Acute pancreatitis associated with pleural effusion: MDCT manifestations and anatomical basis.

BACKGROUND: Acute pancreatitis (AP) is a severe condition with complications that can impact multiple organ systems throughout the body. Specifically, the diffusion of peripancreatic effusion to the pleural cavity is a significant phenomenon in AP. However, its pathways and implications for disease severity are not fully understood. OBJECTIVE: This study aims to investigate the anatomical routes of peripancreatic effusion diffusion into the pleural cavity in patients with AP and to analyze the correlation between the severity of pleural effusion (PE) and the computed tomography severity index (CTSI) and acute physiology and chronic health evaluation II (APACHE II) scoring system. METHODS: 119 patients with AP admitted to our institution were enrolled in this study (mean age 50 years, 74 male and 45 female). Abdominal CT was performed, and the CTSI and APACHE II index were used to evaluate the severity of the AP, Meanwhile, the prevalence and semiquantitative of PE were also mentioned. The anatomical pathways of peripancreatic effusion draining to pleural were analyzed. Finally, the correlation relationship between the severity of AP and the PE was analyzed. RESULTS: In 119 patients with AP, 74.8% of patients had PE on CT. The anatomic pathways of peripancreatic effusion draining to pleural included esophageal hiatus in 33.7% of patients, aortic hiatus in 6.7% of patients and inferior vena cava hiatus in 3.37% of patients. The rating of PE on CT was correlated with CTSI scores (r= 0.449, P= 0.000) and was slightly correlated with the APACHE II scores (r= 0.197, P= 0.016). CONCLUSION: PE is a common complication of AP, which can be caused by anatomic pathways such as diaphragmatic hiatus. Due to its correlation with the CTSI score, the PE may be a supplementary indicator in determining the severity of AP.

Automatic method for individual parcellation of manganese-enhanced magnetic resonance imaging of rat brain.

Aims: To construct an automatic method for individual parcellation of manganese-enhanced magnetic resonance imaging (MEMRI) of rat brain with high accuracy, which could preserve the inherent voxel intensity and Regions of interest (ROI) morphological characteristics simultaneously. Methods and results: The transformation relationship from standardized space to individual space was obtained by firstly normalizing individual image to the Paxinos space and then inversely transformed. On the other hand, all the regions defined in the atlas image were separated and resaved as binary mask images. Then, transforming the mask images into individual space via the inverse transformations and reslicing using the 4th B-spline interpolation algorithm. The boundary of these transformed regions was further refined by image erosion and expansion operator, and finally combined together to generate the individual parcellations. Moreover, two groups of MEMRI images were used for evaluation. We found that the individual parcellations were satisfied, and the inherent image intensity was preserved. The statistical significance of case-control comparisons was further optimized. Conclusions: We have constructed a new automatic method for individual parcellation of rat brain MEMRI images, which could preserve the inherent voxel intensity and further be beneficial in case-control statistical analyses. This method could also be extended to other imaging modalities, even other experiments species. It would facilitate the accuracy and significance of ROI-based imaging analyses.

Molecular clustering based on gene set expression and its relationship with prognosis in patients with lung adenocarcinoma.

Background: Lung adenocarcinoma (LUAD) is a subtype of lung cancer with high morbidity and mortality. While genotyping is an important determinant for the prognosis of LUAD patients, there is a paucity of studies on gene set-based expression (GSE) typing for LUAD. This current study used GSE methodology to perform gene typing of LUAD patients. Methods: Clinical and genomic information of the LUAD patients were downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Patients with LUAD were clustered into different molecular subtypes depending on the clinical and gene set expression characteristics. The survival rate and silhouette widths were compared between each molecular subtype. Differences in survival rate between gene sets were analyzed using Kaplan-Meier survival curves. Cox regression and Lasso regression were used to establish the prognostic gene set model based on the TCGA database, and the results were validated using the GEO dataset. Results: A total of 10 hub genes were finally identified and clustered into 3 subtypes with a mean contour width of 0.96. There were significant differences in survival rates among the 3 subtypes (P<0.05). Gene Ontology (GO) analysis indicated that the related biological processes (BP) were mainly involved in regulation of cell cycle, mitotic cell cycle phase transition, and proteasome-mediated ubiquitin-dependent protein catabolic process. The cellular components (CC) were related to the spindle, chromosomal region, and midbody. Molecular function (MF) mainly focused on ubiquitin-like protein ligase binding, translation regulator activity, and oxidation activity. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that the main pathways included the Epstein Barr virus infection pathway of neurogeneration, the p53 signaling pathway, and the proteome pathways. In addition, the protein-protein interaction network was analyzed using the STRING and Cytospace software, and the top 9 hub genes identified were KIF2C, DLGAP5, KIF20A, PSMC1, PSMD1, PSMB7, SNAI2, FGF13, and BMP2. Conclusions: Patients with LUAD can be clustered into three subtypes based on the expression of gene sets. These findings contribute to understanding the pathogenesis and molecular mechanisms in LUAD, and may lead to potential individualized pharmacogenetic therapy for patients with LUAD.

Gastrointestinal tract involvement in acute pancreatitis: initial findings and follow-up by magnetic resonance imaging.

BACKGROUND: To study the initial and follow up patterns of gastrointestinal tract involvement in acute pancreatitis (AP) using magnetic resonance imaging (MRI). METHODS: A total of 209 patients with AP undergoing abdominal MRI on 1.5 T MRI were compared to 100 control patients selected from our daily clinical caseload who underwent MRI over the same recruitment period and had no other disease which can cause abnormality of gastrointestinal tract. Initial and follow up MRI examinations of gastrointestinal tract abnormalities were noted for AP patients. The severity of AP was graded by the MRSI and APACHE II. Spearman correlation of gastrointestinal tract involvement with MRSI and APACHE II was analyzed. RESULTS: In 209 patients with AP, 63% of the AP patients on their initial MRI exams and 5% of control subjects had at least one gastrointestinal tract abnormality (P<0.05). In the control group, thirty-seven patients were normal on MRI, 24 patients with renal cysts, eighteen patients with liver cysts, eleven patients with liver hemangiomas, and ten patients with splenomegaly. The abnormalities of gastrointestinal tract observed in AP patients included thickened stomach wall (20%), thickened duodenum wall (27%), thickened ascending colon wall (11%), thickened transverse colon wall (15%), and thickened descending colon wall (26%), among others. Gastrointestinal tract abnormalities were correlated with the MRSI score (r=0.46, P<0.05) and APACHE II score (r=0.19, P<0.05). Among 62 patients who had follow up examinations, 26% of patients had gastrointestinal tract abnormality, which was significantly lower than that in the initial exams (P<0.05). Resolution of gastrointestinal tract abnormal MRI findings coincided with symptom alleviation in AP patients. CONCLUSIONS: Gastrointestinal tract abnormalities on MRI are common in AP and they are positively correlated with the severity of AP. It may add value for determining the severity of AP.