Background Spontaneous intracerebral hemorrhage (ICH) is a devastating disease with high mortality rate. This study aimed to predict hematoma expansion in spontaneous ICH from routinely available variables by using support vector machine (SVM) method. Methods We retrospectively reviewed 1157 patients with spontaneous ICH who underwent initial computed tomography (CT) scan within 6 h and follow-up CT scan within 72 h from symptom onset in our hospital between September 2013 and August 2018. Hematoma region was manually segmented at each slice to guarantee the measurement accuracy of hematoma volume. Hematoma expansion was defined as a proportional increase of hematoma volume > 33% or an absolute growth of hematoma volume > 6 mL from initial CT scan to follow-up CT scan. Univariate and multivariate analyses were performed to assess the association between clinical variables and hematoma expansion. SVM machine learning model was developed to predict hematoma expansion. Findings 246 of 1157 (21.3%) patients experienced hematoma expansion. Multivariate analyses revealed the following 6 independent factors associated with hematoma expansion: male patient (odds ratio [OR] = 1.82), time to initial CT scan (OR = 0.73), Glasgow Coma Scale (OR = 0.86), fibrinogen level (OR = 0.72), black hole sign (OR = 2.52), and blend sign (OR = 4.03). The SVM model achieved a mean sensitivity of 81.3%, specificity of 84.8%, overall accuracy of 83.3%, and area under receiver operating characteristic curve (AUC) of 0.89 in prediction of hematoma expansion. Interpretation The designed SVM model presented good performance in predicting hematoma expansion from routinely available variables. Fund This work was supported by , China, , China (LQ15H180002), the , China (Y20180112), Scientific Research Staring Foundation for the Returned Overseas Chinese Scholars of , and , China. The funders had no role in study design, data collection, data analysis, interpretation, writing of the report.

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Several lines of evidence point to alteration in brain metabolic homeostasis in Parkinson's disease (PD) and levodopa-induced dyskinesia (LID), yet the metabolic mechanism in different brain regions underlying PD and LID remains largely unknown. The present study aimed to uncover the metabolic pathways across anatomical regions in the brain of PD and LID. Using an NMR-based metabolomic approach, we generated the metabolomics profiling data from six different brain regions of PD rats and following the onset of LIDs. The diversity of metabolite patterns across the brain and its relation to PD and LID were further investigated through principal component analysis (PCA) and multivariate general linear model. Compared with control rats, dopamine loss in PD rats produced a marked and persistent metabolic disturbance in neurotransmitter metabolism and energy pathway, resulting in a metabolic imbalance among different brain regions. In LID rats, levodopa replacement did not restore the midbrain-striatum metabolic crosstalk and metabolic disturbance throughout the brain was involved in levodopa related involuntary movements. Most notably, the midbrain and right cortex were identified as the primary regions of metabolic abnormalities in PD and LID rats. Neurochemical differences in metabolic phenotypes were mainly defined by various neurotransmitters including glutamate, glutamine and aspartate. Accordingly, we found that the PD and LID rats exhibited lower levels of synaptophysin (SYP), a marker for synaptic plasticity, compared with control rats. These findings provide key insights into the metabolic mechanism underlying PD and LID by defining brain-region specific metabolic phenotype, with implications for developing targeted therapies.

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Background: Tonsil hypertrophy has negative impact on children's health, but its pathogenesis remains obscure despite the fact that numerous bacteriological studies have been carried out. Understanding the innate immune and inflammatory states of hypertrophic tonsils with different clinical manifestations is of great significance for defining the pathogenesis of tonsil hypertrophy and establishing treatment strategies. The present study was undertaken to examine the characteristics of innate immunity and inflammation in children with hypertrophic palatine tonsils and different clinical manifestations. Methods: Tonsil tissues were surgically removed from the patients and classified based on the patients' clinical manifestations. The patients were divided into three groups: 1) Control group; 2) Tonsil Hypertrophy (TH) group; and 3) Tonsil Hypertrophy combined with Recurrent Infection (TH + RI) group. The immune and inflammatory statuses of these tissues were characterized using qRT-PCR and ELISA methods. Results: Viral protein 1 (VP1) was highly expressed in TH group, but not in TH + RI group. In TH group, elevated expression was observed in the innate immune mediators, including retinoic acid-inducible gene I (RIG-I), interferon alpha (IFN-α), mitochondrial antiviral-signaling protein (MAVS), NLR family pyrin domain containing 3 (NLRP3), tolllike receptor (TLR) 4 and TLR7. Consistent with the innate immune profile, the expression of inflammatory markers (IL-1β, NF-κB and IL-7) was also significantly elevated in TH group. Meanwhile, the COX-2/PGE2/EP4 signaling pathway was found to be involved in the inflammatory response and the formation of fibroblasts. Conclusions: Innate immune and inflammatory responses are more active in simple hypertrophic tonsils, rather than hypertrophic tonsils with recurrent inflammation. A local relative immune deficiency in the hypertrophic tonsils may be a causative factor for recurrent tonsillitis in TH + RI. These differences, together with the patient's clinical manifestations, suggest that tonsillar hypertrophy might be regulated by diverse immune and/or inflammatory mechanism through which novel therapeutic strategies might be created.

Objective. We aim to analyze the diagnostic yield, diagnostic accuracy, and delayed diagnosis of patients with terminal ileum lesions, providing follow-up suggestions for suspected patients. Methods. We carried out an analysis of 1099 patients who had terminal ileum lesions in our hospital from 2009 to 2019. The endoscopy reports and histopathology reports of terminal ileal biopsies were recorded. Clinical diagnosis and management were reviewed to determine whether there was a need to correct after a follow-up endoscopy result. Results. A total of 1099 patients were found to have terminal ileum lesions, among which 959 in 1099 patients (87.26%) were diagnosed as benign, 17 in 1099 patients (1.55%) were diagnosed as malignant, and 123 in 1099 patients (11.19%) were diagnosed as suspected. The diagnostic accuracies of terminal ileal polyp, cyst, cancer, eosinophilic enteritis, parasite, lymphofollicular hyperplasia, and amyloidosis were 100%. The diagnosis was delayed in 9.93% of Crohn’s disease (CD) and 12.5% of lymphoma. Among the definite cases, the diagnosis was corrected during the follow-up in 12.5% of the patients, while the clinical treatment was corrected during the follow-up in 17.86% of the patients. Among the suspected cases, the diagnosis and treatment was corrected in 61.11% of the patients during the follow-up. Conclusion. Coincident diagnosis of ileitis and ileum ulcer is low. Delayed diagnosis of Crohn’s disease and lymphoma were observed in a certain proportion of patients with terminal ileum lesions. A follow-up endoscopy was strongly recommended for these suspected patients with terminal ileum lesions.