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1.
冲击波致伤动物模型是原发冲击伤模拟实验研究的前提和保障。目前绝大多数实验模拟冲击波是使用炸药产生冲击波和冲击波生成装置两种方法。早期建立冲击伤模型是使用烈性炸药产生冲击波致伤动物,随着技术的发展,冲击波生成装置取代烈性炸药应用到动物实验研究中。冲击波生成装置常见两种类型:生物激波管装置和激光冲击波发生装置。各种生物激波管装置已发展成熟并被广泛使用,激光冲击波发生装置也显示出独特的优势,大大促进了冲击伤模拟实验研究的开展。  相似文献   

2.
    
To better protect soldiers from blast threat, that principally affect air-filled organs such a lung, it is necessary to develop an adapted injury criterion and, prior to this, to evaluate the response of a biological model against that threat. The objective of this study is to provide some robust data to quantify the chest response of post-mortem swine under blast loadings.7 post-mortem swine (54.5 ± 2.6 kg), placed side-on to the threat and against the ground, were exposed to 5 shock-waves of increasing intensities. Their thorax were instrumented with a piezo-resistive pressure sensor, an accelerometer directly exposed to the shock-wave and a target was mounted on the latter in order to track the chest wall displacement.For incident impulses ranging from 47 kPa ms ± 2% to 173 kPa ms ± 6%, the measured maximum of linear chest wall acceleration (Γmax) goes from 5800 m/s2 ± 16% to 41,000 m/s2 ± 8%, with a duration of 0.8 ms. Chest wall displacements ranging from 5 mm ± 20% to 20 mm ± 15%, with a duration of 9 ms, are reached. These reproducible data were used to find simple relations (linear, 2nd and 3rd order polynomials) between the kinematic parameters (plus the viscous criterion) and the incident and reflected impulses.Correlating the new reproducible data with the prediction from the Bowen curves showed a lung injury threshold in terms of Γmax similar to that of Cooper (10,000 m/s2). However, the limits defined for the viscous criterion in the automobile field and for non-lethal weapons seems not adapted for the blast threat.  相似文献   

3.
Molecules that simultaneously inhibit independent or co-dependent proinflammatory pathways may have advantages over conventional monotherapeutics. OmCI is a bifunctional protein derived from blood-feeding ticks that specifically prevents complement (C)-mediated C5 activation and also sequesters leukotriene B4 (LTB4) within an internal binding pocket. Here, we examined the effect of LTB4 binding on OmCI structure and function and investigated the relative importance of C-mediated C5 activation and LTB4 in a mouse model of immune complex-induced acute lung injury (IC-ALI). We describe two crystal structures of bacterially expressed OmCI: one binding a C16 fatty acid and the other binding LTB4 (C20). We show that the C5 and LTB4 binding activities of the molecule are independent of each other and that OmCI is a potent inhibitor of experimental IC-ALI, equally dependent on both C5 inhibition and LTB4 binding for full activity. The data highlight the importance of LTB4 in IC-ALI and activation of C5 by the complement pathway C5 convertase rather than by non-C proteases. The findings suggest that dual inhibition of C5 and LTB4 may be useful for treatment of human immune complex-dependent diseases.  相似文献   

4.
目的:探讨胸外科手术术后神经病理性疼痛的发生情况及相关危险因素。方法:回顾性分析2015年至2016年就诊于我院行胸外科手术的患者的临床资料,包括患者的年龄、性别、吸烟史、BMI、术前是否使用催眠药物、术前诊断、手术侧别、手术方式、是否为微创、硬膜外自控镇痛泵使用情况、术中失血量、手术持续时间、引流管引流时间及是否发生神经病理性疼痛,对比分析是否发生神经病理性疼痛患者的临床资料,对有差异的临床资料进行多因素Logistic回归分析探讨发生神经病理性疼痛的危险因素。结果:共有123例患者纳入研究,33例(26.8%)患者的患者术后出现神经病理性疼痛,6例(4.9%)患者在术后一年仍有持续性神经性病理疼痛,术后出现神经病理性疼痛的平均时间为术后第7天,平均持续时间为75天,发生神经病理性疼痛的患者吸烟比例(81.8%)、术前使用催眠药比例(57.6%)、开胸手术比例(81.8%)、术中失血量(185 mL)、手术时间(196分钟)、术后引流时间(2.5天)均高于没有发生神经病理性疼痛的患者。多因素分析显示术前使用催眠药(OR=2.322,P<0.001)、手术时间延长(OR=3.703,P<0.001)和术后引流时间延长(OR=2.675,P=0.002)均是神经病理性疼痛发生的危险因素,电视辅助胸腔镜手术方式是保护性因素(OR=0.453,P=0.002)。结论:术前使用催眠药物、延长的手术时间及术后引流时间增加了神经病理性疼痛发生的风险,电视辅助胸腔镜技术可减少其发生率。  相似文献   

5.
目的:研究全凭静脉麻醉复合胸椎旁神经阻滞(TPVB)对胸腔镜下肺病损切除术患者应激反应、血流动力学及术后镇痛的影响。方法:选择2016年6月至2017年12月在我院行胸腔镜下肺病损切除术的80例患者为研究对象。采用简单随机抽样方法,分为对照组(n=40)和观察组(n=40)。对照组行单纯全身麻醉,观察组在超声引导下行TPVB复合全身麻醉。比较两组麻醉前、术毕、术后24 h的血糖、肾上腺素(E)、去甲肾上腺素(NE)及多巴胺(DA)的浓度,以及两组在麻醉时、手术开始时、手术开始后0.5 h、手术开始后1 h、术毕时的平均动脉压(MAP)和心率(HR),同时比较两组术后2 h、6 h、12 h、24 h静息及活动时的视觉模拟评分(VAS)及相关并发症的发生率。结果:两组患者在麻醉前及术毕的各应激反应指标比较无差异(P0.05),而术后24 h比较,观察组低于对照组(P0.05);两组患者麻醉时的MAP、HR比较无差异(P0.05),除手术开始后1 h和术毕的HR外,观察组各时间的MAP、HR均显著低于对照组(P0.05);除静息时24 h外,观察组各时间静息时和活动时的VAS评分均低于对照组(P0.05);两组患者术后各并发症的发生率比较无统计学差异(P0.05)。结论:全凭静脉麻醉复合TPVB在胸腔镜下肺病损切除术中应激反应小,对血流动力学的波动影响小,术后镇痛效果良好,且安全有效。  相似文献   

6.
    
Exposure to mustard gas causes inflammatory lung diseases including acute respiratory distress syndrome (ARDS). A defect in the lung surfactant system has been implicated as a cause of ARDS. A major component of lung surfactant is dipalmitoyl phosphatidylcholine (DPPC) and the major pathway for its synthesis is the cytidine diphosphocholine (CDP-choline) pathway. It is not known whether the ARDS induced by mustard gas is mediated by its direct effects on some of the enzymes in the CDP-choline pathway. In the present study we investigated whether mustard gas exposure modulates the activity of cholinephosphotransferase (CPT) the terminal enzyme by CDP-choline pathway. Adult guinea pigs were intratracheally infused with single doses of 2-chloroethyl ethyl sulfide (CEES) (0.5 mg/kg b.wt. in ethanol). Control animals were injected with vehicles only. The animals were sacrificed at different time and the lungs were removed after perfusion with physiological saline. CPT activity increased steadily up to 4 h and then decreased at 6 h and stabilized at 7 days in both mitochondria and microsomes. To determine the dose-dependent effect of CEES on CPT activity we varied the doses of CEES (0.5-6.0 mg/kg b.wt.) and sacrificed the animals at 1 h and 4 h. CPT activity showed a dose-dependent increase of up to 2.0 mg/kg b.wt. of CEES in both mitochondria and microsomes then decreased at 4.0 mg/kg b.wt. For further studies we used a fixed single dose of CEES (2.0 mg/kg b.wt.) and fixed exposure time (7 days). Lung injury was determined by measuring the leakage of iodinated-bovine serum albumin into lung tissue and expressed as the permeability index. CEES exposure (2.0 mg/kg b.wt. for 7 days) caused a significant decrease of both CPT gene expression (approximately 1.7-fold) and activity (approximately 1.5-fold) in the lung. This decrease in CPT activity was not associated with any mutation of the CPT gene. Previously we reported that CEES infusion increased the production of ceramides which are known to modulate PC synthesis. To determine whether ceramides affect microsomal CPT activity the lung microsomal fraction was incubated with different concentrations of C(2)-ceramide prior to CPT assay. CPT activity decreased significantly with increasing dose and time. The present study indicates that CEES causes lung injury and significantly decreases CPT gene expression and activity. This decrease in CPT activity was not associated with any mutation of the CPT gene is probably mediated by accumulation of ceramides. CEES induced ceramide accumulation may thus play an important role in the development of ARDS by modulating CPT enzyme.  相似文献   

7.
    
In soccer (football), dominant limb kicking produces higher ball velocity and is used with greater frequency than the non-dominant limb. It is unclear whether limb dominance has an effect on injury incidence. The purpose of this systematic review with meta-analysis is to examine the relationship between limb dominance and soccer injuries. Studies were identified from four online databases according to PRISMA guidelines to identify studies of soccer players that reported lower extremity injuries by limb dominance. Relevant studies were assessed for inclusion and retained. Data from retained studies underwent meta-analyses to determine relative risk of dominant versus non-dominant limb injuries using random-effects models. Seventy-four studies were included, with 36 of them eligible for meta-analysis. For prospective lower extremity injury studies, soccer players demonstrated a 1.6 times greater risk of injury to the dominant limb (95% CI [1.3–1.8]). Grouped by injury location, hamstring (RR 1.3 [95% CI 1.1–1.4]) and hip/groin (RR 1.9 [95% CI 1.3–2.7]) injuries were more likely to occur to the dominant limb. Greater risk of injury was present in the dominant limb across playing levels (amateurs RR 2.6 [95% CI 2.1–3.2]; youths RR 1.5 [95% CI 1.26–1.67]; professionals RR 1.3 [95% CI 1.14–1.46]). Both males (RR 1.5 [95% CI 1.33–1.68)] and females (RR 1.5 [95% CI 1.14–1.89]) were more likely to sustain injuries to the dominant limb. Future studies investigating soccer injury should adjust for this confounding factor by using consistent methods for assigning limb dominance and tracking use of the dominant versus non-dominant limb.  相似文献   

8.
目的:分析造成军人前交叉韧带损伤的危险因素,进而指导临床,为前交叉韧带损伤的预防提供理论依据.方法:回顾性分析本院2011年11月-2012年6月的58例前交叉韧带损伤的军人病例,分别以损伤动作及其机制、损伤时所穿鞋子及发生场地、BMI及雌激素水平、运动前有无准备活动为指标,研究生物力学危险因素、外在环境危险因素、内在危险因素、神经肌肉危险因素对前交叉韧带损伤的影响.结果:ACL损伤动作中军事训练23例,篮球22例所占比例最高(总计77.6%).在所有损伤动作中屈膝外翻38例,跳起落地10例,运动急停7例,暴力扭转3例.塑胶场地发生33例(占56.9%)为四大场地中损伤构成比最高的场地;运动时所穿鞋子类型为运动鞋12例(20.7%)、胶底鞋41例(70.6%)时损伤发生构成比明显高于其他类型的鞋子.BMI分组中超重者38例(65.5%)占据首位.雌激素分组中损伤一般发生于排卵期前后.神经肌肉因素调查中56例(96.5%)患者运动前未行专业的准备活动.结论:屈膝外翻位,活动中鞋子与地面摩擦力大,BMI指数高,体内雌激素含量增高,没有专业的运动前准备活动与前交叉韧带损伤的发生有关.诸多危险因素中唯有神经肌肉危险因素可调节控制.  相似文献   

9.
Supplemental oxygen inhalation is frequently used to treat severe respiratory failure; however, prolonged exposure to hyperoxia causes hyperoxic acute lung injury (HALI), which induces acute respiratory distress syndrome and leads to high mortality rates. Recent investigations suggest the possible role of NLRP3 inflammasomes, which regulate IL-1β production and lead to inflammatory responses, in the pathophysiology of HALI; however, their role is not fully understood. In this study, we investigated the role of NLRP3 inflammasomes in mice with HALI. Under hyperoxic conditions, NLRP3−/− mice died at a higher rate compared with wild-type and IL-1β−/− mice, and there was no difference in IL-1β production in their lungs. Under hyperoxic conditions, the lungs of NLRP3−/− mice exhibited reduced inflammatory responses, such as inflammatory cell infiltration and cytokine expression, as well as increased and decreased expression of MMP-9 and Bcl-2, respectively. NLRP3−/− mice exhibited diminished expression and activation of Stat3, which regulates MMP-9 and Bcl-2, in addition to increased numbers of apoptotic alveolar epithelial cells. In vitro experiments revealed that alveolar macrophages and neutrophils promoted Stat3 activation in alveolar epithelial cells. Furthermore, NLRP3 deficiency impaired the migration of neutrophils and chemokine expression by macrophages. These findings demonstrate that NLRP3 regulates Stat3 signaling in alveolar epithelial cells by affecting macrophage and neutrophil function independent of IL-1β production and contributes to the pathophysiology of HALI.  相似文献   

10.
    
Mustard gas exposure causes inflammatory lung diseases. Many inflammatory lung diseases are associated with oxidative stress. Reactive oxygen species (ROS) are involved in the maintenance of physiological functions. In tissues, it is therefore essential to maintain a steady-state level of antioxidant activity to allow both for the physiological functions of ROS to proceed and at the same time preventing tissue damage. We have recently reported that mustard gas exposure decreases the overall activity of superoxide dismutase (SOD). In the present study, we investigated the effects of mustard gas on each of the three isozymes: SOD-1 (Cu/Zn), SOD-2 (Mn), and SOD-3 (extracellular). Adult guinea pigs were intratracheally injected single doses of 2-chloroethyl ethyl sulfide (CEES) (2 mg/kg body weight) in ethanol. Control animals were injected with vehicle in the same way. The animals were sacrificed after 7 days, and lungs were removed after perfusion with physiological saline. Lung injury was established by measuring the leakage of iodinated-BSA into lung tissue. Mustard gas exposure caused a significant increase in the activity of SOD-1 (35%). However, the SOD-3 activity which is the predominant type in lung was significantly decreased (62%), whereas no change was observed in SOD-2 activity. Thus the decrease in the total activity of SOD was primarily due to the SOD-3 isozyme. Northern blot analysis indicated 3.5-fold increased expression of SOD-1 in mustard gas exposed lung, but no significant change in the expression of SOD-2 and SOD-3 was observed. Mustard gas exposure did not cause mutation in the coding region of SOD-1 gene while causing modulation in expression levels. The protein levels of SOD-1, SOD-2, and SOD-3 were not altered significantly in the mustard gas exposed lung. Our results indicate that the overall decrease in the activity of SOD by mustard gas exposure is probably mediated by direct inactivation of the SOD-3 gene or the enzyme itself. This decrease in the activity of SOD-3 may be due to the cleavage of active form of the protein to an inactive form. The existence of active and inactive forms of SOD-3 as a result of shifts in Cys-Cys disulfide bonding has been described in human, recently. Studies are underway in our laboratory to investigate whether mustard gas induced inactivation of SOD-3 in lung is similarly mediated by a change in Cys-Cys disulfide bonding.  相似文献   

11.
    
Cardamonin, a flavone compound isolated from Alpinia katsumadai Heyata seeds, has been reported to possess anti-inflammatory and anticoagulative activities, and it might be beneficial for management of sepsis. This study was conducted to examine the protective effects of cardamonin on experimental sepsis and resultant acute lung injury (ALI). Cardamonin (30 and 100 mg/kg) significantly elevated the survival rate of septic mice, alleviated ALI and lung microvascular leak, and lowered the serum levels of proinflammatory cytokines TNF-α, IL-1β, and IL-6. In vitro, it (25 and 50 μM) concentration dependently inhibited endothelium permeability and downregulated phosphorylation of P38 in rat lung microvascular endothelial cells induced by lipopolysaccharide (LPS). P38 inhibitor inhibited the endothelium permeability. In RAW 264.7 macrophage cells, cardamonin also showed selective inhibition of P38 phosphorylation induced by LPS. These results indicate that cardamonin can protect septic mice from ALI by preventing endothelium barrier dysfunction via selectively inhibiting P38 activation.  相似文献   

12.
目的:总结成功治愈的一例多发巨大肺大泡患者的临床经验,并结合文献报道对肺大泡的治疗方法进行复习,以提高临床对肺大泡治疗方法的认识,为临床肺大泡的治疗提供新的思路与借鉴。方法:采用内科胸腔镜下肺减容术,即在胸腔镜下夹破充气的肺大泡,同时胸腔内注入自体血60 mL及凝血酶1000U一次,嘱患者翻身活动,促进胸膜表面混合均匀,连续行胸腔闭式引流。结果:患者治疗后,右肺复张良好,患者胸膜破口愈合,且康复出院。结论:应用内科胸腔镜下肺减容术,具有经济、疼痛小、自体血来源方便、患者更易接受的优点,疗效确切,值得临床推广。  相似文献   

13.
In humans, disrupted repair and remodeling of injured lung contributes to a host of acute and chronic lung disorders which may ultimately lead to disability or death. Injury-based animal models of lung repair and regeneration are limited by injury-specific responses making it difficult to differentiate changes related to the injury response and injury resolution from changes related to lung repair and lung regeneration. However, use of animal models to identify these repair and regeneration signaling pathways is critical to the development of new therapies aimed at improving pulmonary function following lung injury. The mouse pneumonectomy model utilizes compensatory lung growth to isolate those repair and regeneration signals in order to more clearly define mechanisms of alveolar re-septation. Here, we describe our technique for performing mouse pneumonectomy and sham pneumonectomy. This technique may be utilized in conjunction with lineage tracing or other transgenic mouse models to define molecular and cellular mechanism of lung repair and regeneration.  相似文献   

14.
  总被引:2,自引:0,他引:2  
The lung is a relatively quiescent tissue comprised of infrequently proliferating epithelial, endothelial, and interstitial cell populations. No classical stem cell hierarchy has yet been described for the maintenance of this essential tissue; however, after injury, a number of lung cell types are able to proliferate and reconstitute the lung epithelium. Differentiated mature epithelial cells and newly recognized local epithelial progenitors residing in specialized niches may participate in this repair process. This review summarizes recent discoveries and controversies, in the field of stem cell biology, that are not only challenging, but also advancing an understanding of lung injury and repair. Evidence supporting a role for the numerous cell types believed to contribute to lung epithelial homeostasis is reviewed, and initial studies employing cell-based therapies for lung disease are presented. As a detailed understanding of stem cell biology, lung development, lineage commitment, and epithelial differentiation emerges, an ability to modulate lung injury and repair is likely to follow.  相似文献   

15.
目的:探讨CT引导下经皮肤肺穿刺并发症发生的高危因素.方法:回顾分析93例因肺部肿块行CT引导下经皮肤肺穿刺患者,对其性别、吸烟史、病灶大小、肿块类型、组织学分型、穿刺时体位、进针位置、进针角度和进针深度等因素与穿刺后并发症的相关性进行分析.结果:单因素分析显示吸烟史、病灶大小、肿块类型和进针深度在有并发症患者和无并发症的患者之间存在显著性差异(P<0.05),多因素分析显示病灶大小、肿块类型和进针深度在两组患者间存在显著性差异(P<0.05).结论:病灶大小、肿块类型和进针深度为CT引导下经皮肺穿刺并发症出现的高危因素.  相似文献   

16.
    
Radical radiotherapy of lung cancer with dose escalation has been associated with increased tumor control. However, these attempts to continually improve local control through dose escalation, have met mixed results culminating in the findings of the RTOG trial 0617, where the heart dose was associated with a worse overall survival, indicating a significant contribution to radiation-induced cardiac morbidity. It is, therefore, very likely that poorly understood cardiac toxicity may have offset any potential improvement in overall survival derived from dose escalation and may be an obstacle that limits disease control and survival of patients. The manifestations of cardiac toxicity are relatively common after high dose radiotherapy of advanced lung cancers and are independently associated with both heart dose and baseline cardiac risk. Toxicity following the treatment may occur earlier than previously thought and, therefore, heart doses should be minimized. In patients with lung cancer, who not only receive substantial heart dose, but are also older with more comorbidities, all cardiac events have the potential to be clinically significant and life-threatening.Sophisticated radiation treatment planning techniques, charged particle therapy, and modern imaging methods in radiotherapy planning, may lead to reduction of the heart dose, which could potentially improve the clinical outcomes in patients with lung cancer. Efforts should be made to minimize heart radiation exposure whenever possible even at doses lower than those generally recommended. Heart doses should be limited as much as possible.A heart dosimetry as a whole is important for patient outcomes, rather than emphasizing just one parameter.  相似文献   

17.
目的:探讨重症监护病房(ICU)中心发生胸腔感染的情况及其影响因素,并提出相应的预防对策。方法:选择2015年2月至2017年2月我院ICU中心收治的98例患者进行研究,均为全麻下行开胸术后住ICU者。收集所有患者临床资料,分析胸腔感染的发生情况,通过比较发生/未发生胸腔感染患者的临床资料,探讨ICU中心发生胸腔感染的危险因素,并提出相应的预防对策。结果:在98例患者中,有15例发生胸腔感染,发生率为15.31%,以铜绿假单胞菌所占比例最高,为40.00%。单因素分析结果显示:性别、术前抗菌药物的使用、胸管类型和ICU中心胸腔感染无相关性(P0.05),而年龄、手术时间、术前肺功能、引流管留置时间、手术创口污染、原发病灶蔓延均和ICU中心胸腔感染密切相关(P0.05);多因素logistic回归分析结果显示:年龄≥60岁、手术时间≥2h、术前肺功能、引流管留置时间≥3d、手术创口污染、原发病灶蔓延均是造成ICU中心胸腔感染的独立危险因素(OR=3.485、3.714、3.571、5.731、6.172、6.081,P0.05)。结论:ICU中心发生胸腔感染会对患者病情恢复造成较大影响,在今后临床工作中,需重视围术期管理,积极采取合理的预防措施,降低胸腔感染的发生率。  相似文献   

18.
隋一玲  李皎伦  吴淑莉 《生物磁学》2011,(24):4955-4957
目的:探讨优质整体护理优质服务管理模式对胸外科临床应用中的优势,并对此进行护理效果评价。方法:采用统计比较的方法,依据诊断标准,选取200例肺癌患者,平均分为对照组和普通组,从生活能力、心理状态、病人满意度、平均住院日和住院费用进行统计分析。结果:对照组和普通组间存在较大差异,有统计学意义。结论:整体护理优质服务管理模式对胸科疾病患者的护理康复有促进作用。  相似文献   

19.
    
Better understanding of the acute/chronic inflammation in airways is very important in order to avoid lung injuries for patients undergoing mechanical ventilation for treatment of respiratory problems. Local lung inflammation is triggered by many mechanisms within the lung, including pathogens. In this study, a cellular automata based model (CA) for pulmonary inflammation that incorporates biophysical processes during inflammatory responses was developed. The developed CA results in three possible outcomes related to homeostasis (healing), persistent infection, and resolved infection with high inflammation (inflamed state). The results from the model are validated qualitatively against other existing computational models. A sensitivity analysis was conducted on the model parameters and the outcomes were assessed. Overall, the model results showed possible outcomes that have been seen in clinical practice and animal models. The present model can be extended to include inflammation resulting from damage tissue and eventually to model inflammation resulting from acute lung injury and multiple organ dysfunction syndromes in critical illness and injury.  相似文献   

20.

Background

Acute lung injury (ALI) is a serious respiratory disorder for which therapy is primarily supportive once infection is excluded. Surgical lung biopsy may rule out other diagnoses, but has not been generally useful for therapy decisions or prognosis in this setting. Importantly, tissue and peripheral blood eosinophilia, the hallmarks of steroid-responsive acute eosinophilic pneumonia, are not commonly linked with ALI. We hypothesized that occult eosinophilic pneumonia may explain better outcomes for some patients with ALI.

Methods

Immunohistochemistry using a novel monoclonal antibody recognizing eosinophil peroxidase (EPX-mAb) was used to assess intrapulmonary eosinophil accumulation/degranulation. Lung biopsies from ALI patients (n = 20) were identified following review of a pathology database; 45% of which (i.e., 9/20) displayed classical diffuse alveolar damage (ALI-DAD). Controls were obtained from uninvolved tissue in patients undergoing lobectomy for lung cancer (n = 10). Serial biopsy sections were stained with hematoxylin and eosin (H&E) and subjected to EPX-mAb immunohistochemistry.

Results

EPX-mAb immunohistochemistry provided a >40-fold increased sensitivity to detect eosinophils in the lung relative to H&E stained sections. This increased sensitivity led to the identification of higher numbers of eosinophils in ALI patients compared with controls; differences using H&E staining alone were not significant. Clinical assessments showed that lung infiltrating eosinophil numbers were higher in ALI patients that survived hospitalization compared with non-survivors. A similar conclusion was reached quantifying eosinophil degranulation in each biopsy.

Conclusion

The enhanced sensitivity of EPX-mAb immunohistochemistry uniquely identified eosinophil accumulation/degranulation in patients with ALI relative to controls. More importantly, this method was a prognostic indicator of patient survival. These observations suggest that EPX-mAb immunohistochemistry may represent a diagnostic biomarker identifying a subset of ALI patients with improved clinical outcomes.  相似文献   

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