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101.
Christine Chavez Shinji Sasada Takehiro Izumo Yukiko Nakamura Koji Tsuta Takaaki Tsuchida 《Journal of thoracic disease》2014,6(6):E81-E84
Guided bronchoscopy has been found to be useful for the diagnosis of solid peripheral pulmonary lesions (PPLs) but more evidence on ground glass opacities (GGOs), especially those without a solid component, are lacking. A 69-year-old male, asymptomatic, heavy smoker was referred to our department for non-surgical diagnosis of a focal pure GGO in the right upper lobe that was found incidentally on computed tomography (CT). Transbronchial biopsy (TBB) with the aide of endobronchial ultrasound with a guide sheath (EBUS-GS), virtual bronchoscopic navigation (VBN), and fluoroscopy was performed for sampling. There were no complications after the procedure. The diagnosis of adenocarcinoma with lepidic growth pattern was established from the fourth and fifth TBB specimens and was confirmed on subsequent surgical resection. Image-guided bronchoscopy with TBB was successful for the diagnosis of a pure GGO. Use of a larger biopsy device may be helpful for the histopathologic diagnosis of lung adenocarcinoma with lepidic growth. 相似文献
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103.
Kashio M Sokabe T Shintaku K Uematsu T Fukuta N Kobayashi N Mori Y Tominaga M 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(17):6745-6750
The ability to sense temperature is essential for organism survival and efficient metabolism. Body temperatures profoundly affect many physiological functions, including immunity. Transient receptor potential melastatin 2 (TRPM2) is a thermosensitive, Ca(2+)-permeable cation channel expressed in a wide range of immunocytes. TRPM2 is activated by adenosine diphosphate ribose and hydrogen peroxide (H(2)O(2)), although the activation mechanism by H(2)O(2) is not well understood. Here we report a unique activation mechanism in which H(2)O(2) lowers the temperature threshold for TRPM2 activation, termed "sensitization," through Met oxidation and adenosine diphosphate ribose production. This sensitization is completely abolished by a single mutation at Met-214, indicating that the temperature threshold of TRPM2 activation is regulated by redox signals that enable channel activity at physiological body temperatures. Loss of TRPM2 attenuates zymosan-evoked macrophage functions, including cytokine release and fever-enhanced phagocytic activity. These findings suggest that redox signals sensitize TRPM2 downstream of NADPH oxidase activity and make TRPM2 active at physiological body temperature, leading to increased cytosolic Ca(2+) concentrations. Our results suggest that TRPM2 sensitization plays important roles in macrophage functions. 相似文献
104.
K Taguchi N Fujikawa M Komatsu T Ishii M Unno T Akaike H Motohashi M Yamamoto 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(34):13561-13566
The Kelch-like ECH-associated protein 1 (Keap1)-NF-E2-related factor 2 (Nrf2) system is essential for cytoprotection against oxidative and electrophilic insults. Under unstressed conditions, Keap1 serves as an adaptor for ubiquitin E3 ligase and promotes proteasomal degradation of Nrf2, but Nrf2 is stabilized when Keap1 is inactivated under oxidative/electrophilic stress conditions. Autophagy-deficient mice show aberrant accumulation of p62, a multifunctional scaffold protein, and develop severe liver damage. The p62 accumulation disrupts the Keap1-Nrf2 association and provokes Nrf2 stabilization and accumulation. However, individual contributions of p62 and Nrf2 to the autophagy-deficiency-driven liver pathogenesis have not been clarified. To examine whether Nrf2 caused the liver injury independent of p62, we crossed liver-specific Atg7::Keap1-Alb double-mutant mice into p62- and Nrf2-null backgrounds. Although Atg7::Keap1-Alb::p62(-/-) triple-mutant mice displayed defective autophagy accompanied by the robust accumulation of Nrf2 and severe liver injury, Atg7::Keap1-Alb::Nrf2(-/-) triple-mutant mice did not show any signs of such hepatocellular damage. Importantly, in this study we noticed that Keap1 accumulated in the Atg7- or p62-deficient mouse livers and the Keap1 level did not change by a proteasome inhibitor, indicating that the Keap1 protein is constitutively degraded through the autophagy pathway. This finding is in clear contrast to the Nrf2 degradation through the proteasome pathway. We also found that treatment of cells with tert-butylhydroquinone accelerated the Keap1 degradation. These results thus indicate that Nrf2 accumulation is the dominant cause to provoke the liver damage in the autophagy-deficient mice. The autophagy pathway maintains the integrity of the Keap1-Nrf2 system for the normal liver function by governing the Keap1 turnover. 相似文献
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108.
Y Shindo H Miyatani T Uehara T Ikeya K Yamanaka M Ikeda K Tokai S Ushimaru S Matsumoto T Asano T Takamatsu M Fukunishi T Iwaki Y Sagihara S Asabe Y Yoshida 《Nihon Shokakibyo Gakkai zasshi》2012,109(7):1243-1249
A 78-year-old man with hepatocellular carcinoma treated by chemoembolization and percutaneous ethanol injection was admitted to our hospital because of acute abdomen. The CT scan showed biliary fistula caused by hepatocellular carcinoma protruding from S3. Endoscopic retrograde cholangiopancreatography showed disruption of an intrahepatic duct and the main pancreatic duct, and contrast agent leaked into the peritoneal cavity from each duct. Omental panniculitis with biliary fistula and pancreatic fistula was diagnosed. The symptoms improved by endoscopic nasobiliary drainage and endoscopic pancreatic stenting. On the 13th day after admission, we added endoscopic nasopancreatic drainage because his abdominal pain had been exacerbated by pancreatic juice leakage. Omental panniculitis by hepatocellular carcinoma complicated by biliary fistula and pancreatic fistula is extremely rare. Endoscopic transpapillary pancreaticobiliary drainage was effective for omental panniculitis in this case. 相似文献
109.
Hiroyoshi Adachi MD PhD Shunichiro Shinagawa MD PhD Kenjiro Komori MA Yasutaka Toyota MD PhD Takaaki Mori MD PhD Teruhisa Matsumoto MD PhD Naomi Sonobe MD PhD Tetsuo Kashibayashi MD PhD Tomohisa Ishikawa MD PhD Ryuji Fukuhara MD PhD Manabu Ikeda MD PhD 《Psychiatry and clinical neurosciences》2013,67(3):148-153
110.
Tomokazu Kishiki Tadahiko MasakiHiroyoshi Matsuoka M.D. Takaaki KobayashiYutaka Suzuki M.D. Nobutsugu AbeToshiyuki Mori M.D. Masanori Sugiyama M.D. 《American journal of surgery》2013