Emphysema in Coal Workers' Pneumoconiosis

A correlation survey has been carried out between the pathological, physiological, and radiological findings pertaining to emphysema in 247 deceased coal miners and ex-miners, most of whom had been diagnosed as suffering from coal workers'' pneumoconiosis during life. The pathological findings, which included large lung sections and detailed histology in every case, were compared with similar findings in a contrast non-mining population matched for age and sex.The results indicated that emphysema was much more common among the coal miners, both with simple and with complicated pneumoconiosis, than among the contrast group. In addition the extent of the emphysema as measured by a recognized “counting” method carried out on paper-mounted lung sections was remarkably closely related to ventilatory impairment as evidenced by the forced expiratory volume in one second.Extensive emphysema was more commonly found in those pneumoconiosis cases, both simple and complicated, showing the finer punctiform type of radiological change than in cases showing the larger micronodular and nodular opacities.     

Cross sectional study on cytokine production (TNF-α, IL-8) in German coalminers with progressive massive fibrosis and in control miners using a rapid wholeblood assay

Whole-blood release of tumour necrosis factor (TNF-α) and interleukin 8 (IL-8) was studied in 26 German ex-coalminers with progressive massive fibrosis (≥A, ILO 1980; cases) and 26 ex-miners free of pneumoconiosis (≤ 0/1; controls) using a simple wholeblood assay. Cases and controls were matched individually by age and duration of coalmine dust exposure (5-year window). Whole-blood cytokine release was determined (blinded to case control status) in incubations without additions (spontaneous) and with endotoxin (LPS, 3 ng ml^-1) or with coalmine dust (CMD; 5 mg ml^-1). CMD-stimulated TNF-α release was significantly increased and LPS-induced IL-8 release was significantly decreased in cases (matched t-tests: p < 0.01). No effect of duration of exposure was detectable in an unmatched analysis. No clear relationship with lung function parameters independent from case/control-status was observed, although a possible positive association with central airway resistance was indicated by multiple regression for both CMD stimulated TNF-α and LPS-stimulated IL-8. This study on individually matched coalminers validates previous findings on monocyte TNF release as a marker for pneumoconiosis using a method (whole-blood assay) that is more feasible for epidemiological studies. The different response of TNF-α and IL-8 may be useful in studying the occurrence of different endpoints like pneumoconiosis and lung function decrease.     

Dusts causing pneumoconiosis generate .OH and produce hemolysis by acting as Fenton catalysts

Silicates causing pneumoconiosis function as Fenton catalysts to generate hydroxyl radicals (.OH) when incubated with hydrogen peroxide and a reducing substance. In contrast, silicates which do not cause pneumoconiosis demonstrate no Fenton activity. Catalytic activity is decreased by pretreatment of silicates with the iron chelators deferoxamine or transferrin. Hemolysis from silicates is decreased by interventions which remove superoxide anion or hydrogen peroxide from the medium, or by pretreatment of dusts with iron chelators. Thus, asbestos and nonfibrous silicates may cause pneumoconiosis through a common oxidant mechanism by catalyzing production of toxic .OH radicals in the lung.     

Clinical characteristics and epidemiology of pulmonary pseudallescheriasis

BackgroundSome members of the Pseudallescheria (anamorph Scedosporium) have emerged as an important cause of life-threatening infections in humans. These fungi may reach the lungs and bronchial tree causing a wide range of manifestations, from colonization of airways to deep pulmonary infections. Frequently, they may also disseminate to other organs, with a predilection for the brain. In otherwise healthy patients, the infection is characterized by non-invasive type involvement, while invasive and/or disseminated infections were mostly seen in immunocompromised patients.AimsWe reviewed all the available reports on Pseudallescheria/Scedosporium pulmonary infections, focusing on the geographical distribution, immune status of infected individuals, type of infections, clinical manifestations, treatment and outcome.Results and conclusionsThe main clinical manifestations of the 189 cases of pulmonary pseudallescheriasis reviewed were pneumonia (89), followed by fungus ball (26), and chest abscess (18). Some patients had more than one type of invasive pulmonary manifestations. Among patients with pneumonia, several cases of pneumonia associated with near-drowning (10/89, 11.2%) have also been reported in immunocompetent hosts. Major underlying conditions for non-invasive pulmonary infection were preexisting lung cavities and medical immunosuppression for invasive pulmonary infection. Saprobic airway colonization was mostly seen in patients with mucosal dysfunction, i.e. patients with cystic fibrosis. The mortality rate was closely related to the infection type, being 26.8% in non-invasive type (fungus balls) and 57.2% in invasive type.     

Pulmonary Disability in Coal Workers' Pneumoconiosis

Results from a correlation survey which compared radiological and physiological findings during life with detailed morbid anatomical findings in the lungs of 247 deceased miners and ex-miners with pneumoconiosis were used to assess the extent and significance of their pulmonary disability.Coal workers'' pneumoconiosis usually caused progressive impairment of ventilation, which in the simple type of disease was not related to radiological category. In such cases the presence of emphysema was found to be a more important factor in determining the impairment of ventilation than the radiological category of simple pneumoconiosis.     

Circulating Antinuclear Antibody and Rheumatoid Factor in Coal Pneumoconiosis

Circulating antinuclear antibody and rheumatoid factor have been measured in 109 coal miners with pneumoconiosis whose chest radiograph showed a range of abnormalities varying from simple pneumoconiosis of mild degree to advanced progressive massive fibrosis.At a screening dilution of 1/10 the overall incidence of antinuclear antibody was 17%. In almost half of the positive cases the titre was 1/40 or greater.The prevalence of antinuclear antibody was lowest in those with simple pneumoconiosis (9%) and highest in those with category C progressive massive fibrosis (27%). A similar but less striking trend was seen with rheumatoid factor, ranging from 6% in simple pneumoconiosis to 18% in category C progressive massive fibrosis. The trend of increasing frequency of autoantibodies with advancing radiographic category was most marked when the frequencies of antinuclear antibody and rheumatoid factor were combined. These autoantibodies were found in 13% of the miners with simple pneumoconiosis and 45% of those with category C progressive massive fibrosis (P for the trend=0·01).     

The cellular composition of the bronchoalveolar washing in experimental anthracosis

Bronchoalveolar lavage (BAL) was performed in albino random-bred adult male rats with pneumoconiosis. Fibrotic reaction in the lungs was induced by inhalation coal dust during 6 months. BAL comprised 90.9 +/- 1.2% of macrophages; 4.4 +/- 0.8% of neutrophils and 4.5 +/- 1.0% of lymphocytes. The total cell number in BAL was higher (over 59%) in animals with pneumoconiosis. The number of cells on alveolar surface of the lungs was also higher. Fibrotic reaction in the lungs is probably directly related with the increased number of vital macrophages in the lung.     

Bronchoscopic Diagnosis of Pulmonary Infections—Comparison of Protected-Specimen Brush and Cytology Brush With Lung Aspirates

In a recent study the use of a new plugged double-lumen protected-specimen brush with the flexible fiberoptic bronchoscope was advocated to isolate pathogens in lower respiratory tract infections while avoiding upper respiratory tract contamination. To compare the efficacy of this brush and a standard single-lumen cytology brush in identifying the etiologic agent in lower respiratory tract infections, we studied 18 patients with lung infections. Transthoracic lung aspiration was done in all but two patients in an attempt to identify the specific etiologic agent. In these two cases, cultures of specimens of blood or postmortem lung tissue yielded the causative organism. In 12 patients anaerobic or aerobic bacteria (or both) were identified, whereas one patient had a mixed bacterial and fungal infection. Using the cytology brush and the protected-specimen brush we identified at least one pathogen in 10 of 12 and 10 of 13 cases, whereas both brushes missed one or more causative organisms in 8 of 12 and 8 of 13 cases, respectively. Nonetiologic organisms were found in 8 of 12 cases by the cytology brush and 8 of 13 cases by the protected-specimen brush. Quantitative culture techniques improved the specificity of the brush results in infections where aerobes predominated. Our data show that bronchoscopic cultures of lower respiratory tract infections do not consistently recover the causative agent and are frequently subject to contamination by nonetiologic organisms. There was no difference between the brushes in avoiding contamination.     

Rhinovirus genome variation during chronic upper and lower respiratory tract infections

Routine screening of lung transplant recipients and hospital patients for respiratory virus infections allowed to identify human rhinovirus (HRV) in the upper and lower respiratory tracts, including immunocompromised hosts chronically infected with the same strain over weeks or months. Phylogenetic analysis of 144 HRV-positive samples showed no apparent correlation between a given viral genotype or species and their ability to invade the lower respiratory tract or lead to protracted infection. By contrast, protracted infections were found almost exclusively in immunocompromised patients, thus suggesting that host factors rather than the virus genotype modulate disease outcome, in particular the immune response. Complete genome sequencing of five chronic cases to study rhinovirus genome adaptation showed that the calculated mutation frequency was in the range observed during acute human infections. Analysis of mutation hot spot regions between specimens collected at different times or in different body sites revealed that non-synonymous changes were mostly concentrated in the viral capsid genes VP1, VP2 and VP3, independent of the HRV type. In an immunosuppressed lung transplant recipient infected with the same HRV strain for more than two years, both classical and ultra-deep sequencing of samples collected at different time points in the upper and lower respiratory tracts showed that these virus populations were phylogenetically indistinguishable over the course of infection, except for the last month. Specific signatures were found in the last two lower respiratory tract populations, including changes in the 5'UTR polypyrimidine tract and the VP2 immunogenic site 2. These results highlight for the first time the ability of a given rhinovirus to evolve in the course of a natural infection in immunocompromised patients and complement data obtained from previous experimental inoculation studies in immunocompetent volunteers.     

Polycythaemia in Coal Miners with Chronic Lung Disease

The polycythaemic response to hypoxia was studied in 30 ex-coal miners, comprising 14 patients with complicated pneumoconiosis and 16 with chronic non-specific lung disease. A close correlation was found between arterial oxygen saturation and haemoglobin, packed-cell volume, and the red cell mass.     

Specific dermatoglyphic traits of patients with occupational allergic bronchitis

Dermatoglyphic traits proved to be closely associated with chronic mechanic bronchitis (CMB). With the most informative traits identified, it is possible to estimate the individual predisposition to this occupational disorder and thereby to increase the efficiency of preliminary and follow-up medical examinations. Comparison with data on dermatoglyphic traits predisposed to various types of pneumoconiosis supported the hypothesis on a single mechanical lung disease or "general dust lung disease".     

Nosocomial infection in a children's hospital. A retrospective study

The investigations the frequency of the occurrences of hospital infections were carried in a General Pediatric Ward. Most of the infections (77 per cent) appeared in children up to one year of age. The hospital infections mostly affected children residing in rural areas. The etiological agent was E. coli (36 per cent), Proteus (22.7 per cent) Klebsiella and Staphylococcus. The infections caused by E. coli mainly appeared in girls, others- in boys. The frequency of the occurrences of hospital infections was also analysed with respect to the primary disease of a child. In most cases of additional infections were found in children with upper respiratory tract infections, pneumonia and bronchitis. The above differences are statistically valid.     

老年大肠埃希菌血流感染患者的临床分析

为探讨老年大肠埃希菌血流感染患者的临床特点及药敏结果,回顾性分析徐州医科大学附属医院2013年1月-2016年12月340例大肠埃希菌血流感染老年患者的临床资料及药敏结果,采用SPSS软件进行分析。结果显示,患者均合并基础疾病(恶性肿瘤、高血压病、糖尿病、肺部感染等);感染途径主要为消化道(38.5%)、呼吸道(36.8%)和泌尿道(22.6%);检出产超广谱β-内酰胺酶(extended-spectrum β-lactamase,ESBL)大肠埃希菌96例(28.2%);ESBL阳性菌对氨苄西林、复方磺胺甲恶唑、环丙沙星、哌拉西林、第3代头孢、左氧氟沙星的耐药率均高;所有菌株均对碳青霉烯类敏感。结果提示,该院老年大肠埃希菌血流感染患者均合并基础疾病,常见感染途径是消化道、呼吸道和泌尿道,ESBL阳性大肠埃希菌除对碳青霉烯类抗菌药物敏感外,对多种抗菌药物耐药。     

Nickel and extracellular acidification inhibit the water permeability of human aquaporin-3 in lung epithelial cells

Nickel is a common cause of pneumoconiosis. Here, we show that nickel inactivates aquaporin (AQP)-3, the water channel expressed apically in epithelial cells of human terminal airways. Human AQP3 was transiently transfected into human lung cells, and water permeability was measured in transfected and neighboring untransfected cells. Incubation with NiCl2 rapidly, dose-dependently, and reversibly decreased water permeability in AQP3-expressing cells. Acidification of the extracellular medium also caused rapid, dose-dependent, and reversible inhibition of AQP3. Sensitivity of AQP3 to nickel was lower at alkaline pH than at neutral and acidic pH. Cells transfected with human AQP4 and AQP5, which are also expressed in airway epithelia, were insensitive to nickel and extracellular acidification. Zinc and cadmium, other common causes of pneumoconiosis, had no effect on the water permeability of AQP3. Three extracellular residues, Trp128, Ser152, and His241, were responsible for the blocking effect of nickel on human AQP3. Ser152 was identified as a common site for nickel and pH sensitivity. His53, Tyr124, and His154 were also involved in regulation of AQP3 by extracellular pH. In addition, the aromatic side chain of His154 was shown to be important for the water permeability of AQP3. Our results imply that nickel and extracellular pH may modulate lung water clearance and that defective water clearance may be an early component of nickel-induced lung disease.     

Infecciones por mohos en el trasplante pulmonar

Invasive infections by molds, mainly Aspergillus infections, account for more than 10% of infectious complications in lung transplant recipients. These infections have a bimodal presentation: an early one, mainly invading bronchial airways, and a late one, mostly focused on lung or disseminated. The Aspergillus colonization at any time in the post-transplant period is one of the major risk factors. Late colonization, together with chronic rejection, is one of the main causes of late invasive forms. A galactomannan value of 0.5 in bronchoalveolar lavage is currently considered a predictive factor of pulmonary invasive infection. There is no universal strategy in terms of prophylaxis. Targeted prophylaxis and preemptive treatment instead of universal prophylaxis, are gaining more followers. The therapeutic drug monitoring level of azoles is highly recommended in the treatment. Monotherapy with voriconazole is the treatment of choice in invasive aspergillosis; combined antifungal therapies are only recommended in severe, disseminated, and other infections due to non-Aspergillus molds.     

Roles of bioavailable iron and calcium in coal dust-induced oxidative stress: possible implications in coal workers' lung disease

Marked regional differences in prevalence of pneumoconiosis are apparent in the US despite comparable dust exposure. In the present study, we examined the ability of 28 coal samples to release bioavailable iron (BAI) and calcium, as well as other metals such as Cr, Ni, Cu, and Co, from three coalmine regions in Utah (UT), West Virginia (WV), and Pennsylvania (PA), respectively. BAI is defined as iron (both Fe 2+ and Fe 3+ ) released by the coals in 10 mM phosphate solution, pH 4.5, which mimics conditions of the phagolysosomes in cells. We found that coals from the UT, WV, and PA regions released average levels of BAI of 9.6, 4658.8, and 12149 parts per million (ppm, w/w), respectively, which correlated well with the prevalence of pneumoconiosis from that region (correlation coefficient r =0.92 ). The low levels of BAI in the UT coals were due to the presence of calcite (CaCO 3 ), which was shown to be preferentially acid solubilized before iron compounds. Release of iron by two coal samples from the PA and UT regions was further examined in vitro in human lung epithelial A549 cells. We found that the coal from PA, with a high prevalence of pneumoconiosis, released BAI in a dose-dependent manner, both in tissue culture media and in A549 cells. At 2 μg/cm 2 , levels of lipid peroxidation induced by the PA coal were increased 112% over control cells at 24 h treatment, and were sustained at this level for 3 days. The coal from UT, with a low prevalence of pneumoconiosis, induced a marginal increase in cellular iron at 5 and 10 μg/cm 2 treatments and had no effect on lipid peroxidation. Calcium levels in the cells treated with the PA and UT coals were 8.6 and 11.5 μmoles/10 6 cells, respectively, and were significantly higher than that in the controls (53 μmoles/10 6 cells). Our results suggest that the differences in the BAI content in the coals may be responsible for the observed regional differences in the prevalence of pneumoconiosis. Therefore, BAI may be a useful characteristic of coal for predicting coal's toxicity.     

神经内科住院患者肺部感染的相关危险因素分析及护理对策

目的:确定影响神经内科患者肺部感染的危险因素,为预防和控制住院患者肺部感染提供依据。方法:本研究采用回顾性调查方法,对我院神经内科2010年3月至2011年3月住院患者发生肺部感染的案例进行回顾性调查分析。结果:研究发现,调查的2091名患者中,肺部感染例数为41例,发生率为1.96%。内源性因素包括:年龄,意识障碍,瘫痪,卧床,严重的基础疾病;外源性因素包括:住院日,侵入性检查、人工气道与人工机械通气,不合理使用抗生素以及误吸。结论:外源性的感染,通过科学有效的护理措施,在临床上及早进行预防性的护理干预,采取有针对性的护理措施,预防患者肺部感染的发生,降低患者的发病率和死亡率。     

神经内科住院患者肺部感染的相关危险因素分析及护理对策

目的：确定影响神经内科患者肺部感染的危险因素,为预防和控制住院患者肺部感染提供依据。方法：本研究采用回顾性调查方法,对我院神经内科2010年3月至2011年3月住院患者发生肺部感染的案例进行回顾性调查分析。结果：研究发现,调查的2091名患者中,肺部感染例数为41例,发生率为1．96％。内源性因素包括：年龄,意识障碍,瘫痪,卧床,严重的基础疾病;外源性因素包括：住院日,侵入性检查、人工气道与人工机械通气,不合理使用抗生素以及误吸。结论：外源性的感染,通过科学有效的护理措施,在临床上及早进行预防性的护理干预,采取有针对性的护理措施,预防患者肺部感染的发生,降低患者的发病率和死亡率。     

An immunofluorescent study of lung, hilar lymph nodes and spleen in a series of autopsied cases

Direct immunofluorescence reactions were performed with conjugated antihuman IgA, IgG, and IgM sera on bronchi, lung, lymph nodes and spleen, sampled at 12-72 h after death in a series of 20 cases submitted to autopsy. The IgA cells were preponderent in the lung where they concentrate preferentially in the bronchial tree, whereas the IgG and IgM cells were found in a relative higher proportion in the pulmonary parenchyma. The most intense lung immunofluorescence reactions were identified in pneumonias; in relation of these types they acquire distinct aspects: a bronchio-peribronchial disposition in bronchopneumonia and an interstitial-perivascular one in plasma cell pneumonitis. The lymph nodes and spleen of the same cases presented mostly IgG cells, but also, in a smaller amount, IgA and IgM plasma cells.     

Induction of interleukin-6 by coal containing bioavailable iron is through both hydroxyl radical and ferryl species

Coal mining causes health problems, such as pneumoconiosis. We have previously shown that prevalence of pneumoconiosis in workers from various coalmine regions positively correlates with levels of bioavailable iron (BAI) in the coals from that region. In the present study, the nature of reactive oxygen species formed by BAI in the coals and its mechanisms of the induction of biological responses were investigated. Human lung epithelial cell line, A549 cells, were used to examine the induction of interleukin-6 (IL-6), a pro-inflammatory cytokine, which is known to play a crucial role in the development of pneumoconiosis. We found that levels of IL-6 protein as well as its mRNA were significantly increased in the cells treated for 24 h with 20 microg/cm2 of the BAI-containing Pennsylvania (PA) coal; for example we observed 6.7-fold increase in IL-6 protein. Levels of IL-6 protein in cells treated with the Utah (UT) coal containing low-BAI were only 1.9-fold of the control levels. The enhancing effect on the IL-6 by the PA coal was similar to that caused by hydrogen peroxide. Superoxide dismutase (SOD), catalase (CAT), and N-acetyl-L-cysteine (NAC) all had inhibitory effects on the PA coal-induced IL-6 formation. However, CAT had the least protective effect as compared to SOD and NAC. Our results indicate that BAI in the PA coal may induce IL-6 through both ferryl species (via iron autoxidation) and hydroxyl radicals (via the Fenton/Haber Weiss reactions).