Infrastructure Engineering - Research Publications

Permanent URI for this collection

Search Results

Now showing 1 - 10 of 564
  • Item
    Thumbnail Image
    The carbon footprint of treating patients with septic shock in the intensive care unit
    McGain, F ; Burnham, J ; LAU, R ; Aye, L ; Kollef, MH ; McAlister, S (College of Intensive Care Medicine of Australia and New Zealand, 2018-12-01)
    OBJECTIVE: To use life cycle assessment to determine the environmental footprint of the care of patients with septic shock in the intensive care unit (ICU). DESIGN, SETTING AND PARTICIPANTS: Prospective, observational life cycle assessment examining the use of energy for heating, ventilation and air conditioning; lighting; machines; and all consumables and waste associated with treating ten patients with septic shock in the ICU at BarnesJewish Hospital, St. Louis, MO, United States (US-ICU) and ten patients at Footscray Hospital, Melbourne, Vic, Australia (Aus-ICU). MAIN OUTCOME MEASURES: Environmental footprint, particularly greenhouse gas emissions. RESULTS: Energy use per patient averaged 272 kWh/day for the US-ICU and 143 kWh/day for the Aus-ICU. The average daily amount of single-use materials per patient was 3.4 kg (range, 1.0-6.3 kg) for the US-ICU and 3.4 kg (range, 1.2-8.7 kg) for the Aus-ICU. The average daily particularly greenhouse gas emissions arising from treating patients in the US-ICU was 178 kg carbon dioxide equivalent (CO2-e) emissions (range, 165-228 kg CO2-e), while for the Aus-ICU the carbon footprint was 88 kg CO2-e (range, 77-107 kg CO2-e). Energy accounted for 155 kg CO2-e in the US-ICU (87%) and 67 kg CO2-e in the Aus-ICU (76%). The daily treatment of one patient with septic shock in the US-ICU was equivalent to the total daily carbon footprint of 3.5 Americans' CO2-e emissions, and for the Aus-ICU, it was equivalent to the emissions of 1.5 Australians. CONCLUSION: The carbon footprints of the ICUs were dominated by the energy use for heating, ventilation and air conditioning; consumables were relatively less important, with limited effect of intensity of patient care. There is large opportunity for reducing the ICUs' carbon footprint by improving the energy efficiency of buildings and increasing the use of renewable energy sources.
  • Item
    No Preview Available
    Editorial
    Tse, N ; Rajkowski, R (Informa UK Limited, 2015-06-01)
  • Item
    Thumbnail Image
    A Novel Approach for 3D Modeling and Geovisualization of Easement Rights in Apartments
    Emamgholian, S ; Taleai, M ; Shojaei, D (CMV Verlag, 2018-12-01)
  • Item
    Thumbnail Image
    Very early onset of amiodarone-induced pulmonary toxicity.
    Lee, W ; Ryu, DR ; Han, S-S ; Ryu, S-W ; Cho, BR ; Kwon, H ; Kim, BR (The Korean Society of Cardiology, 2013-10)
    Amiodarone is a widely used antiarrhythmic agent. Among its various adverse effects, amiodarone-induced pulmonary toxicity (APT) is the most life threatening complication, which has been described mostly in patients who have been in treatment with high accumulative doses for a long duration of time. However, amiodarone therapy in short-term duration induced APT was rarely reported. We describe a case of a 54-year-old man who is presented with symptoms of APT after a few days of therapy for post-myocardial infarction ventricular tachycardia. For early diagnosis and successful treatment, awareness and high suspicion of this rare type of early onset APT is crucial in patients with amiodarone therapy.
  • Item
    Thumbnail Image
    Endoplasmic reticulum stress promotes LIPIN2-dependent hepatic insulin resistance.
    Ryu, D ; Seo, W-Y ; Yoon, Y-S ; Kim, Y-N ; Kim, SS ; Kim, H-J ; Park, T-S ; Choi, CS ; Koo, S-H (American Diabetes Association, 2011-04)
    OBJECTIVE: Diet-induced obesity (DIO) is linked to peripheral insulin resistance-a major predicament in type 2 diabetes. This study aims to identify the molecular mechanism by which DIO-triggered endoplasmic reticulum (ER) stress promotes hepatic insulin resistance in mouse models. RESEARCH DESIGN AND METHODS: C57BL/6 mice and primary hepatocytes were used to evaluate the role of LIPIN2 in ER stress-induced hepatic insulin resistance. Tunicamycin, thapsigargin, and lipopolysaccharide were used to invoke acute ER stress conditions. To promote chronic ER stress, mice were fed with a high-fat diet for 8-12 weeks. To verify the role of LIPIN2 in hepatic insulin signaling, adenoviruses expressing wild-type or mutant LIPIN2, and shRNA for LIPIN2 were used in animal studies. Plasma glucose, insulin levels as well as hepatic free fatty acids, diacylglycerol (DAG), and triacylglycerol were assessed. Additionally, glucose tolerance, insulin tolerance, and pyruvate tolerance tests were performed to evaluate the metabolic phenotype of these mice. RESULTS: LIPIN2 expression was enhanced in mouse livers by acute ER stress-inducers or by high-fat feeding. Transcriptional activation of LIPIN2 by ER stress is mediated by activating transcription factor 4, as demonstrated by LIPIN2 promoter assays, Western blot analyses, and chromatin immunoprecipitation assays. Knockdown of hepatic LIPIN2 in DIO mice reduced fasting hyperglycemia and improved hepatic insulin signaling. Conversely, overexpression of LIPIN2 impaired hepatic insulin signaling in a phosphatidic acid phosphatase activity-dependent manner. CONCLUSIONS: These results demonstrate that ER stress-induced LIPIN2 would contribute to the perturbation of hepatic insulin signaling via a DAG-protein kinase C ε-dependent manner in DIO mice.
  • Item
    Thumbnail Image
    Growth differentiation factor 15 is a myomitokine governing systemic energy homeostasis.
    Chung, HK ; Ryu, D ; Kim, KS ; Chang, JY ; Kim, YK ; Yi, H-S ; Kang, SG ; Choi, MJ ; Lee, SE ; Jung, S-B ; Ryu, MJ ; Kim, SJ ; Kweon, GR ; Kim, H ; Hwang, JH ; Lee, C-H ; Lee, S-J ; Wall, CE ; Downes, M ; Evans, RM ; Auwerx, J ; Shong, M (Rockefeller University Press, 2017-01-02)
    Reduced mitochondrial electron transport chain activity promotes longevity and improves energy homeostasis via cell-autonomous and -non-autonomous factors in multiple model systems. This mitohormetic effect is thought to involve the mitochondrial unfolded protein response (UPRmt), an adaptive stress-response pathway activated by mitochondrial proteotoxic stress. Using mice with skeletal muscle-specific deficiency of Crif1 (muscle-specific knockout [MKO]), an integral protein of the large mitoribosomal subunit (39S), we identified growth differentiation factor 15 (GDF15) as a UPRmt-associated cell-non-autonomous myomitokine that regulates systemic energy homeostasis. MKO mice were protected against obesity and sensitized to insulin, an effect associated with elevated GDF15 secretion after UPRmt activation. In ob/ob mice, administration of recombinant GDF15 decreased body weight and improved insulin sensitivity, which was attributed to elevated oxidative metabolism and lipid mobilization in the liver, muscle, and adipose tissue. Thus, GDF15 is a potent mitohormetic signal that safeguards against the onset of obesity and insulin resistance.
  • Item
    Thumbnail Image
    Loss of Sirt1 function improves intestinal anti-bacterial defense and protects from colitis-induced colorectal cancer.
    Lo Sasso, G ; Ryu, D ; Mouchiroud, L ; Fernando, SC ; Anderson, CL ; Katsyuba, E ; Piersigilli, A ; Hottiger, MO ; Schoonjans, K ; Auwerx, J ; Papa, S (Public Library of Science (PLoS), 2014)
    Dysfunction of Paneth and goblet cells in the intestine contributes to inflammatory bowel disease (IBD) and colitis-associated colorectal cancer (CAC). Here, we report a role for the NAD+-dependent histone deacetylase SIRT1 in the control of anti-bacterial defense. Mice with an intestinal specific Sirt1 deficiency (Sirt1int-/-) have more Paneth and goblet cells with a consequent rearrangement of the gut microbiota. From a mechanistic point of view, the effects on mouse intestinal cell maturation are mediated by SIRT1-dependent changes in the acetylation status of SPDEF, a master regulator of Paneth and goblet cells. Our results suggest that targeting SIRT1 may be of interest in the management of IBD and CAC.
  • Item
    Thumbnail Image
    Antibiotic use and abuse: a threat to mitochondria and chloroplasts with impact on research, health, and environment.
    Wang, X ; Ryu, D ; Houtkooper, RH ; Auwerx, J (Wiley, 2015-10)
    Recently, several studies have demonstrated that tetracyclines, the antibiotics most intensively used in livestock and that are also widely applied in biomedical research, interrupt mitochondrial proteostasis and physiology in animals ranging from round worms, fruit flies, and mice to human cell lines. Importantly, plant chloroplasts, like their mitochondria, are also under certain conditions vulnerable to these and other antibiotics that are leached into our environment. Together these endosymbiotic organelles are not only essential for cellular and organismal homeostasis stricto sensu, but also have an important role to play in the sustainability of our ecosystem as they maintain the delicate balance between autotrophs and heterotrophs, which fix and utilize energy, respectively. Therefore, stricter policies on antibiotic usage are absolutely required as their use in research confounds experimental outcomes, and their uncontrolled applications in medicine and agriculture pose a significant threat to a balanced ecosystem and the well-being of these endosymbionts that are essential to sustain health.
  • Item
    Thumbnail Image
    Eliciting the mitochondrial unfolded protein response by nicotinamide adenine dinucleotide repletion reverses fatty liver disease in mice.
    Gariani, K ; Menzies, KJ ; Ryu, D ; Wegner, CJ ; Wang, X ; Ropelle, ER ; Moullan, N ; Zhang, H ; Perino, A ; Lemos, V ; Kim, B ; Park, Y-K ; Piersigilli, A ; Pham, TX ; Yang, Y ; Ku, CS ; Koo, SI ; Fomitchova, A ; Cantó, C ; Schoonjans, K ; Sauve, AA ; Lee, J-Y ; Auwerx, J (Ovid Technologies (Wolters Kluwer Health), 2016-04)
    UNLABELLED: With no approved pharmacological treatment, nonalcoholic fatty liver disease (NAFLD) is now the most common cause of chronic liver disease in Western countries and its worldwide prevalence continues to increase along with the growing obesity epidemic. Here, we show that a high-fat high-sucrose (HFHS) diet, eliciting chronic hepatosteatosis resembling human fatty liver, lowers hepatic nicotinamide adenine dinucleotide (NAD(+) ) levels driving reductions in hepatic mitochondrial content, function, and adenosine triphosphate (ATP) levels, in conjunction with robust increases in hepatic weight, lipid content, and peroxidation in C57BL/6J mice. To assess the effect of NAD(+) repletion on the development of steatosis in mice, nicotinamide riboside, a precursor of NAD(+) biosynthesis, was added to the HFHS diet, either as a preventive strategy or as a therapeutic intervention. We demonstrate that NR prevents and reverts NAFLD by inducing a sirtuin (SIRT)1- and SIRT3-dependent mitochondrial unfolded protein response, triggering an adaptive mitohormetic pathway to increase hepatic β-oxidation and mitochondrial complex content and activity. The cell-autonomous beneficial component of NR treatment was revealed in liver-specific Sirt1 knockout mice (Sirt1(hep-/-) ), whereas apolipoprotein E-deficient mice (Apoe(-/-) ) challenged with a high-fat high-cholesterol diet affirmed the use of NR in other independent models of NAFLD. CONCLUSION: Our data warrant the future evaluation of NAD(+) boosting strategies to manage the development or progression of NAFLD.
  • Item
    Thumbnail Image
    Cancer-Associated Fibroblasts and Desmoplastic Reactions Related to Cancer Invasiveness in Patients With Colorectal Cancer.
    Shin, N ; Son, GM ; Shin, D-H ; Kwon, M-S ; Park, B-S ; Kim, H-S ; Ryu, D ; Kang, C-D (Korean Society of Coloproctology, 2019-02)
    PURPOSE: We evaluated the relationship of cancer-associated fibroblasts (CAFs) and desmoplastic reactions with cancer invasiveness and long-term outcomes in patients with colorectal cancer (CRC). METHODS: Histologic evaluation of mature CAFs and desmoplasia was performed by observing the collagen fiber structure and fibroblast cytomorphology in the intratumoral stroma and invasive front of CRC tissues. Cancer-cell invasiveness was evaluated using lymphatic invasion, vascular invasion, perineural invasion, tumor budding, and tumor growth patterns. Overall survival and systemic recurrence were analyzed. A network analysis was performed between CAF maturation, desmoplastic reaction, and cancer invasiveness. RESULTS: The proportions of mature CAFs in the intratumoral stroma and the invasive front were 57.6% and 60.3%, respectively. Epidermal growth factor receptor (EGFR) overexpression was significantly higher in the mature CAFs in the invasive front as compared to immature CAFs. Lymphatic invasion increased as the number of mature fibroblasts in the intratumoral stroma increased. Tumor budding was observed in almost half of both mature and immature stroma samples and occurred more frequently in infiltrating tumors. On network analysis, well-connected islands were identified that was associated with EGFR overexpression, CAF maturation, and infiltrating tumor growth patterns leading to tumor budding. CONCLUSION: The maturity of CAFs and desmoplastic reactions were associated with cancer invasion. However, the cytomorphologic characteristics of CAFs were insufficient as an independent prognostic factor for patients with CRC.