방음용 실란트를 이용한 틈새 소음 저감에 대한 연구

학위논문(석사) -- 서울대학교대학원 : 공과대학 기계공학부, 2023. 2. 강연준.Lightweight walls can be easily installed for the purpose of separating spaces and blocking noise indoors. These walls are non-bearing walls, —since these structures are installed in addition to the existing structures. Joint sections between old and new structures form apertures. These apertures, which include floors, ceilings, windows, and doors, —hinder soundproofing and fireproofing performance. These defects are reduced by filling these apertures with sealants. Among the sealants, an acoustic sealant serves to block generated noise in this manner. This study conducts a theoretical analysis of acoustic transmission according to the presence or absence of an acoustic sealant for apertures in lightweight walls. Also, it verifies the validity of the theory by measuring transmission loss using the sound intensity technique. The theory uses a Mechel prediction model rather than Gomperts and Kiliman, which have been primarily employed in earlier studies. The proposed model has very good agreement with the measurement value, with a difference of less than 2dB. The theory is restricted when the transmission coefficients of partition and sealant are not significantly different. However, the slit with an acoustic sealant represents an equivalent sound reduction effect, —which is a wall without a slit.실내에 공간을 구분하고 소음을 차단하는 목적으로 쉽게 설치가능한 것이 경량 벽체이다. 경량 벽체는 비내력벽으로 기존 구조물과 별도로 구조물을 설치되기 때문에 접합부에 틈새가 생기기 마련이다. 이 틈새는 천정과 바닥 또는 창문, 문 등이 해당되며, 이 틈새는 방음과 방화성능에 방해가 되기 때문에 실란트 시공을 통해 틈새를 메우게 된다. 실란트 중 방음용 실란트는 벽 틈새를 채워 인접한 공간 상에서 발생하는 소음을 차단하는 역할을 한다. 본 연구는 경량 벽체 상 틈새 소음에 대해서 실란트 유무에 따라 음향 투과를 이론적 분석을 목적으로 실시하였고, Sound intensity technique을 이용한 투과손실 측정을 통해 이론의 타당성을 검증하였다. 이전 연구부터 이론적 모델로 주로 사용되었던 Gomperts와 Kiliman의 예측 모델이 아닌 Mechel의 예측 모델을 활용하였고, 실험결과와 비교하여 어느 모델이 더욱 타당한지도 확인하였다. 중 · 고주파수 대역에서 Mechel의 예측모델이 측정결과에 근접하였고, 이 모델을 통해 측정결과 대비 2dB 이내의 근접한 결과를 예측하였다. 반면, 이론적 모델에서는 벽과 실란트 투과계수가 현저히 차이가 나지 않는다면 투과손실이 예측이 제한되는 점이 식별되었지만 실란트로 틈새를 채웠을 때 틈새가 없는 벽과 유사한 방음성능을 발휘한다는 것을 알 수 있었다.Chapter 1. INTRODUCTION 1 Chapter 2. THEORY 3 2.1 Theoretical model for sound transmission 3 2.2 Theoretical model for a slit 6 Chapter 3. EXPERIMENT 13 3.1 Experimental arrangement 13 3.2 Experimental results 17 Chapter 4. RESULTS AND DISSCUSSION 20 Chpater 5. CONCLUSIONS 23 REFERENCES 24 ABSTRACT IN KOREAN 26석

Protective Effects of Lithospermic Acid B on Diabetic Nephropathy in OLETF Rats Comparing with Amlodipine and Losartan

BACKGROUND: Lithospermic acid B (LAB), an active component isolated from Salvia miltiorrhizae, has been reported to have renoprotective effects in type 1 and type 2 diabetic animal models. We examined the effects of LAB on the prevention of diabetic nephropathy compared with amlodipine, a calcium channel blocker, and losartan, an angiotensin receptor blocker, in Otsuka Long-Evans-Tokushima Fatty (OLETF) rats, an animal model of type 2 diabetes. METHODS: LAB (20 mg/kg), amlodipine (10 mg/kg), or losartan (10 mg/kg) was given orally once daily to 10-week-old male OLETF rats for 28 weeks. RESULTS: None of LAB, losartan, and amlodipine exhibited effects on blood glucose levels. Treatment with amlodipine or losartan resulted in similar reductions in blood pressure; however, LAB was less effective in lowering blood pressure. Albuminuria was markedly suppressed by losartan and LAB, but not by amlodipine. LAB treatment decreased levels of renal lipid peroxidation, monocyte chemoattractant protein-1 (MCP-1), and transforming growth factor-beta1 (TGF-beta1). CONCLUSION: These results suggest that LAB has beneficial effects on the diabetic nephropathy in OLETF rats by decreasing oxidative stress and inflammation as potent as losartanope

Sorafenib acts synergistically in combination with radiotherapy without causing intestinal damage in colorectal cancer

Colorectal cancer; G2-M arrest; Gamma-radiation; Jejunum crypt; Radiosensitive effect; Sorafeni

Sirolimus inhibits platelet-derived growth factor-induced collagen synthesis in rat vascular smooth muscle cells

Vascular smooth muscle cell (VSMC) proliferation and extracellular matrix (ECM) accumulation play key roles in the development and the progression of vascular remodeling such as transplant arteriosclerosis and restenosis. The present study examined the effects of sirolimus (SRL) on platelet-derived growth factor (PDGF)-induced fibronectin secretion, collagen synthesis, and the related signaling pathways including reactive oxygen species (ROS) and mitogen-activated protein kinases (MAPK) in rat VSMCs. Primary rat VSMCs were isolated from male Sprague-Dawley rats. Growth arrested, synchronized cells were treated with various concentrations of SRL before the addition of PDGF at 10 ng/mL. Proliferating cell nuclear antigen expression, fibronectin secretion, and the activation of extracellular signal-regulated protein kinase (ERK) and p38 MAPK were assessed by Western blot analysis, collagen synthesis by [ 3H]-proline incorporation, and cellular ROS by flow cytometry. PDGF (10 ng/mL) increased VSMC proliferation by 1.7-fold, fibronectin secretion by 1.5-fold, collagen synthesis by 2.1-fold, cellular ROS by 1.6-fold, and activation of ERK and p38 MAPK by 3.3- and 3.9-fold compared to controls. SRL above 1 nmol/L inhibited PDGF-induced VSMC proliferation and collagen synthesis but not PDGF-induced fibronectin secretion, cellular ROS, and activation of ERK and p38 MAPK. These data demonstrated that PDGF increased ECM synthesis as well as proliferation through cellular ROS and subsequent MAPK activation and that SRL inhibited PDGF-induced VSMC proliferation and collagen synthesis in a cellular ROS- and MAPK activation-independent way. © 2005 by Elsevier Inc. All rights reserved

Radical approach to diabetic nephropathy

There is increasing evidence that reactive oxygen species (ROS) play a major role in the development of diabetic complications. Oxidative stress is increased in diabetes and in chronic kidney disease (CKD). High glucose upregulates transforming growth factor-β1 (TGF-β1) and angiotensin II (Ang II) in renal cells and high glucose, TGF-β1, and Ang II all generate and signal through ROS. ROS mediate high glucose-induced activation of protein kinase C and nuclear factor-κB in renal cells. Intensive glycemic control and inhibition of Ang II delay the onset and progression of diabetic nephropathy, in part, through antioxidant activity. Conventional and catalytic antioxidants were shown to prevent or delay the onset of diabetic nephropathy. Transketolase activators and poly (ADP-ribose) polymerase inhibitors were shown to block major biochemical pathways of hyperglycemic damage. Combination of strategies to prevent overproduction of ROS, to increase the removal of preformed ROS, and to block ROS-induced activation of biochemical pathways leading to cellular damage may prove to the effective in preventing the development and progression of CKD in diabetes. © 2007 International Society of Nephrology

Rapamycin inhibits platelet-derived growth factor-induced collagen, but not fibronectin, synthesis in rat mesangial cells

Rapamycin, a macrocyclic lactone, is effective in reducing the incidence of acute rejection after renal transplantation. The inhibitory effects of rapamycin on lymphocyte proliferation and the molecular mechanisms that were involved have been described. However, its effects on glomerular mesangial cells have not been clearly understood, and here, we examined the effect of rapamycin on platelet-derived growth factor (PDGF)-induced extracellular matrix synthesis as well as cell proliferation in mesangial cells. Rat mesangial cells were isolated from the glomeruli of Sprague-Dawley rats and cultured with Dulbecco's modified Eagles medium containing 20% fetal bovine serum. Different concentrations of rapamycin were administered 1 hour before the addition of 10ng/ml of PDGF into growth arrested and synchronized cells. Cell proliferation was assessed by [3H]thymidine incorporation, total collagen synthesis by [3H]proline incorporation, and fibronectin secretion into the medium by Western blot analysis. In the mesangial cells, PDGF increased cell proliferation by 4.6-fold, total collagen synthesis by 1.8-fold, and fibronectin secretion by 3.2-fold. Rapamycin above 10 nM significantly inhibited PDGF-induced proliferation and collagen synthesis, but the treatment of rapamycin up to 1 μM did not show any significant effects on PDGF-induced fibronectin secretion. These inhibitory effects of rapamycin on PDGF-induced mesangial cell proliferation and collagen synthesis reflect the potential value of rapamycin in the prevention and treatment of glomerulosclerosis in patients with chronic allograft nephropathy

Glucose-based peritoneal dialysis solution suppresses adiponectin synthesis through oxidative stress in an experimental model of peritoneal dialysis

Objective: Accumulation of visceral fat is one of the major risk factors for the development of cardiovascular disease in peritoneal dialysis (PD) patients. Adiponectin, an adipokine commonly regarded as a negative indicator of metabolic disease, is reported to be downregulated in its gene level in end-stage renal disease patients. Since excessive fat deposit is involved in increased reactive oxygen species (ROS), PD solution (PDS) may contribute to ROS production, resulting in dysregulation of adiponectin. In this study, we tested our hypothesis that oxidative stress induced by PDS may play a role in the regulation of adiponectin. Methods: Commercial PDS containing 3.86% glucose (20 - 30 mL) was administered to SD rats for 12 weeks with and without N-acetylcysteine (NAC; 10 mmol/L). ELISA was used to quantify adiponectin in plasma and spent dialysate. For in vitro studies, fully differentiated 3T3-L1 adipocytes and adipocytes isolated from abdominal fat were treated with a high glucose solution, PDS, and H 2O 2. Adiponectin levels in the conditioned media were measured by ELISA and immunoblot assays. The mRNA levels of adiponectin in mature adipocytes were examined using real-time RT-PCR. Results: The levels of adiponectin in plasma and spent dialysate were significantly downregulated by PDS and this effect was suppressed by NAC. In 3T3-L1 adipocytes, adiponectin secretion was inhibited by 50 mmol/L glucose, PDS diluted 2-fold, and H 2O 2 (200 μmol/L). In addition, H 2O 2 downregulated expression of adiponectin mRNA and secretion of adiponectin oligomer complexes. Conclusions: Our data suggest that ROS induced by con-ventional glucose-based PDS may contribute to pathophysi-ological changes in abdominal fat and downregulate adiponectin secreted from adipocytes during long-term PD. © 2012 International Society for Peritoneal Dialysis

Mycophenolic acid inhibits oleic acid-induced vascular smooth muscle cell activation by inhibiting cellular reactive oxygen species

BACKGROUND. Vascular smooth muscle cell (VSMC) proliferation and matrix protein accumulation play important roles in the development and progression of chronic allograft vasculopathy. Mycophenolic acid (MPA) inhibits various types of mesenchymal cell proliferation and cellular reactive oxygen species (ROS) are involved in the anti-proliferative effect of MPA. In this study, we investigated the effects of MPA on oleic acid (OA)-induced VSMC proliferation and the role of ROS in this process. METHODS. Primary VSMCs from Sprague-Dawley rats were stimulated with 100 μM OA, with or without MPA (0.1- 10 μM) or 5 mM N-acetylcysteine (NAC) for one hour prior to the addition of OA. Cell proliferation was measured by methylthiazoletetrazolium (MTT) assays, proliferating cell nuclear antigen (PCNA) expression, and fibronectin secretion by Western blot analysis, and dichlorofluorescein (DCF)-sensitive cellular ROS by fluorescence-activated cell scanning (FACS). RESULTS. OA (100 μM) increased cell proliferation, as measured by MTT (by 1.6-fold), PCNA expression, fibronectin secretion, and cellular ROS (by 1.6-fold). Treatment with MPA dose-dependently inhibited OA-induced VSMC proliferation, fibronectin secretion, and cellular ROS. Treatment with 5 mM NAC also inhibited OA-induced rat VSMC activation. CONCLUSIONS. These results suggest that MPA inhibits OA-induced VSMC proliferation and matrix protein synthesis partially by inhibiting cellular ROS. © 2007 Lippincott Williams & Wilkins, Inc

Kidney International: Introduction

[No abstract available