Porous tremella-like NiMoP/CoP network electrodes as an efficient electrocatalyst.

The design of efficient, stable and cost-effective electrocatalysts for the hydrogen evolution reaction holds substantial significance in water electrolysis, but it remains challenging. Tremella-like nickel-molybdenum bimetal phosphide encapsulated cobalt phosphide (NiMoP/CoP) with hierarchical architectures has been effectively synthesized on nickel foam (NF) via a straightforward hydrothermal followed by low-temperature phosphating method. Based on the unique structural benefits, it significantly increases the number of redox active centers, enhances the electrical conductivity of materials, and diminishes the ion diffusion path lengths, thereby promoting efficient electrolyte penetration and reducing the inherent resistance. The as-obtained NiMoP/CoP/NF electrocatalyst exhibited remarkable catalytic activity with an ultralow overpotential of 38 mV (10 mA cm-2) and low Tafel slope of 83 mV dec-1. The straightforward synthesis process and exceptional electrocatalytic properties of NiMoP/CoP/NF demonstrate great potential for the HER to replace the precious metal catalyst.

Suppression of Cation Intermixing Highly Boosts the Performance of Core-Shell Lanthanide Upconversion Nanoparticles.

Lanthanide upconversion nanoparticles (UCNPs) have been extensively explored as biomarkers, energy transducers, and information carriers in wide-ranging applications in areas from healthcare and energy to information technology. In promoting the brightness and enriching the functionalities of UCNPs, core-shell structural engineering has been well-established as an important approach. Despite its importance, a strong limiting issue has been identified, namely, cation intermixing in the interfacial region of the synthesized core-shell nanoparticles. Currently, there still exists confusion regarding this destructive phenomenon and there is a lack of facile means to reach a delicate control of it. By means of a new set of experiments, we identify and provide in this work a comprehensive picture for the major physical mechanism of cation intermixing occurring in synthesis of core-shell UCNPs, i.e., partial or substantial core nanoparticle dissolution followed by epitaxial growth of the outer layer and ripening of the entire particle. Based on this picture, we provide an easy but effective approach to tackle this issue that enables us to produce UCNPs with highly boosted optical properties.

2-Hydroxy-3-methylanthraquinone inhibits homologous recombination repair in osteosarcoma through the MYC-CHK1-RAD51 axis.

BACKGROUND: Osteosarcoma is a malignant bone tumor that usually affects adolescents aged 15-19 y. The DNA damage response (DDR) is significantly enhanced in osteosarcoma, impairing the effect of systemic chemotherapy. Targeting the DDR process was considered a feasible strategy benefitting osteosarcoma patients. However, the clinical application of DDR inhibitors is not impressive because of their side effects. Chinese herbal medicines with high anti-tumor effects and low toxicity in the human body have gradually gained attention. 2-Hydroxy-3-methylanthraquinone (HMA), a Chinese medicine monomer found in the extract of Oldenlandia diffusa, exerts significant inhibitory effects on various tumors. However, its anti-osteosarcoma effects and defined molecular mechanisms have not been reported. METHODS: After HMA treatment, the proliferation and metastasis capacity of osteosarcoma cells was detected by CCK-8, colony formation, transwell assays and Annexin V-fluorescein isothiocyanate/propidium iodide staining. RNA-sequence, plasmid infection, RNA interference, Western blotting and immunofluorescence assay were used to investigate the molecular mechanism and effects of HMA inhibiting osteosarcoma. Rescue assay and CHIP assay was used to further verified the relationship between MYC, CHK1 and RAD51. RESULTS: HMA regulate MYC to inhibit osteosarcoma proliferation and DNA damage repair through PI3K/AKT signaling pathway. The results of RNA-seq, IHC, Western boltting etc. showed relationship between MYC, CHK1 and RAD51. Rescue assay and CHIP assay further verified HMA can impair homologous recombination repair through the MYC-CHK1-RAD51 pathway. CONCLUSION: HMA significantly inhibits osteosarcoma proliferation and homologous recombination repair through the MYC-CHK1-RAD51 pathway, which is mediated by the PI3K-AKT signaling pathway. This study investigated the exact mechanism of the anti-osteosarcoma effect of HMA and provided a potential feasible strategy for the clinical treatment of human osteosarcoma.

Antibiotic-loaded bone substitutes therapy in the management of the moderate to severe diabetic foot infection: A meta-analysis.

In recent years, local antibiotic-loaded bone substitutes (ALBS) have been used increasingly in the treatment of diabetic foot infection (DFI). The meta-analysis aimed to analyse the efficacy of ALBS on patients with moderate to severe DFI (with or without osteomyelitis). With an appropriate search strategy, 7 studies were selected for analysis (2 RCTs and 5 cohort studies). The result showed that the application of ALBS effectively reduced the length of hospital stay (WMD -5.55; 95% CI: -9.85 to -1.26; P = 0.01), the recurrence rates (RR 0.33; 95% CI: 0.15 to 0.69; P = 0.003) and the mortality rates (RR 0.22; 95% CI: 0.06 to 0.82; P = 0.02). Compared to the control groups, however, there was no difference in healing rates (RR 1.06; 95% CI: 0.96 to 1.18; P = 0.26), healing time (WMD -1.44; 95% CI: -3.37 to -0.49; P = 0.14), the number of debridement (WMD -1.98; 95% CI: -4.08 to 0.12; P = 0.06) and major amputation rates (RR 0.76; 95% CI: 0.35 to 1.61; P = 0.47). The ALBS appears to have some beneficial effects as an adjunct to standard surgery in the treatment of DFI with or without osteomyelitis, as it reduces recurrence rates, mortality rates, and length of hospital stay, but there was no statistically significant difference in enhancing wound healing.

Management for lower limb malperfusion in acute type a aortic dissection patients.

OBJECTIVE: Acute type A aortic dissection (ATAAD) accompanied with lower limb malperfusion (LLM) is considered to be a catastrophic event, and remains a great challenge for cardiac surgeons. Here we introduce our experience in treating ATAAD patients accompanied with LLM. METHODS: 61 patients diagnosed with ATAAD accompanied by LLM enrolled in this study. All patients received aortic repair (Total-arch replacement or Hemi-arch replacement) as soon as possible on admission. Patients who still suffered LLM were performed extra-anatomic bypass using artificial vessels. All the discharged patients underwent the standard follow-up protocol. RESULTS: 38 patients (38/61, 62.3%) got satisfied reperfusion of the lower limbs after aortic repair while the others did not. Five patients had femorofemoral bypass, 16 received aortofemoral bypass, and two underwent aortofemoral bypass plus femorofemoral bypass. The ICU stay time was 5.4 ± 3.6 days. Fifty-five patients were discharged home successfully, while six patients died postoperatively with hospital mortality of 9.8%. Major postoperative complications included acute kidney injury requiring hemodialysis in seven patients, delayed wake-up (>3 days) in 5, prolonged ventilation (>4 days) in 8, and lower limb ischaemia in 1. Follow-up was successfully conducted in 50 patients with a mean follow-up time 4.9 ± 2.6 years. Five patients died during the follow-up. The estimated 5-year survival rate was 87.5 ± 6.1%. CTA images showed 100% patency of the extra-anatomic bypass. CONCLUSION: Aortic repair plus concomitant extra-anatomic bypass grafting in one operative setting could be a simple, safe and effective treatment on ATAAD patients with LLM.

Boosting the Efficiency of Dye-Sensitized Solar Cells by a Multifunctional Composite Photoanode to 14.13 .

We report a new strategy to fabricate a multifunctional composite photoanode containing TiO2 hollow spheres (TiO2 -HSs), Au nanoparticles (AuNPs) and novel NaYF4 : Yb,Er@NaLuF4 : Eu@SiO2 upconversion nanoparticles (UCNPs). The AuNPs are grown on the photoanode film including TiO2 -HSs and UCNPs by a simple in situ plasmonic treatment. As a result, an impressive power conversion efficiency of 14.13 % is obtained, which is a record for N719 dye-based dye-sensitized solar cells, demonstrating great potential for the solar cells toward commercialization. This obvious enhancement is ascribed to a collaborative mechanism of the TiO2 -HSs exhibiting excellent light-scattering ability, of the UCNPs converting near-infrared photons into visible photons and of the AuNPs presenting outstanding surface plasmon resonance effect. Notably, a steady-state experiment further reveals that the champion cell exhibits 95.33 % retainment in efficiency even after 180 h of measurements, showing good device stability.

Overexpressed DDX3x promotes abdominal aortic aneurysm formation and activates AKT in ApoE knockout mice.

In recent years, abdominal aortic aneurysm (AAA) lesions have become one of the important diseases that threaten public health. Related studies have confirmed that the occurrence of abdominal aortic aneurysms is related to inflammatory stress, cell apoptosis, and elastic fiber degradation. DDX3x is thought to interact with inflammasomes such as NLRP3 to aggravate the process of the inflammatory response, but its role in the occurrence of AAA remains unclear. Since DDX3x is indispensable in animal embryonic growth, we used an adeno-associated virus to construct gene-overexpressing mice to induce aneurysm development through AngII infusion. The results indicated that the incidence of aneurysms, inflammatory cell infiltration, vascular smooth muscle cell transformation, and oxidative stress levels were significantly increased under the condition of DDX3x overexpression. At the signaling level, activation of the AKT pathway exacerbates aneurysm formation. Taken together, we believe that DDX3x plays a key role in the development of aneurysms and may be a new target for the treatment of aneurysm progression.

Stomatin-like protein-2 attenuates macrophage pyroptosis and H9c2 cells apoptosis by protecting mitochondrial function.

Myocytes undergoing hypoxia condition can recruit macrophages and cause pro-inflammation initiation around the injury area. Mitochondrial dysfunction is related to macrophage pyroptosis. Stomatin-like protein-2 (SLP-2) can regulate mitochondrial biogenesis and function. Whether SLP-2 could affect macrophage pyroptosis remains unclear. In this study, bone marrow derived macrophages (BMDMs) were extracted from WT and SLP-2 knocked out mice, then stimulated by LPS/Nigericin. Western blot showed that SLP-2-/- promoted the expression of NLRP3, GSDMD-N, caspase-11 in macrophages, which means the deficiency of SLP-2 augments macrophage pyroptosis. Higher fluorescence intensity of dihydroethidium and TUNEL represented the increased ROS releasing and macrophage programmed death in SLP-2 deficiency groups. The immunofluorescence intensity of MtioTracker Red decreased and that of mitochondrial ROS (mtROS) increased in SLP-2 deletion groups with LPS/Nigericin stimulation, representing the increased mitochondrial damage. The expression level of HIF-1α increased in SLP-2 deletion macrophages with LPS and Nigericin stimulation. The level of Parkin and the ratio of LC3II/I decreased in SLP-2 deficiency macrophages after stimulated by LPS/Nigericin, compared with untreated macrophages. H9c2 cells were cultured in hypoxia condition before being cocultured with macrophage supernatant. The cocultured H9c2 cells were injured due to the serious pyroptosis of SLP-2 deficiency macrophages. According to these results, we suggest that SLP-2 can reduce macrophage pyroptosis and relieve hypoxia H9c2 cells injury through protecting mitochondrial function.

[Clinical outcomes of radial artery as the second arterial conduit in coronary artery bypass].

Objective: To examine the clinical experience and outcomes of coronary artery bypass grafting (CABG) using radial artery as the second arterial graft. Methods: Totally 585 patients in whom both left internal thoracic artery and radial artery as arterial conduits were used in CABG in Department of Cardiovascular Surgery, Nanjing Hospital Affiliated to Nanjing Medical University from April 2008 to August 2019 were consecutively enrolled. There were 436 males and 149 females, aging (63±10) years (range: 36 to 86 years). There were 40.7% (238/585) of patients had diabetes and 75.6% (442/585) of them had multivessel disease (two-vessel or three-vessel diseases). From January 2017, transit time flow measurement was performed on every patient. Demographic and perioperative data were retrospectively collected, as well as follow-up data for patients who underwent CABG from January 2014 to August 2019. Analysis were made on their early and late outcomes. Results: 81.9%(479/585) Most patients in this cohort (81.9%) received on-pump CABG and 11 patients had intraoperative intro-aortic balloon counterpulsation (prior to CABG) support. Forty-three patients had concomitant valve procedures. The number of distal anastomosis was 3.6±0.9 (range: 2 to 6) and number of arterial distal anastomosis was 2.1±0.3. Radial artery was anastomosed to left obtuse marginal artery in 95.8% (560/585) patients. All target vessels for radial artery conduit had significant proximal stenosis (>70%) and 72.5% (424/585) of target vessels had proximal stenosis which was >90%. Intraoperative transit-time flow measurement of 151 cases showed that radial artery conduits had a flow of (29.8±10.2) ml/minutes (range: 10 to 150 ml/min), and pulsatility index of 2.5±1.4 (range: 0.7 to 5.0). There was no operative death. Two in-hospital death occurred more than 30 days after index surgery. There was no perioperative myocardial infarction. There were 188 patients who received CABG from January 2014 to August 2019 followed-up for a median duration of 3.2 years. There were two noncardiac death. No patient had myocardial infarction or to receive myocardial revascularization. Conclusions: Radial artery as the second arterial conduit is a safe and effective strategy for CABG. Good selection of target vessel and intraoperative transit-time flow measurement may help achieve good patency, as well as the short and mid-term outcome.

Therapeutic Effect of Perioperative Mild Hypothermia on Postoperative Neurological Outcomes in Patients with Acute Stanford Type A Aortic Dissection.

BACKGROUND: Postoperative patients of acute Stanford type A aortic dissection (AAAD) often experience complications consisting of nervous system injury. Mild hypothermia therapy has been proven to provide the therapeutic effect of cerebral protection. We aimed to investigate the therapeutic effects of perioperative mild hypothermia on postoperative neurological outcomes in patients with AAAD. METHODS: A prospective randomized controlled study was conducted on adult patients undergoing aortic dissection surgery between February 2017 and December 2017. Patients in the treatment group underwent mild hypothermia (34° to 35°C) immediately after surgery, and in the conventional therapy group, patients were rewarmed to normal body temperature (36° to 37°C). Postoperative time to regain consciousness, postoperative serum neuron-specific enolase (NSE) and S-100ß levels, cerebral tissue oxygen saturation, presence of delirium or permanent neurological dysfunction, intensive care unit (ICU) and hospital stay duration, and 28-day mortality were compared. RESULTS: We enrolled 55 patients who underwent AAAD surgery and were randomly allocated into to 2 groups, 27 patients in the treatment group and 28 patients in the conventional therapy group. Compared with the conventional therapy group, postoperative time to regain consciousness was much shorter for patients in the mild hypothermia group (12.65 hours, interquartile range [IQR] 8.28 to 23.82, versus 25.80 hours, IQR 14.00 to 59.80; P = .02), and the rate of regaining consciousness in 24 hours after surgery was much higher (74.07% versus 46.42%; P = .037). At the same time, the ICU stay of patients in the mild hypothermia therapy group was significantly shorter than that in the conventional therapy group (5.53 ± 3.13 versus 9.35 ± 8.76 days; P = .038). Cerebral tissue oxygen saturation, incidence of delirium or permanent neurological dysfunction, duration of hospital stay, and 28-day mortality showed no statistical difference. Postoperative serum NSE and S-100ß levels increased compared with preoperative baseline values in both groups (P < .05), and the serum NSE levels of patients in the mild hypothermia therapy was significantly lower than the conventional therapy group 1 hour (P = .049) and 6 hours (P = .04) after surgery. There was no difference in the chest drainage volume or shivering between the 2 groups 24 hours after surgery. CONCLUSIONS: Perioperative mild hypothermia therapy is able to significantly reduce brain cell injury and shorten the postoperative time to regain consciousness, thus improving the neurological prognosis of patients with AAAD.

The fate of mild to moderate proximal aortic dilatation after isolated aortic valve replacement in tricuspid aortic valve patients.

BACKGROUND: Proximal aortic dilatation is frequently associated with aortic valve pathology. The treatment of mild to moderate proximal aortic dilatation (maximal diameter: 40-50 mm) at the time of aortic valve replacement (AVR) is still controversial. We retrospectively analyzed the fate and progression of the proximal dilated aorta after isolated AVR in tricuspid aortic valve (TAV) patients, to determine if ascending aortic replacement (AAR) is recommended at the time of the initial AVR. METHODS: The review of our hospital database revealed a subgroup of 127 TAV disease patients with mild to moderate ascending aortic dilatation, who underwent isolated AVR (group I, n = 68) or AVR combined AAR (group II, n = 59) from January 2000 to December 2013. Follow-up was obtained through a telephone interview/outpatient interview. Adverse aortic events were defined as aortic dissection/ rupture, or diameter of proximal aorta ≥55 mm, or re-do aortic surgery contributable to the dilated aorta during follow-up. RESULTS: There were no differences in age, gender, heart function, hypertension, diabetes, smoking, chronic renal failure, and atrium fibrillation between two groups except for the maximum aortic diameter (group I 43.91 ± 2.0 vs group II 45.20 ± 2.63, P < .05). The cross-clamp time and cardiopulmonary bypass time was significantly less in group I than that in group II, owing to the replacement of the proximal aorta. A total of 126 patients were discharged home successfully, with 0.79% hospital mortality. There was no significant difference of hospital mortality and morbidity between the two groups. Follow-up was successfully obtained in 106 patients (84.13%). Mean follow-up time was (9.60 ± 3.47) years. The overall survival at 10-year follow-up was 72.46% ± 6.42% in group I versus 74.55% ± 6.87% in group II ( P = .73). The freedom from adverse aortic events at 10-year was 89.59% ± 4.02% in group I versus 96.88% ± 3.07% in group II ( P = .09). No significant difference in survival rate and freedom from adverse aortic events can be obtained between the two groups. CONCLUSION: Progression of proximal aorta leading to adverse aortic events after isolated AVR in TAV patients is infrequent. AVR alone is acceptable and reasonable in patients with mild to moderate proximal aortic dilatation if connective tissue disorders are not present.

Regulatory role of IKKɑ in myocardial ischemia/reperfusion injury by the determination of M1 versus M2 polarization of macrophages.

The IκB kinase (IKK) complex plays a well-documented role in cancer and immune system. This function has been widely attributed to its role as the master regulator of the NF-κB family. Particularly, IKKɑ, a member of IKK complex, is reported to have various regulating effects in inflammatory and malignant diseases. However, its role as well as its mechanism of function in macrophages following myocardial ischemia and reperfusion (I/R) injury remains unexplored. In vivo, sham or I/R operations were performed on macrophage-specific IKKɑ knockout (mIKKɑ-/-) mice and their IKKɑflox/flox littermates. We ligated the left anterior descending (LAD) coronary artery of I/R groups simulating ischemia for 30 min, followed by a reperfusion period of 3 days and 7 days, respectively. The hearts of mIKKɑ-/- mice exhibited significantly increased inflammation and macrophage aggregation as compared to their IKKɑflox/flox littermates. Moreover, in the mIKKɑ-/- group subjected to I/R macrophages had a tendency to polarize to M1 phenotype. In vitro, we stimulated RAW264.7 cells with Lipopolysaccharides (LPS) after infection by the lentivirus, either knocking-down or overexpressing IKKɑ. We discovered that a deficiency of IKKɑ in RAW264.7 caused increased expression of pro-inflammatory markers compared to normal RAW264.7 after LPS stimulation. Inversely, pro-inflammatory factors were inhibited with IKKɑ overexpression. Mechanistically, IKKɑ directly combined with RelB to regulate macrophage polarization. Furthermore, IKKɑ regulated MEK1/2-ERK1/2 and downstream p65 signaling cascades after LPS stimulation. Overall, our data reveals that IKKɑ is a novel mediator protecting against the development of myocardial I/R injury via negative regulation of macrophage polarization to M1 phenotype. Thus, IKKɑ may serve as a valuable therapeutic target for the treatment of myocardial I/R injury.

Cortistatin attenuates angiotensin II-induced abdominal aortic aneurysm through inactivation of the ERK1/2 signaling pathways.

Abdominal aortic aneurysm (AAA) is a fatal disease that is associated with chronic inflammation in the vessel wall. Cortistatin is implicated in inflammation, vascular smooth muscle cell migration and other cardiovascular pathologies. But, the hypothetical effect of cortistatin on AAA remains uncertain. We investigated the effect of cortistatin administration to angiotensin (Ang) II-induced AAA formation in apolipoprotein E deficient (Apoe-/-) mice. We showed that cortistatin administration significantly suppresses incidence and severity of AAA in Apoe-/- mice. A significant increase in macrophage infiltration, excretion of inflammatory cytokines, activities and expression levels of MMP2 and MMP9, reactive oxygen species levels and cell apoptosis in aneurysmal aortic wall of Apoe-/- mice infused with Ang-II, and these events were significantly alleviated by co-treatment with cortistatin. Mechanistic studies showed that the protective effects of cortistatin were related to the blocking of ERK1/2 signaling pathways, while does not was not actually affect JNK, P38 phosphorylation. In conclusion, cortistatin appears to play an essential role in the formation of AAA and indicate cortistatin may as novel therapeutic option for AAA.

Regulatory role of CARD3 in left ventricular remodelling and dysfunction after myocardial infarction.

Caspase activation and recruitment domain 3 (CARD3) is a caspase recruitment domain (CARD)-containing serine/threonine kinase and plays a pivotal role in apoptosis, immunity, tissue development and proliferation. To date, the causal relationship between CARD3 and myocardial infarction (MI) remains largely unexplored. This study aimed to identify the functional significance of CARD3 in the regulation of cardiac remodelling after MI and the underlying mechanisms of its effects. The levels of CARD3 expression were up-regulated in failing human and mouse post-infarction hearts. In addition, CARD3-knockout (KO) mice and transgenic mice overexpressing CARD3 in the heart were then generated and subjected to MI. Compared with wild-type (WT) control mice, CARD3-KO mice developed smaller infarct sizes, improved survival rates, and preserved left ventricle (LV) function after MI. Significantly, CARD3-KO hearts had less cardiomyocyte apoptosis and inflammatory cell infiltration in the infarct border zone. Attenuated LV remodelling was also observed in the KO hearts following MI, with reduced cardiac hypertrophy and fibrosis. Conversely, CARD3 overexpression resulted in the opposite MI-induced phenotype. Similar results were observed in ex vivo-cultured neonatal rat cardiomyocytes exposed to hypoxia. Mechanistically, we discovered that the CARD3-mediated detrimental effects of MI were associated with the activation of the NF-κB and p38 signalling cascades. Taken together, these data demonstrate that CARD3 serves as a novel positive modulator of ventricular remodelling after MI via the regulation of the NF-κB and p38 signalling. Thus, CARD3 may be a promising therapeutic target for the treatment of heart failure after MI.

A novel nomogram model to predict in-hospital mortality in patients with acute type A aortic dissection after surgery.

BACKGROUND: Acute type A aortic dissection is a dangerous disease that threatens public health. In recent years, with the progress of medical technology, the mortality rate of patients after surgery has been gradually reduced, leading that previous prediction models may not be suitable for nowadays. Therefore, the present study aims to find new independent risk factors for predicting in-hospital mortality and construct a nomogram prediction model. METHODS: The clinical data of 341 consecutive patients in our center from 2019 to 2023 were collected, and they were divided into two groups according to the death during hospitalization. The independent risk factors were analyzed by univariate and multivariate logistic regression, and the nomogram was constructed and verified based on these factors. RESULTS: age, preoperative lower limb ischemia, preoperative activated partial thromboplastin time (APTT), preoperative platelet count, Cardiopulmonary bypass (CPB) time and postoperative acute kidney injury (AKI) independently predicted in-hospital mortality of patients with acute type A aortic dissection after surgery. The area under the receiver operating characteristic curve (AUC) for the nomogram was 0.844. The calibration curve and decision curve analysis verified that the model had good quality. CONCLUSION: The new nomogram model has a good ability to predict the in-hospital mortality of patients with acute type A aortic dissection after surgery.

Morphology controlled synthesis of Fe3+-doped upconversion nanomaterials.

This work details the synthesis of paramagnetic upconversion nanoparticles doped with Fe3+ in various morphologies via the thermal decomposition method, followed by comprehensive characterization of their structures, optical properties and magnetism using diverse analytical techniques. Our findings demonstrate that by precisely modulating the ratio of oleic acid to octadecene in the solvent, one can successfully obtain hexagonal nanodiscs with a consistent and well-defined morphology. Further adjustments in the oleic acid to octadecene ratio, coupled with fine-tuning of the Na+/F- ratio, led to the production of small-sized nanorods with uniform morphology. Significantly, all Fe3+-doped nanoparticles displayed pronounced paramagnetism, with magnetic susceptibility measurements at 1 T and room temperature of 0.15 emu g-1 and 0.14 emu g-1 for the nanodiscs and nanorods, respectively. To further enhance their magnetic properties, we replaced the Y-matrix with a Gd-matrix, and by fine-tuning the oleic acid/octadecene and Na+/F- ratios, we achieved nanoparticles with uniform morphology. The magnetic susceptibility was 0.82 emu g-1 at 1 T and room temperature. Simultaneously, we could control the nanoparticle size by altering the synthesis temperature. These upconversion nanostructures, characterized by both paramagnetic properties and regular morphology, represent promising dual-mode nanoprobe candidates for optical biological imaging and magnetic resonance imaging.

Proteomics analysis of human pericardial fluid.

Pericardial fluid (PF) is considered as a biochemical window of heart. To date, there have been limited attempts to perform an in-depth analysis of the PF proteome. In this study, an SDS-PAGE-LC-MS/MS platform was utilized to explore depleted PF, which showed great coverage of low-abundant proteins. In total, 1007 nonredundant proteins were identified with at least two peptides. This is the first comprehensive analysis of human PF proteome and provides a foundation for further application of PF in cardiovascular research. The data have been deposited to the ProteomeXchange with identifier PXD000194.

Surgical outcomes of total arch replacement with modified elephant trunk technique in type A aortic dissection: insights from single-center experience.

BACKGROUND: Total arch replacement with modified elephant trunk technique plays an important role in treating acute type A aortic dissection in China. We aim to summarize the therapeutic effects of this procedure in our center over a 17-year period. METHODS: Consecutive patients treated at our hospital due to type A aortic dissection from January 2004 to January 2021 were studied. Relevant data of these patients undergoing total arch replacement with modified elephant trunk technique were collected and analyzed. RESULTS: A total of 589 patients were included with a mean age of 53.1 ± 12.2 years. The mean of cardiopulmonary bypass, cross-clamping, and selected cerebral perfusion time were 199.6 ± 41.9, 119.0 ± 27.2, and 25.1 ± 5.0 min, respectively. In-hospital death occurred in 46 patients. Multivariate analysis identified four significant risk factors for in-hospital mortality: preexisting renal hypoperfusion (OR 5.43; 95% CI 1.31 - 22.44; P = 0.020), cerebral malperfusion (OR 11.87; 95% CI 4.13 - 34.12; P < 0.001), visceral malperfusion (OR 4.27; 95% CI 1.01 - 18.14; P = 0.049), and cross-clamp time ≥ 130 min (OR 3.26; 95% CI 1.72 - 6.19; P < 0.001). The 5, 10, and 15 years survival rates were 86.4%, 82.6%, and 70.2%, respectively. CONCLUSIONS: Total arch replacement with modified elephant trunk technique is an effective treatment for acute type A aortic dissection with satisfactory perioperative results. Patients with preexisting renal hypoperfusion, cerebral malperfusion, visceral malperfusion, and long cross-clamp time are at a higher risk of in-hospital death.

Machine learning in the prediction of cardiac surgery associated acute kidney injury with early postoperative biomarkers.

Purpose: To establish novel prediction models for predicting acute kidney injury (AKI) after cardiac surgery based on early postoperative biomarkers. Patients and methods: This study enrolled patients who underwent cardiac surgery in a Chinese tertiary cardiac center and consisted of a discovery cohort (n = 452, from November 2018 to June 2019) and a validation cohort (n = 326, from December 2019 to May 2020). 43 biomarkers were screened using the least absolute shrinkage and selection operator and logistic regression to construct a nomogram model. Three tree-based machine learning models were also established: eXtreme Gradient Boosting (XGBoost), random forest (RF) and deep forest (DF). Model performance was accessed using area under the receiver operating characteristic curve (AUC). AKI was defined according to the Kidney Disease Improving Global Outcomes criteria. Results: Five biomarkers were identified as independent predictors of AKI and were included in the nomogram: soluble ST2 (sST2), N terminal pro-brain natriuretic peptide (NT-proBNP), heart-type fatty acid binding protein (H-FABP), lactic dehydrogenase (LDH), and uric acid (UA). In the validation cohort, the nomogram achieved good discrimination, with AUC of 0.834. The machine learning models also exhibited adequate discrimination, with AUC of 0.856, 0.850, and 0.836 for DF, RF, and XGBoost, respectively. Both nomogram and machine learning models had well calibrated. The AUC of sST2, NT-proBNP, H-FABP, LDH, and UA to discriminate AKI were 0.670, 0.713, 0.725, 0.704, and 0.749, respectively. In addition, all of these biomarkers were significantly correlated with AKI after adjusting clinical confounders (odds ratio and 95% confidence interval of the third vs. the first tertile: sST2, 3.55 [2.34-5.49], NT-proBNP, 5.50 [3.54-8.71], H-FABP, 6.64 [4.11-11.06], LDH, 7.47 [4.54-12.64], and UA, 8.93 [5.46-15.06]). Conclusion: Our study provides a series of novel predictive models and five biomarkers for enhancing the risk stratification of AKI after cardiac surgery.

Research progress of bone metastases: From disease recognition to clinical practice.

Bone metastases, as one of the common types of metastatic tumors, have a great impact on the survival period and quality of life of patients. Bone metastases are usually characterized by bone destruction. Skeletal related events caused by bone destruction often lead to pain, pathological fractures and even paralysis. In this review, we provide a detailed explanation of bone metastases from the epidemiology, clinical features, pathogenesis, and recently developed clinical treatment viewpoints. We concluded that the incidence of bone metastases is increasing gradually, with serious clinical symptoms, complex pathogenesis and diverse clinical treatment. Tumor cells, immune cells, osteoblasts/osteoclasts and other cells as well as cytokines and enzymes all play a key role in the pathogenesis of bone metastases. We believe that the future treatment of bone metastases will be diversified and comprehensive. Some advanced technologies, such as nanomedicine, could be used for treatment, but this depends on understanding how disease occurs. With the development of treatment, the survival time and quality of life of patients will be improved.