Cardiac CT for intraseptal pseudoaneurysm: impending double rupture of ventricular septum and left ventricular free wall.

A 71-year-old woman presented at our hospital with chest discomfort. Cardiac CT showed an impending double rupture; an intraseptal pseudoaneurysm had ruptured into the right ventricle, while the left ventricular free wall remained intact at this stage. After admission, the patient fell into cardiogenic shock. Emergency surgery was performed. The intraoperative findings included a double rupture of the ventricular septum and the left ventricular free wall. Double rupture is a rare but fatal complication of myocardial infarction. Early diagnosis is essential. Recently, cardiac CT has emerged as a valuable tool for patients with possible ischaemic disease. In this case, enhanced cardiac CT showed an impending double rupture of junctional-type. The static and dynamic images of intraseptal pseudoaneurysm by two-dimensional (2-D) CT, 3-D CT and 4-D CT presented here provide insights into the mechanisms behind, and the pathophysiology of, double ruptures. They also demonstrate the significance of cardiac CT for evaluating ischaemic heart disease.

The relative trending accuracy of noninvasive continuous hemoglobin monitoring during hemodialysis in critically ill patients.

The pulse CO-Oximeter (Radical-7; Masimo Corp., Irvine, CA) is a multi-wavelength spectrophotometric method for noninvasive continuous monitoring of hemoglobin (SpHb). Because evaluating the relative change in blood volume (ΔBV) is crucial to avoid hypovolemia and hypotension during hemodialysis, it would be of great clinical benefit if ΔBV could be estimated by measurement of SpHb during hemodialysis. The capability of the pulse CO-Oximeter to monitor ΔBV depends on the relative trending accuracy of SpHb. The purpose of the current study was to evaluate the relative trending accuracy of SpHb by the pulse CO-Oximeter using Crit-Line as a reference device. In 12 patients who received hemodialysis (total 22 sessions) in the intensive care unit, ΔBV was determined from SpHb. Relative changes in blood volume determined from SpHb were calculated according to the equation: ΔBV(SpHb)=[starting SpHb]/[current SpHb] - 1. The absolute values of SpHb and hematocrit measured by Crit-Line (CL-Hct) showed poor correlation. On the contrary, linear regression analysis showed good correlation between ΔBV(SpHb) and the relative change in blood volume measured by Crit-Line [ΔBV(CL-Hct)] (r=0.83; P≤0.001). Bland-Altman analysis also revealed good agreement between ΔBV(SpHb) and ΔBV(CL-Hct) (bias, -0.77%; precision, 3.41%). Polar plot analysis revealed good relative trending accuracy of SpHb with an angular bias of 4.1° and radial limits of agreement of 24.4° (upper) and -16.2° (lower). The results of the current study indicate that SpHb measurement with the pulse CO-Oximeter has good relative trending accuracy.

Dominant-negative hypoxia-inducible factor-1 alpha reduces tumorigenicity of pancreatic cancer cells through the suppression of glucose metabolism.

In the tumor cells exposed to hypoxia, hypoxia-inducible factor-1 (HIF-1)-mediated adaptation responses such as angiogenesis and anaerobic metabolism are induced for their survival. We have recently reported that the constitutive expression of HIF-1 alpha renders pancreatic cancer cells resistant to apoptosis induced by hypoxia and glucose deprivation. We then established dominant-negative HIF-1 alpha (dnHIF-1 alpha) transfectants and examined their susceptibility to apoptosis and growth inhibition induced by hypoxia and glucose deprivation in vitro and their tumorigenicity in SCID mice. We further examined the expressions of aldolase A and Glut-1 in vitro and Glut-1 expression and glucose uptake in the tumor tissues and microvessel counts in the tumor tissues. As a result, dnHIF-1 alpha rendered the pancreatic cancer cells sensitive to apoptosis and growth inhibition induced by hypoxia and glucose deprivation. Also it abrogated the enhanced expression of Glut-1 and aldolase A mRNAs under hypoxia and reduced the expression of Glut-1 and the glucose uptake in the tumor tissues and consequently in vivo tumorigenicity. We found no significant difference in the microvessel counts among the tumor tissues. From these results, we suggest that the disruption of the HIF-1 pathway might be effective in the treatment of pancreatic cancers.

Genes from Pseudomonas sp. strain BS involved in the conversion of L-2-amino-Delta(2)-thiazolin-4-carbonic acid to L-cysteine.

DL-2-amino-Delta(2)-thiazolin-4-carbonic acid (DL-ATC) is a substrate for cysteine synthesis in some bacteria, and this bioconversion has been utilized for cysteine production in industry. We cloned a DNA fragment containing the genes involved in the conversion of L-ATC to L-cysteine from Pseudomonas sp. strain BS. The introduction of this DNA fragment into Escherichia coli cells enabled them to convert L-ATC to cysteine via N-carbamyl-L-cysteine (L-NCC) as an intermediate. The smallest recombinant plasmid, designated pTK10, contained a 2.6-kb insert DNA fragment that has L-cysteine synthetic activity. The nucleotide sequence of the insert DNA revealed that two open reading frames (ORFs) encoding proteins with molecular masses of 19.5 and 44.7 kDa were involved in the L-cysteine synthesis from DL-ATC. These ORFs were designated atcB and atcC, respectively, and their gene products were identified by overproduction of proteins encoded in each ORF and by the maxicell method. The functions of these gene products were examined using extracts of E. coli cells carrying deletion derivatives of pTK10. The results indicate that atcB and atcC are involved in the conversion of L-ATC to L-NCC and the conversion of L-NCC to cysteine, respectively. atcB was first identified as a gene encoding an enzyme that catalyzes thiazolin ring opening. AtcC is highly homologous with L-N-carbamoylases. Since both enzymes can only catalyze the L-specific conversion from L-ATC to L-NCC or L-NCC to L-cysteine, it is thought that atcB and atcC encode L-ATC hydrolase and N-carbamyl-L-cysteine amidohydrolase, respectively.