Comments for Circulation Research Journal Club

Comment on Journal Club, April 13, 2012: Döring et al, Lack of Neutrophil-Derived CRAMP Reduces Atherosclerosis in Mice by Lisa

Lisa — Thu, 24 May 2012 04:37:54 +0000

Well The high LDH indicates some sort of tssiue and cell breakdown or turnover. It’s really nonspecific. The high platelets could be caused by several things, but one thing that is common is inflammation or infection.Has your doctor referred your child to see a hematologist/oncologist. They specialize in blood disorders (neutropenia) and they would be best equipped to diagnose and evaluate your child’s neutropenia. There is a medication called Neupogen that can be used to stimulate the body’s production of neutrophils, but the heme/onc specialists would be best equipped to decide if your child is a good candidate for this drug.

Comment on Journal Club, April 13, 2012: Döring et al, Lack of Neutrophil-Derived CRAMP Reduces Atherosclerosis in Mice by Ashley

Ashley — Tue, 24 Apr 2012 20:53:53 +0000

Good job

Comment on Commentary: “Mitochondria in Control of Cell Fate” by Yusuf

Yusuf — Thu, 08 Mar 2012 21:04:04 +0000

Mitochondria are certainly one bracnh of research into aging, probably exceeding telomeres in current interest. I seem to remember faulty mitochondria being implicated in cancer due to their role in programed cell death. It seems to me though that if one could get some stem cells made with healthy mitochondria, good telomeres and unmutated DNA and you had a fair understanding of how to grow the stem cells in bulk and how to guide the differentiation you would be much closer to ending aging than by trying to reprogram individual cells. Getting something right once and then copying it seems easier than repairing a large number of mistakes. At any rate, it sounds like there is still a lot of work to do. What is described as a simple injection might actually involve thousands of localized injections and the cost will take a while to come down. Exercise, diet and such will still be important for anyone hoping to reach an extended lifespan.I suspect that there will be a lot of people who are asking whether or not ending aging is a good thing. I do understand such objections but I don’t share them in the least. Aside from the general dislike of humanity (which I also understand but usually do not share or at least try not to), the only real objection to extended life is the fear of over population and ecological harm. I feel that lower fertility rates for the planet not just the wealthy and educated, combined with the growing opportunities for human expansion under the sea, into the deserts and ultimately into space will far exceed any pressure for earthly reserves. Having people who have lived for years learning history, politics, economics, science, engineering and such will be of immense benefit to humanity. If even a few of those who gain extended lifespans take advantage of the opportunities that are available they could be of unprecedented benefit to humanity.

Comment on Journal Club Nov 2011: Wolf et al, CD40L-Mac-1 and Atherosclerosis by Amit P Vaghasiya

Amit P Vaghasiya — Sat, 10 Dec 2011 08:49:45 +0000

Hello sir/mam……

this is your good job. thank you but i need your help if you have any research articles related to glucose 6 phosphate dehydrogenase of wolf et al. so, please give me reply on my e mail id.
Thanking you……………

Comment on Commentary: “Widespread Promiscuous Genetic Information Transfer From DNA to RNA” by amarian

amarian — Mon, 21 Nov 2011 22:44:54 +0000

This is a beautifully written Commentary and a classic. My sincere congrats to Dr. Chakravarti for a superbly informative Commentary.

The potential implications of RDD is enormous. When I read this paper first, it occurred to me that we might have missed detection of the causative genetic mutations in our familial cases by focusing on DNA only. If RDD are truly significant- in terms of clinical and biological effects – then we have to screen RNA and/or proteins to identify the causative genes in our patients with genetic disorders. This is likely not to be the case. One would expect that the majority if not most of these RDDs would not have discernible clinical or biological consequences. Most RDDs probably involve a few copies of the transcripts that are detectable only because of high resolution of the modern deep sequencing technologies. This reminds me of detection of MYH7 (slow-fiber muscle specific beta myosin heavy chain) mutations in MYH7 transcripts in circulating lymphocytes, which was done early days of genetic studies of hypertrophic cardiomyopathy. MYH7 mutations could be detected in lymphocytes at low levels (we used to do 60 to 70 cycles of PCR to detect). Few people would believe that detection of mutations in MYH7 transcript impart discernible biological or clinical effects. My guess is that a significant number of RDDs are in this category.

Comment on Journal Club Nov 2011: Wolf et al, CD40L-Mac-1 and Atherosclerosis by AJ Marian

AJ Marian — Sat, 12 Nov 2011 00:33:17 +0000

Congratulations to authors for this fascinating discovery.
Here is my musing (as Jonathan would say) on this interesting manuscript: There is simply no vacuum in the cell. Various cellular (and extracellular) molecules are in constant and often transient state of interactions with various levels of moiety. The findings of this paper and the previous studies further highlight not only the complexity of such interactions but also differential phenotypic consequences. The challenge is whether one can exploit and manipulate such differential interactions to garner clinically meaningful effects. Here, the findings showing dissociation of the pro-inflammatory and thrombotic phenotypes through differential bindings of CD40L to Mac1 and CD40 are quite substantial with potentially considerable clinical implications. To someone uninitiated in the field such as me, the challenging question is how to manipulate the interactions between CD40L and Mac-1 to garner the intended phenotypic consequences (attenuate inflammation/atherosclerosis) while avoiding the untoward phenotypic consequences. It would be curious to know whether there are intracellular cross-talks between CD40L/Mac1 pathway and other intracellular pathways and if so, whether inhibition of one would also perturb the other. The authors have been successful in dissociating the pro-thrombotic events from the atherosclerosis phenotype, which is quite promising in terms of potential phenotypic specificity of the CD40L/Mac1 pathway. These discoveries are exciting and only time will tell whether they ultimately will make it to the beside, which all of us for sure hope so.