Electrochemical Investigation of High-Performance Dye-Sensitized Solar Cells Based on Molybdenum for Preparation of Counter Electrode

In order to improve the photocurrent conversion efficiency of dye-sensitized solar cells (DSSCs), we studied an alternative conductor for the counter electrode and focused on molybdenum (Mo) instead of conventional fluorine-doped tin oxide (FTO). Because Mo has a similar work function to FTO for band alignment, better formability of platinum (Pt), and a low electric resistance, using a counter electrode made of Mo instead of FTO lead to the enhancement of the catalytic reaction of the redox couple, reduce the interior resistance of the DSSCs, and prevent energy-barrier formation. Using electrical measurements under a 1-sun condition (100 mW/cm(2), AM 1.5), we determined that the fill factor (FF) and photocurrent conversion efficiency (eta) of DSSCs with a Mo electrode were respectively improved by 7.75% and 5.59% with respect to those of DSSCs with an FTO electrode. Moreover, we have investigated the origin of the improved performance through surface morphology analyses such as scanning electron microscopy and electrochemical analyses including cyclic voltammetry and impedance spectroscopy

Air-stable n-type operation of Gd-contacted carbon nanotube field effect transistors

We report air-stable n -type operations of the single-walled carbon nanotube field effect transistors (SWNT-FETs) fabricated with Gd electrodes. Unlike previously reported n -type SWNT-FETs, our devices maintained their n -type operation characteristics in ambient atmosphere for more than two months. The shallow Gd films with a thickness below 20 nm are corroded by environmental oxygen, whereas the well-contacted Gd-SWNT interfaces underneath the thick Gd layers are protected from contaminations by air molecules. Theoretical studies based on the first-principles electronic structure calculations confirm that Gd layers have an excellent binding affinity to the SWNTs.open8

Utility of targeted deep sequencing for detecting circulating tumor DNA in pancreatic cancer patients.

Targeted deep sequencing across broad genomic regions has been used to detect circulating tumor DNA (ctDNA) in pancreatic ductal adenocarcinoma (PDAC) patients. However, since most PDACs harbor a mutation in KRAS, sequencing of broad regions needs to be systemically compared to analyzing only KRAS mutations for PDAC. Using capture-based targeted deep sequencing, we detected somatic tumor mutations in 17 fine needle aspiration biopsy and 69 longitudinal cell-free DNA (cfDNA) samples from 17 PDAC patients. KRAS mutations were detected in 10 out of 17 pretreatment patient plasma samples. Next, interrogation of genetic alterations in matched primary tumor samples detected ctDNA in 12 of 17 pretreatment plasma samples and cfDNA sequencing across the 83 target genes identified ctDNA in 15 of 17 cases (88.2% sensitivity). This improved sensitivity of ctDNA detection resulted in enhanced tumor burden monitoring when we analyzed longitudinal plasma samples. We found that cfDNA sequencing detected the lowest mutant allelic fractions and number of variants when complete response or partial response to chemotherapy was achieved. We demonstrated that ctDNA levels measured by targeted deep sequencing sensitively indicate the presence of cancer and correlate well with clinical responses to therapy and disease progression in PDAC patients

Polymorphisms in Apoptosis-Related Genes and TP53 Mutations in Non-Small Cell Lung Cancer

Apoptosis plays an essential role in the elimination of mutated or transformed cells from the body. Therefore, polymorphisms of apoptosis-related genes may lead to an alteration in apoptotic capacity, thereby affecting the occurrence of TP53 mutations in lung cancer. We investigated the relationship between potentially functional polymorphisms of apoptosis-related genes and TP53 mutations in non-small cell lung cancer (NSCLC). Twenty-seven single nucleotide polymorphisms in 20 apoptosis-related genes were genotyped by a sequenome mass spectrometry-based genotyping assay in 173 NSCLCs and the associations with TP53 mutations in the entire coding exons (exons 2-11), including splicing sites of the gene, were analyzed. None of the 27 polymorphisms was significantly associated with the occurrence of TP53 mutations. This suggests that apoptosis-related genes may not play an important role in the occurrence of TP53 mutations in lung cancer

Cystamine induces AIF-mediated apoptosis through glutathione depletion

AbstractCystamine and its reduced form cysteamine showed protective effects in various models of neurodegenerative disease, including Huntington's disease and Parkinson's disease. Other lines of evidence demonstrated the cytotoxic effect of cysteamine on duodenal mucosa leading to ulcer development. However, the mechanism for cystamine cytotoxicity remains poorly understood. Here, we report a new pathway in which cystamine induces apoptosis by targeting apoptosis-inducing factor (AIF). By screening of various cell lines, we observed that cystamine and cysteamine induce cell death in a cell type-specific manner. Comparison between cystamine-sensitive and cystamine-resistant cell lines revealed that cystamine cytotoxicity is not associated with unfolded protein response, reactive oxygen species generation and transglutaminase or caspase activity; rather, it is associated with the ability of cystamine to trigger AIF nuclear translocation. In cystamine-sensitive cells, cystamine suppresses the levels of intracellular glutathione by inhibiting γ-glutamylcysteine synthetase expression that triggers AIF translocation. Conversely, glutathione supplementation completely prevents cystamine-induced AIF translocation and apoptosis. In rats, cysteamine administration induces glutathione depletion and AIF translocation leading to apoptosis of duodenal epithelium. These results indicate that AIF translocation through glutathione depletion is the molecular mechanism of cystamine toxicity, and provide important implications for cystamine in the neurodegenerative disease therapeutics as well as in the regulation of AIF-mediated cell death

Pure red-cell aplasia and autoimmune hemolytic anemia in a patient with acute hepatitis A

Pure red cell aplasia (PRCA) and autoimmune hemolytic anemia (AIHA) have rarely been reported as an extrahepatic manifestation of acute hepatitis A (AHA). We report herein a case of AHA complicated by both PRCA and AIHA. A 49-year-old female with a diagnosis of AHA presented with severe anemia (hemoglobin level, 6.9 g/dL) during her clinical course. A diagnostic workup revealed AIHA and PRCA as the cause of the anemia. The patient was treated with an initial transfusion and corticosteroid therapy. Her anemia and liver function test were completely recovered by 9 months after the initial presentation. We review the clinical features and therapeutic strategies for this rare case of extrahepatic manifestation of AHA

Capicua suppresses hepatocellular carcinoma progression by controlling the ETV4–MMP1 axis

Hepatocellular carcinoma (HCC) is developed by multiple steps accompanying progressive alterations of gene expression, which leads to increased cell proliferation and malignancy. Although environmental factors and intracellular signaling pathways that are critical for HCC progression have been identified, gene expression changes and the related genetic factors contributing to HCC pathogenesis are still insufficiently understood. In this study, we identify a transcriptional repressor Capicua/CIC as a suppressor of HCC progression and a potential therapeutic target. Expression of CIC is posttranscriptionally reduced in HCC cells. CIC levels are correlated with survival rates in patients with HCC. CIC overexpression suppresses HCC cell proliferation and invasion, whereas loss of CIC exerts opposite effects in vivo as well as in vitro. The levels of PEA3 group genes, the best-known CIC target genes, are correlated with lethality in patients with HCC. Among the PEA3 group genes, ETV4 is the most significantly upregulated gene in CIC-deficient HCC cells, consequently promoting HCC progression. Furthermore, ETV4 induces expression of MMP1, the MMP gene highly relevant to HCC progression, in HCC cells, and knockdown of MMP1 completely blocks the CIC deficiency-induced HCC cell proliferation and invasion. CONCLUSION: Our study demonstrates that the CIC-ETV4-MMP1 axis is a novel regulatory module controlling HCC progression. This article is protected by copyright. All rights reserved.113sciescopu

Anaphylaxis caused by latex surgical gloves immediately after starting surgery -A case report-

Anaphylaxis is an acute and fatal systemic allergic reaction to an allergen, and it can be an unpredictable and life-threatening cause during anesthesia. Latex is the second most common cause of anaphylaxis following the use of neuromuscular blocking agents during general anesthesia or surgery. We report on a 67-year-old male who had undergone surgery under general anesthesia without any problem but who presented with severe intraoperative anaphylaxis to latex surgical gloves. This case emphasizes the need for anesthesiologists to quickly diagnose and properly manage an allergic reaction in patients under general anesthesia

CT Findings of Completely Regressed Hepatocellular Carcinoma with Main Portal Vein Tumor Thrombosis after Transcatheter Arterial Chemoembolization

Objective: The objective of this study was to determine the sequential CT findings of controlled hepatocellular carcinoma (HCC) with main portal vein (MPV) thrombosis with the use of transcatheter arterial chemoembolization and additional intra-arterial cisplatin infusion. Materials and Methods: From January 2004 to September 2006, 138 patients with HCC invading MPV were referred to the angiography unit of our institution for chemoembolization and additional intra-arterial cisplatin infusion. Until August 2008, seven (5%) of 138 patients were followed-up and found not to have tumor recurrence. CT scans were retrospectively reviewed by two radiologists, focusing on the following parameters: the extent of portal vein thrombosis, the diameter of the affected portal vein, and enhancement of portal vein thrombosis. Results: The extent of portal vein thrombosis at the initial presentation was variable: left portal vein (LPV) and MPV (n = 1), right portal vein (RPV) and MPV (n = 3), as well as RPV, LPV and MPV (n = 3). The extent and diameter of the affected portal vein decreased during follow-up examinations. In addition, the degree of enhancement for tumor thrombi and serum alpha-feto-protein levels decreased after the transcatheter arterial chemoembolization. Portal vein thrombosis was found to be completely resolved in one patient, whereas residual thrombus without viability was persistent in six patients. Conclusion: If chemoembolization is effective in patients with HCC that invades the portal vein, the extent and enhancement of portal vein thrombosis is reduced, but residual thrombosis frequently persists for months or years, without evidence of a viable tumor.Shin SW, 2009, KOREAN J RADIOL, V10, P425, DOI 10.3348/kjr.2009.10.5.425El-Serag HB, 2008, GASTROENTEROLOGY, V134, P1752, DOI 10.1053/j.gastro.2008.02.090Shah ZK, 2007, AM J ROENTGENOL, V188, P1320, DOI 10.2214/AJR.06.0134JEON UB, 2007, RAD SOC N AM 93 SCIObi S, 2006, CANCER, V106, P1990, DOI 10.1002/cncr.21832MYUNG SJ, 2006, KOREAN J HEPATOL, V12, P107Georgiades CS, 2005, J VASC INTERV RADIOL, V16, P1653, DOI 10.1097/01.RVI.0000182185.47500.7AKim DY, 2005, CANCER, V103, P2419, DOI 10.1002/cncr.21043Llovet JM, 2003, HEPATOLOGY, V37, P429, DOI 10.1053/jhep.2003.50047Bruix J, 2001, J HEPATOL, V35, P421Lee HS, 1997, CANCER, V79, P2087Tublin ME, 1997, AM J ROENTGENOL, V168, P719CHUNG JW, 1995, AM J ROENTGENOL, V165, P315MATHIEU D, 1984, RADIOLOGY, V152, P127YAMADA R, 1983, RADIOLOGY, V148, P397

A Case of Pulmonary Vein Tumor Presenting as a Left Atrial Mass

Primary cardiac tumors are extremely rare and can originate within the heart or be the result of tumor spread from other sites. We report a female patient with a pulmonary vein tumor extending into the left atrium that had a suspicious primary malignant origin with a sacral metastatic carcinoma. The patient was admitted complaining of pain in her buttock area as a result of a sacral tumor. It was believed that the sacral tumor was a metastasis from the imaging study and clinical manifestation. The primary malignant origin was evaluated. The chest CT showed a left atrium thrombus-like lesion without a pulmonary abnormality. After a transesophageal echocardiogram, the patient was diagnosed with a pulmonary vein tumor extending to the left atrium. The patient was given palliative radiotherapy for the sacral pain. Initially, the clinical impression was a metastatic sacral tumor with a thromboembolism of the left atrium. However, this patient was finally diagnosed with a pulmonary vein tumor with a left atrium extension by a transesophageal echocardiogram