The purpose of this study was to explore the policies and practices of nursing homes with respect to the resuscitation of residents who do not have a do-not-resuscitate (DNR) order. Responses from a survey of 36 facilities revealed that most residents had DNR orders and most facilities were capable of providing basic cardiopulmonary resuscitation (CPR). Less than 30% had performed CPR in the past 6 months, and 22.8% had no written CPR policies. More facilities required CPR in witnessed arrests of non-DNR residents (79.3%) than in unwitnessed arrests (24%). Methods for identifying CPR status need improvement to enable accurate identification and prompt resuscitation of residents who want CPR.

Advance Directives↗

PubMedDate not supplied

Hyperthermia decreases cytokine-mediated adhesion molecule expression on human umbilical vein endothelial cells.

Although hyperthermia has been used as an effective cancer treatment modality, its effects on metastasis of tumour cells are not clear. Since adhesion molecules play a key role in metastasis, we evaluated how the expression of adhesion molecules is influenced by hyperthermia. Human umbilical vein endothelial cells were incubated in vitro for 1 h. at 39, 42, 43 and 44 degrees C with and without addition of tumour-necrosis factor (TNF) or interferon-gamma (IFN-gamma) and the expression of endothelial cell leukocyte adhesion molecule-1 (ELAM-1), intercellular adhesion molecule-1 (ICAM-1) and major histocompatibility complex (MHC) class-II molecule was measured. Expression of MHC class-II molecules and expression of unstimulated constituent ICAM-1's was not reduced by heat treatment. In contrast, expression of cytokine-induced ELAM-1's and ICAM-1's was significantly lower after heat treatment. The adhesion to HUVEC in vitro of HL-60 leukemia cells, which express sialyl-Lewis-x antigen as a ligand to ELAM-1, was diminished after incubation at 42 degrees C and totally lost after treatment at 44 degrees C. This suggests that any decrease in metastasis formation after heat treatment, which is occasionally observed, could be due to a reduced action of TNF or related cytokines on adhesion molecule induction and subsequent membrane expression by the endothelial cell. A possible underlying mechanism involved is a heat-induced alteration or blockage of the biosynthetic pathways required for synthesis of ELAM-1 and ICAM-1 proteins.

Cell Adhesion↗

PubMedDate not supplied

Liver-associated toxicity of the HSV-tk/GCV approach and adenoviral vectors.

Intravenous injection of immunodeficient mice with adenoviral vectors carrying the HSV-tk gene led to preferential transduction of liver tissue. Subsequent application of ganciclovir (GCV) resulted in extremely high toxicity with negligible survival rates. This toxicity was only seen when GCV was applied in addition to the adenoviral vector and not if combined with the Ad-beta gal control vector. This indicates a specific Ad-tk/GCV-related toxicity. Low survival rates were seen not only after intravenous administration but also after injection of the vectors into the portal vein, the liver tissue and liver tumors, but not during the treatment of subcutaneous tumors. This, together with extensive signs of liver degeneration occurring as early as one day after the initiation of GCV treatment, strongly suggests a specific liver-associated toxicity. Severe toxicity was observed when animals received GCV treatment as late as 7 weeks after vector administration. Moreover, in vitro survival rates of resting primary hepatocytes treated with Ad-tk and GCV were very low. We therefore suppose a mechanism of toxicity of phosphorylated GCV which is independent from cellular proliferation. Since our results indicate that the Ad-HSV-tk/GCV approach is toxic for the resting liver, additional safety features such as tumor-restricted transgene expression should be included in adenoviral vectors.

Adenoviridae↗