THE AGE OF ACCEPTANCE

After so much of fighting for your way and so much of stress, a time comes in your life when you finally get it … !

When in the midst of all your fears and insanity you stop dead in your tracks and somewhere, the voice inside your head cries out – ENOUGH OF IT … ENOUGH! Enough fighting, enough cribbing, enough crying and, enough struggling to hold on ... !

And, like a child quieting down after a blind tantrum, your sobs begin to subside, … you shudder once or twice, you blink back your tears and … through a mantle of wet lashes, you begin to look at the world through new eyes. A new visions comes to you.

This is your awakening … !

You realize that it’s time to stop hoping and waiting for something to change, or for happiness, safety and security to come galloping over the next horizon. You come to terms with the fact that you are not her Prince Charming and she is not your Cinderella either … And that, in the real world, there aren’t ever fairy tale endings … ! There aren’t beginnings for that matter either … !  And that any guarantee of “happily ever after” must begin with her and must finish where you are standing right now and, in the process, a sense of serenity is born out of acceptance of present situation.

You awaken to the fact that you are not perfect and that not everyone will always love, appreciate or approve of who or what you are and there will, in fact,  always be some who will despise who and what you are… and propagate stories about you that you know and they too know, are incorrect. But, what to do … ?  That’s OK for them. They are entitled to their own views and opinions. You have to learn the importance of loving and championing yourself and, in the process, a sense of new found confidence is born out of self-approval.

You stop complaining and blaming other people for the things they did to you ( … or didn’t do for you!) and you learn that the only thing you can really count on is the unexpected. You learn that people don’t always say what they mean or mean what they say and that not everyone will always be there for you and that it’s not always about you … that you were born alone and that you will be put out alone!

So, you learn to stand on your own and to take care of yourself and in the process, a sense of safety & security is born of self-reliance. Then you learn about love. Romantic love and familial love. How to love, how much to give in love, when to stop giving and when to walk away. You learn not to project your needs or your feelings onto a relationship. You learn that you will not be more smart, more intelligent, more lovable or important because of the woman in your arms or the child that bears your name.

You learn to look at relationships as they really are and not as you would like them to be. You stop trying to control people, situations and outcomes and, you stop being controlled by others also. You learn that just as people grow and change, so is it with love too; and you learn that you don’t have the right to demand love on your terms, just to make you happy.

You come to the realization that you deserve to be treated with love, kindness, sensitivity and respect and you won’t settle for less ... but you stop hankering for it. You allow only the hands of a lover who cherishes you, to glorify you with his touch and in the process, you internalize the meaning of self-respect. Agreed, those selfish people will continue to make stories about you … continue trying to pull you towards themselves for their own means but, you learn to fight for your life and not to squander it living under a cloud of impending doom. You learn that life isn’t always fair, you don’t always get what you think you deserve and, that sometimes bad things happen to unsuspecting, good people. On these occasions, you learn not to personalize things. You learn that God isn’t punishing you or failing to answer your prayers; it’s just life happening.

You learn to be thankful and to take comfort in many of the simple things we take for granted; things that millions of people upon the earth can only dream about; a full refrigerator, clean running water, a soft warm bed, a long hot shower … !

Slowly, you begin to take responsibility for yourself, by yourself and you make yourself a promise to never betray yourself and to never ever settle for less than your heart’s desire. You hang a wind chime outside your window so you can listen to the wind, and you make it a point to keep smiling, to keep trusting and to stay open to every wonderful possibility.

At last, with courage in your heart and with God by your side you take a stand, you take a deep breath and you begin to design the life you want to live as best as you can. The age of acceptance dawns on you … Finally!

 

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Auto immune mechanisms behind Alopecia Areata

July 2, 2010 — Alopecia  areata (AA), a hair-loss disease often considered similar to psoriasis because of the inflammation and T-cell involvement, shares many genetic associations with a broad spectrum of autoimmune diseases, according to a study appearing in the July 1 issue of Nature.

Hair loss in AA results from "collapse of immune privilege" in hair follicles, such that a person's own immune system attacks and destroys cells of their hair follicles. Interestingly, AA attacks pigmented hairs more actively than nonpigmented hairs. Thus, selective loss of pigmented hair, causing people to become "gray overnight," could actually result from acute AA onset during intense stress or grief.

The genome-wide association study (GWAS) involved international researchers, led by a group at Columbia University Medical Center, New York City. Genotypic analysis of 1054 patients with AA and 3278 control individuals found more than 100 single nucleotide polymorphisms (SNPs) associated with AA at a GWAS-significant level (P ≤ 5 × 10⁻⁷). The majority of these SNPs were concentrated in 8 regions, most containing 1 or 2 genes with recognized immune function.

"Finding the initial genes underlying [AA] is a big step forward, but the nature of the genes is even more exciting," observed senior author Angela M. Christiano, PhD, professor, Dermatology and Genetics & Development, and director of the Center for Human Genetics, Columbia University Medical Center, in a Columbia University news release.

Six of the loci contained, respectively, CTLA4, IL-2/IL-21, the HLA region, ULBP genes, IL-2RA (CD25), andIKZF4 and ERBB3; 1 locus was within STX17, and 1 lay near PRDX5. The strongest association (P = 1.38 × 10⁻³⁵) was found for HLA gene DQA2. Outside of the HLA region, the strongest association was for ULBP6 (P = 4.49 × 10⁻¹⁹) and ULBP3 (P = 4.43 × 10⁻¹⁷). Both ULBP3 and ULBP6 are NKG2D-activating ligands.

The ULBP3 protein (referred to as NKG2D ligand 3) is present at low levels in normal hair follicles, but the study found it was highly expressed in the "dermal sheath as well as the dermal papilla" of 2 patients in the early stages of AA. Immunohistochemical analysis found significantly more cells positive for ULBP3 in 16 additional patients with AA. Upregulation of ULBP3 may be important in initiating the immune response at the onset of AA, or it may be part of an "inflammatory cascade."

ULBP3 produced in hair follicle cells binds to the NKG2D receptor on natural killer (NK) cells, activating these cells. NK cells are a major type of lymphocyte in the innate immune system that are able to destroy other cells. As the study explains: "The autoimmune destruction in AA may be mediated in part by CD8⁺ NKG2D⁺ cytotoxic T cells, whose activation may be induced by upregulation of ULBP3 in the dermal sheath of the hair follicle."

ULBP6 and ULBP3 had not previously been associated with autoimmune diseases; STX17 was implicated in premature hair graying, but not autoimmunity. However, most of the other loci were involved in classic autoimmune diseases such as type 1 diabetes and rheumatoid arthritis, and several were associated with celiac disease, multiple sclerosis, systemic lupus erythematosus, Graves' disease, or psoriasis, among others.

The present study suggests that the upregulated ULBP3 in the outermost layer of hair follicles engages NKG2D on the NK cells, initiating an immune response. The NKG2D receptor has already been recognized as important in the development of type 1 diabetes, rheumatoid arthritis, and celiac disease.

"There seems to be a shared mechanism among organs that express NKG2D danger signals as part of the initiating process," said Dr. Christiano. Drugs are already being developed to target those pathways in rheumatoid arthritis, type 1 diabetes, and other diseases where the NKG2D receptor is involved.

"We may soon be able to test these drugs in clinical trials for [AA]," said Dr. Christiano. "Finally, we have the possibility of developing drugs that specifically target the mechanism behind the disease."

The authors of the study have disclosed no relevant financial relationships.

Nature. 2010;466:113-117.

From Medscape Dermatology