Medicine - Science topic

concerning H1N1 i want to ask a question , are t6he vaccines nowadays used efficient and what is bettwer than these vaccines if present , thanks for your time

thanks for your reply. I think if we think of chronic exposure to alloxan, we have to take more precautions.

thanks Antonino, i think your last point is highly valuable

Dear Surekha Praveen, thank you for your nice participation. you are still young researcher, i wish you and others long living and to remember in near future this discussion and how science will jump as never before. i agree with you about nanotechnology. let me imagine microsurgery for positive thinking or anticrime surgery!!!!!!!!!! so strange but could be????

Unpublished data is not peer reviewed and once you "publish" it here, a journal might not accept it as new data.

I think so, recently I read an article about "real-time chemistry". The idea is that you can get input parameters for your programs at the time you are conducting experiments. In this case you wouldn't need to perform ab-initio calculations but you would get precise parameters from experiments. The last will be very helpful when you try to model a system consisting of damaged DNA for instance (which is believed to be a cause of cancer) or misfolding of proteins.

I was involved in both research and treating patients with FMS in the past. From a clinical standpoint there were 2 groups that had to be approached very differently. About 2/3 of patients who met the ACR definition for FMS had no serious psychopathology (and were often being treated as if they had some variant of major depression that caused the pain -a universally ineffective approach in my experience). In this group a multidisciplinary/polymodal program almost always helped as long as it was individualized to the patients needs, abilities etc. However, sleep pattern had to be significantly improved to get the best results (i.e. addressing non-restorative sleep was always a first priority and I thought and still think that those who treat FMS need to have a good understanding of circadian rhythms to treat the sleep problems effectively). Also, in my experience patients who reported some type of "spiritual growth" did better. The other group is much more challenging and psychiatric care plays a greater role, but unfortunately at least in my experience is not nearly as successful. One could argue that the only difference is that the second group has a more severe form of FMS that leads to serious psychopathology, but I suspect that is not the case.

In response to your question, I would say that patients with >T1 stage should undergo a later re-resection if the tumorous cells re-appear.Later, radical cystectomie with a formation of ureterocutaneostomy at both sides should be the therapeutic approach.

Hsp90 has been found necessary for iNOS induction in cultured cells exposed to inflammatory mediators. However, Hsp90 is the main component of the cytosolic molecular chaperone complex that has been implicated in the negative regulation of the heat shock factor 1 (HSF1). HSF1 is responsible for the transcriptional activation of the heat shock genes including Hsp40, Hsp70, and Hsp90, suggesting a regulatory role in Hsp90 synthesis at the transcriptional level. Hsp90 forms a multichaperone complex with Hsp70 and Hsp40 to regulate several regulatory proteins, such as steroid hormone receptors and transcription factors, and to modulate the protein translocation from peroxisomal to organelle. The interplay between these chaperones is of crucial importance for cell function and survival. Recently, Uryu et al. demonstrated that Hsp90 was predominantly increased in PD brains, which was in correlation with the elevated level of insoluble αSN. These alterations of Hsp90 in PD brain were recapitulated by neuropathological findings in αSN mutant transgenic mouse model of PD. Furthermore, exposure of cells to proteasome inhibitors resulted in increased levels of Hsp90. Microglia, which plays a principal role of inflammation in brain express high levels of Hsp90 following excitotoxic lesion in the mouse hippocampus. The protective function of Hsp90 can be very important since inflammation evoked by microglia may increase the risk of PD. Hsp90 is also a chaperone for maintaining an appropriate ligand-binding conformation for steroid receptors, but it also participates in the nuclear-cytoplasmic shuttling of steroid receptors. The role of heat shock protein 90 (hsp90) extends to agonist-dependent eNOS activation. Hsp90 binding stimulates eNOS activity by cooperatively enhancing the affinity of eNOS for binding calmodulin, balancing output of nitric oxide versus superoxide, and possibly facilitating heme binding. Synergistic activation of eNOS can be seen following formation of a ternary complex containing hsp90, Akt, and calmodulin-bound eNOS. NO itself may negatively modulate hsp90 by S-nitrosylation of a cysteine residue that inhibits the hsp90 ATPase function and may disrupt eNOS–hsp90 binding; this mechanism might provide negative feedback to regulate the amount of NO generation and/or facilitate cyclic eNOS activity. So, getting back to iNOS: Hsp90 is required in iNOS induction. Inhibiting Hsp90 function with geldanamycin or radicicol prevented iNOS expression in cells stimulated by both LPS and IFN-γ. HOever, it is not Hsp90 alone, but in conjuction with albumin, LPS, IFN- γ, TNF-alpha, endotoxins and many other cytokines. Taking into cosideration the other roles of Hsp90, it is not surprising that iNOS does not increase in all experimental situations even when Hsp90 is increased, especially in the absence of LPS for example.

One of the reasons might be that chromosomal instability is very often associated to cancer, at least in solid tumors. Hence, to revert cancer you would have to put back every piece of DNA at its original place!

Dear Ahed Thanks a lot.Although it's true that high urinary level of some minerals such as Ca, uric acid and oxalate potentially can induce to microscopic hematuria with or without stone formation, but the role of dietary content is the focus of arguments.Because your interest on oxalate and oxalate containing foods,I emphesize on this mineral.We have to consider some points about dietary oxalate and its role on stone formation and hematuria :1/ only 10-15% of urinary oxalate is from diet and the rest is endogenous. 2/ excretion of oxalate in urine depends on bioavailability of oxalate.Spinach and rhubarb are examples for high availability oxalate containing foods.Interestingly ,tea and coffee are not in this group. 3/Oxalate in foods is in complex with other mineral such as calcium,So effect of oxalate ingestion on urinary oxalate excretion is a complicated concept.In conclusion, it is not completely clear that dietary oxalate manipulation can induce in change in urinary oxalate excretion and it dosen't worth to recommend to patients with stone and/or hamaturia.

Being able to differentiate ischemic from a hemorrhagic stroke is very critical. The question is how reliable is the test. What are its specificity and sensitivity indices?. What is the precision? Once we know that it is a reliable test, then in patients with ischemic stroke, it enables neurologists to decide whether or not to administer tPA. Firstly, one has to know whether or not the patient has any contraindications to fibrinolytic therapy. If the patient has no contraindications, then with all due precautions fibrinolytic therapy may be safely administered. Even if you have that fantastic test at your disposal it does not mean that if the test shows ischemic stroke, one jumps to administer fibrinolytic therapy. Patients have to be evaluated on an individual basis and then consider to administer fibrinolytic therapy. If the test shows hemorrhagic stroke, then again based on the reliability and precision of the test, neurologists can administer recombinant Factor VIIa (Novoseven) in a site-directed delivery system. Again caution should be exercised that if the rFVIIa is not safely administered in a site-directed delivery system, there could be thrombotic complications as a result of this.

Typically, if treatment for infantile spasms is successful in causing cessation of spasms and resolution of hypssarrhythmia (the typical EEG of West Syndrome), treatment is short term for first line agents(weeks to months for ACTH or oral steroids, 6 months for Vigabatrin). That said, there are reports of relapse after VGB discontinuation (in children with cortical dysplasia) (Krolle-Seger et all Epilepsia 2007). With other types of epilepsy, discontinuation of antiepileptic medication is considered after 2 years of seizure freedom, and the majority of patients will not have a relapse though those with a symptomatic etiology (as your patient has) and those with epileptiform abnormalities on EEG (which your patient does not have) tend to have a higher relapse rate(see papers by Shlomo Shinnar, and by Ann Berg, also by Peter and Carol Camfield). Because we do not have Sulthiame in the US and rarely use it, I am not familiar with its specific long term risks. There is considerable debate and not very much data about the long term neurodevelopmental effects of AEDs. All in all, if the child does not have a malformation of cortical development, has a normal EEG and has been seizure free for more than 2 years, I would advise discontinuation of the antiepielptic medication.

A unit of light that interacts with a biological system. This is a very new area of study, and there are a number of resources on upcoming research and experimentation in this field. Check out Omenetto's work : http://ase.tufts.edu/biomedical/unolab/home.html

We also have a Department for medical illustrations, actualy I have made good use of it in the past. Regarding classic illustrations I do think most of them are out of context now days just for the fact that in that time they didn´t have digital software to do this images and when I compare a classic image to a "new" (digital version) one, the difference is astonishing, so in conclusion I do suggest all old images should be brought to the actual form.

The Lichtenstein repair was done 6 years ago the 52 year old male is in chronic pain after only 1 month out of surgery. All mentions of this were ignored by both the surgeon and pain management Dr's in Reno NV. We are finally getting help outside of the region and going to the Lichtenstein Amid Institute in southern California at UCLA. A triple neurectomy of the Ilioinguinal, Iliohypogastric, and genitofemoral nerves look to be promising. Please if anyone is preforming this Operation in the future please be very aware of these nerves, as it can become a very debilitating problem. There are many reports on the subject matter on line.