Pub Date : 2018-10-31DOI: 10.15406/JLPRR.2018.05.00184
Anastacio Palacios-Marmolejo, Gabriela de Luna-Ramírez, Mariana Ornelas-Perea, Daniel Alej, ro Herrera-Le, Ro, Mónica Ortiz-Palos, Juan José Silva-Menchaca
Tuberculosis (TB) is an infectious disease mainly caused by Mycobacterium bacterium (M. tuberculosis) and less frequent by M. bovis (zoonotic disease). Which is an intracellular aerobic bacillus characterized, by the formation of granulomas in tissues.1 According to data from the World Health Organization (WHO), TB is essentially a pulmonary disease that represents 85% of the cases, although it can also affect other organs and tissues (extra pulmonary TB [EPTB]). The mechanism of transmission is through the air when a person suffering from pulmonary TB (PTB) expels the bacteria, through productive cough; although, there is a relatively low relation that a person infected with M. tuberculosis develops TB. The probability of developing TB is much higher in patients infected with the human immunodeficiency virus (HIV) or some other co morbidities such as diabetes.2 There are other forms of transmission or acquisition of the disease, one of them can be trough the skin.3 According to WHO data, TB is the second cause of mortality around the world after acquired human immunodeficiency syndrome (AIDS) due to an infectious agent. In 2013, nine million people became ill with TB and 1.5 million died of this disease. More than 95% of TB deaths occurred in lowincome countries and medium income, is one of the five main causes of death in women between 15 and 44 years. In 2013 it is estimated that 550,000 children became ill with TB and that 80,000 seronegative children died. It is the main cause of death in people infected with HIV, a quarter of them is related to TB. An estimated 480,000 people have developed Multidrug-resistant TB (MDR-TB) and, which would cause 170,000 deaths associated with MDR-TB worldwide.2
{"title":"Diagnosis of extra pulmonary tuberculosis by culture","authors":"Anastacio Palacios-Marmolejo, Gabriela de Luna-Ramírez, Mariana Ornelas-Perea, Daniel Alej, ro Herrera-Le, Ro, Mónica Ortiz-Palos, Juan José Silva-Menchaca","doi":"10.15406/JLPRR.2018.05.00184","DOIUrl":"https://doi.org/10.15406/JLPRR.2018.05.00184","url":null,"abstract":"Tuberculosis (TB) is an infectious disease mainly caused by Mycobacterium bacterium (M. tuberculosis) and less frequent by M. bovis (zoonotic disease). Which is an intracellular aerobic bacillus characterized, by the formation of granulomas in tissues.1 According to data from the World Health Organization (WHO), TB is essentially a pulmonary disease that represents 85% of the cases, although it can also affect other organs and tissues (extra pulmonary TB [EPTB]). The mechanism of transmission is through the air when a person suffering from pulmonary TB (PTB) expels the bacteria, through productive cough; although, there is a relatively low relation that a person infected with M. tuberculosis develops TB. The probability of developing TB is much higher in patients infected with the human immunodeficiency virus (HIV) or some other co morbidities such as diabetes.2 There are other forms of transmission or acquisition of the disease, one of them can be trough the skin.3 According to WHO data, TB is the second cause of mortality around the world after acquired human immunodeficiency syndrome (AIDS) due to an infectious agent. In 2013, nine million people became ill with TB and 1.5 million died of this disease. More than 95% of TB deaths occurred in lowincome countries and medium income, is one of the five main causes of death in women between 15 and 44 years. In 2013 it is estimated that 550,000 children became ill with TB and that 80,000 seronegative children died. It is the main cause of death in people infected with HIV, a quarter of them is related to TB. An estimated 480,000 people have developed Multidrug-resistant TB (MDR-TB) and, which would cause 170,000 deaths associated with MDR-TB worldwide.2","PeriodicalId":91750,"journal":{"name":"Journal of lung, pulmonary & respiratory research","volume":"1 1","pages":"158-162"},"PeriodicalIF":0.0,"publicationDate":"2018-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79837750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-10-17DOI: 10.15406/JLPRR.2018.05.00183
Ramniwas, Gopal Singh Chawla, N. Dutt, N. Chauhan, Priyank Jain
{"title":"Novel approach of rescue ventilation during airway stenting in critical airway obstruction","authors":"Ramniwas, Gopal Singh Chawla, N. Dutt, N. Chauhan, Priyank Jain","doi":"10.15406/JLPRR.2018.05.00183","DOIUrl":"https://doi.org/10.15406/JLPRR.2018.05.00183","url":null,"abstract":"","PeriodicalId":91750,"journal":{"name":"Journal of lung, pulmonary & respiratory research","volume":"462 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82988211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-10-11DOI: 10.15406/JLPRR.2018.05.00182
A. Cheepsattayakorn, R. Cheepsattayakorn
The name of this disease “Pneumonoultra-microscopicsilicovolcanokoniosis”, first description by Ramazzini1 was changed due to the types of exposed dust.2 There are no reliable figures on the silica-inhalation exposed populations. Nevertheless, in 2000, the CAREX registry recorded 3.2 million silica-exposed people in the European Union.3 Silicosis is histologically characterized by hyalinized and fibrotic pulmonary nodules, accumulation of lymphocytes and alveolar macrophages, and thickening of pulmonary alveolar interstitium.4 The disease is caused by continuous inhalation of the silica dust (crystalline silica, SiO2 (Silicon dioxide)) with marked inflammation and irreversible scarring of the lungs with nodules in the upper lobes.5,6 Oxygen and silicon, together amount for 74.32% weight and 83.77% of crustal rocks are the two most occurring common elements on the surface of the earth.7 Silicon dioxide or silica is formed under the conditions of increased pressure and heat that exists in amorphous and crystalline (quartz, a typical component of rocks) form. The risk of developing silicosis is closely associated with the accumulated exposure of a person to respirable crystalline silica during his or her working lifetime. The intensity of accumulated respirable silica exposure can be calculated as the following: Accumulated silica dose = fraction of respirable dust X percentage of free silica in mg/m3 X number of years of exposure.8 Silicosis is the most frequently occurring pneumoconiosis due to wide prevalence in the atmosphere and more common than the other types of dust.1,9,10 Both in Developing and developed world, silicosis is an occupational hazard with greater risk for workers engaged in stone crushing, stone cutting, cement industries, glass manufacturing, mining, agriculture, and construction. Pathogenesis
{"title":"Silicosis: biomarkers and pathogenesis","authors":"A. Cheepsattayakorn, R. Cheepsattayakorn","doi":"10.15406/JLPRR.2018.05.00182","DOIUrl":"https://doi.org/10.15406/JLPRR.2018.05.00182","url":null,"abstract":"The name of this disease “Pneumonoultra-microscopicsilicovolcanokoniosis”, first description by Ramazzini1 was changed due to the types of exposed dust.2 There are no reliable figures on the silica-inhalation exposed populations. Nevertheless, in 2000, the CAREX registry recorded 3.2 million silica-exposed people in the European Union.3 Silicosis is histologically characterized by hyalinized and fibrotic pulmonary nodules, accumulation of lymphocytes and alveolar macrophages, and thickening of pulmonary alveolar interstitium.4 The disease is caused by continuous inhalation of the silica dust (crystalline silica, SiO2 (Silicon dioxide)) with marked inflammation and irreversible scarring of the lungs with nodules in the upper lobes.5,6 Oxygen and silicon, together amount for 74.32% weight and 83.77% of crustal rocks are the two most occurring common elements on the surface of the earth.7 Silicon dioxide or silica is formed under the conditions of increased pressure and heat that exists in amorphous and crystalline (quartz, a typical component of rocks) form. The risk of developing silicosis is closely associated with the accumulated exposure of a person to respirable crystalline silica during his or her working lifetime. The intensity of accumulated respirable silica exposure can be calculated as the following: Accumulated silica dose = fraction of respirable dust X percentage of free silica in mg/m3 X number of years of exposure.8 Silicosis is the most frequently occurring pneumoconiosis due to wide prevalence in the atmosphere and more common than the other types of dust.1,9,10 Both in Developing and developed world, silicosis is an occupational hazard with greater risk for workers engaged in stone crushing, stone cutting, cement industries, glass manufacturing, mining, agriculture, and construction. Pathogenesis","PeriodicalId":91750,"journal":{"name":"Journal of lung, pulmonary & respiratory research","volume":"39 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91261065","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-09-28DOI: 10.15406/JLPRR.2018.05.00181
V. Omote, H. Ukwamedua, Johnson Etaghene, M. Oseji, I. Agwai
Tuberculosis (TB) a chronic pulmonary disease caused by a group of non-motile, rod-shaded, aerobic and acid fast bacteria called the Mycobacterium Tuberculosis Complex (MTC),1 is known to currently infect about one-third of the world’s population with a new infection recorded every second.2 Members of the MTC includes Mycobacteriun tuberculosis, Mycobacterium bovis, Mycobacterium africanum, Mycobacterium microfti and Mycobacterium canetti3
{"title":"Pulmonary tuberculosis (PTB) among suspected cases in delta state, South-Southern Nigeria","authors":"V. Omote, H. Ukwamedua, Johnson Etaghene, M. Oseji, I. Agwai","doi":"10.15406/JLPRR.2018.05.00181","DOIUrl":"https://doi.org/10.15406/JLPRR.2018.05.00181","url":null,"abstract":"Tuberculosis (TB) a chronic pulmonary disease caused by a group of non-motile, rod-shaded, aerobic and acid fast bacteria called the Mycobacterium Tuberculosis Complex (MTC),1 is known to currently infect about one-third of the world’s population with a new infection recorded every second.2 Members of the MTC includes Mycobacteriun tuberculosis, Mycobacterium bovis, Mycobacterium africanum, Mycobacterium microfti and Mycobacterium canetti3","PeriodicalId":91750,"journal":{"name":"Journal of lung, pulmonary & respiratory research","volume":"22 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81685056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-07-23DOI: 10.15406/JLPRR.2018.05.00173
M. Sinaa, M. Oukabli, A. Albouzidi
Diffuse idiopathic pulmonary neuroendocrine cells hyperplasia (diffuse idiopathic pulmonary neuroendocrine cell hyperplasia: DIPNECH) is a rare pulmonary lesion described and named since 1992.1 It is characterized by a proliferation of neuroendocrine cells in the bronchial mucosa not exceeding the basal membrane. It may be associated with typical carcinoid tumors.2 The WHO classification of pulmonary tumors classifies it among pre-neoplastic lung lesions, with an increased risk of carcinoid tumors.2 We report here a case of a patient with pulmonary neuroendocrine hyperplasia, poorly known because of its low prevalence and non-specific presentation.
{"title":"Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH)","authors":"M. Sinaa, M. Oukabli, A. Albouzidi","doi":"10.15406/JLPRR.2018.05.00173","DOIUrl":"https://doi.org/10.15406/JLPRR.2018.05.00173","url":null,"abstract":"Diffuse idiopathic pulmonary neuroendocrine cells hyperplasia (diffuse idiopathic pulmonary neuroendocrine cell hyperplasia: DIPNECH) is a rare pulmonary lesion described and named since 1992.1 It is characterized by a proliferation of neuroendocrine cells in the bronchial mucosa not exceeding the basal membrane. It may be associated with typical carcinoid tumors.2 The WHO classification of pulmonary tumors classifies it among pre-neoplastic lung lesions, with an increased risk of carcinoid tumors.2 We report here a case of a patient with pulmonary neuroendocrine hyperplasia, poorly known because of its low prevalence and non-specific presentation.","PeriodicalId":91750,"journal":{"name":"Journal of lung, pulmonary & respiratory research","volume":"17 9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82936963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-06-19DOI: 10.15406/JLPRR.2018.05.00171
D. Rey, J. González
Pulmonary Alveolar Proteinosis (PAP) is one of the “orphan diseases” of the lung, whose peculiarity consists in an intra-alveolar accumulation of a lipo-proteinaceous material related to surfactant, which interferes with gas exchange, presenting with symptoms and signs varying in intensity. Initially described by Rosen, Castleman and Liebow in 1958, its frequency is very low: both Diksen and Ben Dov estimate an incidence in 0.37 cases/100,000 people and prevalence in 3.7/1,000,000 inhabitants.1‒3
{"title":"Pulmonary alveolar proteinosis secondary to chronic chlorine occupational inhalation","authors":"D. Rey, J. González","doi":"10.15406/JLPRR.2018.05.00171","DOIUrl":"https://doi.org/10.15406/JLPRR.2018.05.00171","url":null,"abstract":"Pulmonary Alveolar Proteinosis (PAP) is one of the “orphan diseases” of the lung, whose peculiarity consists in an intra-alveolar accumulation of a lipo-proteinaceous material related to surfactant, which interferes with gas exchange, presenting with symptoms and signs varying in intensity. Initially described by Rosen, Castleman and Liebow in 1958, its frequency is very low: both Diksen and Ben Dov estimate an incidence in 0.37 cases/100,000 people and prevalence in 3.7/1,000,000 inhabitants.1‒3","PeriodicalId":91750,"journal":{"name":"Journal of lung, pulmonary & respiratory research","volume":"31 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82683881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-05-23DOI: 10.15406/JLPRR.2018.05.00169
Neetu Singh
Non-urgent endotracheal intubation is common in the neonatal intensive care unit (NICU). Previous studies have shown that conscious and awake intubations in neonates are painful and associated with adverse physiologic responses.1‒5 Several trials have demonstrated that premedication significantly improves intubation conditions, decreases the time and number of attempts needed to complete the intubation procedure, and minimizes the potential for intubation related airway trauma.6‒13 The Fetus and Newborn Committee of the American Academy of Pediatrics (2010) and Canadian Pediatric Society (2011) recommend premedication of infants before intubation when time permits.6,10 In addition, the International Evidence-Based Group for Neonatal Pain conclude that “tracheal intubation without the use of analgesia or sedation should be performed only for resuscitation in the delivery room or for life-threatening situations associated with the unavailability of intravenous access”.14 Nevertheless, concerns have also been raised regarding adverse effects related to premedication for neonatal intubation.15
{"title":"Premedication for neonatal intubations: an unrecognized area for improvement","authors":"Neetu Singh","doi":"10.15406/JLPRR.2018.05.00169","DOIUrl":"https://doi.org/10.15406/JLPRR.2018.05.00169","url":null,"abstract":"Non-urgent endotracheal intubation is common in the neonatal intensive care unit (NICU). Previous studies have shown that conscious and awake intubations in neonates are painful and associated with adverse physiologic responses.1‒5 Several trials have demonstrated that premedication significantly improves intubation conditions, decreases the time and number of attempts needed to complete the intubation procedure, and minimizes the potential for intubation related airway trauma.6‒13 The Fetus and Newborn Committee of the American Academy of Pediatrics (2010) and Canadian Pediatric Society (2011) recommend premedication of infants before intubation when time permits.6,10 In addition, the International Evidence-Based Group for Neonatal Pain conclude that “tracheal intubation without the use of analgesia or sedation should be performed only for resuscitation in the delivery room or for life-threatening situations associated with the unavailability of intravenous access”.14 Nevertheless, concerns have also been raised regarding adverse effects related to premedication for neonatal intubation.15","PeriodicalId":91750,"journal":{"name":"Journal of lung, pulmonary & respiratory research","volume":"55 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79060712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-05-17DOI: 10.15406/JLPRR.2018.05.00168
E. Kalkan, A. Mirici, B. Akbas
The term occult pneumothorax (OPTX) is used for the pneumothorax that is not visualized with the aid of CXR, but detected via computed tomography (CT). It is a radiological diagnosis increasingly recognized following the extensive use of CT. The radiological investigation of the cases with thoracic trauma in a supine or seated position may also lead to this false diagnosis. It may be diagnosed by investigations of abdominal, cervical, and most commonly thoracic CT that were applied to patients with multiple traumas in order to evaluate all sites of injury.1‒3
{"title":"Indicators of occult pneumothorax in thoracic trauma: a retrospective descriptive study","authors":"E. Kalkan, A. Mirici, B. Akbas","doi":"10.15406/JLPRR.2018.05.00168","DOIUrl":"https://doi.org/10.15406/JLPRR.2018.05.00168","url":null,"abstract":"The term occult pneumothorax (OPTX) is used for the pneumothorax that is not visualized with the aid of CXR, but detected via computed tomography (CT). It is a radiological diagnosis increasingly recognized following the extensive use of CT. The radiological investigation of the cases with thoracic trauma in a supine or seated position may also lead to this false diagnosis. It may be diagnosed by investigations of abdominal, cervical, and most commonly thoracic CT that were applied to patients with multiple traumas in order to evaluate all sites of injury.1‒3","PeriodicalId":91750,"journal":{"name":"Journal of lung, pulmonary & respiratory research","volume":"31 1","pages":"87-90"},"PeriodicalIF":0.0,"publicationDate":"2018-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78757348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-05-16DOI: 10.15406/JLPRR.2018.05.00167
T. Brodskaya, V. Nevzorova, N. Zakharchuk, N. Repina
Currently the connection between chronic obstructive respiratory disease COPD and some cardiovascular and cerebrovascular diseases has been established Vascular disorders in COPD become evident in the early stages of disease and can manifest from endothelial dysfunction to aortic mechanical property disturbance and cerebral circulation disorders COPD is also known as a disease associated with smoking A number of researchers have described pathophysiological mechanisms of vascular disorders and in particular arterial stiffening in COPD A variety of theories have been proposed to explain these observations Pathophysiological processes that increase arterial stiffness both physiological and pathophysiological involve remodeling cascades leading to disturbance of the structural and functional relationships between collagen and elastin in the arterial vascular wall The main processes involved appear to be inflammatory proteases and oxidative stress New research suggests that the vascular dysfunction observed in COPD is associated with some specific genes New data suggests that this is not just due to endothelial dysfunction but a violation of the mechanical properties of the arterial vasculature which is now considered an important component of the pathogenesis of COPD Surplus aortic stiffness can contribute increasingly to cardiovascular event risk in COPD and is associated with changes in normal cerebral circulation and cognitive function Research is focused on the study of genetic predisposition for vascular dysfunction in COPD Various polymorphisms determining the connective tissue metabolism production of nitric oxide detoxification of xenobiotics and many others are now all thought relevant Increasing of aortic stiffness is an important component of the amplification of cardiovascular risk events coronary disorders and cerebral circulation in patients with COPD Some polymorphisms are considered especially relevant such as COL A polymorphisms It is now important to take into consideration the pathophysiological consequences of increasing arterial stiffness in COPD which are schematically represented in our review
{"title":"Aortic stiffness and polymorphisms of collagen-1 type 1a gene in COPD patients","authors":"T. Brodskaya, V. Nevzorova, N. Zakharchuk, N. Repina","doi":"10.15406/JLPRR.2018.05.00167","DOIUrl":"https://doi.org/10.15406/JLPRR.2018.05.00167","url":null,"abstract":"Currently the connection between chronic obstructive respiratory disease COPD and some cardiovascular and cerebrovascular diseases has been established Vascular disorders in COPD become evident in the early stages of disease and can manifest from endothelial dysfunction to aortic mechanical property disturbance and cerebral circulation disorders COPD is also known as a disease associated with smoking A number of researchers have described pathophysiological mechanisms of vascular disorders and in particular arterial stiffening in COPD A variety of theories have been proposed to explain these observations Pathophysiological processes that increase arterial stiffness both physiological and pathophysiological involve remodeling cascades leading to disturbance of the structural and functional relationships between collagen and elastin in the arterial vascular wall The main processes involved appear to be inflammatory proteases and oxidative stress New research suggests that the vascular dysfunction observed in COPD is associated with some specific genes New data suggests that this is not just due to endothelial dysfunction but a violation of the mechanical properties of the arterial vasculature which is now considered an important component of the pathogenesis of COPD Surplus aortic stiffness can contribute increasingly to cardiovascular event risk in COPD and is associated with changes in normal cerebral circulation and cognitive function Research is focused on the study of genetic predisposition for vascular dysfunction in COPD Various polymorphisms determining the connective tissue metabolism production of nitric oxide detoxification of xenobiotics and many others are now all thought relevant Increasing of aortic stiffness is an important component of the amplification of cardiovascular risk events coronary disorders and cerebral circulation in patients with COPD Some polymorphisms are considered especially relevant such as COL A polymorphisms It is now important to take into consideration the pathophysiological consequences of increasing arterial stiffness in COPD which are schematically represented in our review","PeriodicalId":91750,"journal":{"name":"Journal of lung, pulmonary & respiratory research","volume":"33 1","pages":"81-85"},"PeriodicalIF":0.0,"publicationDate":"2018-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86603658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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