Microclimate is an independent risk factor for the development of intraoperatively acquired pressure ulcers in the park-bench position: A prospective observational study.

Preventing pressure ulcers is important in patients undergoing procedures in the park-bench position. We hypothesized that the microclimate around the skin is a significant risk factor for developing pressure ulcers. This research continuously assessed factors of the microclimate in terms of skin temperature and perspiration as well as the interface pressure in order to determine whether the microclimate is an independent risk factor for the development of park-bench position-related pressure ulcers (PBP-PUs). A prospective observational study was conducted among patients undergoing elective surgery in the park-bench position at a general hospital in the metropolitan area of Japan between April and November 2014. Factors of the microclimate, including skin temperature and perspiration, in addition to the interface pressure were continuously measured throughout surgery. Twenty-nine patients were analyzed (mean age 44.4 ± 13.2 years, male 44.8%). Of these 29 patients, seven (24.1%) developed Category I PBP-PUs. The change in skin temperature from baseline to the end of surgery (2.7 ± 0.3 °C vs. 1.9 ± 0.8 °C) and the average peak pressure (119.1 ± 36.8 mmHg vs. 94.5 ± 23.1 mmHg) were significantly higher in the patients with PBP-PUs than in those without PBP-PUs. There were no significant differences in the amount of perspiration between the two groups. A hierarchical logistic regression analysis showed that the change in skin temperature was significantly related to the development of PBP-PUs (unit = 0.1 °C: odds ratio 1.44, 95% confidential interval 1.09-2.33) when adjusted for the average peak pressure and length of surgery. Our results suggest that a change in skin temperature toward a higher value is an independent risk factor for the development of PBP-PUs. Proper intraoperative management of skin temperature may therefore be a promising candidate as a preventive method against PBP-PU development.

An apical expression signal of the renal type IIc Na+-dependent phosphate cotransporter in renal epithelial cells.

The type IIc Na(+)-dependent phosphate cotransporter (NaPi-IIc) is specifically targeted to, and expressed on, the apical membrane of renal proximal tubular cells and mediates phosphate transport. In the present study, we investigated the signals that determine apical expression of NaPi-IIc with a focus on the role of the N- and the C-terminal tails of mouse NaPi-IIc in renal epithelial cells [opossum kidney (OK) and Madin-Darby canine kidney cells]. Wild-type NaPi-IIc, the cotransporter NaPi-IIa, as well as several IIa-IIc chimeras and deletion mutants, were fused to enhanced green fluorescent protein (EGFP), and their cellular localization was analyzed in polarized renal epithelial cells by confocal microscopy and by cell-surface biotinylation. Fluorescent EGFP-fused NaPi-IIc transporter proteins are correctly expressed in the apical membrane of OK cells. The apical expression of N-terminal deletion mutants (deletion of N-terminal 25, 50, or 69 amino acids) was not affected by truncation. In contrast, C-terminal deletion mutants (deletion of C-terminal 45, 50, or 62 amino acids) did not have correct apical expression. A more detailed mutational analysis indicated that a domain (amino acids WLHSL) in the cytoplasmic C terminus is required for apical expression of NaPi-IIc in renal epithelial cells. We conclude that targeting of NaPi-IIc to the apical cell surface is regulated by a unique amino acid motif in the cytoplasmic C-terminal domain.

Unique uptake and efflux systems of inorganic phosphate in osteoclast-like cells.

During bone resorption, a large amount of inorganic phosphate (P(i)) is generated within the osteoclast hemivacuole. The mechanisms involved in the disposal of this P(i) are not clear. In the present study, we investigated the efflux of P(i) from osteoclast-like cells. P(i) efflux was activated by acidic conditions in osteoclast-like cells derived by the treatment of RAW264.7 cells with receptor activator of nuclear factor-kappaB ligand. Acid-induced P(i) influx was not observed in renal proximal tubule-like opossum kidney cells, osteoblast-like MC3T3-E1 cells, or untreated RAW264.7 cells. Furthermore, P(i) efflux was stimulated by extracellular P(i) and several P(i) analogs [phosphonoformic acid (PFA), phosphonoacetic acid, arsenate, and pyrophosphate]. P(i) efflux was time dependent, with 50% released into the medium after 10 min. The efflux of P(i) was increased by various inhibitors that block P(i) uptake, and extracellular P(i) did not affect the transport of [(14)C]PFA into the osteoclast-like cells. Preloading of cells with P(i) did not stimulate P(i) efflux by PFA, indicating that the effect of P(i) was not due to transstimulation of P(i) transport. P(i) uptake was also enhanced under acidic conditions. Agents that prevent increases in cytosolic free Ca(2+) concentration, including acetoxymethyl ester of 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, 2-aminoethoxydiphenyl borate, and bongkrekic acid, significantly inhibited P(i) uptake in the osteoclast-like cells, suggesting that P(i) uptake is regulated by Ca(2+) signaling in the endoplasmic reticulum and mitochondria of osteoclast-like cells. These results suggest that osteoclast-like cells have a unique P(i) uptake/efflux system and can prevent P(i) accumulation within osteoclast hemivacuoles.