Correlation between gastritis cystica profunda and the risk of lymph node metastasis in early gastric cancer.

In early gastric cancer (EGC) patients, lymph node metastasis (LNM) risk assessment is particularly important for the selection of surgical methods. In this study, we investigated the correlation between gastritis cystica profunda (GCP) and the risk of LNM in EGC. From January 2014 to December 2019, EGC patients who underwent curative radical gastrectomy were enrolled in this study. The clinicopathological features were analyzed, and the correlation between GCP and the risk of lymph node metastasis was assessed. Data for 180 EGC patients were analyzed, and 17.8% (32/180) had LNM. The incidence of LNM was 2.6% in the GCP-positive group and 21.8% in the GCP-negative group. Univariate analysis revealed that GCP, depth of tumor invasion, and lymphovascular invasion were the risk factors of LNM in EGC patients. Multiple regression analysis showed that GCP was associated with the risk of LNM in EGC patients (OR=0.097, 0.121, 0.100, p<0.05). The curve fitting results showed that there was a negative correlation between the GCP and LNM in EGC, which was consistent between different tumor sites, size, ulceration, differentiation types, depth of tumor invasion, lymphovascular invasion, and no significant interaction was found among these factors (p for interaction range 0.224-0.717). GCP is closely related to LNM in EGC. Preoperative assessment of whether EGC is combined with GCP is beneficial for the assessment of the risk of LNM.

Using quantitative imaging to determine the correlation between hypothalamic inflammation and anxiety and depression in young patients with obesity.

BACKGROUND: To investigate the incidence of anxiety and depressive disorders in young adults with obesity and the correlation between the severity of these disorders and hypothalamic inflammation. METHODS: The severity of anxiety and depressive disorders was assessed using the Self-Rating Anxiety Scale (SAS) and Self-Rating Depression Scale (SDS), respectively. Hypothalamic inflammation was evaluated by measuring the hypothalamus/amygdala (H/A) signal intensity (SI) ratio in T2-weighted phase quantitative magnetic resonance imaging (MRI). RESULTS: The incidence of depressive disorders in young (18-45 years) patients with obesity (n=66) was higher than that in the control group (n=44); anxiety disorder incidence did not differ significantly between groups. The bilateral H/A SI ratio in the obesity group was significantly higher than that in the control group. In the obesity group, there was no significant correlation between bilateral H/A SI ratio and body mass index (BMI) (right: r=-0.145, P=0.721; left: r=0.102, P=0.415) or SAS scores (right: r=-0.118, P=0.444; left: r=-0.295, P=0.052); SDS scores were significantly correlated with left H/A SI ratio (r=-0.353, P=0.019), but not right H/A SI ratio (r=-0.031, P=0.843). CONCLUSIONS: Patients with obesity had a higher incidence of depressive disorders. Left hypothalamus inflammation may be one of the links between obesity and depressive disorders.

Ankaflavin ameliorates steatotic liver ischemia-reperfusion injury in mice.

BACKGROUND: It is well-known that steatotic liver is more susceptible to ischemia-reperfusion (I/R) injury during liver transplantation, liver resection and other liver surgeries. The increasing incidence of non-alcoholic fatty liver disease (NAFLD) decreases the availability of liver donors. Although steatotic liver is now accepted as a source of liver for transplantation, NAFLD exacerbates the liver injury after liver surgery. The present study was to investigate the protective role of ankaflavin in steatotic liver I/R injury. METHODS: The model of fatty liver mice was induced with high fat diet in four weeks, ankaflavin or vehicle (saline) was administrated by gavage once a day for one week. The animals were subjected to partial hepatic I/R. Blood samples were collected to measure serum aminotransferases. The liver tissues were used to examine liver steatosis, apoptosis of hepatocytes, hepatic oxidative stress, Kupffer cells and inflammatory cytokines. The effects of ankaflavin on inflammatory cytokines were evaluated in isolated Kupffer cells from the steatotic liver. RESULTS: Ankaflavin reduced liver steatosis in high fat diet mice. Compared with normal mice, I/R induced more damage to the mice with steatosis, such as hepatocyte apoptosis, inflammatory cytokines (TNF-alpha, IL-6 and IL-1 beta), serum aminotransferases and thiobarbituric acid reactive substances. Importantly, ankaflavin administration significantly attenuated these changes. In addition, ankaflavin significantly decreased the proliferation of Kupffer cells and the expression of TNF-alpha, IL-6 and IL-1 beta protein in isolated Kupffer cells stimulated by TNF-alpha. CONCLUSION: Ankaflavin has protective effects against I/R injury through anti-inflammatory, anti-oxidant and anti-apoptotic mechanisms in fatty livers, these effects are at least partially mediated by inhibiting Kupffer cell functions.