human biology - Can a color-deficient person be made to visualize the missing colors?

It is a very interesting question and I did some efforts to investigate the literature on this topic, but yet I don't have a definitive answer for you. But let's start from the beginning.

First of all, the reason for color deficiency can be not only lack (rare) or impairment (more often) of certain types of color-perceiving cells (cones) in retina, but also brain injures: the central color blindness can develop after head trauma or as a result of some neurodegenerative deceases, like Parkinson's decease. In case of brain origin of the color blindness it is usually the complete color blindness (no color is percieved), whereas congenical primary color blindness (receptor-based) is usually just the unability to distinguish one or two colors, whereas the rest can be more or less separated.

I searched Pubmed for the literature on the topic and found a recent PNAS paper about the simulation of primary and secondary visual cortex on humans using intracranial electrodes. As they describe their results (bold font by me):

When percepts were elicited from late areas, subjects reported that
they were simple shapes and colors....

But the paper investigated only healthy humans, no color impaired subjects were used for the tests, so cannot conclude from here whether we can elicit the perception of the color the person is incapable to see with the eyes using these stimulations.

I took this paper as the starting point and did some reference research, looking for the paper referenced there and for newer publications referencing this one: PNAS is one of the top journals in this area with very high impact factor and if there were a publication about brain stimulation and color blindness I would have definitely identified it.

During my investigations I came accross a series of interesting articles devoted to "cortical visual neuroprosthesis for the blind" (read this paper^<1> from 2005 for review on this topic), but this is the treatment of conventional blindness, not the color blindness. There was no intersection in keywords or titles for color blindness and brain stimulation, both in the referenced articles and in the complete article database.

So, I would suggest that you address some talented experimentalist with your question and maybe one day, who knows, we will read your name under the Nature article dedicated to the novel way to cure color blindness.

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^<1> -- unfortunately not available publicly for free, I am sorry.

human biology - Does cooking ginger reduce its anti-nausea effect?

There seems to be strong evidence to support the hypothesis that eating ginger helps reduce nausea e.g. during pregnancy (e.g. Vutyavanich et al.). It seems that gingerol is the active ingredient in preventing nausea (cf. Qian et al.). Wikipedia writes: "Cooking ginger transforms gingerol into zingerone...". Presumably, zingerone does not affect nausea.

Question: Does cooking ginger reduce its anti-nausea effect?

A Google search will reveal numerous suggestions for giving ginger tea to pregnant women to help with morning sickness. But boiling the ginger could conceivably defeat the purpose of taking the ginger in the first place (and any effects are primarily due to the placebo).

There's an article (Basirat et al.) which describes an experiment in which biscuits with ginger were given to patients (instead of ginger tablets), although their results alone have not convinced me one way or the other. The authors conclude that their results indicate an anti-nausea effect, but some of their tests do not match that conclusion (i.e. a placebo was comparably effective). Also, the group given the ginger biscuits started off with worse conditions on average.

neuroscience - Latency to audition in human beings?

There are several ways to infer into the propagation delays of auditory system in vivo that is applicable to humans (i.e. leaves the subjects intact).

One of them is so-called ABR that stands for Auditory Brainstem Response. As it is clear from its name this method allows you to derive the brainstem response to an auditory stimulus (so, you can track the auditory pathway up to its input into thalamus), but its resolution is so fine that you can separate single components ("waves") for the following path segments (from Wikipedia):

Wave I – generated by the peripheral portion of cranial nerve VIII
Wave II – generated by the central portion of cranial nerve VIII
Wave III – generated by the cochlear nucleus
Wave IV – generated by the superior olivary complex/lateral lemniscus
Wave V – generated by the lateral lemniscus/inferior colliculus

So, it takes only 10 ms for the signal to reach the input into thalamus. This correlates well with some auditory signal based activities, like startle reflex, which was also shown to have about 10 ms latency.

I tried to search for some electrophysiological recordings from auditory cortex (temporal lobe) paired with auditory stimuli, but the first paper I came accross that is available for free (and which I can also link from my answer) is this work done on monkeys.

If you look at Figure 1:

This is the results from multiunit recordings and you see that the initial activity in the cortex starts approximately 20 ms after the stimulus onset with a short activity pattern, followed by some short break and then longer period of activity with broader frequences spectrum.

In my opinion the delays in signal propagation are not due to complex signal processing in the olivary nucleus or any other brainstem structures, rather they are due to electro-chemical transformations in CNS synapses.

The initial arrival of the signal into the cortex does not mean the perception of the sound, it definitely takes hundreds of millisecond until the conditioned cortex-mediated response to this stimulus.

Which cells are responsible for the extracellular matrix remodeling?

Taken from The role of matrix metalloproteinases (MMPs) in the pathophysiology of chronic obstructive pulmonary disease

Metalloelastase (MMP-12) is (as the name suggests) capable of
degrading elastin, as well as other extra-cellular matrix components.
It is produced predominantly by infiltrating macrophages and appears
essential for macrophage migration through extra-cellular matrix

Matrix Metalloproteinases in Cancer Cell Invasion gives a more thorough description of the various MMP and TIMP types

MMPs are mainly produced by nonmalignant stromal cells in malignant
tumors. Tumor cells also secrete factors, such as extracellular MMP
inducer (EMMPRIN), which enhance the expression of MMPs by stromal
fibroblasts (see Toole, in this book). In addition, growth factors and
cytokines secreted by tumor-infiltrating inflammatory cells as well as
by tumor or stromal cells modulate MMP expression.

zoology - How is the blood volume of a living organism measured without killing it?

Polynomial gives a good hint. By adding in a known tracer of known amount that should only circulate in the blood stream, the concentration of the tracer when completely distributed will give the volume of distribution.

If the tracer only stays in the bloodstream (and that's a fairly large IF), then the V_D will be equal to the V_Blood. However, as many pharmacologists know, interactions with proteins and cells can skew that number. The blood volume is also reduced by the volume of the blood cells. However, using Andrei's method of dilution, one can merely swap the cell counts with the tracer concentration.

zoology - How do porcupines keep from pricking each other while mating?

The female stood with the tail held sharply to one side, and the quills on
the back lying very flat. The male stood on his hind legs, while the
front legs grasped the sides of the female. There was no repetition of the act.

The male's urethra is 115-120 mm long, and his penis is 75 mm, so the he doesn't need to be as close to the female as one might think. The retractor muscles are attached to the lower portion of the pelvis, which is likely well below the level at which the male's quills end.

Apparently, a dozen or so porcupines will den up in close quarters for the winter, so one can probably guess they have a good sense of whether their spines are hurting another, but that's only conjecture.

I suppose the take-home message is, nature will find a way.

Struthers, P.H. (1928) Breeding Habits of the Canadian Porcupine (Erethizon dorsatum). Journal of Mammalogy, 9(4), 300-308. http://www.jstor.org/pss/1374084

Mirand,E.A., Shadle,A.R.(1953). Gross anatomy of the male reproductive system of the porcupine
Journal of Mammalogy, 34(2), 210-220. http://www.jstor.org/pss/1375622

How should I ship plasmids?

Summary

• the 10 uL of plasmid miniprep may have been splattered in the cap of the tube (AnnaF)


• the eppendorf tube may have depressurized during air shipment and allowed the 10 uL to escape and evaporate


• solution: try air-drying or blotting (Jonas) your minipreps prior to air shipment

Details

As AnnaF wrote, the 10 uL of your plasmid could have been hidden in the cap or dispersed around the tube, making appear empty. You should check with your collaborators to be sure they centrifuged it.

According to a fedex document on shipping perishables (pdf) and a paper measuring the temp and pressure of air shipments (pdf), fedex and ups air shipments may experience low pressure environments around 0.56 - 0.74 atmospheres (atm). At these relatively low pressures, perhaps an eppendorf tube sealed at 1 atm might breach. The papers also note that ground shipments that pass over the rockies (i.e. in Colorado) may experience ~ 0.64 atm.

So perhaps your 1.5 ml eppendorf tube depressurized during the shipment?

It would be interesting to do some tests on the pressure-worthiness of eppendorf tubes.

Regarding the original question, in 2007 I prepared and shipped (fedex) a library of thousands of minipreps to hundreds of users. 1uL of miniprep was dispensed into wells of 384-well plates and airdried, then sealed with aluminum, then mailed. Users rehydrate a well with 10 uL of water. Generally it works.