blazinfury

I understand the idea of how anergy happens but I cannot find a clear explanation for why it happens and why there is no co-stimulation? What regulatory mechanism is preventing the B7 and CD28 receptors from interacting? I ask because at least in the thymus, the T cells are in an isolated and controlled environment and they have a hard time leaving if they have receptors against self. However, the peripheral tissues are like an open area. So what is the regulation that is occurring there?

When a virus infects a cell it undergoes recombination with cell genome. I understand how recombination happens. So in the process, is a gene from virus delivered into human genome or human genome into viral genome or both can happen? I know that SRC is often transduced into the virus. Does that mean when a SRC virus enters a cell, the virus uses host machinery to rapidly proliferate and so in the process, the SRC, which is located after the 3 viral genes gag, pol, env, gets transcribed and translated using the viral LTR? Now I am confused how that leads to cancer. Is it that there is excessive proliferation of SRC and so what once was a proto-oncogene now has no control and becomes an oncogene?

I read that X-inactivation doesn't tend to happen in males, but then when someone is XXY, they are a male because of the Y. However these individuals tend to live. So does that mean that x-inactivation happens in males or else these individuals would die?

I understand that the human body when performing Fatty Acid Synthesis can synthesize only until C16 (palmitate). However the ER has desaturases and elongases. I know that elongases are used to add double bonds, but do humans have desaturases to add even more Carbons to a double bond? If so, then this would mean that the human body can synthesize fats longer than C16? Lets take a hypothetical case and say that humans have both desaturases and elongases. Would it be feasible to add double bonds to palmitate via desaturases, then add more carbons to the chain via elongases and then add more double bonds via desaturases? This way, the resulting fatty acid will have an increased length and more unsaturated character (ie more d-bonds than the prescribed 4 that humans can add at positions 4, 5, 6, and 9)?

I was recently reading about the mechanism of gene targeting using single-stranded oligonucleotides. I am familiar with the targeting using TALENs, ZFNs, CRISPR, etc, but my issue is with understanding the mechanism. With the latter targeting technologies, they bind to a particular locus, induce a break and then with a donor plasmid, one can promote repair. However, how does a single stranded oligo induce targeting? Is a particular enzyme or something to that effect added when transfection occurs?

Thanks for the very clear explanation.

Is there a difference between anoxia and hypoxia because I checked the Internet and all I got was that hypoxia is an extreme form of anoxia where there is an inadequate O2 supply despite an adequate blood supply. Then why have 2 terms that mean the same thing.

This is for school. Sorry if I am a bother.

Since hydrostatic pressure depends on arteriole resistance, wouldn't dilating arterioles decrease hydrostatic pressure in the capillaries? As a result less fluid will be transferred to the tissues.

I am trying to understand the purpose of this feature that bacterial possess. Based in what I have read, they are typically found in gram neg bacteria and protect against desiccation and phagocytosis. Is it present all of the time on the bacterial surface or only in times of profound stress? Now when one does a gram stain, does the capsule absorb the gram stain since it is the outer layer of the cell wall or does it seep through it? If so why-- does it have to do with the molecule composition of the capsule structure?

Well I was reading about an instance where human antibodies can be made in an animal, such as a rabbit because the human has some kind of genetic deficiency and was unable to synthesize it. So my quest was what modifications if any have to be made in the animal to then safety transplant those antibodies to the human and/or does the human recipient need to take any drugs or something to prevent the body from seeing those antibodies as foreign.

I was referring to there being a potential immune response against potential foreign substances.

Awesome. Thanks for the great explanation

Thanks for the insight. I am actually referring to the device used here ( ). I understand the mechanics and theory of the photoelectric effect but never heard of Stopping Voltage. So I just wanted some clarification about its purpose and why it is important to calculate it.

The stopping voltage is the voltage that one would apply to stop the electrons from migrating to the cathode. My quest is what purpose does this serve and what does the stopping voltage tell us?

If a person is dehydrated he has low blood volume. As such his blood osmol will increase and thus you have a bigger concentration of particles in blood due to same number of particles but in lower volume. Now since your blood is more viscous it moves slower and as such would there be more or less oxygen exchange with the tissues?

I read somewhere that diabetics have an increases risk of developing kidney failure. I was just trying to understand what is meant by this. The role of the kidney is filtration of blood, reabsorption of ions and molecules that the body needs, control blood volume, and of course excrete wastes as urine. So in diabetes, the glomeruli have a chance of being broken down and so as a result, the patient pees out glucose which is normally reaborbed. At the same time, is he unable to also reabsorb ions and molecules that he needs like Na?

Greatly appreciate it.

So basically this is happening all of the time. But I would assume that there would be a feedback mechanism to balance out the differentiated and nondifferentiated sperm. Thanks for the clarification. I was just trying to see the similarities between males and females. I understand the female and now wish to gain greater insight about the male reproductive system.

I was reading about how antibodies are something produced in animals for humans who are unable to synthesize them. However, I am confused about how scientists ensure that an immune reaction doesn't occur from the recipient? Are those antibodies modified somehow and/or is the animals modified as well to ensure that no immune reaction occurs. Thanks.

I was looking online but was unable to get a clear understanding of the differences between them. Would anyone be able to clarify them.. Thanks so much.

I am comparing oogenesis and spermatogenesis. I was wondering if sperm are arrested as primary spermatocytes like primary oocytes are until puberty? In addition, is there a stimulus that forces spermatagonia to secrete a certain amount of sperm over a set time period like a primary oocyte becomes a secondary oocyte each month? Or do spermatagonia just randomly shift between mitosis and meiosis to constantly create more sperm that first matures on seminiferous tubules and then stored in the epididymis until needed?

One cause of reduced state of oxygen delivery to internal tissues during excessive sweating is a. increased blood viscosity b. increased blood pH c. decreased blood viscosity d. decreased blood pH The answer was A. Now I understand that during extreme sweating one would experience decreased blood volume. As such, the blood osmol would increase because you have a higher concentration of particles in a smaller volume. However, won't blood travel slower and as such there would be a chance of greater exchange of O2 for CO2 or is the concentration of O2 less in the blood as well?

Thank you so much for your clarification. However I was confused when you said that DNA is not transferred through the pillus but the pillus is necessary for conjugation isn't the whole purpose of the pillus to transfer DNA, first of the plasmid, and then chromosomal?

The rate constant in a rxn rate in based on the Arrhenius equation. In this equation, two factors can change and thus influence "k"-- temp and Ea. I was always taught that temp increases the rate if a rxn and this makes sense based on the Arrhenius eq but Ea is also a factor. Now catalysts increase the rate of a rxn by decreasing the Ea if both the fwd and rev rxn. So can we say that a catalyst influences the rate constant and thus influences the rate of a rxn by increasing the value of "k"?