pT1-2 gastric cancer with lymph node metastasis predicted by tumor morphologic features on contrast-enhanced computed tomography

PURPOSETo investigate the value of tumor morphologic features of pT1-2 gastric cancer (GC) on contrast-enhanced computed tomography (CT) in assessing lymph node metastasis (LNM) with reference to histopathological results.METHODSEighty-six patients seen from October 2017 to April 2019 with pT1‐2 GC proven by histopathology were included. Tumor volume and CT densities were measured in the plain scan and the portal-venous phase (PVP), and the percent enhancement was calculated. The correlations between tumor morphologic features and the N stages were analyzed. The diagnostic capability of tumor volume and enhancement features in predicting the LN status of pT1-2 GCs was further investigated using receiver operating characteristic (ROC) analysis.RESULTSTumor volume, CT density in the PVP, and tumor percent enhancement in the PVP correlated significantly with the N stage (rho: 0.307, 0.558, and 0.586, respectively). Tumor volumes were significantly lower in the LNM− group than in the LNM+ group (14.4 mm3 vs. 22.6 mm3, P = 0.004). The differences between the LNM− and LNM+ groups in the CT density in the PVP and the percent enhancement in the PVP were also statistically significant (68.00 HU vs. 87.50 HU, P < 0.001; and 103.06% vs. 179.19%, P < 0.001, respectively). The area under the ROC curves for identifying the LNM+ group was 0.69 for tumor volume and 0.88 for percent enhancement in the PVP, respectively. The percent enhancement in the PVP of 145.2% and tumor volume of 17.4 mL achieved good diagnostic performance in determining LNM+ (sensitivity: 71.4%, 82.1%; specificity: 91.4%, 58.6%; and accuracy: 84.9%, 66.3%, respectively).CONCLUSIONTumor volume and percent enhancement in the PVP of pT1-2 GC could improve the diagnostic accuracy of LNM and would be helpful in image surveillance of these patients

White Matter Injury After Intracerebral Hemorrhage

Spontaneous intracerebral hemorrhage (ICH) accounts for 15% of all stroke cases. ICH is a devastating form of stroke associated with high morbidity, mortality, and disability. Preclinical studies have explored the mechanisms of neuronal death and gray matter damage after ICH. However, few studies have examined the development of white matter injury (WMI) following ICH. Research on WMI indicates that its pathophysiological presentation involves axonal damage, demyelination, and mature oligodendrocyte loss. However, the detailed relationship and mechanism between WMI and ICH remain unclear. Studies of other acute brain insults have indicated that WMI is strongly correlated with cognitive deficits, neurological deficits, and depression. The degree of WMI determines the short- and long-term prognosis of patients with ICH. This review demonstrates the structure and functions of the white matter in the healthy brain and discusses the pathophysiological mechanism of WMI following ICH. Our review reveals that the development of WMI after ICH is complex; therefore, comprehensive treatment is essential. Understanding the relationship between WMI and other brain cells may reveal therapeutic targets for the treatment of ICH

The correlation of hippocampal T2-mapping with neuropsychology test in patients with Alzheimer's disease.

OBJECTIVES: 1) To deduce T2, the inverse of the transverse relaxation rate (R2), in the hippocampus of healthy adults; 2) to investigate the brain iron deposition in Alzheimer's disease (AD) patients and age-matched healthy controls using T2-values. METHODS: T2-weighted data from the bilateral-hippocampi of ten AD patients and sixty healthy controls were collected at six echo time points using multi-slice multi-echo turbo spin echo (MSME-TSE) imaging on a 3.0 T MR-scanner, followed by the neuropsychological testing. The correlations between T2-values and Mini-Mental State Examination (MMSE) scores were investigated on group-wise basis (covariates in the group-wise analyses: gender, age, side and healthy/AD). RESULTS: There were no significant differences in hippocampal T2-values on intra-gender and inter-gender basis (P > 0.05). Hippocampal T2-values of both sides were similar (right: 85.2±2.4 milliseconds; left: 85.3±2.5 milliseconds). The bilateral hippocampal T2 values correlated moderately with age (right: r = -0.59; left: -0.58; P < 0.001). The AD-group had significantly lower T2-values in the hippocampus when compared to normal controls (P < 0.001) and such low T2-values had a strong positive correlation with the MMSE score (R (2) = 0.97; P < 0.05). CONCLUSION: Patients with AD showed significantly lower T2 values, which can be attributed to the increased iron depositions in the hippocampus. A positive correlation between T2-values and cognition scores suggests that quantitative T2 can be used in the early diagnosis of AD and in the monitoring of the treatment response

Scatter plot of T₂ (or R₂)-values of hippocampus vs. MMSE score.

<p>Scatter plot shows the T₂ (or R₂)-values of the hippocampus and the MMSE score in AD patients were positively (or negatively) correlated with a coefficient of determination of 0.97 (or 0.95) (<i>P</i> < 0.05 for both) controlling for the age related bias.</p

Scatter plots of T₂-values in bilateral hippocampus of normal controls at various ages.

<p>Scatter plots illustrate T₂ values on both sides of hippocampus correlated moderately with age in normal controls. The correlation coefficients are -0.59 and -0.58 for right side (A) and left side (B), respectively at <i>P</i> < 0.001.</p

T₂-weighted images at various echo time-points and resultant T₂-map.

<p>Row 1 & Row 2 consist of six T₂-weighted images, taken at echo times of 20, 40, 60, 80, 100, and 120 ms, covering the entire hippocampus of an AD patient and an elderly control. The single image in Row 3 is the corresponding T₂ map. The bilateral hippocampal atrophy was visually found accompanied with a varied degree of decreased T₂ values (or increased R₂ values) in the AD patient. Illustration of the ROI selection on the representative spin-echo images (TE = 60, 80, 100 and 120 milliseconds) of a patient with AD and an elderly control. The hippocampal region for which T₂ data were acquired is shown as representative regions of interest. Note: ROIs required include the hippocampal contours to be as large as possible but not involving its boundaries, and avoiding visible cystic areas and CSF in the hippocampal fissure.</p

Activation of Nurr1 with Amodiaquine Protected Neuron and Alleviated Neuroinflammation after Subarachnoid Hemorrhage in Rats

Background. Nurr1, a member of the nuclear receptor 4A family (NR4A), played a role in neuron protection, anti-inflammation, and antioxidative stress in multidiseases. We explored the role of Nurr1 on subarachnoid hemorrhage (SAH) progression and investigated the feasibility of its agonist (amodiaquine, AQ) as a treatment for SAH. Methods. SAH rat models were constructed by the endovascular perforation technique. AQ was administered intraperitoneally at 2 hours after SAH induction. SAH grade, mortality, weight loss, neurological performance tests, brain water content, western blot, immunofluorescence, Nissl staining, and qPCR were assessed post-SAH. In vitro, hemin was introduced into HT22 cells to develop a model of SAH. Results. Stimulation of Nurr1 with AQ improved the outcomes and attenuated brain edema. Nurr1 was mainly expressed in neuron, and administration of AQ alleviated neuron injury in vivo and enhanced the neuron viability and inhibited neuron apoptosis and necrosis in vitro. Besides, AQ reduced the amount of IL-1β+Iba-1+ cells and inhibited the mRNA level of proinflammatory cytokines (IL-1β and TNF-α) and the M1-like phenotype markers (CD68 and CD86). AQ inhibited the expression of MMP9 in HT22 cells. Furthermore, AQ reduced the expression of nuclear NF-κB and Nurr1 while increased cytoplasmic Nurr1 in vivo and in vitro. Conclusion. Pharmacological activation of Nurr1 with AQ alleviated the neuron injury and neuroinflammation. The mechanism of antineuroinflammation may be associated with the Nurr1/NF-κB/MMP9 pathway in the neuron. The data supported that AQ might be a promising treatment strategy for SAH