Application of an expandable metallic Z-type stent for stenosis of the left main bronchus following tuberculosis--a case report]

A 32-year-old man had been suffering from dyspnea on exertion and stridor, which were due to stenosis of the left main bronchus as a complication of bronchial tuberculosis. A three-connection stent, 1.2 cm in diameter and 4.5 cm in length was placed at the site of the bronchial stenosis. Dyspnea disappeared 2 days after the procedure, and the pulmonary function 3 weeks later showed considerable improvements in %FVC, FEV1 and MMF.     

Expression of the cell surface antigen detected by the monoclonal antibody A7 in pancreatic carcinoma cell lines

In a previous study, we used a murine monoclonal antibody, A7, against human colon carcinoma as a drug-carrier to treat colorectal cancer.¹ In the present study, we found that MAb A7 also reacted immunohistochemically with 73% of human pancreatic carcinoma cell lines, with the A7 antigen mainly being detected on the cell surface. However, the A7 antigen was found in only 9% of the spent media of these human pancreatic carcinoma cell lines by ELISA. On the other hand, the positive incidence of CA19-9, POA, ferritin, CEA, DU-PAN-2 and SLX in those spent media was 100%, 64%, 64%, 55%, 55% and 36%, respectively. These results suggest that the A7 antigen may only rarely be shed into the sera of pancreatic cancer patients, in which case MAb A7 could be a suitable drug-carrier in targeting chemotherapy for pancreatic cancer patients.     

In vitro reactivity and in vivo biodistribution of the monoclonal antibody A7 using human gastric carcinoma cell lines.

The monoclonal antibody (MAb) A7 has been used to treat patients with colorectal or pancreatic carcinoma with encouraging results. We therefore determined if MAb A7 would also react with gastric carcinoma cell lines. MAb A7 reacted with seven of eight gastric carcinoma cell lines tested. The intensity of the reaction, measured by flow cytometry, was equal to that of WiDr (colon) and HPC-YS (pancreas) cell lines. In nude mice bearing xenografts of the MAb A7-reactive gastric cancer line MKN45, the percentage injected dose of MAb A7 per g of tumour tissue on day 7 was 9.79; this value was 77% of that on day 1. The in vivo tumour-to-blood ratio of MAb A7 was 2.77 on day 7. Therefore, MAb A7 has long-term retention at binding sites as well as a high probability, high intensity and high specificity of reactivity against gastric cancer, which make it an ideal drug carrier for immunotargeted chemotherapy and immunodiagnosis.     

Absolute lymphocyte count and C-reactive protein-albumin ratio can predict prognosis and adverse events in patients with recurrent esophageal cancer treated with nivolumab therapy

Predicting the prognosis and adverse events (AEs) of nivolumab therapy for recurrent esophageal cancer is very important. The present study investigated whether a simple blood biochemical examination could be used to predict prognosis and AEs following nivolumab treatment for relapse of esophageal cancer. A total of 41 patients who received nivolumab treatment for recurrent esophageal cancer after esophagectomy were analyzed. The absolute lymphocyte count (ALC), neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR), monocyte-lymphocyte ratio (MLR) and C-reactive protein-albumin ratio (CAR) were assessed at the time of nivolumab induction as indices that can be calculated by blood biochemical examinations alone. Median values were 1,015 for ALC, 3.401 for NLR, 242.6 for PLR, 0.458 for MLR and 0.119 for CAR, and patients were divided into two groups according to values. A high ALC, low NLR, low PLR, low MLR and low CAR were associated with a better response to nivolumab. In addition, patients with the aforementioned indices, with the exception of low PLR, or better response were more likely to develop AEs in univariate analysis. In multivariate analysis, a high ALC [odds ratio (OR): 4.857, P=0.043] and low CAR (OR: 9.099, P=0.004) were identified as independent risk factors for AEs. Survival analysis revealed that overall survival and progression-free survival (PFS) rates after nivolumab treatment differed significantly between the high and low groups of ALC, NLR, PLR, MLR and CAR. The multivariate analysis identified a low ALC [hazard ratio (HR): 3.710, P=0.003] and high CAR (HR: 2.953, P=0.007) as independent poor prognostic factors of PFS. In conclusion, ALC and CAR have potential as biomarkers for outcomes of recurrent esophageal cancer following nivolumab treatment.     

Monophasic transmitral flow pattern with less increase in heart rate indicates left ventricular dysfunction.

When heart rate (HR) increases, mitral flow can become monophasic. Prolonged isovolumic contraction and relaxation time (ICT and IRT), directly related to left ventricular (LV) function, can potentially influence the HR with monophasic mitral flow. The present study investigated the relation between HR that causes monophasic flow and LV function. During diagnostic catheterization, HR was increased using right atrial pacing by 2 beats/min every 2 min in a stepwise manner until the development of monophasic mitral flow in 17 patients with normal sinus rhythm. ICT, IRT, end-diastolic and end-systolic LV volumes, LV ejection fraction, LV peak + and -dP/dt, peak (+dP/dt)/P, and the relaxation time constant (tau) were measured by Doppler echocardiography or catheterization when monophasic mitral flow developed. The monophasic HR varied from 74 to 106 beats/min. By univariate analysis, ICT (p<0.01, r2=0.73), LV peak +dP/dt (p<0.05, r2=0.37), peak (+dP/dt)/P (p<0.01, r2=0.71), peak -dP/dt (p<0.05, r2=0.25), and tau (p<0.05, r2=0.33) had a significant correlation with monophasic HR. By multivariate analysis, prolonged ICT and reduced LV peak -dP/dt independently contributed to monophasic mitral flow with less increase in HR. Monophasic mitral flow with less increase in HR indicates impaired LV systolic and diastolic function during isovolumic contraction and relaxation.     

A set of genes selectively expressed in murine dendritic cells: utility of related cis-acting sequences for lentiviral gene transfer

Professional antigen presenting cells such as dendritic cells (DC) and macrophages (Mphi) share similar characteristics; however, they differ in their ability to initiate an immune response. DCs are much more potent in priming and stimulating nai;ve T-cells. Thus, DCs are good targets for the expression of foreign genes to elicit and specifically modify immune responses. To identify DC markers cDNA subtraction was performed using murine MHC class II(high), B7(high) bone marrow derived DCs as tester and interferon-gamma/E. coli lipopolysaccaride (LPS) treated bone marrow derived macrophages as driver. Analysis of 114 resulting clones revealed a diverse pattern of DC selective (DC(DeltaMphi)) gene expression including known genes whose expression in DCs had not been previously demonstrated as well as multiple novel genes. For several identified DC(DeltaMphi) genes, proximal promoter elements were isolated and incorporated into self-inactivating lentiviral GFP reporter vectors. Promoter activity was measured in bone marrow derived macrophages or dendritic cells. Of the promoters analyzed those for B7-DC and CCL17 drove strong GFP expression in DCs but not in resting or activated macrophages. The CCL17 promoter offered the highest level of expression in DCs and was further activated by culture with LPS or interleukin-4 (IL-4). In contrast, the B7-DC promoter was induced by IL-4 but not by LPS. Endogenous CCL17 and B7-DC mRNAs were increased similarly in IL-4 cultured DCs but only CCL17 was induced by LPS. Additionally, IL-4 increased cell surface expression of B7-DC in both immature and mature DCs.     

Limitation of angiography to identify the culprit plaque in acute myocardial infarction with coronary total occlusion utility of coronary plaque temperature measurement to identify the culprit plaque.

OBJECTIVES: The purpose of this study was to test the hypothesis that the maximal temperature (Tmax) site, as measured by thermal wire, coincides with the culprit plaque by intravascular ultrasound (IVUS) in patients with acute myocardial infarction (AMI). BACKGROUND: Subsequent thrombosis developing to the proximal region from the site of plaque rupture or erosion can potentially complicate the ability of coronary angiography to identify the accurate culprit plaque in patients with coronary total occlusion. METHODS: In 45 consecutive patients with a first anterior AMI, the Tmax site by thermal wire and the culprit plaque by IVUS were evaluated in the left anterior descending coronary artery (LAD). RESULTS: Twenty-five patients had LAD total occlusion, and the remaining 20 had LAD reperfusion. In both groups of patients, the Tmax site was significantly more distal to the angiographically most stenotic site or occlusive site (reperfusion: mean distance [MD] = 1.1 mm distal, 95% confidence interval [CI] 0.3 to 1.9 mm, p = 0.01; total occlusion: MD = 8.8 mm distal, 95% CI 8.0 to 9.6 mm, p < 0.0001). The culprit plaques by IVUS approximately coincided with those by angiography or thermal wire in patients with reperfusion. However, the angiographic occlusive site was significantly more proximal to the culprit plaque by IVUS (MD = 9.2 mm, 95% CI 7.9 to 10.6 mm, p < 0.0001), but the Tmax site coincided with the culprit plaque by IVUS (MD = 0.3 mm distal, 95% CI 0.3 mm proximal to 1.0 mm distal, p = 0.293) in patients with total occlusion. CONCLUSIONS: Temperature measurement of coronary plaque enables accurate localization of the culprit plaque in AMI with coronary total occlusion.     

Reproducibility of intravenous intermittent triggered myocardial contrast echocardiography in healthy subjects

Few data have been published on the reproducibility of baseline subtracted peak intensity obtained from intravenous intermittent triggered myocardial contrast echocardiography. We investigated the reproducibility of the peak intensity measured from intravenous intermittent triggered myocardial contrast echocardiography in 10 young healthy males. The contrast echocardiography was obtained using the second harmonic mode with an intravenous bolus injection of Levovist (first study). The same myocardial contrast echocardiography was repeated after the first study (second study). The myocardial opacification and peak intensity in the 12 segments of the apical 4 and 2 chamber views were assessed visually and quantitatively. The differences in the peak intensity between the initial and repeated measurements in the first study (intraobserver reproducibility) and between the initial measurements in the first and second studies (interinjection reproducibility) were assessed using the Bland and Altman method. The degree of opacification was good or intermediate in 207/228 (91%) of the segments. The agreement of myocardial opacification between the first and second studies was 87/114 (76%). However, significantly higher peak intensity was obtained in apical septal (8200 +/- 6300 au2) and mid septal (8500 +/- 6000 au2) segments in the 4 chamber view and in the mid inferior (12400 +/- 9300 au2) and apical inferior (10700 +/- 6300 au2) segments in the 2 chamber view compared with other segments. The mean differences of the peak intensities according to the Bland and Altman analysis was -1600 +/- 5000 au2 in the intraobserver reproducibility study, and -1100 +/- 5300 au2 in the interinjection reproducibility study. Thus, the measurement error was determined to range from 8400 au2 to 9500 au2 in both studies. We conclude that the peak intensity obtained from intravenous intermittent triggered myocardial contrast echocardiography using Levovist varies significantly among segments in the left ventricular myocardium. Large intraobserver and interinjection variability exists in the measurement of peak intensity, suggesting that the reproducibility of this technique is limited for quantitative assessment of myocardial perfusion.