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41.
Magnifying endoscope with NBI to predict the depth of invasion in laryngo‐pharyngeal cancer
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Ichiro Tateya MD PhD Shuko Morita MD Manabu Muto MD PhD Shin'ichi Miyamoto MD PhD Tomomasa Hayashi MD PhD Makiko Funakoshi MD Ikuo Aoyama MD Shigeru Hirano MD PhD Morimasa Kitamura MD PhD Seiji Ishikawa MD PhD Yo Kishimoto MD PhD Mami Morita MD Patnarin Mahattanasakul MD Satoshi Morita PhD Juichi Ito MD PhD 《The Laryngoscope》2015,125(5):1124-1129
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Yu Sato Akiomi Yoshihisa Yusuke Kimishima Takatoyo Kiko Shunsuke Watanabe Yuki Kanno Satoshi Abe Makiko Miyata Takamasa Sato Satoshi Suzuki Masayoshi Oikawa Atsushi Kobayashi Takayoshi Yamaki Hiroyuki Kunii Kazuhiko Nakazato Takafumi Ishida Yasuchika Takeishi 《The Canadian journal of cardiology》2018,34(1):80-87
Background
It is widely recognized that overt hyper- as well as hypothyroidism are potential causes of heart failure (HF). Additionally it has been recently reported that subclinical hypothyroidism (sub-hypo) is associated with atherosclerosis, development of HF, and cardiovascular death. We aimed to clarify the effect of sub-hypo on prognosis of HF, and underlying hemodynamics and exercise capacity.Methods
We measured the serum levels of thyroid stimulating hormone (TSH) and free thyroxine (FT4) in 1100 consecutive HF patients. We divided these patients into 5 groups on the basis of plasma levels of TSH and FT4, and focused on euthyroidism (0.4 ≤ TSH ≤ 4 μIU/mL and 0.7 ≤ FT4 ≤ 1.9 ng/dL; n = 911; 82.8%) and sub-hypo groups (TSH > 4 μIU/mL and 0.7 ≤ FT4 ≤ 1.9 ng/dL; n = 132; 12.0%). We compared parameters of echocardiography, cardiopulmonary exercise testing, and cardiac catheterization, and followed up for cardiac event rate and all-cause mortality between the 2 groups.Results
Although left ventricular ejection fraction did not differ between the 2 groups, the sub-hypo group had lower peak breath-by-breath oxygen consumption and higher mean pulmonary arterial pressure than the euthyroidism group (peak breath-by-breath oxygen consumption, 14.0 vs 15.9 mL/min/kg; P = 0.012; mean pulmonary arterial pressure, 26.8 vs 23.5 mm Hg, P = 0.020). In Kaplan-Meier analysis (mean 1098 days), the cardiac event rate and all-cause mortality were significantly higher in the sub-hypo group than those in the euthyroidism group (log rank, P < 0.01, respectively). In Cox proportional hazard analysis, sub-hypo was a predictor of cardiac event rate and all-cause mortality in HF patients (P < 0.05, respectively).Conclusions
Sub-hypo might be associated with adverse prognosis, accompanied by impaired exercise capacity and higher pulmonary arterial pressure, in HF patients. 相似文献43.
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45.
Ayako Inoshita Takatoshi Kasai Makiko Takahashi Hiroyuki Inoshita Satoshi Kasagi Fusae Kawana Sugao Ishiwata Minoru Ohno Tetsu Yamaguchi Koji Narui Katsuhisa Ikeda 《Sleep & breathing》2014,18(2):439-445
Purpose
Obstructive sleep apnea (OSA) is complicated with heart failure (HF); however, the reason for this is not well understood. Craniofacial anatomic risk factors may contribute to OSA pathogenesis in HF patients. However, there are no data about cephalometric findings among OSA patients with HF.Methods
Consecutive patients with HF and OSA (defined as total apnea–hypopnea index (AHI) ≥15/h) were enrolled. As controls, OSA patients without HF but matching the test group in age, BMI, and obstructive AHI were also enrolled.Results
Overall, 17 OSA patients with HF and 34 OSA patients without HF were compared. There are no significant differences in the characteristics or polysomnographic parameters between 2 groups. In the cephalometric findings, compared with patients without HF, patients with HF showed a significantly greater angle between the line SN to point “A” (SNA) and a longer inferior airway space and greater airway area. However, the tongue area of patients with HF was more than those without HF.Conclusions
The craniofacial structures of OSA patients with HF were different from those without HF. OSA patients with HF had an upper airway anatomy that is more likely to collapse when sleeping while recumbent, despite having a larger airway space. 相似文献46.
Nobuaki Sakamoto Huanhuan Hu Akiko Nanri Tetsuya Mizoue Masafumi Eguchi Takeshi Kochi Tohru Nakagawa Toru Honda Shuichiro Yamamoto Takayuki Ogasawara Naoko Sasaki Akiko Nishihara Teppei Imai Toshiaki Miyamoto Makoto Yamamoto Hiroko Okazaki Kentaro Tomita Akihiko Uehara Ai Hori Makiko Shimizu Taizo Murakami Keisuke Kuwahara Ami Fukunaga Isamu Kabe Tomofumi Sone Seitaro Dohi 《Journal of diabetes investigation.》2020,11(3):719-725
47.
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
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49.
Hashizume O Shimizu A Yokota M Sugiyama A Nakada K Miyoshi H Itami M Ohira M Nagase H Takenaga K Hayashi J 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(26):10528-10533
It has been hypothesized that respiration defects caused by accumulation of pathogenic mitochondrial DNA (mtDNA) mutations and the resultant overproduction of reactive oxygen species (ROS) or lactates are responsible for aging and age-associated disorders, including diabetes and tumor development. However, there is no direct evidence to prove the involvement of mtDNA mutations in these processes, because it is difficult to exclude the possible involvement of nuclear DNA mutations. Our previous studies resolved this issue by using an mtDNA exchange technology and showed that a G13997A mtDNA mutation found in mouse tumor cells induces metastasis via ROS overproduction. Here, using transmitochondrial mice (mito-mice), which we had generated previously by introducing G13997A mtDNA from mouse tumor cells into mouse embryonic stem cells, we provide convincing evidence supporting part of the abovementioned hypothesis by showing that G13997A mtDNA regulates diabetes development, lymphoma formation, and metastasis--but not aging--in this model. 相似文献
50.