48 research outputs found

    Citizen Sensors for SHM: Use of Accelerometer Data from Smartphones

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    Ubiquitous smartphones have created a significant opportunity to form a low-cost wireless Citizen Sensor network and produce big data for monitoring structural integrity and safety under operational and extreme loads. Such data are particularly useful for rapid assessment of structural damage in a large urban setting after a major event such as an earthquake. This study explores the utilization of smartphone accelerometers for measuring structural vibration, from which structural health and post-event damage can be diagnosed. Widely available smartphones are tested under sinusoidal wave excitations with frequencies in the range relevant to civil engineering structures. Large-scale seismic shaking table tests, observing input ground motion and response of a structural model, are carried out to evaluate the accuracy of smartphone accelerometers under operational, white-noise and earthquake excitations of different intensity. Finally, the smartphone accelerometers are tested on a dynamically loaded bridge. The extensive experiments show satisfactory agreements between the reference and smartphone sensor measurements in both time and frequency domains, demonstrating the capability of the smartphone sensors to measure structural responses ranging from low-amplitude ambient vibration to high-amplitude seismic response. Encouraged by the results of this study, the authors are developing a citizen-engaging and data-analytics crowdsourcing platform towards a smartphone-based Citizen Sensor network for structural health monitoring and post-event damage assessment applications

    Increased nitric oxide levels in exhaled air of rat lung allografts

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    AbstractIn organ transplantation nitric oxide has been reported to be involved in allograft rejection. We examined in a rat lung transplantation model whether nitric oxide is overproduced in acute rejection and can be detected in exhaled air. Thirteen rat right lung transplants were separated into three groups: group 1 (n = 5), untreated allografts (Brown-Norway [RT1n] to Lewis [RT1l]); group 2 (n = 4), cyclosporine-treated allografts; and group 3 (n = 4), isografts (Lewis to Lewis). We examined exhaled nitric oxide levels with a chemiluminescence analyzer and chest roentgenograms on days 2 through 5. Histologic samples were obtained on days 3 and 5. On day 5, the recipients were killed and we measured exhaled nitric oxide from the right and left lungs separately. Blood samples were also obtained for measurement of serum nitrite/nitrate. The exhaled nitric oxide level in untreated allografts increased significantly from day 5 (63.9 ± 39.2 ppb, p = 0.0095) and was significantly higher than that in treated allografts (9.1 ± l.6 ppb) (p = 0.0085) and isografts (6.9 ± 0.5 ppb) (p = 0.0068). The nitric oxide level in untreated allografts (826.5 ± 416.1 ppb) was 75 times as high as that from the contralateral normal left lungs (11.2 ± 2.6 ppb) (p = 0.0118). The level of exhaled nitric oxide correlated significantly with the histologic rejection grade (p = 0.0001). There was no significant difference in the serum nitrite/nitrate levels between allografts and isografts. These data suggest that increased exhaled nitric oxide levels might reflect acute rejection in lung transplants. (J Thorac Cardiovasc Surg 1997;113:830-5

    PERK-mediated translational control is required for collagen secretion in chondrocytes

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    As chondrocytes are highly secretory and they experience a variety of stresses, physiological unfolded protein response (UPR) signalling is essential for extracellular matrix (ECM) secretion and chondrogenesis. In the three branches of the UPR pathway, PERK governs the translational attenuation and transcriptional upregulation of amino acid and redox metabolism and induction of apoptosis. It was previously demonstrated that a defect of the PERK branch of the UPR signalling pathway causes the accumulation of unfolded proteins, leading to cell death without perturbing endoplasmic reticulum (ER)-to-Golgi transport in pancreatic β cells. However, little is known about the role of PERK in chondrocytes. In this study, we found that PERK signalling is activated in chondrocytes, and inhibition of PERK reduces collagen secretion despite causing excessive collagen synthesis in the ER. Perk−/− mice displayed reduced collagen in articular cartilage but no differences in chondrocyte proliferation or apoptosis compared to the findings in wild-type mice. PERK inhibition increases misfolded protein levels in the ER, which largely hinder ER-to-Golgi transport. These results suggest that the translational control mediated by PERK is a critical determinant of ECM secretion in chondrocytes

    Hepatocellular Carcinoma with Direct Invasion to the Duodenal Bulb, Presenting with Gastrointestinal Bleeding

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    Hemorrhage from hepatocellular carcinoma (HCC) directly invading the gastrointestinal tract is very rare. A 71-yearold man, who had been treated with transcatheter arterial embolization and percutaneous ethanol injection for HCC in the right hepatic lobe, presented with melena. Endoscopic examination showed a crater-like ulceration coated with blood clot in the duodenal bulb, and microscopic examination of a biopsy specimen from the duodenal lesion confirmed HCC. Abdominal computed tomography (CT) revealed that the HCC mass containing air-density invaded the duodenum. Recurrent bleeding continued from the lesion and the patient died of liver failure. Postmortem examination revealed massive HCC with hepatoduodenal fistula caused by direct tumor invasion into the duodenum

    Efficacy of SGLT2 inhibitors in IgA nephropathy associated with alcoholic liver cirrhosis accompanied by nephrotic syndrome: a case report

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    We present a 51-year-old male patient with a history of Child-Pugh Grade B alcoholic liver cirrhosis (ALC) who developed renal impairment (serum creatinine of 2.00 mg/dL) and nephrotic syndrome (a urinary protein level of 4.35 g/gCr). The patient was diagnosed with immunoglobulin A nephropathy (IgAN) associated with ALC based on findings from comprehensive evaluations, including markedly elevated serum IgA levels (883.7 mg/dL), a kidney biopsy revealing significant IgA deposition in the para-mesangial area, and a liver diagnosis showing long-standing advanced ALC. Our treatment approach involved initiating dapagliflozin therapy, a sodium-glucose cotransporter-2 (SGLT2) inhibitor, alongside strict alcohol abstinence. Remarkably, the patient demonstrated a dramatic reduction in proteinuria within one week of dapagliflozin administration. No hypoglycemic events were observed. This case adds valuable clinical insights into the potential therapeutic role of SGLT2 inhibitors in IgAN associated with ALC. Specifically, in cases where conventional steroid therapies may be contraindicated due to coexisting comorbidities such as diabetes or obesity, dapagliflozin emerges as a potentially efficacious alternative. Further investigations are warranted to validate these preliminary observations
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