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Protease inhibitor deficiency as molecular basis for emphysema

Maher M. AlQuaimi (2012)
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Maher AlQuaimi

on 8 December 2012

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Transcript of Protease inhibitor deficiency as molecular basis for emphysema

Maher M. AlQuaimi Protease inhibitor deficiency
as
molecular basis for emphysema Introduction Pathophysiology Serum level of 11 uml/L is a good start definition Physiology History is very important when diagnosing it Introduction Physiology Pathophysiology Structure, location, and mutation of A1AT History Diagnosis Treatment Statistics more than (Kochanek et al) 2009 deaths in 2009 An estimated 64 million people have COPD worldwide in 2004 (WHO,2008) More than 12 millions American are diagnosed with COPD (NIH) CLRD Asthma COPD Bronchitis Emphysema Emphysema
Caused
by
A1ATD Proteases Anti
Proteases Proteins Generates
Protects
Degrades Proliferation
Migration
Digestion
Blood clotting
DEATH ! Proteases
(NE) Anti
Proteases
(serpin) Proteases are classified into 4 main groups: Serine X ser-p-in
Aspartyl
Metalloproteases
Cysteine A1ATD Smoking
Irritants
pollution Carl-Bertil Laurell (1919 – 2001) In 1963, Lurell and Eriksson discovered A1AT http://www.ealta.eu Conclusion Structure, location, and mutation of A1AT A1AT gene is located at the q arm of chromosome 14 It has 12.2 Kilobase pair gene containing seven exons and six introns. A1AT produces 418 amino acid protein Post translation modification in the endoplasmic reticulum produces a 52-KDa-glycosylated protein Mutation of glutamic acid to lysine at position of 342 results in A1ATD Diagnosis General specific Isoelectric focusing Genotyping Serum level of 11 umol/L Treatment General specific Bronchodilators BHT Pulmonary rehabilitation O2 Augmentation therapy Petrache et al (2009) Conclusion A1ATD is an inherited disease, leading to emphysema. Augmentation therapy Thank you chronic lower airway respiratory diseases
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