Dislayer

This is probably not the place to get safety information about infectious agents. There should be safety protocols as part of your lab/centre/university for dealing with these bacteria. Alternatively, asking your supervisor or centres safety officer is probably a better idea.

Omentin-1 appears to be an Adipokine (adipose cytokine) that can also be called inelectin-1 (ITLN1). It seems to be a very popular molecule right now in obesity/diabetes research (couple hundred hits on Pubmed [omentin-1 + diabetes]). Some research seems to suggest that its levels are down in the blood of obese patients or patients with diabetes It also seems to have a cardioprotective effect and may be beneficial in type 2 diabetes This review give a good overview of the anti-inflammatory effects of omentin-1 and other adipokines (Role of anti-inflammatory adipokines in obesity-related diseases). Briefly, they indicate that omentin-1 is abundantly expressed in the visceral fat and is detectable circulating in the blood. Some work has shown that omentin-1 stimulates glucose uptake in cultured adipose cells. It may also enhance dilation of the blood vessels through the production of endothelial NO. Omentins anti-inflammatory effects seem to be through the suppression of immune cell adhesion to the endothelial walls. Seems like this protein holds some promise in finding a way to treat diabetes and obesity. Don't know if this answered your question. The literature out there is still fairly new.

To me it sounds like you have repeated the experiment in each condition 6 times (3 repetitions done twice) is that right? If so you have an n of 6 which is a good sized number to start with. All of the values of what ever you are measuring will need to be averaged and you will need to calculate a standard deviation. To compare the difference between the five different concentrations in one protein (asking the question how does the increasing concentration of a given protein affect the cell) you would need to use a one-way ANOVA. To test the difference between a given concentration of protein between the other two proteins (how does the maximum concentration of protein A affect the cell compared to protein B and C?), a one way ANOVA would be used too. The one way ANOVA would give you differences between individual concentrations or proteins but it would also let you know if the general trend is significant (ie. does the proliferation of the cell increase as the concentration of the protein increases? In a dose dependent manner) You still need to identify what variable you are testing though. Is it the effect of the proteins on cell proliferation? Growth? Secretion of another protein? Cell death? Once you identify what variable you want to test you will need an appropriate control (treatment with a vehicle) to determine significance against. Generally you can download a stats program (something like Prism Graphpad or Sigmaplot). Don't try to use excel stats, they are not correct often and are very limited in their use.

I believe it is still very much debated in the research field. We know what the signals for starting mitosis are: 1) the levels of cylins and cyclin dependent kinases within the cell. 2) presence of the M-phase promoting factor (MPF). 3) Cell is large enough to divide and has the necessary nutrients (G1 checkpoint). 4) Ensuring DNA replication has occurred correctly (G2 checkpoint) 5) Density and anchorage dependence. 6) Some external signal triggering the movement to M phase (for example PDGF in fibroblasts). I would hazard a guess that some, maybe all of these are at play as well as some more specific signals. Since meiosis doesn't occur in humans till after puberty, there is likely involvement of some of the sex hormones and other specific proteins that trigger the initiation of meiosis at the gonads. Some other proteins suggested to be important in meiosis are RME1 and IME1 (at least in yeast). RME1 is suggested to inhibit IME1 and IME1 is a positive regulator of meiosis. Similar proteins are likely conserved in humans. Still is very much a black box and a hot topic in research.

Like you said, there is no "growth gene" as human growth (both weight and height) are controlled by a variety of genes and environmental cues. There is a gene; however that when mutated, can lead to excess uncontrolled growth. That gene is codes for the protein for growth hormone. However, its levels are controlled by various other proteins in the body and it is not as simple as modifying the gene. Mutations could occur in the gene itself, in the promoter for the gene, in the suppressor of the gene, in non-coding regions of the gene, in proteins that interact with the gene or in signalling pathways for the protein (or in any other part of the gene) so it is not as simple and changing the gene to get taller. The changes made could have unintended consequences such as stunting of growth or development of cancer. All of this is not even considering the environmental cues that affect height. Things like nourishment, exercise, socio-economic status or history of medication. As said by others before me, no you cannot just change your growth gene because there isn't just one growth gene and even if you targeted one of the growth genes, you would need to be able to change it in every single cell in your body (of which you have approximately 100 trillion). Unfortunately, the only thing you can do to affect your height is eat properly when you're young or wear shoes with big heels...

All university degrees can be difficult since unlike school you will not have constant reminders or "hand holding" to help you along. The biggest piece of advice I can give you is that if you do not understand something, do not be afraid to ask the professor, teaching aide, peer or tutors. The reason you are in school is to learn and so therefore there really is no stupid question. Another helpful thing will be to make sure you get into a routine and make a schedule. If you study the same way and on a schedule then it will not feel like a chore. Lots of times you have breaks between classes (sometimes 30 minutes sometimes a couple hours). Use this time to review what you learned in class, write out your notes (iPads/laptops make note taking easier but you do not retain the info as much as if you write them out). One final piece of info that will definitely help you with whatever you plan on doing after your degree is make sure you get involved. Volunteer in the community, volunteer at the university. Become part of the culture. Look for research opportunities. Many research centres like mine have spots for summer students (usually in their 2nd/3rd year) to come in and get involved in the lab. Best of luck! It is not as bad as you may think.

Interesting article. It seems to me that the problem doesn't solely lie with the doctors but with the way these statistics are presented and the lack of education about them in the public. As the article says, it would be better to express risks/survival/mortality rates as numbers and not percentages. It would likely help to express these sometimes confusing stats in lay language (like most other science needs to do in order to get funded). On another note, don't like the title of the article. Little misleading in the fact that is isn't whether doctors understand tests but rather do they understand statistics.

You can also join Research Gate (http://www.researchgate.net/) which is basically a facebook for scientists. Many researchers (myself included) put up full pdf versions of their manuscripts for people to read.

All the more reason that there needs to be more clinician scientists who understand research and the flaws in it. Most doctors unfortunately are giant stores of memorized information with the ability to apply it but not to critically think about these problems themselves.

No offence taken, just hoping to stimulate discussion. I research asthma and find this question provides interesting talking points in our center. Just wanted to gauge others opinion on the topic. On the note of funding, I think one of the problems is this desire to have a tangible patient benefit by the end of a grant or fellowship when in reality it would take many grant cycles to get to the point of having a relevant treatment developed. The government wants science to move quickly but my experience is that science is slow and methodical. It needs time to be precise so we avoid problems with retraction.

While that is true it does not add to the discussion about this topic. How must we approach the problems in order to gain better understanding of them.

I wanted to start a discussion about complex diseases (atherosclerosis, asthma, multiple sclerosis, etc.) and why we have had a difficult time figuring them out. Is it because we are searching for that one cause (either gene or exposure) that we hope can explain the prevalence of the disorder, like cystic fibrosis. Or is it because we group people with similar symptoms under there syndromes but in fact their diseases have different etiologies and are not the same disorder. I do research on the genetics of asthma and the field is shifting towards better phenotyping of patients to better understand how different asthmas come to be. There is a general belief that large scale genome wide association studies (GWAS) have a hard time turning up results because the 'disease' group is a heterogeneous mix of different disease. I believe there is a need to better integrate research disciplines (molecular, physiology, modelling and epidemology) in order to start understanding these disorders better in the hopes of one day developing a cure. The reductionist approach taken thus far (that worked well for simple Mendelian disorders) probably will not bring us answers or meaning full cures. What does everyone else think? Why have we not been able to make significant progress in understanding complex disorders?

What you just described is CSF. If you take out the cells from blood, all the proteins and make it sterile you end up with something similar to CSF. That is probably how CSF evolved over time.

I would argue that the function of CSF and blood is not the same. Yes they both function to maintain homeostatic regulation but CSF is acellular with cell counts on average of 0-5 white blood cells and functions to cushion the brain and remove waste. Blood is full of cells and its main function is oxygen and nutrient delivery to the bodies cells. CSF is meant to be sterile because it comes in contact with the brain while blood (which is not sterile) is not in direct contact with the brain. In order for blood to take the job of CSF you would need to remove all the cells, make it sterile, remove proteins and platellets. If you do all that you have CSF.

Insulin is a protein made my beta cells within the pancreas. You cannot just eat all the components of insulin to get insulin. Those components (amino acids) need to be linked together in a certain sequence and then folded in a specific manner (often times with the help of other proteins) in order to function. In essence this is what your body does when you eat protein. It breaks down the protein into amino acids and then uses those to build every protein in your body, however this is different then what you are trying to describe. If the point you are trying to make is that you can get the beneficial effects of aspirin by eating willow bark for example (salicylic acid) you might be able to however you would need to consume an excessive quantity and would probably have adverse reactions to the other compounds within the leaf. Part of the reason medicine began distilling these ingredients and selling them in pill form is so we could get an effective dose that would not be attainable if we were trying to get it from the plant/leafs.