Detection of Delaminations Located at Ceramic/Metal Jointed Interface by Scanning Acoustic Microscopy

Since ceramic/metal joints currently play an important role of the structural parts for applications in electrical, electronic or aerospace industries, techniques must be developed for evaluating the integrity of these joints. Such techniques as collimated X-ray beam radiography [1], indentation fracture, and laser speckle imaging have been developed with limited success. No truly nondestructive techniques for evaluating joint strength have been established to date. If a conventional C-scan mode apparatus could be applied directly for detecting a defect such as a delamination on a joint interface, it might be an attractive solution in terms of visualizing the defect as a first step in the evaluation. The shape of the standard specimen of the ceramic/metal joint is essentially a rectangular bar. When the C-scan mode apparatus is used to visualize the jointed interface, an acoustic wave is required to be incident from the ceramic side of the specimen. When considering the attenuation of an ultrasonic wave in the frequency range from 10 to 100 MHz and the thickness of the ceramic portion of the specimen, the wave may not reach the interface, or the wave reflected from the interface may not be detected. When using frequencies lower than 10 MHz, the interface may be imaged, but with limited resolution. Moreover, the contrast may be poor because of water diffusing into the crack in the surface of the specimen. When a conventional A-mode apparatus such as a digital oscilloscope is used to obtain quantitative data, reflected waveforms might be collected. However, the data might not be good enough to analyze details of a defect, such as caused by a fracturing process. Recent studies have shown that delaminations at a ceramic/metal joint, such as a Si3N4/Cu/Steel joint, originate along the periphery of the interface [2]

Line-Focus Acoustic Mcroscopy Measurements of Thin-Film Elastic Constants

Thin film materials are widely used as hard, protective coatings for softer surfaces. It is known that fracture strength and hardness are related to the elastic and plastic properties [1]. The elastic constants of the film deposited on a substrate are, however, difficult to measure. By a technique which was recently discussed [2] the elastic constants of amorphous (isotropic) films and single-crystal (anisotropic) films can be obtained by measuring the velocities of surface acoustic waves (SAWs) propagating over a thin-film/ substrate specimen by the use of a line-focus acoustic microscope

Nondestructive Evaluation of Surface Properties of Sintered Si3N4 Ceramics with Surface Wave Dispersion

Elastic properties of high-performance ceramics is usually measured with ultrasonic bulk waves [1]. However, the bulk waves gives us only properties averaged over sample thickness. Sintered ceramics often have properties at the surface different from in the middle. Thus we need a method which distinguishes near surface property from the averaged one. Surface wave technique has been applied for nondestructive characterization of ceramics [2–4]. The depth-dependent properties of ceramics, however, has never been reported. Surface wave propagates in subsurface layer of about one wavelength. Therefore we’ll be able to estimate the depth-dependent properties of the ceramics, if we’ll use surface waves of different frequency or wavelength

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.

Centromeric instability in human cells undergoing immortalization

Chromosomal instability is an important pathway for cells to generate new chromosome aberrations, which may contribute to carcinogenesis. Of various forms of chromosomal instability, centromeric instability remains particularly poorly understood. In the present study, we found that centromeric instability, evidenced by dynamic formation of centromeric or pericentromeric rearrangements, breaks, deletions or iso-chromosomes, was a general phenomenon in human cells undergoing immortalization by various methods, including expressions of human papillomavirus oncogenes (HPV 16-E6E7), human telomerase reverse transcriptase (hTERT) plus HPV 16-E6E7, and hTERT accompanied by p16INK4a inactivation. In particular, centromeric instability cooperated with telomeric instability in pre-immortal HPV 16-E6E7-expressing cells. This was evidenced by: (1) the progressive formation of centromeric deletions or rearrangements on specific chromosomes carrying critically short (signal-free) telomeres in cell lines of different epithelial cell types expressing HPV16-E6E7, suggesting that centromeric or pericentromeric regions were fragile and prone to be broken after chromosomal end-to-end fusions; and (2) preferential fusions between centromeric and telomeric ends of chromosomes with critically short telomeres. Since HPV16-E6 and E7 inactivate p53 and RB proteins, respectively, and most human cancers have p53 and RB pathway defects, the cell systems are relevant to cancer. Considering that cellular immortalization is a prerequisite for cancer initiation, our results suggest that centromeric instability might play an important role in the early process of cancer development

Living donor versus deceased donor liver transplantation for early unresectable hepatocellular carcinoma: same criteria, different outcome

Invited lectureINTRODUCTIONANDAIM: Hypothetical studies that supported the role of living donor liver transplantation (LDLT) for early unresectable hepatocellular carcinoma (HCC) assumed the same outcome as deceased donor liver transplantation (DDLT).Wetested this assumption with a clinical study. PATIENTS AND METHODS: We studied 60 consecutive patients who met the Milan or UCSF criteria on pretransplant imaging and underwent LDLT (LD group, n=43) or DDLT (DD group, n=17). RESULTS: Compared to the DD group, the LD group had fewer incidental tumors or pretransplant transarterial chemoembolization but more salvage transplantation for recurrence. There was a shorter waiting time and lower graft-weight-to-standard-liver-weight (GW/SLW) ratio. The perioperative course was the same in terms of transfusion, morbidity, mortality and hospital stay. Histopathologic analysis showed similar tumor size, number, grade, and stage. At a median follow-up of 28 months (range: 4–111), 7 (16%) patients of the LD group and none (0%) of the DD group recurred. The 1-, and 5-year cumulative recurrence rate was 9%, and 25%, respectively, for the LD group, and all 0%, for the DD group (p=0.05). The corresponding patient survival was 97% and 55%, respectively, for the LD group, and 94% and 94%, respectively, for the DD group (p=0.279). Apart from tumor factors including vascular permeation, tumor nodules 43, and a pathologic stage beyond UCSF criteria, GW/SLW ratio 50.6 and salvage transplantation were also risk factors for recurrence. CONCLUSION: Despite standard selection criteria, patients who undergo LDLT for early unresectable HCC have different clinical characteristics and inferior oncologic outcome