Verbal Communication of an Orally Intubated Patient in the Intensive Care Unit: A Case Report.

BACKGROUND: Effective interaction with orally intubated patients is important for critical care rehabilitation. An electrolarynx (EL) has reportedly proven useful for facilitating verbal communication during oral intubation. The EL allows patients to express their wishes instantly. Nevertheless, this method is not commonly applied, probably because articulation is often unsatisfactory. Here, we report a case of successful EL-based communication during early mobilization and describe the key factors involved in this success. CASE: An 82-year-old man, who was intubated and undergoing mechanical ventilation for the treatment of acute respiratory failure caused by severe pneumonia, was referred to the rehabilitation department for early mobilization. The patient tried to speak during the spontaneous awakening trials and breathing trials for weaning off mechanical ventilation. However, he was frustrated by communication difficulties and consequently exhibited negative behavior toward physical therapy. We attempted to use an EL to facilitate communication, but initially the patient failed to achieve intelligible articulation. We eventually established that the intubation tube should be located at the corner of the mouth to minimize the restriction of tongue movement. Intelligible sounds were recognized and successful communication between the patient and staff was subsequently achieved. DISCUSSION: The use of an EL is worthy of consideration during early mobilization of orally intubated patients. To achieve successful communication with an EL, both patient selection (Richmond Agitation-Sedation Scale score of 0 or -1) and the proper placement of the intubation tube are necessary to ensure intelligible articulation.

Identification of inflammatory gene modules based on variations of human endothelial cell responses to oxidized lipids.

Oxidized phospholipids are thought to promote atherogenesis by stimulating endothelial cells (ECs) to produce inflammatory cytokines, such as IL-8. In studies with mouse models, we previously demonstrated that genetic variation in inflammatory responses of endothelial cells to oxidized lipids contributes importantly to atherosclerosis susceptibility. We now show that similar variations occur in cultured aortic ECs derived from multiple heart transplant donors. These variations were stably maintained between passages and, thus, reflect either genetic or epigenetic regulatory differences. Expression array analysis of aortic EC cultures derived from 12 individuals revealed that >1,000 genes were regulated by oxidized phospholipids. We have used the observed variations in the sampled population to construct a gene coexpression network comprised of 15 modules of highly connected genes. We show that several identified modules are significantly enriched in genes for known pathways and confirm a module enriched for unfolded protein response (UPR) genes using siRNA and the UPR inducer tunicamycin. On the basis of the constructed network, we predicted that a gene of unknown function (MGC4504) present in the UPR module is a target for UPR transcriptional activator ATF4. Our data also indicate that IL-8 is present in the UPR module and is regulated, in part, by the UPR. We validate these by using siRNA. In conclusion, we show that interindividual variability can be used to group genes into pathways and predict gene-gene regulatory relationships, thus identifying targets potentially involved in susceptibility to common diseases such as atherosclerosis.

Matrix GLA protein, a regulatory protein for bone morphogenetic protein-2.

Matrix GLA protein (MGP) has been identified as a calcification inhibitor in cartilage and vasculature. Part of this effect may be attributed to its influence on osteoinductive activity of bone morphogenetic protein-2 (BMP-2). To detect binding between MGP and BMP-2, we performed immunoprecipitation using MGP and BMP-2 tagged with FLAG and c-Myc. The results showed co-precipitation of BMP-2 with MGP. To quantify the effect of MGP on BMP-2 activity, we assayed for alkaline phosphatase activity and showed a dose-dependent effect. Low levels of MGP relative to BMP-2 (<1-fold excess) resulted in mild enhancement of osteoinduction, whereas intermediate levels (1-15-fold excess) resulted in strong inhibition. High levels of MGP (>15-fold excess), however, resulted in pronounced enhancement of the osteoinductive effect of BMP-2. Cross-linking studies showed that inhibitory levels of MGP abolished BMP-2 receptor binding. Immunoblotting showed a corresponding decrease in activation of Smad1, part of the BMP signaling system. Enhancing levels of MGP resulted in increased Smad1 activation. To determine the cellular localization of BMP-2 in the presence of MGP, binding assays were performed on whole cells and cell-synthesized matrix. Inhibitory levels of MGP yielded increased matrix binding of BMP-2, suggesting that MGP inhibits BMP-2 in part via matrix association. These results suggest that MGP is a BMP-2 regulatory protein.