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Alpha-1 Antitrypsin as a Regulatory Protease Inhibitor Modulating Inflammation and Shaping the Tumor Microenvironment in Cancer.

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January 2025

Shum Yiu Foon Shum Bik Chuen Memorial Centre for Cancer and Inflammation Research, School of Chinese Medicine, Hong Kong Baptist University, Hong Kong SAR, China.

Alpha-1 antitrypsin (AAT) is a key serine protease inhibitor for regulating proteases such as neutrophil elastase. AAT restrains the pulmonary matrix from enzymatic degradation, and a deficiency in AAT leads to inflammatory tissue damage in the lungs, resulting in chronic obstructive pulmonary disease. Due to the crucial biological function of AAT, the emerging research interest in this protein has shifted to its role in cancer-associated inflammation and the dynamics of the tumor microenvironment.

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Serum α1-AT Levels and Molecular Analysis in Breast Cancer: An Experimental and Computational Study.

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December 2024

División de Genética, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Independencia Oriente, Guadalajara 44340, Jalisco, Mexico.

Background/objectives: Breast cancer (BC) is a heterogeneous disease with multifactorial origins, including environmental, genetic, and immunological factors. Inflammatory cytokines, such as alpha 1 antitrypsin (α1-AT), are increased in BC and affect physiological and pathological conditions. This study aimed to evaluate the serum levels of α1-AT and perform a computational analysis of in BC, as well as their association with molecular subtypes and clinical features.

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Making Proteins with Electricity.

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January 2025

Institute of Medical Sciences, University of Aberdeen, Aberdeen, Scotland, UK.

Ribosomes use multiple electrical forces to regulate new protein construction, to ensure efficient protein cotranslation, chaperoning, and folding. When these electrical regulatory forces are disrupted as in point charge mutations, specific disease occurs from aberrantly folded proteins. α1 antitrypsin deficiency is perhaps the best-known misfolded protein disease and is covered in some detail.

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Introduction: Non-cystic fibrosis bronchiectasis is a complex medical condition with multiple etiologies, characterized by chronic productive cough and radiologic evidence of airway lumen dilation and wall thickening. Associated exacerbations and declining lung function contribute to increasing disability and mortality. There are no data about the prevalence of non-cystic fibrosis bronchiectasis etiologies in the Colombian population.

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A 16-year-old boy was diagnosed from multiple sclerosis (MS) after suffering from paresthesia in upper limbs and VI cranial nerve paresis. Corticosteroids and fingolimod were started. After 13 months a worsening of liver biochemical tests (LBT) was noticed: ALP 787 U/L, GGT 737 U/L, AST 195, ALT 321, Bi 0.

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