Pleural effusions in lung transplant recipients: image-guided small-bore catheter drainage

PURPOSE: To assess the efficacy of treating pleural effusions in lung transplant recipients with small-bore catheter drainage. MATERIALS AND METHODS: Chest radiographs and computed tomographic (CT) scans obtained in 31 lung transplant recipients who had pleural effusions treated with catheter drainage were retrospectively reviewed. Duration of drainage and volume of fluid drained were recorded. Results were evaluated 1 and 3 months after chest tube removal. There was complete response (CR) when no pleural fluid remained, partial response (PR) when fluid remaining was less than the pretreatment level, and no response (NR) when fluid recurred to a level at or above the pretreatment level. Associations between cause of effusion (empyema, parapneumonic effusion, rejection, other), response (CR, PR, NR), and type of transplantation (unilateral, bilateral) were examined by using chi2 tests. RESULTS: Of 31 patients, 25 had bilateral effusions; eight of these 25 patients had small-bore catheters inserted bilaterally. Nine patients had multiple sequential catheter insertions. Duration of drainage ranged from 2 to 44 days (median, 6 days). Fluid output was 110-9,726 mL (median, 1,350 mL). One-month follow-up data were available for 31 of 39 treated pleural effusions: 11 (35%) had CR, 18 (58%) had PR, and two (6%) had NR (percentages do not add up to 100% due to rounding). Three-month follow-up data were available for 28 of 39 treated effusions: 22 (79%) had CR, five (18%) had PR, and one (4%) had NR (percentages do not add up to 100% due to rounding). One- and 3-month response rates, respectively, were not related to cause of effusion (P =.82 and.535) or type of transplantation (P =.568 and >.999). CONCLUSION: Small-bore catheter drainage of persistent pleural effusions in lung transplant recipients is usually successful, but drainage is often prolonged and may require multiple catheter placements.     

甲硝唑葡萄糖注射液细菌内毒素检查法的研究

目的;以细菌内毒素检查法对甲硝唑葡萄糖注射液进行试验研究。方法;采用抑制或增强试验,并将细菌内毒素检查法与家兔法检测结果作对比。结果：该注射液经一定稀释后对测定无干扰。结论：细菌内毒素检查法适用于检测该注射液。     

Positron emission tomography imaging in lung cancer

Over the past several years, positron emission tomography (PET) has become a clinically useful, noninvasive study which complements conventional imaging (chest radiographs, computed tomography [CT], and magnetic resonance imaging [MRI]) in the evaluation of patients with lung cancer. PET imaging of lung cancer is typically performed with the radiopharmaceutical 18F-2-deoxy-D-glucose (FDG), a d-glucose analog. Increased glucose metabolism by malignant cells results in increased uptake and accumulation of FDG, which serves as the basis for tumor detection. This review will focus on the current applications of FDG-PET in lung cancer patients including evaluation of focal pulmonary abnormalities, staging lung cancer, determining tumor recurrence, and in assessing prognosis.     

SELECTIVE IgA DEFICIENCY PRESENTING WITH HYPERSPLENISM

SUMMARY A young patient presenting with splenomegaly and hypersplenism was inadvertently found to have selective IgA deficiency. There were no symptoms of immunodeficiency and the patient responded well to splenectomy, with return of blood counts to normal without adverse effects. No other cause for the hypersplenism was found. We postulate selective IgA deficiency as a cause of splenomegaly and hypersplenism.     

恶性肿瘤淋巴管生成与转移的研究进展

淋巴道转移是肿瘤转移的重要途径,也是判断预后的重要依据. 随着淋巴管生成因子及许多淋巴管特异性标记物的发现,肿瘤新生淋巴管调控与淋巴道转移机制研究得以深入开展. 大量的研究发现,恶性肿瘤和瘤周组织内存在新生的淋巴管,新生的淋巴管密度和淋巴管标记物的表达强度均与淋巴结转移密切相关. 这为揭示恶性肿瘤淋巴道转移机制和开发淋巴管靶向治疗提供了重要的研究途径. 现就近年来肿瘤淋巴管生成与转移的研究进展作一综述.     

A Phase I/II Study Combining Erlotinib and Dasatinib for Non‐Small Cell Lung Cancer

Background.

EGFR and Src are frequently activated in non-small cell lung cancer (NSCLC). In preclinical models, combining EGFR and Src inhibition has additive synergistic effects. We conducted a phase I/II trial of the combination of Src inhibitor dasatinib with EGFR inhibitor erlotinib to determine the maximum tolerated dose (MTD), pharmacokinetic drug interactions, biomarkers, and efficacy in NSCLC.

Methods.

The phase I 3+3 dose-escalation study enrolled patients with solid tumors to determine the MTD. The phase II trial enrolled patients with advanced NSCLC who had undergone no previous treatments to determine progression-free survival (PFS) and response. Pharmacokinetic and tissue biomarker analyses were performed.

Results.

MTD was 150 mg of erlotinib and 70 mg of dasatinib daily based on 12 patients treated in the phase I portion. No responses were observed in phase I. The 35 NSCLC patients treated in phase II had an overall disease control rate of 59% at 6 weeks. Five patients (15%) had partial responses; all had activating EGFR mutations. Median PFS was 3.3 months. Epithelial-mesenchymal transition markers did not correlate with outcomes.

Conclusion.

The combination of erlotinib and dasatinib is safe and feasible in NSCLC. The results of this study do not support use of this combination in molecularly unselected NSCLC.     

Myocardial infarct size quantification by MR imaging early after coronary artery occlusion in dogs

The feasibility of using magnetic resonance (MR) imaging to estimate myocardial infarct size was explored in an in vitro model using only the inherent differences in contrast between infarcted and noninfarcted myocardium. Eight dogs underwent coronary occlusion; their hearts were removed 6 hours later. Estimates of T2 for normal and infarcted myocardium were derived from MR images. Infarct size was quantified anatomically using triphenyltetrazolium-chloride (TTC) staining and compared with MR estimates. The T2 values derived from the images clearly discriminated between infarcted (126 +/- 22 msec) and normal myocardium (88 +/- 10 msec, P less than .05), providing images with good contrast between normal and infarcted myocardium. Comparable differences in T2 values were also noted from spectrometric determinations. Estimates of infarct size by MR imaging compared well with TTC estimates (r = 0.98) over a wide range of infarct sizes from 3% to 29% of the left ventricular mass. These results suggest the potential for in vivo quantification of infarct size based on the inherent contrast difference between infarcted and normal myocardium.     

Cloning and expression of the gene involved in Sanfilippo B syndrome (mucopolysaccharidosis III B)

Sanfilippo B syndrome is caused by a deficiency of alpha-N- acetylglucosaminidase, a lysosomal enzyme involved in the degradation of heparan sulphate. Accumulation of the substrate in lysosomes results in degeneration of the central nervous system with progressive dementia often combined with hyperactivity and aggressive behaviour. In order to clone the deficient gene, we purified the enzyme from human placenta and obtained amino acid sequence information. Alignment of one of the CNBr generated internal peptides to sequence from the database revealed the chromosomal location of the gene in the 5' upstream flanking region of the gene for 17-beta-hydroxysteroid-dehydrogenase at 17q21.1. The available DNA sequence was used to clone the cDNA coding for alpha-N- acetylglucosaminidase and analyse its gene structure. The gene is fully contained in the 5' upstream flanking region of the gene for 17-beta- hydroxysteroid-dehydrogenase and interrupted by five introns. The cDNA clone has a length of 2575 bp and encodes a protein of 743 amino acids. Chinese hamster ovary cells transfected with the cDNA construct show alpha-N-acetylglucosaminidase activity about 17-fold over background. This will allow correction studies with NAG deficient Sanfilippo B cell lines and facilitate the development of enzyme replacement therapy for these patients.