FETs are further divided into depletion-mode and enhancement-mode types, depending on whether the channel is turned on or off with zero gate-to-source voltage. For enhancement mode, the channel is off at zero bias, and a gate potential can "enhance" the conduction. For the depletion mode, the channel is on at zero bias, and a gate potential (of the opposite polarity) can "deplete" the channel, reducing conduction. For either mode, a more positive gate voltage corresponds to a higher current for n-channel devices and a lower current for p-channel devices. Nearly all JFETs are depletion-mode because the diode junctions would forward bias and conduct if they were enhancement-mode devices; most IGFETs are enhancement-mode types.
If it is possible to answer this question, answer it for me (else, reply "unanswerable"): At what point is a channel on in depletion-mode?
Ah, so.. at zero bias

Expansion caused controversy about Yale's new roles. Noah Porter, moral philosopher, was president from 1871 to 1886. During an age of tremendous expansion in higher education, Porter resisted the rise of the new research university, claiming that an eager embrace of its ideals would corrupt undergraduate education. Many of Porter's contemporaries criticized his administration, and historians since have disparaged his leadership. Levesque argues Porter was not a simple-minded reactionary, uncritically committed to tradition, but a principled and selective conservative. He did not endorse everything old or reject everything new; rather, he sought to apply long-established ethical and pedagogical principles to a rapidly changing culture. He may have misunderstood some of the challenges of his time, but he correctly anticipated the enduring tensions that have accompanied the emergence and growth of the modern university.
If it is possible to answer this question, answer it for me (else, reply "unanswerable"): What caused agreement about Yale's new position?
Ah, so.. unanswerable

Obesity can unfavourably alter hormonal and metabolic status via resistance to the hormone leptin, and a vicious cycle may occur in which insulin/leptin resistance and obesity aggravate one another. The vicious cycle is putatively fuelled by continuously high insulin/leptin stimulation and fat storage, as a result of high intake of strongly insulin/leptin stimulating foods and energy. Both insulin and leptin normally function as satiety signals to the hypothalamus in the brain; however, insulin/leptin resistance may reduce this signal and therefore allow continued overfeeding despite large body fat stores. In addition, reduced leptin signalling to the brain may reduce leptin's normal effect to maintain an appropriately high metabolic rate.
If it is possible to answer this question, answer it for me (else, reply "unanswerable"): In the so called vicious cycle, what aggravates obesity to continue the cycle?
Ah, so..
insulin/leptin resistance