Radiation-induced Cochlea Hair Cell Death: Mechanisms and Protection

Tan, Pei-Xin,Du, Sha-Sha,Ren, Chen,Yao, Qi-Wei,Yuan, Ya-Wei Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.10

Cochlea hair cell death is regarded to be responsible for the radiation-induced sensorineural hearing loss (SNHL), which is one of the principal complications of radiotherapy (RT) for head and neck cancers. In this mini-review, we focus on the current progresses trying to unravel mechanisms of radiation-induced hair cell death and find out possible protection. P53, reactive oxygen species (ROS) and c-Jun N-terminal kinase (JNK) pathways have been proposed as pivotal in the processes leading to radiation hair cell death. Potential protectants, such as amifostine, N-acetylcysteine (NAC) and epicatechin (EC), are claimed to be effective at reducing radiation-inducedhair cell death. The RT dosage, selection and application of concurrent chemotherapy should be pre-examined in order to minimize the damage to cochlea hair cells.

Design a Laboratory Rotating Test Bench for the Multi-Channel Dryer Experiment

Sha Wang,Jixian Dong,Changke Tan,Bo Wang,Lijie Qiao,Huan Liu 한국펄프·종이공학회 2019 펄프.종이기술 Vol.51 No.5

The dryer of paper machine has problem in discharging condensate water. When the dryer rotates at a high speed, the condensate water that is not discharged in time will form a water ring, resulting in low drying efficiency and high energy consumption. Thus, based on the multi-channel dryer proposed by others, a series of experiments was carried out on multi-channel dryer under static condition. However, due to the fact that the research condition of condensation and heat transfer of multi-channel dryer is not exactly the same as the actual working condition, the multi-channel dryer has not been introduced to the market. To address the above problems, this paper presented a rotating test bench which can better simulate the actual working condition of dryer and expounded the working principle of the test bench, as well as the design and calculation of rotary device of the test bench. Finite element analysis software was used to analyze the stress on the dryer channel. In order to avoid resonance problems, modal numerical analysis was conducted on the test bench, which provided experimental conditions for the further study of multi-channel dryer.

Long Noncoding RNA NEAT1 Aggravates Aβ-Induced Neuronal Damage by Targeting miR-107 in Alzheimer’s Disease

Sha Ke,Zhaohui Yang,Fei Yang,Xiaoming Wang,Juan Tan,Bo Liao 연세대학교의과대학 2019 Yonsei medical journal Vol.60 No.7

Purpose: Alzheimer’s disease (AD) is the most common neurodegenerative disease, with a rising prevalence worldwide. Longnoncoding RNAs (lncRNAs) have been found to play important roles in the development and treatment of AD. However, the exactrole of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in neuronal damage in AD is largely unknown. Materials and Methods: The AD model was established in SH-SY5Y and SK-N-SH cells via treatment with amyloid β1-42 (Aβ). Theexpression of NEAT1 and microRNA-107 (miR-107) was measured by quantitative real-time polymerase chain reaction. Cell viabilityand apoptosis were detected by MTT assay, immunocytochemistry, and flow cytometry. The expression of phosphorylated tauprotein (p-Tau) was measured by Western blot. The interaction between NEAT1 and miR-107 was explored by bioinformaticsanalysis, luciferase activity, and RNA immunoprecipitation assays. Results: NEAT1 expression was enhanced in Aβ-treated SH-SY5Y and SK-N-SH cells, and its knockdown attenuated Aβ-inducedinhibition of viability and promotion of apoptosis and p-Tau levels. NEAT1 was indicated as a decoy of miR-107. miR-107 abundancewas reduced in Aβ-treated cells, and its overexpression reversed Aβ-induced injury. Moreover, interference of miR-107 abatedsilencing of NEAT1-mediated inhibition of neuronal damage in Aβ-treated SH-SY5Y and SK-N-SH cells. Conclusion: LncRNA NEAT1 aggravated Aβ-induced neuronal damage by sponging miR-107, indicating a novel avenue for treatmentof AD.

Naloxone Postconditioning Alleviates Rat Myocardial Ischemia Reperfusion Injury by Inhibiting JNK Activity

Anzhou Xia,Zhi Xue,Tan Zhang,Tiantian Wei,Xingzhi Sha,Yixun Ding,Weidong Zhou 대한약리학회 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.1

To investigate the alteration of c-Jun N-terminal kinase (JNK) activity after myocardial ischemiareperfusion injury (MIRI) and further explore the effect of naloxone postconditioning on MIRI. Fortymale Sprague Dawley rats were randomly divided into five groups: sham operation (sham, n=8);ischemia reperfusion (IR, n=8); IR+naloxone 0.5 mg/kg (Nal L, n=8); IR+naloxone 1.0 mg/kg (Nal M,n=8); IR+naloxone 2.0 mg/kg (Nal H, n=8). Pathological changes of myocardial tissue were visualizedby HE staining. The expression of p-JNK, and the apoptosis of cardiomyocytes were investigated withWestern blotting and the TUNEL assay, respectively. Irregular arrangement and aberrant structureof myocardial fibers, cardiomyocytes with granular or vacuolar degeneration, and inflammatory cellsinfiltrating the myocardial interstitial regions characterized MIRI in the IR group. Signs of myocardialinjury and inflammatory infiltration were less prominent in the Nal-treated groups. The expressionof p-JNK in the sham group and in all Nal-treated groups was significantly lower than that in theIR group (p<0.01). The apoptosis index of cardiomyocytes in the IR group was significantly higherthan in the sham group (p< 0.01). The apoptosis indices of cardiomyocytes in all Nal-treated groupswere significantly reduced to 55.4%, 26.2%, and 27.6%, respectively, of the IR group (p< 0.01). Thisstudy revealed that Naloxone postconditioning before reperfusion inhibits p-JNK expression anddecreases cell apoptosis, thus alleviating MIRI.

Naloxone Postconditioning Alleviates Rat Myocardial Ischemia Reperfusion Injury by Inhibiting JNK Activity

Xia, Anzhou,Xue, Zhi,Wang, Wei,Zhang, Tan,Wei, Tiantian,Sha, Xingzhi,Ding, Yixun,Zhou, Weidong The Korean Society of Pharmacology 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.1

To investigate the alteration of c-Jun N-terminal kinase (JNK) activity after myocardial ischemia reperfusion injury (MIRI) and further explore the effect of naloxone postconditioning on MIRI. Forty male Sprague Dawley rats were randomly divided into five groups: sham operation (sham, n=8); ischemia reperfusion (IR, n=8); IR+naloxone 0.5 mg/kg (Nal L, n=8); IR+naloxone 1.0 mg/kg (Nal M, n=8); IR+naloxone 2.0 mg/kg (Nal H, n=8). Pathological changes of myocardial tissue were visualized by HE staining. The expression of p-JNK, and the apoptosis of cardiomyocytes were investigated with Western blotting and the TUNEL assay, respectively. Irregular arrangement and aberrant structure of myocardial fibers, cardiomyocytes with granular or vacuolar degeneration, and inflammatory cells infiltrating the myocardial interstitial regions characterized MIRI in the IR group. Signs of myocardial injury and inflammatory infiltration were less prominent in the Nal-treated groups. The expression of p-JNK in the sham group and in all Nal-treated groups was significantly lower than that in the IR group (p<0.01). The apoptosis index of cardiomyocytes in the IR group was significantly higher than in the sham group (p<0.01). The apoptosis indices of cardiomyocytes in all Nal-treated groups were significantly reduced to 55.4%, 26.2%, and 27.6%, respectively, of the IR group (p<0.01). This study revealed that Naloxone postconditioning before reperfusion inhibits p-JNK expression and decreases cell apoptosis, thus alleviating MIRI.

Graphitization of PAN-based carbon fibers by CO₂ laser irradiation

Liangbo Yao,Weimin Yang,Sanyang Li,Yang Sha,Jing Tan,Ying An,Haoyi Li 한국탄소학회 2017 Carbon Letters Vol.24 No.-

Experimental analysis on the main contents of Rhizoma gastrodiae extract and inter-transformation throughout the fermentation process of Grifola frondosa

Na Wang,Tian-xiang Wu,Yong Zhang,Xiao-bao Xu,Sha Tan,Hong-wei Fu 대한약학회 2013 Archives of Pharmacal Research Vol.36 No.3

Gastrodin (GA), p-hydroxylbenzaldehyde (HBA),p-hydroxybenzyl alcohol (gastrodigenin, HA) and parishin notonly are the major active ingredients of Rhizoma gastrodiae,but exist transformed relations from each other throughout thefermentation process of Grifola frondosa in this work.We hadfound that parishin (non-free gastrodin) almost could completelytransformed into gastrodin (GA, free gastrodin) afterR. gastrodiae alcohol extract was sterilized by moist heat(121 C, 30 min), but before was added into submerged cultivationof G. frondosa. However, interestingly and importantly,gastrodin re-synthesized of parishin after R. gastrodiaealcohol extract’s addition into submerged cultivation ofG. frondosa. In addition, the reduction of p-hydroxylbenzaldehydeand p-hydroxybenzyl alcohol in G. frondosa fermentationprocess reconfirmed that the G. frondosa strain 51616really could synthesize gastrodin into parishin by submergedfermentation. This paper firstly also reported G. frondosa’seffects on R. gastrodiae.

Numerical optimization of transmission bremsstrahlung target for intense pulsed electron beam

Xiao Yu,Jie Shen,Shijian Zhang,Jie Zhang,Nan Zhang,Ivan Sergeevich Egorov,Sha Yan,Chang Tan,Gennady Efimovich Remnev,Xiaoyun Le 한국원자력학회 2022 Nuclear Engineering and Technology Vol.54 No.2

The optimization of a transmission type bremsstrahlung conversion target was carried out with MonteCarlo code FLUKA for intense pulsed electron beams with electron energy of several hundred keV formaximum photon fluence. The photon emission intensity from electrons with energy ranging from300 keV to 1 MeV on tungsten, tantalum and molybdenum targets was calculated with varied targetthicknesses. The research revealed that higher target material element number and electron energy leadsto increased photon fluence. For a certain target material, the target thickness with maximum photonemission fluence exhibits a linear relationship with the electron energy. With certain electron energy andtarget material, the thickness of the target plays a dominant role in increasing the transmission photonintensity, with small target thickness the photon flux is largely restricted by low energy loss of electronsfor photon generation while thick targets may impose extra absorption for the generated photons. Thespatial distribution of bremsstrahlung photon density was analyzed and the optimal target thicknessesfor maximum bremsstrahlung photon fluence were derived versus electron energy on three targetmaterials for a quick determination of optimal target design