Coupling vibration analysis of heat exchanger tube bundles under different stiffness conditions.

A two-dimensional tube bundles fluid-structure coupling model was developed using the CFD approach, with a rigid body motion equation and the Newmark integral method. The numerical simulations were performed to determine the vibration coupling properties between various tube bundles of stiffness. Take the corner square tube bundles with a pitch ratio of 1.28 as the research object. The influence of adjacent tubes with different stiffness on the vibration of the central target tube was analyzed. The research results show that the vibration characteristic of tube bundles is affected by the flow field dominant frequency and the inherent frequency of tube bundles. The vibration of adjacent tube bundles significantly impacts the amplitude and frequency of the central target tube. The equal stiffness and large stiffness tubes upstream or downstream inhibit the vibration displacement of the target tube to some extent. The low-stiffness tubes upstream or downstream significantly enhanced the amplitude of the target tube. The findings can be used to provide a basis for reasonable design and vibration suppression of shell-and-tube heat exchangers.

Stromal-derived MAOB promotes prostate cancer growth and progression.

Prostate cancer (PC) develops in a microenvironment where the stromal cells modulate adjacent tumor growth and progression. Here, we demonstrated elevated levels of monoamine oxidase B (MAOB), a mitochondrial enzyme that degrades biogenic and dietary monoamines, in human PC stroma, which was associated with poor clinical outcomes of PC patients. Knockdown or overexpression of MAOB in human prostate stromal fibroblasts indicated that MAOB promotes cocultured PC cell proliferation, migration, and invasion and co-inoculated prostate tumor growth in mice. Mechanistically, MAOB induces a reactive stroma with activated marker expression, increased extracellular matrix remodeling, and acquisition of a protumorigenic phenotype through enhanced production of reactive oxygen species. Moreover, MAOB transcriptionally activates CXCL12 through Twist1 synergizing with TGFß1-dependent Smads in prostate stroma, which stimulates tumor-expressed CXCR4-Src/JNK signaling in a paracrine manner. Pharmacological inhibition of stromal MAOB restricted PC xenograft growth in mice. Collectively, these findings characterize the contribution of MAOB to PC and suggest MAOB as a potential stroma-based therapeutic target.

Long-term exposure to PM1 is associated with increased prevalence of metabolic diseases: evidence from a nationwide study in 123 Chinese cities.

Exposure to particulate matter (PM) has been linked to metabolic diseases. However, the effects of PM with an aerodynamic diameter ≤ 1.0 µm (PM1) on metabolic diseases remain unclear. This study is aimed at assessing the associations of PM1 with metabolic disease risk and quantifying the concentration-response (C-R) relationship of PM1 with metabolic disease risk. A national cross-sectional study was conducted, including 12,495 middle-aged and older adults in 123 Chinese cities. The two-year average concentration of PM1 was evaluated using satellite-based spatiotemporal models. Metabolic diseases, including abdominal obesity, diabetes, hypertension, dyslipidemia, and metabolic syndrome, were identified based on physical examination, blood standard biochemistry examination, and self-reported disease histories. Generalized linear models and C-R curves were used to evaluate the associations of PM1 with metabolic diseases. A total of 12,495 participants were included in this study, with a prevalence of 45.73% for abdominal obesity, 20.22% for diabetes, 42.46% for hypertension, 41.01% for dyslipidemia, and 33.78% for metabolic syndrome. The mean ± standard deviation age of participants was 58.79 ± 13.14 years. In addition to dyslipidemia, exposure to PM1 was associated with increased risks of abdominal obesity, diabetes, hypertension, and metabolic syndrome. Each 10 µg/m3 increase in PM1 concentrations was associated with 39% (odds ratio (OR) = 1.39, 95% confidence interval (CI) 1.33, 1.46) increase in abdominal obesity, 18% (OR = 1.18, 95%CI 1.12, 1.25) increase in diabetes, 11% (OR = 1.11, 95%CI 1.06, 1.16) increase in hypertension, and 25% (OR = 1.25, 95%CI 1.19, 1.31) in metabolic syndrome, respectively. C-R curves showed that the OR values of abdominal obesity, diabetes, hypertension, and metabolic syndrome were increased gradually with the increase of PM1 concentrations. Subgroup analysis indicated that exposure to PM1 was associated with increased metabolic disease risks among participants with different lifestyles and found that solid fuel users were more susceptible to PM1 than clean fuel users. This national cross-sectional study indicated that exposure to higher PM1 might increase abdominal obesity, diabetes, hypertension, and metabolic syndrome risk, and solid fuel use might accelerate the adverse effects of PM1 on metabolic syndrome risk. Further longitudinal cohort studies are warranted to establish a causal inference between PM1 exposure and metabolic disease risk.

STAB2: an updated spatio-temporal cell atlas of the human and mouse brain.

The brain is constituted of heterogeneous types of neuronal and non-neuronal cells, which are organized into distinct anatomical regions, and show precise regulation of gene expression during development, aging and function. In the current database release, STAB2 provides a systematic cellular map of the human and mouse brain by integrating recently published large-scale single-cell and single-nucleus RNA-sequencing datasets from diverse regions and across lifespan. We applied a hierarchical strategy of unsupervised clustering on the integrated single-cell transcriptomic datasets to precisely annotate the cell types and subtypes in the human and mouse brain. Currently, STAB2 includes 71 and 61 different cell subtypes defined in the human and mouse brain, respectively. It covers 63 subregions and 15 developmental stages of human brain, and 38 subregions and 30 developmental stages of mouse brain, generating a comprehensive atlas for exploring spatiotemporal transcriptomic dynamics in the mammalian brain. We also augmented web interfaces for querying and visualizing the gene expression in specific cell types. STAB2 is freely available at https://mai.fudan.edu.cn/stab2.

Telomere dysfunction in Tert knockout mice delays BrafV600E -induced melanoma development.

Telomerase activation is a crucial step in melanomagenesis, often occurring because of ultraviolet radiation (UVR)-induced mutations at the telomerase gene (TERT) promoter and rendering TERT transcription in response to the activated Raf-MAP kinase pathway by BRAFV600E mutation. Due to the excessively long telomeres in mice, this process does not occur during melanomagenesis in mouse models. To investigate the impact of telomere dysfunction on melanomagenesis, BrafV600E was induced in generations 1 and 4 (G1 and G4) of Tert-/- mice. Our findings revealed that, regardless of UVR exposure, melanoma development was delayed in G4 mice, which had shorter telomeres compared to G1 and wild-type C57BL/6J (G0) mice. Moreover, many G4 tumors displayed an accumulation of excessive DNA damage, as evidenced by increased γH2A.X staining. Tumors from UVR-exposed mice exhibited elevated p53 protein expression. Cultured tumor cells isolated from G4 mice displayed abundant chromosomal fusions and rearrangements, indicative of telomere dysfunction in these cells. Additionally, tumor cells derived from UVB-exposed mice exhibited constitutively elevated expression of mutant p53 proteins, suggesting that p53 was a target of UVB-induced mutagenesis. Taken together, our findings suggest that telomere dysfunction hampers melanomagenesis, and targeting telomere crisis-mediated genomic instability may hold promise for the prevention and treatment of melanoma.

Extra-anatomic revascularization and a new cannulation strategy for preoperative cerebral malperfusion due to severe stenosis or occlusion of supra-aortic branch vessels in acute type A aortic dissection.

Objectives: Acute type A aortic dissection (ATAAD) with severe stenosis or occlusion of the true lumen of aortic arch branch vessels often leads to an increased incidence of severe postsurgical neurological complications and mortality rate. In this study, we aimed to introduce our institutional extra-anatomic revascularization and cannulation strategy with improved postoperative outcomes for better management of patients with cerebral malperfusion in the setting of ATAAD. Methods: Twenty-eight patients with ATAAD complicated by severe stenosis or occlusion of the aortic arch branch vessels, as noted on combined computed tomography angiography of the aorta and craniocervical artery, between January 2021 and June 2022 were included in this study. Basic patient characteristics, surgical procedures, hospitalization stays, and early follow-up results were analyzed. Results: The median follow-up duration was 16.5 months (interquartile range: 11.5-20.5), with a 100% completion rate. The 30-day mortality rates was 7.1% (2/28 patients); two patients had multiple cerebral infarctions on preoperative computed tomography and persistent coma. Postoperative transient neurological dysfunction occurred in 10.7% (3/28) of the patients, and no new permanent neurological dysfunction occurred. Of all the patients, 3.6% (1/28) had novel acute renal failure. No other deaths, secondary surgeries, or serious complications occurred during the early follow-up period. Conclusions: Use of extra-anatomic revascularization and a new cannulation strategy before cardiopulmonary bypass is safe and feasible and may reduce the high incidence of postoperative neurological complications in patients with ATAAD and cerebral malperfusion.

Prioritizing genes associated with brain disorders by leveraging enhancer-promoter interactions in diverse neural cells and tissues.

BACKGROUND: Prioritizing genes that underlie complex brain disorders poses a considerable challenge. Despite previous studies have found that they shared symptoms and heterogeneity, it remained difficult to systematically identify the risk genes associated with them. METHODS: By using the CAGE (Cap Analysis of Gene Expression) read alignment files for 439 human cell and tissue types (including primary cells, tissues and cell lines) from FANTOM5 project, we predicted enhancer-promoter interactions (EPIs) of 439 cell and tissue types in human, and examined their reliability. Then we evaluated the genetic heritability of 17 diverse brain disorders and behavioral-cognitive phenotypes in each neural cell type, brain region, and developmental stage. Furthermore, we prioritized genes associated with brain disorders and phenotypes by leveraging the EPIs in each neural cell and tissue type, and analyzed their pleiotropy and functionality for different categories of disorders and phenotypes. Finally, we characterized the spatiotemporal expression dynamics of these associated genes in cells and tissues. RESULTS: We found that identified EPIs showed activity specificity and network aggregation in cell and tissue types, and enriched TF binding in neural cells played key roles in synaptic plasticity and nerve cell development, i.e., EGR1 and SOX family. We also discovered that most neurological disorders exhibit heritability enrichment in neural stem cells and astrocytes, while psychiatric disorders and behavioral-cognitive phenotypes exhibit enrichment in neurons. Furthermore, our identified genes recapitulated well-known risk genes, which exhibited widespread pleiotropy between psychiatric disorders and behavioral-cognitive phenotypes (i.e., FOXP2), and indicated expression specificity in neural cell types, brain regions, and developmental stages associated with disorders and phenotypes. Importantly, we showed the potential associations of brain disorders with brain regions and developmental stages that have not been well studied. CONCLUSIONS: Overall, our study characterized the gene-enhancer regulatory networks and genetic mechanisms in the human neural cells and tissues, and illustrated the value of reanalysis of publicly available genomic datasets.

SEVERE BURN-INDUCED MITOCHONDRIAL RECRUITMENT OF CALPAIN CAUSES ABERRANT MITOCHONDRIAL DYNAMICS AND HEART DYSFUNCTION.

ABSTRACT: Mitochondrial damage is an important cause of heart dysfunction after severe burn injury. However, the pathophysiological process remains unclear. This study aims to examine the mitochondrial dynamics in the heart and the role of µ-calpain, a cysteine protease, in this scenario. Rats were subjected to severe burn injury treatment, and the calpain inhibitor MDL28170 was administered intravenously 1 h before or after burn injury. Rats in the burn group displayed weakened heart performance and decreased mean arterial pressure, which was accompanied by a diminishment of mitochondrial function. The animals also exhibited higher levels of calpain in mitochondria, as reflected by immunofluorescence staining and activity tests. In contrast, treatment with MDL28170 before any severe burn diminished these responses to a severe burn. Burn injury decreased the abundance of mitochondria and resulted in a lower percentage of small mitochondria and a higher percentage of large mitochondria. Furthermore, burn injury caused an increase in the fission protein DRP1 in the mitochondria and a decrease in the inner membrane fusion protein OPA1. Similarly, these alterations were also blocked by MDL28170. Of note, inhibition of calpain yielded the emergence of more elongated mitochondria along with membrane invagination in the middle of the longitude, which is an indicator of the fission process. Finally, MDL28170, administered 1 h after burn injury, preserved mitochondrial function and heart performance, and increased the survival rate. Overall, these results provided the first evidence that mitochondrial recruitment of calpain confers heart dysfunction after severe burn injury, which involves aberrant mitochondrial dynamics.

Associations of long-term exposure to air pollution, physical activity with blood pressure and prevalence of hypertension: the China Health and Retirement Longitudinal Study.

Background: Long-term exposure to air pollution and physical activity (PA) are linked to blood pressure and hypertension. However, the joint effect of air pollution and PA on blood pressure and hypertension are still unknown in Chinese middle-aged and older adults. Methods: A total of 14,622 middle-aged and older adults from the China Health and Retirement Longitudinal Study wave 3 were included in this study. Ambient air pollution [particulate matter with diameter ≤ 2.5 µm (PM2.5), or ≤10 µm (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbonic oxide (CO)] were estimated using satellite-based spatiotemporal models. PA was investigated using International Physical Activity Questionnaire. Generalized linear models were used to examine the associations of air pollution, PA score with blood pressure [systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP)], and the prevalence of hypertension. Subgroup analysis was conducted to investigate the effects of air pollution on blood pressure and the prevalence of hypertension in different PA groups. Results: The results showed that for each inter-quartile range (IQR) increase in PM2.5 (25.45 µg/m3), PM10 (40.56 µg/m3), SO2 (18.61 µg/m3), NO2 (11.16 µg/m3), CO (0.42 mg/m3) and PA score (161.3 MET/h-week), the adjusted odd ratio (OR) of hypertension was 1.207 (95% confidence interval (CI): 1.137, 1.281), 1.189 (95%CI: 1.122, 1.260), 1.186 (95%CI: 1.112, 1.266), 1.186 (95%CI: 1.116, 1.260), 1.288 (95%CI: 1.223, 1.357), 0.948 (95%CI: 0.899, 0.999), respectively. Long-term exposure to PM2.5, PM10, SO2, NO2, and CO was associated with increased SBP, DBP, and MAP levels. For example, each IQR increase in PM2.5 was associated with 1.20 mmHg (95%CI: 0.69, 1.72) change in SBP, 0.66 mmHg (95%CI: 0.36, 0.97) change in DBP, and 0.84 mmHg (95%CI: 0.49, 1.19) change in MAP levels, respectively. Each IQR increase in PA score was associated with -0.56 mmHg (95%CI: -1.03, -0.09) change in SBP, -0.32 mmHg (95%CI: -0.59, -0.05) change in DBP, and -0.33 mmHg (95%CI: -0.64, -0.02) change in MAP levels, respectively. Subgroup analysis found that the estimated effects in the sufficient PA group were lower than that in the insufficient PA group. Conclusion: Long-term exposure to air pollutants is associated with increased blood pressure and hypertension risk, while high-level PA is associated with decreased blood pressure and hypertension risk. Strengthening PA might attenuate the adverse effects of air pollution on blood pressure and hypertension risk.

GPR30 Alleviates Pressure Overload-Induced Myocardial Hypertrophy in Ovariectomized Mice by Regulating Autophagy.

The incidence of heart failure mainly resulting from cardiac hypertrophy and fibrosis increases sharply in post-menopausal women compared with men at the same age, which indicates a cardioprotective role of estrogen. Previous studies in our group have shown that the novel estrogen receptor G Protein Coupled Receptor 30 (GPR30) could attenuate myocardial fibrosis caused by ischemic heart disease. However, the role of GPR30 in myocardial hypertrophy in ovariectomized mice has not been investigated yet. In this study, female mice with bilateral ovariectomy or sham surgery underwent transverse aortic constriction (TAC) surgery. After 8 weeks, mice in the OVX + TAC group exhibited more severe myocardial hypertrophy and fibrosis than mice in the TAC group. G1, the specific agonist of GPR30, could attenuate myocardial hypertrophy and fibrosis of mice in the OVX + TAC group. Furthermore, the expression of LC3II was significantly higher in the OVX + TAC group than in the OVX + TAC + G1 group, which indicates that autophagy might play an important role in this process. An in vitro study showed that G1 alleviated AngiotensionII (AngII)-induced hypertrophy and reduced the autophagy level of H9c2 cells, as revealed by LC3II expression and tandem mRFP-GFP-LC3 fluorescence analysis. Additionally, Western blot results showed that the AKT/mTOR pathway was inhibited in the AngII group, whereas it was restored in the AngII + G1 group. To further verify the mechanism, PI3K inhibitor LY294002 or autophagy activator rapamycin was added in the AngII + G1 group, and the antihypertrophy effect of G1 on H9c2 cells was blocked by LY294002 or rapamycin. In summary, our results demonstrate that G1 can attenuate cardiac hypertrophy and fibrosis and improve the cardiac function of mice in the OVX + TAC group through AKT/mTOR mediated inhibition of autophagy. Thus, this study demonstrates a potential option for the drug treatment of pressure overload-induced cardiac hypertrophy in postmenopausal women.

Systematic Identification and Expression Analysis of the Sorghum Pht1 Gene Family Reveals Several New Members Encoding High-Affinity Phosphate Transporters.

Sorghum (Sorghum bicolor) is known to have a more robust capability of phosphorus uptake than many other cereal plants, which could be attributed to its phosphate transporter 1 (Pht1) that has a high phosphorus affinity. There are eleven SbPht1 genes in the sorghum genome, nine of which are expressed in sorghum roots or shoots in response to phosphorus deficiency (low-P). The molecular features of these nine genes were investigated by gene expression analysis, subcellular localization, and a yeast mutant complementation growth assay. They were found to be induced in response to low-P stress in root or shoot. All these SbPht1 proteins were found to be localized on the cell membrane, and SbPht1;8 was also detected in the endoplasmic reticulum. These SbPht1s were able to complement the yeast mutant EY917 that lacks all the functional phosphate transporters, and, among them, SbPht1;5, SbPht1;6 and SbPht1;8 could partially complement the yeast mutant strain EY917 in low-P conditions. Overall, these findings demonstrate that SbPht1;5, SbPht1;6, and SbPht1;8 are high-affinity phosphate transporters. SbPht1;5, in particular, is specifically involved in phosphorus uptake in the roots, whilst SbPht1;6 and SbPht1;8 are key players in both P uptake and P transport in response to low-P stress in sorghum.

Irisin inhibits NLRP3 inflammasome activation in HG/HF incubated cardiac microvascular endothelial cells with H/R injury.

PURPOSE: NLRP3 inflammasome mediates myocardial ischemia/reperfusion (MI/R) injury and diabetic vascular endothelia dysfunction. However, the role of NLRP3 inflammasome in MI/R injury with diabetes has not been fully described. Irisin plays an important role in anti-inflammation and improves endothelial function in type 2 diabetes. The current study aimed to investigate the effect of irisin on regulating NLRP3 inflammasome activation in diabetic vascular endothelia dysfunction. METHODS: Cardiac microvascular endothelial cells (CMECs) were cultured and subjected to high glucose/high fat (HG/HF) receiving hypoxia/reoxygenation (H/R) with irisin incubation or not. Then, apoptosis, viability, migration, NO secretion, and inflammasome activation were examined. RESULTS: The hypoxic CMECs exhibited increased apoptosis, impaired viability, and migration, even decreased NO secretion and enhanced inflammasome activation. Moreover, irisin incubation decreased NLRP3 activation and attenuated cell injury in HG/HF cultured CMECs subjected to H/R injury, which was abolished by NLRP3 inflammasome activation. Meanwhile, NLRP3 inflammasome siRNA also attenuated H/R injury in CMECs under HG/HF condition. CONCLUSION: The current study demonstrated for the first time that irisin inhibits NLRP3 inflammasome activation in CMECs as a novel mechanism in myocardial ischemia/reperfusion injury in diabetes.

STAT3-mediated upregulation of LINC00520 contributed to temozolomide chemoresistance in glioblastoma by interacting with RNA-binding protein LIN28B.

A considerable number of glioblastoma (GBM) patients developed drug resistance to Temozolomide (TMZ) during chemotherapy, resulting in therapeutic failure and tumor recurrence. However, the exact mechanism of TMZ chemoresistance in GBM is still poorly clarified. As a novel identified lncRNA, LINC00520 was located on chromosome 14 and overexpressed in multiple human cancers. This study was designed and conducted to investigate the role and underlying mechanism of LINC00520 in GBM chemoresistance to TMZ. The qRT-PCR assay demonstrated that LINC00520 was significantly overexpressed in TMZ-sensitive and/or TMZ-resistant GBM cells (P < 0.001). The silencing of LINC00520 markedly reduced the cell viability, suppressed colony formation, induced cell apoptosis and G1/S phase arrest in TMZ-resistant cells (P < 0.001). In contrast, overexpression of LINC00520 conferred TMZ-resistant phenotype of GBM cells in vitro (P < 0.001). The orthotopic xenograft model was established and the results indicated that the volume of tumor xenografts in vivo was markedly inhibited by TMZ treatment after the silencing of LINC00520 (P < 0.001). Luciferase reporter assay and chromatin immunoprecipitation (ChIP) assay revealed a strong affinity of transcription factor STAT3 to the promoter regions of LINC00520, suggesting that STAT3 mediated the aberrant expression of LINC00520 in GBM. Further experiments demonstrated that LINC00520 could interact with RNA-binding protein LIN28B to inhibit autophagy and reduce DNA damage, thereby contributing to TMZ chemoresistance in GBM. These findings suggested that STAT3/LINC00520/LIN28B axis might be a promising target to improve TMZ chemoresistance of GBM.

A real-time multi-function digital coincidence spectrometer for neutron copper activation diagnostics.

Copper activation has been a standard diagnostic for measuring 14.1-MeV neutron yields in deuterium-tritium fusion experiments, which is essential to evaluate their performance for potential ignition in the future. Copper-activation equipment, especially data-acquisition systems, is updated constantly thanks to the rapid developments in electronics. Here, a multi-function digital coincidence spectrometer for neutron copper-activation diagnostics was developed. The digital pulse processing includes pulse shaping, multichannel pulse analysis, coincidence event picks, and coincidence multichannel time analysis were implemented on a single field-programmable gate array (FPGA) chip. The results demonstrate that the coincidence background is 0.013 counts per second. By using the multi-function digital coincidence spectrometer, the copper-activation diagnostics could be performed at the SG-III Laser facility when the neutron yield is ≥ 1.0 × 1010/hit.

MtWRP1, a Novel Fabacean Specific Gene, Regulates Root Nodulation and Plant Growth in Medicago truncatula.

Fabaceans symbiotically interact with nitrogen-fixing rhizobacteria to form root nodules. Some fabacean specific proteins play important roles in the symbiosis. WRKY-related Protein (WRP) is a novel fabacean specific protein, whose functions have not been well characterized. In this study, MtWRP1 was functionally characterized in Medicago truncatula. It contains a WRKY domain at C-terminal and a novel transmembrane (TM) domain at N-terminal, and its WRKY domain was highly similar to the N-terminal WRKY domain of the group I WRKY proteins. The TM domain was highly homologous to the eukaryotic cytochrome b561 (Cytb561) proteins from birds. Subcellular localization revealed that MtWRP1 was targeted to the Golgi apparatus through the novel TM domain. MtWRP1 was highly expressed in roots and nodules, suggesting its possible roles in the regulation of root growth and nodulation. Both MtWRP1-overexpression transgenic M. truncatula and MtWRP1 mutants showed altered root nodulation and plant growth performance. Specifically, the formation of root nodules was significantly reduced in the absence of MtWRP1. These results demonstrated that MtWRP1 plays critical roles in root nodulation and plant growth.

Modified Burr-Hole Craniostomy for the Treatment of Chronic Subdural Hematoma in Adults.

BACKGROUND: Burr-hole craniostomy (BHC) is considered to be the most effective method for the treatment of chronic subdural hematoma (CSDH), and middle meningeal artery embolization is a new therapy used in clinical practice in recent years to treat CSDH. However, the optimal therapeutic effect of these 2 procedures is still controversial. This study prospectively designed a modified burr-hole craniostomy (mBHC) with drainage to treat CSDH. METHODS: A total of 101 patients diagnosed with CSDH from January 2019 to April 2020 were prospectively included in this study. They were divided into BHC and mBHC groups. Among them, 40 selected CSDH patients received mBHC treatment. For comparison, 61 CSDH patients who received BHC treatment were used as the control group. Primary outcomes were hematoma recurrence and postoperative complications. Secondary outcomes included midline recovery, hematoma clearance, operation time, and hospital stay. The Chi-square test was used to compare the 6-month follow-up results between the 2 groups. RESULTS: Among patients treated with mBHC, 39 patients had a good prognosis, and one 87-year-old patient with bilateral hematoma died of postoperative heart failure. Of the patients treated with BHC, 52 patients had good prognoses, and one 53-year-old patient with unilateral hematoma died of postoperative acute intracranial bleeding. During the 6-month follow-up period, no relapse occurred in the patients treated with mBHC, whereas 8 (13%) of the patients treated with BHC relapsed. There was a significant difference in the recurrence rate between the 2 groups (P < 0.05). In addition, midline recovery, hematoma clearance rate, operation time, and complications were found to be significantly different statistically (P < 0.05), and other characteristics of operation and outcome were not significantly different (P > 0.05) between the 2 groups. CONCLUSIONS: Modified burr-hole craniostomy has a positive therapeutic effect on patients with CSDH and is more effective than conventional BHC therapy.

Extracellular vesicles derived from astrocytes facilitated neurite elongation by activating the Hippo pathway.

Spinal cord injury (SCI) often causes severe neurological dysfunction, and facilitating neurite elongation is particularly important in its treatment. Astrocytes (AS) play an important role in the central nervous system (CNS), and their high plasticity and versatility provide a feasible entry point for relevant research. Our purpose was to explore whether extracellular vesicles (EVs) from astrocytes (AS-EVs) and lipopolysaccharide (LPS)-preactivated astrocytes (LPAS-EVs) facilitate neurite elongation, to explore the underlying mechanism, and to verify whether these EVs promote locomotor recovery in rats. We used LPS to preactivate astrocytes and cocultured them with PC12 cells to observe neurite changes, then extracted and identified AS-EVs and LPAS-EVs and the role and mechanism of these EVs in facilitating neurite elongation was examined in vivo and vitro. We demonstrated that AS-EVs and LPAS-EVs facilitated the elongation of neurites and the recovery of rats with SCI. LPAS-EVs had a stronger effect than AS-EVs, by activating the Hippo pathway, promoting monopole spindle binding protein 1 (MOB1) expression, and reducing Yes-associated protein (YAP) levels. The data also suggest a feedback regulation between MOB1 and p-YAP/YAP. In sum, AS-EVs and LPAS-EVs can play an active role in facilitating neurite elongation by activating the Hippo pathway. These findings provide a new strategy for treating SCI and other CNS-related injuries.

miR-381-3p Involves in Glioma Progression by Suppressing Tumor-Promoter Factor ANTXR1.

Accumulating studies revealed association between development of glioma and miRNA dysregulation. A case in point is miR-381-3p, but its mechanism in glioma is unclear yet. In this work, we confirmed that overexpressed miR-381-3p repressed biological functions of glioma cells. Additionally, we also discovered that upregulated anthrax toxin receptor 1 (ANTXR1) was negatively mediated by miR-381-3p. We further proved that miR-381-3p-targeted ANTXR1 was able to counteract the suppression of miR-381-3p on biological functions of glioma. We concluded that miR-381-3p and ANTXR1 were both important factors in modulating glioma progression. miR-381-3p/ANTXR1 axis is expected to be a molecular target for glioma.

FPGA implementation of a real-time digital pulse processing analysis for radiation detectors.

A new universal, flexible firmware has been implemented on field -programmable gate array (FPGA) for gamma-ray spectroscopy. The firmware of the FPGA runs on a digitizer that we developed ourselves. The present paper describes the detailed architecture of the firmware, including the trapezoidal shaper, peak detection, pulse height analyzer, and pile-up rejection. Gamma-ray spectroscopy measurements are made using a NaI(Tl) detector, CdZnTe detector, and HPGe detector.