A novel framework for tongue feature extraction framework based on sublingual vein segmentation.

The features of the sublingual veins, including swelling, varicose patterns, and cyanosis, are pivotal in differentiating symptoms and selecting treatments in Traditional Chinese Medicine (TCM) tongue diagnosis. These features serve as a crucial reflection of the human blood circulation status. Nevertheless, the automatic and precise extraction of sublingual vein features remains a formidable challenge, constrained by the scarcity of datasets for sublingual images and the interference of noise from non-tongue and non-sublingual vein elements. In this paper, we present an innovative tongue feature extraction method that relies on focusing specifically on segmenting the sublingual vein rather than the entire tongue base. To achieve this, we have developed a sublingual vein segmentation framework utilizing a Polyp-PVT network, effectively eliminating noise from the surrounding regions of the sublingual vein. Furthermore, we pioneer the utilization of a transformer-based approach, such as the Swin-Transformer network, to extract sublingual vein features, leveraging the remarkable capabilities of transformer networks. To complement our methodology, we have constructed a comprehensive dataset of sublingual vein images, facilitating the segmentation and classification of sublingual veins. Experimental results have demonstrated that our tongue feature extraction method, coupled with sublingual vein segmentation, significantly outperforms existing tongue feature extraction techniques.

EGFR Cooperates with EGFRvIII to Recruit Macrophages in Glioblastoma.

: Amplification of the EGFR gene and its truncation mutant EGFRvIII are hallmarks of glioblastoma. Although coexpression of EGFR and EGFRvIII confers a growth advantage, how EGFR and EGFRvIII influence the tumor microenvironment remains incompletely understood. Here, we show that EGFR and EGFRvIII cooperate to induce macrophage infiltration via upregulation of the chemokine CCL2. EGFRvIII was significantly enriched in glioblastoma patient samples with high CCL2, and knockout of CCL2 in tumors coexpressing EGFR and EGFRvIII led to decreased infiltration of macrophages. KRAS was a critical signaling intermediate for EGFR- and EGFRvIII-induced expression of CCL2. Our results illustrate how EGFR and EGFRvIII direct the microenvironment in glioblastoma. SIGNIFICANCE: Full-length EGFR and truncated EGFRvIII work through KRAS to upregulate the chemokine CCL2 and drive macrophage infiltration in glioblastoma.

The Prognostic Value of HRAS mRNA Expression in Cutaneous Melanoma.

This study aimed to investigate the prognostic value of HRAS mRNA expression in cutaneous melanoma. Cutaneous melanoma is an aggressive cancer with an increasing incidence. Few studies have focused on the transcriptional level of RAS isoforms (KRAS, NRAS, and HRAS) in cutaneous melanoma. To gain further insight into RAS isoforms at transcriptional level, we obtained the cutaneous melanoma data from cBioPortal and investigated the RAS mRNA expression levels in different stages of melanoma and evaluated their correlation with clinical characteristics and patients' survival. Furthermore, we retrieved and analyzed the coexpression data and performed pathway enrichment analysis. Totally, 452 cutaneous melanoma cases were included in this study. We found that lower HRAS expression level was associated with longer patient survival. 206 genes that negatively correlated with HRAS expression were positively correlated with KRAS and NRAS expression. In contrast, no gene that positively correlated with HRAS expression was positively correlated with KRAS and NRAS expression. In conclusion, our data showed that transcriptional regulation was different for the three RAS isoforms in cutaneous melanoma. This study highlighted the prognostic value of HRAS mRNA expression and revealed that HRAS greatly differs from KRAS and NRAS at the transcriptional level.

Evaluation of a magnetic particles-based chemiluminescence enzyme immunoassay for Golgi protein 73 in human serum.

BACKGROUND: Golgi protein 73 (GP73) is regarded as a potential serum biomarker for early diagnosis of hepatocellular carcinoma (HCC). We developed a rapid magnetic particles-based chemiluminescence enzyme immunoassay (MPs-CLEIA) for the determination of serum GP73. METHODS: Fluorescein isothiocyanate (FITC) and alkaline phosphatase (ALP) were used to label 2 different monoclonal antibodies to GP73. Serum GP73 was captured with labeled antibodies and formed a sandwiched immunoreaction. The magnetic particles (MPs) coated with anti-FITC antibody were used as a means of separation of the GP73 protein from other serum proteins. After adding the enzyme substrate solution, the relative light unit (RLU) was measured. A MPs-CLEIA for serum GP73 was established and evaluated. RESULTS: The RLU was directly proportional to the concentration of GP73. The method linearity was 5-600 µg/l. Limit of the blank was 2.19 µg/l. The intra- and inter-assay imprecision was <3% and <5%, respectively. The average recoveries were between 95% and 105%. The proposed method showed a good correlation with a commercial ELISA assay (r=0.983, p<0.001). We also evaluated the efficiency of serum GP73 measurement for the diagnosis of HCC using this assay. The area under the receiver operating characteristic curve was 0.822 (95% CI, 0.73-0.89), and the sensitivity and specificity, with cut-off value of 115.6 µg/l, were 75.4% and 92.1%, respectively. CONCLUSIONS: The proposed method demonstrates an acceptable performance for quantifying serum GP73. This assay could be appropriate for routine use in clinical laboratories.

Human endogenous retroviral K element encodes fusogenic activity in melanoma cells.

INTRODUCTION AND HYPOTHESIS: Nuclear atypia with features of multi nuclei have been detected in human melanoma specimens. We found that the K type human endogenous retroviral element (HERV K) is expressed in such cells. Since cellular syncytia can form when cells are infected with retroviruses, we hypothesized that HERV K expressed in melanoma cells may contribute to the formation of multinuclear atypia cells in melanoma. EXPERIMENTS AND RESULTS: We specifically inhibited HERV K expression using RNA interference (RNAi) and monoclonal antibodies and observed dramatic reduction of intercellular fusion of cultured melanoma cells. Importantly, we identified loss of heterozygosity (LOH)of D19S433 in a cell clone that survived and proliferated after cell fusion. CONCLUSION: Our results support the notion that proteins encoded by HERV K can mediate intercellular fusion of melanoma cells, which may generate multinuclear cells and drive the evolution of genetic changes that provide growth and survival advantages.

Ten-year survey on oncology publications from China and other top-ranking countries.

BACKGROUND: Cancer is a global disease that knows no borders. Over the past decade, oncology research had developed rapidly worldwide. The aim of this study was to evaluate the publication characteristics in oncology journals from China and other top-ranking countries. METHODS: The present study was designed to study publication characteristics in oncology journals from China and other top-ranking countries, the United States (USA), Japan, Germany, the United Kingdom (UK) and France, from 2001 to 2010. We also examined the research output from the three different regions of China: the mainland of China, Hong Kong and Taiwan. RESULTS: Articles published in 163 journals related to oncology were retrieved from the PubMed database. The number of articles showed significantly positive trends for the six countries. The percentage of articles in the world output showed a significantly positive increase in contributions from China, especially the mainland of China. China contributed 4.5% of the total 163 journals, and 2.5% of the journals with the top 10% impact factor (IF) scores. USA contributed 31.4% of the total world output, 40.5% of the top 10% IF score journals and ranked the first. CONCLUSIONS: This analysis described the research output from each country and region of China, and revealed the positive trend in China during 2001 and 2010. Also, by contrast with other top-ranking countries, these results imply that China falls behind the others in conducting high-quality oncology research.

Golgi protein 73(GP73), a useful serum marker in liver diseases.

BACKGROUND: This study was performed to quantify the expression of Golgi protein-73 (GP73) in healthy controls and in patients with liver disease, and to evaluate the correlations between GP73 and other serum markers in different liver diseases. METHODS: Serum GP73 was measured in 478 healthy controls and 296 patients with different types of liver disease. Quantitative hepatitis B virus (HBV) DNA was determined in two chronic hepatitis B (CHB) groups. Other serum liver fibrosis markers were measured in the liver fibrosis group and α-fetoprotein (AFP) was measured in hepatocellular carcinoma (HCC) group. The correlations between GP73 and these markers were evaluated. RESULTS: The GP73 value in hepatitis B e antigen (HBeAg)-positive CHB group, HBeAg-negative CHB group, liver fibrosis group and HCC group was significantly higher (p<0.001) than that in healthy controls. GP73 showed significant correlation with other markers in the liver fibrosis group and with AFP in the HCC group. CONCLUSIONS: Compared with healthy controls, GP73 in patients with liver disease was significantly increased. With the progression of liver disease, GP73 showed a significantly increasing trend. These results suggest that GP73 might be used as a serum marker for the diagnosis of liver diseases and for monitoring disease progression.

Expression of HERV-K correlates with status of MEK-ERK and p16INK4A-CDK4 pathways in melanoma cells.

The dysregulated ERK and RB pathways often coexist in melanoma cells. The K-type human endogenous retrovirus (HERV-K) is implicated in melanomagenesis. Some of the phenotypes that are modified by HERV-K (e.g., changes in cell shape, melanin production, and anchorage-dependent growth) overlap with those that are regulated by ERK and RB pathways. As ERK signaling can regulate retroviruses, we hypothesized that HERV-K expression is controlled by ERK-RB pathways. We found that the levels of HERV-K GAG and EVE correlated with the activation of ERK and loss of p16INK4A and that inhibition of MEK or CDK4, especially in combination, reduced HERV-K EVE in melanoma cells.

[Relationship between copper injury and apoptosis and the effect of curcumin on copper-injured BRL cells].

OBJECTIVE: To study the relationship between copper-induced apoptosis and reactive oxygen species (ROS) in BRL cells and the effect of curcumin, a plant-derived polyphenol, on copper-injured BRL cells. METHODS: BRL cells were treated with CuSO4 (100 micromol/L) or curcumin + CuSO4. The BRL cells without any treatment were used as controls. Flow cytometry was applied to detect the production of ROS with fluorescent probe DCFH-DA. MTT colorimetry was used to evaluate cell activity. Apoptosis was measured using Hoechst 33258 staining and Annexin V-FITC and propidiumiodide (PI) staining. JNK/SAPK protein level was detected using Western blot. RESULTS: ROS levels (711.70 +/- 68.33 vs 87.22 +/- 7.58) and apoptosis rate (45.08 +/- 1.87% vs 8.23 +/- 2.56%) of BRL cells reached to a peak after 6 hrs of CuSO4 treatment, which were significantly higher than controls (P < 0.01). JNK/SAPK levels increased significantly after 6 hrs of CuSO4 treatment and peaked at 24 hrs of CuSO4 treatment compared with controls (P < 0.01). Curcumin pretreatment decreased significantly ROS and JNK/SAPK levels as well as the apoptosis rate when compared with the CuSO4-treated alone group (P < 0.01). CONCLUSIONS: Copper may induce apoptosis of BRL cells. ROS participated in apoptosis induced by copper. Curcumin produced protections on copper-injured BRL cells possibly by anti-oxidation and inhibition of p-JNK expression.