Information Network Modeling and Mining

We are living in an Internet world with huge amounts of information. For example, online Question-and-Answer (Q&A) websites include different kinds of informational objects, i.e., questions, answers and users. Web search logs contain queries and clicked webpages. These online infrastructures usually represent information in various forms. An urgent challenge is to discover meaningful knowledge from massive information that can empower online platforms from different perspectives. Motivated by this trend, my research addresses the modeling and mining tasks for several online platforms, including the Q&A websites, the search engines and the social media. Proposing information network based modeling and mining framework regarding to heterogeneous data sources is the major goal of my research. The frameworks, by extracting interconnected objects, modeling them into information networks, and designing network based learning algorithms, help improve the service offered by different online platforms. The methodology of the information network based modeling and mining is proved to be effective on a series of knowledge discovery topics, including the co-ranking problem in large-scale Q&A sites, the learning of entity types from massive search query logs, and the detection of emerging relationships from news and knowledge graphs. The future work is to explore the network base modeling and mining techniques on more online platforms and study how they can fit for new situations

Data_Sheet_1_Increased central auditory gain in 5xFAD Alzheimer’s disease mice as an early biomarker candidate for Alzheimer’s disease diagnosis.PDF

Alzheimer’s Disease (AD) is a neurodegenerative illness without a cure. All current therapies require an accurate diagnosis and staging of AD to ensure appropriate care. Central auditory processing disorders (CAPDs) and hearing loss have been associated with AD, and may precede the onset of Alzheimer’s dementia. Therefore, CAPD is a possible biomarker candidate for AD diagnosis. However, little is known about how CAPD and AD pathological changes are correlated. In the present study, we investigated auditory changes in AD using transgenic amyloidosis mouse models. AD mouse models were bred to a mouse strain commonly used for auditory experiments, to compensate for the recessive accelerated hearing loss on the parent background. Auditory brainstem response (ABR) recordings revealed significant hearing loss, a reduced ABR wave I amplitude, and increased central gain in 5xFAD mice. In comparison, these effects were milder or reversed in APP/PS1 mice. Longitudinal analyses revealed that in 5xFAD mice, central gain increase preceded ABR wave I amplitude reduction and hearing loss, suggesting that it may originate from lesions in the central nervous system rather than the peripheral loss. Pharmacologically facilitating cholinergic signaling with donepezil reversed the central gain in 5xFAD mice. After the central gain increased, aging 5xFAD mice developed deficits for hearing sound pips in the presence of noise, consistent with CAPD-like symptoms of AD patients. Histological analysis revealed that amyloid plaques were deposited in the auditory cortex of both mouse strains. However, in 5xFAD but not APP/PS1 mice, plaque was observed in the upper auditory brainstem, specifically the inferior colliculus (IC) and the medial geniculate body (MGB). This plaque distribution parallels histological findings from human subjects with AD and correlates in age with central gain increase. Overall, we conclude that auditory alterations in amyloidosis mouse models correlate with amyloid deposits in the auditory brainstem and may be reversed initially through enhanced cholinergic signaling. The alteration of ABR recording related to the increase in central gain prior to AD-related hearing disorders suggests that it could potentially be used as an early biomarker of AD diagnosis.</p

Image_1_Increased central auditory gain in 5xFAD Alzheimer’s disease mice as an early biomarker candidate for Alzheimer’s disease diagnosis.TIF

Alzheimer’s Disease (AD) is a neurodegenerative illness without a cure. All current therapies require an accurate diagnosis and staging of AD to ensure appropriate care. Central auditory processing disorders (CAPDs) and hearing loss have been associated with AD, and may precede the onset of Alzheimer’s dementia. Therefore, CAPD is a possible biomarker candidate for AD diagnosis. However, little is known about how CAPD and AD pathological changes are correlated. In the present study, we investigated auditory changes in AD using transgenic amyloidosis mouse models. AD mouse models were bred to a mouse strain commonly used for auditory experiments, to compensate for the recessive accelerated hearing loss on the parent background. Auditory brainstem response (ABR) recordings revealed significant hearing loss, a reduced ABR wave I amplitude, and increased central gain in 5xFAD mice. In comparison, these effects were milder or reversed in APP/PS1 mice. Longitudinal analyses revealed that in 5xFAD mice, central gain increase preceded ABR wave I amplitude reduction and hearing loss, suggesting that it may originate from lesions in the central nervous system rather than the peripheral loss. Pharmacologically facilitating cholinergic signaling with donepezil reversed the central gain in 5xFAD mice. After the central gain increased, aging 5xFAD mice developed deficits for hearing sound pips in the presence of noise, consistent with CAPD-like symptoms of AD patients. Histological analysis revealed that amyloid plaques were deposited in the auditory cortex of both mouse strains. However, in 5xFAD but not APP/PS1 mice, plaque was observed in the upper auditory brainstem, specifically the inferior colliculus (IC) and the medial geniculate body (MGB). This plaque distribution parallels histological findings from human subjects with AD and correlates in age with central gain increase. Overall, we conclude that auditory alterations in amyloidosis mouse models correlate with amyloid deposits in the auditory brainstem and may be reversed initially through enhanced cholinergic signaling. The alteration of ABR recording related to the increase in central gain prior to AD-related hearing disorders suggests that it could potentially be used as an early biomarker of AD diagnosis.</p

Data_Sheet_2_Increased central auditory gain in 5xFAD Alzheimer’s disease mice as an early biomarker candidate for Alzheimer’s disease diagnosis.PDF

Alzheimer’s Disease (AD) is a neurodegenerative illness without a cure. All current therapies require an accurate diagnosis and staging of AD to ensure appropriate care. Central auditory processing disorders (CAPDs) and hearing loss have been associated with AD, and may precede the onset of Alzheimer’s dementia. Therefore, CAPD is a possible biomarker candidate for AD diagnosis. However, little is known about how CAPD and AD pathological changes are correlated. In the present study, we investigated auditory changes in AD using transgenic amyloidosis mouse models. AD mouse models were bred to a mouse strain commonly used for auditory experiments, to compensate for the recessive accelerated hearing loss on the parent background. Auditory brainstem response (ABR) recordings revealed significant hearing loss, a reduced ABR wave I amplitude, and increased central gain in 5xFAD mice. In comparison, these effects were milder or reversed in APP/PS1 mice. Longitudinal analyses revealed that in 5xFAD mice, central gain increase preceded ABR wave I amplitude reduction and hearing loss, suggesting that it may originate from lesions in the central nervous system rather than the peripheral loss. Pharmacologically facilitating cholinergic signaling with donepezil reversed the central gain in 5xFAD mice. After the central gain increased, aging 5xFAD mice developed deficits for hearing sound pips in the presence of noise, consistent with CAPD-like symptoms of AD patients. Histological analysis revealed that amyloid plaques were deposited in the auditory cortex of both mouse strains. However, in 5xFAD but not APP/PS1 mice, plaque was observed in the upper auditory brainstem, specifically the inferior colliculus (IC) and the medial geniculate body (MGB). This plaque distribution parallels histological findings from human subjects with AD and correlates in age with central gain increase. Overall, we conclude that auditory alterations in amyloidosis mouse models correlate with amyloid deposits in the auditory brainstem and may be reversed initially through enhanced cholinergic signaling. The alteration of ABR recording related to the increase in central gain prior to AD-related hearing disorders suggests that it could potentially be used as an early biomarker of AD diagnosis.</p

Image_2_Increased central auditory gain in 5xFAD Alzheimer’s disease mice as an early biomarker candidate for Alzheimer’s disease diagnosis.TIF

Alzheimer’s Disease (AD) is a neurodegenerative illness without a cure. All current therapies require an accurate diagnosis and staging of AD to ensure appropriate care. Central auditory processing disorders (CAPDs) and hearing loss have been associated with AD, and may precede the onset of Alzheimer’s dementia. Therefore, CAPD is a possible biomarker candidate for AD diagnosis. However, little is known about how CAPD and AD pathological changes are correlated. In the present study, we investigated auditory changes in AD using transgenic amyloidosis mouse models. AD mouse models were bred to a mouse strain commonly used for auditory experiments, to compensate for the recessive accelerated hearing loss on the parent background. Auditory brainstem response (ABR) recordings revealed significant hearing loss, a reduced ABR wave I amplitude, and increased central gain in 5xFAD mice. In comparison, these effects were milder or reversed in APP/PS1 mice. Longitudinal analyses revealed that in 5xFAD mice, central gain increase preceded ABR wave I amplitude reduction and hearing loss, suggesting that it may originate from lesions in the central nervous system rather than the peripheral loss. Pharmacologically facilitating cholinergic signaling with donepezil reversed the central gain in 5xFAD mice. After the central gain increased, aging 5xFAD mice developed deficits for hearing sound pips in the presence of noise, consistent with CAPD-like symptoms of AD patients. Histological analysis revealed that amyloid plaques were deposited in the auditory cortex of both mouse strains. However, in 5xFAD but not APP/PS1 mice, plaque was observed in the upper auditory brainstem, specifically the inferior colliculus (IC) and the medial geniculate body (MGB). This plaque distribution parallels histological findings from human subjects with AD and correlates in age with central gain increase. Overall, we conclude that auditory alterations in amyloidosis mouse models correlate with amyloid deposits in the auditory brainstem and may be reversed initially through enhanced cholinergic signaling. The alteration of ABR recording related to the increase in central gain prior to AD-related hearing disorders suggests that it could potentially be used as an early biomarker of AD diagnosis.</p

Image_1_Fully automated detection and localization of clinically significant prostate cancer on MR images using a cascaded convolutional neural network.tiff

PurposeTo develop a cascaded deep learning model trained with apparent diffusion coefficient (ADC) and T2-weighted imaging (T2WI) for fully automated detection and localization of clinically significant prostate cancer (csPCa).MethodsThis retrospective study included 347 consecutive patients (235 csPCa, 112 non-csPCa) with high-quality prostate MRI data, which were randomly selected for training, validation, and testing. The ground truth was obtained using manual csPCa lesion segmentation, according to pathological results. The proposed cascaded model based on Res-UNet takes prostate MR images (T2WI+ADC or only ADC) as inputs and automatically segments the whole prostate gland, the anatomic zones, and the csPCa region step by step. The performance of the models was evaluated and compared with PI-RADS (version 2.1) assessment using sensitivity, specificity, accuracy, and Dice similarity coefficient (DSC) in the held-out test set.ResultsIn the test set, the per-lesion sensitivity of the biparametric (ADC + T2WI) model, ADC model, and PI-RADS assessment were 95.5% (84/88), 94.3% (83/88), and 94.3% (83/88) respectively (all p > 0.05). Additionally, the mean DSC based on the csPCa lesions were 0.64 ± 0.24 and 0.66 ± 0.23 for the biparametric model and ADC model, respectively. The sensitivity, specificity, and accuracy of the biparametric model were 95.6% (108/113), 91.5% (665/727), and 92.0% (773/840) based on sextant, and were 98.6% (68/69), 64.8% (46/71), and 81.4% (114/140) based on patients. The biparametric model had a similar performance to PI-RADS assessment (p > 0.05) and had higher specificity than the ADC model (86.8% [631/727], pConclusionThe cascaded deep learning model trained with ADC and T2WI achieves good performance for automated csPCa detection and localization.</p

Additional file 1 of Identifying functional dysregulation of NOD2 variant Q902K in patients with Yao syndrome

Additional file 1: Supplementary Table 1. TOP 30 pathways of GSEA Enrichment in PBMCs from patient 1. Supplementary Table 2. Leading edge subset of NOD-like receptor signaling pathway

DataSheet1_Investigation on the efficiency of Brucea javanica oil emulsion injection with chemotherapy for treating malignant pleural effusion: A meta-analysis of randomized controlled trials.docx

Introduction: Systematic evaluation of the clinical efficacy and safety of Brucea javanica oil emulsion injection (BJOEI) in combination with chemotherapy in the treatment of malignant pleural effusion (MPE).Methods: The study searched CNKI, Wanfang database, VIP database, SinoMed, PubMed, Embase, the Cochrane Library, and the Web of Science database and retrieved randomized controlled trials (RCTs) on the treatment of MPE with BJOEI in combination with chemotherapy from seven electronic databases from inception to 31 March 2022. Meta-analysis and sensitivity analysis were performed using Revman 5.4 and Stata 13.0 software.Results: Ultimately, 30 RCTs with 2035 patients were included, including 1002 cases in the control group and 1033 cases in the treatment group. The results of the meta-analysis showed that the overall efficacy rate of BJOEI combined with chemotherapy was higher in the treatment of MPE compared with chemotherapy alone (RR = 1.45, 95%CI: 1.36–1.54, p Conclusion: BJOEI combined with chemotherapy has better clinical efficacy than chemotherapy alone in the treatment of MPE. It can further improve KPS score, improve patients’ quality of life, and reduce the occurrence of adverse reactions. However, the conclusions of this study need to be confirmed by further randomized, double-blind, controlled trials with large sample size, reasonable design, and strict implementation.</p

Table_1_Association of homocysteine and polymorphism of methylenetetrahydrofolate reductase with early-onset post stroke depression.DOCX

BackgroundHomocysteine (Hcy) has been indicated to be involved in pathophysiology of post stroke depression (PSD). There is a lack of research to study the relationship between Hcy metabolism genes and PSD. Our study aims to investigate the relationship among Hcy metabolism genes, Hcy, and early-onset PSD.Materials and methodsWe recruited 212 patients with stroke and collected their peripheral blood sample, clinical data, and laboratory test on admission. 12 single nucleotide polymorphisms (SNPs) in methylenetetrahydrofolate reductase (MTHFR), methionine synthase reductase (MTRR), and methionine synthase (MTR) genes were genotyped by high-resolution melt analysis. PSD was diagnosed by DSM-V at 2 weeks after stroke. Binary logistic regression and haplotype analysis were used to examine the association between Hcy metabolism genes and PSD. Mediation analysis was performed to clarify whether the SNPs exerted their effect on PSD by affecting the Hcy level.Results81 patients were diagnosed with PSD, and the incidence rate was 38.2%. Hcy level in PSD group was significantly higher than it in non-PSD group (p = 0.019). MTHFR rs1801133 AA genotype an A allele were associated with an elevated risk of PSD after adjustment for some confounding factors (OR = 4.021, 95% CI: 1.459∼11.080, p = 0.007 for AA genotype; OR = 1.808, 95% CI: 1.172∼2.788, p = 0.007 for A allele). Furthermore, the effect of MTHFR rs1801133 AA genotype on PSD was mediated by Hcy (OR = 1.569, 95% CI: 0.013∼3.350, p ConclusionMTHFR rs1801133 and Hcy were associated with PSD, and MTHFR rs1801133 may exert an effect on PSD via mediating Hcy level. This offers a new perspective for treating PSD and understanding the mechanism of PSD.</p

Additional file 13 of Circulating tumor DNA integrating tissue clonality detects minimal residual disease in resectable non-small-cell lung cancer

Additional file 13. Supplementary results