Cushion Valve Research Articles

Evolution of cardiac tissue and flow mechanics in developing Japanese Medaka.

The effects of pressure drop across cardiac valve cushion regions and endocardial wall strain in the early developmental stages of a teleost species heart are poorly understood. In the presented work, we utilize microscale particle image velocimetry (μPIV) flow measurements of developing medaka hearts from 3 to 14 dpf (n = 5 at each dpf) to quantify the pressure field and endocardial wall strain. Peak pressure drop at the atrioventricular canal (ΔPAVC) and outflow tract (ΔPOFT) show a steady increase with fish age progression. Pressure drops when non-dimensionalized with blood viscosity and heart rate at each dpf are comparable with measurements in zebrafish hearts. Retrograde flows captured at these regions display a negative pressure drop. A novel metric, Endocardial Work (EW), is introduced by analyzing the ΔPAVC-strain curves, which is a non-invasive measure of work required for ventricle filling. EW is a metric that can differentiate between the linear heart stage (< 100 Pa-%), cardiac looped chamber stage (< 300 Pa-%), and the fully formed chamber stage (> 300 Pa-%).

Research on Steering Vibration Analysis of Wheel Loader and Cushion Valve Design

At present, the wheel loaders on the market have steering vibration problems, which can be summarized as follows: the front frame and the cab vibrate violently at the beginning and at the end of steering. This paper analyzed the steering vibration mechanism by collecting the pressure at different positions of the hydraulic steering system and AMESim simulation. A cushion valve was designed to solve the problem of steering vibration. Finally, the prototype test was carried out and it was concluded that the cushion valve reduced the steering pressure starting shock by 50%, the stop vibration was reduced by 75%, and the suction problem no longer occurred. Further, the analysis provides theoretical and experimental basis for research on the steering system of loaders, and also provides new ideas for the design and optimization of vehicle steering systems.

Developmental origins for semilunar valve stenosis identified in mice harboring congenital heart disease-associated GATA4 mutation.

ABSTRACTCongenital heart defects affect ∼2% of live births and often involve malformations of the semilunar (aortic and pulmonic) valves. We previously reported a highly penetrant GATA4 p.Gly296Ser mutation in familial, congenital atrial septal defects and pulmonic valve stenosis and showed that mice harboring the orthologous G295S disease-causing mutation display not only atrial septal defects, but also semilunar valve stenosis. Here, we aimed to characterize the role of Gata4 in semilunar valve development and stenosis using the Gata4G295Ski/wt mouse model. GATA4 is highly expressed in developing valve endothelial and interstitial cells. Echocardiographic examination of Gata4G295Ski/wt mice at 2 months and 1 year of age identified functional semilunar valve stenosis predominantly affecting the aortic valve with distal leaflet thickening and severe extracellular matrix (ECM) disorganization. Examination of the aortic valve at earlier postnatal timepoints demonstrated similar ECM abnormalities consistent with congenital disease. Analysis at embryonic timepoints showed a reduction in aortic valve cushion volume at embryonic day (E)13.5, predominantly affecting the non-coronary cusp (NCC). Although total cusp volume recovered by E15.5, the NCC cusp remained statistically smaller. As endothelial to mesenchymal transition (EMT)-derived cells contribute significantly to the NCC, we performed proximal outflow tract cushion explant assays and found EMT deficits in Gata4G295Ski/wt embryos along with deficits in cell proliferation. RNA-seq analysis of E15.5 outflow tracts of mutant embryos suggested a disease state and identified changes in genes involved in ECM and cell migration as well as dysregulation of Wnt signaling. By utilizing a mouse model harboring a human disease-causing mutation, we demonstrate a novel role for GATA4 in congenital semilunar valve stenosis.This article has an associated First Person interview with the joint first authors of the paper.

Analysis of failure of helical tomotherapy multi-leaf collimator system

Objective To analyze the failure and processing methods of helical tomotherapy multi-leaf collimator (MLC) and summarize relevant maintenance experience, aiming to accurately identify the faulty parts, shorten the downtime and enhance the work time. Methods The failure data of the helical tomotherapy MLC system in the past 48 months were analyzed to identify the common faulty parts, causes and processing methods. Results During the previous 48 months, the MLC failure occurred for 20 times, 11 times for air compressor failure, 4 times for position verification board failure, twice for leaf driver failure, twice for cushion valve failure and once for the slip of leaf position verification rod. The MLC failure was significantly correlated with the humidity of high-pressure gas. The work time of machine exerted significant effect upon the service time of MLC parts. Conclusions The structure of the helical tomotherapy MLC system is complex. The high-intensity work increases the failure rate. The humidity of high-pressure gas affects the normal operation of the MLC equipment. The faulty parts can be identified, the downtime can be reduced and the work time can be enhanced by summarizing the experience of MLC maintenance. Key words: Tomotherapy; Multi-leaf collimator; Binary pneumatic blade; Failure processing

TGF-β Signaling in Control of Cardiovascular Function.

Genetic studies in animals and humans indicate that gene mutations that functionally perturb transforming growth factor β (TGF-β) signaling are linked to specific hereditary vascular syndromes, including Osler-Rendu-Weber disease or hereditary hemorrhagic telangiectasia and Marfan syndrome. Disturbed TGF-β signaling can also cause nonhereditary disorders like atherosclerosis and cardiac fibrosis. Accordingly, cell culture studies using endothelial cells or smooth muscle cells (SMCs), cultured alone or together in two- or three-dimensional cell culture assays, on plastic or embedded in matrix, have shown that TGF-β has a pivotal effect on endothelial and SMC proliferation, differentiation, migration, tube formation, and sprouting. Moreover, TGF-β can stimulate endothelial-to-mesenchymal transition, a process shown to be of key importance in heart valve cushion formation and in various pathological vascular processes. Here, we discuss the roles of TGF-β in vasculogenesis, angiogenesis, and lymphangiogenesis and the deregulation of TGF-β signaling in cardiovascular diseases.

Endothelial Notch1 Is Required for Proper Development of the Semilunar Valves and Cardiac Outflow Tract.

BackgroundCongenital heart disease is the most common type of birth defect, affecting ≈2% of the population. Malformations involving the cardiac outflow tract and semilunar valves account for >50% of these cases predominantly because of a bicuspid aortic valve, which has an estimated prevalence of 1% in the population. We previously reported that mutations in NOTCH1 were a cause of bicuspid aortic valve in nonsyndromic autosomal‐dominant human pedigrees. Subsequently, we described a highly penetrant mouse model of aortic valve disease, consisting of a bicuspid aortic valve with thickened cusps and associated stenosis and regurgitation, in Notch1‐haploinsufficient adult mice backcrossed into a Nos3‐null background.Methods and ResultsHere, we described the congenital cardiac abnormalities in Notch1 +/− ;Nos3 −/− embryos that led to ≈65% lethality by postnatal day 10. Although expected Mendelian ratios of Notch1 +/− ;Nos3 −/− embryos were found at embryonic day 18.5, histological examination revealed thickened, malformed semilunar valve leaflets accompanied by additional anomalies of the cardiac outflow tract including ventricular septal defects and overriding aorta. The aortic valve leaflets of Notch1 +/− ;Nos3 −/− embryos at embryonic day 15.5 were significantly thicker than controls, consistent with a defect in remodeling of the semilunar valve cushions. In addition, we generated mice haploinsufficient for Notch1 specifically in endothelial and endothelial‐derived cells in a Nos3‐null background and found that Notch1 fl/+;Tie2‐Cre +/− ;Nos3 −/− mice recapitulate the congenital cardiac phenotype of Notch1 +/− ;Nos3 −/− embryos.ConclusionsOur data demonstrate the role of endothelial Notch1 in the proper development of the semilunar valves and cardiac outflow tract.

Regular heartbeat rhythm at the heartbeat initiation stage is essential for normal cardiogenesis at low temperature

BackgroundThe development of blood flow in the heart is crucial for heart function and embryonic survival. Recent studies have revealed the importance of the extracellular matrix and the mechanical stress applied to the valve cushion that controls blood flow to the formation of the cardiac valve during embryogenesis. However, the events that trigger such valve formation and mechanical stress, and their temperature dependence have not been explained completely. Medaka (Oryzias latipes) inhabits a wide range of East Asia and adapts to a wide range of climates. We used medaka embryos from different genomic backgrounds and analyzed heartbeat characteristics including back-and-forth blood flow and bradyarrhythmia in embryos incubated at low temperature. We also used high-speed imaging analysis to examine the heartbeat of these animals after transient exposure to low temperature.ResultsEmbryos of the Hd-rR medaka strain exhibited back-and-forth blood flow in the heart (blood regurgitation) after incubation at 15°C. This regurgitation was induced by exposure to low temperature around the heartbeat initiation period and was related to abnormalities in the maintenance or pattern of contraction of the atrium or the atrioventricular canal. The Odate strain from the northern Japanese group exhibited normal blood flow after incubation at 15°C. High-speed time-lapse analysis of the heartbeat revealed that bradyarrhythmia occurred only in Hd-rR embryos incubated at 15°C. The coefficient of contraction, defined as the quotient of the length of the atrium at systole divided by its length at diastole, was not affected in either strain. The average heart rate after removing the effect of arrhythmia did not differ significantly between the two strains, suggesting that the mechanical stress of individual myocardial contractions and the total mechanical stress could be equivalent, regardless of the presence of arrhythmia or the heart rate. Test-cross experiments suggested that this circulation phenotype was caused by a single major genomic locus.ConclusionsThese results suggest that cardiogenesis at low temperature requires a constant heartbeat. Abnormal contraction rhythms at the stage of heartbeat initiation may cause regurgitation at later stages. From the evolutionary viewpoint, strains that exhibit normal cardiogenesis during development at low temperature inhabit northern environments.

Sox9bIs Required for Epicardium Formation and Plays a Role in TCDD-Induced Heart Malformation in Zebrafish

Activation of the transcription factor aryl hydrocarbon receptor by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) prevents the formation of the epicardium and leads to severe heart malformations in developing zebrafish (Danio rerio). The downstream genes that cause heart malformation are not known. Because TCDD causes craniofacial malformations in zebrafish by downregulating the sox9b gene, we hypothesized that cardiotoxicity might also result from sox9b downregulation. We found that sox9b is expressed in the developing zebrafish heart ventricle and that TCDD exposure markedly reduces this expression. Furthermore, we found that manipulation of sox9b expression could phenocopy many but not all of the effects of TCDD at the heart. Loss of sox9b prevented the formation of epicardium progenitors comprising the proepicardium on the pericardial wall, and prevented the formation and migration of the epicardial layer around the heart. Zebrafish lacking sox9b showed pericardial edema, an elongated heart, and reduced blood circulation. Fish lacking sox9b failed to form valve cushions and leaflets. Sox9b is one of two mammalian Sox9 homologs, sox9b and sox9a. Knock down of sox9a expression did not cause cardiac malformations, or defects in epicardium development. We conclude that the decrease in sox9b expression in the heart caused by TCDD plays a role in many of the observed signs of cardiotoxicity. We find that while sox9b is expressed in myocardial cells, it is not normally expressed in the affected epicardial cells or progenitors. We therefore speculate that sox9b is involved in signals between the cardiomyocytes and the nascent epicardial cells.

Simulation on the Dynamic Characteristics of an Electromagnetic Relief Valve with High Pressure and Large Flow Rate

The use of electromagnetic relief valve with high pressure and large flow rate in hydraulic system is usually easy to bring vibration and noise issues, especially while water or high water based fluid (HWBF) is used as the fluid medium. In this paper, a HWBF electromagnetic relief valve with a cushion valve was presented and its simulation model was built based on AMESim software. Through simulation, it is found that the cushion valve can significantly reduce the peak pressure gradient of the electromagnetic relief valve during unloading process compared with that without a cushion valve. This research provides a new solution for solving the vibration and noise issues of a hydraulic system with electromagnetic relief valve.

Cardiac expression of Brn-3a and Brn-3b POU transcription factors and regulation of Hsp27 gene expression

The Brn-3 family of transcription factors play a critical role in regulating expression of genes that control cell fate, including the small heat shock protein Hsp27. The aim of this study was to investigate the relationship between Brn-3a and Brn-3b and Hsp27 expression in the developing rodent heart. Brn-3a and Brn-3b were detected from embryonic days 9.5-10.5 (E9.5-E10.5) in the mouse heart, with significant increases seen later during development. Two isoforms (long and short) of each protein were detected during embryogenesis and postnatally. Brn-3a messenger RNA (mRNA) and protein were localized by E13.0 to the atrio-ventricular (AV) valve cushions and leaflets, outflow tract (OFT), epicardium and cardiac ganglia. By E14.5, Brn-3a was also localised to the septa and compact ventricular myocardium. An increase in expression of the long Brn-3a(l) isoform between E17 and adult coincided with a decrease in expression of Brn-3b(l) and a marked increase in expression of Hsp27. Hearts from Brn-3a-/- mice displayed a partially penetrant phenotype marked by thickening of the endocardial cushions and AV valve leaflets and hypoplastic ventricular myocardium. Loss of Brn-3a was correlated with a compensatory increase in Brn-3b and GATA3 mRNA but no change in Hsp27 mRNA. Reporter assays in isolated cardiomyocytes demonstrated that both Brn-3a and Brn-3b activate the hsp27 promoter via a consensus Brn-3-binding site. Therefore, Brn-3 POU factors may play an important role in the development and maintenance of critical cell types and structures within the heart, in part via developmental regulation of myocardial Hsp27 expression. Furthermore, Brn-3a may be necessary for correct valve and myocardial remodelling and maturation.

Ubiquitin fusion degradation 1–like gene dysregulation in bicuspid aortic valve

Bicuspid aortic valve, the most common congenital cardiac malformation, is caused by fusion of valve cushions at the onset of valvulogenesis. Although its exact pathogenesis is still unclear, a genetic basis is appearing more and more likely. Search for a potential candidate gene by reviewing semilunar valve morphogenesis led us to the ubiquitin fusion degradation 1-like gene (UFD1L), which is highly expressed in the cardiac outflow tract during embryogenesis. Aortic valves were collected during surgery from 39 patients with bicuspid aortic valve (mean age 56.8 +/- 18.1 years) and from 38 patients with tricuspid aortic valve (mean age 61.7 +/- 16.1 years). Fluorescence in situ hybridization was performed for detection of microdeletion, quantitative reverse transcriptase-polymerase chain reaction to measure gene expression, and Western blotting to analyze the amount of UFD1L gene product. No microdeletion was found in either group in the critical region of chromosome 22 containing the UFD1L gene. UFD1L gene expression, however, was significantly reduced in bicuspid aortic valve samples (median 787-fold) relative to tricuspid aortic valve samples (median 10,887-fold, P = .001). The amount of UFD1L gene product was also significantly diminished in bicuspid aortic valve samples (3.9 +/- 2.6 vs 8.4 +/- 4.8 optical density units, P < .05). Bicuspid aortic valve was associated with downregulation of UFD1L gene expression, supporting the hypothesis that bicuspid aortic valve is a genetic disorder, with the UFD1L gene as a potential candidate gene.

Control of endocardial cushion and cardiac valve maturation by BMP signaling pathways

Congenital heart defects, the leading cause of deaths from birth defects, are estimated to occur in close to 1% of live newborns. Among these, abnormal septation of the heart and valve anomalies are the most frequent forms. Despite progress defining several genes involved in normal heart development, we still have a limited understanding of the signaling pathways involved in morphogenesis of the outflow tract (OFT) and, to date, very few genes have been identified that are responsible for defects in humans. Bone Morphogenetic Protein (BMP) signaling pathways are emerging as vital regulators of multiple aspects of cardiogenesis, including the septation of the OFT and valve maturation. Genetic and other in vivo evidence is now supporting the role for BMPs as inducers of endocardial cushion epithelial-to-mesenchymal transformation that was suggested by in vitro explant studies as well as by their patterns of expression in the developing heart. Here, we review briefly the in vitro data, and detail the novel mouse models where perturbed BMP signaling pathways result in impaired OFT septation and semilunar valvulogenesis. We propose that growth of the OFT valve cushions is regulated by the level of BMP signaling, under the control of other signaling pathways.

Anatomy and formation of congenital bicuspid and quadricuspid pulmonary valves in Syrian hamsters.

Congenital bicuspid and quadricuspid pulmonary valves have received little attention because of their limited clinical relevance. However, knowledge of the mechanisms by which these anomalous valves develop is essential to obtain a more accurate survey of the etiological factors implicated in the malformations of the cardiac outflow tract in mammals. The present study was designed to assess the anatomical features of bicuspid and quadricuspid pulmonary valves in Syrian hamsters as well as to elucidate the mechanisms involved in the formation of these defective valves. The sample examined consisted of 206 adults and 28 embryos belonging to a laboratory-inbred family of Syrian hamsters with a high incidence of congenital anomalies of the pulmonary and aortic valves. The study was carried out using histological techniques for light microscopy, semithin sections, and scanning electron microscopy. The pulmonary valve was tricuspid in 140 of the 206 adult hamsters, and in 124 of these tricuspid valves the dorsal commissure was more or less extensively fused. Another 45 hamsters possessed a bicuspid pulmonary valve with the sinuses oriented ventrodorsally. In 43 of these bicuspid valves, a raphe was located in the dorsal pulmonary sinus. The pulmonary valve was quadricuspid in a further nine specimens. The remaining 12 hamsters had a tricuspid pulmonary valve with a raphe-like ridge located in the right pulmonary sinus. In seven of these valves, the dorsal commissure showed a more or less extensive fusion. The embryos examined, aged between 11 days, 3 hours and 12 days, 6 hours postcoitum, were at the beginning of the valvulogenesis. In five of the 28 embryos, the pulmonary valve consisted of three mesenchymal valve cushions, right, left, and dorsal. In a further 17 embryos, the right and left valve cushions were more or less fused toward the lumen of the pulmonary artery. In the remaining six embryos, the left and dorsal valve cushions were normal, whereas the right cushion was divided into two lobes. The present findings suggest that in the Syrian hamster: (1) bicuspid pulmonary valves result from the extensive fusion of the right and left pulmonary valve cushions at the beginning of the valvulogenesis, (2) the partial fusion of the right and left pulmonary valve cushions leads to the formation of tricuspid pulmonary valves with a more or less extensive fusion of the dorsal commissure, (3) quadricuspid pulmonary valves result from the partition of one of the three valve cushions at a very early stage of the valvulogenesis, and (4) the partial division of the right pulmonary valve cushion may lead to the development of tricupsid pulmonary valves with a raphe-like ridge located in the right pulmonary sinus. In addition, the present findings, together with previous observations in Syrian hamsters, indicate that in this species the mechanisms by which bicuspid and quadricuspid pulmonary valves develop are similar to those by which bicuspid and quadricuspid aortic valves form, respectively. However, the primary factor or factors that induce the malformations of the pulmonary valve operate independently from those inducing the malformations of the aortic valve.

Anatomy and formation of congenital bicuspid and quadricuspid pulmonary valves in Syrian hamsters

Background Congenital bicuspid and quadricuspid pulmonary valves have received little attention because of their limited clinical relevance. However, knowledge of the mechanisms by which these anomalous valves develop is essential to obtain a more accurate survey of the etiological factors implicated in the malformations of the cardiac outflow tract in mammals. The present study was designed to assess the anatomical features of bicuspid and quadricuspid pulmonary valves in Syrian hamsters as well as to elucidate the mechanisms involved in the formation of these defective valves. Methods The sample examined consisted of 206 adults and 28 embryos belonging to a laboratory-inbred family of Syrian hamsters with a high incidence of congenital anomalies of the pulmonary and aortic valves. The study was carried out using histological techniques for light microscopy, semithin sections, and scanning electron microscopy. Results The pulmonary valve was tricuspid in 140 of the 206 adult hamsters, and in 124 of these tricuspid valves the dorsal commissure was more or less extensively fused. Another 45 hamsters possessed a bicuspid pulmonary valve with the sinuses oriented ventrodorsally. In 43 of these bicuspid valves, a raphe was located in the dorsal pulmonary sinus. The pulmonary valve was quadricuspid in a further nine specimens. The remaining 12 hamsters had a tricuspid pulmonary valve with a raphe-like ridge located in the right pulmonary sinus. In seven of these valves, the dorsal commissure showed a more or less extensive fusion. The embryos examined, aged between 11 days, 3 hours and 12 days, 6 hours postcoitum, were at the beginning of the valvulogenesis. In five of the 28 embryos, the pulmonary valve consisted of three mesenchymal valve cushions, right, left, and dorsal. In a further 17 embryos, the right and left valve cushions were more or less fused toward the lumen of the pulmonary artery. In the remaining six embryos, the left and dorsal valve cushions were normal, whereas the right cushion was divided into two lobes. Conclusions The present findings suggest that in the Syrian hamster: (1) bicuspid pulmonary valves result from the extensive fusion of the right and left pulmonary valve cushions at the beginning of the valvulogenesis, (2) the partial fusion of the right and left pulmonary valve cushions leads to the formation of tricuspid pulmonary valves with a more or less extensive fusion of the dorsal commissure, (3) quadricuspid pulmonary valves result from the partition of one of the three valve cushions at a very early stage of the valvulogenesis, and (4) the partial division of the right pulmonary valve cushion may lead to the development of tricupsid pulmonary valves with a raphe-like ridge located in the right pulmonary sinus. In addition, the present findings, together with previous observations in Syrian hamsters, indicate that in this species the mechanisms by which bicuspid and quadricuspid pulmonary valves develop are similar to those by which bicuspid and quadricuspid aortic valves form, respectively. However, the primary factor or factors that induce the malformations of the pulmonary valve operate independently from those inducing the malformations of the aortic valve. Anat. Rec. 250:70–79, 1998. © 1998 Wiley-Liss, Inc.

Fusion of valve cushions as a key factor in the formation of congenital bicuspid aortic valves in Syrian hamsters.

Bicuspid aortic valve is the most frequent congenital cardiac malformation in humans. However, the morphogenesis of the defect is still unknown. Previous work showed that, in the Syrian hamster, congenital bicuspid aortic valves with the aortic sinuses arranged in ventrodorsal orientation are expressions of a trait the variation of which takes the form of a continuous phenotypic spectrum, ranging from a tricuspid aortic valve with no fusion of the ventral commissure to a bicuspid aortic valve devoid of any raphe. The present study was designed to elucidate the mechanism involved in the formation of bicuspid aortic valves in Syrian hamsters as a possible starting point for further investigation of this process in humans. The sample examined consisted of 80 embryos, aged between 10 days, 16 hours and 13 days, 1 hour postcoitum. Most (n = 59) of the embryos belonged to a laboratory-inbred family of Syrian hamsters with a high incidence of bicuspid aortic valves. The study was carried out using scanning electron microscopy and histological techniques for light microscopy. Twenty-three embryos showed a still undivided conotruncus. In all of these cases there were six mesenchymal semilunar valve primordia protruding into the lumen of the conotruncus. In a further 29 embryos, the conotruncus had just divided into the aortic and pulmonary channels; the embryos were at the beginning of the valvulogenesis. In 13 of these 29 embryos there were three well-defined aortic valve cushions, right, left, and dorsal, whereas in the other 16, the right and left valve cushions were more or less fused toward the lumen of the aorta; when they were completely fused, only two aortic valve cushions, a ventral and a dorsal, could be identified. In the remaining 28 embryos, the aortic valve cushions showed a marked degree of excavation. In 23 of these cases, the valve exhibited a basically tricuspid architecture, whereas it was unequivocally bicuspid in the other five. All variants of the aortic valve morphologic spectrum occurring in the Syrian hamster develop from three mesenchymal valve cushions, right, left, and dorsal, after normal septation of the conotruncus. The bicuspid condition of the aortic valve is not the consequence of improper development of the conotruncal ridges, conotruncal malseptation, valve cushion agenesis, or lesions acquired after a normal valvulogenesis. Fusion of the right and left valve cushions at the beginning of the valvulogenesis appears to be a key factor in the formation of bicuspid aortic valves. Each aortic valve acquires its specific morphology prior to the end of the valvulogenetic process.

Fusion of valve cushions as a key factor in the formation of congenital bicuspid aortic valves in Syrian hamsters

Fusion of valve cushions as a key factor in the formation of congenital bicuspid aortic valves in Syrian hamsters

Embryological evidence for the formation of a quadricuspid aortic valve in the Syrian hamster

Congenital quadricuspid aortic valve is a rare anomaly, the morphogenesis of which remains unclear. In this study we report the case of a Syrian hamster embryo that presented an aortic valve with four valve cushions instead of three. The embryo, aged 12 days and 2 hours postcoitum, was at an early stage of valvulogenesis. It was examined using semithin sections of the heart. Two of the four valve cushions were located, one in the dorsal and the other in the left-ventral position, corresponding, respectively, to the dorsal and left valve cushions of a normal aortic valve. The remaining two cushions were situated in the right-ventral position. They were joined at the level of their basal portions and were less developed in size than the other cushions. This report seems to be the first embryological evidence for the formation of a quadricuspid aortic valve. The present findings strongly suggest that the anomalous valve originated from three mesenchymal anlagen and that the supernumerary valve cushion resulted from the division of the anlagen that normally gives rise to the right valve cushion.

Characterization and ergonomic design modifications for pneumatic percussive rivet tools

This paper presents an intensive study on the ergonomic design modifications for pneumatic percussive rivet tools, i.e. rivet hammers and bucking bars. Detailed discussions are provided on the vibration characteristics, measurements, and methods of analyzing the multiple impulsive signals generated by the rivet tools. Recommendations arising from the study include design modifications using a recoilless concept, as well as other mechanical improvements, both for the rivet hammers and the bucking bars. It was found that the vibration transmitted to the worker's hands can be reduced by using a nose bushing, a low-stiffness spring, a valve cushion, and a coated cylinder in the rivet hammer. In addition, the recoilless method used in the bucking bars appears to be effective in diminishing the vibration to the workers.