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.

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".

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?

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).

thermodynamics - How do warm-blooded animals keep their temperatures constant?

Since there seems to be several distinct sub-topics in your question, I will answer them one-by-one:

1). There are a variety of mechanisms that allow endothermic animals to maintain thermal homeostasis in a cold environment. The main ones are:

a). The shivering response: When the core body temperature of a endotherm drops below a critical value (36.8C in humans), it causes the posterior hypothalamus to stimulate certain skeletal muscle groups (especially around vital organs) to start to "shiver" rapidly, generating heat.

b). Compared to ectotherms, endotherms have more mitochondria per cell, thus allowing them to have a higher metabolism. Since metabolism always generates heat, an [general] increase in cellular metabolism will cause an increase in body heat.

c). Many endotherms have layers of insulating matter, such as fur, blubber, feathers…etc, allowing them to preserve body heat. In addition, endotherms can also route blood away from capillaries via vasoconstriction of arterioles, reducing the area in which heat can be lost.

d). As mentioned by Memming, brown adipose tissue also plays a role in temperature regulation. Thermoregulation-based metabolism in brown fat causes the P+ in the electron transport chain to go through thermogenin instead of ATP synthase. This process generates heat, but no ATP.

e). Some endotherms, such as penguins and arctic wolves have countercurrent exchange in their capillaries. This is when warm arterial blood "passes" some of its heat to cooler veinous blood. This feature allows some of the heat normally "wasted" into the air to be recycled back into the body.

Note: Though it is true that endotherms are able to keep their body temperature constant irrespective of their surroundings (ignoring extremes), they do this at a cost of requiring significant amounts sustenance. Most endotherms require much more sustenance than ectotherms.

2). Your second sub-question is very interesting. Though it is true that generating heat will require substantial amounts of carbohydrates/fats/...etc, it does not necessarily mean that the net consumption of sustenance in cold environments is greater than that in normal environments. In most cases, endotherms in cold environments will have exhibit significantly less activity than when in an optimal environment. The decrease in activity when in a cold environment will likely balance out the increase in thermo-regulation based metabolism. This likely explains why people tend to drink equal or slightly less amounts of water when in cold environments. One more thing: some reactions heat-generating reactions (like the alternate ETC pathway) do not require water. Glycolysis and Krebs actually generates water (not to say that there is a net gain in the body :))

3). In truth, nothing "prevents" ectotherms from generate heat. They simply do not have the cellular "machinery". Ectotherms metabolize in ways very similar to other organisms, using molecules like ATP, glucose, fat…etc. Unlike endotherms however, they spend very little of their energy on temperature regulation. As a consequence, their overall metabolic rates are dependent on the external temperature. The point is this: A substantial portion of endotherm sustenance is used to generate heat. Only a small (if any) portion of ectotherm sustenance is used to regulate heat. As a result, endotherms require much more nourishment than ectotherms.

4). I am not entirely certain what you mean by "evolutionary path", but I will just say this: In many ways, endotherms and ectotherms are organisms that have found different ways to the same problem; how to regulate body heat for maximal survival and reproduction. Basically,

ectotherm- more dependent on environmental temperature, requires less sustenance

endotherm- less dependent on environmental temperature, requires more sustenance

5). You are quite correct. The cellular and genetic components are very similar. Some morphological aspects seem to be shared as well.

Sources:

Cambell & Reece (2010) Biology (9th ed)

Swan, K. G.; R. E. Henshaw (March 1973), "Lumbar sympathectomy and
cold acclimatization by the arctic wolf", Analysis of Surgery 177 (3):
286–292,

Guyton & Hall (2006) Textbook of Medical Physiology. (11th ed)

Romanovsky AA. (2007). Thermoregulation: some concepts have changed.
Functional architecture of the thermoregulatory system. Am J Physiol
Regul Integr Comp Physiol. 292(1):R37-46.

chromosome - Coiling of chromatids during cell division

What is exactly coiling of chromosomes?
I just heard about the names i.e paranemic, plectonemic, orthostichious, anorthospiral.
I have ecaxtly no idea of what phenomenon is this.
Also what type of coiling occurs during meiosis and mytosis type of cell division.
Could it be explained in detail....?

cell biology - Experiments in vitro vs those with dead organisms and fixated tissue

Does the term in vitro necessarily imply that the organism/organs/cells of study are dead?

If not, is there an alternative latin term to refer to studies of dead biological matter ? (e.g. in Connectomics where the tissue is biologically dead, and has been fixated and sectioned with a microtome)

genetics - Non-monotonic knock-out effects in prokaryotes

Typically, when performing gene-knockout, the experimenters select one gene to remove/replace-with-junk and then see if the prokaryote can still undergo fission. If it continues to reproduce then the gene is labeled as non-essential; if the organism cannot reproduce then the gene is labeled as essential; and some-times (if the organism can reproduce but only for a certain number of generations) the gene is labeled as quasi-essential.

Typically, if gene X is essential, and you knock-out both gene X and some other gene Y then the organism still dies; this is an example of monotonic behavior. However, this doesn't always have to be the case, it could be that gene X is essential only in the presence of gene Y (for instance if the two proteins produced are in a delicate feedback loop). Is there examples when knocking out gene X makes the organism nonviable, but knocking out gene X and Y maintains viability? In the most extreme case, is there an example where both gene X and Y are essential, but if both are knocked-out then the organism is still viable? I am primarily interested in simple prokaryotes (an answer for Mycoplasma genitalium or Escherichia coli would be best) but more complicated organisms are preferred over no answer.

bioinformatics - Expanding the SETI initiative to seek intelligent data within DNA sequences?

Let's extend your idea a bit... Ok, there are conserved sequences that we may not know what their function is. Let's assume that they are indeed not functional and are some kind of message left by an ancient form of intelligence.

How would you go about detecting that? It is already given that they are highly non-random, but this is not surprising and many "non-message" sequences have this property. Also consider that these sequences are quite short, meaning that they will have low information content. This means that if you check enough conversion codes and use imagination, you would probably be able to find several "messages" which are "hidden" there (e.g. "bible codes" etc). In other words, as I am a scientist that deals with probability and pattern recognition frequently, you will have a very hard time trying to convince me that you found a real hidden message... Formally, you don't have a satisfying background model.

The main difference from SETI is that there they know that their background is essentially random noise, so it is much easier to detect "intelligent" messages.

microbiology - How do I measure bacterial growth in agar dishes (either by cell mass or by cell count)?

The most simple way is seeding the plates with a suspension of bacteria ensuring that you spread the solution properly. Then you can count the number of colonies, wich would be equal to the number of single cells.

If you want to mesure the growth speed, usually it's simpler to just measure the diameter of the colonies, always ensuring you inoculate the plates with the same amount of inoculum.

Lastly, it's even easier to estimate the growth if your culture is un liquid media and you measure the optic density with an spectophotometer.