Abnormal brain functional network dynamics in amyotrophic lateral sclerosis patients with depression.

Since depression is common in amyotrophic lateral sclerosis (ALS) patients, we aimed to explore the specific brain functional network dynamics in ALS patients with depression (ALS-D) compared with healthy controls (HCs) and ALS patients without depressive symptoms (ALS-ND). According to the DSM-V, 32 ALS-D patients were selected from a large and newly diagnosed ALS cohort. Then, 32 demographic- and cognitive-matched ALS-ND patients were also selected, and 64 HCs were recruited. These participants underwent resting-state fMRI scans, and functional connectivity state analysis and dynamic graph theory were applied to evaluate brain functional network dynamics. Moreover, the Hamilton Depression Rating Scale (HDRS) was used to quantify depressive symptoms in the ALS-D patients. Four distinct states were identified in the ALS-D patients and controls. Compared with that in HCs, the fraction rate (FR) in state 2 was significantly decreased in ALS-D patients, and the FR in state 4 was significantly increased in ALS-D patients. Compared with that of HCs, the dwell time in state 4 was significantly increased in the ALS-D patients. Moreover, compared with that in the ALS-D patients, the FR in state 3 was significantly decreased in the ALS-ND patients. Among the ALS-D patients, there was the suggestion of a positive association between HDRS scores and dwell time of state 4, but this association did not reach statistical significance (r = 0.354; p = 0.055). Depression is an important feature of ALS patients, and we found a special pattern of brain functional network dynamics in ALS-D patients. Our findings may play an important role in understanding the mechanism underlying depression in ALS patients and help develop therapeutic interventions for depressed ALS patients.

Choroid plexus enlargement in amyotrophic lateral sclerosis patients and its correlation with clinical disability and blood-CSF barrier permeability.

BACKGROUND: Using in vivo neuroimaging techniques, growing evidence has demonstrated that the choroid plexus (CP) volume is enlarged in patients with several neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease. However, although animal and postmortem findings suggest that CP abnormalities are likely important pathological mechanisms underlying amyotrophic lateral sclerosis (ALS), the third most common neurodegenerative disease, no available study has been conducted to thoroughly assess CP abnormalities and their clinical relevance in vivo in ALS patients to date. Thus, we aimed to determine whether in vivo CP enlargement may occur in ALS patients. We also aimed to identify the relationships of CP volume with clinical disabilities and blood-CSF barrier (BCSFB) permeability in ALS patients. METHODS: In this retrospective study, based on structural MRI data, CP volume was assessed using a Gaussian mixture model and underwent further manual correction in 155 ALS patients and 105 age- and sex-matched HCs from October 2021 to April 2023. The ALS Functional Rating Scale-Revised (ALSFRS-R) was used to assess clinical disability. The CSF/serum albumin quotient (Qalb) was used to assess BCSFB permeability. Moreover, all the ALS patients completed genetic testing, and according to genetic testing, the ALS patients were further divided into genetic ALS subgroup and sporadic ALS subgroup. RESULTS: We found that compared with HCs, ALS patients had a significantly higher CP volume (p < 0.001). Moreover, compared with HCs, CP volume was significantly increased in both ALS patients with and without known genetic mutations after family-wise error correction (p = 0.006 and p < 0.001, respectively), while there were no significant differences between the two ALS groups. Furthermore, the CP volume was significantly correlated with the ALSFRS-r score (r = -0.226; p = 0.005) and the Qalb (r = 0.479; p < 0.001) in ALS patients. CONCLUSION: Our study first demonstrates CP enlargement in vivo in ALS patients, and continues to suggest an important pathogenetic role for CP abnormalities in ALS. Moreover, assessing CP volume is likely a noninvasive and easy-to-implement approach for screening BCSFB dysfunction in ALS patients.

The Clinical Significance and the Potential Regulatory Mechanism of the LncRNA OIP5-AS1 in Paediatric Severe Community-Acquired Pneumonia Blood Through the MiR-150-5p/PDCD4 Axis.

BACKGROUND: This study aimed to elucidate the clinical significance and regulatory mechanism of the long non-coding RNA OIP5-AS1 in severe community-acquired pneumonia (SCAP) among paediatric patients. METHODS: qRT-PCR was used to assess the mRNA levels of OIP5-AS1. ROC curve analysis was used to assess the diagnostic significance of OIP5-AS1. Short-term prognostic significance was evaluated through Kaplan-Meier survival. An in vitro cell model was developed using LPS-induced MRC-5 cells. CCK-8, flow cytometry, and ELISA were conducted to measure cell viability, apoptosis, and inflammatory factor levels. The association between miR-150-5p and PDCD4 was confirmed through DLR assays. RESULTS: Elevated OIP5-AS1 were observed in paediatric patients with SCAP, which enabled effective differentiation from healthy individuals. High expression of OIP5-AS1 correlated with reduced survival rates. OIP5-AS1 knockdown attenuated cell viability suppression and the promotion of apoptosis and inflammatory factors induced by LPS. However, this attenuation was reversed by reduced levels of miR-150-5p. miR-150-5p was identified as a target of PDCD4 and OIP5-AS1. CONCLUSION: Increased OIP5-AS1 levels show potential as a valuable diagnostic and prognostic biomarker for paediatric patients with SCAP. This study illustrates its role in regulating cell viability, apoptosis, and the inflammatory response via the miR-150-5p/PDCD4 axis, acting as a ceRNA.

Glymphatic dysfunction in patients with early-stage amyotrophic lateral sclerosis.

Recently, an astrocytic aquaporin 4-dependent drainage system, that is, the glymphatic system, has been identified in the live murine and human brain. Growing evidence suggests that glymphatic function is impaired in patients with several neurodegenerative diseases, including Alzheimer's and Parkinson's disease. As the third most common neurodegenerative disease, although animal studies have indicated that early glymphatic dysfunction is likely an important pathological mechanism underpinning amyotrophic lateral sclerosis (ALS), no available study has been conducted to thoroughly assess glymphatic function in vivo in ALS patients to date, particularly in patients with early-stage ALS. Thus, using diffusion tensor imaging analysis along the perivascular space (ALPS) index, an approximate measure of glymphatic function in vivo, we aimed to explore whether glymphatic function is impaired in patients with patients with early-stage ALS, and the diagnostic performance of the ALPS index in distinguishing between patients with early-stage ALS and healthy subjects. We also aimed to identify the relationships between glymphatic dysfunction and clinical disabilities and sleep problems in patients with early-stage ALS. In this retrospective study, King's Stage 1 ALS patients were defined as patients with early-stage ALS. We enrolled 56 patients with early-stage ALS and 32 age- and sex-matched healthy control subjects. All participants completed clinical screening, sleep assessment and ALPS index analysis. For the sleep assessment, the Pittsburgh Sleep Quality Index, Epworth Sleepiness Scale and polysomnography were used. Compared with healthy control subjects, patients with early-stage ALS had a significantly lower ALPS index after family-wise error correction (P < 0.05). Moreover, receiver operating characteristic analysis showed that the area under the curve for the ALPS index was 0.792 (95% confidence interval 0.700-0.884). Partial correlation analyses showed that the ALPS index was significantly correlated with clinical disability and sleep disturbances in patients with early-stage ALS. Multivariate analysis showed that sleep efficiency (r = 0.419, P = 0.002) and periodic limb movements in sleep index (r = -0.294, P = 0.017) were significant predictive factors of the ALPS index in patients with early-stage ALS. In conclusion, our study continues to support an important role for glymphatic dysfunction in ALS pathology, and we provide additional insights into the early diagnostic value of glymphatic dysfunction and its correlation with sleep disturbances in vivo in patients with early-stage ALS. Moreover, we suggest that early improvement of glymphatic function may be a promising strategy for slowing the neurodegenerative process in ALS. Future studies are needed to explore the diagnostic and therapeutic value of glymphatic dysfunction in individuals with presymptomatic-stage neurodegenerative diseases.

The Abnormal Alternations of Brain Imaging in Patients with Chronic Obstructive Pulmonary Disease: A Systematic Review.

Background: Cognitive impairment (CI) is an important extrapulmonary complication in patients with chronic obstructive pulmonary disease (COPD). Multimodal Neuroimaging Examination can display changes in brain structure and functions in patients with COPD. Objective: The purpose of this systematic review is to provide an overview of the variations in brain imaging in patients with COPD and their potential relationship with CI. Furthermore, we aim to provide new ideas and directions for future research. Methods: Literature searches were performed using the electronic databases PubMed, Scopus, and ScienceDirect. All articles published between January 2000 and November 2021 that met the eligibility criteria were included. Results: Twenty of the 23 studies focused on changes in brain structure and function. Alterations in the brain's macrostructure are manifested in the bilateral frontal lobe, hippocampus, right temporal lobe, motor cortex, and supplementary motor area. The white matter microstructural changes initially appear in the bilateral frontal subcortical region. Regarding brain function, patients with COPD exhibited reduced frontal cerebral perfusion and abnormal alterations in intrinsic brain activity in the bilateral posterior cingulate cortex, precuneus, right lingual gyrus, and left anterior central gyrus. Currently, there is limited research related to brain networks. Conclusion: CI in patients with COPD may present as a type of dementia different from Alzheimer's disease, which tends to manifest as frontal cognitive decline early in the disease. Further studies are required to clarify the neurobiological pathways of CI in patients with COPD from the perspective of brain connectomics based on the whole-brain system in the future.

A therapy that modulates T lymphocyte subsets in patients infected with Epstein-Barr virus: Ganciclovir combined with interferon atomization inhalation.

To investigate the effect of ganciclovir combined with interferon atomization inhalation on T lymphocyte subsets in patients with Epstein-Barr virus (EBV) infection and its efficacy. Fifty patients with EBV infection who received ganciclovir combined with interferon atomization inhalation were selected as the observation group, and 50 healthy people were selected as the control group. The changes of T lymphocyte subsets in peripheral blood were detected by flow cytometry before treatment and at the 1st, 2nd, 3rd and 4th cycle after treatment. Before treatment, the CD3+, CD4+, CD4+/CD8+ indexes of the patients were significantly lower than those of the control group (P < .05), and the CD8+ level was significantly increased (P < .05). After one cycle of treatment, there was no significant difference in the changes of T lymphocyte subsets compared with those before treatment. After 2 and 3 cycles of treatment, CD3+, CD4+, CD4+/CD8+ values were higher than those before treatment (P > .05), and CD8+ index was lower than that before treatment (P < .05). After the 4th cycle of treatment, CD3+, CD4+, CD4+/CD8+ values were significantly improved (P < .05), and CD8+ index was significantly decreased (P < .05). Ganciclovir combined with interferon atomization inhalation can regulate the changes of T lymphocyte subsets in patients with EBV infection, improve the patient's condition, and has no obvious adverse reactions. Monitoring the changes of T lymphocyte subsets during treatment is more meaningful to predict the therapeutic effect of patients with EB virus infection.

Transcriptome analysis identifies the role of Class I histone deacetylase in Alzheimer's disease.

Epigenetics modification is a process that does not change the sequence of deoxyribonucleic acid (DNA) in disease progression but can alter the genetic expression of the brain in Alzheimer's disease (AD). In this study, we deployed the weighted gene co-expression network analysis (WGCNA) to explore the role of Class I histone deacetylases (HDACs) in AD, which included HDAC1, HDAC2, HDAC3, and HDAC8. The aim of the study was to find how Class I HDACs affected AD pathology by analyzing the Gene Expression Omnibus (GEO) microarray datasets GSE33000. We found that HDAC1 and HDAC8 were more highly expressed in the cortex of AD patients than in Controls, while HDAC2 and HDAC3 were lower expressed. By WGCNA analysis, we found the blue module was associated with HDAC1 and HDAC8, and the turquoise module was related to HDAC2 and HDAC3. Functional enrichment analysis revealed that the Wnt signaling pathway and synaptic plasticity played an important role in the modification of HDAC1 and HDAC8 while gap junction and cell-cell junction were involved in the regulation of HDAC2 and HDAC3 in the disease progression of AD. By Receiver Operating Characteristics (ROC) analysis, we concluded that HDAC1 might be the most probable diagnostic biomarker of Class I HDACs for AD. Our study provided a comprehensive understanding of Class I HDACs and provided new insight into the function of HDAC1 in AD disease progression.

Disconnection of Network Hubs Underlying the Executive Function Deficit in Patients with Ischemic Leukoaraiosis.

BACKGROUND: Cognitive impairment is the most common clinical manifestation of ischemic leukoaraiosis (ILA), but the underlying neurobiological pathways have not been well elucidated. Recently, it was thought that ILA is a "disconnection syndrome". Disorganized brain connectome were considered the key neuropathology underlying cognitive deficits in ILA patients. OBJECTIVE: We aimed to detect the disruption of network hubs in ILA patients using a new analytical method called voxel-based eigenvector centrality (EC) mapping. METHODS: Subjects with moderate to severe white matters hyperintensities (Fazekas score ≥3) and healthy controls (HCs) (Fazekas score = 0) were included in the study. The resting-state functional magnetic resonance imaging and the EC mapping approach were performed to explore the alteration of whole-brain network connectivity in ILA patients. RESULTS: Relative to the HCs, the ILA patients exhibited poorer cognitive performance in episodic memory, information processing speed, and executive function (all ps < 0.0125). Additionally, compared with HCs, the ILA patients had lower functional connectivity (i.e., EC values) in the medial parts of default-mode network (i.e., bilateral posterior cingulate gyrus and ventral medial prefrontal cortex [vMPFC]). Intriguingly, the functional connectivity strength at the right vMPFC was positively correlated with executive function deficit in the ILA patients. CONCLUSION: The findings suggested disorganization of the hierarchy of the default-mode regions within the whole-brain network in patients with ILA and advanced our understanding of the neurobiological mechanism underlying executive function deficit in ILA.

Sex differences in the effects of sleep disorders on cognitive dysfunction.

Sleep is an essential physiological function that sustains human life. Sleep disorders involve problems with the quality, duration, and abnormal behaviour of sleep. Insomnia is the most common sleep disorder, followed by sleep-disordered breathing (SDB). Sleep disorders often occur along with medical conditions or other mental health conditions. Of particular interest to researchers is the role of sleep disorders in cognitive dysfunction. Sleep disorder is a risk factor for cognitive dysfunction, yet the exact pathogenesis is still far from agreement. Little is known about how sex differences influence the changes in cognitive functions caused by sleep disorders. This narrative review examines how sleep disorders might affect cognitive impairment, and then explores the sex-specific consequences of sleep disorders as a risk factor for dementia and the potential underlying mechanisms. Some insights on the direction of further research are also presented.

Intestinal dysbiosis mediates cognitive impairment via the intestine and brain NLRP3 inflammasome activation in chronic sleep deprivation.

Growing evidence suggests the involvement of the microbiota-gut-brain axis in cognitive impairment induced by sleep deprivation (SD), however how the microbiota-gut-brain axis work remains elusive. Here, we discovered that chronic SD induced intestinal dysbiosis, activated NLRP3 inflammasome in the colon and brain, destructed intestinal/blood-brain barrier, and impaired cognitive function in mice. Transplantation of "SD microbiota" could almost mimic the pathological and behavioral changes caused by chronic SD. Furthermore, all the behavioral and pathological abnormalities were practically reversed in chronic sleep-deprived NLRP3-/- mice. Regional knockdown NLRP3 expression in the gut and hippocampus, respectively. We observed that down-regulation of NLRP3 in the hippocampus inhibited neuroinflammation, and ameliorated synaptic dysfunction and cognitive impairment induced by chronic SD. More intriguingly, the down-regulation of NLRP3 in the gut protected the intestinal barrier, attenuated the levels of peripheral inflammatory factors, down-regulated the expression of NLRP3 in the brain, and improved cognitive function in chronic SD mice. Our results identified gut microbiota as a driver in chronic SD and highlighted the NLRP3 inflammasome as a key regulator within the microbiota-gut-brain axis.

Sleep disorders affect cognitive function in adults: an overview of systematic reviews and meta-analyses.

Sleep disorders frequently result in poor memory, attention deficits, as well as a worse prognosis for neurodegenerative changes, such as Alzheimer's disease. The purpose of this study is to investigate the impact of sleep disorders on cognition. We screened four databases for all meta-analyses and systematic reviews from the establishment through March 2022. We have carried out quality evaluation and review the eligible systematic reviews. Evidence grading and quality assessment were performed on 22 eligible articles. Sleep deprivation primarily affects simple attention, complex attention, and working memory in cognition and alertness. The moderate-to-high-quality evidence proves optimal sleep time as 7-8 h. Sleep time outside this range increases the risk of impaired executive function, non-verbal memory, and working memory. Sleep-related breathing disorders is more likely to cause mild cognitive impairment and affects several cognitive domains. In older adults, insomnia primarily affects working memory, episodic memory, inhibitory control, cognitive flexibility, problem-solving, operational ability, perceptual function, alertness, and complex attention, and maintaining sensitivity. Sleep disturbances significantly impair cognitive function, and early detection and intervention may be critical steps in reducing poor prognosis. A simple neuropsychological memory test could be used to screen people with sleep disorders for cognitive impairment. Supplementary Information: The online version contains supplementary material available at 10.1007/s41105-022-00439-9.

Submucosal esophageal abscess evolving into intramural submucosal dissection: A case report.

BACKGROUND: Here we report a rare case of submucosal esophageal abscess evolving into intramural submucosal dissection. CASE SUMMARY: An 80-year-old woman was admitted to our emergency department with a chief complaint of dysphagia and fever. Laboratory tests showed mild leukocytosis and elevated C-reactive protein level. Computed tomography showed thickening of the esophageal wall. Upper endoscopy showed a laceration of the esophageal mucosa and a submucosal mass. Spontaneous drainage occurred, and we could see purulent exudate from the crevasse. We closed the laceration with endoscopic clips. The patient did not remember swallowing a foreign body; however, she ate crabs before the symptoms occurred. We prescribed the patient with antibiotic, and the symptoms were gradually relieved. Two months later, upper endoscopy showed that the laceration was healed, and the submucosal abscess disappeared. However, intramural esophageal dissection was formed. We performed endoscopic incision of the septum using dual-knife effectively. CONCLUSION: In conclusion, we are the first to report the case of esophageal submucosal abscess evolving into intramural esophageal dissection. The significance of this case lies in clear presentation of the evolution process between two disorders. In addition, we recommend that endoscopic incision be considered as one of the routine therapeutic modalities of intramural esophageal dissection.

Autogenous and Tunable CNTs for Enhanced Polarization and Conduction Loss Enabling Sea Urchin-Like Co3ZnC/Co/C Composites with Excellent Microwave Absorption Performance.

ZIF-67-derived magnetic metal/carbon composites are considered prospective candidates for use as microwave absorption (MA) materials owing to their magnetoelectric synergy. However, the structure of ZIF-67-derived MA materials mainly depends on the morphology and composition of pristine metal-organic frameworks (MOFs), and their microstructures lack a rational design. Herein, a multidimensional sea urchin-like carbon nanotubes (CNTs)-grafted carbon polyhedra-encapsulated Co3ZnC/Co nanoparticle composite was prepared by one-step catalytic pyrolysis of ZIF-67/ZnO using a rational structural design. The autogenous and tunable CNTs obtained with the assistance of zinc evaporation not only overcome the limitation of homogeneous dispersion but also endow the Co3ZnC/Co/C composite with outstanding MA properties owing to the conduction loss provided by CNTs, polarization loss caused by multiple components, and electromagnetic wave trap composed of a special sea urchin-like structure. Consequently, the minimum reflection loss of ZZ0.1-600 reaches -60.3 dB at 1.6 mm, the maximum absorption bandwidth of ZZ0.05-600 is 6.24 GHz (covering nearly the entire Ku band) at 1.9 mm, and the structure has a low weight ratio (30 wt %). Compared with Z-600 and pure ZnO, the MA performance of the sea urchin-like Co3ZnC/Co/C composite obtained by rational structural design has been greatly improved; this strategy offers a new approach for optimizing the MA performance of materials according to their structural design.

DI-3-n-butylphthalide mitigates stress-induced cognitive deficits in mice through inhibition of NLRP3-Mediated neuroinflammation.

Our previous study has demonstrated that chronic stress could cause cognitive deficits and tau pathology. However, the underlying mechanism and whether/how DI-3-n-Butylphthalide (NBP) ameliorates these effects are still unclear. Here, Wild-type mice were subjected to chronic unpredictable and mild stress (CUMS) for 8 weeks. Following the initial 4 weeks, the stressed animals were separated into susceptible (depressive) and unsusceptible (resilient) groups based on behavioral tests. Then, NBP (30 mg/kg i.g) was administered for 4 weeks. Morris water maze (MWM), Western-blot, Golgi staining, immunofluorescence staining and ELISA were used to examine behavioral, biochemical, and pathological changes. The results showed that both depressive and resilient mice displayed spatial memory deficits and an accumulation of tau in the hippocampus. Activated microglia and NLRP3 inflammasome were found after 8-week chronic stress. We also found a decreased level of postsynaptic density (PSD) related proteins (PSD93 and PSD95) and decreased the number of dendritic spines in the hippocampus. Interestingly, almost all the pathological changes in depressive and resilient mice previously mentioned could be reversed by NBP treatment. To further investigate the role of NLRP3 inflammasome in chronic stress-induced cognitive deficits, NLRP3 KO mice were also exposed to chronic stress. And these changes induced by chronic stress could not be found in NLRP3 KO mice. These results show an important role for the NLRP3/caspase-1/IL-1ß axis in chronic stress-induced cognitive deficits and NBP meliorates cognitive impairments and selectively attenuates phosphorylated tau accumulation in stressed mice through regulation of NLRP3 inflammatory signaling pathway.

Differentiation of Parkinson's disease and Parkinsonism predominant multiple system atrophy in early stage by morphometrics in susceptibility weighted imaging.

Background and purpose: We previously established a radiological protocol to discriminate multiple system atrophy-parkinsonian subtype (MSA-P) from Parkinson's disease (PD). However, we do not know if it can differentiate early stage disease. This study aimed to investigate whether the morphological and intensity changes in susceptibility weighted imaging (SWI) of the lentiform nucleus (LN) could discriminate MSA-P from PD at early stages. Methods: We retrospectively enrolled patients with MSA-P, PD and sex- and age-matched controls whose brain MRI included SWI, between January 2015 and July 2020 at the Movement Disorder Center. Two specialists at the center reviewed the medical records and made the final diagnosis, and two experienced neuroradiologists performed MRI analysis, based on a defined and revised protocol for conducting morphological measurements of the LN and signal intensity. Results: Nineteen patients with MSA-P and 19 patients with PD, with less than 2 years of disease duration, and 19 control individuals were enrolled in this study. We found that patients with MSA- P presented significantly decreased size in the short line (SL) and corrected short line (cSL), ratio of the SL to the long line (SLLr) and corrected SLLr (cSLLr) of the LN, increased standard deviation of signal intensity (SIsd_LN, cSIsd_LN) compared to patients with PD and controls (P < 0.05). With receiver operating characteristic (ROC) analysis, this finding had a sensitivity of 89.5% and a specificity of 73.7% to distinguish MSA- P from PD. Conclusion: Compared to PD and controls, patients with MSA-P are characterized by a narrowing morphology of the posterior region of the LN. Quantitative morphological changes provide a reference for clinical auxiliary diagnosis.

Amygdala abnormalities across disease stages in patients with sporadic amyotrophic lateral sclerosis.

To examine selective atrophy patterns and resting-state functional connectivity (FC) alterations in the amygdala at different stages of amyotrophic lateral sclerosis (ALS), and to explore any correlations between amygdala abnormalities and neuropsychiatric symptoms. We used the King's clinical staging system for ALS to divide 83 consecutive patients with ALS into comparable subgroups at different disease stages. We explored the pattern of selective amygdala subnucleus atrophy and amygdala-based whole-brain FC alteration in these patients and 94 healthy controls (HCs). Cognitive and emotional functions were also evaluated using a neuropsychological test battery. There were no significant differences between ALS patients at King's stage 1 and HCs for any amygdala subnucleus volumes. Compared with HCs, ALS patients at King's stage 2 had significantly lower left accessory basal nucleus and cortico-amygdaloid transition volumes. Furthermore, ALS patients at King's stage 3 demonstrated significant reductions in most amygdala subnucleus volumes and global amygdala volumes compared with HCs. Notably, amygdala-cuneus FC was increased in ALS patients at King's stage 3. Specific subnucleus volumes were significantly associated with Mini-Mental State Examination scores and Hamilton Anxiety Rating Scale scores in ALS patients. In conclusions, our study provides a comprehensive profile of amygdala abnormalities in ALS patients. The pattern of amygdala abnormalities in ALS patients differed greatly across King's clinical disease stages, and amygdala abnormalities are an important feature of patients with ALS at relatively advanced stages. Moreover, our findings suggest that amygdala volume may play an important role in anxiety and cognitive dysfunction in ALS patients.

Imaging features of dermatofibrosarcoma protuberans.

Aims: The study highlights diffusion-weighted imaging (DWI) and dynamic enhancement features of DFSP and characterizes unenhanced and enhanced computed tomography (CT) and magnetic resonance imaging (MRI) scans. Settings and Design: Image findings and clinical histories of 23 patients with DFSP were reviewed. Nine patients underwent CT before and after intravenous administration of contrast material. MRI was performed for 17 patients. CT and MRI findings were analyzed using location, size, edge, shape, infiltration sign, density and signal enhancement mode, and degree. Results: Patients showed 26 superficial and one deep lesion. Ten superficial lesions bulged onto the skin surface. Fourteen lesions were well-defined and 13 ill-defined. All lesions were nodular, with nine being multilobular. Thirteen showed infiltration to adjacent skin, fat, and fascia. Seven lesions on CT were iso- or hypo-dense to muscle without calcification. Contrast-enhanced CT showed inhomogeneous moderate and progressive enhancement in the arterial phase. Small tortuous vessels were seen in the arterial phase in one case. Sixteen tumors displayed signals that were similar to muscle by T1WI. Ten lesions were either hyper-intense to muscle or iso-intense to fat; the deep DFSP was hypo-intense by T2WI. All lesions were hyper-intense homogeneously or heterogeneously under fat-suppressed T2WI. Twelve superficial lesions showed high-intermediate signal, and one deep lesion showed low-intermediate signal with DWI. Seven cases showed low signal diffusion coefficient (ADC) images. Dynamic enhancement and signal intensity-time (SI-T) curves of four tumors showed rapid SI increases followed by steady or slightly rising SI. All lesions showed inhomogeneous, progressive enhancement in the arterial phase. Conclusions: This report is the first on dynamic curves and highlights DWI and T2WI features of DFSP. DFSP can be correctly diagnosed by combining a patient's clinical manifestations with imaging characteristics.

A Pilot Study of Radiomic Based on Routine CT Reflecting Difference of Cerebral Hemispheric Perfusion.

Background: To explore the effectiveness of radiomics features based on routine CT to reflect the difference of cerebral hemispheric perfusion. Methods: We retrospectively recruited 52 patients with severe stenosis or occlusion in the unilateral middle cerebral artery (MCA), and brain CT perfusion showed an MCA area with deficit perfusion. Radiomics features were extracted from the stenosis side and contralateral of the MCA area based on precontrast CT. Two different region of interest drawing methods were applied. Then the patients were randomly grouped into training and testing sets by the ratio of 8:2. In the training set, ANOVA and the Elastic Net Regression with fivefold cross-validation were conducted to filter and choose the optimized features. Moreover, different machine learning models were built. In the testing set, the area under the receiver operating characteristic (AUC) curve, calibration, and clinical utility were applied to evaluate the predictive performance of the models. Results: The logistic regression (LR) for the triangle-contour method and artificial neural network (ANN) for the semiautomatic-contour method were chosen as radiomics models for their good prediction efficacy in the training phase (AUC = 0.869, 0.873) and the validation phase (AUC = 0.793, 0.799). The radiomics algorithms of the triangle-contour and semiautomatic-contour method were implemented in the whole training set (AUC = 0.870, 0.867) and were evaluated in the testing set (AUC = 0.760, 0.802). According to the optimal cutoff value, these two methods can classify the vascular stenosis side class and normal side class. Conclusion: Radiomic predictive feature based on precontrast CT image could reflect the difference of cerebral hemispheric perfusion to some extent.

Radiomics for predicting revised hematoma expansion with the inclusion of intraventricular hemorrhage growth in patients with supratentorial spontaneous intraparenchymal hematomas.

BACKGROUND: Previous radiomics analyses of hematoma expansion have been based on the traditional definition, which only focused on changes in intraparenchymal volume. However, the ability of radiomics-related models to predict revised hematoma expansion (RHE) with the inclusion of intraventricular hemorrhage expansion remains unclear. To develop and validate a noncontrast computed tomography (NCCT)-based clinical- semantic-radiomics nomogram to identify supratentorial spontaneous intracerebral hemorrhage (sICH) patients with RHE on admission. METHODS: In this double-center retrospective study, data from 376 patients with sICH (training set: n=299; test set: n=77; external validation cohort: n=91) were reviewed. A radiomics model, a clinical-semantic model, and a combined model were then constructed based on the logistic regression machine learning approach. Radiomics features were extracted and selected by least absolute shrinkage and selection operator (LASSO) with 5-fold cross validation. Furthermore, the classical BRAIN scoring system was also constructed to predict RHE. Discriminative performance of the models was evaluated on the training and test set with area under the curve (AUC) and decision curve analysis (DCA). RESULTS: The addition of radiomics to clinical-semantic factors significantly improved the prediction performance of RHE compared with the clinical-semantic model alone in the training (AUC, 0.94 vs. 0.81, P<0.05) and test (AUC, 0.84 vs. 0.71, P<0.05) sets, with similar results in the validation set (AUC, 0.83 vs. 0.69, P<0.05). Moreover, the discrimination efficacy of the BRAIN score was significantly lower than the other 3 models (AUC of 0.71 in the training set, P<0.05). CONCLUSIONS: The clinical-semantic-radiomics combined model had the greatest potential for discriminating RHE, and significantly outperformed the classical BRAIN scoring system.