http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Experimental investigation of impact behaviour of shear deficient RC beam to column connection
Murat Aras,Tolga Yılmaz,Özlem Çalışkan,Özgür Anıl,R. Tuğrul Erdem,Turgut Kaya 국제구조공학회 2022 Structural Engineering and Mechanics, An Int'l Jou Vol.84 No.5
Reinforced concrete (RC) structures may be subjected to sudden dynamic impact loads such as explosions occurring for different reasons, the collision of masses driven by rockfall, flood, landslide, and avalanche effect structural members, the crash of vehicles to the highway and seaway structures. Many analytical, numerical, and experimental studies focused on the behavior of RC structural elements such as columns, beams, and slabs under sudden dynamic impact loads. However, there is no comprehensive study on the behavior of the RC column-beam connections under the effect of sudden dynamic impact loads. For this purpose, an experimental study was performed to investigate the behavior of RC column-beam connections under the effect of low-velocity impact loads. Sixteen RC beam-column connections with a scale of 1/3 were manufactured and tested under impact load using the drop-weight test setup. The concrete compressive strength, shear reinforcement spacing in the beam, and input impact energy applied to test specimens were taken as experimental variables. The time histories of impact load acting on test specimens, accelerations, and displacements measured from the test specimens were recorded in experiments. Besides, shear and bending crack widths were measured. The effect of experimental variables on the impact behavior of RC beam-column connections has been determined and interpreted in detail. Besides, a finite element model has been established for verification and comparison of the experimental results by using ABAQUS software. It has been demonstrated that concrete strength, shear reinforcement ratio, and impact energy significantly affect the impact behavior of RC column-beam connections.
Sen, Halil Murat,Guven, Mustafa,Aras, Adem Bozkurt,Cosar, Murat The Korean Neurosurgical Society 2017 Journal of Korean neurosurgical society Vol.60 No.3
Dural injury during spinal surgery can subsequently give rise to a remote cerebellar hemorrhage (RCH). Although the incidence of such injury is low, the resulting hemorrhage can be life threatening. The mechanism underlying the formation of the hemorrhage is not known, but it is mostly thought to develop after venous infarction. Cerebellar mutism (CM) is a frequent complication of posterior fossa operations in children, but it is rarely seen in adults. The development of CM after an RCH has not been described. We describe the case of a 65-year old female who lost cerebrospinal fluid after inadvertent opening of the dura during surgery. Computerized tomography performed when the patient became unable to speak revealed a bilateral cerebellar hemorrhage.
Hwang, Ara B.,Ryu, Eun-A,Artan, Murat,Chang, Hsin-Wen,Kabir, Mohammad Humayun,Nam, Hyun-Jun,Lee, Dongyeop,Yang, Jae-Seong,Kim, Sanguk,Mair, William B.,Lee, Cheolju,Lee, Siu Sylvia,Lee, Seung-Jae National Academy of Sciences 2014 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.111 No.42
<P><B>Significance</B></P><P>Reactive oxygen species (ROS) have long been thought to cause aging and considered to be toxic byproducts generated during mitochondrial respiration. Surprisingly, recent studies show that modestly increased ROS levels lengthen lifespan, at least in the roundworm <I>Caenorhabditis elegans</I>. It was unclear how the levels of potentially toxic ROS are regulated and how ROS promote longevity. Here we demonstrate that ROS activate two proteins, AMP-activated kinase (AMPK) and hypoxia-inducible factor 1 (HIF-1), to promote longevity by increasing immunity. Further, we find that internal ROS levels are reduced by AMPK while being amplified by HIF-1 when animals are stimulated to have higher ROS levels. Thus, balancing ROS at optimal levels appears to be crucial for organismal health and longevity.</P><P>Mild inhibition of mitochondrial respiration extends the lifespan of many species. In <I>Caenorhabditis elegans</I>, reactive oxygen species (ROS) promote longevity by activating hypoxia-inducible factor 1 (HIF-1) in response to reduced mitochondrial respiration. However, the physiological role and mechanism of ROS-induced longevity are poorly understood. Here, we show that a modest increase in ROS increases the immunity and lifespan of <I>C</I>. <I>elegans</I> through feedback regulation by HIF-1 and AMP-activated protein kinase (AMPK). We found that activation of AMPK as well as HIF-1 mediates the longevity response to ROS. We further showed that AMPK reduces internal levels of ROS, whereas HIF-1 amplifies the levels of internal ROS under conditions that increase ROS. Moreover, mitochondrial ROS increase resistance to various pathogenic bacteria, suggesting a possible association between immunity and long lifespan. Thus, AMPK and HIF-1 may control immunity and longevity tightly by acting as feedback regulators of ROS.</P>
Dursun Aras,Ozcan Ozeke,Serkan Cay,Firat Ozcan,Kazım Baser,Umuttan Dogan,Murat Unlu,Burcu Demirkan,Omac Tufekcioglu,Serkan Topaloglu 한국심초음파학회 2015 Journal of Cardiovascular Imaging (J Cardiovasc Im Vol.23 No.3
The clinical diagnosis of right ventricular (RV) cardiomyopathies is often challenging. It is difficult to differentiate the isolatedleft ventricular (LV) noncompaction cardiomyopathy (NC) from biventricular NC or from coexisting arrhythmogenic ventricularcardiomyopathy (AC). There are currently few established morphologic criteria for the diagnosis other than RV dilation andpresence of excessive regional trabeculation. The gross and microscopic changes suggest pathological similarities between, orcoexistence of, RV-NC and AC. Therefore, the term arrhythmogenic right ventricular cardiomyopathy is somewhat misleading asisolated LV or biventricular involvement may be present and thus a broader term such as AC should be preferred. We describe anunusual case of AC associated with a NC in a 27-year-old man who had a history of permanent pacemaker 7 years ago due tosecond-degree atrioventricular block.
Some notes on compact sets in soft metric spaces
Cigdem Gunduz Aras,Murat Ibrahim Yazar,Sadi Bayramov 원광대학교 기초자연과학연구소 2017 ANNALS OF FUZZY MATHEMATICS AND INFORMATICS Vol.14 No.4
The first aim of this study is to define soft sequential compact metric spaces and to investigate some important theorems on soft sequential compact metric space. Second is to introduce $\tilde{\varepsilon}-$net and totally bounded soft metric space and study properties of this space. Third is to define Lebesque number for soft sets and soft uniformly continuous mapping and investigate some theorems in detail.
Mitochondrial chaperone HSP ‐60 regulates anti‐bacterial immunity via p38 MAP kinase signaling
Jeong, Dae‐,Eun,Lee, Dongyeop,Hwang, Sun‐,Young,Lee, Yujin,Lee, Jee‐,Eun,Seo, Mihwa,Hwang, Wooseon,Seo, Keunhee,Hwang, Ara B,Artan, Murat,Son, Heehwa G,Jo, Jay‐,Hyun,Baek, Haes Published for the European Molecular Biology Organ 2017 The EMBO journal Vol.36 No.8
<P>Mitochondria play key roles in cellular immunity. How mitochondria contribute to organismal immunity remains poorly understood. Here, we show that HSP-60/HSPD1, a major mitochondrial chaperone, boosts anti-bacterial immunity through the up-regulation of p38 MAP kinase signaling. We first identify 16 evolutionarily conserved mitochondrial components that affect the immunity of Caenorhabditis elegans against pathogenic Pseudomonas aeruginosa (PA14). Among them, the mitochondrial chaperone HSP-60 is necessary and sufficient to increase resistance to PA14. We show that HSP-60 in the intestine and neurons is crucial for the resistance to PA14. We then find that p38 MAP kinase signaling, an evolutionarily conserved anti-bacterial immune pathway, is down-regulated by genetic inhibition of hsp-60, and up-regulated by increased expression of hsp-60. Overexpression of HSPD1, the mammalian ortholog of hsp-60, increases p38 MAP kinase activity in human cells, suggesting an evolutionarily conserved mechanism. Further, cytosol-localized HSP-60 physically binds and stabilizes SEK-1/MAP kinase kinase 3, which in turn up-regulates p38 MAP kinase and increases immunity. Our study suggests that mitochondrial chaperones protect host eukaryotes from pathogenic bacteria by up-regulating cytosolic p38 MAPK signaling.</P>