Enhancing subcellular protein localization mapping analysis using Sc2promap utilizing attention mechanisms.

BACKGROUND: Aberrant protein localization is a prominent feature in many human diseases and can have detrimental effects on the function of specific tissues and organs. High-throughput technologies, which continue to advance with iterations of automated equipment and the development of bioinformatics, enable the acquisition of large-scale data that are more pattern-rich, allowing for the use of a wider range of methods to extract useful patterns and knowledge from them. METHODS: The proposed sc2promap (Spatial and Channel for SubCellular Protein Localization Mapping) model, designed to proficiently extract meaningful features from a vast repository of single-channel grayscale protein images for the purposes of protein localization analysis and clustering. Sc2promap incorporates a prediction head component enriched with supplementary protein annotations, along with the integration of a spatial-channel attention mechanism within the encoder to enables the generation of high-resolution protein localization maps that encapsulate the fundamental characteristics of cells, including elemental cellular localizations such as nuclear and non-nuclear domains. RESULTS: Qualitative and quantitative comparisons were conducted across internal and external clustering evaluation metrics, as well as various facets of the clustering results. The study also explored different components of the model. The research outcomes conclusively indicate that, in comparison to previous methods, Sc2promap exhibits superior performance. CONCLUSIONS: The amalgamation of the attention mechanism and prediction head components has led the model to excel in protein localization clustering and analysis tasks. GENERAL SIGNIFICANCE: The model effectively enhances the capability to extract features and knowledge from protein fluorescence images.

Fast Real-Time Brain Tumor Detection Based on Stimulated Raman Histology and Self-Supervised Deep Learning Model.

In intraoperative brain cancer procedures, real-time diagnosis is essential for ensuring safe and effective care. The prevailing workflow, which relies on histological staining with hematoxylin and eosin (H&E) for tissue processing, is resource-intensive, time-consuming, and requires considerable labor. Recently, an innovative approach combining stimulated Raman histology (SRH) and deep convolutional neural networks (CNN) has emerged, creating a new avenue for real-time cancer diagnosis during surgery. While this approach exhibits potential, there exists an opportunity for refinement in the domain of feature extraction. In this study, we employ coherent Raman scattering imaging method and a self-supervised deep learning model (VQVAE2) to enhance the speed of SRH image acquisition and feature representation, thereby enhancing the capability of automated real-time bedside diagnosis. Specifically, we propose the VQSRS network, which integrates vector quantization with a proxy task based on patch annotation for analysis of brain tumor subtypes. Training on images collected from the SRS microscopy system, our VQSRS demonstrates a significant speed enhancement over traditional techniques (e.g., 20-30 min). Comparative studies in dimensionality reduction clustering confirm the diagnostic capacity of VQSRS rivals that of CNN. By learning a hierarchical structure of recognizable histological features, VQSRS classifies major tissue pathological categories in brain tumors. Additionally, an external semantic segmentation method is applied for identifying tumor-infiltrated regions in SRH images. Collectively, these findings indicate that this automated real-time prediction technique holds the potential to streamline intraoperative cancer diagnosis, providing assistance to pathologists in simplifying the process.

Unveiling precision: a data-driven approach to enhance photoacoustic imaging with sparse data.

This study presents the Fourier Decay Perception Generative Adversarial Network (FDP-GAN), an innovative approach dedicated to alleviating limitations in photoacoustic imaging stemming from restricted sensor availability and biological tissue heterogeneity. By integrating diverse photoacoustic data, FDP-GAN notably enhances image fidelity and reduces artifacts, particularly in scenarios of low sampling. Its demonstrated effectiveness highlights its potential for substantial contributions to clinical applications, marking a significant stride in addressing pertinent challenges within the realm of photoacoustic acquisition techniques.

Modified Transannular Patching Palliation versus Modified Blalock-Taussig-Thomas Shunt in Infants with Severe Tetralogy of Fallot with Diminutive Pulmonary Arteries.

OBJECTIVE: The purpose of this study was to compare pulmonary arterial (PA) growth and morbidity, mortality, reintervention and complete repair rates after modified transannular patching palliation (mTAP) versus modified Blalock-Taussig-Thomas shunt (mBTS) for palliation in infants with severe tetralogy of Fallot (TOF) with diminutive pulmonary arteries. METHODS: This was a retrospective case review study of 107 patients (64 males) with severe TOF who underwent staged repair with either mTAP (n = 55) or mBTS (n = 52) over an 8-year period. Procedure-related PA growth and morbidity, mortality, reintervention and complete repair rates were compared. RESULTS: Two deaths occurred in the mBTS group due to sudden cardiac arrest, and five patients needed reintervention after the mBTS procedure because of shunt thrombosis or stenosis. Postoperative complications of mBTS included sudden cardiac arrest, shunt thrombosis/stenosis, vocal cord palsy and diaphragmatic palsy. Unlike in the mBTS group, no death, severe complications or reintervention occurred in the mTAP group. Oxygen saturations post mTAP and mBTS were significantly higher, which improved from 67.73 ± 4.36% to 94.33 ± 2.19% in the mTAP group and from 68.24 ± 3.87% to 86.87 ± 3.38% in the mBTS group. The increase in oxygen saturation and pulmonary artery growth (from pre- to post palliation) was significantly better with mTAP than with mBTS palliation (p < 0.01). All 55 patients showed complete repair after mTAP, and the time from palliation to complete repair was significantly shorter in the mTAP group. CONCLUSIONS: In a severe form of TOF with the hypoplastic PA tree, mTAP seems to be a better strategy that is safe and better facilitates satisfactory pulmonary arterial growth until complete repair than the mBTS procedure.

3DCNAS: A universal method for predicting the location of fluorescent organelles in living cells in three-dimensional space.

Cellular biology research relies on microscopic imaging techniques for studying the complex structures and dynamic processes within cells. Fluorescence microscopy provides high sensitivity and subcellular resolution but has limitations such as photobleaching and sample preparation challenges. Transmission light microscopy offers a label-free alternative but lacks contrast for detailed interpretation. Deep learning methods have shown promise in analyzing cell images and extracting meaningful information. However, accurately learning and simulating diverse subcellular structures remain challenging. In this study, we propose a method named three-dimensional cell neural architecture search (3DCNAS) to predict subcellular structures of fluorescence using unlabeled transmitted light microscope images. By leveraging the automated search capability of differentiable neural architecture search (NAS), our method partially mitigates the issues of overfitting and underfitting caused by the distinct details of various subcellular structures. Furthermore, we apply our method to analyze cell dynamics in genome-edited human induced pluripotent stem cells during mitotic events. This allows us to study the functional roles of organelles and their involvement in cellular processes, contributing to a comprehensive understanding of cell biology and offering insights into disease pathogenesis.

Pixel-level multimodal fusion deep networks for predicting subcellular organelle localization from label-free live-cell imaging.

Complex intracellular organizations are commonly represented by dividing the metabolic process of cells into different organelles. Therefore, identifying sub-cellular organelle architecture is significant for understanding intracellular structural properties, specific functions, and biological processes in cells. However, the discrimination of these structures in the natural organizational environment and their functional consequences are not clear. In this article, we propose a new pixel-level multimodal fusion (PLMF) deep network which can be used to predict the location of cellular organelle using label-free cell optical microscopy images followed by deep-learning-based automated image denoising. It provides valuable insights that can be of tremendous help in improving the specificity of label-free cell optical microscopy by using the Transformer-Unet network to predict the ground truth imaging which corresponds to different sub-cellular organelle architectures. The new prediction method proposed in this article combines the advantages of a transformer's global prediction and CNN's local detail analytic ability of background features for label-free cell optical microscopy images, so as to improve the prediction accuracy. Our experimental results showed that the PLMF network can achieve over 0.91 Pearson's correlation coefficient (PCC) correlation between estimated and true fractions on lung cancer cell-imaging datasets. In addition, we applied the PLMF network method on the cell images for label-free prediction of several different subcellular components simultaneously, rather than using several fluorescent labels. These results open up a new way for the time-resolved study of subcellular components in different cells, especially for cancer cells.

Aortic regurgitation after closure of ventricular septal defect by transcatheter device: the long-term complication.

Ventricular septal defect is the most common type of CHD, and transcatheter ventricular septal defect closure has been shown to be an alternative to surgical closure with acceptable mortality and morbidity as well as encouraging results. Short-term and mid-term follow-ups have indicated the safety and efficacy of transcatheter closure, but long-term follow-up results were rare. In this report, we first found that aortic regurgitation occurred in patients 9-12 years following transcatheter closure and regurgitation were gradually increased. The findings indicate that the long-term outcome of transcatheter closure of ventricular septal defect may not be as satisfied as expected.

Activation of AMPK alleviates cardiopulmonary bypass-induced cardiac injury via ameliorating acute cardiac glucose metabolic disorder.

Recent years, studies have demonstrated that hyperglycemia is one of the main manifestations after cardiac surgeries, which contributes to myocardial injuries and increases the chance of subsequent complications and mortality in such patients. However, strategies targeting at glucose metabolic disorder after cardiac surgeries to attenuate myocardial injuries are inadequately studied. In this study, a rat model of cardiopulmonary bypass (CPB) was applied to investigate the role of Adenosine 5'-monophosphate-activated protein kinase (AMPK) in modulating myocardial glucose metabolic-induced cardiac injuries after cardiac surgery. The results revealed that CPB elicited significant cardiac dysfunction, and pronouncedly elevated the markers of myocardial injuries including serum creatine kinase MB and cardiac troponin I. Additionally, blunted myocardial glucose uptake after CPB was associated with decreased membrane glucose transporter 4 (GLUT4) content. However, pretreatment of AMPK agonist 5-aminoimidazole-4-carboxamide1-ß-D-ribofuranoside (AICAR) at the beginning of CPB activated AMPK, enhanced phosphorylation of Akt substrate 160 (AS160), and increased myocardial membrane content of GLUT4. Meanwhile, improved myocardial glucose uptake and more importantly alleviated cardiac injury were also observed after CPB pretreated with AICAR. Moreover, the application of a mutant form of AS160 (AS160-4P) abolished the beneficial effect of AICAR, as evidenced by impaired cardiac glucose uptake, reduced myocardial membrane GLUT-4 translocation, increased cardiac injury markers, and deterioration of cardiac function after CPB. In conclusion, it was suggested in this study that preactivation of AMPK by AICAR improved myocardial glucose uptake by promoting AS160 dependent myocardial membrane GLUT-4 translocation, which ultimately provided a potent cardioprotective effect.

One-stage surgical correction in pentalogy of Cantrell with left ventricular diverticulum.

The pentalogy of Cantrell is a rare and fatal malformation. A left ventricular diverticulum is a common finding of this pentalogy. The present report summarizes our experience with three patients who suffered from pentalogy of Cantrell. All three cases had a left ventricular diverticulum. The intracardiac malformations and the left ventricular diverticulum were corrected simultaneously. All patients recovered uneventfully. One-stage surgical correction could improve short-term outcomes in selected patients with pentalogy of Cantrell.

Relationships of adiponectin with markers of systemic inflammation and insulin resistance in infants undergoing open cardiac surgery.

BACKGROUND: Insulin resistance and systemic inflammation frequently occur in infants undergoing cardiac surgery with cardiopulmonary bypass, while adiponectin has been demonstrated to have insulin-sensitizing and anti-inflammatory properties in obesity and type 2 diabetes mellitus. In this prospective study, we aimed to investigate the association of adiponectin with insulin resistance and inflammatory mediators in infants undergoing cardiac surgery with cardiopulmonary bypass. METHODS AND RESULTS: From sixty infants undergoing open cardiac surgery, blood samples were taken before anesthesia, at the initiation of cardiopulmonary bypass and at 0, 6, 12, 24, and 48 hours after the termination of cardiopulmonary bypass. Plasma interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF- α ), and adiponectin levels were assessed in blood samples. Insulin resistance was measured by assessment of the insulin requirement to maintain euglycaemia and repeated measurements of an insulin glycaemic index. Insulin glycaemic index, IL-6, and TNF- α increased up to 3-8-fold 6 h after the operation. Adiponectin is negatively correlated with markers of systemic inflammation 6 h after CPB. CONCLUSIONS: Although the level of serum adiponectin decreased significantly, there was a significant inverse association of adiponectin with markers of systemic inflammation and insulin resistance in infants undergoing open cardiac surgery.

Carboxy terminus of heat shock protein (HSP) 70-interacting protein (CHIP) inhibits HSP70 in the heart

Heat shock protein (HSP) 70 plays a critical role in protecting the heart from various stressor-induced cell injuries; the mechanism remains to be further understood. The present study aims to elucidate the effect of a probiotics-derived protein, LGG-derived protein p75 (LGP), in alleviating the ischemia/reperfusion (I/R)-induced heart injury. We treated rats with the I/R with or without preadministration with LGP. The levels of HSP70 and carboxy terminus of HSP70-interacting protein (CHIP) in the heart tissue were assessed by enzyme-linked immunosorbent assay (ELISA) and Western blotting. The effect of CHIP on suppression of HSP70 and the effect of LGP on suppression of CHIP were investigated with an I/R rat model and a cell culture model. The results showed that I/R-induced infarction in the heart could be alleviated by pretreatment with LGP. HSP70 was detected in naïve rat heart tissue extracts. I/R treatment significantly suppressed the level of HSP70 and increased the levels of CHIP in the heart. A complex of CHIP/HSP70 was detected in heart tissue extracts. The addition of recombinant CHIP to culture inhibited HSP70 in heart cells. LGP was bound CHIP in heart cells and prevented the CHIP from binding HSP70. In summary, I/R can suppress HSP70 and increase CHIP in heart cells. CHIP can suppress HSP70 that can be prevented by pretreatment with LGP. The results imply that CHIP may be a potential target in the prevention of I/R-induced heart cell injury (AU)

Quadruple valve replacement with mechanical valves: an 11-year follow-up study.

BACKGROUND: We performed the first quadruple valve replacement with mechanical valves, combined with the correction of complex congenital heart disease on November 17, 1999. We report here the 11-year follow-up study. METHODS: A 47-year-old man with subacute rheumatic endocarditis, a ventricular septal defect, and an obstruction of the right ventricular outflow tract required replacement of the aortic, mitral, tricuspid, and pulmonary valves; repair of the ventricular septal defect; and relief of the obstruction of the right ventricular outflow tract. The surgery was done on November 17, 1999, after careful systemic preparation of the patient. Warfarin therapy with a target international normalized ratio (INR) range of 1.5 to 2.0 was used. Follow-up included monitoring the INR, recording the incidences of thromboembolic and bleeding events, electrocardiography, radiography, and echocardiography evaluations. RESULTS: The patient's INR was maintained between 1.5 and 2.0. All 4 mechanical prosthetic heart valves worked well. He is in generally good health without any thromboembolic or bleeding complications. CONCLUSIONS: Long-term management is challenging for patients who have experienced quadruple valve replacement with mechanical valves; however, promising results could mean that replacement of all 4 heart valves in 1 operation is feasible in patients with quadruple valve disease, and an INR of 1.5 to 2.0 could be appropriate for Chinese patients with undergoing valve replacement with mechanical valves.

Carboxy terminus of heat shock protein (HSP) 70-interacting protein (CHIP) inhibits HSP70 in the heart.

Heat shock protein (HSP) 70 plays a critical role in protecting the heart from various stressor-induced cell injuries; the mechanism remains to be further understood. The present study aims to elucidate the effect of a probiotics-derived protein, LGG-derived protein p75 (LGP), in alleviating the ischemia/reperfusion (I/R)-induced heart injury. We treated rats with the I/R with or without preadministration with LGP. The levels of HSP70 and carboxy terminus of HSP70-interacting protein (CHIP) in the heart tissue were assessed by enzyme-linked immunosorbent assay (ELISA) and Western blotting. The effect of CHIP on suppression of HSP70 and the effect of LGP on suppression of CHIP were investigated with an I/R rat model and a cell culture model. The results showed that I/R-induced infarction in the heart could be alleviated by pretreatment with LGP. HSP70 was detected in naïve rat heart tissue extracts. I/R treatment significantly suppressed the level of HSP70 and increased the levels of CHIP in the heart. A complex of CHIP/HSP70 was detected in heart tissue extracts. The addition of recombinant CHIP to culture inhibited HSP70 in heart cells. LGP was bound CHIP in heart cells and prevented the CHIP from binding HSP70. In summary, I/R can suppress HSP70 and increase CHIP in heart cells. CHIP can suppress HSP70 that can be prevented by pretreatment with LGP. The results imply that CHIP may be a potential target in the prevention of I/R-induced heart cell injury.

Connexin40 modulates pulmonary permeability through gap junction channel in acute lung injury after thoracic gunshot wounds.

BACKGROUND: The permeability of pulmonary microvessel endothelial cells increases markedly after acute lung injury via paracellular gap. Connexin40 is a primary component of pulmonary microvessel endothelial cells gap junction channel and mediates intercellular communication. However, the relationship between connexin40 and the permeability of pulmonary microvessel endothelial cells is still unknown. Therefore, we determined whether connexin40 affected rabbits' pulmonary microvessel endothelial cells permeability after acute lung injury induced by gunshot trauma. METHODS: We used an acute lung injury model in New Zealand rabbits following gunshot chest trauma and correlated connexin40 immunohistochemistry in gunshot lung tissue with Evans blue leak rate. Cultured pulmonary microvessel endothelial cells were divided into three groups, control (G control), injured serum (G serum), and blocker agent (G blocker). Gap junction channel function was assessed by scrape-loading and dye transfer techniques. Pulmonary microvessel endothelial cells permeability was measured by Evans blue-labeled albumin transfer. RESULTS: Connexin40 expression decreased time dependently, whereas Evans blue leak rate increased. Connexin40 expression and Evans blue leak rate exhibited a strong inverse correlation (gamma = -0.934, p < 0.05). Injured serum decreased gap junction channel function, and the gap junction channel blocker aggravated this effect. Similarly, pulmonary microvessel endothelial cells permeability increased significantly in G serum and G blocker. CONCLUSIONS: Connexin 40 expression in pulmonary microvasculature endothelial cells is downregulated after acute lung injury induced by gunshot trauma. This is associated with impaired gap junction channel function and increased pulmonary microvessel endothelial cells permeability.

Gap junction channel modulates pulmonary vascular permeability through calcium in acute lung injury: an experimental study.

BACKGROUND: Increased pulmonary vascular permeability is a hallmark of acute lung injury (ALI). Gap junction channels (GJCs) connect adjacent cells and facilitate ion exchange. It remained unclear whether GJCs modulate pulmonary permeability in ALI through intracellular calcium. OBJECTIVES: This study aimed to verify if GJCs in pulmonary microvessel endothelial cells (PMVECs) modulate pulmonary vascular permeability in ALI via intracellular calcium. METHODS: Firstly, an animal model of ALI was studied using connexin 40 (Cx40) immunohistochemistry in the lung with Evans' blue (EB) leakage. Then cultured PMVECs were divided into three groups: G(control), G(serum) and G(blocker). Serum was obtained from animals with ALI following gunshot injury (injured serum). Initially, G(blocker) was treated with the blocker of GJCs, and then G(serum) and G(blocker) were stimulated with the injured serum, respectively. GJCs, the permeability of cell monolayers and intracellular Ca(2+) were assessed. RESULTS: Cx40 time-dependently decreased, whereas EB leakage increased. Cx40 and EB leakage exhibited a strong inverse correlation (rho = -0.934, p < 0.05). Injured serum decreased GJCs and expression of Cx40, whereas the blocker aggravated this effect. Similarly, when PMVEC monolayer was treated with injured serum, both permeability and intracellular Ca(2+) increased. These effects were also aggravated with the blocker. CONCLUSIONS: Depression of GJCs of PMVECs increased pulmonary vascular permeability in ALI; this effect may be mediated by the overload of intracellular calcium.

Antegrade cerebral perfusion during deep hypothermia circulatory arrest attenuates the apoptosis of neurons in porcine hippocampus.

BACKGROUND: Cerebral damage is a major problem after reconstructive surgery of the aortic arch and the descending aorta. Current protective strategies, including deep hypothermia and antegrade cerebral perfusion (ACP), are used to prolong the tolerated duration of circulatory arrest. The aim of the study was to observe the influence of deep hypothermic circulatory arrest (DHCA) and ACP on neuronal apoptosis in the hippocampus. To further elucidate the mechanisms of neurologic injury and protection, we assessed the expression of the antiapoptotic protein Bcl-2 and the proapoptotic protein Bax. METHODS: We randomly divided 18 pigs into 3 groups: The control group (n = 6) received normal-temperature cardiopulmonary bypass (CPB), the DHCA group (core temperature, 18 degrees C; n = 6) received DHCA for 90 minutes, and the third group (DHCA + ACP) (core temperature, 18 degrees C; ACP, flow rate of 30 mL/kg per minute at a pressure of 15-25 mm Hg; n = 6) received DHCA for 90 minutes. Hippocampal tissue was sampled 2 hours after CPB was finished. Bcl-2 and Bax expression was examined by immunohistochemistry. Morphologic changes in hippocampal tissue were measured with transmission electron microscopy. RESULTS: Bax protein levels were significantly higher in the DHCA group than in the other 2 groups (P < .05), whereas Bcl-2 protein levels were significantly higher in the DHCA + ACP group than in the other 2 groups (P < .05). Obvious neuronal apoptosis was observed in the DHCA group but not in the controls, and few apoptotic neurons were seen in the DHCA + ACP group. CONCLUSIONS: DHCA can induce neuronal apoptosis in the hippocampus. ACP during the DHCA period protects cerebral tissue by suppressing apoptosis through decreasing Bax expression and increasing Bcl-2 expression.

Surgical treatment of giant coronary artery aneurysm secondary to Kawasaki disease.

AIM: To investigate the clinical features and surgical management of giant coronary artery aneurysm during end-stage Kawasaki disease. METHODS: From May 2006 to October 2007, 5 patients, 2 to 57 years old, presented with giant coronary artery aneurysm and underwent surgical correction. The coronary aneurysm diameters were 1.5 to 2.5 cm. The coronary aneurysm lesion sites included the right main coronary artery in 1 case, the left main coronary artery in 2 cases, and both the left and right coronary arteries in 2 cases. Preoperative electrocardiogram revealed altered S-T segments in 5 cases and reduced ejection fraction values in 3 cases, resulting in 1 emergency admission for congestive heart failure. Surgical treatments included thromboendarterectomy, thrombectomy, and aneurysmal reconstruction under the orthophoria of extracorporeal circulation. RESULTS: There were no operative deaths. All patients recovered and received dopamine 2 to 4 microg/min per kg and nitroglycerine 0.3 to 0.5 microg/min per kg. Time spent by patients in intensive care was uneventful. Following surgery, 4 patients showed ischemic improvement of the S-T segment on electrocardiograms, and 4 patients presented with increased ejection fraction, according to cardiac ultrasound inspection. The improvement of ejection fraction value was not significant in only 1 case. CONCLUSION: Surgery is necessary for stage-3 Kawasaki disease patients that have giant coronary artery aneurysm complications. Surgical treatment includes thromboendarterectomy, thrombus clearing, aneurysmal reconstruction, and coronary artery bypass grafting, followed by postoperative anticoagulation and immunotherapy. Myocardial ischemia and cardiac function can be greatly improved through surgery.

Age-dependent mobilization of circulating endothelial progenitor cells in infants and young children undergoing cardiac surgery with cardiopulmonary bypass.

This study was designed to find the effects of age on circulating endothelial progenitor cells (EPCs) and their mobilization in infants and young children following surgical correction of congenital heart defects. In 60 consecutive infants and young children (1month to 3years old) undergoing repair of atrial/ventricular septal defect, the numbers of EPCs and plasma levels of IL-6, -8, -10, TNF-alpha, VEGF and G-CSF were determined preoperatively, at the end of cardiopulmonary bypass (CPB), as well as 6, 12, 24, 48, 72 and 96h following surgery. Preoperative EPCs were reduced with increased age, similar to changes in plasma VEGF and G-CSF levels. Rapid mobilizations of EPCs and plasma VEGF, G-CSF were induced by cardiac surgery with CPB in all infants and young children, and the increased volumes of EPCs, VEGF and G-CSF decreased with age decreasing. The increased volumes of IL-6, -8, -10 and TNF-alpha were similar in different age groups. However, mobilization of EPCs, plasma VEGF and G-CSF were limited in infants <6months old, which did not correlate with change in inflammatory IL activation. Preoperative EPCs and plasma levels of VEGF and G-CSF were reduced with increasing age in infants and young children. Although a significant increase in EPCs and release of cytochemokines were observed in infants undergoing CPB, the mobilization of EPCs of the infants <6months old are limited.

Calcification resistance of procyanidin-treated decellularized porcine aortic valves in vivo.

OBJECTIVES: Conventional glutaraldehyde fixation is conducive to calcification of bioprosthetic tissues. The aim of this study was to test calcification resistance of procyanidin-treated decellularized porcine aortic valve in a rat model. MATERIALS AND METHODS: We performed cross-linking of the decellularized porcine aortic heart valves by procyanidins and observed morphologic performance and examined the tensile strength and cross-linking index. Then we implanted subcutaneous samples of procyanidin cross-linking decellularized valves, glutaraldehyde cross-linking decellularized valves, and decellularized valves in rats. The retrieved grafts were stained with hematoxylin-eosin and von Kossa and were analyzed with scanning electron microscopy and x-ray energy dispersive spectroscopy (EDS) after 21 and 63 days. RESULTS: After decellularized and cross-linking pretreatment, the procyanidin cross-linked leaflets were soft and stretchable. In addition, the cellular components of the porcine aortic heart valve leaflets were completely removed, and the extracelluar matrix was maintained completely. Examination of tensile strength revealed a significantly higher tissue resistance to tension in procyanidin cross-linked tissue than in other tissues, including the glutaraldehyde group (P< .05), even though the extents of cross-linking of each group were roughly the same at approximately 90%. Histopathologic examination showed that the procyanidin cross-linked valve matrix had no significant calcification, and there were no calcium peaks in the EDS profile of procyanidin cross-linked samples in the 21-day and 63-day rat studies. CONCLUSION: This study demonstrated that procyanidin cross-linked decellularized heart valves can resist calcification to some extent.

Pulse oxygen saturation measured in standing and squatting positions may be useful in evaluating tetralogy of Fallot.

BACKGROUND: Left-ventricular end-diastolic volume index (LVEDVI) and Nakata index, which in most cases are evaluated by echocardiography and cardiac catheterization, are 2 important predictors for the prognosis of surgical correction of tetralogy of Fallot (TOF). Nonetheless, performing these procedures on TOF patients is not always feasible. We therefore investigated whether the difference in transcutaneous pulse oxygen saturation between the standing position and squatting position (DeltaSPO2) reflected the LVEDVI and Nakata index, allowing DeltaSPO2 to be used as a supplement to echocardiography and cardiac catheter evaluation. METHODS: Nineteen TOF patients (11 boys, 8 girls; median age 6 years) were randomly selected for this study. In each patient, we used a pulse oximeter placed on the left index finger to measure transcutaneous pulse oxygen saturation, first with the patient in a standing position and then with the patient in a squatting position. We then performed correlational analyses of DeltaSPO2 and the LVEDVI or Nakata index. RESULTS: The mean SPO2 was 79%+/-4% in standing patients and 84%+/-4% in squatting patients, and the mean DeltaSPO2 was 5%+/-3%. The LVEDVI was 41+/-5 mL/m2, and the Nakata index was 188+/-37 mm2/m2. DeltaSPO2 correlated with both LVEDVI (gamma=0.854, P< .05) and the Nakata index (gamma=0.641, P< .05). CONCLUSION: For patients with TOF, the DeltaSPO2 between SPO2 measured in a standing and squatting position has a positive correlation with the LVEDVI and Nakata index. Thus these measurements may be used as supplemental factors in evaluating LV function and performing a preoperative assessment of the pulmonary artery.