astrobiology - In our solar system which other planet could have been in the "habitable zone" in the past?

This answer is also speculative, but according to the planetary habitable zone models proposed by "Habitable zone for Earth-like planets in the solar system" (Franck et al. 2000), a key finding was that:

an Earth-like planet at Martian distance
would have been habitable up to about 500 Ma ago while the position of Venus was always outside the habitable zone.

So, Mars could have been habitable, but as it is much smaller than Earth, it has a smaller gravitational field presumably a major factor in how it lost much of its atmosphere.

molecular biology - Termination of translation

Shigeta's got a point: the ribosome is latched onto the mRNA so those two are intrinsically linked. You're really asking whether the ribosome comes off first or whether the tRNA does, but it's actually the new polypeptide, which makes sense:

The stop codon is recognized by a protein, the polypeptide chain release factor (RF), which triggers the hydrolytic release of the nascent polypeptide chain from the P-site-bound peptidyl-tRNA.

This minireview puts forth a model (see below) where, in E. coli at least, the 50S ribosome subunit is then dissociated from the mRNA/30S subunit/tRNA complex, following which the final tRNA is removed. An in-depth review from a few years later gives more context.

Effect of extracellular molecules on membrane potential

The absolute answer would depend on a lot of factors, but the basics of it would be that - Yes, the volume does change and Yes, it would have an affect on the membrane potential.

By adding mass to any liquid solution, you are changing the volume. Plain and simple. Liquids are not compressible, and the only way to maintain volume while adding mass would be to increase the density of the liquid. [Edit] I'm wondering if you don't mean increase the volume of the cell - in which case, in extreme conditions where the cell cannot maintain water and salt concentrations, the cell would lose volume as water and salts move out. In a hypotonic solution (much more water than solutes), the cell would lyse as osmotic pressure favors water moving into the cell

The membrane potential would change, but how much depends on a lot of factors. It would most likely change due to the movement of ionic solvents down their concentration gradients. Osmosis would move water out of the cell and into the extracellular environment, and ultimately reduce the membrane potential as more water outside the cell would essentially decrease the molarity of the solution. The cell would have to pump more ions out in order to regain the membrane potential.

The exception might be if you added so many hydrophobic molecules outside the cell that you basically saturate the environment, which could prevent exchange of all charged or partially charged atoms and molecules.

biochemistry - Why is absorbance at 280 nm for protein solution going up when I measure repeatedly?

It looks like your protein concentrations are right on the limit of detection of the spectrophotometer, and changing the diluent buffer changed their concentrations. The samples may not have been thoroughly mixed after dilution and before measurement, so the varying measurements may simply be the solution coming to equilibrium. Temperature can also affect absorbance, so you should verify that your samples have equilibrated before drawing any conclusions. If the absorbance of your phosphate buffer is 0.03, I'd try to keep the sample absorbances above 0.075 or higher to avoid getting too close to the limit of detection. Also, make sure your buffer isn't too old or contaminated with something which could be affecting its absorbance characteristics.

I would suggest taking one or two protein samples and doing a dilution series (1:1, 1:5, 1:10, 1:20) in a large-ish volume (say 400 ul each, if you can spare it), vortex briefly to mix well, then measure triplicates of each dilution on your reader, along with appropriate blanks (buffer only). You will see differences between each measurement, but it should be quite small, depending on the accuracy and precision of your instrument.

Measured values will not be exactly the same from measurement to measurement, and it would take a lot more than three repetitions to determine if there was an actual drift trend occurring. Measure your sample plate every 5 minutes for an hour and plot the values (don't just eyeball them) to see if the machine may need to be serviced.

genetics - How do circulating androgens contribute to higher rates of hirsuteness in some women?

I was reading up on ethnic groups in which the women are naturally more hirsute (such as South Asian women) in the context of evolving standards of beauty. I came across this statement on a forum:

Hirsutism is much more common in South Asian women (particularly North Indians such as Punjabi Sikhs) asymptomatically because they tend to have higher levels of circulating androgens than your typical [North or Western European ethnic group]. This is also true of Eastern European women to an extent.

Per Wikipedia, I learned:

Circulating levels of androgens can influence human behavior because some neurons are sensitive to steroid hormones. Androgen levels have been implicated in the regulation of human aggression and libido. Indeed, androgens are capable of altering the structure of the brain in several species, including mice, rats, and primates, producing sex differences.

So: do circulating androgens trigger higher testosterone production in some women? Is this what yields higher instances of "hirsutism" among certain populations? How are some women more prone to this than others? (That is, per the forum post, why are South Asian women more likely to have this than Western European women?)

neuroscience - The Operation of tuning in the S1 layer of ventral model

According to my previous question in ventral Stream pathway and architecture, I want now to get a brief example about how the S1 layer is constructed. In other words, how all the simple units are tuned with the gaussian-Like tuning (for example). I am only interested to get such a cartoon example in step by step how this operation can be achieved in given of inputs (which inputs? and what we mean about these inputs?) in order to obtain the tuned simple units.

We all know that each simple unit is obtained after a tuning operation around their inputs (Subunits) in order to select an optimal output which corresponds to the preferred orientation for such a simple unit.

Moreover, I know that the S1 layer units perform a convolution on regions of the raw input image using gabor filters at different orientations and sizes. The entire population of S1 units represents a convolution map of Gabor filters of different sizes and orientations with the entire raw image (really I didn't understand this point) you can read the subsection 2.2 in this article

The image below contains the image to be recognized by the brain and some simple units obtained after the tuning operation. So what I want is to obtain a brief example which can include the details (step by step) of how the operation of tuning can be achieved.

i didn't understand well the concept. That's why i need a real example with a specific image which can contains all the steps described in my attached image (step by step) because i still don't understand what we mean about inputs x, etc.
So please if anyone can give me a real example with a specific image which can respond briefly to this attached image

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.