Central cancer of the lung in MR image

The paper analyzes the authors' own material based on the data of chest magnetic resonance imaging (MRI) in 48 patients with verified central cancer of the lung. The algorithm of chest MRI optimized by the authors is presented. The MRI signs of lung cancer in exo- and peribronchial forms of cancer are systematized. The MRI semiotics of chest structural damages are given in the extent of a tumor when progressing, and a metastatic lesion. The MRI signs of complications of this disease are specified.     

小细胞肺癌发生阻塞性肺炎相关因素分析

目的通过对小细胞肺癌患者是否发生阻塞性肺炎的相关因素对比分析,了解伴有阻塞性肺炎小细胞肺癌患者临床特点。方法采用回顾性分析方法,收集2003年1月至2013年1月大连医科大学附属第二医院所收治的经组织学或细胞学确诊的小细胞肺癌患者共450例。经核查资料后,进入统计学的伴有阻塞性肺炎组100例,不伴有阻塞性肺炎组112例,均为初治。对以下因素进行分析：性别、年龄、居住环境、吸烟情况、分期、肿瘤位置、病理类型、初始疗效、NSE（神经元特异性烯醇化酶）。计数资料率和构成比的比较采用卡方检验。结果本组研究中伴有阻塞性肺炎组患者100例中,吸烟患者占76%,小细胞未分化癌患者占81%,中心型癌患者占52%,广泛期患者占57%,NSE阳性率为92%,均高于不伴有阻塞性肺炎组患者。不伴有阻塞性肺炎组的小细胞癌患者初始疗效有效率明显高于伴有阻塞性肺炎组患者。两组在性别、年龄、居住环境方面差异无统计学意义。结论伴有阻塞性肺炎组的小细胞肺癌患者NSE阳性率高于不伴有阻塞性肺炎组。吸烟是小细胞肺癌患者发生阻塞性肺炎的高危因素。阻塞性肺炎降低小细胞癌患者化疗初始疗效。     

Potentialities of MRI in the differential diagnosis of peripheral lung cancer and inflammatory changes

The paper analyzes the authors' own data of chest magnetic resonance imaging (MRI) in 62 patients with verified peripheral lung cancer and different inflammatory changes (round pneumonic focuses, abscesses, etc.). The MRI signs of peripheral lung cancer are systematized. The additional capacities of contrast enhancement are analyzed. The MRI semiotics of different inflammatory changes has been developed. The differential diagnostic criteria for recognizing peripheral lung cancer and inflammatory changes have been also elaborated.     

TGF-beta1 在不同类型特发性间质性肺炎患者肺组织中的表达及其意义

目的:探讨TGF-β1在不同类型特发性间质性肺炎患者肺组织中的表达及其意义。方法:选取2010年2月至2013年12月在我院就诊的72例经支气管镜肺活检的不同类型的特发性间质性肺炎患者的组织标本,对其转化生长因子-β1表达程度进行评定。结果:寻常型(普通型)、非特异性、脱屑性、急性等ⅡP、呼吸性细支气管炎并间质性肺疾病以及隐原性机化性肺炎患者肺组织中TGF-β1表达强度评分均显著高于对照组;脱屑性ⅡP和呼吸性细支气管炎并间质性肺疾病患者肺组织中TGF-β1表达强度评分均显著高于其他类型ⅡP患者;非特异性ⅡP、急性ⅡP、淋巴细胞性ⅡP以及隐原性机化性肺炎组患者肺组织中TGF-β1表达强度评分均显著低于寻常型(普通型)ⅡP组;隐原性机化性肺炎、淋巴细胞性ⅡP组患者肺组织中TGF-β1表达强度评分分别为(0.93±0.34)分、(0.82±0.27)分,显著低于急性ⅡP组患者的(1.64±0.05)分。差异均有统计学意义(P<0.05)。结论:TGF-β1表达过度可能是ⅡP患者的重要特征,在肺纤维化的过程中发挥着重要作用,但在不同类型ⅡP中的作用机制并不相同。     

CD47 deficiency protects mice from lipopolysaccharide-induced acute lung injury and Escherichia coli pneumonia

CD47 modulates neutrophil transmigration toward the sites of infection or injury. Mice lacking CD47 are susceptible to Escherichia coli (E. coli) peritonitis. However, less is known concerning the role of CD47 in the development of acute lung inflammation and injury. In this study, we show that mice lacking CD47 are protected from LPS-induced acute lung injury and E. coli pneumonia with a significant reduction in pulmonary edema, lung vascular permeability, and bacteremia. Reconstitution of CD47(+/-) mice with CD47(-/-) neutrophils significantly reduced lung edema and neutrophil infiltration, thus demonstrating that CD47(+) neutrophils are required for the development of lung injury from E. coli pneumonia. Importantly, CD47-deficient mice with E. coli pneumonia had an improved survival rate. Taken together, deficiency of CD47 protects mice from LPS-induced acute lung injury and E. coli pneumonia. Targeting CD47 may be a novel pathway for treatment of acute lung injury.     

多层螺旋计算机断层扫描联合磁共振成像对早期中央型肺癌及术后复发的诊断价值

目的:探讨多层螺旋计算机断层扫描(MSCT)联合磁共振成像(MRI)对早期中央型肺癌及术后复发的诊断价值。方法:选取2015年8月到2017年2月我院收治的早期中央型肺癌患者98例,所有患者均经MSCT和MRI检查。分析并对比单独MSCT的诊断结果及MSCT联合MRI的诊断结果。随访1年,观察并比较疑似复发的患者单独MSCT的诊断结果及MSCT联合MRI的诊断结果,并比较其对复发诊断的灵敏度、特异度。结果:MSCT联合MRI对早期中央型肺癌诊断的准确率、误诊率、漏诊率分别为94.90%、1.02%、4.08%,与单独MSCT诊断的82.65%、9.18%、8.16%比较,MSCT联合MRI诊断的准确率明显升高,误诊率明显降低(P0.05),而两种诊断方法的漏诊率比较差异无统计学意义(P0.05)。随访1年后,98例患者共复查122例次,共有49例复发。MSCT联合MRI诊断早期中央型肺癌患者术后复发的灵敏度、特异度分别为97.96%、93.15%,均高于单独MSCT诊断的83.67%、82.19%(P0.05)。结论:MSCT联合MRI诊断早期中央型肺癌准确率较高,且在诊断术后复发中可提高灵敏度、特异度。     

Diagnosis of Legionella micdadei pneumonia from cytologic specimens

Legionella micdadei is a recently described opportunistic pulmonary pathogen that produces an acute, suppurative pneumonia in patients receiving steroid therapy. Most prospective diagnoses have been made by open lung biopsy. We present a case in which the diagnosis was made from cytologic material. The clinicopathologic features of L. micdadei pneumonia are discussed, and criteria for diagnosis from cytologic specimens are presented.     

Hyperoxia mediates acute lung injury and increased lethality in murine Legionella pneumonia: the role of apoptosis

Legionella pneumophila is a major cause of life-threatening pneumonia, which is characterized by a high incidence of acute lung injury and resultant severe hypoxemia. Mechanical ventilation using high oxygen concentrations is often required in the treatment of patients with L. pneumophila pneumonia. Unfortunately, oxygen itself may propagate various forms of tissue damage, including acute lung injury. The effect of hyperoxia as a cofactor in the course of L. pneumophila pneumonia is poorly understood. In this study, we show that exposure to hyperoxic conditions during the evolution of pneumonia results in a marked increase in lethality in mice with Legionella pneumonia. The enhanced lethality was associated with an increase in lung permeability, but not changes in either lung bacterial burden or leukocyte accumulation. Interestingly, accelerated apoptosis as evidenced by assessment of histone-DNA fragments and caspase-3 activity were noted in the infected lungs of mice exposed to hyperoxia. TUNEL staining of infected lung sections demonstrated increased apoptosis in hyperoxic mice, predominantly in macrophages and alveolar epithelial cells. In vitro exposure of primary murine alveolar epithelial cells to Legionella in conjunction with hyperoxia accelerated apoptosis and loss of barrier function. Fas-deficient mice demonstrated partial resistance to the lethal effects of Legionella infection induced by hyperoxia, which was associated with attenuated apoptosis in the lung. These results demonstrate that hyperoxia serves as an important cofactor for the development of acute lung injury and lethality in L. pneumophila pneumonia. Exaggerated apoptosis, in part through Fas-mediated signaling, may accelerate hyperoxia-induced acute lung injury in Legionella pneumonia.     

When is pneumonia not pneumonia: a clinicopathologic study of the utility of lung tissue biopsies in determining the suitability of cadaveric tissue for donation

Healthcare-associated pneumonia (HCAP) represents a major diagnostic challenge because of the relatively low sensitivity and specificity of clinical criteria, radiological findings, and microbiologic culture results. It is often difficult to distinguish between pneumonia, underlying pulmonary disease, or conditions with pulmonary complications; this is compounded by the often-subjective clinical diagnosis of pneumonia. We conducted this study to determine the utility of post-mortem lung biopsies for diagnosing pneumonia in tissue donors diagnosed with pneumonia prior to death. Subjects were deceased patients who had been hospitalized at death and diagnosed with pneumonia. Post-mortem lung biopsies were obtained from the anatomic portion of the cadaveric lung corresponding to chest radiograph abnormalities. Specimens were fixed, stained with hematoxylin and eosin, and read by a single board-certified pathologist. Histological criteria for acute pneumonia included intense neutrophilic infiltration, fibrinous exudates, cellular debris, necrosis, or bacteria in the interstitium and intra-alveolar spaces. Of 143 subjects with a diagnosis of pneumonia at time of death, 14 (9.8 %) had histological evidence consistent with acute pneumonia. The most common histological diagnoses were emphysema (53 %), interstitial fibrosis (40 %), chronic atelectasis (36 %), acute and chronic passive congestion consistent with underlying cardiomyopathy (25 %), fibro-bullous disease (12 %), and acute bronchitis (11 %). HCAP represents a major diagnostic challenge because of the relatively low sensitivity and specificity of clinical criteria, radiological findings, and microbiologic testing. We found that attending physician-diagnosed pneumonia did not correlate with post-mortem pathological diagnosis. We conclude that histological examination of cadaveric lung tissue biopsies enables ascertainment or rule out of underlying pneumonia and prevents erroneous donor deferrals.     

肺腺癌发生阻塞性肺炎的临床分析

目的研究阻塞性肺炎与肺腺癌发病的关系以及对预后的影响。方法对2003年12月至2013年1月于大连医科大学附属二院确诊的436例肺腺癌患者病历进行回顾,根据患者临床特征进行分组,并进行统计学分析。结果晚期肺腺癌患者更易出现阻塞性肺炎（χ2=5．662,P=0．017）;中心型肺腺癌较周围型更易出现阻塞性肺炎（χ2=4．432,P=0．035）;在肺腺癌中,性别、年龄、吸烟史以及体重下降与否与阻塞性肺炎的发生经比较差异无统计学意义（P〉0．05）。结论阻塞性肺炎的发生与晚期肺腺癌以及中心型肺腺癌有关,重视筛查对肺腺癌的诊断和预后有重要意义。     

The bactericidal/permeability-increasing protein (BPI) in the innate defence of the lower airways

The human BPI (bactericidal/permeability-increasing protein), stored in primary azurophilic granula of neutrophil granulocytes and produced by mucosal epithelia, has been known for decades to bind LPS (lipopolysaccharide) with very high affinity and to efficiently kill Gram-negative bacteria. Thus BPI potentially represents a central component of the innate immune system to directly combat microbes and modulate subsequent adaptive immune responses. Especially in the lungs, which are frequently exposed to a variety of inhaled pathogens, antimicrobial innate defence molecules such as BPI, are of exceptional relevance. In the present review, we highlight possible functions of BPI during acute pneumonia and CF (cystic fibrosis)-associated chronic infections in the lung.     

A case of fire-eater's pneumonia in an active-duty soldier

Fire-eater's pneumonia is an acute, intense hydrocarbon pneumonitis resulting from aspiration of volatile hydrocarbons such as kerosene, gasoline, or turpentine. The vast majority of patients have resolution of their acute lung injury with supportive care only, avoiding the need for surgical lung reduction procedures. We describe a case of severe hydrocarbon pneumonitis secondary to aspiration of JP-8 jet fuel. The presentation, management, and prognosis of fire-eater's pneumonia are reviewed.     

肺炎型肺癌的影像学特点及误诊分析

目的:探讨肺炎型肺癌影像学特点,深入肺炎型肺癌认识,提高诊断水平,降低临床误诊率。方法:随机选取2013年1月份至2014年2月份我院胸外科住院治疗的36例肺炎型肺癌患者作为研究对象,回顾性分析全部患者的影像学资料及病理检查结果。结果:患者病变部位在各肺段均有分布,局限性及弥漫性分布均可见,其中局灶性分布较大,未出现跨越肺段侵袭肺叶的病例。影像表现主要为边缘不清云絮状肿块影、云絮状影伴结节、肺段实变影、肺实变伴空泡及蜂窝状影、肺炎纤维样化及混合阴影。其中,单纯性磨玻璃影10例;磨玻璃结节肿块10例;肺段分布实变影7例;肺叶及肺段实变伴空泡或蜂窝状影6例;肺炎样纤维化及肿块10例;混合阴影(4种或4种以上阴影并存)3例。结论:肺炎型肺癌患者影像学检查结果多具有肺炎样改变,极易误诊肺炎性疾病,临床诊断中结合活检检查技术,有利于改善临床诊断正确率。     

磁共振成像对非小细胞肺癌的诊断价值分析

目的:探讨磁共振成像(Magnetic resonance imaging,MRI)对非小细胞肺癌的诊断价值。方法:选择2016年9月-2019年4月南京医科大学附属脑科医院(胸科院区)放射科收治的肺部结节患者74例,包括病理证实为肺部良性病变54例(良性组)和非小细胞肺癌20例(肺癌组)。所有患者都给予常规MRI、增强MRI与磁共振扩散加权成像(Diffusion weighted imaging,DWI),记录影像学特征并评估其诊断价值。结果:肺癌组的病灶形态、边缘等MRI特征与良性组对比差异无统计学意义(P0.05)。在b值=0、600、800、1000 s/mm~2条件下,肺癌组的病灶表观扩散系数(Apparent diffusion coefficient,ADC)值都显著低于良性组(P0.05)。肺癌组的病灶MRI增强Ⅰ型+Ⅱ型比例显著高于良性组(P0.05)。MRI鉴别诊断非小细胞肺癌的敏感性与特异性为98.1%和94.4%。结论:MRI用于非小细胞肺癌的诊断能反映病灶组织的血流动力学与水分子活动状况,具有较高的诊断敏感性与特异性。     

Differential MicroRNAs Expression in Serum of Patients with Lung Cancer, Pulmonary Tuberculosis, and Pneumonia

MicroRNAs (miRNAs) play critical regulatory roles in the physiological and pathological processes. The high stability of miRNAs in human serum represents attractive novel diagnostic biomarkers of clinical conditions. Several studies have shown that aberrant expression of miRNAs in human cancer including lung cancer, but little is known about their effects on some infectious lung diseases such as pulmonary tuberculosis (TB) and pneumonia. In this study, we investigated miRNA expression pattern in serum of Egyptian patients with lung cancer, TB, and pneumonia compared with matched healthy controls. Using microarray-based expression profiling followed by real-time quantitative polymerase chain reaction validation, we compared the levels of a series of circulating miRNAs (miR-21, miR-155, miR-182, and miR-197) in serum from patients with lung cancer (n = 65), pulmonary tuberculosis (n = 29), pneumonia (n = 29), and transudate (n = 16) compared with matched healthy controls (n = 37). MiRNA SNORD68 was the housekeeping endogenous control. We found that the serum levels of miR-21, miR-155, and miR-197 were significantly elevated in the patients with lung cancer and pneumonia whereas miR-182 and miR-197 levels were increased only in patients with lung cancer and TB, respectively, compared with controls. Receiver operating characteristic analysis revealed that miR-182, miR-155, and miR-197 have superior diagnostic potential in discriminating patients with lung cancer, pneumonia, and TB, respectively, from controls. Our results conclude that the differential expression of the four studied miRNAs can be potential non-invasive biomarkers for patients with lung cancer, TB and pneumonia.     

Enhanced expression of Duffy antigen in the lungs during suppurative pneumonia.

Duffy antigen is a chemokine binding protein expressed on the surface of erythrocytes and postcapillary venular endothelial cells. It binds selective CXC and CC chemokines with high affinity. Although Duffy antigen is present in the normal pulmonary vascular bed, it is not known whether its expression is altered by innate inflammatory responses in the lungs. We studied Duffy antigen expression by immunohistochemistry in autopsy lung specimens from 16 cases of suppurative pneumonia, 11 cases of acute lung injury, and seven normal lungs. In lungs with suppurative pneumonia, Duffy antigen was expressed in higher numbers of pre- and postcapillary parenchymal vessels compared to normal specimens or specimens with acute lung injury (p<0.03 and p<0.02, respectively). Lungs with suppurative pneumonia also showed Duffy antigen expression on the alveolar septa, whereas this was a rare finding in normal specimens or in acute lung injury (p<0.02). Furthermore, Duffy antigen labeling of the alveolar septa localized to regions with airspace accumulation of neutrophil-rich exudates. In summary, Duffy antigen expression is increased in the vascular beds and alveolar septa of the lung parenchyma during suppurative pneumonia, suggesting that Duffy antigen may have a functional role in the lung parenchyma during inflammation.     

Protective effect of endogenous beta-adrenergic tone on lung fluid balance in acute bacterial pneumonia in mice

Some investigators have reported that endogenous beta-adrenoceptor tone can provide protection against acute lung injury. Therefore, we tested the effects of beta-adrenoceptor inhibition in mice with acute Escherichia coli pneumonia. Mice were pretreated with propranolol or saline and then intratracheally instilled with live E. coli (10(7) colony-forming units). Hemodynamics, arterial blood gases, plasma catecholamines, extravascular lung water, lung permeability to protein, bacterial counts, and alveolar fluid clearance were measured. Acute E. coli pneumonia was established after 4 h with histological evidence of acute pulmonary inflammation, arterial hypoxemia, a threefold increase in lung vascular permeability, and a 30% increase in extravascular lung water as an increase in plasma catecholamine levels. beta-Adrenoceptor inhibition resulted in a marked increase in extravascular lung water that was explained by both an increase in lung vascular permeability and a reduction in net alveolar fluid clearance. The increase in extravascular lung water with propranolol pretreatment was not explained by an increase in systemic or vascular pressures. The increase in lung vascular permeability was explained in part by anti-inflammatory effects of beta-adrenoceptor stimulation because plasma macrophage inflammatory protein-2 levels were higher in the propranolol pretreatment group compared with controls. The decrease in alveolar fluid clearance with propranolol was explained by a decrease in catecholamine-stimulated fluid clearance. Together, these results indicate that endogenous beta-adrenoceptor tone has a protective effect in limiting accumulation of extravascular lung water in acute severe E. coli pneumonia in mice by two mechanisms: 1) reducing lung vascular injury and 2) upregulating the resolution of alveolar edema.     

Bench to bedside: targeting coagulation and fibrinolysis in acute lung injury

Substantial progress has been made in understanding the contribution of alterations in coagulation and fibrinolysis to the pathogenesis of acute lung injury (ALI). Findings from mouse, rat, baboon, and human studies indicate that alterations in coagulation and fibrinolysis may be of major pathogenetic importance in ALI and other inflammatory conditions in the lung including pneumonia, sepsis, and ventilator-induced lung injury. Therapies targeted at both activation of coagulation through the extrinsic coagulation cascade and modulation of coagulation through the protein C system have the potential to favorably impact clinical ALI/acute respiratory distress syndrome.     

Pneumocystis jirovecii colonization in chronic pulmonary disease

Pneumocystis jirovecii causes pneumonia in immunosuppressed individuals. However, it has been reported the detection of low levels of Pneumocystis DNA in patients without signs and symptoms of pneumonia, which likely represents colonization. Several studies performed in animals models and in humans have demonstrated that Pneumocystis induces a local and a systemic response in the host. Since P jirovecii colonization has been found in patients with chronic pulmonary diseases it has been suggested that P jirovecii may play a role in the physiopathology and progression of those diseases. In this report we revise P. jirovecii colonization in different chronic pulmonary diseases such us, chronic obstructive pulmonary disease, interstitial lung diseases, cystic fibrosis and lung cancer.     

Stat3/IL-6 signaling mediates sustained pneumonia induced by Agiostrongylus cantonensis

Angiostrongylus cantonensis (AC) is well-documented that parasitizes the host brain and causes eosinophilic meningitis. The migration route of AC in permissive hosts is well demonstrated, while in nonpermissive hosts, it remains to be fully defined. In the present study, we exploited live imaging technology, morphological and pathological configuration analysis, and molecular biological technologies to explore the migration route of AC and the accompanying tissue damage in nonpermissive and permissive hosts. Our data indicated that, in nonpermissive host mouse, AC larvae migrated from intestinal wall to liver at 2 hours post-infection (hpi), from liver to lung at 4 hpi and then from lung to brain at 8 hpi. AC larval migration caused fatal lung injury (pneumonia) during acute and early infection phases, along with significant activation of Stat3/IL-6 signaling. In addition, AC induce sustained interstitial pneumonia in mouse and rat and pulmonary fibrosis only in rat during late infection phase. Moreover, during the early and late infection phases, Th2 cytokine expression and Stat3 and IL-6 signaling were persistently enhanced and myeloid macrophage cells were notably enriched in host lung, and administration of Stat3 and IL-6 inhibitors (C188-9 and LMT-28) attenuated AC infection-induced acute pneumonia in mice. Overall, we are the first to provide direct and systemic laboratory evidence of AC migration route in a nonpermissive host and report that infection with a high dose of AC larvae could result in acute and fatal pneumonia through Stat3/IL-6 signaling in mice. These findings may present a feasible to rational strategy to minimize the pathogenesis induced by AC.