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Predictive Value of Recent QuantiFERON Conversion for Tuberculosis Disease in Adolescents.

CONCLUSION: Recent QFT conversion was indicative of approximately 8-fold higher risk of progression to tuberculosis disease (compared to non-converters) within 2 years of conversion in a cohort of adolescents in a high tuberculosis burden population. PMID: 22955316 [PubMed - as supplied by publisher] (Source: American Journal of Respiratory and Critical Care Medicine)

Immune/Inflammatory Cell Involvement in the Pathology of Idiopathic Pulmonary Arterial Hypertension.

CONCLUSIONS: Our findings reveal altered immune/inflammatory cell infiltration in pulmonary vascular lesions of idiopathic pulmonary arterial hypertension patients. Thus, targeting immune/inflammatory cells and their secretory molecules may be a novel approach to treat this condition and can be used to monitor the disease process. PMID: 22955318 [PubMed - as supplied by publisher] (Source: American Journal of Respiratory and Critical Care Medicine)

Muscle function in COPD: a complex interplay.

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Muscle function in COPD: a complex interplay.

Int J Chron Obstruct Pulmon Dis. 2012;7:523-35

Authors: Donaldson AV, Maddocks M, Martolini D, Polkey MI, Man WD

Abstract
The skeletal muscles play an essential role in life, providing the mechanical basis for respiration and movement. Skeletal muscle dysfunction is prevalent in all stages of chronic obstructive pulmonary disease (COPD), and significantly influences symptoms, functional capacity, health related quality of life, health resource usage and even mortality. Furthermore, in contrast to the lungs, the skeletal muscles are potentially remedial with existing therapy, namely exercise-training. This review summarizes clinical and laboratory observations of the respiratory and peripheral skeletal muscles (in particular the diaphragm and quadriceps), and current understanding of the underlying etiological processes. As further progress is made in the elucidation of the molecular mechanisms of skeletal muscle dysfunction, new pharmacological therapies are likely to emerge to treat this important extra-pulmonary manifestation of COPD.

PMID: 22973093 [PubMed - in process]

Effects of second hand smoke on airway secretion and mucociliary clearance.

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Effects of second hand smoke on airway secretion and mucociliary clearance.

Front Physiol. 2012;3:342

Authors: Liu Y, Di YP

Abstract
The airway acts as the first defense against inhaled pathogens and particulate matter from the environment. One major way for the airway to clear inhaled foreign objects is through mucociliary clearance (MCC), an important component of the respiratory innate immune defense against lung disease. MCC is characterized by the upward movement of mucus by ciliary motion that requires a balance between the volume and composition of the mucus, adequate periciliary liquid (PCL) volume, and normal ciliary beat frequency (CBF). Airway surface fluid (ASL) is a thin layer liquid that consists of the highly viscous mucus upper "gel" layer, and the watery lubricating lower "sol" layer. Mucus production, secretion and clearance are considered to play a critical role in maintenance of airway health because it maintains hydration in the airway and traps particulates, bacteria, and viruses. Different types of epithelial cells, including secretory cells, and ciliated cells, contribute to the MCC function. Cigarette smoke (CS) contains chemicals and particulates that significantly affect airway secretion. Active and passive CS-induced chronic obstructive pulmonary disease (COPD) is frequently associated with hyperplasia of goblet cells and submucosal glands (SMGs), thus increasing the secretory capacity of the airways that impairs MCC.

PMID: 22973232 [PubMed - in process]

Pathogenic mechanism of second hand smoke induced inflammation and COPD.

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Pathogenic mechanism of second hand smoke induced inflammation and COPD.

Front Physiol. 2012;3:348

Authors: Birru RL, Di YP

Abstract
Second hand smoke (SHS) introduces thousands of toxic chemicals into the lung, including carcinogens and oxidants, which cause direct airway epithelium tissue destruction. It can also illicit indirect damage through its effect on signaling pathways related to tissue cell repair and by the abnormal induction of inflammation into the lung. After repeated exposure to SHS, these symptoms can lead to the development of pulmonary inflammatory disorders, including chronic obstructive pulmonary disease (COPD). COPD is a severe pulmonary disease characterized by chronic inflammation and irreversible tissue destruction. There is no causal cure, as the mechanism behind the development and progression of the disease is still unknown. Recent discoveries implicate genetic predisposition associated with inflammatory response contributed to the development of COPD, linked to irregular innate and adaptive immunity, as well as a risk factor for cancer. The use of animal models for both cigarette smoke (CS) and SHS associated in vivo experiments has been crucial in elucidating the pathogenic mechanisms and genetic components involved in inflammation-related development of COPD.

PMID: 22973236 [PubMed - in process]

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