Myocardial viability in chronic ischemic heart disease: comparison of delayed-enhancement magnetic resonance imaging with 99mTc-sestamibi and 18F-fluorodeoxyglucose single-photon emission computed tom

Nucl Med Commun. 2009 May 30; Liu Q, Zhao S, Yan C, Lu M, Jiang S, Zhang Y, Li S, Liu Y, Yang M, He ZOBJECTIVES: We sought to compare delayed-enhancement MRI (DE-MRI) with Tc-sestamibi and F-fluorodeoxyglucose (F-FDG) single-photon emission computed tomography (SPECT) for the assessment of myocardial viability. METHODS: Thirty-four patients with prior myocardial infarction underwent DE-MRI and Tc-sestamibi/F-FDG SPECT. The area of delayed enhancement by DE-MRI was defined as scar tissue. The region with concordantly reduced perfusion and glucose metabolism was defined as nonviable myocardium. In a 17-segment model, the segmental extent of hyperenhancement was compared with segmental Tc-sestamibi and F-FDG uptake defect. All segments were divided into five different severities by segmental extent of hyperenhancement in DE-MRI and were classified into different viability situations by segmental Tc-sestamibi and F-FDG uptake in SPECT. RESULTS: A total of 578 segments were studied. Sensitivity and specificity of DE-MRI in identifying segments with flow/metabolism match were 61.32 and 95.35%, respectively. Semiquantitatively assessed relative MRI scar tissue correlated well with Tc-sestamibi and F-FDG SPECT (r = 0.63, P = 0.0284). However, of the 431 segments defined as normal by DE-MRI, 82 segments (19%) were scored as nonviable by F-FDG SPECT. During these segments, 48 showed less than 50% reduced F-FDG uptake, 25 showed 50-75% reduced F-FDG uptake, and nine showed no F-FDG uptake. CONCLUSION: MRI hyperenhancement as a marker of myocardial scar closely agrees with Tc-sestamibi and F-FDG SPECT. Nuclear technology and DE-MRI show their own predominance and limitation in assessment of myocardial viability and detecting irreversibly injured tissue.

Peritoneal Ultrafiltration: Physiology and Failure.

Contrib Nephrol. 2009; 163: 7-14Flessner MFNet ultrafiltration in peritoneal dialysis results from a complex set of forces within the tissue space surrounding the peritoneal cavity. Hydrostatic pressure due to the large volume of fluid drives water and solute into the surrounding tissue, and therefore a high osmotic pressure must be maintained in the cavity to draw fluid from blood capillaries distributed in the tissue adjacent to the peritoneum. The osmotic pressure in the interstitium decreases from that of the cavity to equilibration with the plasma in the first millimeter of tissue below the peritoneum. Osmotic pressure differences at the blood capillary produce a solute free ultrafiltrate via aquaporin 1 that is approximately 50% of the total filtration. The remainder of the fluid is filtered via interendothelial gaps lined with negatively charged glycocalyx, which alters the traditional Starling forces and is easily damaged by inflammation or ischemia. Ultrafi ltration failure occurs when intraperitoneal pressure is too high, the inflamed peritoneum dissipates the osmotic agent rapidly because of hyperpermeable angiogenic vessels, or peritoneal scarring lowers the osmotic pressure near the blood supply and there is no force for fluid transport through the scar to the cavity. To remedy problems in net ultrafiltration, lowering the volume lowers the intraperitoneal pressure and often solves the problem of excessive pressure. Preventative measures to decrease infl ammation and peritonitis are important for preservation of the barrier. Experimental measures such as peritoneal stem-cell transplants may someday permit reclamation of damaged barrier systems and allow patients to continue the dialytic technique.

Mode of vegetative reproduction of the bipolar budding yeast species Wickerhamomyces pijperi and related strains.

Microbiology. 2009 Jun 4; Imanishi Y, Jindamorakot S, Limtong S, Nakase TTo clarify the budding pattern of Wickerhamomyces pijperi, the vegetative cells were observed by scanning electron microscopy (SEM). The cells grew by bipolar budding, but cells that budded from the shoulder of a mother cell were occasionally observed. We examined the cell morphology and phylogeny of 5 W. pijperi strains isolated in Thailand as well as 10 W. pijperi strains and related species that were preserved in culture collections. Phylogenetic analysis based on 3 different nucleotide sequences (D1/D2 domain of 26S ribosomal DNA, the actin gene ACT1, and the elongation factor 2 gene EF2) indicated that all the strains belonged to the genus Wickerhamomyces and were neighbors of the type strain W. pijperi NBRC 1290(T). In addition, the strains fell into 2 groups. The budding patterns of the strains were carefully observed by staining the bud scars, and these patterns were categorized into 3 groups: Types I-III. Type I included cells that grew by bipolar budding and formed multiple scars, type III included cells that grew by multilateral budding and formed a single scar, and type II included cells that exhibited a mixture of type I and type III patterns. Among the 15 strains, 12 strains, including W. pijperi NBRC 1290(T), mainly exhibited type I or type II budding patterns, and the remaining 3 strains exhibited either type II or type III patterns. This finding indicates that the separation of the strains into 2 groups was based on the mode of budding. Thus, the phylogenetic relationship and budding patterns are related. Moreover, some cells also exhibited budding characteristics that were intermediate between bipolar and multilateral budding.