Xalatan

Aside from better diagnostic tools, screening for cancer will also introduce lead-time bias. Ie. a lot more cases of cancer will be picked up at an earlier asymptomatic stage, so it may seem more people are living with cancer.

This is how I understand autoimmune diseases and relevant pathophysiology that you have mentioned: 1. Anti-dsDNA antibody is pathognomonic of systemic lupus erythematosus, not rheumatoid arthritis. Rheumatoid factor is classically described as an anti-IgG IgM autoantibody. 2. Both SLE and RA are type 3 hypersensitivities, which means the underlying pathology involves immune complexes. Ie. Circulating pre-existent antibodies binding to the relevant antigens (dsDNA in the case of SLE, IgG in the case of RA), triggering immune-complex deposition and inflammation in areas of high vascular resistance, such as serosa, glomeruli, small vessels. 3. The pathophysiology you are describing involving B cells, antigen presentation, class switching and plasma cell production of auto-antibodies is defined as class 2 hypersensitivity. More classical examples of type 2 hypersensitivities include ABO incompatibility, Myasthenia gravis etc, not SLE and RA. 4. To directly answer your question on an immunological level, while it is true that antigens presented on MHC II molecules are peptides, B cells can actually undergo T-cell independent activation without the need for MHC II presentation. This is how IgM is produced as part of the innate first response without the need for isotope switching and IgG production. B cells can use their BCR to bind to PAMPs or DAMPs like foreign polysaccharide or DNA; the second signal is from macrophages rather than T cells, or in the case of a large bacterial antigen, extensive cross-linking to repetitive bacterial epitopes can also trigger the second signal in the B cell.

Yes, recombinant DNA technology is in place for different clinical applications. For example, recombinant human insulin is synthesised by inserting the human insulin gene into E. coli, which produces insulin for human use.

It seems rather reductionist to think of hypothalamus as the origin of sexual orientation. Yes, GnRH drives pituitary hormone release to control sex hormone production in the gonads, and it controls the autonomic nervous system that governs the mechanics of penile erection. I don't know if it's this simple though. Is there a cortical component to sexual arousal? Maybe there is visual or Olfactory Stimulation that relay via the brainstem and pelvic splanic nerve bypassing the hypothalamus. Also, I am unaware of a hypothalamic lesion that alters the sexual orientation of a patient.

Maybe there is still residual ethanol from the precipitation step that's preventing dissolution.

The proteins related to the brain has already been mapped a posteriori. For the sake of forum discussion it's interesting to read the results and reason which proteins are not related, but I wouldn't misinterpret it as "Proposing an exercise to try to find proteins that are not expressed in the brain a priori". If the subject is close to your research interest you can propose your own exercises.

The empirical experiment has already been done, these authors may answer your question best. http://science.sciencemag.org/content/347/6220/1260419 The editors at Science seemed to think the exercise was worthwhile enough to publish in their journal.

Quoting the National Institute of Neurological Disorders and Stroke, "At least a third of the approximately 20,000 different genes that make up the human genome are active (expressed) primarily in the brain. This is the highest proportion of genes expressed in any part of the body. These genes influence the development and function of the brain, and ultimately control how we move, think, feel, and behave". http://www.ninds.nih.gov/disorders/brain_basics/genes_at_work.htm The human protein Atlas quotes 67% http://www.proteinatlas.org/humanproteome/brain Hmm what's the best way to exclude proteins not present in the brain? The common origin of Neuroectoderm and possibly neural crest makes it difficult... perhaps proteins of endodermal, yolk sac, or extraembryonic mesoderm origin? For example, alpha Fetoprotein is produced by the developing world yolk sac and liver.

It would be interesting to measure tangible electrophysiological parameters like brain waves to see if perhaps there is a tendency for beta to alpha transition. Also neuroendocrine parameters like cortisol, melatonin etc to see if there is any effect on hypothalamic function.

That's an interesting question. Wikipedia says there are an estimated 20,000-25,000 protein-coding genes in the human genome. What percentage of this regulates brain function? Another way to think about it may be to exclude functions that the brain doesn't perform. Eg. Secrete insulin, exocrine digestive enzymes, turn over urea, secrete surfactant, produce renin, ACE, aldosterone, cortisol, androgens. Structurally there may be less collagen and muscle fibres in the brain matrix since glia fulfils the role but meninges would be composed of connective tissue.

Yep I mean, with hypoxia you could say the same, that oxygen is present as part of general homeostasis to maintain cellular and organelle function (the mitochondria). On the other hand the discovery of HIF and EPO provides specific oxygen sensing mechanism that highlights the potential for tumourigenesis. So perhaps there is a means for intracellular protons to influence processes like proliferation, apoptosis, renewal in a specific way (though 30min of acid bath to turn white cells into iPS cells seems too good to be true - even the Yamanaka factors don't work that fast).

Does anyone think intracellular pH is an important physiological factor that regulates cellular function? The STAP papers have been retracted but perhaps intracellular pH may still have physiological relevance outside of stem reprogramming?

Wikipedia says that meldonium inhibits γ-butyrobetaine hydroxylase (IC50 = 62mcM), carnitine biosynthesis, and beta oxidation. How does this mechanistically link up with improved exercise tolerance in stable angina (and athletic performance)? Supposedly myocardial work is reduced decreased by the lack of beta oxidation feeding acetyl CoA into the Kreb's cycle, and this improves cardiac endurance?

My advice would be to listen to your advisor(s) and let them guide you. Chances are they would have had a lot more experience than you and I in terms of preparing and publishing manuscripts. A friend of mine published his first paper writing an invited review for his advisor. Another's first was a manuscript for conference attendance. Most others' were middle authors doing some parts of the experiments.

Yeah I often wondered about this myself. My guess is both digestion and absorption would be decreased in the event of gastroenteritis - gut fluid secretion and motility may both be increased by the gastroenteritic process, which may shorten the gut transit time (i.e. diarrhoea). Digestive enzymes and nutrient transporters may not function as effectively given the less transit time available. On the other hand, there may be enough residual capacity in the gut to fully digest the food in spite of the gastroenteritis. The answer may come down to the severity of the gastroenteritis and the virulence of pathogens involved in each case.

Question about P. aeruginosa - question talks about it being an obligate aerobe, so C may be the best answer. An obligate aerobe would need an ETC and the inorganic final electron acceptor likely refers to molecular oxygen. Generating NADH2 from NAD by making alcohol and lactic acid is a property of anaerobes, so B is incorrect. Since alcohol and lactic acid are not produced, A may also be incorrect. A molecule of glucose produces 38 molecules of ATP under obligate aerobic conditions so D is also incorrect. Last question - A; DNA polymerase carries out DNA replication; RNA polymerase is what is responsible for transcription.

https://en.m.wikipedia.org/wiki/Coding_strand https://www.google.com.tw/search?q=coding+strand&oq=coding+strand&aqs=chrome..69i57j0l3j69i60.4917j0j4&client=ms-android-htc-rev&sourceid=chrome-mobile&ie=UTF-8#imgrc=N_H8uoPZ_vi3aM%3A

Yeah it's fine, the background will be stronger with the EtBr on the second run but if you just want to check for a band it is still useable. Maybe drop the exposure time a bit and see if it's more optimised. Let the gel cool down a bit though, you don't want the gel to melt if it overheats.

That's a lot of work for you if there is no answer key. The answer to the second question should be C - enhancer first, then polymerase then mRNA processing, followed by protein synthesis. There may be rules here about posting homework etc, maybe ask a moderator to see if the content can be posted this way?

My understanding of ptsd is that the diagnosis is based on the perceived threat of an event to self, typically for the fear of losing life, a limb, or loved ones. The job of an executioner may not necessarily exposes the person to threat of such catastrophic or dangerous nature, though that's not to say given the right context cases can't exist, especially if the symptomology is present. Acute stress disorder may be a plausible differential for novice executioners.

Dunno about Ebola but for influenza A, the the haemagglutinin and neurominidase antigens influence species tropism. Perhaps some surface proteins also govern Ebola behaviour by the host proteins they interact with.

I also think thermogenin may be the answer here. When the proton channel is physiologically uncoupled from atp synthase heat may be generated by the ETC. Also since aerobic glycolysis and cell respiration are catabolic in nature some heat may be given off by these chemical reactions. Shivering on the other hand is an autonomic neural reflex that loops the hypothalamus and spinal cord. This is different to the metabolic heat production from glucose use.

Unfortunately no. 5'-->3' is the coding strand, while 3'-->5' is the template strand. RNA pol binds to the template strand, and transcribes in the complementary 5'-->3' direction, so the resultant mRNA reads 5'-->3', the same as the coding strand (which is why the coding strand is so named). The mRNA should read the same as the coding strand, except U subbed for T.

Interesting idea, artemisinin conjugated to iron and transferrin may be a good way to target red cells and hepatocytes, perhaps an improved antimalarial? How would this artemisinin conjugate target tumour cells is what I would like to find out, if you wouldn't mind kindly sharing your good ideas.

Physiology is the study of how the body functions.