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RISS 인기검색어
- 검색키워드
- 저자 : Nilius, Bernd (검색결과 4 건)
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Nilius, Manfred,Mueller, Charlotte,Nilius, Minou Helene,Haim, Dominik,Leonhardt, Henry,Lauer, Guenter The Korean Dental Society of Anesthsiology 2020 Journal of Dental Anesthesia and Pain Medicine Vol.20 No.6
Background: Intraosseous anesthesia (IO) allows the anesthetic solution to be injected directly into the cancellous bone. The anesthetic solution immediately reaches the periapical region, and thus the axonal area of the nerve, where it can temporarily disable the sodium pump. The effect is felt almost without any time delay, and only a small amount of anesthetic solution is required. Methods: This study aims to investigate the efficacy of IO using the AnestoⓇ device after infiltration anesthesia (IA) and/or inferior alveolar nerve block anesthesia (IANB) failed to work in symptomatic irreversible pulpitis (hot tooth). The 33 patients included in the study were treated additionally with 1.7 ml articaine hydrochloride with 1:100,000 epinephrine hydrochloride (UltracainⓇ D-S, Sanofi-Aventis, Frankfurt, Germany) IO. Results: The electrical pulp test showed that 95.76% of the volunteers reacted positively to the combination of IANB or IA with the IO. In women, the additive IO was effective at 97.22%. In men, the IO led to pain elimination in 94.00% of cases. The duration of the IO was less than a quarter of an hour (13.03 min). The IO worked longer in women than in men (13.61 min vs. 12.33 min). Overall, more than every third tooth that needed trepanation was located in the posterior area of the mandible (36.4%). Treatment of hot teeth in this area was associated with an increased pulse rate and increased residual pain. There was a moderate correlation (Spearman-Rho [IRI] = 0.280) between the Visual Analog Scale (VAS) score and bone density, and a significant correlation (IRI = 0.612) between subjective residual pain and bone width. The IO resulted in a moderate, transient increase in the pulse rate by approximately 20 bpm. This is similar to the temporary increase in heart rate after conventional anesthesia techniques in non-preloaded patients and can be considered clinically irrelevant. Conclusion: IO with the AnestoⓇ device as an extension and deepening of local pain elimination is recommended for the treatment of hot teeth.
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Current and upcoming mitochondrial targets for cancer therapy
Kim, Hyoung Kyu,Noh, Yeon Hee,Nilius, Bernd,Ko, Kyung Soo,Rhee, Byoung Doo,Kim, Nari,Han, Jin HARCOURT BRACE JOVANOVICH 2017 SEMINARS IN CANCER BIOLOGY Vol.47 No.-
<P><B>Abstract</B></P> <P>Mitochondria are essential intracellular organelles that regulate energy metabolism, cell death, and signaling pathways that are important for cell proliferation and differentiation. Therefore, mitochondria are fundamentally implicated in cancer biology, including initiation, growth, metastasis, relapse, and acquired drug resistance. Based on these implications, mitochondria have been proposed as a major therapeutic target for cancer treatment. In addition to classical view of mitochondria in cancer biology, recent studies found novel pathophysiological roles of mitochondria in cancer. In this review, we introduce recent concepts of mitochondrial roles in cancer biology including mitochondrial DNA mutation and epigenetic modulation, energy metabolism reprogramming, mitochondrial channels, involvement in metastasis and drug resistance, and cancer stem cells. We also discuss the role of mitochondria in emerging cancer therapeutic strategies, especially cancer immunotherapy and CRISPR-Cas9 system gene therapy.</P>
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Kim, Hyoung Kyu,Youm, Jae Boum,Lee, Sung Ryul,Lim, Se Eun,Lee, Sun-Young,Ko, Tae Hee,Long, Le Thanh,Nilius, Bernd,Won, Du Nam,Noh, Jung-Hyun,Ko, Kyung Soo,Rhee, Byoung Doo,Kim, Nari,Han, Jin Springer-Verlag 2012 Pfl ugers Arch Vol.464 No.6
<P>Telmisartan is an angiotensin II receptor blocker and partial peroxisome proliferator-activated receptor gamma agonist that modulates the renin-angiotensin-aldosterone system. It is used primarily to manage hypertension, diabetic nephropathy, and congestive heart failure. Recent studies have reported that myocardial infarction (MI) has occurred in telmisartan-treated patients. The purpose of the study was to investigate the specific conditions and underlying mechanisms that may result in telmisartan-induced MI. We evaluated the effect of telmisartan on whole hearts, cardiomyocytes, and cardiac sarcolemmal ion channels. Hearts of 8-week-old male Sprague-Dawley rats were perfused with 3, 10, 30, or 100?μM telmisartan or losartan or with normal Tyrode's solution (control) for 3?h. We found that telmisartan induced myocardial infarction, with an infarct size of 21?% of the total at 30?μM (P?<?0.0001) and 63?% of the total area at 100?μM (P?<?0.001). Telmisartan also induced cardiac dysfunction (e.g., decreased heart rate, diminished coronary flow, hypercontracture, and arrhythmia). Confocal microscopy demonstrated that 30?μM telmisartan significantly elevated the intracellular Ca(2+) level, leading to hypercontracture and cell death. Patch clamp analysis of isolated cardiomyocytes revealed that telmisartan induced Na(+) overload by slowing the inactivation of voltage-gated Na(+) current (I (Na)), activating the reverse mode of Na(+)-Ca(2+) exchanger activity, and causing Ca(2+) overload. Telmisartan significantly delayed the inactivation of the voltage-gated Na(+) channel, causing cytosolic Na(+) overload, prolonged action potential duration, and subsequent Ca(2+) overload. Above 30?μM, telmisartan may potentially cause cardiac cell death and MI.</P>
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