Identifying diabetes from conjunctival images using a novel hierarchical multi-task network.

Diabetes can cause microvessel impairment. However, these conjunctival pathological changes are not easily recognized, limiting their potential as independent diagnostic indicators. Therefore, we designed a deep learning model to explore the relationship between conjunctival features and diabetes, and to advance automated identification of diabetes through conjunctival images. Images were collected from patients with type 2 diabetes and healthy volunteers. A hierarchical multi-tasking network model (HMT-Net) was developed using conjunctival images, and the model was systematically evaluated and compared with other algorithms. The sensitivity, specificity, and accuracy of the HMT-Net model to identify diabetes were 78.70%, 69.08%, and 75.15%, respectively. The performance of the HMT-Net model was significantly better than that of ophthalmologists. The model allowed sensitive and rapid discrimination by assessment of conjunctival images and can be potentially useful for identifying diabetes.

Optical Coherence Tomography Angiography as a Noninvasive Assessment of Cerebral Microcirculatory Disorders Caused by Carotid Artery Stenosis.

PURPOSE: Using retinal optical coherence tomography angiography (OCTA), we aimed to investigate the changes in important indicators of cerebral microcirculatory disorders, such as the properties of the radial peripapillary capillaries, vascular complexes, and the retinal nerve fiber layer, caused by carotid stenosis and postoperative reperfusion. METHODS: In this prospective longitudinal cohort study, we recruited 40 carotid stenosis patients and 89 healthy volunteers in the First Affiliated Hospital of Harbin Medical University (Harbin, China). Eyes with ipsilateral carotid stenosis constituted the experimental group, while the fellow eyes constituted the contralateral eye group. Digital subtraction angiography, CT perfusion imaging (CTP), and OCTA examinations were performed in all subjects. The vessel density of the radial peripapillary capillaries (RPC), superficial retinal vascular complexes (SVC), deep vascular complexes (DVC), choriocapillaris (CC), and the thickness of the retinal nerve fiber layer (RNFL) were assessed. Propensity-matched analysis was undertaken to adjust for covariate imbalances. Intergroup comparative analysis was conducted, and the paired sample t-test was used to evaluate the preoperative and postoperative changes in OCTA variables. RESULTS: The ocular vessel density in the experimental group was significantly lower than that in the control group (RPC: 55.95 vs. 57.24, P = 0.0161; SVC: 48.65 vs. 52.22, P = 0.0006; DVC: 49.65 vs. 57.50, P < 0.0001). Participants with severe carotid stenosis have reduced contralateral ocular vessel density (RPC 54.30; SVC 48.50; DVC 50.80). Unilateral stenosis removal resulted in an increase in vessel density on both sides, which was detected by OCTA on the 4th day (RPC, P < 0.0001; SVC, P = 0.0104; DVC, P = 0.0104). Moreover, the ocular perfusion was consistent with that established by CTP. CONCLUSION: OCTA can be used for sensitive detection and accurate evaluation of decreased ocular perfusion caused by carotid stenosis and may thus have the potential for application in noninvasive detection of cerebral microcirculation disorders. This trial is registered with NCT04326842.

Quantitative analysis of retinal vessel density and thickness changes in diabetes mellitus evaluated using optical coherence tomography angiography: a cross-sectional study.

BACKGROUND: Diabetic retinopathy is the most common microvascular complication of diabetes; however, early changes in retinal microvessels are difficult to detect clinically, and a patient's vision may have begun to deteriorate by the time a problem is identified. Optical coherence tomography angiography (OCTA) is an innovative tool for observing capillaries in vivo. The aim of this study was to analyze retinal vessel density and thickness changes in patients with diabetes. METHODS: This was a retrospective, observational cross-sectional study. Between August 2018 and February 2019, we collected OCTA data from healthy participants and diabetics from the First Affiliated Hospital of Harbin Medical University. Analyzed their retinal vessel density and thickness changes. RESULTS: A total of 97 diabetic patients with diabetes at different severity stages of diabetic retinopathy and 85 controls were involved in the experiment. Diabetic patients exhibited significantly lower retinal VD (particularly in the deep vascular complexes), thickening of the neurosensory retina, and thinning of the retinal pigment epithelium compared with controls. In the control group, nondiabetic retinopathy group and mild diabetic retinopathy group, superficial VD was significantly correlated with retinal thickness (r = 0.3886, P < 0.0001; r = 0.3276, P = 0.0019; r = 0.4614, P = 0.0024, respectively). CONCLUSIONS: Patients with diabetes exhibit ischemia of the retinal capillaries and morphologic changes in vivo prior to vision loss. Therefore, OCTA may be useful as a quantitative method for the early detection of diabetic retinopathy.

Long Noncoding RNA LINC01485 Promotes Tumor Growth and Migration via Inhibiting EGFR Ubiquitination and Activating EGFR/Akt Signaling in Gastric Cancer.

BACKGROUND: Although several long non-coding RNAs (lncRNAs) have been found to be involved in gastric cancer tumorigenesis, the more comprehensive contributions of lncRNAs to gastric cancer require further investigation. Here, we identify a cytoplasmic lncRNA, LINC01485, which promotes tumor growth and migration in gastric cancer. MATERIALS AND METHODS: Microarray and computational analysis were utilized to identify differential expression in LINC01485 and EGFR. Real-time PCR and Western blotting assays were used to confirm the expression of LINC01485 and EGFR in gastric cancer cells. Cell proliferation, wound-healing and transwell assays were performed to measure cell growth, migration and invasion. Immunoprecipitation, RNA pull-down, and RNA fluorescence in situ hybridization (RNA-FISH) assays were used to test the interaction of c-Cbl with LINC01485 and EGFR. Furthermore, tumor xenograft in nude mice was performed to test tumor growth in vivo. RESULTS: LINC01485 was upregulated and associated with tumor size, lymphatic metastasis and advanced pathological stage in gastric cancer. LINC01485 promoted gastric cancer cell proliferation, migration and invasion in vitro and in vivo. Furthermore, LINC01485 levels were positively correlated with EGFR expression in gastric cancer tissues and significantly increased the expression and phosphorylation (Tyr1045) of EGFR in gastric cancer cells. Mechanistically, LINC01485 competes with c-Cbl for binding to phosphorylated Tyr1045 site of EGFR, thus interfering with c-Cbl-mediated ubiquitination and subsequent degradation of EGFR. CONCLUSION: LINC01485 promoted EGFR stabilization and activation of EGFR/Akt signaling in gastric cancer. Our findings illustrate the diversity of cytoplasmic lncRNAs in signal transduction and highlight the important roles of lncRNAs in gastric cancer.

Cell-free DNA as a biomarker for colorectal cancer: a retrospective analysis in patients before and after surgery.

This study was aimed at investigating the potential of cell-free DNA (cfDNA) as a biomarker for colorectal cancer prognosis. Sixty patients with colorectal cancer who had not undergone surgery were enrolled as study group. Their peripheral blood samples were collected, and peripheral blood of 30 healthy volunteers (control) was collected. The cfDNA concentration and integrity were determined using q-PCR so as to ascertain if cfDNA was associated with clinical presentations of the disease. Then, the specificities and sensitivities of cfDNA, CFA and CA199 were determined with ROC curve. The level and integrity of cfDNA in patients with colorectal cancer before surgery were significantly higher than those in patients with colorectal cancer after surgery, and cfDNA concentration of colorectal cancer patients after surgery was also significantly higher than that in healthy control group. However, the integrity was not significantly different from that of control group. There was a significant correlation between cfDNA concentration and TNM stage, differentiation degree and CEA expression, while cfDNA integrity was significantly correlated with TNM stage and degree of differentiation. Moreover, specificity and sensitivity of cfDNA concentration and integrity were higher than those of CEA and CA199. The TNM stage and cfDNA concentration were independent risk factors for progression-free survival (PFS) in colorectal cancer patients. In conclusion, cfDNA concentration and integrity were more sensitive and specific than traditional tumor markers (CA199, CEA). Thus, changes in cfDNA changes can be effectively used to determine the prognosis of postoperative colorectal cancer patients.

Long noncoding RNA KCNQ1OT1 induces pyroptosis in diabetic corneal endothelial keratopathy.

Diabetic corneal endothelial keratopathy is an intractable ocular complication characterized by corneal edema and endothelial decompensation, which seriously threaten vision. It has been suggested that diabetes is associated with pyroptosis, a type of programmed cell death via the activation of inflammation. Long noncoding RNA KCNQ1OT1 is commonly associated with various pathophysiological mechanisms of diabetic complications, including diabetic cardiomyopathy and diabetic retinopathy. However, whether KCNQ1OT1 is capable of regulating pyroptosis and participates in the pathogenesis of diabetic corneal endothelial keratopathy remains unknown. The aim of this study was to investigate the mechanisms of KCNQ1OT1 in diabetic corneal endothelial keratopathy. Here, we reveal that KCNQ1OT1 and pyroptosis can be triggered in diabetic human and rat corneal endothelium, along with the high glucose-treated corneal endothelial cells. However, miR-214 expression was substantially decreased in vivo and in experiments with cultured cells. LDH assay was also used to verify the existence of pyroptosis in high glucose-treated cells. Bioinformatics prediction and luciferase assays showed that KCNQ1OT1 may function as a competing endogenous RNA binding miR-214 to regulate the expression of caspase-1. To further analyze the KCNQ1OT1-mediated mechanism, miR-214 mimic and inhibitor were introduced into the high glucose-treated corneal endothelial cells. The results showed that upregulation of miR-214 attenuated pyroptosis; conversely, knockdown of miR-214 promoted it. In addition, KCNQ1OT1 knockdown by a small interfering RNA decreased pyroptosis factors expressions but enhanced miR-214 expression in corneal endothelial cells. To understand the signaling mechanisms underlying the prepyroptotic properties of KCNQ1OT1, si-KCNQ1OT1 was cotransfected with or without miR-214 inhibitor. The results showed that pyroptosis was repressed after silencing KCNQ1OT1 but was reversed by cotransfection with miR-214 inhibitor, suggesting that KCNQ1OT1 mediated pyroptosis induced by high glucose via targeting miR-214. Therefore, the KCNQ1OT1/miR-214/caspase-1 signaling pathway represents a new mechanism of diabetic corneal endothelial keratopathy progression, and KCNQ1OT1 could potentially be a novel therapeutic target.

Linc00441 interacts with DNMT1 to regulate RB1 gene methylation and expression in gastric cancer.

Recent studies revealed that several Long noncoding RNAs (LncRNAs) are associated with progression of gastric cancer (GC), while the functional role and molecular mechanism of many GC-associated lncRNAs remain undetermined. The tumor suppressor-gene retinoblastoma gene (RB1) was decreased in several human cancers including gastric cancer (GC). In this study, we investigated whether Linc00441 was involved in the suppression of RB1. Our findings showed that the up-regulated Linc00441 was inversely correlated with RB1 expression in human GC tumor samples. The gain- and loss-of-function investigation revealed that Linc00441 could promote the proliferation of GC cells. Furthermore, RNA pull down and RIP assays demonstrated that Linc00441 could recruit DNMT1 to the RB1 promoter and suppressed RB1 expression in GC cells. In conclusion, our findings revealed that Linc00441 played crucial role in GC progression and suggested that Linc00441 was potentially an effective target for GC therapy in the future.

The polymorphism in miR-25 attenuated the oncogenic function in gastric cancer.

miR-25 was identified as an essential oncogene by promoting the growth and metastasis through TOB1 in gastric cancer (GC). The function of the single nucleotide polymorphism (SNP) located in the mature region of miR-25 (rs41274221) has not been investigated. In this study, we aimed to explore the involvement of rs41274221 in miR-25 in gastric cancer. We found that SNP rs41274221 in miR-25 was participated in the occurrence of GC by acting as a tumor protective factor associating with the tumor growth and metastasis. Besides, further investigation found that upregulation of miR-25 with AA genotype could attenuate the proliferation and invasion of tumor cells caused by wild-type miR-25. The dual-luciferase reporter assay also confirmed that miR-25 harbored the A allele which caused an incapacitation of binding at the TOB1. In conclusion, rs41274221 in miR-25 was a subgroup which may protect the patients from further growth and metastasis of gastric cancer and might serve as a novel biomarker for the disease.

[Co-inhibition effect of 17-DMAG and oxaliplatin on proliferation and invasion of colorectal cancer cells].

OBJECTIVE: To explore the effect of heat shock protein 90 (HSP90) inhibitor (17-DMAG) and oxaliplatin on the proliferation and invasion of colorectal cancer. METHODS: After 17-DMAG, oxaliplatin and half-dose combination of 2 drugs processing colorectal cancer SW480 and HCT116 cell lines, CCK8 assay was applied to detect cell viability. RT-PCR and Western blot were used to detect the expression level of the apoptosis-related molecules. Transwell chemokine axis experiment and Western blot were employed to detect cell invasion ability and the expression level of tumor metastasis-associated protein. RESULTS: The growth of SW480 and HCT116 cells was inhibited after the administration of 17-DMAG and oxaliplatin(P<0.05) in dose- and time-dependent manner. Processed by 17-DMAG 100 nmol/L, oxaliplatin 50 mg/L and half-dose combination of 2 drugs, transcription level of the apoptosis inhibitory gene (Bcl-2) in SW480 and HCT116 cells was decreased, the level of apoptosis promoting gene (Bax) transcription and protein PARP-1 spliceosome expression was increased, and the above trend was more obvious when using half-dose combination of 2 drugs. Transwell chemokine axis experiments showed the penetrating relative percentage and expression level of MMP9 and integrin ß3 decreased, especially for half-dose combination of 2 drugs. CONCLUSION: 17-DMAG and oxaliplatin can co-inhibit the proliferation and invasion of colorectal cancer.

Cullin1 is a novel prognostic marker and regulates the cell proliferation and metastasis in colorectal cancer.

PURPOSE: To investigate the precise function of Cullin1 (CUL1) in colorectal cancer (CRC). METHODS: Immunohistochemistry was performed to test the expression of CUL1 on a CRC tissue microarray containing the tumor and corresponding normal tissues. Simultaneously, the correlation of CUL1 expression with clinicopathological parameters and survival was evaluated. CUL1 was over-expressed or knocked down in HCT116 and SW480 cells, then the cell proliferation, migration and invasion assays in vitro and in vivo were performed. RESULTS: In this study, we found that CUL1 expression was significantly up-regulated in CRC compared with normal colon tissues. High CUL1 expression was positively associated with lymph node metastasis (P = 0.007) and tumor diameter (P = 0.052). Multivariate Cox regression analysis revealed that high CUL1 expression was an independent unfavorable prognostic factor for CRC patients (HR = 13.9, 95% confidence interval = 5.89-32.6, P < 0.001). Moreover, we found that CUL1 over-expression induced CRC cell proliferation and the growth of xenografts in nude mice via the changing of cell-cycle proteins. In addition, increased CUL1 expression in CRC cells significantly promoted cell migration and invasion abilities in vitro and peritoneal metastasis in vivo through inducing high expression of MMPs. CONCLUSION: Our findings imply that CUL1 may serve as promising prognostic markers in CRC patients.

PKM2 gene regulates the behavior of pancreatic cancer cells via mitogen-activated protein kinase pathways.

The aim of the current study was to investigate the effect of the PKM2 gene on the proliferation, invasion, migration and apoptosis of Panc­1 and Sw1990 pancreatic cancer cells via its interaction with the mitogen­activated protein kinases (MAPKs) signaling pathways. The expression levels of PKM2 protein in pancreatic cancer cells and the corresponding normal tissues was determined with western blot analysis. Immunohistochemical analysis of PKM2 expression was carried out in paraffin­embedded sections of pancreatic cancer tissue. Two human pancreatic cancer cell lines were cultured in vitro, and a small interfering RNA (siRNA) was designed for the PKM2 gene and transfected into the cells. Cell proliferation was measured via an MTT assay, cell migration and invasion was measured via Transwell® chambers, and the effect of PKM2 on apoptosis was detected from B­cell lymphoma 2 (Bcl­2) and Bcl­2­associated X protein expression levels. Protein expression levels of the MAPK pathway proteins extracellular signal­regulated kinase 1/2 (ERK1/2), p38 and c­Jun N­terminal kinase (JNK) and their phosphorylated forms were measured via western blot analysis. The expression level of PKM2 was significantly upregulated in the pancreatic cancer tissue compared with that of the corresponding normal tissue. Downregulation of PKM2 expression reduced the proliferation, migration and invasion of pancreatic cancer cell lines, while increasing the levels of apoptosis. Additionally, the expression levels of the phosphorylated­(p­)ERK1/2 and p­p38 of the MAPK pathway in the PKM2 siRNA groups were markedly downregulated compared with those of the controls; however, the expression levels of ERK1/2, p38, JNK, p­p38 and p­JNK had no significantly changes compared with those of the control groups. In summary, the PKM2 gene has an important role in the proliferation, invasion, migration and apoptosis of Panc­1 and Sw1990 pancreatic cancer cells, which may be associated with the expression of ERK1/2 and p38 of the MAPK signaling cascade.

JWA gene regulates PANC-1 pancreatic cancer cell behaviors through MEK-ERK1/2 of the MAPK signaling pathway.

The present study aimed to investigate the role of JWA gene in the proliferation, apoptosis, invasion and migration of PANC-1 pancreatic cancer cells and the effect on the MAPK signaling pathway. Human PANC-1 pancreatic cancer cells were cultured in vitro, and small interfering RNA (siRNA) was designed for the JWA gene. The siRNA was transfected into PANC-1 cells. Subsequently, the cell proliferation was measured by MTT assay; cell apoptosis was detected by analyzing BAX and Bcl-2 protein expression; cell migration and invasion were measured using Transwell® chambers; and the protein expression of JWA and ERK1/2, JNK and p38 and their phosphorylated forms were measured by western blotting. By utilizing the MTT assay, the results showed that when JWA protein expression was inhibited, the proliferation of PANC-1 cells was enhanced. In addition, the expression of apoptosis-associated protein (AAP) BAX was substantially decreased, while the expression of the apoptosis inhibitor gene, Bcl-2, was significantly enhanced. Using Transwell chambers, it was found that the number of penetrating PANC-1 cells was significantly increased after transfection with JWA siRNA, suggesting that the migration and invasion of the cells was substantially increased. By studying the association between JWA and the MAPK pathway in PANC-1 cells, it was found that the expression of p-ERK1/2 of the MAPK pathway was significantly downregulated following JWA siRNA transfection. However, the expression levels of ERK1/2, JNK, p38, p-JNK and p-p38 showed no significant differences. In conclusion, it was shown that JWA affects the proliferation, apoptosis, invasion and migration of PANC-1 pancreatic cancer cells which could be attributed to effects on the expression of ERK1/2 in the MAPK pathway.

Clinicopathological and prognostic significance of galectin-1 and vascular endothelial growth factor expression in gastric cancer.

AIM: To evaluate the expression of galectin-1 and vascular endothelial growth factor (VEGF) in gastric cancer and investigate their relationships with clinicopathologic factors and prognostic significance. METHODS: Galectin-1 and VEGF were immunohistochemically investigated in tumor samples obtained from 214 gastric cancer patients with all tumor stages. Immunohistochemical analyses for galectin-1 and VEGF expression were performed on formalin-fixed, paraffin-embedded sections of surgical specimens. The relationship between the expression and staining intensity of galectin-1 and VEGF, clinicopathologic variables, and patient survival were analyzed. All patients underwent follow-up until cancer-related death or more than five years after tumor resection. P values < 0.05 were considered statistically significant. RESULTS: Immunohistochemical staining demonstrated that 138 of 214 gastric cancer samples (64.5%) were positive for galectin-1, and 116 out of 214 gastric cancer samples (54.2%) were positive for VEGF. There was a significant association between galectin-1 and VEGF expression; VEGF was detected in 60.1% of galectin-1-positive samples and 43.4% of galectin-1-negative samples (P < 0.05). Galectin-1 expression was associated with tumor size, tumor location, stage, lymph node metastases, and VEGF expression (all P < 0.05). VEGF expression was related to tumor size, stage, and lymph node metastases (all P < 0.05). The 5-year survival rate was 56.6% for galectin-1-positive patients and 69.2% for galectin-1-negative patients, and the prognosis for galectin-1-positive patients was significantly poorer compared with galectin-1-negative patients (χ² = 13.880, P = 0.000). The 5-year survival rates for VEGF-positive and VEGF-negative patients were 53.4% and 70.5%, respectively (χ² = 4.619, P = 0.032). The overall survival rate of patients with both galectin-1 and VEGF overexpression in gastric cancer tissue samples was significantly poorer than other groups (both P < 0.05). CONCLUSION: Galectin-1 expression was positively associated with VEGF expression. Both galectin-1 and VEGF can serve as independent prognostic indicators of poor survival for gastric cancer after gastrectomy.

Temporary ileostomy versus colostomy for colorectal anastomosis: evidence from 12 studies.

OBJECTIVE: To assess the safety and efficacy of temporary ileostomy and temporary colostomy after a low anterior resection for rectal cancer by comparing the postoperative complications, then investigate which type of stoma is better. MATERIAL AND METHODS: Studies comparing temporary ileostomy with colostomy for colorectal anastomosis were searched. The rates of complications (i.e., clinical anastomotic leak or fistula, stoma prolapse, parastomal hernia, wound infection related to stoma closure, obstruction following stoma closure, and skin trouble) were pooled and compared using a meta-analysis. The risk ratios (RRs) were calculated with 95% confidence intervals (CIs). RESULTS: The study included five randomized controlled trials (RCTs) and seven non-randomized studies involving 1687 patients. The meta-analysis of the RCTs demonstrated a lower risk of stoma prolapse (RR 0.15; 95% CI: 0.04-0.48) in the temporary ileostomy group. Meta-analysis of the non-randomized studies showed a lower risk of stoma prolapse and wound infection after stoma closure in the temporary ileostomy group (both p < 0.05). CONCLUSIONS: Temporary ileostomy has a minor impact on patients; we endorse temporary ileostomy over colostomy after a low anterior resection for rectal cancer.

Expression of ADAM8 and its clinical values in diagnosis and prognosis of hepatocellular carcinoma.

ADAM8 behaves as an active metalloprotease in vitro, hydrolyzing myelin basic protein and a variety of peptide substrates based on the cleavage sites of membrane-bound cytokines, growth factors, and receptors. Other studies have demonstrated overexpression of some ADAM family proteins in a variety of human tumors, but no report is available on the actual expression of ADAM8 and the correlation between clinicopathologic features and prognosis of hepatocellular carcinoma (HCC) patients. In this study, serum levels of ADAM8 were measured by ELISA in 126 patients with HCC, 50 patients with liver cirrhosis (LC), and 50 healthy individuals. The expression of ADAM8 in liver tissue was further studied using Western blotting in 126 patients with HCC and 50 with LC. The correlations between ADAM8 status and various clinicopathological parameters including survival were analyzed. Survival analysis was performed using the Kaplan-Meier method and Cox's proportional hazards model. The ELISA assay showed that the serum levels of ADAM8 in the HCC, LC, and healthy groups were 136.4 ± 34.5, 64.2 ± 20.1, and 63.2 ± 22.7 U/ml, respectively. Analysis of variance was used for inter-group comparison, and differences were found between the HCC group and the other two groups (both P < 0.001), while no difference was found between the LC group and the healthy group (P = 0.365). Western blotting assay showed that ADAM8 protein expression was detected in 62.7 % (79/126) HCC and in 32 % (16/50) LC tissues. Further, ADAM8 expression was associated closely with serum AFP elevation, tumor size, histological differentiation, tumor recurrence, tumor metastasis, and tumor stage. Kaplan-Meier survival analysis showed that patients with ADAM8-positive tumors had a shorter postoperative survival time than those with ADAM8-negative tumors (P < 0.001). Multivariate analysis revealed that ADAM8 expression was an independent prognostic parameter for the overall survival rate of HCC patients. These findings provide evidence that the expression of ADAM8 serves as a poor prognostic biomarker for HCC. ADAM8 may be a potential target of antiangiogenic therapy for HCC.

High RIN1 expression is associated with poor prognosis in patients with gastric adenocarcinoma.

The aim of this study was to investigate the expression and prognostic significance of RIN1 in gastric adenocarcinoma. RIN1 expression was analyzed using quantitative real-time PCR (qRT-PCR), Western blotting, and immunohistochemical staining on tissue samples from a consecutive series of 315 gastric adenocarcinoma patients who underwent tumor resections between 2003 and 2006. The relationship between RIN1 expression, clinicopathological factors, and patient survival was investigated. qRT-PCR results showed that the RIN1 mRNA expression was higher in tumor tissue samples than in the adjacent normal tissues, and a corresponding increase in protein expression was confirmed by Western blotting. Immunohistochemical staining indicated that RIN1 is highly expressed in 54.3 % of gastric adenocarcinomas. RIN1 expression levels were closely associated with tumor size, histological differentiation, tumor stage, and lymph node involvement. Kaplan-Meier survival analysis showed that high RIN1 expression exhibited a significant correlation with poor prognosis for gastric adenocarcinoma patients. Multivariate analysis revealed that RIN1 expression is an independent prognostic parameter for the overall survival rate of gastric adenocarcinoma patients. Our data suggest that RIN1 plays an important role in gastric adenocarcinoma progression and that a high RIN1 expression predicts an unfavorable prognosis in gastric adenocarcinoma patients.

Relationship between computed tomography manifestations of thymic epithelial tumors and the WHO pathological classification.

OBJECTIVE: To explore the relationship between computed tomography (CT) manifestations of thymoma and its WHO pathological classification. METHODS: One hundred and five histopathologically confirmed cases were collected for their pathological and CT characteristics and results were statistically compared between different pathological types of thymoma. RESULTS: Tumor size, shape, necrosis or cystic change, capsule integrity, invasion to the adjacent tissue, lymphadenopathy, and the presence of pleural effusion were significantly different between different pathological types of thymomas (P<0.05). Type B2, B3 tumors and thymic carcinomas were greater in size than other types. More than 50% of type B3 tumors and thymic carcinomas had a tumor size greater than 10 cm. The shape of types A, AB, and B1 tumors were mostly round or oval, whereas 75% of type B3 tumors and 85% of thymic carcinomas were irregular in shape. Necrosis or cystic change occurred in 67% of type B3 thymomas and 57% of thymic carcinomas, respectively. The respective figures for capsule destruction were 83% and 100%. Increases in the degree of malignancy were associated with increases in the incidence of surrounding tissue invasion: 33%, 75%, and 81% in type B2, type B3, and thymic carcinomas, respectively. Pleural effusion occurred in 48% of thymic carcinomas, while calcification was observed mostly in type B thymomas. CONCLUSIONS: Different pathological types of thymic epithelial tumors have different CT manifestations. Distinctive CT features of thymomas may reflect their pathological types.