoline is a D2 agonist.
How do these compounds enter the physical synapses? Are they simply lipid soluble and diffuse throughout all cells?

The answer is that cabergoline does not need to enter a cell in order to function.
Cabergoline (as well as most (possibly all?) other drugs that target synapses) interact with proteins on the surfaces of the synapses. For example, the D2 receptor that you mention is a dopamine receptor which in its active form is expressed on the surface of neurons near the synaptic cleft.


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Are different eye colors indicative of chimerism?
If an animal or person has different colored eyes, does that mean they are a chimera?

You will find this wiki entry [1] informative.
While chimerism is one possible explanation, it is certainly not the only one.
[1] https://en.wikipedia.org/wiki/Heterochromia_iridum

A possibly easier to understand explanation of eye color here. One thing to consider thats not mentioned in the wiki article in answer is incomplete penetrance


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Part of a fish outside the intestinal sac on the back?
I saw an expert Japanese chef fillet a mackerel (Scomber scombrus). He cut off the head and the whole intestinal sac came out with it as a single unit. Then he took the knife and scraped something from inside on the back. The object(s) were dark and bloody. Would those have been the kidneys?
You can see the video here: https://www.youtube.com/watch?v=udTHiRg34KI. The moment is at 2:20.

Yes, those are the kidneys. They're quite different from mammalian kidneys.
This is a picture highlighting the kidneys in a salmon dissection from the Pacific Streamkeepers Federation (http://www.pskf.ca/sd/). A very different fish, but similar enough to show the kidneys.

You can also see a dissection of the fish urogenital system here: http://necropsymanual.net/en/teleosts-anatomy/excretory-and-osmo-regulatory-system/, though I can't tell what fish species they're dissecting.

Are you going to upvote my question considering that you took the time to answer it?

I just did. Sorry, I'm new here-- is that generally expected?

@Kara welcome to bio.SE! Like any community-driven Q&A site, we hope that you vote frequently so as to acknowledge the efforts of others (or help to downvote bad/wrong answers once you have enough rep). However,  you should only vote when and how you want to -- no  one should pressure  you to do so.  It's perfectly acceptable to answer a question that you don't think qualifies for an upvote (or even one that you downvote). See here for more info.


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How does translational immunotherapy work?
I skimmed an article on a recent experiment which suggested that it was effective to inject induced colon cancer tumors with an attenuated salmonella variant. According to the article, this stimulated an immune response which suppressed metastasis of the cancer. How exactly does this work?

Tumors are commonly infiltrated with lymphocytes, including T cells, macs, DCs and B cells. The crux of the paper is that their attenuated virus secretes TLR ligands (Toll-like receptor) that resulted in an activation of tumor-suppressive M1 macrophages, a concomitant reduction in immune-suppressive M2 macrophage activity, and an influx of immune infiltrate to the tumor.
So M1 macs are activated typically by IFN-y and LPS stimulation, which is typically through TLR4. Their salmonella is attenuated and causes no disease, check one. It's gram-negative and thus has LPS, check two. It's engineered to secrete bacterial flagellin, a TLR5 agonist, check three.
M1 macs secrete IL12, important for polarizing T cells to TH1/TC1 phenotypes that are oncolytic, and IL10 which can elicit anti-tumor immunity though it's reputation is that of an immunosuppressant. M1 macs can also kill tumors of their own accord by producing nitric oxide which is cytotoxic to tumor cells. TLR4 agonsim on it's own accord also activates T cells in an NF-kB-dependent manner.
Whats also interesting is the inflammatory signal actuated by the macrophages actually tells other immune cells "hey come check this out," and potentially makes for a more robust anti-tumor response. The idea is that inflamed tissues secrete signalling or chemotactic molecules called chemokines which are picked up by chemokine receptors on leukocytes, telling them to enter the zone of infection (and thus the malignancy).
You'll also find, however, that despite immunological advances, modulating cells is a challenge due to the nature of each type of cancer's TME (tumor microenvironment). And so in your paper they tested it in a murine system in bladder cancer, but will it work in a human melanoma must be qualified, for example.