Background. Although researchers have consistently demonstrated systemic inflammation in chronic obstructive pulmonary disease (COPD), its origin is yet unknown. We aimed to compare the lung bronchial and parenchymal tissues as potential sources of major acute-phase reactants in COPD patients and resistant smokers.Methods. Consecutive patients undergoing elective surgery for suspected primary lung cancer were considered for the study. Patients were categorized as COPD or resistant smokers according to their spirometric results. Lung parenchyma and bronchus sections distant from the primary lesion were obtained. C-reactive protein (CRP) and serum amyloid A (SAA1, SAA2 and SAA4) gene expressions were evaluated by RT-PCR. Protein levels were evaluated in paraffin embedded lung tissues by immunohistochemistry and in serum samples by nephelometry.Results. Our study included 85 patients with COPD and 87 resistant smokers. In bronchial and parenchymal tissues, both CRP and SAA were overexpressed in COPD patients. In the bronchus, CRP, SAA1, SAA2, and SA4 gene expressions in COPD patients were 1.89-fold, 4.36-fold, 3.65-fold, and 3.9-fold the control values, respectively. In the parenchyma, CRP, SAA1, and SAA2 gene expressions were 2.41-, 1.97-, and 1.76-fold the control values, respectively. Immunohistochemistry showed an over-stained pattern of these markers on endovascular cells of COPD patients. There was no correlation with serum protein concentration.Conclusions. These results indicate an overexpression of CRP and SAA in both bronchial and parenchymal tissue in COPD, which differs between both locations, indicating tissue/cell type specificity. The endothelial cells might play a role in the production of theses markers.

Background Asthma, a chronic condition characterized by airway inflammation and airflow obstruction, is one of the most prevalent diseases in the United State (US) and worldwide [1, 2]. Obesity is a well-established risk factor for new onset asthma, asthma morbidity and poorer asthma-related quality of life [3-6]. Potential mechanisms underlying the relationship between obesity and poor asthma outcomes may include enhanced inflammation, increased level of oxidative stress, and decreased response to standard asthma medication (e.g., inhaled corticosteroids [ICS]) [4, 23, 24, 26] increased prevalence of comorbidities such as gastro-esophageal reflux, sleep disorders, and depression associated with obesity [7-9], also worsen asthma control. The prevalence of obesity in the US has increased steadily during the past 30 years, reaching an overall rate of 36.5% in the general population in 2014 [10, 18, 19, 21, 22]. However, less is known about the trajectory of obesity and overweight among individuals with asthma. This information is important to estimate the extent that obesity contributes to the burden of asthma and to develop policy interventions to curve the negative impact of obesity in this vulnerable group of patients. In this study, we used data from the nationally representative U.S. Behavioral Risk Factor Surveillance System (BRFSS) to assess the trends of obesity and overweight in patients with asthma and to identify the subgroups of patients at higher risk of increased weight.

Introduction: Global Burden of Tuberculosis Mycobacterium Tuberculosis is an ancient and highly harmful successful human pathogen. Despite the advent of effective antimicrobial drugs, tuberculosis (TB) is still the most important infectious disease in humans and remains a leading cause of mortality worldwide [1, 2]. In 1993, the World Health Organization (WHO) declared TB a global public health emergency [3]. Since then, TB incidence has fallen by an average of 1.5% per year and is now 18% lower than in 2000. However, the 2015 update of the WHO Global Tuberculosis Report [2] estimated that there were still approximately 10.4 million (5.9 million men, 3.5 million women, and 1 million children) incident cases worldwide and TB was considered the underlying cause of 1.8 million deaths, 400,000 of whom were among HIV-positive individuals [4]. TB is relatively simple and inexpensive to diagnose, in most cases can be cured with well-tolerated, effective, and low-cost treatments [5, 6, 7]. It has been estimated that 37 million patients were cured between 2000 and 2013, ascribed to advanced diagnostic methods in conjunction with effective treatments [2]. However, multidrug resistant tuberculosis (MDR-TB) remains a major challenge to achieving complete disease control. The development of drug resistant TB strains is multifactorial. When TB bacteria replicate, some naturally mutate and become resistant to anti-TB drugs. TB treatment subsequent kills the non-mutated bacteria, leading to a selective survival of mutated, drug-resistant organisms. In 2015, it was estimated that approximately 580,000 individuals were carriers of rifampicin (RIF) and/or isoniazid (INH) and rifampicin-resistant (MDR) TB strains globally and that about 250,000 deaths were caused by those strains [2]. Moreover, only 25% of those cases were reported and just the 52% were successfully treated [2, 8, 9]. In 2006, extensively drug-resistant TB (XDR-TB; MDR plus resistance to any fluoroquinolone and, at least, one of the three second line injectable drug) also emerged as a more serious form of multidrug-resistant TB and a severe threat to public health, especially in countries with a high prevalence of HIV. Through 2015, XDR-TB cases have been reported in 105 countries and it is estimated 10% of cases of MDR-TB are XDR-TB [10, 11]. Diagnosing TB: Conventional Methods and Molecular Procedures WHO's global strategy for TB control prioritizes early diagnosis, which should include systematic screening of latent TB (contacts and high-risk groups) [12] and universal availability of drug susceptibility testing (DST). Unfortunately, of the 10.4 million TB cases estimated in 2015, more than 4 million remain undiagnosed and thus, continue to spread the disease [2]. Achieving global TB control requires that all of those cases be identified and effectively treated. Nowadays, TB diagnosis is still based in many countries on clinical suspicion, radiography and microbiological tests, performed by microscopic examination of sputum, a 120-year-old method. Bacilloscopy ba...

Improving World Trade Center-related asthma outcomes will require multifactorial approaches such as supporting adherence to controller medications and other self-management behaviors. This study identified several modifiable beliefs that may be the target of future efforts to support self-management in this patient population.

A large number of World Trade Center (WTC) rescue and recovery workers are affected by asthma. While physical and mental health comorbidities have been associated with poor asthma control in this population, the potential role of allergen sensitization is unknown. This study examined the association of indoor sensitization and exposure as a risk factor for increased asthma morbidity in WTC workers. We used data from a prospective cohort of 331 WTC workers with asthma. Sensitization to indoor allergens was assessed by measurement of antigen-specific serum immunoglobulin E (IgE) levels. We used validated tools to evaluate the exposure to indoor allergens. Asthma morbidity outcomes included level of control (Asthma Control Questionnaire, ACQ), quality of life (Asthma Quality of Life Questionnaire, AQLQ) and acute resource utilization. The prevalence of sensitization to cat, dog, mouse, dust mite, cockroach, and mold allergens were 33%, 21%, 17%, 40%, 17%, and 17%, respectively. Unadjusted and regression analyses showed no significant relationship between sensitization and increased asthma morbidity (p > 0.05 for all comparisons), except for sensitization to Aspergillus Fumigatus, cat and mouse epithelium, which were associated with decreased morbidity.