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건축물 건설단계에서의 에너지소비량 및 CO₂배출량 원단위 산출
김종엽,이승언,손장열 대한건축학회 2004 대한건축학회논문집 Vol.20 No.10
The purpose of this study is to establish the database that could be applied to the building LCA Firstly, in this paper, the methodologies of building LCA and energy based I/O model for estimating embodied energy of building materials were examined Then, the intensity of energy consumption and CO₂ emission for building materials and construction stage were estimated The intensity database for building materials calculated by the I/O table published in 2000 was compared with the database by the I/O table published in 1995 According to the result of comparison, there were a little differences between the results calculated by the new and the previous data, and two results showed nearly the same patterns So, it could be said that the industrial activity change has little effect on the energy intensity of building materials during the past 5 years For the calculation of the energy intensity in the construction stages, the payment documents of an ad and electricity consumptions during construction for the sample buildings were surveyed and the intensity per a building gross area were calculated The database presented in this paper could be applied to the building LCA process as the basic data for analysing global worming effect caused by building construction
Jang, Jeon Yeob,Koh, Young Jun,Lee, Seung-Hun,Lee, Junyeop,Kim, Kyoo Hyun,Kim, Daesoo,Koh, Gou Young,Yoo, Ook Joon American Society of Hematology 2013 Blood Vol.122 No.13
<P>To unveil the organotypic role and vulnerability of lymphatic vessels, we generated a lymphatic vessel endothelial hyaluronan receptor-1 (LYVE-1)-Cre/iDTR double-transgenic mouse and ablated LYVE-1–expressing lymphatic vessels in adult mice in a diphtheria toxin (DT)–inducible manner based on selective expression of LYVE-1 in most lymphatic vessels. Strikingly, lymphatic vessels in the small intestine and lymph nodes were rapidly ablated, but lymphatic vessels in the other organs were relatively intact at 24 hours after DT administration. Unexpectedly, LYVE-1-Cre/iDTR mice died of sepsis without visible edema at 24 and 60 hours after DT administration. The cause of death appeared to be related to acute failure of immune surveillance systems in the small intestine and draining lymph nodes. Of note, acute loss of lymphatic lacteals in intestinal villi appeared to trigger distortion of blood capillaries and the whole architecture of the villi, whereas acute loss of lymphatic vessels in lymph nodes caused dysfunction of lymph drainage and abnormal distribution of dendritic cells and macrophages. Thus, intact lymphatic vessels are required for structural and functional maintenance of surrounding tissues in an organotypic manner, at least in the intestine and lymph nodes.</P>
Jang, Jeon Yeob,Choi, Sung Yong,Park, Intae,Park, Do Young,Choe, Kibaek,Kim, Pilhan,Kim, Young Keum,Lee, Byung‐,Joo,Hirashima, Masanori,Kubota, Yoshiaki,Park, Jeong‐,Won,Cheng, Sheueȁ John Wiley and Sons Inc. 2017 EMBO molecular medicine Vol.9 No.6
<P><B>Abstract</B></P><P>Thyroid gland vasculature has a distinguishable characteristic of endothelial fenestrae, a critical component for proper molecular transport. However, the signaling pathway that critically governs the maintenance of thyroid vascular integrity, including endothelial fenestrae, is poorly understood. Here, we found profound and distinct expression of follicular epithelial VEGF‐A and vascular VEGFR2 that were precisely regulated by circulating thyrotropin, while there were no meaningful expression of angiopoietin–Tie2 system in the thyroid gland. Our genetic depletion experiments revealed that VEGFR2, but not VEGFR3, is indispensable for maintenance of thyroid vascular integrity. Notably, blockade of VEGF‐A or VEGFR2 not only abrogated vascular remodeling but also inhibited follicular hypertrophy, which led to the reduction of thyroid weights during goitrogenesis. Importantly, VEGFR2 blockade alone was sufficient to cause a reduction of endothelial fenestrae with decreases in thyrotropin‐responsive genes in goitrogen‐fed thyroids. Collectively, these findings establish follicular VEGF‐A–vascular VEGFR2 axis as a main regulator for thyrotropin‐dependent thyroid angiofollicular remodeling and goitrogenesis.</P>
하부식도 괄약근과 식도 연동운동에 미치는 Nicotine의 효과
장영운 ( Jang Yeong Un ),나득영 ( Na Deug Yeong ),천호기 ( Cheon Ho Gi ),김구엽 ( Kim Gu Yeob ),김효종 ( Kim Hyo Jong ),김병호 ( Kim Byeong Ho ),이정일 ( Lee Jeong Il ),장린 ( Jang Lin ) 대한내과학회 1992 대한내과학회지 Vol.42 No.5
연구배경 : 흡연시 체내로 흡수되는 nicotine은 하부식도 괄약근압을 떨어뜨려 위식도 역류성 질환을 초래하는 것으로 알려져 있다. 지금까지는 흡연가를 대상으로 담배를 피우게 하면서 흡연데 의한 즉각적인 효과와 수년간에 걸쳐 장기적인 효과를 담배를 피우지 못하는 비흡연가와 비교 관찰하는 데에는 어려움이 없었다. 저자등은 흡연가뿐만 아니라 담배를 피우지 못하는 비흡연가에게 담배대신 nicotine gum을 씹게하여 하부식도 괄약근과 식도 연동운동에 미치는 nicotine의 즉각적인 효과와 장기적인 효과를 함께 알아보았다. 방법 : 양군 모두에게 2㎎의 nicotine이 함유된 nicotine gum 1개를 15분간에 걸쳐 천천히 씹게 하였다. 식도내압검사는 nicotine 투여전과, 투여 25분후, 그리고 35분후의 각각의 하부식도 괄약근압과 하부식도의 연동운동을 triple lumen catheter와 pneumohy-draulic capillary infusion system을 이용하여 측정하였다. 결과 : 흡연군에서 하부식도 괄약근압의 기저치가 29.3±6.52㎜Hg에서 nicotine 투여 25분 후에는 23.6±7.23㎜Hg, 35분후에는 24.4±4.97㎜Hg으로 각각 통계적인 유의성은 없었지만 감소가 있었다(p<0.001). 비흡연군에서도 하부식도 괄약근압의 기저치는 26.6±5.44㎜Hg이었지만, 25분후에 20.0±4.40㎜Hg, 35분후에 18.5±4.95㎜Hg로 각각 유의한 감소가 관찰되었다(p<0.001, p<0.005). 따라서 nico-tine의 즉각적인 효과는 양군 모두에서 괄약근압의 감소를 유도하였으며, 이러한 효과는 비흡연군에서 더욱 뚜렷하였다. 그러나 흡연군이 nicotine에 전혀 노출되니 않았던 비흡연군에 비하여 괄약근압의 기저치가 예상과는 달리 낮지 않았고, 양군 모두 정상범위내에 있었다. 하부식도에서 측정한 nicotine 투여전의 연동파의 진폭도 양군에서 유사한 소견을 보였으며, niocitine 투여에 의해서도 영향을 받지 않았다. 결론 : 만성적인 흡연과 위식도 역류성 질환과의 상호연관 관계는 아직까지 확실치 않을 것으로 생각된다. Background : Cigarette smoking has been reported to cause a reduction in the lower esophageal sphincter (LES) pressure, which may predispose to gastroesophageal reflux and esophagitis. The inhibitory effect of smoking on the LES, like many other acute effects of smoking, may due to its nicotine content. Most investigators have studied the acute effect, but not the chronic effect, of smoking on the LES. We studied both acute and chronic effects of 2 ㎎ nicotine in a chewing gum on the LES and esophageal peristaltic motility in 20 healthy volunteers, 10 smokers and 10 nonsmokers. Methods : Parameters measured by pneumohy-draulic capillary infusion system were LES pressure and esophageal peristaltic amplitude. We obtained manometric readings before nicotine ingestion after 25 minutes, and after 35 minutes. Results: The mean basal LES pressure of smokers was 29.3±6.52㎜Hg, 23.6±7.23㎜Hg after 25 minutes, and 24.4±4.97㎜Hg after 35 minutes. In nonsmokers, the mean basal LES pressure was 26.6±5.44 ㎜Hg, 20.0+ 4.40 ㎜Hg after 25 minutes, and 18.5±4.95 ㎜Hg after 35 minutes. Acute effect of nicotine reduced LES pressure in both smokers and nonsmokers, but the effect was greater in nonsmokers. Unexpectedly, the mean basal LES pressure of smokers was not lower than that of nonsmokers. And, there was no significant difference in the mean basal esophageal peristaltic amplitude between both groups. Therefore, chronic effect of nicotine did not decrease basal LES pressure and peristaltic amplitude. And the peristaltic amplitude was not influenced by nicotine ingestion in both groups. Conclusions : The relationship between chronic nicotinic effect and gastroesophageal reflux disease is not certain.
Mice 소장의 Cajal 세포에서 기록되는 향도잡이 전류의 특성
장성종 ( Jang Seong Jong ),조은택 ( Jo Eun Taeg ),허광식 ( Heo Gwang Sig ),박찬국 ( Park Chan Gug ),김만우 ( Kim Man U ),장인엽 ( Jang In Yeob ),신무경 ( Sin Mu Gyeong ),차경훈 ( Cha Gyeong Hun ),염철호 ( Yeom Cheol Ho ),전제열 ( 대한소화기학회 2003 대한소화기학회지 Vol.42 No.2
Background/Aims: Gastrointestinal motility is initiated by the periodic generation of slow waves. Interstitial cells of Cajal (ICC) are pacemaker cells that generate slow waves and drive spontaneous mechanical contractions of the gastrointestinal smooth muscle. Slow waves generate the periodic activation of spontaneous inward currents (pacemaker currents). The aim of this study was to investigate the characterization of pacemaker currents of ICC. Methods: The ICC in mice small intestine were cultured with stem cell factor for 2 days, and then we recorded pacemaker currents and slow waves using a whole-cell patch clamp technique. Results: Under voltage clamp at -80 mV of holding potential, ICC generated pacemaker currents. Tetrodotoxin and nifedipine did not affect on the pacemaker currents. In addition, tetraethylammonium, 4-aminopyridine and glibenclamide did not affect on the pacemaker currents. The reduction of external Na+ concentrations inhibited pacemaker currents. Moreover, these currents were completely abolished in the external Ca2+-free condition. Gadolinium and flufenamic acid, inhibitors of non-selective cationic currents, inhibited pacemaker currents. Thapsigargin and cyclopiazoic acid, inhibitors of Ca2+-ATPase in endoplasmic reticulum, abolished pacemaker currents. Carbachol depolarized membrane potential and increased inward currents. Conclusions: These results suggest that pacemaker currents are mediated by the activation of non-selective cation channel and become a target of neurotransmitters in regulation of intestinal motility. (Korean J Gastroenterol 2003;42:121-127)