Right ventricular function evaluated by volumetric analysis during left heart bypass in a canine model of postischemic cardiac dysfunction

AbstractRight ventricular function during left heart bypass was evaluated by volumetric analysis with a conductance catheter in 12 dogs with postischemic cardiac dysfunction. The conductance catheter was used to assess the volumetric status of the right ventricle and thereby allowed a right ventricular pressure-volume curve to be obtained, in which transient volume loading on the right ventricle was applied. The following right ventricular properties during left heart bypass were assessed and compared with properties measured without left heart bypass, by means of load-independent parameters: maximum elastance, stroke work/end-diastolic volume relation, end-diastolic pressure/volume relation, and stroke work/end-diastolic pressure relation. The stroke volume derived from the conductance catheter and the electromagnetic flow probe showed good linear correlation (r2 = 0.733 to 0.975). After initiation of left heart bypass, maximum elastance did not change significantly, although volume intercept significantly increased, from 1.2 ± 7.3 to 3.6 ± 7.9 ml ( p < 0.05). End-diastolic pressure/volume relation was well fitted to the exponential curve (EDP = e (k1 · EDV+k2) ) and was shifted to the right and downward during left heart bypass; the slope k1 significantly decreased, from 0.12 ± 0.06 to 0.10 ± 0.07 ( p < 0.01). Stroke work/end-diastolic volume relation and stroke work/end-diastolic pressure relation were closely fitted to the linear regression, and their slopes were significantly increased during left heart bypass, from 0.14 ± 0.08 to 0.18 ± 0.08 ( p < 0.05) and from 0.22 ± 0.15 to 0.34 ± 0.19 ( p < 0.01), respectively. These results suggest that the decompression of the left ventricle and septal shifting by left heart bypass provide good diastolic compliance and good systolic performance because of afterload unloading of the right ventricle. Thus the left heart bypass improved the overall right ventricular performance, particularly at higher end-diastolic pressures, in dogs with postischemic cardiac dysfunction. (J THORAC CARDIOVASC SURG 1995;109:796-803

Inspection Method by Comparing CAD Figure with Processed Image

We propose the recognition method of bridge soldering base metal on the circuits by comparing CAD figure and input image of image processing to locate the soldering iron tip accurately to secure the high quality Firstly, three dimensional CAD assembly drawing of circuits which are assembled perpendicularly in each other is projected on an imaginary two dimensional screen which is vertical to the optical axis of the camera The projected image is used as the standard CAD figure to inspect the location of the bridge soldering base metal. The positions among the bridge soldering base metals show the line state. So this line (connecting line) is used as the reference line to inspect the location of the bridge soldering base metal. The characteristics of the standard figure are represented by the connecting line, edge line and center points of base metal. Secondly, the position and gradient of connecting line among bridge soldering base metals in the input image is estimated. And the position of base metal and assembly accuracy of circuit units are calculated by comparing the shape and position of each base metal with its standard figure based on the connecting line Furthermore, the length between the opposite edges of the base metals are calculated to inspect the positions and the assemble accuracy of circuit units

Renoprotective Action of a Matrix Metalloproteinase Inhibitor in Progressive Mesangioproliferative Nephritis

Background/Aim: Matrix metalloproteinases (MMPs) play pivotal roles in extracellular matrix turnover and are involved in chronic kidney disease. The renoprotective action of a synthetic MMP inhibitor, compound A, was investigated in chronic nephritis. Methods: Nephritis was induced by a single injection of anti-Thy1.1 antibody to unilaterally nephrectomized rats. The effects of compound A on proteinuria, blood urea nitrogen, and matrix-related gene expressions were evaluated. Collagen accumulation, as assessed by periodic acid-Schiff staining and hydroxyproline content, was determined. The integrity of glomerular epithelial cells and glomerular basement membrane was evaluated with desmin immunohistochemistry and electron microscopic detection of anionic charge sites, respectively. Results: Treatment with compound A notably attenuated proteinuria, ameliorated blood urea nitrogen, and prevented glomerulosclerosis. Gene upregulation of collagen and transforming growth factor β1 in the cortex was prevented in the treated animals. Glomerular epithelial cell injury was milder, and glomerular basement membrane anionic sites were protected with the treatment. Conclusion: A novel MMP inhibitor, compound A, exerts protective effects in progressive glomerulonephritis. Compound A ameliorates various aspects of renal injuries and may have therapeutic potential toward kidney diseases

Effect of Boron Incorporation on Slow Interface Traps in SiO2/4H-SiC Structures

The reason for the effective removal of interface traps in SiO2/4H-SiC (0001) structures by boron (B) incorporation was investigated by employing low-temperature electrical measurements. Low-temperature capacitance–voltage and thermal dielectric relaxation current measurements revealed that the density of electrons captured in slow interface traps in B-incorporated oxide is lower than that in dry and NO-annealed oxides. These results suggest that near-interface traps can be removed by B incorporation, which is considered to be an important reason for the increase in the field-effect mobility of 4H-SiC metal–oxide–semiconductor devices. A model for the passivation mechanism is proposed that takes account of stress relaxation during thermal oxidation

The Possible Role of TASK Channels in Rank-Ordered Recruitment of Motoneurons in the Dorsolateral Part of the Trigeminal Motor Nucleus.

Because a rank-ordered recruitment of motor units occurs during isometric contraction of jaw-closing muscles, jaw-closing motoneurons (MNs) may be recruited in a manner dependent on their soma sizes or input resistances (IRs). In the dorsolateral part of the trigeminal motor nucleus (dl-TMN) in rats, MNs abundantly express TWIK (two-pore domain weak inwardly rectifying K channel)-related acid-sensitive-K(+) channel (TASK)-1 and TASK3 channels, which determine the IR and resting membrane potential. Here we examined how TASK channels are involved in IR-dependent activation/recruitment of MNs in the rat dl-TMN by using multiple methods. The real-time PCR study revealed that single large MNs (&gt;35 μm) expressed TASK1 and TASK3 mRNAs more abundantly compared with single small MNs (15-20 μm). The immunohistochemistry revealed that TASK1 and TASK3 channels were complementarily distributed in somata and dendrites of MNs, respectively. The density of TASK1 channels seemed to increase with a decrease in soma diameter while there were inverse relationships between the soma size of MNs and IR, resting membrane potential, or spike threshold. Dual whole-cell recordings obtained from smaller and larger MNs revealed that the recruitment of MNs depends on their IRs in response to repetitive stimulation of the presumed Ia afferents. 8-Bromoguanosine-cGMP decreased IRs in small MNs, while it hardly changed those in large MNs, and subsequently decreased the difference in spike-onset latency between the smaller and larger MNs, causing a synchronous activation of MNs. These results suggest that TASK channels play critical roles in rank-ordered recruitment of MNs in the dl-TMN

Smad6/Smurf1 overexpression in cartilage delays chondrocyte hypertrophy and causes dwarfism with osteopenia

Biochemical experiments have shown that Smad6 and Smad ubiquitin regulatory factor 1 (Smurf1) block the signal transduction of bone morphogenetic proteins (BMPs). However, their in vivo functions are largely unknown. Here, we generated transgenic mice overexpressing Smad6 in chondrocytes. Smad6 transgenic mice showed postnatal dwarfism with osteopenia and inhibition of Smad1/5/8 phosphorylation in chondrocytes. Endochondral ossification during development in these mice was associated with almost normal chondrocyte proliferation, significantly delayed chondrocyte hypertrophy, and thin trabecular bone. The reduced population of hypertrophic chondrocytes after birth seemed to be related to impaired bone growth and formation. Organ culture of cartilage rudiments showed that chondrocyte hypertrophy induced by BMP2 was inhibited in cartilage prepared from Smad6 transgenic mice. We then generated transgenic mice overexpressing Smurf1 in chondrocytes. Abnormalities were undetectable in Smurf1 transgenic mice. Mating Smad6 and Smurf1 transgenic mice produced double-transgenic pups with more delayed endochondral ossification than Smad6 transgenic mice. These results provided evidence that Smurf1 supports Smad6 function in vivo

Class IA Phosphatidylinositol 3-Kinase in Pancreatic β Cells Controls Insulin Secretion by Multiple Mechanisms

SummaryType 2 diabetes is characterized by insulin resistance and pancreatic β cell dysfunction, the latter possibly caused by a defect in insulin signaling in β cells. Inhibition of class IA phosphatidylinositol 3-kinase (PI3K), using a mouse model lacking the pik3r1 gene specifically in β cells and the pik3r2 gene systemically (βDKO mouse), results in glucose intolerance and reduced insulin secretion in response to glucose. β cells of βDKO mice had defective exocytosis machinery due to decreased expression of soluble N-ethylmaleimide attachment protein receptor (SNARE) complex proteins and loss of cell-cell synchronization in terms of Ca2+ influx. These defects were normalized by expression of a constitutively active form of Akt in the islets of βDKO mice, preserving insulin secretion in response to glucose. The class IA PI3K pathway in β cells in vivo is important in the regulation of insulin secretion and may be a therapeutic target for type 2 diabetes