Saturday, 30 December 2006

genetics - What makes a gene dominant or recessive

Generally if one of the genes' biochemical functions becomes knocked out completely, the other copy will fill in for it, making the trait recessive - requiring both copies being knocked out.



An example of such a recessive trait is Albinism - if both copies of the enzyme participating in melanin biosynthesis are ineffective, the result is someone with no pigment.



Dominant genes are often variant genes which convey a new ability (phenotype) and as such the trait can show up with just one copy has this variant. Phenylthiocarbamide tasting is an example of this dominance. If both copies of the gene were the variant, the original ability might disappear - making the original trait dominant as well. On the molecular level, genes most often encode proteins which perform some function for the cell: For example, they could be enzymes and catalyze chemical reactions. They could also have some structural function, such as make up the "muscle" part of your muscle cells... You get the idea.



In the most simple case, the dominant allele encodes a protein that can perform its function. For example, the dominant allele for the CFTR gene encodes a channel that can let chloride into and out of the cells. The recessive allele, on the other hand encodes a protein that cannot do its job correctly (this also called a loss-of-function mutation). So if you inherit a functional copy from one parent and a non-functional copy from the other parent, you will still have one copy of the protein that can do its job. Only if you get a nonfunctional copy from both parents will you have a recessive condition called cystic fybrosis.

Wednesday, 27 December 2006

microbiology - If a human takes antibiotics are all bacteria in the body killed?

No



There are several reasons why this might not be true, as Alexander has discussed. An antibiotic often has a molecular target that isn't present in all bacteria, it's extremely hard to get antibiotics to certain parts of your body, and some bacteria will be defended against a antibiotic attack by biofilms, resistance mechanisms, and sheer statistical probability.



That is not to say that many don't die. Indeed, one of the major causes of Clostridium difficile infection is that antibiotics kill most of your gut bacteria, allowing the somewhat better protected C. diff to proliferate, start producing toxins, and send you to the hospital with symptoms ranging from diarrhea to perforated colon and worse. That disease is a direct consequence of "Antibiotics kill some but not all bacteria in you".

Tuesday, 26 December 2006

microbiology - How to Diagnose this hepatitis A, B and C case?

The last sentence of the question doesn't make it clear what's being asked. But it seems to be asking: What version of Hepatitis did he get from the contaminated blood?



To that end...




Serum antigen of HB tells us about the levels of IgM and IgG. If vaccinated, then IgG should be positive, I think? What does HBsAg tell you?




HBsAg gives you the knowledge of whether or not there's an acute infection of Hep-B. Hep-B IgM antibodies indicate an acute infection, whilst IgG antibodies would show up due to his previous exposure/immunization. If the patient has Hep-B IgM, the icteric illness was probably a re-infection of Hep-B.




Why do we need to detect anti-HCV? If they are found, what does it mean? I think that then it means if found that he does not have hepatitis C then.




That would my assumption as well.



You run the HBsAg and can get two outcomes: IgM(+)/IgG(+) or IgM(-)/IgG(+). The former indicates the icteric illness was probably a reinfection of Hep-B.



You run the anti-HCV and get two outcomes: (+) or (-). The former indicates a present infection, the latter indicates no Hep-C.



What might throw you off is the wife's anti-HepC antibodies. If she was formerly infected and infected the patient (or vice versa) then you'd expect to find a (+) anti-HCV result.



I might come back to this after thinking on it a bit more, but that's the best I have for now.

zoology - Does sleep duration vary for animals based on time of the year?

I'm interested in the sleep patterns of wild animals, that still use sun for controlling their biological clock.



Animals entrain their biological clock to the day/night cycle using light as the entrainment signal. The biological clock follows the day/night cycle: dim light initiates melatonin secretion, while bright morning light stops melatonin production. Melatonin is involved in sleep regulation



Here, I have plotted the day duration over the course of the year for Northeast US, around Washington DC.



My question is given the day duration plot below, would the total sleep duration for wild animals vary over the course of the year?



In other words, would animals sleep longer in the winter time and shorter in the summer time?



enter image description here

Monday, 18 December 2006

If I graft two trees together while young, will they grow as one plant?

If two trees grow close enough together so that their trunks touch each other anywhere along the length of the tree, then they will eventually fuse. This generally only happens at the trunk because, unlike small branches, the trunk really can't be pushed out of the way as easily. It doesn't necessarily need to be two trees of the same species either.



There used to be a fused sycamore-maple on my school campus (it was damaged in Sandy and was cut down). They weren't completely fused together, but you could see a joint at the base and about 20 feet below the canopy where the trunks essentially became the same. There was no distinction between the two separate trunks.



But to finally answer your question; when the trees fuse they pretty much become conjoined twins. I'm not sure if they transfer genetics to each other, but they do share resources.

human biology - Lactose Intolerance

The lactose intolerance Wikipedia page explains the problem fairly well, so I'll refer you to that for a more detailed explanation.



Briefly, the most common cause of lactose intolerance is primary lactase deficiency, which affects the majority of the world's population. This only affects adults: the majority of people do not produce lactase as adults.




Congenital lactase deficiency, instead is a very rare, autosomal recessive genetic disorder that prevents lactase expression from birth.
[...]
Congenital lactase deficiency (CLD), where the production of lactase is inhibited from birth, can be dangerous in any society because of infants' nutritional reliance on human breast milk during their first months. Before the 20th century, babies born with CLD often did not survive, but death rates decreased with soybean-derived infant formulas and manufactured lactose-free dairy products. Beyond infancy, individuals affected by CLD usually have the same nutritional concerns as any lactose-intolerant adult.




A couple of good references:



Lactose intolerance in infants, children, and adolescents. - Heyman, Pediatrics 2006



Genetics of lactase persistence and lactose intolerance. - Swallow, Annu Rev Genet. 2003

neuroscience - Number of MHCs in neurons

Antigen presentation by MHC will induce a cytotoxic response by the immune system, which is usually a good thing in the body since most cells can just divide and replicate again. Neurons, however, are particularly ineffective at regenerating from such an attack, and are not easy to come by; they are also rather important! Better not to risk it, eh?



That being said, neuronal expression of MHC is actually a pretty complex case, and this open-access article is a good start down the rabbit hole (see also here, here, and here if you have access).