[A project to improve the "do not resuscitation" consent completeness rate for terminal cancer patients].

BACKGROUND: Signed do-not-resuscitate (DNR) consent is the essential first step for terminal cancer patients to choose palliative care and a quality marker of terminal care. DNR consent completeness helps deliver correct information, ensure consent legal validity, reduce medical disputes, and protect patient and family rights. The DNR consent completeness rate during May and June 2005 was only 33.9% in our hospital. Reasons indicated for this low rate included: (1) lack of a standard operating procedure for DNR consent; (2) multiple DNR consent versions; (3) lack of DNR-related education; and (4) lack of monitoring procedures. Our team developed a project to resolve these problems and improve terminal care quality. PURPOSE: The goal of this project was to increase the rate of DNR consent completeness from 33.9% to 80%. RESOLUTION: The plan, implemented between August and December 2009, included the following components: (1) establish standard guidelines for DNR consent; (2) simplify and unify DNR consent procedures; (3) provide DNR education for hospital staff; and (4) establish a DNR consent monitoring system. RESULTS: The DNR consent completeness rate rose from 33.9% to 90%. The goal of this project was thus achieved. CONCLUSION: This project effectively improved the DNR consent completeness rate at our hospital. The project ensured patients a good death and enhanced terminal care quality and patient satisfaction. Our experience may provide a reference to help other hospitals increase DNR their consent completeness rates.

A dedicated small-angle X-ray scattering beamline with a superconducting wiggler source at the NSRRC.

At the National Synchrotron Radiation Research Center (NSRRC), which operates a 1.5 GeV storage ring, a dedicated small-angle X-ray scattering (SAXS) beamline has been installed with an in-achromat superconducting wiggler insertion device of peak magnetic field 3.1 T. The vertical beam divergence from the X-ray source is reduced significantly by a collimating mirror. Subsequently the beam is selectively monochromated by a double Si(111) crystal monochromator with high energy resolution (DeltaE/E approximately 2 x 10(-4)) in the energy range 5-23 keV, or by a double Mo/B4C multilayer monochromator for 10-30 times higher flux ( approximately 10(11) photons s(-1)) in the 6-15 keV range. These two monochromators are incorporated into one rotating cradle for fast exchange. The monochromated beam is focused by a toroidal mirror with 1:1 focusing for a small beam divergence and a beam size of approximately 0.9 mm x 0.3 mm (horizontal x vertical) at the focus point located 26.5 m from the radiation source. A plane mirror installed after the toroidal mirror is selectively used to deflect the beam downwards for grazing-incidence SAXS (GISAXS) from liquid surfaces. Two online beam-position monitors separated by 8 m provide an efficient feedback control for an overall beam-position stability in the 10 microm range. The beam features measured, including the flux density, energy resolution, size and divergence, are consistent with those calculated using the ray-tracing program SHADOW. With the deflectable beam of relatively high energy resolution and high flux, the new beamline meets the requirements for a wide range of SAXS applications, including anomalous SAXS for multiphase nanoparticles (e.g. semiconductor core-shell quantum dots) and GISAXS from liquid surfaces.

X-ray beamlines for structural studies at the NSRRC superconducting wavelength shifter.

Using a superconducting-wavelength-shifter X-ray source with a photon flux density of 10(11)-10(13) photons s(-1) mrad(-1) (0.1% bandwidth)(-1) (200 mA)(-1) in the energy range 5-35 keV, three hard X-ray beamlines, BL01A, BL01B and BL01C, have been designed and constructed at the 1.5 GeV storage ring of the National Synchrotron Radiation Research Center (NSRRC). These have been designed for structure-related research using X-ray imaging, absorption, scattering and diffraction. The branch beamline BL01A, which has an unmonochromatized beam, is suitable for phase-contrast X-ray imaging with a spatial resolution of 1 microm and an imaging efficiency of one frame per 10 ms. The main beamline BL01B has 1:1 beam focusing and a medium energy resolution of approximately 10(-3). It has been designed for small-angle X-ray scattering and transmission X-ray microscopy, used, respectively, in anomalous scattering and nanophase-contrast imaging with 30 nm spatial resolution. Finally, the branch beamline BL01C, which features collimating and focusing mirrors and a double-crystal monochromator for a high energy resolution of approximately 10(-4), has been designed for X-ray absorption spectroscopy and high-resolution powder X-ray diffraction. These instruments, providing complementary tools for studying multiphase structures, have opened up a new research trend of integrated structural study at the NSRRC, especially in biology and materials. Examples illustrating the performances of the beamlines and the instruments installed are presented.

Levamisole modulates prostaglandin E2 production and cyclooxygenase II gene expression in human colonic cancer cells.

BACKGROUND: Colorectal adenocarcinoma is one of the leading causes of cancer mortality in the world. Recent studies have demonstrated that prostaglandin E(2) (PGE(2)) and cyclooxygenase (COX) are involved in the early development of colorectal cancer. Levamisole together with 5-fluorouracil has been shown to improve the survival of patients with Duke's C colon cancer. This study examined the effect of levamisole on PGE(2) production and COX-2 gene activation in immortalized human colon cells. MATERIALS AND METHODS: Colon 205 cells, a human colonic cancer cell line, were exposed to Escherichia coli LPS (1 microg/mL) in the presence of levamisole (1 microm to 1 mm). The PGE(2) production was determined by enzyme-linked immunosorbent assay. In addition, cyclooxygenase II (COX-2) mRNA expression and COX-2 protein were measured by the real-time reverse transcription polymerase chain reaction and Western blot assay, respectively. Transcription factor nuclear factor (NF)-kappaB activity of the nuclear and cytoplasmic proteins was determined by Western blot assay with a P65 antibody. RESULTS: Colon 205 cells produced significantly more PGE(2) when stimulated by LPS. Levamisole inhibited PGE(2) production by LPS-stimulated colon 205 cells in a dose-dependent fashion. In addition, COX-2 mRNA expression and COX-2 protein induced by LPS were also reduced by levamisole. Finally, NF-kappaB activation of LPS-stimulated colon cells was inhibited by levamisole. CONCLUSION: Levamisole inhibits PGE(2) production by LPS-stimulated colon 205 cells. The inhibition of levamisole occurs at the transcription level of COX-2 gene and is regulated through NF-kappaB activation.

Lysophosphatidylcholine alters vascular tone in rat aorta by suppressing endothelial [Ca(2+)](I) signaling.

The detailed mechanism of how lysophosphatidylcholine (LPC) suppresses endothelium-dependent vasodilatation is unclear at present. We investigated the effects of LPC on endothelial intracellular calcium (EC [Ca(2+)](i)) signaling and vascular tone simultaneously using a new technique we developed. Fura-2-labeled rat aortic specimens were mounted in a tissue flow chamber and precontracted with phenylephrine (5 x 10(-8) M). Under either basal or agonist-stimulated conditions, the EC [Ca(2+)](i) level was calculated from fura 2 fluorescence ratio images, and the vascular tone was estimated by measuring the relative displacement of the fluorescence images. Although both acetylcholine (ACh)-induced EC [Ca(2+)](i) elevation and the concomitant vasorelaxation were partially suppressed in specimens pretreated with LPC (20 microM), the quantitative relationship between EC [Ca(2+)](i) elevation and the corresponding vasorelaxation was unaffected. A high concentration of LPC (40 microM) completely eliminated ACh-evoked [Ca(2+)](i) elevation and vasodilatation. It has been reported that exposing vascular tissue to a calcium-free buffer causes a reduction in the EC [Ca(2+)](i) level and the accompanying vasoconstriction. Pretreatment with 20 microM LPC reduced the basal EC [Ca(2+)](i) level and abolished the calcium-free solution-induced EC [Ca(2+)](i) reduction and vasoconstriction. We conclude that LPC impairs endothelium-dependent vasorelaxation mainly by reducing the basal EC [Ca(2+)](i) level and suppressing agonist-evoked EC [Ca(2+)](i) signaling.