A Novel tsRNA, m7G-3' tiRNA LysTTT, Promotes Bladder Cancer Malignancy Via Regulating ANXA2 Phosphorylation.

Emerging evidence indicates that transfer RNA (tRNA)-derived small RNAs (tsRNAs), originated from tRNA with high abundance RNA modifications, play an important role in many complex physiological and pathological processes. However, the biological functions and regulatory mechanisms of modified tsRNAs in cancer remain poorly understood. Here, it is screened for and confirmed the presence of a novel m7G-modified tsRNA, m7G-3'-tiRNA LysTTT (mtiRL), in a variety of chemical carcinogenesis models by combining small RNA sequencing with an m7G small RNA-modified chip. Moreover, it is found that mtiRL, catalyzed by the tRNA m7G-modifying enzyme mettl1, promotes bladder cancer (BC) malignancy in vitro and in vivo. Mechanistically, mtiRL is found to specifically bind the oncoprotein Annexin A2 (ANXA2) to promote its Tyr24 phosphorylation by enhancing the interactions between ANXA2 and Yes proto-oncogene 1 (Yes1), leading to ANXA2 activation and increased p-ANXA2-Y24 nuclear localization in BC cells. Together, these findings define a critical role for mtiRL and suggest that targeting this novel m7G-modified tsRNA can be an efficient way for to treat BC.

Enhancing m6A modification of lncRNA through METTL3 and RBM15 to promote malignant progression in bladder cancer.

Objective: Bladder cancer is one of the most prominent malignancies affecting the urinary tract, characterized by a poor prognosis. Our previous research has underscored the pivotal role of m6A methylation in the progression of bladder cancer. Nevertheless, the precise relationship between N6-methyladenosine (m6A) regulation of long non-coding RNA (lncRNA) and bladder cancer remains elusive. Methods: This study harnessed sequencing data and clinical records from 408 bladder cancer patients in the TCGA database. Employing R software, we conducted bioinformatics analysis to establish an m6A-lncRNA co-expression network. Analyzing the differences between high and low-risk groups, particularly at the immunological level, and subsequently investigating the primary regulatory factors of these lncRNA, validating the findings through experiments, and exploring their specific cellular functions. Results: We identified 50 m6A-related lncRNA with prognostic significance through univariate Cox regression analysis. In parallel, we employed a LASSO-Cox regression model to pinpoint 11 lncRNA and calculate risk scores for bladder cancer patients. Based on the median risk score, patients were categorized into low-risk and high-risk groups. The high-risk cohort exhibited notably lower survival rates than their low-risk counterparts. Further analysis pointed to RBM15 and METTL3 as potential master regulators of these m6A-lncRNA. Experimental findings also shed light on the upregulated expression of METTlL3 and RBM15 in bladder cancer, where they contributed to the malignant progression of tumors. The experimental findings demonstrated a significant upregulation of METTL3 and RBM15 in bladder cancer specimens, implicating their contributory role in the oncogenic progression. Knockdown of METTL3 and RBM15 resulted in a marked attenuation of tumor cell proliferation, invasion, and migration, which was concomitant with a downregulation in the cellular m6A methylation status. Moreover, these results revealed that RBM15 and METTL3 function in a synergistic capacity, positing their involvement in cancer promotion via the upregulation of m6A modifications in long non-coding RNAs. Additionally, this study successfully developed an N-methyl-N-nitrosourea (MNU)-induced rat model of in situ bladder carcinoma, confirming the elevated expression of RBM15 and METTL3, which paralleled the overexpression of m6A-related- lncRNAs observed in bladder cancer cell lines. This congruence underscores the potential utility of these molecular markers in in vivo models that mirror human malignancies. Conclusion: This study not only offers novel molecular targets,but also enriches the research on m6A modification in bladder cancer, thereby facilitating its clinical translation.

Development of a new Cox model for predicting long-term survival in hepatitis cirrhosis patients underwent transjugular intrahepatic portosystemic shunts.

BACKGROUND: Transjugular intrahepatic portosystemic shunt (TIPS) placement is a procedure that can effectively treat complications of portal hypertension, such as variceal bleeding and refractory ascites. However, there have been no specific studies on predicting long-term survival after TIPS placement. AIM: To establish a model to predict long-term survival in patients with hepatitis cirrhosis after TIPS. METHODS: A retrospective analysis was conducted on a cohort of 224 patients who underwent TIPS implantation. Through univariate and multivariate Cox regression analyses, various factors were examined for their ability to predict survival at 6 years after TIPS. Consequently, a composite score was formulated, encompassing the indication, shunt reasonability, portal venous pressure gradient (PPG) after TIPS, percentage decrease in portal venous pressure (PVP), indocyanine green retention rate at 15 min (ICGR15) and total bilirubin (Tbil) level. Furthermore, the performance of the newly developed Cox (NDC) model was evaluated in an internal validation cohort and compared with that of a series of existing models. RESULTS: The indication (variceal bleeding or ascites), shunt reasonability (reasonable or unreasonable), ICGR15, postoperative PPG, percentage of PVP decrease and Tbil were found to be independent factors affecting long-term survival after TIPS placement. The NDC model incorporated these parameters and successfully identified patients at high risk, exhibiting a notably elevated mortality rate following the TIPS procedure, as observed in both the training and validation cohorts. Additionally, in terms of predicting the long-term survival rate, the performance of the NDC model was significantly better than that of the other four models [Child-Pugh, model for end-stage liver disease (MELD), MELD-sodium and the Freiburg index of post-TIPS survival]. CONCLUSION: The NDC model can accurately predict long-term survival after the TIPS procedure in patients with hepatitis cirrhosis, help identify high-risk patients and guide follow-up management after TIPS implantation.

Serum metabolome and gut microbiome alterations are associated with low handgrip strength in older adults.

Handgrip strength (HGS), which represents global muscle strength, is a powerful indicator of disability and mortality in older adults; it is also used for the diagnosis of possible- or probable- sarcopenia and physical frailty. This study aimed to explore the metabolic mechanisms and potential biomarkers associated with declining HGS among older adults. We recruited 15 age- and environment-matched inpatients (age, 77-90 years) with low or normal HGS. Liquid chromatography-mass spectrometry (LC-MS) and 16S ribosomal DNA (rDNA) gene sequencing were performed to analyze the metabolome of serum and stool samples and the gut microbiome composition of stool samples. Spearman's correlation analysis was used to identify the potential serum and fecal metabolites associated with HGS. We assessed the levels of serum and fecal metabolites belonging to the class of cinnamic acids and derivatives and reported that the levels of carboxylic acids and their derivatives decreased in the low-HGS group. Serum levels of microbial metabolites, including cinnamoylglycine, 4-methoxycinnamic acid, and (e)-3,4,5-trimethoxycinnamic acid, were positively correlated with HGS. We found that gut microbial α-diversity was significantly higher in the low-HGS group, whereas higher ß-diversity was observed in the normal group. The relative abundances of the genera Parabacteroides and Intestinibacter increased significantly in the low-HGS group and were negatively correlated with the serum levels of cinnamoylglycine. The identified metabolites whose levels were markedly altered, and intestinal flora associated with these metabolites suggest the potential metabolic underpinnings for HGS and provide a basis for the further identification of biomarkers of muscle strength decline in older adults.

Genome-wide analysis of FRF gene family and functional identification of HvFRF9 under drought stress in barley.

FHY3 and its homologous protein FAR1 are the founding members of FRS family. They exhibited diverse and powerful physiological functions during evolution, and participated in the response to multiple abiotic stresses. FRF genes are considered to be truncated FRS family proteins. They competed with FRS for DNA binding sites to regulate gene expression. However, only few studies are available on FRF genes in plants participating in the regulation of abiotic stress. With wide adaptability and high stress-resistance, barley is an excellent candidate for the identification of stress-resistance-related genes. In this study, 22 HvFRFs were detected in barley using bioinformatic analysis from whole genome. According to evolution and conserved motif analysis, the 22 HvFRFs could be divided into subfamilies I and II. Most promoters of subfamily I members contained abscisic acid and methyl jasmonate response elements; however, a large number promoters of subfamily II contained gibberellin and salicylic acid response elements. HvFRF9, one of the members of subfamily II, exhibited a expression advantage in different tissues, and it was most significantly upregulated under drought stress. In-situ PCR revealed that HvFRF9 is mainly expressed in the root epidermal cells, as well as xylem and phloem of roots and leaves, indicating that HvFRF9 may be related to absorption and transportation of water and nutrients. The results of subcellular localization indicated that HvFRF9 was mainly expressed in the nuclei of tobacco epidermal cells and protoplast of arabidopsis. Further, transgenic arabidopsis plants with HvFRF9 overexpression were generated to verify the role of HvFRF9 in drought resistance. Under drought stress, leaf chlorosis and wilting, MDA and O2 - contents were significantly lower, meanwhile, fresh weight, root length, PRO content, and SOD, CAT and POD activities were significantly higher in HvFRF9-overexpressing arabidopsis plants than in wild-type plants. Therefore, overexpression of HvFRF9 could significantly enhance the drought resistance in arabidopsis. These results suggested that HvFRF9 may play a key role in drought resistance in barley by increasing the absorption and transportation of water and the activity of antioxidant enzymes. This study provided a theoretical basis for drought resistance in barley and provided new genes for drought resistance breeding.

Identification of MGMT promoter methylation as a specific lipid metabolism biomarker, reveals the feasibility of atorvastatin application in glioblastoma.

BACKGROUND: Glioblastoma is one of the deadliest tumors, and limited improvement in managing glioblastoma has been achieved in the past decades. The unmethylated promoter area of 6-O-Methylguanine-DNA Methyltransferase (MGMT) is a significant biomarker for recognizing a subset of glioblastoma that is resistant to chemotherapy. Here we identified MGMT methylation can also work as a specific biomarker to classify the lipid metabolism patterns between methylated and unmethylated glioblastoma and verify the potential novel therapeutic strategy for unmethylated MGMT glioblastoma. METHODS: Liquid Chromatograph Mass Spectrometer has been applied for non-targeted metabolome and targeted lipidomic profiling to explore the metabolism pattern correlated with MGMT promoter methylation. Transcriptome has been performed to explore the biological differences and the potential mechanism of lipid metabolism in glioblastoma samples. In vivo and ex vivo assays were performed to verify the anti-tumor activity of atorvastatin in the administration of glioblastoma. RESULTS: Multi-omics assay has described a significant difference in lipid metabolism between MGMT methylated and unmethylated glioblastoma. Longer and unsaturated fatty acyls were found enriched in MGMT-UM tumors. Lipid droplets have been revealed remarkably decreased in MGMT unmethylated glioblastoma. In vivo and ex vivo assays revealed that atorvastatin and also together with temozolomide showed significant anti-tumor activity, and atorvastatin alone was able to achieve better survival and living conditions for tumor-hosting mice. CONCLUSIONS: MGMT promoter methylation status might be a well-performed biomarker of lipid metabolism in glioblastoma. The current study can be the basis of further mechanism studies and implementation of clinical trials, and the results provide preclinical evidence of atorvastatin administration in glioblastoma, especially for MGMT unmethylated tumors.

m6A modification mediates SLC3A2/SLC7A5 translation in 3-methylcholanthrene-induced uroepithelial transformation.

3-Methylcholanthracene (3-MC) is one of the most carcinogenic polycyclic aromatic hydrocarbons (PAHs). Long-term exposure to PAHs has been thought of as an important factor in urothelial tumorigenesis. N6-methyladenosine (m6A) exists widely in eukaryotic organisms and regulates the expression level of specific genes by regulating mRNA stability, translation efficiency, and nuclear export efficiency. Currently, the potential molecular mechanisms that regulate m6A modification for 3-MC carcinogenesis remain unclear. Here, we profiled mRNA, m6A, translation and protein level using "-omics" methodologies, including transcriptomes, m6A profile, translatomes, and proteomics in 3-MC-transformed urothelial cells and control cells. The key molecules SLC3A2/SLC7A5 were screened and identified in 3-MC-induced uroepithelial transformation. Moreover, SLC7A5/SLC3A2 promoted uroepithelial cells malignant phenotype in vitro and in vivo. Mechanically, METTL3 and ALKBH5 mediated m6A modification of SLC3A2/SLC7A5 mRNA in 3-MC-induced uroepithelial transformation by upregulating the translation of SLC3A2/SLC7A5. Furthermore, programmable m6A modification of SLC3A2/SLC7A5 mRNA affected the expression of its proteins. Taken together, our results revealed that the m6A modification-mediated SLC3A2/SLC7A5 translation promoted 3-MC-induced uroepithelial transformation, suggesting that targeting m6A modification of SLC3A2/SLC7A5 may be a potential therapeutic strategy for bladder cancer related to PAHs.

Targeted m6A demethylation of ITGA6 mRNA by a multisite dCasRx-m6A editor inhibits bladder cancer development.

INTRODUCTION: N6-methyladenosine (m6A) modification contributes to the pathogenesis and development of various cancers, including bladder cancer (BCa). In particular, integrin α6 (ITGA6) promotes BCa progression by cooperatively regulating multisite m6A modification. However, the therapeutic effect of targeting ITGA6 multisite m6A modifications in BCa remains unknown. OBJECTIVES: We aim to develop a multisite dCasRx- m6A editor for assessing the effects of the multisite dCasRx-m6A editor targeted m6A demethylation of ITGA6 mRNA in BC growth and progression. METHODS: The multisite dCasRx- m6A editor was generated by cloning. m6A-methylated RNA immunoprecipitation (meRIP), luciferase reporter, a single-base T3 ligase-based qPCR-amplification, Polysome profiling and meRIP-seq experiments were performed to determine the targeting specificity of the multisite dCasRx-m6A editor. We performed cell phenotype analysis and used in vivo mouse xenograft models to assess the effects of the multisite dCasRx-m6A editor in BC growth and progression. RESULTS: We designed a targeted ITGA6 multi-locus guide (g)RNA and established a bidirectional deactivated RfxCas13d (dCasRx)-based m6A-editing platform, comprising a nucleus-localized dCasRx fused with the catalytic domains of methyltransferase-like 3 (METTL3-CD) or α-ketoglutarate-dependent dioxygenase alkB homolog 5 (ALKBH5-CD), to simultaneously manipulate the methylation of ITGA6 mRNA at four m6A sites. The results confirmed the dCasRx-m6A editor modified m6A at multiple sites in ITGA6 mRNA, with low off-target effects. Moreover, targeted m6A demethylation of ITGA6 mRNA by the multisite dCasRx-m6A editor significantly reduced BCa cell proliferation and migration in vitro and in vivo. Furthermore, the dCasRx-ALKBH5-CD and ITGA6 multi-site gRNA delivered to 5-week-old BALB/cJNju-Foxn1nu/Nju nude mice via adeno-associated viral vectors significantly inhibited BCa cell growth. CONCLUSION: Our study proposes a novel therapeutic tool for the treatment of BC by applying the multisite dCasRx-m6A editor while highlighting its potential efficacy for treating other diseases associated with abnormal m6A modifications.

Magnetic Resonance Perfusion-Weighted Imaging in Predicting Hemorrhagic Transformation of Acute Ischemic Stroke: A Retrospective Study.

Hemorrhagic transformation (HT) is one of the common complications in patients with acute ischemic stroke (AIS). This study aims to investigate the value of different thresholds of Tmax generated from perfusion-weighted MR imaging (PWI) and the apparent diffusion coefficient (ADC) value in the prediction of HT in AIS. A total of 156 AIS patients were enrolled in this study, with 55 patients in the HT group and 101 patients in non-HT group. The clinical baseline data and multi-parametric MRI findings were compared between HT and non-HT groups to identify indicators related to HT. The optimal parameters for predicting HT and the corresponding cutoff values were obtained using the receiver operating characteristic curve analysis of the volumes of ADC < 620 × 10-6 mm2/s and Tmax > 6 s, 8 s, and 10 s. The results showed that the volumes of ADC < 620 × 10-6 mm2/s and Tmax > 6 s, 8 s, and 10 s in the HT group were all significantly larger than that in the non-HT group and were all independent risk factors for HT. Early measurement of the volume of Tmax > 10 s had the highest value, with a cutoff lesion volume of 10.5 mL.

Subcutaneous adipose tissue alteration in aging process associated with thyroid hormone signaling.

BACKGROUND: Functional changes in subcutaneous adipose tissue (SAT) occur earlier in the aging process and play an important role in the occurrence and development of age-related metabolic diseases. The mechanism of this phenomenon is still unclear, and the change in adipose tissue with age is poorly understood. METHODS: We used transcriptome sequencing (RNA seq) to screen differentially expressed genes at the mRNA level, and analyzed the functional characteristics of the differential genes through GO and KEGG analysis in human SAT of all ages. In order to clarify the specific mechanism of the functional change, we analyzed the chromatin accessibility in the promoter region in the same SAT used in the RNA seq by the assay for transposase-accessible chromatin with high throughput sequencing (ATAC-seq) and obtained the functional genes in SAT changed with age. To verify these changes, we enlarged our sample content of human SAT. The primary mice adipocytes were extracted and stimulated by thyroid hormone of different concentration to construct an animal model, and the expression of the genes were determined through real-time Polymerase Chain Reaction(RT-PCR). The oxygen consumption test and immunofluorescence staining were used to determine the mitochondrial function of SAT. RESULTS: RNA-seq showed characteristic gene expression of young and old human SAT, in which 331 genes were up-regulated and 349 genes were down-regulated. ATAC-seq, RNA-seq, combined with the mouse prediction model, determined the functional changed characteristics of seven genes. All these genes expressed differently in SAT of different ages, in which, NCF1, NLRP3, DUOX1 showed positive correlation with age; The expression of IFI30, P2RX1, P2RX6, PRODH, however, decreased with age. And all these genes showed dose dependent alternations under treatment of triiodothyroxine in mice SAT. The oxygen consumption rate revealed significant changes of the mitochondrial function and ROS accumulation in human SAT of different ages. CONCLUSION: In elderly individuals, the function, in addition to distribution, of SAT undergoes significant changes, primarily in mitochondria, which may be due to insensitivity to thyroid hormone signaling. These results identified seven novel genes regulated by thyroid hormone, exhibiting significant changes in SAT of different age, and are probably related to the dysfunction of the aged SAT due to the mitochondrial damage and ROS accumulation.

Surgical site infections after elective craniotomy for brain tumor: a study on potential risk factors and related treatments.

BACKGROUND: Surgical site infection (SSI) is a common complication following craniotomy that increases morbidity, mortality, and medical expenses. The objectives of this study were to determine the relevant risk factors associated with SSI after elective craniotomy for brain tumor and analyse the treatments for SSI. METHODS: A retrospective nested case‒control study was conducted using data from patients who underwent craniotomy for brain tumor resection at the Neurosurgical Oncology Department No. 6 of Beijing Tiantan Hospital, Capital Medical University, between January 2019 and December 2021. Risk factors for SSI were determined using multivariate logistic regression analysis. We analyzed microbiological and related treatment data for different SSI types. RESULTS: Among 2061 patients who underwent craniotomy for brain tumor, 31 had SSI (1.50%). In the multivariate logistic regression analysis, body mass index (BMI) and operative duration were identified as independent risk factors for SSI. The most common microorganism isolated from SSIs was Staphylococcus epidermidis (22.9%), and drug sensitivity results showed that gram-positive bacteria were sensitive to linezolid, vancomycin and tigecycline, whereas gram-negative bacteria were sensitive to meropenem, cefepime and ceftazidime. Six of the seven patients who underwent bone flap removal due to osteomyelitis were infected with gram-negative bacteria. CONCLUSIONS: BMI and operative duration were identified as independent risk factors for SSI. Diabetes mellitus, previous ratio therapy, type of incision, recurrence tumor and other risk factors were not found to be associated with the occurrence of SSI in this study.

Asymmetric Non-Fullerene Acceptor Derivatives Incorporated Ternary Organic Solar Cells.

Incorporating ITIC derivatives as guest acceptors into binary host systems is an effective strategy for constructing high-performance ternary organic solar cells (TOSCs). In this work, we introduced A-D-A type ITIC derivatives PTBTT-4F (asymmetric) and PTBTP-4F (symmetric) into the PM6:BTP-BO-4F (Y6-BO) binary blend and investigated the impacts of two guest acceptors on the performance of TOSCs. Differentiated device performance was observed, although PTBTT-4F and PTBTP-4F presented similar chemical structures and comparable absorptions. The PTBTT-4F ternary devices exhibited an improved power conversion efficiency (PCE) of 17.67% with increased open circuit (VOC) and current density (JSC), whereas the PTBTP-4F-based ternary devices yielded a relatively lower PCE of 16.34%. PTBTT-4F showed much better compatibility with the host acceptor BTP-BO-4F, so that they formed a well-mixed alloy phase state; more precise phase separation and increased crystallinity were thus induced in the ternary blends, leading to reduced molecular recombination and improved charge mobilities, which contributed to improved fill factors of the ternary devices. In addition, the optimized PTBTT-4F devices exhibited good performance tolerance of the photoactive layer thickness, as they even delivered a PCE of 15.25% when the active layer was as thick as up to ∼300 nm.

Distinct response of adipocyte progenitors to glucocorticoids determines visceral obesity via the TEAD1-miR-27b-PRDM16 axis.

OBJECTIVE: Visceral obesity contributes to obesity-related complications; however, the intrinsic mechanism of depot-specific adipose tissue behavior remains unclear. Despite the pro-adipogenesis role of glucocorticoids (GCs) in adipogenesis, the role of GCs in visceral adiposity rather than in subcutaneous adipose tissue is not established. Because adipocyte progenitors display a striking depot-specific pattern, the regulatory pathways of novel progenitor subtypes within different depots remain unclear. This study describes a cell-specific mechanism underlying visceral adiposity. METHODS: A diverse panel of novel depot-specific adipose progenitors was screened in mice and human samples. The transcriptome distinction and various responses of novel progenitor subtypes of GCs were further measured using the GC receptor-chromatin immunoprecipitation assay and RNA sequencing. The mechanism of novel subtypes was identified using transposase-accessible chromatin analysis and bisulfite sequencing and further confirmed using precise editing of CpG methylation. RESULTS: Platelet-derived growth factor receptor α (PDGFRα+ ) progenitors, which were dominant in the visceral adipose tissue, were GC-sensitive beige adipose progenitors, whereas CD137+ progenitors, which were dominant in the subcutaneous adipose tissue, were GC-passive beige adipose progenitors. Expression of miR-27b, an inhibitor of adipocyte browning, was significantly increased in PDGFRα+ progenitors treated with GCs. Using transposase-accessible chromatin analysis, bisulfite sequencing, and precise editing of CpG methylation, TEA domain transcription factor 1 (TEAD1) was discovered to be uniquely hypomethylated in PDGFRα+ progenitors. CONCLUSIONS: GCs inhibited the PDGFRα+ progenitors' browning process via miR-27b, which was transcriptionally activated by the collaboration of TEAD1 with the GC receptor. These data provide insights into the mechanism of depot-specific variations in high-fat diet-induced obesity.

TROP2 translation mediated by dual m6A/m7G RNA modifications promotes bladder cancer development.

RNA modifications, including adenine methylation (m6A) of mRNA and guanine methylation (m7G) of tRNA, are crucial for the biological function of RNA. However, the mechanism underlying the translation of specific genes synergistically mediated by dual m6A/m7G RNA modifications in bladder cancer (BCa) remains unclear. We demonstrated that m6A methyltransferase METTL3-mediated programmable m6A modification of oncogene trophoblast cell surface protein 2 (TROP2) mRNA promoted its translation during malignant transformation of bladder epithelial cells. m7G methyltransferase METTL1 enhanced TROP2 translation by mediating m7G modification of certain tRNAs. TROP2 protein inhibition decreased the proliferation and invasion of BCa cells in vitro and in vivo. Moreover, synergistical knockout of METTL3/METTL1 inhibited BCa cell proliferation, migration, and invasion; however, TROP2 overexpression partially abrogated its effect. Furthermore, TROP2 expression was significantly positively correlated with the expression levels of METTL3 and METTL1 in BCa patients. Overall, our results revealed that METTL3/METTL1-mediated dual m6A/m7G RNA modifications enhanced TROP2 translation and promoted BCa development, indicating a novel RNA epigenetic mechanism in BCa.

Cerebral cortical regions always connect with each other via the shortest paths.

In human society, the choice of transportation mode between two cities is largely influenced by the distance between the regions. Similarly, when neurons communicate with each other within the cerebral cortex, do they establish their connections based on their physical distance? In this study, we employed a data-driven approach to explore the relationships between fiber length and corresponding geodesic distance between the fiber's two endpoints on brain surface. Diffusion-MRI-derived fiber streamlines were used to represent extra-cortical axonal connections between neurons or cortical regions, while geodesic paths between cortical points were employed to simulate intra-cortical connections. The results demonstrated that the geodesic distance between two cortical regions connected by a fiber streamline was greater than the fiber length most of the time, indicating that cortical regions tend to choose the shortest path for connection; whether it be an intra-cortical or extra-cortical route, especially when intra-cortical routes within cortical regions are longer than potential extrinsic fiber routes, there is an increased probability to establish fiber routes to connect the both regions. These findings were validated in a group of human brains and may provide insights into the underlying mechanisms of neuronal growth, connection, and wiring.

Efficient and Stable ß-CsPbI3 Solar Cells through Solvent Engineering with Methylamine Acetate Ionic Liquid.

CsPbI3, an all-inorganic perovskite material with suitable band gap and excellent thermal stability, has garnered significant attention for its potential in perovskite solar cells (PSCs). However, CsPbI3 is susceptible to phase changes from photoactive to photoinactive in humid environments. Hence, it is crucial to achieve controllable growth of CsPbI3 perovskite thin films with the desired ß-crystal phase and compact morphology for efficient and stable PSCs. Herein, MAAc was used as a solvent for the CsPbI3 precursor to fabricate ß-CsPbI3 perovskite. An intermediate compound of CsxMA1-xPbIxAc3-x was initially formed in the MAAc solution, and during annealing, the MA+ and Ac- ions were replaced by Cs+ and I- ions, respectively. Furthermore, the incorporation of strong C═O···Pb coordination stabilized the black-phase ß-CsPbI3 and facilitated the growth of crystals with a narrow vertical orientation and large grain size. As a result, the PSCs with an efficiency of 18.9% and improved stability (less than 10% decay after 2000 h of storage in N2 and less than 30% decay after 500 h of storage in humid air without any encapsulation) were achieved.

Novel Bilayer SnO2 Electron Transport Layers with Atomic Layer Deposition for High-Performance α-FAPbI3 Perovskite Solar Cells.

Perovskite solar cells (PSCs) based on the SnO2 electron transport layer (ETL) have achieved remarkable photovoltaic efficiency. However, the commercial SnO2 ETLs show various shortcomings. The SnO2 precursor is prone to agglomeration, resulting in poor morphology with numerous interface defects. Additionally, the open circuit voltage (Voc ) would be constrained by the energy level mismatch between the SnO2 and the perovskite. And, few studies designed SnO2 -based ETLs to promote crystal growth of PbI2 , a crucial prerequisite for obtaining high-quality perovskite films via the two-step method. Herein, we proposed a novel bilayer SnO2 structure that combined the atomic layer deposition (ALD) and sol-gel solution to well address the aforementioned issues. Due to the unique conformal effect of ALD-SnO2 , it can effectively modulate the roughness of FTO substrate, enhance the quality of ETL, and induce the growth of PbI2 crystal phase to develop the crystallinity of perovskite layer. Furthermore, a created built-in field of the bilayer SnO2 can help to overcome the electron accumulation at the ETL/perovskite interface, leading to a higher Voc and fill factor. Consequently, the efficiency of PSCs with ionic liquid solvent increases from 22.09% to 23.86%, maintaining 85% initial efficiency in a 20% humidity N2 environment for 1300 h.

Structural optimisation for controlled deflections of additively manufactured single material beams.

Closely controlling the mechanical behaviour and characterization of the deflection of a beam structure is a well-known and widely studied engineering problem. The progress in additive manufacturing methods and the possibilities to closely control the material property variations with the controlled placement of materials further widen the opportunities to achieve given beam deflection criteria. The multi-material additive manufacturing solutions suffer from the lack of real engineering material options, and the quality and performance of the printed parts are usually unsuitable for producing functional parts. A novel cellular structured solution is proposed here, which utilises optimisation of geometries of individual cells of a single material structured beam to obtain deflection profiles closely matched with preset conditions under different loading conditions. The cellular geometry of the structured beam is continually altered for searching and converging on the optimal structure of the cells by the covariance matrix adaptation evolution strategy algorithm in an iterative manner. The optimised beam structures could also be physically produced with single material additive manufacturing methods and the experimental and numerical beam deflection responses correlated closely.

Accurate corresponding fiber tract segmentation via FiberGeoMap learner with application to autism.

Fiber tract segmentation is a prerequisite for tract-based statistical analysis. Brain fiber streamlines obtained by diffusion magnetic resonance imaging and tractography technology are usually difficult to be leveraged directly, thus need to be segmented into fiber tracts. Previous research mainly consists of two steps: defining and computing the similarity features of fiber streamlines, then adopting machine learning algorithms for fiber clustering or classification. Defining the similarity feature is the basic premise and determines its potential reliability and application. In this study, we adopt geometric features for fiber tract segmentation and develop a novel descriptor (FiberGeoMap) for the corresponding representation, which can effectively depict fiber streamlines' shapes and positions. FiberGeoMap can differentiate fiber tracts within the same subject, meanwhile preserving the shape and position consistency across subjects, thus can identify common fiber tracts across brains. We also proposed a Transformer-based encoder network called FiberGeoMap Learner, to perform segmentation based on the geometric features. Experimental results showed that the proposed method can differentiate the 103 various fiber tracts, which outperformed the existing methods in both the number of categories and segmentation accuracy. Furthermore, the proposed method identified some fiber tracts that were statistically different on fractional anisotropy (FA), mean diffusion (MD), and fiber number ration in autism.

Surgical Resection of Large Primary Intraosseous Meningiomas (6 Case Reports).

OBJECTIVE: The clinical features and surgical techniques related to patients undergoing resection of extracranial large primary intraosseous meningiomas are studied. METHODS: The clinical characteristics, treatment, and prognosis of 6 patients with primary intraosseous meningiomas larger than 5 cm in diameter were retrospectively reviewed in the 10th Neurosurgical Department of Beijing Tiantan Hospital, Capital Medical University. RESULTS: Five males and one female (18-57 years old) suffered from large primary intraosseous meningiomas. The main symptoms were headaches accompanied by head swelling. CT showed irregular thickening of the bone diploe with increased density and uneven surface. MRI showed partial bone destruction of the skull, local thickening of the internal and external plates, shell and palisade changes of the external cranial plate, and enhancement of the adjacent meninges. A horseshoe or coronary incision plus the "Mercedes-Benz" incision were chosen to expose the skull bone, and drilling was performed in the normal skull bone at the transition zone between abnormal and normal skull bone. After drilling, the sub flap dura was dissected, the hyperplastic skull was dissected with a milling cutter, and the residual tumor was then resected. A cranioplasty was performed 6 months to 1 year later. CONCLUSIONS: Surgical treatment and precise perioperative management can achieve a better prognosis for large intraosseous meningiomas.