beautifull girl

Beautiful girl, wherever you are
I knew when I saw you, you had opened the door
I knew that I'd love again after a long, long while
I'd love again.
You said "hello" and I turned to go
But something in your eyes left my heart beating so
I just knew that I'd love again after a long, long while
I'd love again.

Refrain : It was destiny's game
For when love finally came on
I rushed in line only to find
That you were gone.

Whenever you are, I fear that I might
Have lost you forever like a song in the night
Now that I've loved again after a long, long while
I've loved again.

*Repeat Refrain

Beautiful girl, I'll search on for you
'Til all of your loveliness in my arms come true
You've made me love again after a long, long while
In love again
And I'm glad that it's you
Hmm, beautiful girl

Christian Bautista - Beautiful Girl

you are my Lee Donghae

The loneliness of nights alone
the search for strength to carry on
my every hope has seemed to die
my eyes had no more tears to cry
then like the sun shining up above
you surrounded me with your endless love
Coz all the things I couldn’t see are now so clear to me

You are my everything
Nothing your love won’t bring
My life is yours alone
The only love I’ve ever known
Your spirit pulls me through
When nothing else will do
Every night I pray
On bended knee
That you will always be
My everything

Now all my hopes and all my dreams
are suddenly reality
you’ve opened up my heart to feel
a kind of love that’s truly real
a guiding light that’ll never fade
there’s not a thing in life that I would ever trade
for the love you give it won’t let go
I hope you’ll always know

You’re the breath of life in me
the only one that sets me free
and you have made my soul complete
for all time (for all time)

You are my everything (you are my everything)
Nothing your love won’t bring (nothing your love won’t bring)
My life is yours alone (alone)
The only love I’ve ever known
Your spirit pulls me through (your spirit pulls me through)
When nothing else will do (when nothing else will do)
Every night I pray (I pray)
On bended knee (on my knee)
That you will always bebe my everything

[almost spoken:] Every night I pray
down on bended knee
that you will always be
my everything
oh my everything



Adaptor protein (AP) complexes regulate clathrin-coated vesicle assembly, protein cargo sorting, and vesicular trafficking between organelles in eukaryotic cells. Because disruption of the various subunits of the AP complexes is embryonic lethal in the majority of cases, characterization of their function in vivo is still lacking. Here, we describe the first mutation in the human AP1S1 gene, encoding the small subunit [sigma]1A of the AP-1 complex. This founder splice mutation, which leads to a premature stop codon, was found in four families with a unique syndrome characterized by mental retardation, enteropathy, deafness, peripheral neuropathy, ichthyosis, and keratodermia (MEDNIK). To validate the pathogenic effect of the mutation, we knocked down Ap1s1 expression in zebrafish using selective antisens morpholino oligonucleotides (AMO). The knockdown phenotype consisted of perturbation in skin formation, reduced pigmentation, and severe motility deficits due to impaired neural network development. Both neural and skin defects were rescued by co-injection of AMO with wildtype (WT) human AP1S1 mRNA, but not by co-injecting the truncated form of AP1S1, consistent with a loss-of-function effect of this mutation. Together, these results confirm AP1S1 as the gene responsible for MEDNIK syndrome and demonstrate a critical role of AP1S1 in development of the skin and spinal cord.

UNTUK LEBIH JELAS,.... Click here

rheumatoid arthritis


Nearly 12% of children and 6% of adults in Canada have been diagnosed with asthma. Although in most patients symptoms are controlled by inhaled steroids, a subpopulation (~ 10%) characterized by excessive airway neutrophilia, is refractory to treatment; these patients exhibit severe disease, and account for more than 50% of asthma health care costs. These numbers underscore the need to better understand the biology of severe asthma and identify pro-asthma mediators released by cells, such as neutrophils, that are unresponsive to common steroid therapy. This review focuses on a unique protein complex consisting of S100A8 and S100A9. These subunits belong to the large [Ca.sup.2+]-binding S100 protein family and are some of the most abundant proteins in neutrophils and macrophages. S100A8/A9 is a damage-associated molecular pattern (DAMP) protein complex released in abundance in rheumatoid arthritis, inflammatory bowel disease, and cancer, but there are no definitive studies on its role in inflammation and obstructive airways disease. Two receptors for S100A8/A9, the multiligand receptor for advanced glycation end products (RAGE) and Toll-like receptor4 (TLR4), are expressed in lung. TLR4 is linked with innate immunity that programs local airway inflammation, and RAGE participates in mediating fibroproliferative remodeling in idiopathic pulmonary fibrosis. S100A8/A9 can induce cell proliferation, or apoptosis, inflammation, collagen synthesis, and cell migration. We hypothesize that this capacity suggests S100A8/A9 could underpin chronic airway inflammation and airway remodeling in asthma by inducing effector responses of resident and infiltrating airway cells. This review highlights some key issues related to this hypothesis and provides a template for future research.

mau liat lebih jelas, here