Thursday, October 01, 2009

Publicizing Publications

As usual, in my vain attempt to compensate my lack of time to blog during after my work, here's a quick entry to keep this blog going...



As some of you might know, part of my current job scope deals with publications arising from researchers in National University Health System (AKA NUH + NUS School of Medicine + NUS Faculty of Dentistry).

Thankfully, I am not required to read every single article but dabble with those that fall under Tier 1. Like graded examinations, these papers have been appraised and classified into different tiers, gauged mainly by their impact factor.
The impact factor, often abbreviated IF, is a measure reflecting the average number of citations to articles published in science and social science journals. It is frequently used as a proxy for the relative importance of a journal within its field, with journals with higher impact factors deemed to be more important than those with lower ones.
Most unfortunately, being the usual impatient me, I was inclined to make a premature judgement, just by reading the titles of the publications.

Here is a sampling of publication titles...

Consequences of incomplete repair of acute type A aortic dissection.
Verdict: Normal

Danqi Piantang Jiaonang (DJ), a traditional Chinese medicine, in poststroke recovery.
Verdict: Potentially herbal but interesting

Potential pharmacological control of the NF-kappaB pathway.
Verdict: Potentially normal... NOT.

Aspirin and dry eye?
Verdict: Short title, must be brilliant.

Would you perform thrombolysis in this acute ischemic stroke patient?
Verdict: No.

The influence of birth size on intelligence in healthy children.
Verdict: Eat more, women!

Premarital sexual intercourse among adolescents in an Asian country: multilevel ecological factors
Verdict: We need more papers like these.

Synergistic antileukemic effects between ABT-869 and chemotherapy involve downregulation of cell cycle regulated genes and c-Mos-mediated MAPK pathway.
Verdict: Title too long, FAIL

Surface functionalization of titanium with hyaluronic acid/chitosan polyelectrolyte multilayers and RGD for promoting osteoblast functions and inhibiting bacterial adhesion.
Verdict: This is not the abstract, Mister. DOUBLE FAIL.

Protein kinase SGK1 enhances MEK/ERK complex formation through the phosphorylation of ERK2: implication for the positive regulatory role of SGK1 on the ERK function during liver regeneration.
Verdict: Stop it. FAIL FAIL FAIL.

Monocyte chemoattractant protein-1 (MCP-1) produced via NF-kappaB signaling pathway mediates migration of amoeboid microglia in the periventricular white matter in hypoxic neonatal rats.
Verdict: ... ...

Stimulation of N-terminal truncated isoform of androgen receptor stabilizes human ether-รก-go-go-related gene-encoded potassium channel protein via activation of extracellular signal regulated kinase 1/2.
Verdict: I quit.


Ever so rarely, once in a very blue moon, one of NUHS researchers would be involved in a SUPER TIER PUBLICATION. By their definition, impact factor would have to exceed 15 (which is really high).

This super researcher would then be confered a God-like status, causing the whole Research Office and Corporate Communications to cease normal work activities. Massive whoring to the Mass Media would go on an overdrive, at least to gain some cheap publicity.

Just one a week ago, we were informed of one super such paper. And with bated breath, I present... ...


WORLD BLOG PREMIERE!

Title: Specific LysRS serine 207 phosphorylation regulates Ap(4)A production in immunologically stimulated mast cells, thus implying that LysRS is a key mediator in gene regulation.
SuperAuthors: Yannay-Cohen N, Carmi-Levy I, Kay G, Yang CM, Han JM, Kemeny DM, Kim S, Nechushtan H, Razin E.

Abstract
Lysyl-tRNA synthetase (LysRS) was found to produce diadenosine tetraphosphate (Ap(4)A) in vitro more than two decades ago. Here, we used LysRS silencing in mast cells in combination with transfected normal and mutated LysRS to demonstrate in vivo the critical role played by LysRS in the production of Ap(4)A in response to immunological challenge. Upon such challenge, LysRS was phosphorylated on serine 207 in a MAPK-dependent manner, released from the multisynthetase complex, and translocated into the nucleus. We previously demonstrated that LysRS forms a complex with MITF and its repressor Hint-1, which is released from the complex by its binding to Ap(4)A, enabling MITF to transcribe its target genes. Here, silencing LysRS led to reduced Ap(4)A production in immunologically activated cells, which resulted in a lower level
of MITF inducible genes. Our data demonstrate that specific LysRS serine 207 phosphorylation regulates Ap(4)A production in immunologically stimulated mast cells, thus implying that LysRS is a key mediator in gene regulation.


By the time, I read the last line of the abstract, I was convinced that my past, present and future insomnia was, is and will be certainly cured.


BONUS WALLPAPER GRAPHICS
Cool Wallpapers for your handheld devices!


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