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Why is Chromosome 1 called Chromosome 1?
Chromosome 1 is the designation for the largest human chromosome. Humans have two copies of chromosome 1, as they do with all of the autosomes, which are the non-sex chromosomes. Chromosome 1 spans about 249 million nucleotide base pairs, which are the basic units of information for DNA. It represents about 8% of the total DNA in human cells.
Why is Chromosome 1 called Chromosome 1? Is being the largest human chromosome the only reason?

If they had started with the smallest, then what if one is found later that was missed because of its small size? If you start from the largest, that's less of a problem.

Because biologists aren't  C-language coders  :-)

@forest But it would have been much more embarrassing if they'd started with the largest and then found a larger one! (I'm looking at you, zeroth law of thermodynamics.)

@user1136 Is there some reason it's written "any body" (this is the actual title of the paper) or do I need to write a follow-up called "Can Anybody Spell?"

@user1136 Thanks -- that makes a lot of sense. I agree that it's a very good title, now that I understand it.

Chromosomes were first known about from karyograms (that's the word for chromosome pictures like these) sort of like this one (1)(2):

The scientists looking at these chromosomes didn't know much about them at first. They were discovered before anything was understood about genes, but by 1922 it was thought they were the carriers of genes. Without much understanding of the chromosomes, and certainly no understanding of what they carried, scientists needed an easy way to order and compare them. They chose a straight forward option - size - and paired them up and then lined them up biggest to smallest. Because the sex chromosomes didn't fit into this scheme of matching pairs they were left to the end.
Hence Chromosome 1 is Chromosome 1 because it is the largest autosomal chromosome.
Notes:

The actual first karyogram was of a plant, this one is of a human male.
The image above is public domain, obtained from Wikipedia, and originally made by the National Human Genome Research Institute.

This also works for chromosomes in other species, but sometimes with complications due to interspecific phylogenetics. Chromosome 2 turned out to be two smaller primate chromosomes fused, and these half-chromosomes are now called 2A and 2B. In particular, in non-human primates this has required a renaming of chromosomes, and one that isn't as simple for them as numbering by size.

@user1136: double checking, I see that it was the first observation of chromosomes that was in 1842 but Karyograms were presumably a bit later. Human chromosomes are not the easiest to see so the science advanced in other organisms earlier

Size is a difficult one to judge when chromosomes are similar sizes, and it was more difficult before staining of the bands.
Because of this, some chromosome naming systems group chromosomes into different categories of the centromere type (acrocentric, telocentric), so the largest do not always necessarily descend in order of size. Some genomes still use a sub-classification system, such as Feline (A1, A2, B1, B2), though it is a lot easier to treat chromosomes numerically in programs.

Welcome to Biology.SE! While interesting, this doesn't really answer the OP question. ——— Please take the [tour] and then consult the help pages on the standards for [answer] effectively. Thanks!


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Why do people say that smallpox has been eradicated?
I keep reading things like “smallpox has been eradicated” or “there are only two samples of the virus left in existence in a lab somewhere”, but couldn’t there be a bunch of smallpox viruses in an alleyway where some infected person sneezed years ago? Is there some reason the virus can’t exist without a human host?

You may want to read this.

The viruses that caused smallpox (Variola major and Variola minor) are generally not stable in the environment (<24 hours as an aerosol), though they may persist for more than a decade within scabs Reviewed: Sinclair et. al., 2008 OSHA.
UV light is an excellent disinfectant, so typically any virus exposed to sunlight will lose rapidly infectiousness.
You may also find this answer to a related question of interest:
https://biology.stackexchange.com/a/59165/46609

source: Stack Exchange

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How did Aposematism evolve?
Disclaimer: I know nearly nothing about biology.
My understanding is that camouflage evolved gradually with individuals that looked more like their environment even slightly being less likely to be eaten.
I might be understanding this wrong, but it seems aposematism could not have evolved like this because you really can't distinguish slight aposematism from just being bad at camouflage.

@MaximilianPress  are you saying there was a period of very low evolutionary pressure when  aposematism  evolved?

@MaximilianPress aposematism is not a "bad" trait it is a direct advantageous adaptation, the question is completely valid.

@John Fair enough, I seem to have misunderstood the original question.

The noxious element of aposematism evolves first.
Take a second to think about how  aposematism works, you will notice the underlying mechanism works even without distinctive coloration.
Bad at camouflage means more likely to be spotted which also means more likely to be identified.
If a wolf eats a pale green frog and gets sick it is likely to avoid pale green frogs. Avoidance works by itself regardless as long as the thing doing the avoiding can identify the toxic animal, aposematism just makes it work better by making identification easier. Even if the frog is well camouflaged avoidance still works if it is toxic, but it works better if the wolves can easily tell what it is.
If the coloration is distinctive enough, or is used my several toxic organisms, predators just start avoiding that color or pattern entirely.
https://www.sciencedirect.com/science/article/abs/pii/S0169534705002521
https://royalsocietypublishing.org/doi/abs/10.1098/rspb.2004.2968

Another really interesting aspect of aposematism, from an animal behavior perspective, is that some predators seem to evolve a genetic predisposition to avoid the aposematic prey, while others still need to learn through experience. I suppose it has to do with whether the poison is deadly to the predator or simply noxious and unpleasant.

Then there are 2 problems 1) animals that look poisonous but aren't  and 2) wouldn't it take several generations to be able to look distinctive enough  before you're just bad at cameoflauge?  During which time you still get eaten more often?

@user122938 mimicry is a separate issue, but yes is should reduce the effectiveness of aposematism. and many predators can identify animals even when they are camouflaged before they eat them, so yes you still get eaten but less often than if you were not noxious in the first place. like anything in evolution the advantage does not have to be huge to be favored. even making your camouflage worse can keep you from getting attacked as often since for many predators attack and eat are not the same action.

But isn't not being spotted better than spotted and recognized? Since it's guaranteed survival vs not guaranteed survival.
Clearly a 0% chance of being spotted is best so what you are claiming is that while 0% being spotted is best 1% chance of being spotted isn't better than 2% or 3% etc  why would that be?

@user122938 but a zero chance of being spotted is impossible, you still need to move around to find resources so there is no such thing as a zero percent chance of being discovered. So it is better to be avoided than risk being seen as prey, consider 20% chance to be spotted vs 30% to be spotted but 50% chance to be avoided.  also evolutions is about good enough not hypothetically perfect.

@John that wasn't the point it was that   while 0% being spotted is best 1% chance of being spotted isn't better than 2% or 3% etc why would that be?
You can't assume the percentage of avoidance that's some function of the the percentage of being spotted.

@user122938 even the best camo has a solid chance to be spotted, all that needs to happen is for avoidance to result in less chance of being eaten. remember aposematism usually evolves with something kind of defense like a sting or poison but an organisms can still be injured or killed while having those before the predator realizes that is why aposematism evolves because being avoided reduces this. no camouflage is perfect and it can work against you if you are noxious. aposematism and camouflage have to part of the same equation, they have to be linked. Have you read the sources I provided.

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Why am I finding peculiar B cell population when pbmcs are cultured for 3 days with CD40L?
While performing intracellular cytokine assay on B cells, I am finding a peculiar population.
I use 2*10^6 cells for studying each functional marker. The pbmcs are cultured for 72 hours, with CD40L dose being given in 0 hour after plating and BFA in the 48th hour. When analysed, I am getting two CD19+ populations from the lymphocytes. Can anyone enlighten me about what actually is happening?

Have you phenotyped the populations further, other than using CD19 after presumably gating on CD3-? How are you detecting the two populations of CD19+? Are you plotting CD19 vs another marker, or is it simply CD19 intensity? Can you share your plots and gating strategy, comparing untreated vs treated? Also, what is BFA - brefeldin A?


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regarding evolution of ears and sense organs
How could we(or any other organism) have developed ears through evolution when before having ears we did not know that sound waves existed or there was anything such as hearing? How did the first hearing organ develop? The same can be asked for the other sense organs as well.

I tried to answer below. Your question is very broad currently - if my answer is not targeting your main concern, or is opaque, please comment on the answer, and try to sharpen your question so i (and other users) can try to better fit your question.

I think this is, in principle, a duplicate of a question that is quite commonly asked here, but I can't find a prototype - I suspect that most of these questions get closed as "Too broad". The real problem is of course that the question is based on a profound but common misunderstanding of evolution, the notion that there's some plan or direction to it. Remi.b's answer here addresses this, but perhaps there should be a more detailed, canonical answer to point newcomers to.

Possible duplicate of How does the creative process of Biological Evolution work?

When you are asking about the evolution of organs, you are already five steps ahead of yourself. To have sensory organs, you need cells that react to some stimulus:

Hearing, Touch: Mechanical stimulus
Smell, some pain: Chemical stimulus
Sight: Optic stimulus
Other (non-human) organisms can also sense electric fields, magnetic fields, ...

As soon as you have those, having 'organs' that house a lot of those cells surrounded by tissues that aid in the reception of these stimuli, is relatively trivial.
But isn't a sensory cell totally complicated? It is. But: A simple neuron already is a sensory cell of sorts: It reacts to electrical and chemical imbalances.
But isn't then a neuron totally comlicated? It is. But: A simple non-neuronal cell already has a lot of the intricate machinery that a neuron does - a neuron mostly has some special parts and structures that make it a neuron. A simple cell also does react to chemical and other stimuli (this is why hormones work, and how little one-celled animals can orient themselves towards the light or food, or away from dangerous chemicals)
But isn't a run-of-the-mill cell totally complicated? It is. But it actually is just the workings of several archaic cells crammed into one (one of the more popular theories on Eukaryote evolution has them result from a very intense partnership of several more basic cells). And those archaic cells can also react to stimuli (they manage their metabolism according to the available food, for instance)
But isn't a basic cell totally complicated? It is. But is actually is just the interaction of several molecules that have some very interesting properties - DNA/RNA can function as an information storage, but are at the same time tools that can cowork with other DNA/RNA, and also interfaces/interferes with proteins in interesting ways.
But aren't big molecules totally complicated? They are. We still need supercomputers to reliably model all of the intricacies of any given Protein-Protein or Protein-RNA interaction. Many proteins behave differently in different environments (electromagnetic field strengths, chemical environment, temperature and mechanical factors (e.g. ultrasound)) - they could be said to 'react' to certain triggers. But they are actually just chains of repetitive elements (so called polymers of so called monomers).
But aren't those monomers totally complicated? Some are, but here we slowly get into the realm of 'mostly modellable on a hefty home computer'.
So we have systems of systems of systems... All of them very complicated.
But evolution is not a process that involves understanding ot planning. It is simply the result of coincidences and inheritance. You can see colors that many animals cannnot. You have the requisite molecules in your sensory cells in your eyes. Some people can see more colors than you, an inheritable trait. Some people can see less colors. Currently those people have no evolutionary profit from this - they reproduce and die with the same probability as the rest of us. Likewise there are a million (possibly billion?) such traits in every human. Traits that are different from the rest. Little things. Ineffective things (= having no net effect). But there might come a time where seeing one color or not seeing it (= not being distracted by it) will give a continuous net positive or net negative effect on the reproduction of those people carrying that trait. That is the time when that trait will start to  be present in a larger piece of the population (over many generations). The people carrying that trait will also be different from one another. And the ones carrying the traits with the most positive net effect will multiply the most, etc. Humans in some distant future then can eye-sense some X-factor we cannot even describe currently (try describing different colors to a blind person) and thus have, say, Xeyes.

Organism don't have any intention to evolve a certain. As soon as a mutation creates a protein that can change conformation in response to a given sound frequency, then the organism carrying this information has opportunity for making use of this new signal. If this new mutation is beneficial, then it can be selected for and will increase in frequency in the population.


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Why exactly does UMN lesion cause hypertonia?
The corticospinal tracts are excitatory in nature (Glutaminergic). So damage of the CST would mean less excitatory input to the LMN. By this logic, there should not be hypertonia. What is the mechanism behind this spastic (hypertonic) state of the muscle in UMN type of lesion?

The main idea is that most Corticospinal tracts end up in inhibitory (GABA releasing) inter-neutrons, which then synapse directly into the Lower Motor neurons. This means that positive stimulation of inhibitory neurons occurs, which leads to overall negative regulation of Lower motor neurons.(1)
And the book goes on to say,

The corticospinal tracts are not the sole pathway for serving voluntary movement. Rather, they form the pathway that confers speed and agility to volun- tary movements and is thus used in performing rapid skilled movements. Many of the simple, basic voluntary movements are mediated by other descending tracts.

Note that the other descending tracts would be the extra-pyramidal tracts, which, are responsible for the most evident signs of UMN lesions, which include spasticity, hyper-reflexia, hyper-tonicity and severe paralysis.
Here is the list of symptoms of lesions localised to the pyramidal/coricospinal tracts:

Positive Babinski sign.
Absence of Cremasteric reflexes.
Absence of Superficial abdominal reflexes.

1- South Asian Edition Of Snell's Clinical Neuroanatomy


text:
Why does warfarin decrease biological activity of protein C?
Warfarin inhibits VKOR. Hence it disrupts vitamin K dependent $\gamma$-carboxylation of Fc- II, VII, IX, X.
But what exactly it does to Protein C and Protein S? How does it also affect anticoagulant system?
[Ref. Kim, Yesel, and Oh Young Bang. “Paradoxical Procoagulant Effect of Early Doses of Warfarin: Possible Role of Non-Vitamin K Oral Anticoagulant in Patients with Atrial Fibrillation-Related Stroke.” Journal of stroke vol. 17,2 (2015): 216-8. doi:10.5853/jos.2015.17.2.216
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4460341/]
I couldn't find an article regarding the mechanism of this inhibition. Any help will be appreciated.


text:
Why is syphilis not resistant to penicilin?
How is it that we are dealing with so many antiobiotic resistant infections in iatrogenic settings, and yet this very old bacterial pathogen has still not acquired resistance to penicilin (the oldest antibiotic to which it has had the longest relative exppsure to)??

While rare, it does happen--reports of penicillin-resistance go back to at least 1949

First off, Treponema Pallidum-the bacteria which causes Syphilis-is EXTREMELY SENSITIVE to Pencillin; even a small does can wipe them out! Secondly, since Syphilis has been around for centuries without mutating into a form immune to Pencillin this suggests TP doesn’t have ANY protective measures against antibiotics-making it highly susceptible. Lastly, resistance rates remain low globally, meaning strains which develop immunity don’t survive long against antibiotic treatment


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Can plants produce oxygen at night (without light)?
I accidentally clicked on a "Top n X's that Y" result in google and found Top 9 Plants that gives (sic) off Oxygen at night as well (best for indoors).
In this helpful answer I've found a nice, concise description that I'm just going to reproduce here:

Photosynthesis consists of two general steps, one that requires light and one that does not. The first step occurs in the thylakoid membrane, and splits water into oxygen, hydrogen ions, and energy. The second step is the carbon fixation step, which occurs in the chloroplasts and uses energy to convert the carbon dioxide into carbohydrates.
Step 1: $\ce{2 H2O + light → 2 H+ + O2 + energy}$
Step 2: $\ce{3 CO2 + 6 H+ + energy → C3H6O3-P + 3 H2O}$

In general, the oxygen released from plants comes from water splitting which is driven (in a multi-step process) by photons. From what I remember, the oxygen molecules ($\ce{O2}$) are usually produced and released to the air within seconds, and certainly within minutes after all of the necessary photons for it have been absorbed.
So I am asking; are there plants that really make meaningful, or even just measurable amounts of oxygen without light?
(Or is the idea here that you leave your lights on at night and so actually any plant can make oxygen at night?)

@AlwaysConfused what are CAM plants? Could you include a link in your comment - or expand to an answer? This sounds like a very plausible scenario.

@AlwaysConfused you can write answer anytime you want...write now, I am writing one (though it doesn't involve your point :)

@another'Homosapien' et al remember the question is primarily about oxygen production in the dark, not what the advertisers may have been confused about.

To the unclear what you're asking voter - I am asking if plants can make oxygen at night or not. Yes or no. I'll remove the word "these" from the title.

@tomd I'll do the reading you mentioned, thanks. I need to ease myself into photosynthesis slowly, from the edges. I know I should follow the electrons, but I'm curious how the two oxygens meet up. I wish I could see an animation, or read a description of what happens to the two oxygen atoms in the two initial water molecules.

@tomd wow - too many big words for me! :)

@tomd this sounds really interesting! There are a lot of big words here, and some of them seem important: https://www.researchgate.net/post/How_CAM_plants_handle_the_O2_evolved_in_photosynthesis_during_daytime My title says "...produce oxygen... without light" and the restatement at the end of the question says "...make...
oxygen without light..." so I think the answer as I wrote it is still "no" — but now I regret that I didn't say "...release oxygen..."

Short Answer: Any plant can produce oxygen at night, but plants cannot produce oxygen without light.
Longer Answer: It all comes down to spontaneity of a reaction i.e. whether a reaction can occur without input of energy or not.
Before we talk about spontaneity, I feel it better to first know about the process we're talking about here. In photosynthesis, the water-splitting reaction occurs in the oxygen-evolving complex through a process known as Joliot-Kok cycle (or simply, Kok cycle)1. Although, the complete mechanism of this process is not understood yet, the basic reaction can be depicted in a diagram as2:

(Pay attention that in the diagram, the time taken is in microseconds and even nanoseconds. So, at molecular level, oxygen evolution does not take minutes or even seconds! However, at larger scale, release of oxygen might take longer time since the formed oxygen has to pass through many fluids, like thylakoid membrane, stroma, chloroplast membrane, cytoplasm, etc. before finally coming out in atmosphere)
To know where the photons are required (since the above diagram doesn't talk about that), I'll let in another diagram involving the steps where photons come in (as depicted by Rutherford et al, 1989):

As you can see, Kok cycle does not get direct input of energy through photons. Rather, it is the high energy P680+ which oxidizes a redox active tyrosine (YZ), which drives the reaction forward (the actual process is much more complex, see another answer or Halverson et al, 2003 for details).
Now, talking about spontaneity of this reaction, oxidation of water into hydrogen and oxygen is an endothermic process i.e. it is non-spontaneous in nature. In fact, the process requires 475 kJ/mol energy for occurring (Wikipedia). This energy barrier is so large that in the Kok cycle too, 4 photons are required to bring about oxidation of 1 water molecule (generally, catalysts are used so that they bring down the energy barrier of a non-spontaneous reaction so that it can be performed under normal conditions). Nilsson et al, 1857 talks about free energy change ($\Delta G_0$) of the cycle. See the graph for free energy change:

As is clearly visible from the graph, a higher amount of energy is needed to oxidize water ($E_P^+, S_2 \rightarrow S_3$) and even higher for liberation of dioxygen from the complex ($S_4 \rightarrow S_0$) (though the free energy change is negative for the last step i.e. liberation of oxygen is spontaneous, still the overall energy is larger than that at S3). Thus, since the reaction requires overall energy input, plants cannot produce oxygen without light. Also, as you suspect already, the point here is the abundance of light from man-made sources which makes some plants able to produce oxygen at night.
BONUS: I'll add some details about the thermodynamics of the system (skip this part if you're not interested in maths). The basic equations I will use here are Gibbs Fundamental Equation ($\Delta G = \Delta H - T\Delta S$), Arrhenius Equation ($k = A \times e^{-E_a/RT}$) and Eyring Equation ($k = k_BT/h \times e^{-\Delta G^\ddagger/RT}$) and used data will be from Nilsson et al, 1857.
From $\Delta G = \Delta H - T\Delta S$, to make a reaction spontaneous ($\Delta G < 0$), either there should be release of heat ($\Delta H < 0$) or increase in entropy ($\Delta S > 0$). As we know now, the reaction is endothermic i.e. there is absorption of heat. So, there must be increase in overall entropy to drive the reaction forward. If you look at the graph for free energy change in different steps of reaction, it comes out to be like this:

In this, $\Delta G_0$ is overall energy change, $\Delta G_{in}$ is the required energy input (given by photons), $\Delta G_{ex}$ is final free energy change and $\Delta G^\ddagger$ is Gibbs energy of activation. Here, $\Delta G_{ex}$ (shown in blue) corresponds to only the entropy change when final products (oxygen and protons) are released from the system as there is no enthalpy change here.
In release intermediate stage, the mole fraction $x = 1$ for oxygen, whereas in dissociated product stage mole fraction for water $x_1 = 56 /( [O_2]_0 + 56)$ and for oxygen $x_2 = [O_2]_0 / ([O_2]_0 + 56)$ (assuming molarity of water = 56 M) since in the final stage, water or oxygen or both can remain binded to the active site.
For release of oxygen: $[O_2]_0 = 273~\mu M$ and $T = 298~K$
which gives $\Delta G_1 = -~T\Delta S_1 = -~314~meV$
For release of proton: $\Delta G_2 = -~T\Delta S_2 = -~516~meV$ (since there is no enthalpy change, $\Delta H$ is neglected)
Now, $\Delta G_{ex} = \Delta G_1 + \Delta G_2 = -~314 - 516 = -~830~meV$
Also $\Delta G_0 = \Delta G_{in} + \Delta G_{ex}$
Since $\Delta G_{ex} > \Delta G_0$ therefore $\Delta G_{in} > 0$ i.e. energy is supplied.
Now, for the reaction $~~P_{680}Y_Z^{ox}M_3 \rightarrow P_{680}Y_ZM_0 + O_2$ (for which we've made the above graph)
Time constant $\tau \approx 10^{-3}~s$
i.e. $1/k = 10^{-3}~s$
or $k = 10^3~s^{-1}$
Using Eyring equation $k = k_BT/h \times e^{-\Delta G^\ddagger /RT}$
We get $\Delta G^\ddagger = -~580~meV$
In other words $\Delta G_{in} \leq -~580~meV$
Again $\Delta G_0 = \Delta G_{in} + \Delta G_{ex}$
On solving, $\Delta G_0 \leq -~250~meV$
Again, from Eyring equation, we get $k \geq 10^4~s^{-1}$
The large rate constant shows that there is a strong driving force for release of oxygen from the system, which is very likely due to increased entropy of the final product.
Thus, the enzyme brings down the free energy of the reaction, but at the expense of an increased activation energy barrier. Coming back to the main point, since energy is supplied to the system for the reaction, the reaction is non-spontaneous. However, the last step of the reaction is spontaneous (as also seen in the first graph) because of increase in translational and rotational entropy of final products when they are released (in above calculations, we neglected rotational entropy because of lack of data). Also, the above calculations were only for the last step of reaction ($S_4 \rightarrow S_0$) to show its spontaneity. In all other steps, energy has to be supplied to the system to drive the reaction forward (as shown in both first and second graphs above), making the overall reaction endergonic. I hope this helps now.
References:
 1. Wikipedia contributors. "Oxygen-evolving complex." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 1 Jan. 2017. Web. 18 Apr. 2017.
 2. Oxygen Evolution - 1996, Antony Crofts, University of Illinois at Urbana-Champaign
 3. A.W. Rutherford, Photosystem II, the water-splitting enzyme, Trends in Biochemical Sciences, Volume 14, Issue 6, 1989, Pages 227-232, ISSN 0968-0004, http://dx.doi.org/10.1016/0968-0004(89)90032-7.
 4. Halverson, Kelly M., and Bridgette A. Barry. “Evidence for Spontaneous Structural Changes in a Dark-Adapted State of Photosystem II.” Biophysical Journal 85.4 (2003): 2581–2588. Print.
 5. Wikipedia contributors. "Heterogeneous water oxidation." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 18 Apr. 2017. Web. 18 Apr. 2017.
 6. Håkan Nilsson, Laurent Cournac, Fabrice Rappaport, Johannes Messinger, Jérôme Lavergne, Estimation of the driving force for dioxygen formation in photosynthesis, Biochimica et Biophysica Acta (BBA) - Bioenergetics, Volume 1857, Issue 1, January 2016, Pages 23-33, ISSN 0005-2728, http://doi.org/10.1016/j.bbabio.2015.09.011.

Oh my goodness this is very helpful, thank you. I'll take some time to read through it. Is the $\ce{O2}$ released in milliseconds all the way to the air, or does it have to diffuse through some fluid first?

And if you catch your breath, I've asked another photosynthesis question as well.

I would like to add CAM plants, they open their stomata only during the night, to absorb CO2. For the rest of the day it is closed. So the O2 produced through calvin cycle is not released during the day, does it release at night, is the question. I couldn't find much research on this, possibly not much has been done. I didn't check if the plants enlisted in OP's website are CAM. They might be. Interesting though. Researchgate has a discussion on this.

I'm sorry, not Calvin cycle, through photolysis.

Won't be writing answers anymore. It just takes too much time.

I've just seen the "enhancements" here - will need a bit longer to read it all, but wow! In the mean time, I have this affliction that causes me to spot tiny errors without even looking - the units here should be inverse seconds: $k = 10^3~s$

Junior high physics teacher was obsessive about units, taught us to look at the units before looking at the equation. Now it's just a reflex I must live with ;)

Can you please stop excessive commenting and move over into the chat for this?

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text:
Is C. elegans always observed with precisely 302 neurons? Are there ever individual viable exceptions?
This answer mentions that the C. elegans hermaphrodite has exactly 302 distinct neurons. This has made it a very effective model for a variety of types of biological research, including neurology and cell differentiation. It is also currently the only organism with a completely mapped connectome.
But the word "always" made me wonder - has a viable specimen ever been verified to naturally have a number of neurons other than 302? Not as a result of an experiment, just naturally?

tag suggestions?

Well, at the most trivial level, males have 385 neurons compared to the 302 in hermaphrodites but I don't think that's what you mean.

@JackAidley Thanks - I've made an edit to reflect that. Assistance always appreciated!

Your comment to an answer made your question confusing. Are you asking whether wild-type C. elegans can develop with more or less neurons or whether natural mutants have been observed that have more or less neurons?

@canadianer The question is worded as intended, and doesn't try to pre-specify how or why it might happen beyond "(n)ot as a result of an experiment, just naturally." I'll add a comment below the one you've mentioned to make sure it doesn't affect interpretation of the question. Thanks for pointing it out!

The mutation studied in this paper prevents apoptosis and leads to mature worms with extra neurons. However, the mutation was induced chemically. https://www.ncbi.nlm.nih.gov/m/pubmed/3955651/

According to the highly respected WORMATLAS: A Database of Behavioral and Structural Anatomy of Caenorhabditis elegans, the number is invariable in this animal, one of the most studied in the world.

There are 302 neurons in the nervous system of C. elegans; this number is invariant between animals. Each neuron has a unique combination of properties, such as morphology, connectivity and position, so that every neuron may be given a unique label. Groups of neurons that differ from each other only in position have been assigned to classes. There are 118 classes that have been made using these criteria, the class sizes ranging from 1 to 13. Thus C. elegans has a rich variety of neuron types in spite of having only a small total complement of neurons. (Emphasis mine)

From the above, you might guess that the number of synapses are not, however.

The full list of synapses for hermaphrodite (including larval stages) and adult male are currently being reviewed and revised for the Wormwiring Project. All data comes from re/analysis of the sections for the hermaphrodite N2U, N2T, N2W and JSE animals, and male N2Y and n930 animals. The total counts of both electrical and chemical synapses are likely to be substantially higher than what was reported in the Mind of a Worm.

Would I be surprised if someone found a different number in a particular  specimen? No more so than when people are born with four kidneys, a parasitized twin, etc.
Edited to Add:
An article, Mutations that affect neural cell lineages and cell fates during the development of the nematode Caenorhabditis elegans has identified mutations with more or fewer neurons:

Specifically, unc-83 and unc-84 mutations affect certain precursor cells that generate both neural and nonneural descendants; lin-22 and lin-26 mutants lead to the generation of supernumerary neural cells with a concomitant loss of nonneural cells; lin-4, lin-14, lin-28, and lin-29 mutants perturb global aspects of developmental timing, altering the time of appearance (or preventing the appearance) of both neural and nonneural cells...

However, access to the paper is restricted, and I don't know if these mutations were induced (most likely were.)
HT to @canadianer for the link that led to my link.

Thanks, this is helpful, and the issue of synapse number and its variation is very interesting. But "I wouldn't be surprised" is not really a satisfying answer to my yes or no question.

That's because people like "yes or no" questions. But the truth is that there is very little in life that can be answered by "yes or no". An oft-quoted maxim in English is, "Nothing is certain but death and taxes." However, even that can't be relied upon. Will you die? Yes. Will you have to pay taxes? It depends.

Have you rarely given yes or no answers in stackexchange?

That is irrelevant to your question.

Rats! I started counting them - you have several high-fliers with very explicit yeses and nos, and was going to create an incredibly eloquent comment pointing them out, but then you brought in logic, and my flow is lost. Hopefully along the way, someone has published an account of a wild-type with an other-than-302 neuron number. I say hopefully because its a lot harder to defend a no in this case, but a yes just needs one example. I saw a four leaf clover once, that's all it took to know they can happen.

The comment above shouldn't have used the term wild type as it speaks too specifically to genetics. The point there is that a yes would require a single example, but a no would be more challenging to support, thus the four-leaf clover example.

@uhoh - Ha! I hope you see the irony of the above edit. It satisfies both of us. ;)

I'll come back again after having sufficient coffee firing neuron number, and see if I can.

Not only is the exact number of cells in C.elegans known but the lineages of each and every cell are known and traced back to the fertilized egg. Neuron map http://www.wormbook.org/chapters/www_specnervsys.2/neurogenesis_fig2.jpg
They are an easy model organism to work with. You can perform RNAi experiments by feeding the worms bacteria transformed with the construct for your RNA. They are transparent, making live imaging easier. Hermaphrodites will produce exact clones of themselves. Plus, if you feel like going home or taking the weekend off, you can freeze the plates and pick it up later.

@anongoodnurse my goodness that's a lot of mutations, and even a lot of mutation-naming citations! I see your point now - it would be surprising not to find an occasional individual hermaphrodite with a neuron number other than 302 if one looked hard enough. That may not be as rewarding as finding a four-leaf clover, so won't be doing any searching very soon. Thanks! - I've now asked the four leaf clover question.

Male C. elegans have 385 neurons http://www.wormatlas.org/male/neuronalsupport/Neuroframeset.html

Many Nematodes do not use traditional hox genes instead the have a strange set up which controls cell placement directly. This means individual adults of many nematode species have the exact same number of cells, it can even be used to identify species. So having the exact same number of neurons is what one should expect in nematodes. https://www.ncbi.nlm.nih.gov/books/NBK26861/
Although they may have two different but none the less exact cell counts due to gender, for instance you often see it written that C. elegans as about ~1000 somatic cells, what they actually mean is males have 959 somatic cells and hermaphrodites (there are no females)have exactly 1031 somatic cells. They count this by number of nuclei since the cell size can vary.
Note that this is also in ADULT specimens newly hatched specimens have only 558 cells, so you could look at newly hatched ones for a smaller neuron count.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Kitchen sponge microbiomes; management versus replacement versus "don't use sponges"?
I have unfortunately just skimmed through the recent open access paper Microbiome analysis and confocal microscopy of used kitchen sponges reveal massive colonization by Acinetobacter, Moraxella and Chryseobacterium species (M. Cardinale et al. Scientific Reports 7, Article number: 5791 (2017) doi:10.1038/s41598-017-06055-9)
It reports an extensive analysis of a group of kitchen sponge specimines. From the abstract:

Two of the ten dominant OTUs, closely related to the RG2-species Chryseobacterium hominis and Moraxella osloensis, showed significantly greater proportions in regularly sanitized sponges, thereby questioning such sanitation methods in a long term perspective. FISH–CLSM showed an ubiquitous distribution of bacteria within the sponge tissue, concentrating in internal cavities and on sponge surfaces, where biofilm–like structures occurred. Image analysis showed local densities of up to 5.4 * 1010 cells per cm3, and confirmed the dominance of Gammaproteobacteria. Our study stresses and visualizes the role of kitchen sponges as microbiological hot spots in the BE, with the capability to collect and spread bacteria with a probable pathogenic potential. (emphasis added)

A quick take-home message from the paper is that typical efforts to try to re-sanitize used sponges may only shift the sponges bacterial population toward a more potentially pathogenic population, and that it is probably a better idea to simply dispose of the sponge perhaps weekly and get a fresh one instead of microwaving it.
There's a nice write-up in the NYTimes science section, Cleaning a Dirty Sponge Only Helps Its Worst Bacteria, Study Says:

Stop. Drop the sponge and step away from the microwave.
That squishy cleaning apparatus is a microscopic universe, teeming with countless bacteria. Some people may think that microwaving a sponge kills its tiny residents, but they are only partly right. It may nuke the weak ones, but the strongest, smelliest and potentially pathogenic bacteria will survive.
Then, they will reproduce and occupy the vacant real estate of the dead. And your sponge will just be stinkier and nastier and you may come to regret having not just tossed it, suggests a study published last month in Scientific Reports.

Personally I've always hated the whole concept of kitchen sponges and now feel vindicated. Isn't something that can trap biomatter (bacteria, food particles) and keep it moist for extended periods of time the antithesis of what you would want to clean your dishes with?
Question: Aren't sponges simply a bad idea for washing dishes in the first place?
I'm not looking for opinion, rather I'm asking about policy and practice. Since what we do in the privacy of our own kitchen sink is our own, I'd like to ask if kitchen sponges are generally approved for use in restaurants or institutional food preparation settings? Do they have sterilization protocols? Does this paper speak to those?

Background:

above: "(A) Kitchen sponges, due to their porous nature (evident under the binocular; (B)) and water-soaking capacity, represent ideal incubators for microorganisms. Scale bar (B): 1 mm. (C) Pie charts showing the taxonomic composition of the bacterial kitchen sponge microbiome, as delivered by pyrosequencing of 16S rRNA gene libraries of 28 sponge samples (top and bottom samples of 14 sponges, respectively). For better readability, only the 20 most abundant orders and families are listed." From here.

above: "Neighbor-joining phylogenetic tree of the ten most abundant OTUs in the analyzed kitchen sponges, as retrieved by pyrosequencing of 16S rRNA gene amplicon libraries. The relative abundance (percentage of the total sequence dataset) and the detection frequency (number of sponges where they were detected) are given in parenthesis after the OTU number. The most similar reference sequences retrieved by BLAST and EzTaxon alignment (type strains only) were included in the tree, followed by the corresponding accession numbers. Red circles indicate risk group 2 organisms, according to the German Technical Rule for Biological Agents No. 466 (TRBA 46631). Numbers at the nodes indicate percentage values of 1000 bootstrap re–samplings (only percentages ≥ 50 are shown). Scale bar represents substitution rate per nucleotide position." From here.

I vote to close. This isn't a question but a review.

@David the section at the end with the sentences that end in question marks would be the question, as would the title (also has a question mark). How can you say this is not a question. I will add Question: to the question, in bold, to help you find the sentences that are ending in question marks (besides the title). There is nothing wrong with summarizing a small part of a recent paper as background to a question. It happens all the time. There is a big difference between a summary and a review, and this is not a review in any way. Your stated reasons for closing are not in line with SE.

@David you could also consider making some positive recommendations how to further improve the question, rather than reaching for the "insta-close" button. Public health and sanitary procedures are certainly on-topic here. If you'd like to see some improvement in the question, why not take a moment and explain what you'd recommend?

@uhoh - I don't think most of us can answer what restaurants do or don't do. There are probably not a lot of health inspectors on the site. As such, your major questions are probably as easy for you to google as for us. Norovirus is the most likely agent to cause illness from a restaurant; that's a virus, not a bacteria. Salmonella is high, as is listeria, campylobacter and e. coli. Other fecal-to-oral transmissions are harmful. If those aren't grown in the sponge, then you have a cruddy but not dangerous sponge.

Putting things into perspective (again, not a health inspector), you're less likely to get sick from food if employees wash their hands well after relieving themselves, if the public isn't allowed to touch/serve themselves the food (those tongs!), and the kitchen is kept clean.

@anongoodnurse thanks, but I'm asking about the nature of sponges, and if it's a good idea to use them to wash dishes and I'd like to stay focused on that. Wouldn't a non-porous mesh or scrubber be better than something that provides an ideal medium for growth? The same way that reusable wooden kitchen implements are discouraged or in some cases against code compared to plastic/teflon/metal.

@anongoodnurse I'm not interested in what "most of us" can answer. It would not make sense to hold back on question because "most of us" can't answer them, would it? In fact wouldn't "I don't think most of us can answer..." be equally valid on perhaps half of all the questions in any SE site, and particularly on the good and/or challenging questions? How is saying that helpful in this case?

Your question as stated seems to be about kitchen hygiene and not biology. Good questions in this area may or may not be appropriate on SE Health. 2. However, as posed "Aren't...a bad idea", the negation presupposes the answer "yes" and the word "idea" invites subjective discussion rather than fact. As such this falls into categories described in questions to avoid asking. So if you do post on Health, try to ask a precise question in a neutral way, e.g. "Is there any evidence that kitchen sponges are a source of disease?"

@David OK thanks! That's very helpful! Now that you've initiated the close process, I'm not sure if it makes sense to revise the question now, or wait until the whole thing runs its course. I'm probably a bit unusual in that I try to babysit my question and respond to helpful suggestions in real time to avoid closing, but once it's started it's often like trying to stop a train. Plus it's getting a bit late here for me to do some "inspired" rewriting, so maybe letting it run its course might be the best way to proceed.

I'm voting to close this question as off-topic because it is about healthy policy and not biology.

If your question is, indeed,

I'm asking about the nature of sponges, and if it's a good idea to use them to wash dishes and I'd like to stay focused on that.

I can answer that.
I like the sponge+mesh scrubber for washing dishes (not countertops or other) because the sponge conforms to the shape of things and reaches into crevices (with dishsoap and water) that I normally can't reach without more effort, and the mesh, well, scrubs. I don't care how grungy it gets; I rinse it out till it looks clean, throw it in the dishwasher when I run a load, which isn't often, and reuse until it's falling apart. Is it an ideal home for bacteria? Yep. You may think this is a red herring, but so is your toothbrush. Yet no one tells you to use a new toothbrush every week.
What is important is not what's in the sponge (or the toothbrush), but 1) how much of that bacteria stays deposited on the dishes washed with a sponge and rinsed with clean water, and 2) are any of the said bacteria dangerous to one's health?
Unfortunately, while the microbiome of the sponge was analyzed, the more important questions were not. There isn't a study yet that answers that aspect. So, until there is, I'll keep using my sponge without fear, as I do my toothbrush.
For example, the most common organisms grown from sponges were from the class Gammaproteobacteria. The important question is, is Gammaproteobacteria a pathogen?
What has been shown is that lack of Gammaproteobacteria in one's environment predisposes an individual to asthma and allergies. Also worth mentioning is that the mouth has a very high density microbiome itself,

The oral microbiome is comprised of over 600 prevalent taxa at the species level, with distinct subsets predominating at different habitats.

The oral microbiome is largely still unknown, but includes some of the species found in the kitchen sponge (chicken or egg situation?) Or is it that the prevalence of these organisms in our environment (including our hands) seeds the sponge and the mouth?

While the similarities suggest a kitchen sponge core-microbiome, the more variable fractions might differ from region to region. Clearly, more data from different regions are needed to support this hypothesis, but apparently bacteria affiliated with the Moraxellaceae seem “typical” for kitchen sponges. Interestingly, Moraxellaceae have been consistently detected on sink surfaces, faucets, refrigerator doors and stoves30, i.e. surfaces that might be regularly cleaned with kitchen sponges, suggesting them as source for these surface contaminations. However, Moraxellaceae also represent typical human skin bacteria, suggesting also other sources for the contamination of kitchen surfaces. In turn, human skin (hands) might represent a source for the contamination of the sponges with Moraxellceae during use. Recently it has been shown that in particular Moraxellaceae get significantly enriched on cotton laundry during a domestic washing process.

Should we stop laundering out cotton clothing?
As a physician (a shameless appeal to authority here), I'll worry when studies show that dishes washed with a sponge are colonized by harmful bacteria. So I'll continue to use my sponge to wash dishes partly because I like studies to be meaningful to health and disease, partly because I like my dishwashing sponge, and partly because whatever I use to wash my dishes (except my bare hands, which I deem insufficient to the task) will become a breeding ground for all manner of bacteria.
For all other kitchen cleanup, I use a cloth, which is doubtlessly packed with bacteria as well, but I can fool myself into thinking it is cleaner because I launder them every couple of days, or immediately after a relatively dirtier task.

Thank you for the wonderful answer! I appreciate you taking the time to put these results into perspective. There are all kinds of bacteria in all kinds of places, and if one looks, one will find them, so I was wondering if this article which touts the "massive colonization" of kitchen sponges in the title was scaring me more than it should. Indeed it's the rinsed dishes that matter, and I'm only guessing, but a few individuals of any of these bacteria on a plate is just not something to be afraid of in the grand scheme of things.

Why do you think it appropriate to answer a question on washing dishes on this list?

@David - It's about microbiomes. Where should I answer said question when it was asked here? Or are you trying to tell me you don't approve of an answer to a question you think deserves no answer? If so, that's your problem, not mine. I'm just obviously much nicer than you are.

I'm sure you are. But sometimes being nice isn't nice.

@David - I think that would make a good meta question.

I want to ask in Biology SE about the level of soapiness necessary to prevent this from happening... but I keep remembering your answer here and hesitating. I did ask Can some bacteria eat soap molecules in soapy water rather than get killed by it? How do they hang on to their surface lipids? Evolutionary advantage? and feel there is more answering possible there.

Hey, @uhoh! Yeah, I agree that the soapiness question would probably not be well received. I don't think soapiness is helpful for health reasons; soapiness addresses grease, which isn't as big a hit with bacteria as watery food particles. So, I think increased soapiness will help get rid of grease on dishes, but not bacteria. It also means more water wasting (it takes more water to rinse) and is much harder on your skin (breaks down protective skin lipids more.) Does this help?

@uhoh - I just realized I didn't address the effect of soap on bacterial cell walls. Sorry! I'd have to research that a bit to answer authoritatively. Again, sorry.

@anongoodnurse thanks for your help! I've read a little bit about alcohol on some kinds of viruses but soap vs bacteria seems like a much more complicated scenario.

@uhoh - Oh, yes, much more complicated!

Buy a jug of hydrogen peroxide. A nice big one. Rinse the sponge with the peroxide before use and then wait 5 minutes while the bacteria bleach out and die.
THEN stick it in boiling water to kill any that are left, if you REALLY hate germs. (Although the peroxide should do the job on its own).
Science behind this:
Hydrogen peroxide is a free radical/oxidizer. It desperately wants to oxidize something, and anything will do. It will oxidize the cell wall, weakening it, it will oxidize the phospholipid bilayer of the bacteria, which will pop the microbe, and even if the microbe has an unbreakable will to live, and can somehow stay intact up to this point, it will destroy the DNA and RNA inside. Seriously. If you actually want to see this happen, drop a piece of raw chicken into peroxide and see what happens.

Why the crap was this downvoted? It's a good solution. Looks like there's an anti-sanitizer propaganda/fake news/witch-hunt movement going around and downvoting everyone who suggest sanitizers and similar, spinning their own unproven opinion while putting the burden on proof on people who actually posted a constructive solution. Upvoted in opposition against #FakeDownvotes!

Lol that's funny

@user1258361 ps, I think your comment if funny. but... what IS anti-sanitizer propaganda? did you make that word up?

The best solution is to keep the bacteria in an incredibly hostile environment to prevent bacterial growth in the first place rather than letting the sponges rot and re-sanitizing them after the fact. Additionally, keep unused sponges in a container of aqueous fluid - bacteria grow best in moist/slightly damp conditions rather than a pond.
If you're going to use sponges in the kitchen, put an open plastic container next to the sink containing dilute benzalkonium chloride or cetylpyridinium chloride (quaternary ammonium compounds), and perhaps some extra swimming pool grade chlorine. Soak the sponge in the container when it isn't being actively used. That should largely prevent bacteria and mold from growing.

Dilute benzalkonium chloride (.07% to .11%) is used as a suitable alternative to alcohol-based sanitizers and generally considered safe (although you obviously will have problems if you get it in the eyes or accidentally drink large amounts of it - then again the same is true for regular dishwashing soap). Dilute cetylpyridinium chloride is readily available as antibacterial mouthwash. What I posted works, yet I get downvoted despite neither of you proving that it doesn't work. Dishonest and crooked downvotes with a hidden anti-sanitizer agenda. #FakeDownvotes!


text:
How do the three mechanisms of the 1000X improved "new" vancomycin work together?
The BBC News article Ultra-tough antibiotic to fight superbugs says (in part):

One hard-to-treat infection that has been worrying doctors is vancomycin-resistant enterococci or VRE.
It has been found in hospitals, can cause dangerous wound and bloodstream infections and is considered by the WHO to be one of the drug-resistant bacteria that pose the greatest threat to human health.
Some antibiotics still work against VRE, but the 60-year-old drug vancomycin is now powerless.
The Scripps team set out to see if they could revamp vancomycin to restore its killing ability.
They made some strategic modifications to the molecular structure of the old drug to make it better at attacking bacteria where it hurts - destroying cell walls.
Three changes in particular seem to be important, increasing the strength and durability of the drug.
Lead researcher Dr Dale Boger explained: "We made one change to the molecule vancomycin that overcomes what is the present resistance to vancomycin. And then we added to the molecule, two small changes that built into the molecule, two additional ways in which it can kill bacteria. So the antibiotic has three different, we call them 'mechanisms', by which it kills bacteria. And resistance to such an antibiotic would be very difficult to emerge. So it's a molecule designed specifically to address the emergence of resistance." (emphasis added)

Unfortunately I haven't been able to see the PNAS paper. The link in the BBC article just gives me this:

However the title in PNAS seems to be stated in the Genetic Engineering & Biotechnology News article Vancomycin Modified to Combat Growing Antibiotic Resistance Threat as "Peripheral Modifications of [Ψ[CH2NH]Tpg4]Vancomycin with Added Synergistic Mechanisms of Action Provide Durable and Potent Antibiotics"
It sounds to me that the first change was to keep the original vancomycin's original mode of action but to make it more robust against adaptations in the vancomycin-resistant strain, but I'm not sure if that's correct.
The other two differences sound to me like two new mechanisms that were not there before - it almost sounds like they could just as well be on different molecules administered simultaneously, and that their presence on the vancomycin molecule is primarily for issues of delivery.
Are these two new changes essentially independent modes of actions that could be on separate molecules, or do they need to reside on the same molecule as the primary mechanism?
The article puts the word "mechanism" in quotes. I'm trying to understand if these are independent or work together at the molecular level - in other words do they operate together in such a way that they need to be on the same molecule?

Unfortunately we have to wait until this paper is published and then see what the exact mechanism and the modifications are. My guess is that they chemically modified Vancomycin, but this can be wrong.

@Chris Oh, so it is not just me - nobody can see the paper yet? I thought it was just paywalled. I can't see how "They made some strategic modifications to the molecular structure..." could be interpreted in any other way than "chemically modified".

You can't see this paper unless you are a registered journalist. It is still under embargo until it is released - journalists only get access to it to get some more publicity. But I found some interesting information, I "only" have to write up the answer...

you can find some information about it on the "In the Pipeline" blog from Derek Lowe (http://blogs.sciencemag.org/pipeline/archives/2017/05/30/antibiotic-progress-and-not-a-moment-too-soon), but the link there also fails for me, so it looks like the embargo date is wrong for some reason.

@Chris et al. This seems related; same research group, but published a few years ago http://pubs.acs.org/doi/ipdf/10.1021/ja507009a

@MadScientist The blog is interesting reading, certainly some clues there at least. "...and in this new work they’ve got a compound that combines greatly improved potency with three separate mechanisms of action."

Since PNAS comes out weekly, my guess would be that the article is included in the issue which comes out today or the one next week. I will have a look at it.

@Chris thank you for your attention - I will "stay tuned."

Answer updated. :-)

This is typically for a paper under embargo - it can be accessed by registered journalists so they can cover the original article when it is published. The paper is now published, so I changed the first answer.
Before I go into the details, it is necessary to have a short look at the working mechanism of Vancomycin and the way bacteria got around it (which took exceptionally long given that the drug is used since 1959 in the clinic):
Vancomycin works by inhibiting the proper crosslinking of the bacterial peptidoglycan in the cell wall. This is achieved by binding to the substrate for the peptido glycane synthesis, a D-alanyl-D-alanine end of a peptide. Cells then burst due to osmotic pressure.
Resistant cells have a D-alanyl-D-lactate ending of this peptide (all details can be found here or in the introduction of the paper) which lowers the effictivity of the drug by a factor of 1000. Interestingly, this resistance mechanism seems not to have evolved in pathogen bacteria itself, but has been "borrowed" from bacteria which produce Vancomycin and need this as a self-defense (for more, see reference 2).
Vancomycin forms a pocket around the d-Ala-d-Ala substrate, which is impaired in the resistant form. Overcoming the resistance means finding a variation of Vancomycin which effectively binds both of the variants and thus inhibits proper cell wall crosslinking.
To achieve this, Okano and his colleagues chemically modified the structure of Vancomycin with several different functional groups at different sites of the molecule, see this figure from the paper (figure 4 from reference 1):

Changing these residues changes the sensitivity against these modified Vancomycine quite a lot, as can be seen in the sensitivity table in the figure.

When they changed the molecule, they did not only change the binding pocket to allow binding to the different peptide substrates, they also introduced two other independent mechanisms against the bacteria. The most active compound (named 18 in the paper, seen above from figure 11) shows:

Compound 18, which incorporates the redesigned pocket modification for
  dual d-Ala-d-Ala/d-Ala-d-Lac binding (blocks cell wall synthesis by
  ligand binding, including inhibition of transpeptidase-catalyzed
  cross-linking), the CBP disaccharide modification (blocks cell wall
  synthesis by direct transglycosylase inhibition without
  d-Ala-d-Ala/d-Ala-d-Lac binding), and the C1 quaternary ammonium salt
  C-terminal modification (induces membrane permeability), exhibited the
  most potent inhibition of cell wall synthesis in the assay of all
  compounds assessed.

Okano and colleagues also tested the different modifications one by one to see, which one has which effect and also tested the effectivity on resistant bacteria. The resulting table shows that the strongest effect is only achieved when all three modifications are present in the molecule.

Since these are independent mechanisms, it will also prolong the time until resistance against the new version of Vancomycin (given that is has a tolerable toxicity in humans and can be introduced into the clinic) will take a while to develop. Despite the optimism in parts of the paper this resistance will eventually develop, although it is quite complicated to overcome three different mechanisms.
References:

Peripheral modifications of [Ψ[CH2NH]Tpg4]vancomycin with added
synergistic mechanisms of action provide durable and potent
antibiotics
Glycopeptide antibiotic resistance genes in glycopeptide-producing
organisms.

My goodness! Did you have this already written and ready to go? This was quick, thanks! Certainly helps to have further reading. It will take me a while to read these. In the mean time, it it  likely that these changes must all be on the same molecule to work together, as compared to simply dosing with three drugs, each with one of the changes?

+1 I don't get to read papers like this anymore, so it was a refreshing answer. Now the cynical me wonders how many more thousands of times more expensive this new and improved vancomycin will cost to use. :-/

@uhoh Nope, I looked this up. Googling the the compound named helped, finding and pinning down information is critical and something I learned over the years in research :-) Plus: This topic interests me, so I read about it every now and then.

@anongoodnurse We haven't reached the clinics yet - but my guess (driven by my experience in the costs of the new cancer therapies) is also that this will be expensive.

@Chris - Sorry, a side question: I would guess this is all in vitro antimicrobial testing. Do you know if any in vivo testing for toxicity has been undertaken? It seems to me that would have been considered in developing this drug before releasing the information that there's a new vanc in the works.

@anongoodnurse I don't know, but I can have a look. It is probably also in this embargoed paper...

Thanks! Don't go to too much trouble, tho; it's really not in the OP's question. :)

@anongoodnurse It certainly may be in there to a trained eye, but I don't see "they have to all be on the same molecule" or "they could be on different molecules." If I say that I need some clarification, why not take it in good faith and help me understand?

@anongoodnurse I think you can say "if we want to decrease hemoglobin's affinity to CO, do we need to add some other molecule to it? No, you need a modified version of hemoglobin OR would just putting in a modified version of hemoglobin completely solve this? No, you also need to modify the molecules already in there". Maybe this won't work either (or maybe its just my lack of confidence :P)

The paper is out now and they use the components mentioned above. I will update the answer tomorrow. @anongoodnurse They mention no lytic activity against RBC, and also see no growth inhibition in cell based assays. Animal experiments as well as toxicity and tolerance studies in humans of course need to be done, but it looks pretty much like there is not much toxicity.

If I follow correctly (I could be wrong, I have primitive knowledge of ochem) the logic is something like this: protein binding is like fitting together two complicated jigsaw pieces, if they don't fit together properly they don't bind.  Binding to part of a molecule only works if there's a "space" and potentially produces other issues besides.  You could have two molecules to bind to the two types, but why not have one molecule to do it if you can get away with that?

@Kaithar This is exactly the problem. Getting Vancomycin to bind the actual two possible structures and prevent the crosslinking.

Thank you for the update! I'll head to the library and take a look in the next few days. It seems one can be exposed to a number of different concepts and issues from this particular example. So for example, the mechanism related to the CBP disaccharide modification also has antibiotic activity, and there's nothing in the paper that says it necessarily has to be on the same molecule as the other modifications, is that correct? The mechanisms seem to work independently and it's more of a convenience to put them on the same molecule versus a "cocktail" of one-at-a-time modified variants?

@uhoh The different mechanisms work independently, and it makes the component more potent. The 1000x more activity comes from the combination of all three. Nevertheless, the other two (not the substrate binding) could be of interest in similar antibiotics.

@uhoh - I finally realized what you were asking! I'm so sorry I misunderstood.

@anongoodnurse no problem! Through itteration and patience, stackexchange can make amazing things happen :)


text:
Why crystal violet inhibits growth of gram positive bacteria?
In microbiology lab, we use MacConkey agar to selectively grow Gram-Negative bacilli. Crystal violet is used as a component of MacConkey agar for inhibiting growth of Gram Positive bacteria.
However I can't associate this action of crystal violet on Gram positive bacteria specifically. What is the probable mechanism?


text:
Is there a way to derive Bazett's formula to correct QT interval in ECG?
As we know that QT interval in ECG is a function of heart rate (HR) and to comment on the pathology associated with altered QT interval, we must neutralise the effect of HR. For this Bazett's formula is broadly accepted, i.e. $QT_c=\dfrac{QT}{\sqrt{RR}}$.
Is it purely based on experimental data? Or, there is some mathematical logic behind it?
Here, $QT_c$ = correcred QT interval; $QT$ = measured in original ECG; $RR$ = RR interval.

Would anyone like to share their personal insight into this question?


text:
Is water movement across cell membrane purely diffusive or it always requires channels?
If we see nephrons, in the descending part of Loop of Henle (LoH), water movement is allowed but solute movement is not. On the contrary, in ascending LoH, solute movement is allowed but not water. What exactly restricts this movement?
I am particularly interested in understanding the movement of water across cell membranes and then answering the above query.

Water across cell membranes occurs due to osmosis( which is based on a concentration gradient). so water diffuses through the cell membrane. sometimes water channels called aquaporins can be found.
https://www.anaesthesiamcq.com/FluidBook/fl1_2.php
https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/aquaporin
In the loop of Henle, the water, and Na+ & Cl- exchange occurs due to the counter-current principle takes place. the interstitial fluid has a certain sodium chloride concentration. the filtrate that is entering the descending limb of the loop of Henle, has a particularly low NaCl concentration.so because of that water moves from the loop of Henle to the interstitial fluid.simultaneously, at the ascending limb of the loop of Henle just adjacent to that particular point, water concentration is high in the interstitial fluid. so because of that NaCl moves to the interstitial fluid (Na+ actively, and for ion balance, Cl- passively.) this happens along the length of the loop of Henle. what restricts water movement from the ascending limb of the loop of Henle is that that limb has no aquaporins and the descending limb has numerous (with relative to other places in the nephron). anyway, here's a link for you.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3468499/

Actually osmosis is based on a chemical potential difference, which is not quite the same as a concentration gradient.

So it means water movement is very minimal through physical diffusion. It requires an Aquaporin for transport across cell membrane. (Inspite of the fact that water is a tiny molecule)

yes. "The cell membranes of a variety of different bacteria, fungi, animal and plant cells contain aquaporins through which water can flow more rapidly into and out of the cell than by diffusing through the phospholipid bilayer". I got this from Wikipedia https://en.wikipedia.org/wiki/Aquaporin

As @Roshelle Perera points out, the textbook reason for differential solute and water movement in different parts of the LoH is osmolarity, which is nicely explained in this wikipedia article.

Coming to an interesting point, about the movement of water across cell membranes through aquaporins, this is helpful:{1}

The discovery of aquaporin membrane water channels by Agre and co-workers (6, 7, 191, 192) answered a long-standing biophysical question of how water crosses biological membranes specifically, and provided insight, at the molecular level, into the fundamental physiology of water balance and the pathophysiology of water balance disorders. Out of at least 10 aquaporin isoforms, at least 7 are known to be present in the kidney at distinct sites along the nephron and collecting duct.
Aquaporin-1 (AQP1) is extremely abundant in the proximal tubule and descending thin limb where it appears to be the main site for proximal nephron water reabsorption. It is also present in the descending vasa recta. AQP2 is abundant in the collecting duct principal cells and is the chief target for the regulation of collecting duct water reabsorption by vasopressin.

The journal further elaborates on these APQ's and their function in detail, do read it if you are interested, but the following diagram sums it up pretty well, so I am just going to expand on this:

A: schematic representation of the structural organization of aquaporin-1 (AQP1) monomers in the membrane (top and bottom).

Aquaporins have six membrane-spanning regions, both intracellular NH2 and COOH termini, and internal tandem repeats that, presumably, are due to an ancient gene duplication (top). The topology is consistent with an obverse symmetry for the two similar NH2- and COOH-terminal halves (bottom).

The tandem repeat structure with two asparagine-proline-alanine (NPA) sequences has been proposed to form tight turn structures that interact in the membrane to form the pathway for translocation of water across the plasma membrane.

Of the five loops in AQP1, the B and E loops dip into the lipid bilayer, and it has been proposed that they form “hemichannels” that connect between the leaflets to form a single aqueous pathway within a symmetric structure that resembles an “hourglass.”

B: AQP1 is a multisubunit oligomer that is organized as a tetrameric assembly of four identical polypeptide subunits with a large glycan attached to only one.

The direcrion of flow of water, again, depends on osmolarity.

...Only inward water flow (swelling) was examined, but it was predicted that the direction of water flow through AQP1 is determined by the orientation of the osmotic gradient. Consistent with this, it was later demonstrated that AQP1-expressing oocytes swell in hyposmolar buffers but shrink in hyperosmolar buffers.

Please note that the linked journal is brilliantly detailed, so there are several points that I have skimmed over. I recommend reading it if you have time.
{1}-https://journals.physiology.org/doi/full/10.1152/physrev.00024.2001#:~:text=Aquaporin%2D1%20(AQP1)%20is,for%20proximal%20nephron%20water%20reabsorption.&text=AQP2%20is%20abundant%20in%20the,duct%20water%20reabsorption%20by%20vasopressin.


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How are Current Sources and Sinks for Postsynaptic Potentials defined?
I am currently reading "Electric Fields of the Brain" by Paul Nunez, and encountered this passage:

The synaptic inputs to a neuron are of two types: those that
produce excitatory postsynaptic potentials (EPSPs) across the membrane of
the target neuron, thereby making it easier for the target neuron to fire an
action potential and the inhibitory postsynaptic potentials (IPSPs), which act in
the opposite manner on the output neuron. EPSPs produce local membrane current sinks with corresponding distributed passive sources to
preserve current conservation. IPSPs produce local membrane current
sources with more distant distributed passive sinks.

Can somebody explain why EPSPs would produce current sinks instead of sources (and likewise why IPSPs would produce a source)? I was under the impression that EPSPs would propagate a signal, instead of terminating them, making them act more like a source.

Sinks and sources just refer to the sign of the local field potential measured with extracellular electrodes.
Excitation involves positive charges entering cells, depolarizing them. When positive charges move into a cell, there is less positive charge outside the cell where the electrode is, so it becomes more negative. This is called a "sink" because the electrode records a negative deflection.
Inhibition is a bit more complicated because shunting inhibition does not involve much net movement of ions, rather it involves opening chloride channels with reversal potential near the resting membrane potential, which prevents cation channels from contributing to depolarization (sodium coming in the cation channels is balanced by chloride coming in the inhibitory channels).
Charge flows in circuits, so when you get negativity in one place you get positivity elsewhere and vice versa. If you stimulate a cell near its soma such that positive charge enters the cell there, the positive charge will flow into the rest of the cell but also attract negative charges towards it. The result is that membranes out on distal portions of the cell become slightly (because this is over a wide space) more positive inside, which in turn repels positive charge outside the membrane so an electrode near the fringes of a cell but not near the stimulation site will actually record a source. Generally in CSD recordings these types of sources dominate over inhibition, it's very difficult to record a "current source" and attribute it to inhibition.
I attached a few references below; I think the Olejniczak paper is a good place to start. It's focused on EEG but will help understand how what goes on inside neurons affects what we measure outside of them. Nicholson & Freeman talk about the theory behind current source density and is probably a straightforward read if you're familiar with the physics/math of electricity. Mitzdorf is a longer review article that talks more about the information you can get from a CSD and talks about the difficulty in interpreting sources that I mention.

Mitzdorf, U. (1985). Current source-density method and application in cat cerebral cortex: investigation of evoked potentials and EEG phenomena. Physiological reviews, 65(1), 37-100.
Nicholson, C., & Freeman, J. A. (1975). Theory of current source-density analysis and determination of conductivity tensor for anuran cerebellum. Journal of neurophysiology, 38(2), 356-368.
Olejniczak, P. (2006). Neurophysiologic basis of EEG. Journal of clinical neurophysiology, 23(3), 186-189.


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Can a species include only one subspecies?
Wikipedia says: A single subspecies cannot be recognized independently: a species is either recognized as having no subspecies at all or at least two, including any that are extinct. I do not understand this concept, please explain.

Heard today (TV) that red pandas are considered a single species .

it might be possible if a known specie goes extinct so only a subspecie remain,but then the subspecie will become the main specie and your whole question falls apart :)

Think about it like this:

How can a you subdivide 1 individual and still get a whole?

The answer is, you can't.
For there to be subspecies you need to have defining characteristics that can be used to separate individuals within the population into groups. This means that you need at least 2 to divide into.
Now there's a little tricky ground here - you could have an extinct subspecies as one of the subspecies (e.g. Homo sapiens neanderthalensis, if you follow the trend that Neanderthals are not a separate species) - meaning that the humans you see around you can't be subdivided into subspecies, but can still a subspecies that could be called Homo sapiens sapiens

In biological classification, the term subspecies refers to one of two or more populations of a species living in different subdivisions of the species' range and varying from one another by morphological characteristics. A single subspecies cannot be recognized independently: a species is either recognized as having no subspecies at all or at least two, including any that are extinct.

Thst is, subspicies are defined by opposition to each other: e.g., taller vs. shorter, bright vs. bleak, etc. Such a definition logically implies (at least) two types of specimen.


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How related are trees?
I was surprised to see how far apart macadamia and hazelnuts are from each other. I always thought all trees had a common ancestor that was also a tree. But that doesn't seem to be the case? Did wood evolve multiple times?

Welcome to Biology.SE. You seem to be assuming that the first flowering plant wasn't a woody plant. IIRC at least one hypothesis about the origin of angiosperms contradicts this assumption. Wikipedia looks like a reasonable place to start checking what the latest thinking on this is, but if that is correct then herbaceous angiosperms have lost "treeness". Also, please edit your title — it doesn't seem to reflect your actual question because trees occur outside the angiosperms!

WRT evolving multiple times, consider bamboo, which is botanically a grass, even though some varieties can be tree-sized, and the stems are to all appearances a kind of wood.

The word "tree" is a not a taxonomic classification, but a human perceptual clustering based on form and size. The word "fish" has a similar problem, covering a vast collection of taxa, some of which are less closely related to one another than they are to us.
Becoming tree-like often has a strong evolutionary value, because plants compete for sunlight and taller plants shade shorter plants. Thus, we should not be surprised that "tree" forms have evolved independently in a number of different lineages.
The common evolutionary lineage for all of these, however, is tracheophyta, the vascular plants.  These are plants that have differentiated xylem (which is the wood of a tree) and phloem tissues for transport of water and minerals. Most such plants are not trees, of course, but these tissues provide an effective means of vertical transport and the basis for hard woody material, which  appears to have been the key differentiator between plants capable of evolving into trees and plants that are not able do to so.


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If stomata is closed at night ,how does exchange of oxygen take place at night?
In this article in the second paragraph, it is written that the stomata remains closed at night to reduce water loss. We know that the plants respire and take in oxygen at night. Then how do plants take in oxygen i.e. respiration takes place at night?
Again in this article, it is written that the oxygen during respiration is taken through stomata. Which is correct ??

What does the bar-graph in the first article show about the gaseous exchange at the "closed" stomata?

I can't see where it's written ''closed at night to prevent water loss''? Article is very clear, that stomata closes due to extreme conditions faced by plants. suggest to read it again.

It's clearly written " In leaves, they typically open during the day to favor CO2 diffusion when light is available for photosynthesis, and close at night to limit transpiration and save water". Please read the second paragraph's second line properly..

I recommend looking at figure 1 here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4940480/. Plants don't run out of O2 overnight, they can store it!

Apart from what's written in the article, stomata typically close at night as there's no sunlight so no photosynthesis. Respiration however continues 24/7 but the rates vary. During the night, the rate of respiration drops since stomata are closed. But it never drops to 0. Respiration still happens as oxygen exchange can still be done through the following three routes:
. Direct diffusion of oxygen through the waxy cuticle in minute amounts
. There are small pores in the stem region called lenticels which allow the exchange of oxygen
. Some small open spaces left in the stomata even after the closure of stomata
Here's a link for reference: https://bio.libretexts.org/Bookshelves/Introductory_and_General_Biology/Book%3A_Biology_(Kimball)/16%3A_The_Anatomy_and_Physiology_of_Plants/16.02%3A_Plant_Physiology/16.2D%3A_Gas_Exchange_in_Plants#:~:text=the%20plasma%20membrane.-,Leaves,stomata%20(singular%20%3D%20stoma).&text=Normally%20stomata%20open%20when%20the,and%20close%20during%20the%20night.
Hope it helps.


text:
Are the complementary base pairs known as genes?
In my text book ,it is written that a chromosome has 1000s of genes and it is distributed throughout the chromatids except in the centromere. But we know that the chromosomes have DNAs inside them which have complementary base pairs. Then are these base pairs known as genes??

A chromatid is a single hundred of million bases DNA molecules, glued to its complement and a chromosome is two identical copies of that chromatid.  You might want to look at https://www.ncbi.nlm.nih.gov/nuccore/NC_000001.11?from=1000&to=100000 you can see that the region 10875..13410 encodes a gene named DDX11L1 whose sequence is given below. So the genes are those kind of annotated pieces of the chromosome sequence, mainly dedicated to understanding the mRNA whence the proteins that will be produced from it.

what do you think is meant by "complementary base pairs"? Have you researched this term at all?

Don't assume a chromosome to be some X-shaped box that contains DNA inside it and DNA as a container of genes.
DNA, genes, Chromatid, Chromosomes are just different names at different levels of the same thing.
In molecular biology, you'll find multiple definitions of certain terms because as new insights are gained by any researcher, the definition gets modified. So one has to always make their concept clear so that they don't get confused between the same yet uniquely different terms.
So, Let's first look at how different their definitions can be:

DNA is a molecule inside cells that contains the genetic information responsible for the development and function of an organism. DNA molecules allow this information to be passed from one generation to the next. DNA is made up of a double-stranded helix held together by weak hydrogen bonds between purine-pyrimidine nucleotide base pairs: adenine (A) paired with thymine (T), and guanine (G) paired with cytosine (C). Also called deoxyribonucleic acid.

GENE, For many years the HGNC has maintained the definition of a gene as “a DNA segment that contributes to phenotype/function. In the absence of demonstrated function a gene may be characterized by sequence, transcription, or homology”. As there is still no universally agreed alternative we continue to use this definition.

Chromosome is a highly coiled structure of DNA molecule. Often observed in X-shaped only. Along with DNA, some proteins are also make up chromosomes.

But Why does DNA need to be coiled tightly into chromosomes?
DNA double helix is like a telephone wire. If length is to be measured, it will go beyond 60 miles. Some even say it can make a trip to the moon more than 150,000 times. Such a long DNA molecule is not only the part of each organism's cell nucleus but also it's invisible to the naked eye. This happens just because of the high packaging and coiling of this long DNA molecule.
Let's see the diagram to get an idea.
At the bottom  of the diagram there is a sequence of nucleotides (ATGC) in different combinations. This can be considered as a gene if it codes for certain protein which is required for the growth or any other function of the body.
Returning back to your question, Complimentary base pairs are not genes.
Genes are the segments of DNA which is a long sequence of nucleotide base pairs that code for any protein or RNA transcript that contributes to any trait/phenotype/function of an individual.
With the tight packaging of DNA double helix along with help of packaging proteins(Histones and Non-histones), the chromatid and chromosomes are made. The packaging of DNA to chromosomes is highly controlled and is a whole different topic in itself.

Firstly, even in the centromere region, complementary base pairs are found, so, if base pairs were to be known as genes, then genes would also be present in the centromeric region.
Secondly, Genes are functional units of DNA made of one or more codons which store information to make protein which gives an organism a certain characteristics.
Basically, DNA is made of two complementary strands of nitrogenous bases [ Adenine(A), Thymine(T), Guanine(G) and Cytosine(C) ]. Read/ Watch
Now that you know the structure of DNA, realize that information may be stored by the order in which the Nitrogenous bases are placed. Exactly this strategy is used by your cells, to build your body, in other words, you.
I am not writing about the process by which that information is interpreted by your body, since that is beyond the scope of the question, still, you can Read/ Watch about it.


text:
How to memorize Transcription and Translation?
I often get confused between transcription and translation. Is there any way to memorize them easily like a mnemonic??

I prefer a conceptual distinction rather than a mnemonic in this case.
I've always thought of a transcript as an exact copy of record - that's the meaning of the word in English, and an RNA transcript is effectively an exact copy of the DNA message. Sure, there are complications like the uracil in RNA, and that the strand that is actually copied from has the complementary bases, but you still have a molecule containing the same message and you could easily go backward to DNA if you wanted.
A translation, however, is moving to another "language". When you make a translation of a document, you're not making an exact copy, you're taking the meaning of a source document and representing it in another form. Similarly, translation of mRNA into protein is moving from the language of nucleic acids to the language of amino acids. Once you've translated, you can't go back to an exact copy of the original. You could get pretty close, but the redundancy of triplet codes means you can never get the exact RNA/DNA bases back from just the protein.


text:
In phloems, does the sap move through the sieve element cytoplasm?
We know that in xylems, the water move through the lumen of the vessel elements and move to the other vessel element through a pit. As the vessel elements are dead , there is no cytoplasm to block their way. The water can move through the cell walls(apoplastic pathway) or through the cytoplasm (symplastic pathway).
Phloems are living tissue and made up of sieve elements and companion cells. I have a doubt regarding the movement of sap in phloems.
In phloems, does the sap move through the sieve element and move to the other seive element through sieve plate pore? If yes, does the sap move through the sieve element's cytoplasm (like symplastic pathway) ? If no, then how does the sap move?
I guess there is no function of companion cells in the transportation. Their only function is to carry metabolic activities in sieve elements.

In phloem, the sieve tube elements are not lignified so no concept of 'pits' and since cell wall is permeable (cellulose) and also has plasmodesmata, substances can easily transfer through diffusion and/or osmosis. Sieve tube elements are living cells having reduced cytoplasm restricted to the sides and the sieve pores in the sieve plates are modified versions of plasmodesmata. This allows a nearly empty lumen for continuous bulk transport of organic food solution.
Companion cells keep the sieve tube elements alive and help them in their transport act.
For further details visit the following website:
https://academic.oup.com/jxb/article/64/16/4839/593231
You can also find many books explaining the whole process.
Hope it helps.


text:
Trouble in understanding graph of pressure time in different chambers of heart

In the book, it is written that from 0 s to 0.125 s-Atrial Systole; 0.125 s to 0.325 s-Ventricular Systole; 0.325 s to 0.6 s-Ventricular Diastole
Why a bump is there from 0.125 s to about 0.175 s in the pressure-time graph of left atrial pressure and why is the pressure in the left auricle increasing during the ventricular systole and ventricular diastole stage (from 0.175 s to 0.45 s)?

A previous Biology.SE question has a diagram with a bit more information on it...

When the ventricles starts to contract, the AV valves close as the pressure rises very quickly in the ventricle and exceeds that of the atria; the blood in the atrium is going to be squeezed a bit at that point between the atrial wall and AV valve, that's the little uptick "0.125 s to 0.325 s".
From 0.175 s to 0.45 s the AV valves are still closed but blood is trickling into the atria and they're getting passively distended. You can see the pressure drops again when the AV valves open and the ventricles begin to fill from the atria.


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What is the name of this mosquito-like insect?
While I was studying, this insect fell down from the ceiling. It was alone and not in a swarm. It looked much like a mosquito but is quite larger compared to a mosquito..
I live in the Indian subcontinent (India).

Can anyone identify it??

It is a Crane fly (Tipulidae), which is a large, cosmopolitan family of flies in the order Diptera (true flies). There are about 15,000 species according to Wikipedia and some 500-odd genera.
The crane flies are sometimes known as "daddy longlegs" though this name is more commonly associated with arachnids in the order Opiliones. Both the harvestmen and the crane flies have long, jointed legs. Crane fly legs fall off fairly easily, so if you brush one off a curtain or your clothes, you are often left with a loose leg.
They are harmless, despite appearing like a giant mosquito. They like damp environments, but can be found almost anywhere there is pasture or forest nearby. They typically need a fresh water source or moisture for the larvae to mature.