First record of the complete mitochondrial genome of Botyodes diniasalis (Walker, 1859) (Lepidoptera: Crambidae).

We performed the first sequencing of the complete mitogenome of Botyodes diniasalis by high-throughput sequencing. A circular DNA molecule of 15,219 bp in size, encoding 2 rRNAs, 22 tRNAs, and 13 PCGs, contains a non-coding AT-rich region. The overall nucleotide composition of the genome is A (39.5%), T (41.3%), C (11.3%), and G (7.8%). Phylogenetic analysis based on mitogenomic data suggest that the species B. diniasalis has a close evolutionary relationship with B. principalis in Margaroniini. The complete mitogenome of B. diniasalis will serve as a valuable resource for future studies on evolution, taxonomy, genetic conservation, and utilization of Botyodes.

Assessment of compensated advanced chronic liver disease based on serum bile acids in chronic hepatitis B patients.

Patients with chronic liver disease progressed to compensated advanced chronic liver disease (cACLD), the risk of liver-related decompensation increased significantly. This study aimed to develop prediction model based on individual bile acid (BA) profiles to identify cACLD. This study prospectively recruited 159 patients with hepatitis B virus (HBV) infection and 60 healthy volunteers undergoing liver stiffness measurement (LSM). With the value of LSM, patients were categorized as three groups: F1 [LSM ≤ 7.0 kilopascals (kPa)], F2 (7.1 < LSM ≤ 8.0 kPa), and cACLD group (LSM ≥ 8.1 kPa). Random forest (RF) and support vector machine (SVM) were applied to develop two classification models to distinguish patients with different degrees of fibrosis. The content of individual BA in the serum increased significantly with the degree of fibrosis, especially glycine-conjugated BA and taurine-conjugated BA. The Marco-Precise, Marco-Recall, and Marco-F1 score of the optimized RF model were all 0.82. For the optimized SVM model, corresponding score were 0.86, 0.84, and 0.85, respectively. RF and SVM models were applied to identify individual BA features that successfully distinguish patients with cACLD caused by HBV. This study provides a new tool for identifying cACLD that can enable clinicians to better manage patients with chronic liver disease.

Dynamic response of deepwater test string under fluctuations in axial force and internal pressure.

In this study, a mechanical model suitable for deepwater test string was proposed. An analysis of the dynamic response of the test string under different frequencies, different water depths and different fluctuation amplitudes was carried out by using the finite element method based on the change in the internal pressure and axial force measured. The results of the analysis showed that the response parameters (maximum stress and maximum deformation) tended to be stable after one period of fluctuation in the axial force and half a period of fluctuation in the internal pressure, respectively. When a sine waveform fluctuation in the internal pressure and axial force occurred, the response parameters increased with an increase in the amplitude of the fluctuation and increased with an increase in the frequency of fluctuation, and the amplitude of variation decreased with an increase in the fluctuation period. Under fluctuation in the axial force, the response parameter decreased with an increase in the water depth. The response parameter decreased first and then increased with an increase in the water depth when the fluctuation in the internal pressure occurred with a sine waveform. The maximum deformation and stress of the test string always changed with a change in the load when the fluctuation in the internal pressure and axial force had a sine waveform, and the test string under a load with a sine waveform was prone to periodic fatigue failure. The relevant conclusions provide a basis for the analysis and prevention of fatigue failure in test strings.

Green-Light Responsive Perylene Bisimides for Atom-Economic Thiol Generation and Click-Ligation.

Novel methylthiophene/benzo[b]thiophene perylene bisimide thiol-precursors that would generate thiols via a green-light-induced (λexc = 530 nm, φre = 0.33) photorearrangement are presented herein. The "no-wash", photoreleased thiols thus enabled a subsequent thiol-ene click ligation with electron-deficient substrates. Moreover, by virtue of the intrinsic fluorescence evolution from the rearrangement of perylene bisimide scaffolds, the whole process of thiol formation could be self-reported, further potentiating themselves with application versatilities.

Nano-silica anti-icing coatings for protecting wind-power turbine fan blades.

Wind power is a promising electricity source. Nevertheless, wind turbine blade icing can cause severe problems in turbine operation. In this study, SiO2 spherical nanoparticles (∼90 nm), produced by RF (radio frequency) plasma spheroidization, were mixed with E51, PDMS, and ethyl acetate, and sprayed on the surface of aluminum plates and regular power windmill fan blades which were already coated with polyurethane primer. XPS and IR spectroscopies revealed the development of SiC and SiPh (Ph = phenolic ring) bonds, whose formation should be favored by the ultrasound and curing processes at 50 °C. The integrity of the coating/substrate interface, whose strength is ascribed to hydrogen bonds, was maintained after 100 icing-melting cycles. The coatings display superhydrophobic behavior and excellent anti-icing performance, along with stability in abrasion, sunlight and self-cleaning ability towards solid pollutants.

Kukoamine A activates Akt/GSK-3ß signaling pathway to inhibit oxidative stress and relieve myocardial ischemia-reperfusion injury.

PURPOSE: Myocardial ischemia/reperfusion (MI/R) injury refers to a pathological condition of treatment of myocardial infarction. Oxidative stress and inflammation are believed to be important mechanisms mediating MI/R injury. Kukoamine A (KuA), a sperm, is the main bioactive component extracted from the bark of goji berries. In this study, we wanted to investigate the possible effects of KuA on MI/R injury. METHODS: In this experiment, all rats were divided into sham operation group, MI/R group, KuA 10 mg + MI/R group, KuA 20 mg + MI/R group. After 120 min of ischemia/reperfusion treatment, left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), maximal rates of rising and fall of left ventricular pressure (±dp/dtmax), and ischemic area were detected. Serum samples of rats in each group were collected. The enzyme activities of catalase (CAT), glutathione peroxidase (GSH-PX), superoxide dismutase (SOD), levels of malondialdehyde (MDA), CK muscle/brain (CK-MB), tumor necrosis factor (TNF), interleukin-1ß (IL-1ß), and interleukin-6 (IL-6) were detected using enzyme-linked immunosorbent assay (ELISA). The apoptosis of myocardium in each group was detected according to the instructions of the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The expressions of mammalian target of glycogen synthase kinase-3ß (GSH-3ß) and protein kinase B (Akt) mRNA level in myocardial tissues were detected via reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: MI/R rats showed a significant increase in oxidative stress and inflammation. In addition, we showed that KuA significantly improved the myocardial function such as LVSP, left ventricular ejection fraction, +dp/dt, and -dp/dt. Here, it attenuated dose-dependent histological damage in ischemia-reperfused myocardium, which is associated with the enzyme activities of SOD, GSH-PX, and levels of MDA, IL-6, TNF-α, L-1ß. CONCLUSIONS: KuA inhibited gene expression of Akt/GSK-3ß, inflammation, oxidative stress and improved MR/I injury. Taken together, our results allowed us to better understand the pharmacological activity of KuA against MR/I injury.

Coupling mechanism and parameter optimization of sewage sludge dewatering jointly assisted by electric field and mechanical pressure.

Pressurized electro-dewatering technology is considered to be one of the most effective methods for improving dewatering performance of sewage sludge. In this paper, four dewatering protocols were developed to further explore the coupling mechanism of sludge dewatering through mechanical pressure, electric field and their joint. The results showed that the dewatering performance of the four dewatering protocols were as follows: pressurized electro-dewatering with constant voltage gradient mode (G-PEDW) > first mechanical dewatering then electro-dewatering > mechanical dewatering > electro-dewatering. The coupling mechanism was revealed from the perspectives of pore structure and moisture distribution of sludge cakes. The pore structure was discussed in detail from the whole pore size distribution and fractal dimension. The fractal dimension could quantitatively describe the change of pore structure. The moisture distribution was analyzed by the thermogravimetric differential scanning calorimetry test. The results showed that the electric field could reduce bound strength of moisture and produce new micro-pores to build more water flow paths, the water was discharged through interior capillary channels, and mechanical pressure could accelerate the water removing process. Response surface method was used to establish an empirical prediction model of G-PEDW, and discussed the selection of optimal parameters. The R-square values of mathematical models of moisture content and energy consumption were as high as 0.9863 and 0.9838, respectively, which was more advanced than other mathematical models. Experiments showed that G-PEDW could reduce the time to 20 min or reduce the energy consumption to 7.1 Wh/kg•H2O when the target moisture content was set to 41.7%.

Sirtuin 6 regulates macrophage polarization to alleviate sepsis-induced acute respiratory distress syndrome via dual mechanisms dependent on and independent of autophagy.

BACKGROUND AIMS: Sepsis-induced acute respiratory distress syndrome (ARDS) can be mediated by an imbalance in macrophage polarization; however, the underlying mechanisms remain poorly understood. This study aimed to investigate the modulatory role of sirtuin 6 (SIRT6) in macrophage polarization during sepsis-induced ARDS. METHODS: A mouse ARDS model was established using cecal ligation and puncture. Isolated alveolar macrophages (AMs) and lipopolysaccharide (LPS)-stimulated bone marrow-derived macrophages (BMDMs) were adopted as in vitro models. Macrophage polarization was evaluated by measuring M1 and M2 macrophage percentages via flow cytometry and expression of specific markers. The expression of microtubule-associated light chain protein 3I/II and beclin-1 was detected for assessing macrophage autophagy. Binding between specificity protein 1 (SP1) and the target gene promoter was evaluated using a chromatin immunoprecipitation assay. RNA expression was analyzed by quantitative reverse transcription polymerase chain reaction and western blotting. RESULTS: Treatment with the SIRT6 activator UBCS039 significantly alleviated lung injury in the mouse ARDS model and enhanced autophagy and M2 polarization in isolated AMs. M2 polarization and autophagy in LPS-challenged BMDMs were also effectively promoted by UBCS039 treatment or SIRT6 overexpression. An adenosine monophosphate-activated protein kinase inhibitor (Compound C) or autophagy inhibitor (3-methyladenine) partially abrogated M2 polarization mediated by SIRT6 overexpression upon LPS exposure. SIRT6 induced autophagy and M2 polarization of BMDMs partially via its deacetylase activity. SIRT6 inhibited mammalian target of rapamycin transcription by modulating SP1 to promote BMDM M2 polarization, which was independent of autophagy. CONCLUSIONS: SIRT6 promotes M2 polarization of macrophages to alleviate sepsis-induced ARDS in an autophagy-dependent and -independent manner.

Ginsenoside Rg3 alleviates septic liver injury by regulating the lncRNA TUG1/miR-200c-3p/SIRT1 axis.

BACKGROUND: Studies have shown that ginsenoside R3 (Rg3) plays a protective role in sepsis-induced organ injuries and mitochondrial dysfunction. Long noncoding RNA (lncRNA) taurine-upregulated gene 1 (TUG1) is regarded as a regulator in sepsis. However, the association between TUG1 and Rg3 remains elusive. METHODS: A sepsis mouse model was established by caecal ligation and puncture (CLP), and liver injury was induced by haematoxylin-eosin (H&E) staining. Lipopolysaccharide (LPS) was used to induce hepatocyte damage. The expression levels of TUG1, microRNA (miR)-200a-3p, and silencing information regulator 1 (SIRT1) were examined by quantitative real-time polymerase chain reaction (qRT-PCR) assays. Cell viability was monitored using the Cell Counting Kit-8 (CCK-8) assay. MitoSOX Red staining and CBIC2 (JC-1) dye were employed to detect mitochondrial reactive oxygen species (ROS) and mitochondrial transmembrane potential (MTP) levels, respectively. The interaction between miR-200a-3p and TUG1 or SIRT1 was confirmed via dual-luciferase reporter or RNA immunoprecipitation (RIP) assay. RESULTS: Rg3 upregulated TUG1 expression in liver tissues of CLP mice and LPS-induced hepatocytes. Rg3 could activate autophagy to improve mitochondrial dysfunction in LPS-treated hepatocytes, which was partially reversed by TUG1 depletion or miR-200a-3p overexpression. Importantly, TUG1 targeted miR-200a-3p to activate the SIRT1/AMP-activated protein kinase (AMPK) pathway in LPS-treated hepatocytes. Moreover, gain of TUG1 ameliorated mitochondrial dysfunction in LPS-treated hepatocytes by sequestering miR-200a-3p. CONCLUSION: Our study revealed that Rg3 increased TUG1 expression and reduced miR-200a-3p expression to stimulate the SIRT1/AMPK pathway, thereby enhancing autophagy to improve sepsis-induced liver injury and mitochondrial dysfunction.

ROCK1 regulates sepsis-induced acute kidney injury via TLR2-mediated endoplasmic reticulum stress/pyroptosis axis.

BACKGROUND: It has been reported that ROCK1 participates in the progression of multiple diseases, including septic intestinal barrier, cardiac dysfunction and acute lung injury. However, its regulatory role and specific mechanism in sepsis-induced acute kidney injury (AKI) remain unclear. METHODS: Cecal ligation puncture (CLP) was conducted to establish sepsis mouse model, and in vitro model was achieved by lipopolysaccharide (LPS) stimulation. Genes expression was evaluated by qRT-PCR, western blot or ELISA was conducted to assess the levels of proteins. Hoechst staining was performed to evaluate cell pyroptosis. LDH activity assay was detected to assess cytotoxicity. Immunohistochemistry was conducted to detect Ly-6G expression and neutrophils distribution in kidney tissues of mice. H&E and TUNEL staining were carried to evaluate kidney injury of mice. RESULTS: Our findings illuminated that ROCK1 was highly expressed in sepsis-induced AKI, and ROCK1 knockdown inhibited NLRP3-mediated cell pyroptosis in LPS-induced HK-2 cells. Moreover, ROCK1 modulated HK-2 cell pyroptosis by regulating endoplasmic reticulum stress (ERS). TLR2 inhibitor could suppress ERS mediated cell pyroptosis under LPS treatment. Further, TLR2 activator partially reversed the effects of ROCK1 inhibition on ERS mediated pyroptosis in LPS-treated HK-2 cells and CLP mice. CONCLUSION: In conclusion, ROCK1 may regulate sepsis-induced AKI via TLR2-mediated ERS/pyroptosis axis. Our data demonstrated the role and underlying mechanism of ROCK1 in septic AKI, providing theoretical basis for sepsis-induced AKI treatment.

Numerical Simulation Study on the Mechanism of Formation of Apical Aneurysm in Hypertrophic Cardiomyopathy With Midventricular Obstruction.

Apical aneurysm was observed to be associated with midventricular obstruction (MVO) in hypertrophic cardiomyopathy (HCM). To investigate the genesis of the apical aneurysm, the idealized numerical left ventricular models (finite-element left ventricle models) of the healthy left ventricle, subaortic obstruction, and midventricular obstruction in HCM of left ventricle were created. The mechanical effects in the formation of apical aneurysm were determined by comparing the myofiber stress on the apical wall between these three models (healthy, subaortic obstruction, and midventricular obstruction models). In comparing the subaortic obstruction model and MVO model with HCM, it was found that, at the time of maximum pressure, the maximum value of myofiber stress in MVO model was 75.0% higher than that in the subaortic obstruction model (654.5 kPa vs. 373.9 kPa). The maximum stress on the apex of LV increased 79.9, 69.3, 117.8% than that on the myocardium around the apex in healthy model, subaortic obstruction model, and MVO model, respectively. Our results indicated that high myofiber stress on the apical wall might initiate the formation process of the apical aneurysm.

Long Non-coding RNA AFAP1-AS1 Facilitates Prostate Cancer Progression by Regulating miR-15b/IGF1R Axis.

BACKGROUND: Prostate cancer (PCa) is a commonly diagnosed malignant cancer and is the second- highest cause of cancer death in men worldwide. Enzalutamide is the second-generation inhibitor of androgen receptor signaling and is the fundamental drug for the treatment of advanced PCa. However, the disease will eventually progress to metastatic castration-resistant prostate cancer (CRPC) and aggressive neuroendocrine prostate cancer (NEPC) because of androgen-deprivation therapy (ADT) resistance. The aim of the study was to investigate the role of long non-coding RNA (lncRNA) AFAP1-AS1 in ADT resistance. METHODS: Quantitative real-time PCR analysis (qPCR) was used to assess the expression of AFAP1-AS1 in PCa cell lines and tissues. Cell proliferation and invasion were assessed after AFAP1-AS1 knockdown using Cell Counting Kit (CCK)-8 and Transwell assay, respectively. A dual-luciferase reporter gene assay was carried out to validate the regulatory relationship among AFAP1-AS1, microRNA (miR)-15b, and insulin-like growth factor1 receptor (IGF1R). RESULTS: AFAP1-AS1 level was markedly increased in castration-resistant C4-2 cells and NE-like cells (PC3, DU145, and NCI-H660), compared with androgen-sensitive LNCaP cells. Enzalutamide treatment increased the expression of AFAP1-AS1 in vitro and in vivo. Functionally, AFAP1-AS1 knockdown repressed tumor cell proliferation and invasion. Mechanistically, AFAP1-AS1 functioned as an oncogene in PCa through binding to miR-15b and destroying its tumor suppressor function. Finally, we identified that AFAP1-AS1 up-regulated IGF1R expression by competitively binding to miR-15b to de-repress IGF1R. CONCLUSION: AFAP1-AS1 facilitates PCa progression by regulating miR-15b/IGF1R axis, indicating that AFAP1-AS1 may serve as a diagnostic biomarker and therapeutic target for PCa.

Expression and prognostic significance of thrombospondin gene family in gastric cancer.

BACKGROUND: Thrombospondins (THBSs) are glycoproteins expressed in the extracellular matrix (ECM) and have critical roles in tumor development and metastasis. However, the diverse expression patterns and prognostic roles of distinct THBS genes in gastric cancer have not been fully elucidated. In the current study, we aimed to investigate the expression patterns of THBSs in gastric cancer (GC) and determine whether they are prognostic markers for this malignancy. METHODS: mRNA expression status and genetic mutations of THBS family members were performed by using ONCOMINE, UCSC Xena browser, GEPIA, and cBioPortal databases. Prognostic values and function enrichment analysis of the members were assessed via Kaplan-Meier plotter and Metascape. RESULTS: we found that the mRNA expression of THBS1, THBS2, THBS4, and COMP were higher in patients with GC tissues than those in normal gastric mucosa and there was no difference in the mRNA expression of THBS3 between GC and normal tissue. Survival analysis revealed that mRNA levels of THBSs were strongly related to worse OS in GC patients (P<0.05). Overexpression of THBSs indicated poor OS in stage III/IV GC and high expression of THBS1, THBS3, THBS4, and COMP were related to worse OS in stage II GC. CONCLUSIONS: Bioinformatics analysis revealed a better understanding the value of THBS family members in GC and suggest that THBSs might serve as potential prognostic biomarkers for GC.

Influence of operator volume on early outcomes of septal myectomy for isolated hypertrophic obstructive cardiomyopathy.

BACKGROUND: Guidelines on the diagnosis and management of hypertrophic cardiomyopathy (HCM) recommend that septal myectomy be performed by experienced operators. However, the impact of operator volume on surgical treatment outcomes for isolated HCM has been poorly investigated. METHODS: From 2002 to 2014, 435 consecutive patients with isolated HCM undergoing myectomy at the Fuwai Hospital were retrospectively enrolled. All 29 surgeons were divided into beginner surgeons (operator volume ≤20) and experienced surgeons (operator volume >20) according to the guidelines for the diagnosis and treatment of HCM. Propensity score matching of patients in the two groups was performed. RESULTS: Baseline differences included advanced New York Heart Association classification and older age in the experienced surgeon group. After matching, in the beginner surgeon group (107 cases), residual obstruction (18.7% vs. 0.9%, P<0.001) was more common, and the postoperative left ventricular outflow tract pressure gradient (20.7±15.1 vs. 14.3±7.4 mmHg, P<0.001) was higher than that of the experienced surgeon group. In the experienced surgeon group (107 cases), the incidence of mitral valve replacement (1.9% vs. 11.2%, P<0.001) and permanent pacemaker implantation (1.9% vs. 3.7%, P<0.001) was significantly lower than that in the beginner surgeon group. However, there was no difference in procedural mortality (1.9% vs. 1.9%) between the two groups. CONCLUSIONS: Operator volume is an important factor in achieving better obstruction obliteration after septal myectomy in patients with isolated HCM.

Surgical treatment of pulmonary artery sarcoma: a report of 17 cases.

Pulmonary artery sarcoma (PAS) is a rare and devastating disease. The diagnosis is often delayed, and optimal treatment remains unclear. The aim of this study is to report our experience in the surgical management of this disease. Between 2000 and 2018, 17 patients underwent operations for PAS at our center. The medical records were retrospectively reviewed to evaluate the clinical characteristics, operative findings, the postoperative outcomes, and the long-term results. The mean age at operation was 46.0 ± 12.4 years (range, 26-79 years), and eight (47.1%) patients were male. Six patients underwent tumor resection alone, whereas the other 11 patients received pulmonary endarterectomy (PEA). There were two perioperative deaths. Follow-up was completed for all patients with a mean duration of 23.5 ± 17.6 months (1-52 months). For all 17 patients, the median postoperative survival was 36 months, and estimated cumulative survival rates at 1, 2, 3, and 4 years were 60.0%, 51.4%, 42.9%, and 21.4%, respectively. The mean survival was 37.0 months after PEA and 14.6 months after tumor resection only (p = 0.046). Patients who had no pulmonary hypertension (PH) postoperatively were associated with improved median survival (48 vs. 5 months, p = 0.023). In conclusion, PAS is often mistaken for chronic pulmonary thromboembolism. The prognosis of this very infrequent disease remains poor. Early detection is essential for prompt and best surgical approach, superior to tumor resection alone, and PEA surgery with PH relieved can provide better chance of survival.

lncRNA PVT1 modulates NLRP3­mediated pyroptosis in septic acute kidney injury by targeting miR­20a­5p.

Acute kidney injury (AKI) is the most common complication of sepsis. The current incidence of sepsis is high (0.3% of total population) worldwide, and septic AKI may cause death in patients. Long non­coding (lnc)RNAs serve important roles in the pathogenesis of AKI. Therefore, the present study investigated the mechanism underlying lncRNA plasmacytoma variant translocation 1 (PVT1)­mediated regulation of pyroptosis in septic AKI. Septic kidney injury was induced in mice using the caecal ligation and puncture method, and lipopolysaccharide (LPS)­induced HK­2 cell models were also established. Haematoxylin­eosin staining was performed to assess pathological alterations of kidney tissues in the mice. The levels of IL­1ß, IL­18 and lactate dehydrogenase were determined by conducting ELISAs. Reverse transcription­quantitative PCR was used to detect the expression levels of PVT1 and microRNA (miR)­20a­5p. To assess pyroptosis, the protein expression levels of nucleotide­binding oligomerization domain­like receptor protein 3 (NLRP3), IL­1ß, IL­18, apoptosis­associated speck­like protein containing a CARD and cleaved caspase­1 were measured via western blotting. Flow cytometry was performed to assess the rate of cell pyroptosis. Dual luciferase reporter assays were used to assess the binding relationships of PVT1/miR­20a­5p and miR­20a­5p/NLRP3. PVT1 expression was significantly increased, whereas miR­20a­5p expression was significantly decreased in sepsis model mice and LPS­induced HK­2 cells compared with sham mice and control HK­2 cells, respectively. PVT1 knockdown significantly suppressed cell pyroptosis and downregulated the expression of inflammatory factors in LPS­induced HK­2 cells. The results also indicated that PVT1 served as a sponge of miR­20a­5p, and miR­20a­5p directly targeted NLRP3. miR­20a­5p knockdown significantly promoted LPS­induced cell pyroptosis. Moreover, PVT1 knockdown inhibited LPS­induced cell pyroptosis by targeting the miR­20a­5p/NLRP3 signalling pathway. The results of the present study suggested that PVT1 modulated NLRP3­mediated pyroptosis in septic AKI by targeting miR­20a­5p, which might suggest significant potential therapeutic targets for septic AKI.

Comparisons of simulation results between passive and active fluid structure interaction models for left ventricle in hypertrophic obstructive cardiomyopathy.

BACKGROUND: Patient-specific active fluid-structure interactions (FSI) model is a useful approach to non-invasively investigate the hemodynamics in the heart. However, it takes a lot of effort to obtain the proper external force boundary conditions for active models, which heavily restrained the time-sensitive clinical applications of active computational models. METHODS: The simulation results of 12 passive FSI models based on 6 patients' pre-operative and post-operative CT images were compared with corresponding active models to investigate the differences in hemodynamics and cardiac mechanics between these models. RESULTS: In comparing the passive and active models, it was found that there was no significant difference in pressure difference and shear stress on mitral valve leaflet (MVL) at the pre-SAM time point, but a significant difference was found in wall stress on the inner boundary of left ventricle (endocardium). It was also found that pressure difference on the coapted MVL and the shear stress on MVL were significantly decreased after successful surgery in both active and passive models. CONCLUSION: Our results suggested that the passive models may provide good approximated hemodynamic results at 5% RR interval, which is crucial for analyzing the initiation of systolic anterior motion (SAM). Comparing to active models, the passive models decrease the complexity of the modeling construction and the difficulty of convergence significantly. These findings suggest that, with proper boundary conditions and sufficient clinical data, the passive computational model may be a good substitution model for the active model to perform hemodynamic analysis of the initiation of SAM.

Ultrafine- and uniform-grained biodegradable Zn-0.5Mn alloy: Grain refinement mechanism, corrosion behavior, and biocompatibility in vivo.

An ultrafine- and uniform-grained Zn-0.5Mn alloy (D3 alloy, stands for deformation rate of 99.5%) is fabricated via multi-pass drawing. The alloy features excellent ductility and elongation properties (up to 245.0% ± 9.0% at room temperature). Zn-0.5Mn alloys are composed of two phases, namely, Zn and MnZn13. The MnZn13 phase confers multiple effects during refinement by inducing and pinning low-angle boundaries within grains. Meanwhile, the presence of these phases along grain boundaries prevents the growth of new refined grains. D3 shows uniform corrosion behaviors in c-SBF solution on account of the even distribution of the MnZn13 phase in its microstructure. Animal implantation experiments indicate that D3 has good biocompatibility; it does not cause damage to bone tissue or other organs. Taking the results together, D3 may be developed into a new type of biodegradable material with remarkable elongation and corrosion properties and satisfactory biocompatibility for medical applications.