Congenital absence of left atrial appendage combined with type A Wolff-Parkinson-White syndrome diagnosed by multimodal imaging.

The absence of left atrial appendage (LAA) is relatively rare, especially with type A Wolff-Parkinson-White syndrome. Secondly, we diagnosed it by multimodal imaging including two-dimensional (2D) and three-dimensional (3D) transesophageal echocardiography (TEE), CT, electrophysiological examination, and 3D electro anatomical mapping system, which is more comprehensive.

Dynamic Changes in Plasma Urotensin II and Its Correlation With Plaque Stability.

ABSTRACT: Urotensin II (UII) is involved in the formation of atherosclerosis, but its role in the stability of atherosclerotic plaques is unknown. The purpose of this study was to observe the dynamic changes in plasma UII and analyze its relationship to the stability of atherosclerotic plaques. One hundred thirty-five consecutive patients with acute coronary syndrome (ACS) were enrolled. The plasma UII levels were measured immediately after admission and during three-month follow-up. A vulnerable plaque model was established using local transfection of a recombinant P53 adenovirus into plaques in rabbits fed with a high-cholesterol diet and subjected to balloon arterial injury. The levels of plasma UII were measured weekly. The changes in plasma UII during the formation of atherosclerotic plaques and before and after plaque transfection were observed. The morphology of the plaques and the expression, distribution, and quantitative expression of UII in the plaques also were observed. Our results showed that the levels of plasma UII in patients with ACS at admission were lower than levels observed at the three-month follow-up. UII dynamic changes and its correlation with plaque stabilities were further verified in rabbits with atherosclerotic vulnerable plaques. The UII levels in rabbits were significantly decreased immediately after the P53 gene transfection, which led to plaque instability and rupture. These results suggested that UII expression was down-regulated in ACS, which may be related to its ability to modulate mechanisms involved in plaque stability and instability.

Robust 4d-5f Bimetal-Organic Framework for Efficient Removal of Trace SO2 from SO2/CO2 and SO2/CO2/N2 Mixtures.

Herein, we report a highly rare robust 4d-5f bimetal-organic framework that shows high porosity and thermal/chemical stability and thus is capable of removing trace SO2 from a SO2/CO2/N2 mixture even under humid conditions. This work not only shows a novel adsorbent for SO2 removal but also extends the function of actinium-based coordination compounds.

Microencapsulation of low-passage poorly-differentiated human mucoepidermoid carcinoma cells by alginate microcapsules: in vitro profiling of angiogenesis-related molecules.

BACKGROUND: Human mucoepidermoid carcinoma (MEC) is regarded as the most common primary salivary malignancy. High-grade MEC has a high risk of recurrence and poor prognosis. Tumor angiogenesis, induced by poorly differentiated cancer cells of high-grade MEC, contributes to tumor growth and metastasis. Therefore, elucidating molecular mechanisms underlying the pro-angiogenic ability of poorly differentiated MEC cells is critical for the understanding of high-grade MEC progression. It is well known that three-dimensional (3D) cell culture, in contrast with conventional two-dimensional (2D) culture, provides a better approach to in vitro recapitulation of in vivo characteristics of cancer cells and their surrounding microenvironment. The purpose of this study was to model a 3D environment for in vitro gene expression profiling of key molecules in poorly differentiated MEC cells for cancer neovascularization and compared them with traditional 2D cell culture. METHODS: Low-passage poorly differentiated MEC cells, derived from human patient samples of high-grade MEC, were microencapsulated in sodium alginate gel microcapsules (3D culture) and compared with cells grown in 2D culture. Cancer cell proliferation was determined by MTT assays for 1 week, and gene expression of VEGF-A, bFGF and TSP-1 was analyzed by western blotting or ELISA. The hypoxic environment in 3D versus 2D culture were assessed by western blotting or immunofluorescence for HIF1α, and the effect of hypoxia on VEGF-A gene expression in 3D cultured cancer cells was assessed by western blotting with the use of the HIF1α inhibitor, 2-methoxyestradiol (2-MeOE2). RESULTS: When encapsulated in alginate gel microcapsules, low-passage poorly differentiated human MEC cells grew in blocks and demonstrated stronger and relatively unlimited proliferation activities. Moreover, significant differences were found in gene expression, with 3D-grown cancer cells a significant increment of VEGF-A and bFGF and a drastic reduction of TSP-1. Consistently, 3D-grown cancer cells secreted significantly more VEGF-A than 2D culture cancer cells. Furthermore, 3D-grown cancer cells showed significantly higher expression of HIF1α, a molecular indicator of hypoxia; the increased expression of VEGF-A in 3D cultured cancer cells was shown to be dependent on the HIF1α activities. CONCLUSIONS: The present work shows the effects of 3D culture model by alginate microencapsulation on the proangiogenic potentials of low-passage poorly differentiated human MEC cells. Cancer cells in this 3D system demonstrate significant intensification of key molecular processes for tumor angiogenesis. This is due to a better modeling of the hypoxic tumor microenvironment during 3D culture.

A Fluorescence Sensor for Lead (II) Ions Determination Based on Label-Free Gold Nanoparticles (GNPs)-DNAzyme Using Time-Gated Mode in Aqueous Solution.

This paper describes a label-free 17E DNAzyme-based time-gated fluorescence sensor for Pb2+ detection by unmodified gold nanoparticles (GNPs) and a terbium ternary complex. The fluorophore that used in this paper is a terbium ternary complex. Its signal can be measured in a time-gated manner which could eliminate most of the unspecific fluorescent background. It is well known that unfolded single-stranded DNA (ssDNA) could be adsorbed on GNPs while double-stranded DNA could not. The cleavage of the substrate by the 17E DNAzyme in the presence of Pb2+ causes the release of ssDNA from the 17E-17S duplex to be absorbed onto GNPs, preventing the aggregation of GNPs and then leading to a fluorescence decrease of terbium ternary complex. By means of this method, the authors have successfully detected Pb2+ over a range of 10 nM to 2500 nM with a detection limit of 1.7 nM. The sensor also exhibited good selectivity. The sensor provided a simple, cost-effective, rapid and sensitive measurement tool for Pb2+ detection.

GDF8 inhibits bone formation and promotes bone resorption in mice.

Growth Differentiation Factor 8 (GDF8), also called myostatin, is a member of the transforming growth factor (TGF)-ß super-family. As a negative regulator of skeletal muscle growth, GDF8 is also associated with bone metabolism. However, the function of GDF8 in bone metabolism is not fully understood. Our study aimed to investigate the role of GDF8 in bone metabolism, both in vitro and in vivo. Our results showed that GDF8 had a negative regulatory effect on primary mouse osteoblasts, and promoted receptor activator of nuclear factor κB ligand (RANKL)-induced osteoclastogenesis in vitro. Intraperitoneal injection of recombinant GDF8 repressed bone formation and accelerated bone resorption in mice. Furthermore, treatment of aged mice with a GDF8 neutralizing antibody stimulated new bone formation and prevented bone resorption. Thus, our study showed that GDF8 plays a significant regulatory role in bone formation and bone resorption, thus providing a potential therapeutic pathway for osteoporosis.

Molecular Characteristics of Methicillin-Resistant Staphylococcus epidermidis on the Abdominal Skin of Females before Laparotomy.

Staphylococcus epidermidis, especially methicillin-resistant strains, may be the source of surgical site infections and may be a reservoir of staphylococcal cassette chromosome mec (SCCmec) for S. aureus. The aim of this study was to investigate the prevalence of methicillin-resistant S. epidermidis (MRSE) on the abdominal skin of females before laparotomy and determine the molecular characteristics and antimicrobial susceptibility patterns of these isolates. MRSE was found in 54 of 157 isolates based on mecA gene detection, and there was no difference in icaA gene carriage rate between MRSE and methicillin-susceptible S. epidermidis (MSSE) isolates. Antimicrobial susceptibility profiles were determined by broth microdilution antimicrobial susceptibility testing according to the latest CLSI manuals. All MRSE isolates had unfavorable antimicrobial susceptibility patterns. Twenty-three MRSE strains (42.6%) were multi-drug resistant. SCCmec typing and pulsed field gel electrophoresis (PFGE) typing was performed. Thirty-nine (72.2%) had a single SCCmec type, whereas 1.9% had two types. Fourteen strains (25.9%) were non-typeable (NT). The most frequent MRSE genotype was SCCmec type IVa. High diversity with PFGE patterns was obtained for MRSE, and there were no isolates exhibiting identical pulsotype. The results confirm that methicillin-resistant strains are frequently present among S. epidermidis on the abdominal skin of females before laparotomy. Moreover, resistance profiles seem to have no association with the SCCmec types or PFGE types for most common antibiotics.

MiR-125a TNF receptor-associated factor 6 to inhibit osteoclastogenesis.

MicroRNAs (miRNAs) play important roles in osteoclastogenesis and bone resorption. In the present study, we found that miR-125a was dramatically down-regulated during macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor-κB ligand (RANKL) induced osteoclastogenesis of circulating CD14+ peripheral blood mononuclear cells (PBMCs). Overexpression of miR-125a in CD14+ PBMCs inhibited osteoclastogenesis, while inhibition of miR-125a promoted osteoclastogenesis. TNF receptor-associated factor 6 (TRAF6), a transduction factor for RANKL/RANK/NFATc1 signal, was confirmed to be a target of miR-125a. EMSA and ChIP assays confirmed that NFATc1 bound to the promoter of the miR-125a. Overexpression of NFATc1 inhibited miR-125a transcription, and block of NFATc1 expression attenuated RANKL-regulated miR-125a transcription. Here, we reported that miR-125a played a biological function in osteoclastogenesis through a novel TRAF6/ NFATc1/miR-125a regulatory feedback loop. It suggests that regulation of miR-125a expression may be a potential strategy for ameliorating metabolic disease.

[Use of Ultrasound in the Follow-up of Professional Athletes Receiving Conservative Treatment of Patellar Tendon Enthesiopathy].

OBJECTIVE: To investigate the role of high-frequency ultrasound (HFUS) in evaluating in the effectiveness of conservative treatment for professional athletes with patellar tendon enthesiopathy. METHODS: According to different treatment intensities, 24 professional athletes with patellar tendon enthesiopathy were randomly divided into painless group, slightly-painful group and extremely-painful group. Then changes of the HFUS findings [including ranges of two-dimensional diseases and blood conditions by Color Doppler Flow Imaging (CDFI)] of patellar tendon before and after the treatment were recorded. The results were also compared with conventional clinical treatment evaluations. RESULTS: After two courses of treatment,the percentage of athletes whose pain was resolved or disappeared was 37.5% in painless group, 87.5% in slightly-painful group, and 62.5% in extremely-painful group. The pain score was 4.50 ± 2.07, 4.88 ± 1.13, and 6.13 ± 1.55 in painless group,slightly-painful group,and extremely-painful group, respectively,before treatment and 4.88 ± 2.17, 3.00 ± 1.77,and 5.13 ± 2.36 after treatment. The average pain score remarkably decreased in the slightly-painful group and extremely-painful group,and such difference was statistically significant in the slightly-pain group (P<0.05). The effective rate (defined as thinner patellar,decreased hypoecho area and fewer blood distribution in the lesion) was 38%, 50%, and 62% in the painless group, slightly-painful group,and extremely-painful group, and the rates in the slightly-painful group and extremely-painful group were significantly higher than that in painless group (both P<0.05). CONCLUSIONS: HFUS can display the ultrasonographic changes of patellar tendon enthesiopathy after conservative treatments in an objective and quantitative manner. Compared with conventional clinical evaluations, it can more accurately reflect the disease recovery status.

Association between Ambient Air Pollution and Outpatient Visits for Acute Bronchitis in a Chinese City.

OBJECTIVE: To investigate the short-term association between outdoor air pollution and outpatient visits for acute bronchitis, which is a rare subject of research in the mainland of China. METHODS: A time-series analysis was conducted to examine the association of outdoor air pollutants with hospital outpatient visits in Shanghai by using two-year daily data (2010-2011). RESULTS: Outdoor air pollution was found to be associated with an increased risk of outpatient visits for acute bronchitis in Shanghai. The effect estimates of air pollutants varied with the lag structures of the concentrations of the pollutants. For lag06, a 10 µg/m(3) increase in the concentrations of PM10, SO(2), and NO(2) corresponded to 0.94% (95% CI: 0.83%, 1.05%), 11.12% (95% CI: 10.76%, 11.48%), and 4.84% (95% CI: 4.49%, 5.18%) increases in hospital visits for acute bronchitis, respectively. These associations appeared to be stronger in females (P<0.05). Between-age differences were significant for SO(2) (P<0.05), and between-season differences were also significant for SO(2) (P<0.05). CONCLUSION: Our analyses have provided the first evidence that the current air pollution level in China has an effect on acute bronchitis and that the rationale for further limiting air pollution levels in Shanghai should be strengthened.

Protective effect of alizarin on vascular endothelial dysfunction via inhibiting the type 2 diabetes-induced synthesis of THBS1 and activating the AMPK signaling pathway.

BACKGROUND: In this study, we investigated the protective effects of alizarin (AZ) on endothelial dysfunction (ED). AZ has inhibition of the type 2 diabetes mellitus (T2DM)-induced synthesis of thrombospondin 1 (THBS1). Adenosine 5'-monophosphate- activated protein kinase (AMPK), particularly AMPKα2 isoform, plays a critical role in maintaining cardiac homeostasis. PURPOSE: The aim of this study was to investigate the ameliorative effect of AZ on vascular injury caused by T2DM and to reveal the potential mechanism of AZ in high glucose (HG)-stimulated human umbilical vein endothelial cells (HUVECs) and diabetic model rats. STUDY DESIGN: HUVECs, rats and AMPK-/- transgenic mice were used to investigate the mitigating effects of AZ on vascular endothelial dysfunction caused by T2DM and its in vitro and in vivo molecular mechanisms. METHODS: In type 2 diabetes mellitus rats and HUVECs, the inhibitory effect of alizarin on THBS1 synthesis was verified by immunohistochemistry (IHC), immunofluorescence (IF) and Western blot (WB) so that increase endothelial nitric oxide synthase (eNOS) content in vitro and in vivo. In addition, we verified protein interactions with immunoprecipitation (IP). To probe the mechanism, we also performed AMPKα2 transfection. AMPK's pivotal role in AZ-mediated prevention against T2DM-induced vascular endothelial dysfunction was tested using AMPKα2-/- mice. RESULTS: We first demonstrated that THBS1 and AMPK are targets of AZ. In T2DM, THBS1 was robustly induced by high glucose and inhibited by AZ. Furthermore, AZ activates the AMPK signaling pathway, and recoupled eNOS in stressed endothelial cells which plays a protective role in vascular endothelial dysfunction. CONCLUSIONS: The main finding of this study is that AZ can play a role in different pathways of vascular injury due to T2DM. Mechanistically, alizarin inhibits the increase in THBS1 protein synthesis after high glucose induction and activates AMPKα2, which increases NO release from eNOS, which is essential in the prevention of vascular endothelial dysfunction caused by T2DM.

The distinguishing cellular features of pulmonary artery smooth muscle cells from chronic thromboembolic pulmonary hypertension patients.

In chronic thromboembolic pulmonary hypertension (CTEPH), central thrombi are the most likely disease initiators, and progressive pulmonary vascular remodeling, which is characterized by marked proliferation of pulmonary artery smooth muscle cells (PASMCs), may also contribute to the long-term progression of CTEPH. This study was designed to investigate the cellular characteristics of PASMCs isolated from the organized thrombotic tissues of CTEPH. In the present study, analysis of PASMCs isolated from five CTEPH patients and three control subjects showed that cells from CTEPH patients had certain characteristics that distinguished them from control cells, including inferior or no cell-cell contact inhibition growth, increased sensitivity to hypoxia-induced proliferation, resistance to serum starvation-induced apoptosis, and mitochondrial metabolism disorder. These differences in the PASMCs in endarterectomized tissue of CTEPH patients may prove useful in understanding the pathobiology of CTEPH.

Development of a molecularly imprinted polymer for prometryne clean-up in the environment.

Molecularly imprinted polymers (MIPs) are prepared on the surface of modified silica gel using prometryne as a template, methacrylic acid as the functional monomer, ethylene glycol dimethacrylate as a crosslinker, and 2,2-azobisisobutyronitrile as an initiator. The structure of the MIPs was characterized using SEM and FTIR spectroscopy. The selectivity of the MIPs for the template molecule prometryne was proven by adsorption experiments. Highly selective SPE cartridges of MIP particles were developed and an optimized prometryne procedure was developed for the enrichment and clean-up of prometryne residues in water, soil, and wheat samples. The concentrations of prometryne in the samples were analyzed by HPLC. The average recoveries of prometryne spiked for water at 0.05∼0.8 mg/L were 101.47-106.65% and the RSD was 2.63-4.71%. The average recoveries of prometryne spiked for soil at 0.05∼0.8 mg/L were 87.34-94.91% with the RSD being 2.77-8.41%. The average recoveries of prometryne spiked for wheat plant at 0.2∼2.0 mg/kg were 91.04-97.76% with the RSD being 6.53-10.69%. The method developed here can be regenerated and repeatedly used more than two dozen times.

[Increased survival of free fat grafts with adipose-derived stem cells and platelet-rich plasma in nude mice].

OBJECTIVE: To investigate the impact of combined adipose-derived stem cells (ASCs) and platelet-rich plasma (PRP) on the survival of transplanted fat. METHODS: The ASCs were isolated and cultured from fat tissues by enzyme digestion; and the PRP was prepared by two-step ultracentrifugation. The grafts of fat granules were divided into test groups (ASCs + PRP + fat granules, PRP + fat granules, ASCs + fat granules) and control groups (PBS + fat granules). The grafts were injected into the left and right dorsal subcutaneous areas of nude mice. General observations, volume measurements and microscope examinations were conducted 10 d, 30 d, 60 d and 90 d after transplantation. RESULTS: The grafts of the mice in the ASCs + PRP group showed soft structure, with light yellow color and closer to normal adipose tissue compared with those in other groups. Greater survival volumes (P < 0.05) and better histology were also observed in the grafts of the mice in the ASCs + PRP group. CONCLUSION: The fat grafts consisting of PRP and ASCs constitute an ideal transplant strategy, which could provide a valuable and needed tool in plastic and reconstructive surgery.

ADCY6 is a potential prognostic biomarker and suppresses OTSCC progression via Hippo signaling pathway.

Oral tongue squamous cell carcinoma (OTSCC) is a malignant tumor. Recently, studies have found that adenylate cyclase 6 (ADCY6) plays a pivotal role in many lethal tumors formation processes. The role of ADCY6 in OTSCC remains unknown. The expression of ADCY6 in OTSCC tissue samples was detected. The clinical significance of ADCY6 in OTSCC was analyzed by statistical methods. OTSCC cell lines were selected to analyze the biological function of ADCY6. Meanwhile, the effect of ADCY6 on the growth of OTSCC in vivo was explored using subcutaneous tumorigenesis assay. WB assay was used to detect the underlying signaling pathway. Cell function recovery test used to investigate the mechanism of ADCY6-promoting OTSCC malignant biological behavior via Hippo signaling pathway. We report that ADCY6 was obviously downregulated in OTSCC tissue samples and cell lines. Importantly, lower expression of ADCY6 indicates a poorer prognosis in patients with OTSCC, and its expression is significantly correlated with TNM stage and tumor size. Functionally, forced expression of ADCY6 can significantly inhibit the proliferation, migration, invasion, and promote apoptosis of OTSCC cells. Mechanistically, we demonstrated that ADCY6 upregulation impaired Hippo signaling pathway to reduce the malignant biological behavior of OTSCC. Generally, our findings suggest that ADCY6 suppressed Hippo signaling pathway to regulate malignant biological behavior in OTSCC, which provide new cues for further exploring the mechanism of occurrence and development of OTSCC.

Perillaldehyde improves diabetic cardiomyopathy by upregulating miR-133a-3p to regulate GSK-3ß.

Diabetic cardiomyopathy (DCM) is part of the most important causes of death from cardiovascular disease. Perillaldehyde (PAE), a major component of the herb perilla, has been shown to ameliorate doxorubicin-induced cardiotoxicity, but it is unclear whether PAE exerts beneficial effects on DCM. Exploring the potential molecular mechanisms of PAE for the treatment of DCM through network pharmacology and molecular docking. The SD rat type 1 diabetes model was established by a single intraperitoneal injection of streptozotocin (60 mg/kg), the cardiac function indexes of each group were detected by echocardiography; the morphological changes, apoptosis, protein expression of P-GSK-3ß (S9), collagen I (Col-Ⅰ), collagen III (Col-Ⅲ) and alpha-smooth muscle actin (α-SMA), and miR-133a-3p expression levels were detected. An DCM model of H9c2 cells was established in vitro and transfected with Mimic and Inhibitor of miR-133a-3p. The results showed that PAE ameliorated cardiac dysfunction, reduced fasting glucose and cardiac weight index, and improved myocardial injury and apoptosis in DCM rats. It reduced high glucose-induced apoptosis, promoted migration and improved mitochondrial division injury in H9c2 cells. PAE decreased P-GSK-3ß (S9), Col-Ⅰ, Col-Ⅲ and α-SMA protein expression and upregulated miR-133a-3p expression levels. After miR-133a-3p Inhibitor treatment, the expression of P-GSK-3ß (S9) and α-SMA expression were significantly increased; after miR-133a-3p Mimic treatment, the expression of P-GSK-3ß (S9) and α-SMA decreased significantly in H9c2 cells. It suggests that the mechanism of action of PAE to improve DCM may be related to the upregulation of miR-133a-3p and inhibition of P-GSK-3ß expression.

Amorphous selenium inhibits oxidative stress injury of neurons in vascular dementia rats by activating NMDAR pathway.

Vascular dementia (VD) is one of the most common causes of dementia, taking account for about 20% of all cases. Although studies have found that selenium supplementation can improve the cognitive ability of Alzheimer's patients, there is currently no research on the cognitive impairment caused by VD. This study aimed to investigate the role and mechanism of Amorphous selenium nanodots (A SeNDs) in the prevention of VD. The bilateral common carotid artery occlusion (BCCAO) method was used to establish a VD model. The neuroprotective effect of A SeNDs was evaluated by Morris water maze, Transcranial Doppler TCD, hematoxylin-eosin (HE) staining, Neuron-specific nuclear protein (Neu N) staining and Golgi staining. Detect the expression levels of oxidative stress and Calcium-calmodulin dependent protein kinase II (CaMK II), N-methyl-D-aspartate receptor subunit NR2A, and postsynaptic dense protein 95 (PSD95). Finally, measure the concentration of calcium ions in neuronal cells. The results showed that A SeNDs could significantly improve the learning and memory ability of VD rats, restore the posterior arterial blood flow of the brain, improve the neuronal morphology and dendritic remodeling of pyramidal cells in hippocampal CA1 area, reduce the level of oxidative stress in VD rats, increase the expression of NR2A, PSD95, CaMK II proteins and reduce intracellular calcium ion concentration, but the addition of selective NR2A antagonist NVP-AAMO77 eliminated these benefits. It suggests that A SeNDs may improve cognitive dysfunction in vascular dementia rats by regulating the NMDAR pathway.

A Runx2/miR-3960/miR-2861 regulatory feedback loop during mouse osteoblast differentiation.

Our recent study showed that miR-2861 promotes osteoblast differentiation by targeting histone deacetylase 5, resulting in increased runt-related transcription factor 2 (Runx2) protein production. Here we identified another new microRNA (miRNA) (miR-3960) that played a regulatory role in osteoblast differentiation through a regulatory feedback loop with miR-2861. miR-3960 and miR-2861 were found clustered at the same loci. miR-3960 was transcribed during bone morphogenic protein 2 (BMP2)-induced osteogenesis of ST2 stromal cells. Overexpression of miR-3960 promoted BMP2-induced osteoblastogenesis. However, the inhibition of miR-3960 expression attenuated the osteoblastogenesis. Homeobox A2 (Hoxa2), a repressor of Runx2 expression, was confirmed to be a target of miR-3960. Electrophoretic mobility shift assay and chromatin immunoprecipitation experiments confirmed that Runx2 bound to the promoter of the miR-3960/miR-2861 cluster. Furthermore, overexpression of Runx2 induced miR-3960/miR-2861 transcription, and block of Runx2 expression attenuated BMP2-induced miR-3960/miR-2861 transcription. Here we report that miR-3960 and miR-2861, transcribed together from the same miRNA polycistron, both function in osteoblast differentiation through a novel Runx2/miR-3960/miR-2861 regulatory feedback loop. Our findings provide new insights into the roles of miRNAs in osteoblast differentiation.

Nadir Oxygen Delivery During Pediatric Bypass as a Predictor of Acute Kidney Injury.

BACKGROUND: Cardiac surgery-associated acute kidney injury (CS-AKI) is common in infants and is associated with negative outcomes. Nadir indexed oxygen delivery (DO2i) during cardiopulmonary bypass (CPB) is associated with the occurrence of postoperative CS-AKI, with critical thresholds for DO2i reported to be 262 to 300 mL/min/m2 in adults. However, given that infants have a higher metabolic rate and oxygen demand, the critical DO2i in infants is not comparable with existing adult standards. This study aimed to explore the critical DO2i threshold during pediatric CPB. METHODS: Between March 2019 and April 2020, 106 consecutive infants undergoing cardiac surgery with CPB were admitted to this prospective observational cohort study. The DO2i levels of each patient were monitored during CPB. Pre- and intraoperative factors were tested for independent association with CS-AKI. The postoperative outcomes of patients with or without CS-AKI were compared. RESULTS: In our patient population (n = 83), we identified 25 patients (38.5%) with postoperative CS-AKI. Multivariate analysis revealed 2 independent risk factors for onset of CS-AKI: CPB duration and nadir DO2i. The lowest suitable DO2i during CPB in the present population was 353 mL/min/m2 (sensitivity, 65.6%; specificity, 74.5%). CS-AKI during pediatric CPB remained significantly associated with an increased morbidity, related mainly to a postoperative low cardiac output syndrome, but not to mortality. CONCLUSIONS: The lowest suitable DO2i during CPB in the infant population undergoing cardiac surgery was 353 mL/min/m2. Below this threshold, there was a high probability of inducing CS-AKI.

Potential Therapeutic Effect of Citronellal on Diabetic Cardiomyopathy in Experimental Rats.

Diabetic cardiomyopathy (DCM), a cardiovascular complication of patients with diabetes, is a special cardiomyopathy that is independent of coronary heart disease, hypertension, and valvular disease. Citronellal (CT) is a monoterpene compound generated by the secondary metabolism of plants. In this work, the therapeutic effect and mechanism of CT in DCM were investigated. Experimental diabetic rat models were constructed through a high-fat and high-carbohydrate diet combined with low-dosage streptozotocin (STZ) treatment. CT was intragastrically administered at the dosage of 150 mg/kg/day. The cardiac functions of the rats were evaluated via cardiac Doppler ultrasound. Changes in myocardial structure were analyzed through histopathology. Changes in the representative indices of oxidative stress, namely, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were detected on the basis of a biochemical test. Related protein levels were assayed via immunofluorescence and Western blot analyses. The DCM rats in the nontreatment group experienced diastolic and systolic dysfunctions, associated with myocardial hypertrophy, fibrosis, and cardiomyocyte apoptosis. Moreover, this condition was concurrent with metabolic disorders, the degradation of SOD activity in myocardial tissues, the increase in MDA content, the abnormal activation of sodium-hydrogen exchanger 1 (NHE1), and the aggravation of cell apoptosis (Bax levels were elevated, whereas Bcl-2 levels decreased). Myocardial hypertrophy, fibrosis, oxidative stress, and cell apoptosis were obviously inhibited after treatment with CT (150 mg/kg/day). The abnormal activation of NHE1 was recovered under the action of CT. Our study results showed that CT might play a protective role in the treatment of DCM by repressing the abnormal activation of NHE1.