2 research outputs found
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Eliminating Medical Waste Liabilities Through Mobile Maceration and Disinfection
Commercial medical waste treatment technologies include incineration, melting, autoclaving, and chemical disinfection. Incineration disinfects, destroys the original nature of medical waste, and reduces the waste volume by converting organic waste content to carbon dioxide and water, leaving only residual inorganic ash. However, medical waste incinerator numbers have plummeted from almost 2,400 in 1995 to 115 in 2003 and to about 62 in 2005, due to negative public perception and escalating compliance costs associated with increasingly strict regulations. High-temperature electric melters have been designed and marketed as incinerator alternatives, but they are also costly and generally must comply with the same incinerator emissions regulations and permitting requirements. Autoclave processes disinfect medical waste at much lower operating temperatures than incinerators operate at, but are sometimes subject to limitations such as waste segregration requirements to be effective. Med-Shred, Inc. has developed a patented mobile shredding and chemical disinfecting process for on-site medical waste treatment. Medical waste is treated on-site at customer facilities by shredding and disinfecting the waste. The treated waste can then be transported in compliance with Health Insurance Portability and Accountability Act of 1996 (HIPAA) requirements to a landfill for disposal as solid municipal waste. A team of Idaho National Laboratory engineers evaluated the treatment process design. The process effectiveness has been demonstrated in mycobacterium tests performed by Analytical Services Incorporated. A process description and the technical and performance evaluation results are presented in the paper. A treatment demonstration and microbiological disinfecting tests show that the processor functions as it was intended
Soluble CD44 Interacts with Intermediate Filament Protein Vimentin on Endothelial Cell Surface
CD44 is a cell surface glycoprotein that functions as hyaluronan receptor. Mouse and human serum contain substantial amounts of soluble CD44, generated either by shedding or alternative splicing. During inflammation and in cancer patients serum levels of soluble CD44 are significantly increased. Experimentally, soluble CD44 overexpression blocks cancer cell adhesion to HA. We have previously found that recombinant CD44 hyaluronan binding domain (CD44HABD) and its non-HA-binding mutant inhibited tumor xenograft growth, angiogenesis, and endothelial cell proliferation. These data suggested an additional target other than HA for CD44HABD. By using non-HA-binding CD44HABD Arg41Ala, Arg78Ser, and Tyr79Ser-triple mutant (CD443MUT) we have identified intermediate filament protein vimentin as a novel interaction partner of CD44. We found that vimentin is expressed on the cell surface of human umbilical vein endothelial cells (HUVEC). Endogenous CD44 and vimentin coprecipitate from HUVECs, and when overexpressed in vimentin-negative MCF-7 cells. By using deletion mutants, we found that CD44HABD and CD443MUT bind vimentin N-terminal head domain. CD443MUT binds vimentin in solution with a Kd in range of 12–37 nM, and immobilised vimentin with Kd of 74 nM. CD443MUT binds to HUVEC and recombinant vimentin displaces CD443MUT from its binding sites. CD44HABD and CD443MUT were internalized by wild-type endothelial cells, but not by lung endothelial cells isolated from vimentin knock-out mice. Together, these data suggest that vimentin provides a specific binding site for soluble CD44 on endothelial cells