Greippi

I'm sorry I phrased the cholesterol thing wrong really. Yes, it's a major factor in many cases, but there are other factors that come in to play in the initiation and progression of atherosclerosis, and research has moved on from primarily focusing on cholesterol. Also, cholesterol increases expression of VCAM-1 (I'll find the reference for that later) integrin molecule. Meaning that inflammatory cells are more likely to adhere to the vessel wall and start the whole process. While they seem to arise at increases in LDL content (i.e. fatty streaks), most patients with atheroscleorisis have cholesterol levels within the normal range (the Nature paper I cited above). These fatty streaks tend to develop in children. What is universally acknowledged is that they are more prone to developing in areas of sher stress and lower blood flow (making it easier for the adhesion of leukocytes I assume). Really interesting review, if you're interested I suggest you read it if you have time: Inflammation in atherosclerosis. Peter Libby NATURE VOL 420 19/26 DECEMBER 2002 Hemodynamic parameters regulating vascular inflammation and atherosclerosis: A brief update Ridgers et al Biomedicine & Pharmacotherapy 62 (2008) 536e540 But I LIKE debating. Debate is good, I wanna share ideas! It's interesting because you're from a medical background and I'm a biochemist.

Shame, I thought this was gonna be about tummy buttons.

Well then, I would say the MS then MBA is your best option (or could you just do the MBA?), especially if the MS will give you more lab experience.

Seems baffling from the info you've given, and I don't have much to suggest. You could perhaps try a completely new batch of plasmid (seems unlikely that would be the problem, but you've gotta troubleshoot everything I suppose).

I'm not sure what an MS or MBA are (I'm from England).=, but here's what I think: You seem pretty much definite that you don't want to continue lab work, and one of the main advantages of a PhD is that you get more lab experience. If you were in England and a PhD was only a 3-year commitment, I would say you might as well do it because of your long-term career prospects. But if you're in America (PhDs are 7 years?) that might not be such a good idea. I assume you've looked around at the sorts of jobs you'd like to do and see what they require - a lot of jobs like that only require a degree, and it sounds like you have a good background for that.

Confused here. If an atherosclerotic plaque ruptures, it can cause a thrombus. How can you then say it's not related to thrombosis? The idea of atherosclerosis primarily being caused by aging and LDL levels is a little out-dated.

If you check the review I cited: Cytokines in Atherosclerosis: Pathogenic and Regulatory Pathways. ALAIN TEDGUI AND ZIAD MALLAT Physiol Rev 86: 515–581, 2006; doi:10.1152/physrev.00024.2005. There's a good section there, along with references to other papers.

Is this homework? We're not meant to feed you answers. What's the definition of a reducing sugar? That should help you get some of the way there. Look up the structures of the sugars. It should then be very easy to find the number of the carbon atom that way.

Take a look at the molecular structure of some common dyes: Coomassie blue: Carminic acid (cochineal) Methyl red: Notice anything similar? I can explain why they're coloured when I have more time

Yup As for bacteria, I assume it's just floating around free in the blood stream. But I am not entirely sure about that one. Maybe it produces toxins that irritate the artery wall. Yah, I know your question wasn't specifically related to atherosclerosis, but it's one way in which a thrombus can form. And the only way I know much about Merged post follows: Consecutive posts mergedHere's something else: Cytokines, such as TNF are secreted in response to infection (innate immune system, many cell types can recognise infection and release cytokines). Resident macrophages recognise LPS (bacterial lipopolysaccharides) and can release TNF alpha. One local effect of TNF is the influx of platelets to cause blood clotting in capillaries as a barrier to prevent spread of infection. This can produce a microthrombus, and sometimes this can lead to coronary thrombosis.

If you're concerned, put bleach on it. that should blatter it.

There are thousands of types of mold hanging around, so it could be anything. Without a proper test in the lab I doubt you could identify it. As for throwing it away, just throw it away as you would normally!

Is it soaked in nutrients in case of emergency?

It is towel day today.

Sounds like some sort of mold/fungus to me. Very understandable it would only appear on this bread - by the window is a different environment from the others! Can't tell you anything else without a picture.

A dative bond (aka dipolar bond) is where one atom donates both electrons to a bond. This commonly happens with hydrogen ions - with no electrons. They can accept two electrons to complete their electron shell from e.g. NH3 to form the ammonium ion. It's no different from a covalent bond as the end result you can't tell where the electrons came from.

TEMED (Tetramethylethylenediamine) is yucky.

Gaga is awesome, but then again I would say that, I'm a girl.

Atherosclerosis is one disease that can cause thrombosis. Incidentally, I have an exam tomorrow on atherosclerosis so I've just been reading about this! Atherosclerosis basically occurs when damage to the arterial endothelial cells provokes an immune response, causing inflammation. This can lead to the formation of a plaque covered by a fibrous cap - if the cap breaks, the contents of the plaque is released, causing thrombosis. If you look up atherosclerosis, e.g. the wikipedia page basically explains how slight damage to the artery wall can lead to thrombosis. As for infection: the classical view would be that an infection, or some sort of trauma lead to the production of cytokines by the endothelial cells of an artery and thus inflammation, plaque formation, thrombosis etc. There was evidence that Chlamydia pneumoniae and cytomegalovirus (CMV) were triggers for provoking this response. The infectious agents could be circulating in the blood then infect the endothelial cells maybe. However, more recent research shows that you're just as likely to get atherosclerosis if you don't have an infection - infection isn't necessary for initiation or progression of the disease. Infectious agents may have a part to play in exacerbating the atherosclerotic process. Chlamydia pneumoniae can infect the various immune cells involved in the inflammation response. It can also promote the expression of adhesion molecules on cells, meaning that immune cells are more likely to bind to the endothelial cells on an artery and cause an immune reaction. There are various viruses that can make atherosclerosis worse, including the herpes viruses. Source: Cytokines in Atherosclerosis: Pathogenic and Regulatory Pathways. ALAIN TEDGUI AND ZIAD MALLAT Physiol Rev 86: 515–581, 2006; doi:10.1152/physrev.00024.2005.

It's hard not to use the "technical" language because that's what I think puts a lot of people off being willing to understand science. Being confronted with lots of long words that they don't know the meanings of can be off putting and daunting. So yes, it is a bit like translating to another language.

I disagree, but then again I suppose it depends on the format of the masters course. My masters will make me a more attractive prospect when applying for a PhD as it will give me more training.

Since I want to end up being a lecturer to undergraduates (amongst other things), being able to explain things clearly is an important skill for me. I am able to explain exactly what I get up to in the lab to both my boyfriend and my mother, who are English majors with no background in science. While they couldn't then go on to give a distinguished lecture on the subject, they understand the basic concepts. But, as has been previously mentioned, the interest of the listener is vitally important!

How about taking a masters while you decide what you want to do. As farmboy said, it would make most sense to do a PhD if you were seriously considering going in to research. I think you should be aware of what whatever job you go for will entail - for example if you're working for a pharmaceutial company in drug design you're not necessarily going to be involved in rational drug design, but more likely doing endless repetitive assays.

My name is Katie Grape. "Greippi" means "grapefruit" in Finnish, and it amuses me that it does not, in fact, mean just "grape". The number of Finnish people I get informing me that I've got grape in Finnish wrong is insane.

The mutations don't change what protein it has. It's still the same protein, just subtly different. Different enough to stop the immune system recognizing it for a second time/for a vaccine to be effective against it. HIV's reverse transcriptase is extremely error-prone. (our replication enzymes make errors too, but we have effective proof-reading mechanisms).