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?