Impact of premorbid hypertension and renin-angiotensin-aldosterone system inhibitors on the severity of aneurysmal subarachnoid haemorrhage: a multicentre study.

BACKGROUND: Hypertension is widely acknowledged as a significant contributory factor to the heightened risk of intracranial aneurysm rupture. Nevertheless, the impact of hypertension management on the outcomes subsequent to aneurysmal subarachnoid haemorrhage (aSAH), particularly concerning the severity of aSAH, remains an underexplored area. METHODS: We conducted a retrospective analysis using data from a prospectively multicentre cohort of 4545 patients with aSAH in China. Premorbid hypertension status and the utilisation of antihypertensive medications prior to admission were set as key exposure factors. The primary outcomes encompassed unfavourable clinical grading scales observed on admission. Employing multivariable logistic regression, we explored the association between premorbid hypertension status, preadmission use of renin-angiotensin-aldosterone system (RAAS) inhibitors and unfavourable clinical grading scales. RESULTS: In comparison to patients with normal blood pressure, only uncontrolled hypertension demonstrated a significant and independent association with an elevated risk of poor outcomes on the Hunt-Hess scale (OR=1.799, 95% CI 1.413 to 2.291, p<0.001) and the World Federation of Neurological Surgeons (WFNS) scale (OR=1.721, 95% CI 1.425 to 2.079, p<0.001). Furthermore, the antecedent use of RAAS inhibitors before admission was markedly and independently linked to a diminished risk of adverse outcomes on the Hunt-Hess scale (OR=0.653, 95% CI 0.430 to 0.992, p=0.046) and the WFNS scale (OR=0.656, 95% CI 0.469 to 0.918, p=0.014). CONCLUSIONS: Uncontrolled hypertension markedly elevates the risk of adverse clinical outcomes following an aSAH. Conversely, the preadmission utilisation of RAAS inhibitors demonstrates a noteworthy association with a favourable clinical outcome after aSAH.

Hematoma Enlargement After Intracerebral Hemorrhage: A Bibliometric Analysis.

OBJECTIVE: To conduct a quantitative analysis of published studies on hematoma enlargement after intracerebral hemorrhage. METHODS: Studies on hematoma enlargement after cerebral hemorrhage were retrieved from the Web of Science database on June 30, 2023. Microsoft Excel, VOSviewer, and CiteSpace software were used for bibliometric analysis and visualization, focusing on the quantitative characteristics of the literature. RESULTS: A total of 444 articles were published in 161 journals, with 2161 authors from 41 countries and 717 institutions. The most published authors, countries, and institutions were Goldstein, the USA, and Massachusetts General Hospital. Stroke published the most studies, but the average citation number per year of Lancet Neurology far exceeded that of other journals. The research field of hematoma enlargement is mainly divided into 3 focuses, including mechanisms, identification (computed tomography signs, predictive models), and treatment (hemostasis, antihypertensive therapy). Most bursts in publication number have been since 2010, where the highest burst was from research on spot signs, and the latest burst focused on tranexamic acid. Treatment using tranexamic acid based on different computed tomography signs is a focus of current research, but the effectiveness still requires further exploration. CONCLUSIONS: This bibliometric analysis analyzed the research framework and hotspots on hematoma enlargement after cerebral hemorrhage, which can help researchers better understand this field and provide potential suggestions for collaborations and research.

Proteomic and metabolomic analyses illustrate the mechanisms of expression of the O6 -methylguanine-DNA methyltransferase gene in glioblastoma.

AIM: Glioblastoma (GBM) has been reported to be the most common high-grade primary malignant brain tumor in clinical practice and has a poor prognosis. O6 -methylguanine-DNA methyltransferase (MGMT) promoter methylation has been related to prolonged overall survival (OS) in GBM patients after temozolomide treatment. METHODS: Proteomics and metabolomics were combined to explore the dysregulated metabolites and possible protein expression alterations in white matter (control group), MGMT promoter unmethylated GBM (GBM group) or MGMT promoter methylation positive GBM (MGMT group). RESULTS: In total, 2745 upregulated and 969 downregulated proteins were identified in the GBM group compared to the control group, and 131 upregulated and 299 downregulated proteins were identified in the MGMT group compared to the GBM group. Furthermore, 131 upregulated and 299 downregulated metabolites were identified in the GBM group compared to the control group, and 187 upregulated and 147 downregulated metabolites were identified in the MGMT group compared to the GBM group. The results showed that 94 upregulated and 19 downregulated proteins and 20 upregulated and 16 downregulated metabolites in the MGMT group were associated with DNA repair. KEGG pathway enrichment analysis illustrated that the dysregulated proteins and metabolites were involved in multiple metabolic pathways, including the synthesis and degradation of ketone bodies, amino sugar and nucleotide sugar metabolism. Moreover, integrated metabolomics and proteomics analysis was performed, and six key proteins were identified in the MGMT group and GBM group. Three key pathways were recognized as potential biomarkers for recognizing MGMT promoter unmethylated GBM and MGMT promoter methylation positive GBM from GBM patient samples, with areas under the curve of 0.7895, 0.7326 and 0.7026, respectively. CONCLUSION: This study provides novel mechanisms to understand methylation in GBM and identifies some biomarkers for the prognosis of two different GBM types, MGMT promoter unmethylated or methylated GBM, by using metabolomics and proteomics analyses.

The causal relationship between genetically determined telomere length and meningiomas risk.

Background: Studies have shown that longer leukocyte telomere length (LTL) is significantly associated with increased risk of meningioma. However, there is limited evidence concerning the causal association of LTL with benign and malignant meningiomas or with the location of benign tumors. Methods: We used three LTL datasets from different sources, designated by name and sample size as LTL-78592, LTL-9190, and LTL-472174. The linkage disequilibrium score (LDSC) was used to explore the association between LTL and meningioma. We utilized two-sample bidirectional Mendelian randomization (TSMR) to evaluate whether LTL is causally related to meningioma risk. We adjusted for confounders by conducting multivariable Mendelian randomization (MVMR). Results: In the LTL-78592, longer LTL was significantly associated with increased risk of malignant [odds ratio (OR) = 5.14, p = 1.04 × 10-5], benign (OR = 4.81, p < 0.05), benign cerebral (OR = 5.36, p < 0.05), and benign unspecified meningioma (OR = 8.26, p < 0.05). The same results were obtained for the LTL-9190. In the LTL-472174, longer LTL was significantly associated with increased risk of malignant (OR = 4.94, p < 0.05), benign (OR = 3.14, p < 0.05), and benign cerebral meningioma (OR = 3.59, p < 0.05). Similar results were obtained in the MVMR. In contrast, only benign cerebral meningioma displayed a possible association with longer LTL (OR = 1.01, p < 0.05). No heterogeneity or horizontal pleiotropy was detected. Conclusion: In brief, genetically predicted longer LTL may increase the risk of benign, malignant, and benign cerebral meningiomas, regardless of the LTL measure, in European populations.

The CDK inhibitor AT7519 inhibits human glioblastoma cell growth by inducing apoptosis, pyroptosis and cell cycle arrest.

Glioblastoma multiforme (GBM) is the most lethal primary brain tumor with a poor median survival of less than 15 months. However, clinical strategies and effective therapies are limited. Here, we found that the second-generation small molecule multi-CDK inhibitor AT7519 is a potential drug for GBM treatment according to high-throughput screening via the Approved Drug Library and Clinical Compound Library (2718 compounds). We found that AT7519 significantly inhibited the cell viability and proliferation of U87MG, U251, and patient-derived primary GBM cells in a dose-dependent manner. Furthermore, AT7519 also inhibited the phosphorylation of CDK1/2 and arrested the cell cycle at the G1-S and G2-M phases. More importantly, AT7519 induced intrinsic apoptosis and pyroptosis via caspase-3-mediated cleavage of gasdermin E (GSDME). In the glioblastoma intracranial and subcutaneous xenograft assays, tumor volume was significantly reduced after treatment with AT7519. In summary, AT7519 induces cell death through multiple pathways and inhibits glioblastoma growth, indicating that AT7519 is a potential chemical available for GBM treatment.

Microglial Piezo1 senses Aß fibril stiffness to restrict Alzheimer's disease.

The pathology of Alzheimer's disease (AD) is featured with extracellular amyloid-ß (Aß) plaques, whose impact on the mechanical properties of the surrounding brain tissues is unclear. Microglia sense and integrate biochemical cues of the microenvironment. However, whether the microglial mechanosensing pathways influence AD pathogenesis is unknown. Here, we surveyed the elevated stiffness of Aß-plaque-associated tissues and observed the selective upregulation of the mechanosensitive ion channel Piezo1 in Aß-plaque-associated microglia. Piezo1 sensed the stiffness stimuli of Aß fibrils and subsequently induced Ca2+ influx for microglial clustering, phagocytosis, and compacting of Aß plaques. Microglia lacking Piezo1 led to the exacerbation of Aß pathology and cognitive decline, whereas pharmacological activation of microglial Piezo1 ameliorated brain Aß burden and cognitive impairment in 5 × FAD mice. Together, our results reveal that Piezo1, a mechanosensor of Aß fibril stiffness in microglia, represents a potential therapeutic target for AD.

Potential Role of Host Microbiome in Areca Nut-Associated Carcinogenesis and Addiction.

Areca nut (AN) is widely consumed all over the world, bringing great harm to human health and economy. Individuals with AN chewing are at high risk of cardiovascular disease and impaired immune system and metabolic system. Despite a growing number of studies having reported on the adverse effects brought by AN chewing, the exact mechanism of it is limited and the need for additional exploration remains. In recent years, the interaction between microorganisms, especially intestinal microorganism and host, has been extensively studied. AN chewing might disrupt the oral and intestinal microbiota communities through direct connect with the microbes it contains, altering PH, oxygen of oral and intestinal microenvironment, and disturbing the immune homeostasis. These mechanisms provide insights into the interplay between areca nut and host microbiota. Emerging studies have proposed that bidirectional interaction between polyphenols and intestinal microbes might play a potential role in the divergence of polyphenol, extracted from AN, among individuals with or without AN-induced cancer development and progression. Although some AN chewers have been aware of the harmful effects brought by AN, they cannot abolish this habit because of the addiction of AN. Increasing studies have tried to revealed that gut microbiota might influence the onset/development of addictive behaviors. Altogether, this review summarizes the possible reasons for the disturbance of host microbiota caused by areca nut chewing and clarifies the complex interaction between human microbiome and major constituents and the addiction and carcinogenicity of AN, tempting to provide novel insights into the development and utilization of it, and to control the adverse consequences caused by AN chewing.

Effect of Renin-Angiotensin-Aldosterone System Inhibitors on the Rupture Risk Among Hypertensive Patients With Intracranial Aneurysms.

BACKGROUND: Mounting experimental evidence supports the concept that the RAAS (renin-angiotensin-aldosterone system) is involved in the pathogenesis of intracranial aneurysm rupture. However, whether RAAS inhibitors could reduce the rupture risk of intracranial aneurysms remains unclear. METHODS: We performed a chart review of a multicenter, prospectively maintained database of 3044 hypertensive patients with intracranial aneurysms from 20 medical centers in China. The patients were separated into ruptured and unruptured groups. Univariable and multivariable logistical regression analyses were performed to determine the association between the use of RAAS inhibitors and the rupture risk. Sensitivity analyses and subgroup analyses were performed to verify the robustness of the results. RESULTS: In multivariable analyses, female sex, passive smoking, uncontrolled, or unmonitored hypertension, use of over 2 antihypertensive medications, RAAS inhibitors use, antihyperglycemic agents use, hyperlipidemia, ischemic stroke, and aneurysmal location were independently associated with the rupture risk. The use of RAAS inhibitors was significantly associated with a reduced rupture risk compared with the use of non-RAAS inhibitors (odds ratio, 0.490 [95% CI, 0.402-0.597]; P=0.000). Compared with the use of non-RAAS inhibitors, the use of ACE (angiotensin-converting enzyme) inhibitors (odds ratio, 0.559 [95% CI, 0.442-0.709]; P=0.000) and use of ARBs (angiotensin receptor blockers; odds ratio, 0.414 [95% CI, 0.315-0.542]; P=0.000) were both significantly associated with a reduced rupture risk. The negative association of the rupture risk with RAAS inhibitors was consistent across 3 analyzed data and the predefined subgroups (including controlled hypertension). CONCLUSIONS: The use of RAAS inhibitors was significantly associated with a decreased rupture risk independent of blood pressure control among hypertensive patients with intracranial aneurysms.

Identification of ubiquitin-specific protease 32 as an oncogene in glioblastoma and the underlying mechanisms.

Glioblastoma (GBM) patients present poor prognosis. Deubiquitination by deubiquitinating enzymes (DUBs) is a critical process in cancer progression. Ubiquitin-specific proteases (USPs) constitute the largest sub-family of DUBs. Evaluate the role of USP32 in GBM progression and provide a potential target for GBM treatment. Clinical significance of USP32 was investigated using Gene Expression Omnibus databases. Effects of USP32 on cell growth and metastasis were studied in vitro and in vivo. Differentially expressive genes between USP32-knockdown U-87 MG cells and negative control cells were detected using RNA sequencing and used for Gene Ontology and Kyoto Encyclopedia of Genes and Genomic pathway enrichment analyses. Finally, RT-qPCR was used to validate the divergent expression of genes involved in the enriched pathways. USP32 was upregulated in GBM patients, being correlated to poor prognosis. USP32 downregulation inhibited cell growth and metastasis in vitro. Furthermore, USP32 knockdown inhibited tumorigenesis in vivo. In addition, UPS32 was identified as a crucial regulator in different pathways including cell cycle, cellular senescence, DNA replication, base excision repair, and mismatch repair pathways. USP32 acts as an oncogene in GBM through regulating several biological processes/pathways. It could be a potential target for GBM treatment.

Association Between Regular Blood Pressure Monitoring and the Risk of Intracranial Aneurysm Rupture: a Multicenter Retrospective Study with Propensity Score Matching.

Although hypertension is a known risk factor for intracranial aneurysm rupture, the benefit of the management of blood pressure in reducing the rupture risk of intracranial aneurysms remains largely unknown, especially for regular blood pressure monitoring. We conducted a retrospective analysis of a prospectively maintained database of 3965 patients with saccular intracranial aneurysms from 20 medical centers in China. The patients were divided into the non-hypertensive group and hypertensive group. Propensity score matching was applied to identify a cohort of patients with similar baseline characteristics. Univariable and multivariable logistic regression analyses were performed to determine the association between intracranial aneurysm rupture and the management of blood pressure. After matching, hypertension was significantly associated with an increased rupture risk of intracranial aneurysms (OR = 2.559, 95%CI = 2.161-3.030, P = 0.000). For the management of blood pressure, controlled hypertension (OR = 1.803, 95%CI = 1.409-2.307, P = 0.000), uncontrolled hypertension (OR = 2.178, 95%CI = 1.756-2.700, P = 0.000), and hypertension without regular blood pressure monitoring (OR = 5.000, 95%CI = 3.823-6.540, P = 0.000) were all significantly associated with a higher rupture risk compared with the absence of hypertension. Moreover, hypertension without regular blood pressure monitoring was associated with a higher rupture risk compared with either controlled hypertension (OR = 3.807, 95%CI = 2.687-5.395, P = 0.000) or hypertension with regular blood pressure monitoring (including controlled and uncontrolled hypertension) (OR = 2.893, 95%CI = 2.319-3.609, P = 0.000). The absence of regular blood pressure monitoring was significantly associated with an increased risk of intracranial aneurysm rupture, emphasizing the importance of implementation of regular blood pressure monitoring in hypertensive patients with intracranial aneurysms.

Awake craniotomy for removal of gliomas in eloquent areas: An analysis of 21 cases.

OBJECTIVE: To discuss the techniques and methods in respective operation of brain gliomas located in eloquent brain region under awake anesthesia state METHODS: 21 patients admitted into Department of Neurosurgery of the First Affiliated Hospital of Xiamen University were chosen as subject. Diagnosed with brain gliomas, they received operation with neuronavigation, intraoperative ultrasonography for locating the lesion and intraoperative direct electric stimulation for functional mapping of the eloquent brain region after receiving awake anesthesia. All patients were followed up from post-surgical 3 months to 18 months. RESULTS: Applied with MRI scanning during post-surgical 60-90d, resection results shows that 5 cases (23.8%) received total resection of lesions, 10 cases (47.6%) received subtotal resection while 6 cases (28.6%) received partial resection. Post-surgical performance shows 8 cases (38.1%) of transitory postoperative aphasia, 5 cases(23.8%) of transitory postoperative dyskinesia and 1 case(4.8%) of permanent dyskinesia. Recovery was achieved in the patients except for the 1 case of permanent dyskinesia. CONCLUSIONS: Comprehensive application of awake anesthesia, neuronavigation, intraoperative ultrasonography and intraoperative direct electrical stimulation facilitates recognition of clear position relationship between gliomas and eloquent brain region, and maximum safe resection of gliomas in eloquent brain region with maximal protection of brain function.

Complete Freund's adjuvant-induced protein dysregulation correlated with mirror image pain as assessed by quantitative proteomics of the mouse spinal cord.

Inflammation or trauma occurring on one side of the body can cause pathological pain on the contralateral noninjured side in a phenomenon called mirror-image pain (MIP). Although some potential mechanisms involved in MIP have been reported, including those involving the immune system and glial cells as well as neural mechanisms, the molecular mechanisms are not well understood. In this study, we aimed to understand the molecular mechanisms in MIP using quantitative proteomics and whole-cell patch clamp recordings. Behavioral test results showed that complete Freund's adjuvant could induce MIP in the mice. The results of isobaric tags for relative and absolute quantification (iTRAQ) quantitative proteomics showed that 108 proteins were dysregulated, and these proteins may represent potential targets. Furthermore, bioinformatics analysis was applied to explore the potential molecular mechanisms during MIP after complete Freund's adjuvant (CFA) treatment. Parallel reaction monitoring (PRM) results showed that PKCδ and seven other dysregulated proteins were related to MIP after CFA treatment. Patch clamp recording results showed that CFA treatment could increase intrinsic excitability and spontaneous firing in spinal cord neurons during MIP. In summary, we found that CFA could induce MIP. The results of proteomic research on the spinal cord after CFA treatment could provide new insight into the molecular mechanisms of MIP. Moreover, the neuronal activity of spinal cord neurons was upregulated during MIP after CFA treatment. In summary, the results of the spinal cord proteomic profile provide a potential molecular mechanism for understanding MIP.

Electroencephalogram-Based Motor Imagery Classification Using Deep Residual Convolutional Networks.

The classification of electroencephalogram (EEG) signals is of significant importance in brain-computer interface (BCI) systems. Aiming to achieve intelligent classification of motor imagery EEG types with high accuracy, a classification methodology using the wavelet packet decomposition (WPD) and the proposed deep residual convolutional networks (DRes-CNN) is proposed. Firstly, EEG waveforms are segmented into sub-signals. Then the EEG signal features are obtained through the WPD algorithm, and some selected wavelet coefficients are retained and reconstructed into EEG signals in their respective frequency bands. Subsequently, the reconstructed EEG signals were utilized as input of the proposed deep residual convolutional networks to classify EEG signals. Finally, EEG types of motor imagination are classified by the DRes-CNN classifier intelligently. The datasets from BCI Competition were used to test the performance of the proposed deep learning classifier. Classification experiments show that the average recognition accuracy of this method reaches 98.76%. The proposed method can be further applied to the BCI system of motor imagination control.

Deep Convolutional Neural Network With a Multi-Scale Attention Feature Fusion Module for Segmentation of Multimodal Brain Tumor.

As a non-invasive, low-cost medical imaging technology, magnetic resonance imaging (MRI) has become an important tool for brain tumor diagnosis. Many scholars have carried out some related researches on MRI brain tumor segmentation based on deep convolutional neural networks, and have achieved good performance. However, due to the large spatial and structural variability of brain tumors and low image contrast, the segmentation of MRI brain tumors is challenging. Deep convolutional neural networks often lead to the loss of low-level details as the network structure deepens, and they cannot effectively utilize the multi-scale feature information. Therefore, a deep convolutional neural network with a multi-scale attention feature fusion module (MAFF-ResUNet) is proposed to address them. The MAFF-ResUNet consists of a U-Net with residual connections and a MAFF module. The combination of residual connections and skip connections fully retain low-level detailed information and improve the global feature extraction capability of the encoding block. Besides, the MAFF module selectively extracts useful information from the multi-scale hybrid feature map based on the attention mechanism to optimize the features of each layer and makes full use of the complementary feature information of different scales. The experimental results on the BraTs 2019 MRI dataset show that the MAFF-ResUNet can learn the edge structure of brain tumors better and achieve high accuracy.

Downregulation of phosphoglycerate mutase 5 improves microglial inflammasome activation after traumatic brain injury.

Traumatic brain injury (TBI) is considered as the most common cause of disability and death, and therefore an effective intervention of cascade pathology of secondary brain injury promptly can be a potential therapeutic direction for TBI prognosis. Further study of the physiological mechanism of TBI is urgent and important. Phosphoglycerate mutase 5 (Pgam5), a mitochondrial protein, mediate mitochondrial homeostasis, cellular senescence, and necroptosis. This study evaluated the effects of Pgam5 on neurological deficits and neuroinflammation of controlled cortical impact-induced TBI mouse model in vivo and LPS + ATP-induced microglia model in vitro. Pgam5 was overexpressed post-TBI. Pgam5 depletion reduced pyroptosis-related molecules and improved microglia activation, neuron damage, tissue lesion, and neurological dysfunctions in TBI mice. RNA-seq analysis and molecular biology experiments demonstrated that Pgam5 might regulate inflammatory responses by affecting the post-translational modification and protein expression of related genes, including Nlrp3, caspase1, Gsdmd, and Il-1ß. In microglia, Pgam5-sh abrogated LPS + ATP-induced Il-1ß secretion through Asc oligomerization-mediated caspase-1 activation, which was independent of Rip3. The data demonstrate the critical role Pgam5 plays in nerve injury in the progression of TBI, which regulates Asc polymerization and subsequently caspase1 activation, and thus reveals a fundamental mechanism linking microglial inflammasome activation to Asc/caspase1-generated Il-1ß-mediated neuroinflammation. Thus, our data indicate Pgam5 worsens physiological and neurological outcomes post-TBI, which may be a potential therapeutic target to improve neuroinflammation after TBI.

Association Between Body Mass Index and Intracranial Aneurysm Rupture: A Multicenter Retrospective Study.

Background and Aims: It has recently emerged the concept of "obesity paradox," a term used to describe an inverse association between obesity and clinical outcomes in cardiovascular diseases and stroke. The purpose of this study was to investigate the association between body mass index (BMI) and the risk of intracranial aneurysm rupture. Methods: In this study, we conducted a retrospective analysis of a prospectively maintained database of patients with intracranial aneurysms from 21 medical centers in China. A total of 3,965 patients with 4,632 saccular intracranial aneurysms were enrolled. Patients were separated into unruptured (n = 1,977) and ruptured groups (n = 1,988). Univariable and multivariable logistic regression analyses were performed to determine the association between BMI and intracranial aneurysm rupture. Results: Compared to the patients with normal BMI (18.5 to < 24.0 kg/m2), the odds of intracranial aneurysm rupture were significantly lower in patients with BMI 24.0 to < 28.0 kg/m2 (OR = 0.745, 95% CI = 0.638-0.868, P = 0.000) and patients with BMI ≥ 28.0 kg/m2 (OR = 0.628, 95% CI = 0.443-0.890, P = 0.009). Low BMI (<18.0 kg/m2) was not associated with intracranial aneurysm rupture (OR = 0.894, 95% CI = 0.483-1.657, P = 0.505). For males, both the BMI 24.0 to < 28.0 kg/m2 (OR = 0.606, 95% CI = 0.469-0.784, P = 0.000) and the BMI ≥ 28.0 kg/m2 (OR = 0.384, 95% CI = 0.224-0.658, P = 0.001) were associated with a lower rupture risk, whereas the inverse association was not observed in females. Both the BMI 24.0 to < 28.0 kg/m2 (OR = 0.722 for aged 50-60y, 95% CI = 0.554-0.938, P = 0.015; OR = 0.737 for aged >60y, 95% CI = 0.586-0.928, P = 0.009) and the BMI ≥ 28.0 kg/m2 (OR = 0.517 for aged 50-60y, 95% CI = 0.281-0.950, P = 0.0034; OR = 0.535 for aged >60y, 95% CI = 0.318-0.899, P = 0.0018) was associated with a lower rupture risk in patients aged ≥50 years, whereas the association was not significant in patients aged <50 years. Conclusions: Increased BMI is significantly and inversely associated with saccular intracranial aneurysm rupture in males and patients aged ≥50 years.

Increased risk of cerebrovascular mortality in head and neck cancer survivors aged ≥ 65 years treated with definitive radiotherapy: a population-based cohort study.

BACKGROUND: To investigate the relationship between radiotherapy (RT) and the risk of cerebrovascular mortality (CVM) in head and neck cancer (HNC) survivors aged ≥ 65 years. METHODS: Patients with HNC survivors aged ≥ 65 years diagnosed between 2000 and 2012 were included from the Surveillance, Epidemiology, and End Results database. Kaplan-Meier analysis, Log-rank tests, and Cox proportional-hazards regression models were performed for statistical analyses. RESULTS: We included 16,923 patients in this study. Of these patients, 7110 (42.0%) patients received surgery alone, 5041 (29.8%) patients underwent RT alone, and 4772 (28.2%) patients were treated with surgery and RT. With a median follow-up time of 87 months, 1005 patients died with cerebrovascular disease. The 10-years CVM were 13.3%, 10.8%, and 11.2% in those treated with RT alone, surgery alone, and surgery plus RT, respectively (P < 0.001). The mean time for CVM was shorter in RT alone compared to surgery alone and surgery plus RT (52 months vs. 56-60 months). After adjusting for covariates, patients receiving RT alone had a significantly higher risk of developing CVM compared to those receiving surgery alone (hazard ratio [HR] 1.703, 95% confidence interval [CI] 1.398-2.075, P < 0.001), while a comparable risk of CVM was found between those treated with surgery alone and surgery plus RT (HR 1.106, 95% CI 0.923-1.325, P = 0.274). Similar trends were found after stratification age at diagnosis, gender, tumor location, and marital status. CONCLUSIONS: Definitive RT but not postoperative RT can increase the risk of CVM among older HNC survivors. Long-term follow-up and regular screening for CVD are required for HNC patients who received definitive RT to decrease the risk of CVM.

Multi-Source and Multi-Representation Adaptation for Cross-Domain Electroencephalography Emotion Recognition.

Due to the non-invasiveness and high precision of electroencephalography (EEG), the combination of EEG and artificial intelligence (AI) is often used for emotion recognition. However, the internal differences in EEG data have become an obstacle to classification accuracy. To solve this problem, considering labeled data from similar nature but different domains, domain adaptation usually provides an attractive option. Most of the existing researches aggregate the EEG data from different subjects and sessions as a source domain, which ignores the assumption that the source has a certain marginal distribution. Moreover, existing methods often only align the representation distributions extracted from a single structure, and may only contain partial information. Therefore, we propose the multi-source and multi-representation adaptation (MSMRA) for cross-domain EEG emotion recognition, which divides the EEG data from different subjects and sessions into multiple domains and aligns the distribution of multiple representations extracted from a hybrid structure. Two datasets, i.e., SEED and SEED IV, are used to validate the proposed method in cross-session and cross-subject transfer scenarios, experimental results demonstrate the superior performance of our model to state-of-the-art models in most settings.

Programmable patterns in a DNA-based reaction-diffusion system.

Biology offers compelling proof that macroscopic "living materials" can emerge from reactions between diffusing biomolecules. Here, we show that molecular self-organization could be a similarly powerful approach for engineering functional synthetic materials. We introduce a programmable DNA embedded hydrogel that produces tunable patterns at the centimeter length scale. We generate these patterns by implementing chemical reaction networks through synthetic DNA complexes, embedding the complexes in the hydrogel, and triggering with locally applied input DNA strands. We first demonstrate ring pattern formation around a circular input cavity and show that the ring width and intensity can be predictably tuned. Then, we create patterns of increasing complexity, including concentric rings and non-isotropic patterns. Finally, we show "destructive" and "constructive" interference patterns, by combining several ring-forming modules in the gel and triggering them from multiple sources. We further show that computer simulations based on the reaction-diffusion model can predict and inform the programming of target patterns.

[Intestinal dysfunction of spinal cord injury treated with tongdu tiaoshen moxibustion: a randomized controlled trial].

OBJECTIVE: To compare the clinical effect on intestinal dysfunction of spinal cord injury (SCI) between the comprehensive therapy of tongdu tiaoshen moxibustion (moxibustion for opening the governor vessel and regulating the spirit) and rehabilitation training and the simple treatment with rehabilitation training. METHODS: A total of 60 patients with intestinal dysfunction of SCI were randomized into a comprehensive therapy group and a rehabilitation group, 30 cases in each one (3 cases were dropped out in each group). On the base of the routine western medicine treatment and rehabilitation training, the bowel training and rectal function training were provided, once a day in the rehabilitation group. In the comprehensive therapy group, on the base of the treatment as the rehabilitation group, the tongdu tiaoshen moxibustion was exerted at Yaoyangguan (GV 3), Mingmen (GV 4), Zhiyang (GV 9), Dazhui (GV 14) and Baihui (GV 20), etc, once a day, 30 min each time. In both groups, the treatment for 4 weeks was as one course and 3 courses of treatment were required. Separately, before treatment, after 4, 8 and 12 weeks of treatment, the scores of neurogenic bowel dysfunction (NBD) and World Health Organization quality of life scale (WHOQOL-BREF) were observed and the clinical effect was evaluated after 12 weeks of treatment. RESULTS: After treatment, the total effective rate was 88.9% (24/27) in the comprehensive therapy group, which was higher than 74.1% (20/27) in the rehabilitation group (P<0.05). After 4, 8 and 12 weeks of treatment, NBD scores were all reduced obviously as compared with those before treatment in the two groups (all P<0.01). After 8 and 12 weeks of treatment, NBD scores in the comprehensive therapy group were lower than the rehabilitation group (both P<0.05). After 4, 8 and 12 weeks of treatment, the scores of all of the domains (psychology, physiology, social relations and environment) in WHOQOL-BREF were higher than those before treatment in the two groups (all P<0.01). After 4 weeks of treatment, the scores in the psychology and physiology domains in the comprehensive therapy group were higher than the rehabilitation group (all P<0.05). After 8 and 12 weeks of treatment, the scores of all of the domains in the comprehensive therapy group were higher than the rehabilitation group (all P<0.05). CONCLUSION: The comprehensive treatment of tongdu tiaoshen moxibustion and rehabilitation training achieves the better effect on intestinal dysfunction of SCI than the simple rehabilitation training and greatly improves the quality of life in SCI patients.