The Oak Ridge Refrigerant Management Program

For many years, chlorofluorocarbons (CFC's) have been used by the Department of Energy's (DOE) Oak Ridge Y-12 Plant in air conditioning and process refrigeration systems. However, Title 6 of the Clean Air Act Amendments (CAAA) and Executive Order 12843 (Procurement Requirements and Policies for Federal Agencies for Ozone Depleting Substances) signed by President Clinton require, as policy, that all federal agencies maximize their use of safe, alternate refrigerants and minimize, where economically practical, the use of Class 1 refrigerants. Unfortunately, many government facilities and industrial plants have no plan or strategy in place to make this changeover, even though their air conditioning and process refrigeration equipment may not be sustainable after CFC production ends December 31, 1995. The Y-12 Plant in Oak Ridge, Tennessee, has taken an aggressive approach to complying with the CAAA and is working with private industry and other government agencies to solve tough manufacturing and application problems associated with CFC and hydrochlorofluorocarbon (HCFC) alternatives. Y-12 was the first DOE Defense Program (DP) facility to develop a long-range Stratospheric Ozone Protection Plan for refrigerant management for compliance with the CAAA. It was also the first DOE DP facility to complete detailed engineering studies on retrofitting and replacing all air conditioning and process refrigeration equipment to enable operation with alternate refrigerants. The management plan and engineering studies are models for use by other government agencies, manufacturing plants, and private industry. This presentation identifies some of the hidden pitfalls to be encountered in the accelerated phaseout schedule of CFC's and explains how to overcome and prevent these problems. In addition, it outlines the general issues that must be considered when addressing the phase-out of ozone depleting substances and gives some 'lessons learned' by Y-12 from its Refrigerant Management Program. Discussion topics include requirements for developing a refrigerant management plan and establishing priorities for cost-effective compliance with the CAAA, as well as ways in which employees can be empowered to develop a comprehensive refrigerant management plan. The result of this employee empowerment was a cooperative labor-management effort that is beneficial for Y-12, DOE, and the environment

Endothelial Dysfunction and Diabetes: Effects on Angiogenesis, Vascular Remodeling, and Wound Healing

Diabetes mellitus (DM) is a chronic metabolic disorder characterized by inappropriate hyperglycemia due to lack of or resistance to insulin. Patients with DM are frequently afflicted with ischemic vascular disease or wound healing defect. It is well known that type 2 DM causes amplification of the atherosclerotic process, endothelial cell dysfunction, glycosylation of extracellular matrix proteins, and vascular denervation. These complications ultimately lead to impairment of neovascularization and diabetic wound healing. Therapeutic angiogenesis remains an attractive treatment modality for chronic ischemic disorders including PAD and/or diabetic wound healing. Many experimental studies have identified better approaches for diabetic cardiovascular complications, however, successful clinical translation has been limited possibly due to the narrow therapeutic targets of these agents or the lack of rigorous evaluation of pathology and therapeutic mechanisms in experimental models of disease. This paper discusses the current body of evidence identifying endothelial dysfunction and impaired angiogenesis during diabetes

Regulation and Maintenance of Vascular Tone and Patency in Cardiovascular Health and Disease

License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Despite numerous advances in health care practices, cardiovascular disease still remains the leading cause of morbidity and mortality worldwide. Perhaps the most important consequence of cardiovascular disease is the interruption of blood flow to organs such as the heart and brain, resulting in the clinical presentation of a heart attack or stroke. As such, the regulation of vascular tone and the maintenance of vascular patency are vital for the preservation of cardiovascular health. Central to this process is the vascular endothelium. The endothelium is vital for the regulation of vascular tone and the maintenance of vascular homeostasis, as it releases factors such as nitric oxide, hydrogen sulfide, endothelialdependent hyperpolarizing factor, and prostacyclin tha

Photoluminescence Study of Up-Conversion Phosphor La2(MoO4)3 Yb3+, Er3+ Prepared by Precipitation Method

Up-conversion phosphors of La2(MoO4)3: Yb3+, Er3+ with different concentration of Erbium were prepared by a simple precipitation method. The crystal structure, surface morphology, elemental composition, and photoluminescence properties were characterized by X-ray powder diffraction (XRD), Scanning electron microscopy (SEM), Energy-dispersive X-ray Spectroscopy (EDAX) and Photoluminescence spectroscopy respectively. XRD spectra show a high degree of crystallinity in all samples. SEM images show rod-like structures present in the samples. EDAX analysis confirms the presence of dopants (Yb3+ and Er3+) in the host matrix (La2(MoO4)3). Upon excitation by 980 nm infrared radiation, all the samples give emission peaks between 524 – 533 nm in the bluish-green region, 546 – 555 nm in the green region and 659 – 672 nm in the red region which are attributed to the 2H11/2 → 4I15/2, 4S3/2 → 4I15/2 and 4F9/2 → 4I15/2 transitions of Er3+ ions respectively

Cardiac-Specific Inactivation of LPP3 in Mice Leads to Myocardial Dysfunction and Heart Failure

Lipid Phosphate phosphatase 3 (LPP3), encoded by the Plpp3 gene, is an enzyme that dephosphorylates the bioactive lipid mediator lysophosphatidic acid (LPA). To study the role of LPP3 in the myocardium, we generated a cardiac specific Plpp3 deficient mouse strain. Although these mice were viable at birth in contrast to global Plpp3 knockout mice, they showed increased mortality ~ 8 months. LPP3 deficient mice had enlarged hearts with reduced left ventricular performance as seen by echocardiography. Cardiac specific Plpp3 deficient mice had longer ventricular effective refractory periods compared to their Plpp3 littermates. We observed that lack of Lpp3 enhanced cardiomyocyte hypertrophy based on analysis of cell surface area. We found that lack of Lpp3 signaling was mediated through the activation of Rho and phospho-ERK pathways. There are increased levels of fetal genes Natriuretic Peptide A and B (Nppa and Nppb) expression indicating myocardial dysfunction. These mice also demonstrate mitochondrial dysfunction as evidenced by a significant decrease (P \u3c 0.001) in the basal oxygen consumption rate, mitochondrial ATP production, and spare respiratory capacity as measured through mitochondrial bioenergetics. Histology and transmission electron microscopy of these hearts showed disrupted sarcomere organization and intercalated disc, with a prominent disruption of the cristae and vacuole formation in the mitochondria. Our findings suggest that LPA/LPP3-signaling nexus plays an important role in normal function of cardiomyocytes

Investigating cortisol excess or deficiency: a practical approach.

'No abstract

Cystathionine γ-lyase regulates arteriogenesis through NO-dependent monocyte recruitment

AIMS: Hydrogen sulfide (H2S) is a vasoactive gasotransmitter that is endogenously produced in the vasculature by the enzyme cystathionine γ-lyase (CSE). However, the importance of CSE activity and local H2S generation for ischaemic vascular remodelling remains completely unknown. In this study, we examine the hypothesis that CSE critically regulates ischaemic vascular remodelling involving H2S-dependent mononuclear cell regulation of arteriogenesis. METHODS AND RESULTS: Arteriogenesis including mature vessel density, collateral formation, blood flow, and SPY angiographic blush rate were determined in wild-type (WT) and CSE knockout (KO) mice at different time points following femoral artery ligation (FAL). The role of endogenous H2S in regulation of IL-16 expression and subsequent recruitment of monocytes, and expression of VEGF and bFGF in ischaemic tissues, were determined along with endothelial progenitor cell (CD34/Flk1) formation and function. FAL of WT mice significantly increased CSE activity, expression and endogenous H2S generation in ischaemic tissues, and monocyte infiltration, which was absent in CSE-deficient mice. Treatment of CSE KO mice with the polysulfide donor diallyl trisulfide restored ischaemic vascular remodelling, monocyte infiltration, and cytokine expression. Importantly, exogenous H2S therapy restored nitric oxide (NO) bioavailability in CSE KO mice that was responsible for monocyte recruitment and arteriogenesis. CONCLUSION: Endogenous CSE/H2S regulates ischaemic vascular remodelling mediated during hind limb ischaemia through NO-dependent monocyte recruitment and cytokine induction revealing a previously unknown mechanism of arteriogenesis