High-resolution non-confocal non-line-of-sight imaging based on spherical-slice transform from spatial and temporal frequency to space and time.

Current non-confocal non-line-of-sight (NLOS) imaging faces the problems of low resolution and limited scene adaptability. We propose a non-confocal NLOS imaging method based on spherical-slice transform from spatial and temporal frequency to space and time. Simulation and experimental results show that the proposed method has high-resolution reconstruction without artifact interference, shape distortion, and position offset. Furthermore, it has strong scene adaptability. After GPU acceleration, the reconstruction time of the proposed method can be reduced to several hundred milliseconds for the PF32 photon array camera with 32 × 32 detection units. In the future, the proposed method has great potential for application in real-time NLOS imaging systems.

The Safety and Efficacy of Apatinib Treatment in Addition to Concurrent Chemoradiotherapy in Patients with Nonoperative Locally Advanced Esophageal Squamous Cell Carcinoma.

BACKGROUND Esophageal cancer is a common gastrointestinal malignancy in China. We evaluated the efficacy and safety of adding Apatinib to concurrent chemoradiotherapy in patients with locally advanced esophageal squamous cell carcinoma. MATERIAL AND METHODS In this single-center retrospective study, we compared short-term efficacy, long-term efficacy, and adverse events between patients who received Apatinib and concurrent chemoradiotherapy (Apatinib group), and those who received only concurrent chemoradiotherapy (CCRT group). RESULTS Sixty-five patients with stage II and III esophageal squamous cell carcinoma were enrolled (31 in the Apatinib group, 34 in the CCRT group). After treatment, the therapy response rate (the sum of the complete and partial remission rates) was significantly higher in the Apatinib group than in the CCRT group (P=0.045); the complete remission rate was particularly higher in the Apatinib group. Median progression-free survival in the Apatinib group (12 months) was higher than that of the CCRT group (7 months), and the 1- and 2-year progression-free survival rates were significantly higher in the Apatinib group than in the CCRT group (47.0% vs. 30.3% and 20.2% vs. 12.1%, respectively; P=0.040). The main adverse effects of Apatinib treatment were elevated blood pressure, proteinuria, hand-foot syndrome, fatigue, and oral mucositis, all of which were level 1-2. Cox multivariate regression analysis indicated T stage and short-term efficacy were independent prognostic factors for overall and progression-free survival. CONCLUSIONS For patients with locally advanced esophageal squamous cell carcinoma, combining Apatinib with concurrent chemoradiotherapy can improve patient survival and significantly prolong progression-free survival, with tolerable adverse reactions.

Comparative study of dual energy CT iodine imaging and standardized concentrations before and after chemoradiotherapy for esophageal cancer.

BACKGROUND: To compare dual energy CT iodine imaging and standardized iodine concentration before and after chemoradiotherapy (CRT) for esophageal cancer and evaluate the efficacy of CRT for EC by examining DECT iodine maps and standard CT values. METHODS: The clinical data of 45 patients confirmed by pathology with newly diagnosed esophageal cancer who underwent concurrent CRT from February 2012 to January 2017 in our department of radiology were collected. All patients underwent dual-source dual-energy CT (DECT) before and after CRT. Normalized iodine concentration (NIC) and normalized CT (NCT) corresponding to the overall cancer lesion and its maximum cross-sectional area were observed and compared. Additionally, 30 healthy individuals were compared as control group. After treatment, the patients were divided into two groups according to RECIST1.1: treatment effective group and ineffective group. RESULTS: There were 33 patients (CR 9, PR 24) in the effective group and 12 patients (SD 12, PD 0) in the ineffective group. There was no significant difference in the NIC-A, NIC-V, NCT-A and NCT-A indexes between the effective group (B group) and the ineffective group (C group) before treatment (P > 0.05). After the treatment, the above-mentioned indexes in the effective group of patients were significantly lower than before treatment, and compared with the ineffective group, the NIC-A, NIC-V, NCT-A and NCT-V values of the effective group were significantly lower than those of ineffective group (P < 0.05). After treatment, the NIC-V and NCT-V in the ineffective group were lower than before treatment, and the difference was statistically significant (P < 0.05). However, their NIC-A and NCT-A were not statistically different from those before treatment (P > 0.05). CONCLUSION: Using DECT iodine map, the changes of NIC and NIC before and after CRT in patients with esophageal cancer can evaluate the effect of CRT, and does not increase the radiation dose, so it is suitable for clinical use.

[Radiobiological characteristics of cancer stem cells from esophageal cancer cell lines].

OBJECTIVE: To study the cancer stem cell populations in esophageal cancer cell lines KYSE150 and TE1 and identify whether resulting stem-like cell spheres display radiation resistance characteristics. METHODS: Serum-free medium (SFM) suspension was used to culture the esophageal cancer stem cell lines and enrich the esophageal stem-like cell spheres. RT-PCR assay was used to detect the stem cell gene expression in the sphere cells. Radiosensitivity of the sphere cells and parental cells were evaluated by clone formation assay. Different cells after irradiation at different doses were tested to evaluate the changes of sphere formation, and cell cycle and CD44(+)CD271(+) expression of the sphere cells were also analyzed by flow cytometry before and after irradiation. RESULTS: Cancer stem-like cell spheres were generated from KYSE150 and TE1 cells and enriched by culture in serum-free medium, and the number of spheres was increasing alone with the increase of cell passages. The numbers of spheres formed from the 1st, 2nd and 3rd generations of KYSE150 cells were 25 ± 2, 37 ± 2 and 47 ± 3, respectively. The numbers of spheres formed from the 1st, 2nd and 3rd generations of TE1 cells were 15 ± 3, 24 ± 3 and 36 ± 4, respectively. Certain doses of radiation increased the sphere formation rate. The average survival fraction (SF2) of the suspension-cultured KYSE150 stem-like cell spheres after 2 Gy irradiation were 0.81 ± 0.03 and 0.69 ± 0.04, while that of TE1 parental cells were 0.87 ± 0.01 and 0.80 ± 0.03 (P < 0.05 for all). In the esophageal parental KYSE150 and TE1 cells, arrest at G2 phase was induced after irradiation. After the same dose of irradiation, the inhibition of proliferation of the cancer stem cells was lower than that of the parent cells (P < 0.05). After 0, 4 and 8 Gy irradiation, the CD44(+)CD271(+) cell percentage of KYSE150 parental cells were (1.08 ± 0.03)%, (1.29 ± 0.07)% and (1.11 ± 0.09)%; the CD44(+)CD271(+) cell percentage of TE1 parental cells were (1.16 ± 0.11)%, (0.97 ± 0.08)% and (1.45 ± 0.35)% (P > 0.05 for all). After 0, 4 and 8 Gy irradiation, the percentage of CD44(+)CD271(+) cells of KYSE150 stem cell-like spheres were (35.83 ± 1.23)%, (44.90 ± 1.67)% and (57.77 ± 1.88)%, and that of TE1 stem cell-like spheres were (16.07 ± 0.91)%, (22.67 ± 1.12)% and (33.27 ± 1.07)%. Compared the 4 Gy and 8 Gy irradiated KYSE150 and TE1 stem-like cell spheres with the 0 Gy irradiated spheres, the differences were statistically significant (P < 0.05 for all). CONCLUSIONS: The cancer stem cells in KYSE150 and TE1 spheres are more radio-resistant than their parental cells. It may suggest that cancer stem cell populations in the esophageal cancer cells are related to the mechanism of occurrence of radioresistance.

Knowledge domains and emerging trends in radiotherapy in oesophageal cancer from 2004 to 2023: a bibliometric analysis and visualization study.

Esophageal cancer (EC) is a malignant tumour with high morbidity and mortality rates. Recent studies have shown that much progress has been made in the research of radiotherapy in EC. This study aims to provide a comprehensive overview of the knowledge structure and research hotspots of radiotherapy in EC through bibliometrics. Publications related to radiotherapy in EC from 2014 to 2023 were searched on the web of science core collection database. VOSviewers, CiteSpace and R package 'bibliometrix' were used to conduct this bibliometric analysis. In total, 4258 articles from 76 countries led by China and the USA were included. The Chinese Academy of Medical Sciences-Peking Union Medical College has the highest number of publications. International Journal of Radiation Oncology Biology Physics is the most popular journal and also the most co-cited journal in this field. These publications come from 21 972 authors among which Liao Zhongxing had published the most papers and Cooper JS was co-cited most often. Neoadjuvant chemoradiotherapy and strategies based on it are the main topics in this research field. 'IMRT' and 'immunotherapy' are the primary keywords of emerging research hotspots. This is a bibliometric study that comprehensively summarizes the research trends and developments of radiotherapy in EC. This information identifies recent research frontiers and hot directions, which will provide a reference for scholars studying radiotherapy in EC.

The role of tumor-associated macrophages in the radioresistance of esophageal cancer cells via regulation of the VEGF-mediated angiogenic pathway.

Tumor-associated macrophages (TAMs) are known to promote tumor growth, invasion, metastasis, and protumor angiogenesis, but the role of TAMs in evading radiotherapy in esophagus cancer remains unclear. In this study, we first induced TAMs from human monocytes (THP-1) and identified using immunofluorescence and Western blotting assays. We then co-cultured them with human esophageal cancer cell lines. CCK-8, colony formation, Transwell, scratch test, and TUNEL assays showed that TAMs could promote proliferation, survival rate, invasion, migration, and radioresistance and could inhibit apoptosis of the esophageal squamous carcinoma cell lines KYSE-150 and TE-1 before and after radiotherapy both in vivo and in vitro. Using LV-VEGFA-RNAi lentiviral vectors, we also found that TAMs could increase the expression of VEGFA and that inhibition of VEGFA could inhibit the biological function caused by TAMs. Finally, a Western blotting assay was used to evaluate the expression of various factors underlying the mechanism of TAMs. VEGFA, MAPK, P-MAPK, BCL-2, and Snail proteins were found to be overexpressed in co-cultured groups, whereas after VEGFA inhibition, MAPK, P-MAPK, BCL-2, and Snail proteins were found to be significantly downregulated in the radiotherapy group. These study results offer important information regarding the mechanism of radioresistance in esophageal cancer.

Network pharmacology in combination with bibliometrics analysis on the mechanism of compound Kushen injection in the treatment of radiation pneumonia and lung cancer.

Radiation pneumonia is a common adverse reaction during radiotherapy in lung cancer patients, which negatively impacts the quality of life and survival of patients. Recent studies have shown that compound Kushen injection (CKI), a traditional Chinese medicine (TCM), has great anti-inflammatory and anticancer potential, but the mechanism is still unclear. We used CiteSpace, the R package "bibliometrix," and VOSviewers to perform a bibliometrics analysis of 162 articles included from the Web of Science core collection. A network pharmacology-based approach was used to screen effective compounds, screen and predict target genes, analyze biological functions and pathways, and construct regulatory networks and protein interaction networks. Molecular docking experiments were used to identify the affinity of key compounds and core target. The literature metrology analysis revealed that over 90% of the CKI-related studies were conducted by Chinese scholars and institutions, with a predominant focus on tumors, while research on radiation pneumonia remained limited. Our investigation identified 60 active ingredients of CKI, 292 genes associated with radiation pneumonia, 533 genes linked to lung cancer, and 37 common targets of CKI in the treatment of both radiation pneumonia and lung cancer. These core potential targets were found to be significantly associated with the OS of lung cancer patients, and the key compounds exhibited a good docking affinity with these targets. Additionally, GO and KEGG enrichment analysis highlighted that the bioinformatics annotation of these common genes mainly involved ubiquitin protein ligase binding, cytokine receptor binding, and the PI3K/Akt signaling pathway. Our study revealed that the main active components of CKI, primarily quercetin, luteolin, and naringin, might act on major core targets, including AKT1, PTGS2, and PPARG, and further regulated key signaling pathways such as the PI3K/Akt pathway, thereby playing a crucial role in the treatment of radiation pneumonia and lung cancer. Moreover, this study had a certain promotional effect on further clinical application and provided a theoretical basis for subsequent experimental research.

Network Pharmacology Analysis on the Mechanism of Xihuangwan in Treating Rectal Cancer and Radiation Enteritis.

BACKGROUND: Recent studies have shown that XihuangWan (XHW) is a kind of Chinese medicine with significant anti-tumor and anti-inflammatory activities. However, its mechanism for preventing and treating radiation proctitis in rectal cancer patients during radiotherapy remains unclear. METHODS: This study employed the network pharmacology to establish a "drug-active ingredient-target genedisease" network via using TCMSP, SymMap, GeneCard, and OMIM databases. The PPI network was conducted by the String tool. The core targets of XHW in the treatment of rectal cancer and radiation enteritis were identified by topological analysis, and the functional annotation analysis and pathway enrichment analysis were performed. RESULTS: A total of 61 active ingredients of XHW ingredients, 4607 rectal cancer-related genes, 5803 radiation enteritis-related genes, and 68 common targets of XHW in the treatment of rectal cancer and radiation enteritis were obtained. PTGS1 and NR3C2, as identified potential targets, were significantly associated with OS of colorectal cancer patients. GO and KEGG enrichment analysis showed that bioinformatics annotation of these common genes was mainly involved in DNA-binding transcription factor, PI3K/Akt, TNF, HIF-1 signaling pathway, and colorectal cancer pathway. CONCLUSION: The active ingredients of XHW, mainly including Quercetin, Ellagic acid, and Stigmasterol, might act on common targets of rectal cancer and radiation enteritis, such as PTGS1, NR3C2, IL-6, EGFR, HIF-1A, CASP3, BCL2, ESR1, MYC, and PPARG, and regulate multiple signaling pathways like PI3K-Akt, TNF, and HIF-1 to inhibit tumor proliferation, tumor angiogenesis, inflammatory responses, and oxidative stress, thereby achieving prevention and treatment of radiation enteritis in rectal cancer patients during radiotherapy. It provided an important reference for further elucidating the anti-inflammation and anti-tumor mechanism and clinical application of XHW.

Cuckoo Algorithm Based on Global Feedback.

This article proposes a cuckoo algorithm (GFCS) based on the global feedback strategy and innovatively introduces a "re-fly" mechanism. In GFCS, the process of the algorithm is adjusted and controlled by a dynamic global variable, and the dynamic global parameter also serves as an indicator of whether the algorithm has fallen into a local optimum. According to the change of the global optimum value of the algorithm in each round, the dynamic global variable value is adjusted to optimize the algorithm. In addition, we set new formulas for the other main parameters, which are also adjusted by the dynamic global variable as the algorithm progresses. When the algorithm converges prematurely and falls into a local optimum, the current optimum is retained, and the algorithm is initialized and re-executed to find a better value. We define the previous process as "re-fly." To verify the effectiveness of GFCS, we conducted extensive experiments on the CEC2013 test suite. The experimental results show that the GFCS algorithm has better performance compared to other algorithms when considering the quality of the obtained solution.

Qi Fu Yin ameliorates neuroinflammation through inhibiting RAGE and TLR4/NF-κB pathway in AD model rats.

The purpose of this study is to investigate the therapeutic effect of Qi Fu Yin (QFY) on Alzheimer's disease (AD) both computationally and experimentally. Network pharmacology analysis and molecular docking were conducted to identify potential targets and signaling pathways involved in QFY treating AD. Streptozotocin-induced AD rat model was used to verify important targets and predicted pathways. The components of QFY were identified using liquid chromatography-tandem mass spectrometry. The results indicate that the potential targets of QFY are highly enriched for anti-inflammatory pathways. Molecular docking analysis revealed stable structures formed between QFY's active compounds, including stigmasterol, ß-sitosterol, and isorhamnetin, and the identified targets. In vivo, QFY improved cognitive memory in AD rats and reduced the mRNA expression levels of toll-like receptor 4 (TLR4), the receptor for advanced glycation end products (AGER), and the inflammatory factors interleukin-1ß (IL-1ß) and tumor necrosis factor-α (TNF-α) in the brains of AD rats. Furthermore, QFY effectively reduced nuclear translocation of nuclear factor-kappa B (NF-κB) and inhibited NF-κB and microglia activation. In conclusion, QFY can ameliorate neuroinflammation in AD model rats, partly via the inhibition of TLR4 and RAGE/NF-κB pathway and microglia activation, thereby enhancing learning and memory in AD model rats.

Genomewide association study of leprosy.

BACKGROUND: The narrow host range of Mycobacterium leprae and the fact that it is refractory to growth in culture has limited research on and the biologic understanding of leprosy. Host genetic factors are thought to influence susceptibility to infection as well as disease progression. METHODS: We performed a two-stage genomewide association study by genotyping 706 patients and 1225 controls using the Human610-Quad BeadChip (Illumina). We then tested three independent replication sets for an association between the presence of leprosy and 93 single-nucleotide polymorphisms (SNPs) that were most strongly associated with the disease in the genomewide association study. Together, these replication sets comprised 3254 patients and 5955 controls. We also carried out tests of heterogeneity of the associations (or lack thereof) between these 93 SNPs and disease, stratified according to clinical subtype (multibacillary vs. paucibacillary). RESULTS: We observed a significant association (P<1.00x10(-10)) between SNPs in the genes CCDC122, C13orf31, NOD2, TNFSF15, HLA-DR, and RIPK2 and a trend toward an association (P=5.10x10(-5)) with a SNP in LRRK2. The associations between the SNPs in C13orf31, LRRK2, NOD2, and RIPK2 and multibacillary leprosy were stronger than the associations between these SNPs and paucibacillary leprosy. CONCLUSIONS: Variants of genes in the NOD2-mediated signaling pathway (which regulates the innate immune response) are associated with susceptibility to infection with M. leprae.

A Novel Ferroptosis-Related Gene Signature to Predict Prognosis of Esophageal Carcinoma.

Objective: This study aimed to develop a novel ferroptosis-related gene-based prognostic signature for esophageal carcinoma (ESCA). Methods: The TCGA-ESCA gene expression profiles and corresponding clinical data were downloaded from the TCGA database. Ferroptosis-related genes were identified from the literature and public databases, which were intersected with the differentially expressed genes between ESCA and normal samples. After univariate Cox regression and random forest analyses, several ferroptosis-related feature genes were identified and used to construct a prognostic signature. Then, the prognostic value of the complex value and the correlation of the complex value with immune cell infiltration were analyzed. Moreover, function analysis, mutation analysis, and molecular docking on the ferroptosis-related feature genes were performed. Results: Based on the TCGA dataset and ferroptosis pathway genes, 1929 ferroptosis-related genes were preliminarily selected. Following univariate Cox regression analysis and survival analysis, 14 genes were obtained. Then, random forest analysis identified 10 ferroptosis key genes. These 10 genes were used to construct a prognostic complex value. It was found that low complex value indicated better prognosis compared with high complex value. In different ESCA datasets, there were similar differences in the proportion of immune cell distribution between the high and low complex value groups. Furthermore, TNKS1BP1, AC019100.7, KRI1, BCAP31, and RP11-408E5.5 were significantly correlated with ESCA tumor location, lymph node metastasis, and age of patients. KRI1 had the highest mutation frequency. BCAP31 had the strongest binding ability with small molecules DB12830, DB05812, and DB07307. Conclusion: We constructed a novel ferroptosis-related gene signature, which has the potential to predict patient survival and tumor-infiltrating immune cells of ESCA.

KIF26B in the Prognosis and Immune Biomarking of Various Cancers: A Pan-Cancer Study.

KIF26B has been identified as an oncogene in several tumors; however, its utility as a prognostic indicator for various cancers has not yet been comprehensively evaluated. Here, we first examined how KIF26B intervenes in thirty-three cancers within the TCGA database, including potential immunological functions, and how it affects the prognosis. Based on the open databases TCGA, TIMER2, GEPIA2, GTEx, CPTAC, and HPA, we found that, when compared with normal tissues, KIF26B is overexpressed in 22 tumor tissues. Following a survival analysis, a relationship between the expression of KIF26B and the prognosis of various cancers was observed. Among the genetic alterations assessed, mutations were the most frequent. On the contrary, high phosphorylation levels of S977 were detected in breast cancer, KIRC, LUAD, and UCEC. We also found positive or negative correlations between KIF26B and the immune infiltration of endothelial cells and cancer-associated fibroblast infiltration. This could imply that patients may benefit from immunotherapy. Finally, KEGG pathways and GO enrichment analyses were implemented to identify the molecular mechanisms of KIF26B. This study illustrates the function of KIF26B from a pan-cancer perspective and offers a new horizon for cancer prognostic and immunotherapeutic investigations.

Investigating the predictive value of vascular endothelial growth factor in the evaluation of treatment efficacy and prognosis for patients with non-surgical esophageal squamous cell carcinoma.

In this study, we aim to investigate the predictive value of serum vascular endothelial growth factor (VEGF) in evaluating treatment efficacy and long-term prognosis for patients with non-surgical esophageal squamous cell carcinoma (ESCC). The patients diagnosed with ESCC by histopathology who didn't receive surgical treatment were retrospectively analyzed. Through follow-up and prognostic analysis, we explored the value of serum VEGF changes before, during, and after radiotherapy for predicting treatment efficacy, and identified important indicators to construct the predictive model. Eighty-four patients were enrolled in this study, and the objective response rate (ORR) after treatment was 75.0%. The serum VEGF before, during and after radiotherapy were 108.2 ± 38.4, 98.6 ± 20.3 and 96.9 ± 20.0pg/ml, respectively. Staging and serum VEGF during radiotherapy were the independent factors affecting the treatment efficacy of non-surgical ESCC patients (OR=0.182 and 0.959, P<0.05). The median overall survival (OS) and progression-free survival (PFS) were 24.4 and 15.8 months. The 3-year, 5-year, 10-year OS rates and PFS rates were 35.7%, 26.2%, 14.4%, and 26.2%, 22.6%, 12.3%, respectively. By performing COX regression analysis, we found that the TNM stage, changes of VEGF after radiotherapy (∆VEGF2), and endoscopic histopathological response were the independent prognostic factors for OS and PFS (P<0.05). The R2 of the constructed prediction model was 0.328 and 0.362, and the C-index was 0.697 and 0.708, respectively. The follow-up time-dependent AUC showed that the predicted AUC was stable and greater than 0.7 as the follow-up time increased. For patients with non-surgical ESCC, those with low VEGF levels during radiotherapy had better treatment efficacy, and those with significant VEGF reduction after radiotherapy had a better prognosis. In summary, our results demonstrate that it is feasible to construct a model to evaluate and predict the efficacy and prognosis of patients with non-surgical ESCC based on serum VEGF measurement.

Transcriptomic and microRNA Expression Profiles Identify Biomarkers for Predicting Neo-Chemoradiotherapy Response in Esophageal Squamous Cell Carcinomas (ESCC).

Neo-chemoradiotherapy (nCRT) before surgery is a standard treatment for locally advanced esophageal cancers. However, the treatment outcome of nCRT varied with different patients. This study aimed to identify potential biomarkers for prediction of nCRT-response in patients with esophageal squamous cell carcinoma (ESCC). Microarray datasets of nCRT responder and non-responder samples (access number GSE45670 and GSE59974) of patients with ESCC were downloaded from Gene Expression Omnibus (GEO) database. The mRNA expression profiles of cancer biopsies from four ESCC patients were analyzed before and after nCRT. Differentially expressed genes (DEGs) and miRNAs were screened between nCRT responder and non-responder ESCC samples. Functional enrichment analysis was conducted for these DEGs followed by construction of protein-protein interaction (PPI) network and miRNA-mRNA regulatory network. Finally, univariate survival analysis was performed to identify candidate biomarkers with prognostic values in ESCC. We identified numerous DEGs and differentially expressed miRNAs from nCRT responder group. GO and KEGG analysis showed that the dysregulated genes were mainly involved in biological processes and pathways, including "response to stimulus", "cellular response to organic substance", "regulation of signal transduction", "AGE-RAGE signaling pathway in diabetic complications", and "steroid hormone biosynthesis". After integration of PPI network and miRNA-mRNA network analysis, we found eight genes, TNF, AKR1C1, AKR1C2, ICAM1, GPR68, GNB4, SERPINE1 and MMP12, could be candidate genes associated with disease progression. Univariate cox regression analysis showed that there was no significant correlation between dysregulated miRNAs (such as hsa-miR-34b-3p, hsa-miR-127-5p, hsa-miR-144-3p, and hsa-miR-486-5p, et al.) and overall survival of ESCC patients. Moreover, abnormal expression of MMP12 was significantly correlated with pathological degree, TNM stage, lymph nodes metastasis, and overall survival of ESCC patients (p < 0.05). Taken together, our study identified that MMP12 might be a useful tumor biomarker and therapeutic target for ESCC.

Comprehensive Quality Evaluation of American Ginseng for Different Parts and Abnormal Trait Based on the Major Ginsenoside Contents and Morphological Characteristics.

The demand for American ginseng, a famous traditional medicine and high-grade healthy food, has increased dramatically over recent years. However, only the main root is popular among consumers, whereas other parts of American ginseng are rarely available in the market. In this study, the contents of 5 major ginsenosides (Re, Rc, Rg1, Rd, and Rb1) were determined through high-performance liquid chromatography. Our study showed that all these 5 major ginsenosides are found in different parts of American ginseng plants, and the total content in different parts varied significantly in the following order: fibrous root > flower > branch root > main root > leaf > stem. Interestingly, the total content in the fibrous root was approximately 2.24 times higher than that in the main root. Further research indicated that the ginsenoside content in American ginseng with abnormal characteristics (physical deformity caused by disease and discolouration) is similar to that in the normal plant. Interestingly, a positive correlation was observed between the main root diameter and total ginsenoside content, whereas a negative correlation was observed between the main root length and total ginsenoside content. Our comprehensive study revealed that all parts of American ginseng, including the main root with abnormal characteristics, possess medicinal or economic value. Therefore, our results provide feasible evidence to further explore the potential application of American ginseng.

KIF22 promotes progress of esophageal squamous cell carcinoma cells and is negatively regulated by miR-122.

Esophageal squamous cell carcinoma (ESCC) increases at fast rate of all cancer types in China, which urges the investigations of its potential mechanism. In this research, a highly expressed kinesin superfamily protein 22 (KIF22) was founded both in ESCC tissues and cancer cell lines. The following experiments pointed out that down-regulation of KIF22 remarkably restrained the malignant progression of ESCC cells. Besides, KIF22 knockdown promoted ESCC cells apoptosis and arrested cells in G0/G1 phase, while KIF22 also regulated the expression of cell cycle- and EMT-related proteins. Previous research revealed that the aberrant expressions of microRNAs (miRNAs) are related to tumors development. Based on the predict result, KIF22 was considered as the target of miR-122, which was demonstrated by luciferase reporter assay. miR-122 inhibitor could significantly reverse the function of KIF22 knockdown, including cell proliferation, migration and invasion. Furthermore, down-expressed miR-122 altered the function of KIF22 knockdown on cell cycle- and EMT-related proteins. In a word, this work illustrated the regulatory function of KIF22/miR-122 axis in ESSC and provided potential targets for potential targets for ESSC treatment.

Hypofractionated Radiotherapy in Combination With Chemotherapy Improves Outcome of Patients With Esophageal Carcinoma Tracheoesophageal Groove Lymph Node Metastasis.

This study investigated the efficiency and safety of hypofractionated radiotherapy (HFR) combined with paclitaxel chemotherapy for the treatment of postsurgery tracheoesophageal groove lymph node (TGLN) metastasis in patients with esophageal cancer (EC). Fifty-three EC patients with TGLN metastasis after surgery admitted to the Yancheng Third People's Hospital from January 2013 to June 2015 were included in this study. They were randomly divided into the HFR group (n = 25) and conventional fractioned radiotherapy (CFR) group (n = 28) based on the random grouping method. Patients in the HFR group received treatment with radiation of 60 Gy (5 fractions per week, total 20 fractions) combined with paclitaxel chemotherapy at a dose of 50 mg once per week for 4 weeks. Patients in the CFR group received radiation of 60 Gy (5 fractions per week, total 30 fractions) combined with paclitaxel chemotherapy at a dose of 50 mg once per week for 6 weeks. The adverse events and treatment outcomes in these two groups were analyzed. It was found that there was no significant difference in the incidence of radiation esophagitis in the HFR group compared with that of the CFR group (grades 3-4, 44.0 vs. 25.0%; P = 0.149). There was no statistical difference in the incidence of radiation pneumonitis between these two groups (grades 3-4, 16.0 vs. 7.1%; P = 0.314). No statistical difference was noticed in complete response (CR), partial response (PR), and no response (NR) between these two groups. The median overall survival (OS) in the HRF group was significantly longer compared with that of the CRF group (24.2 months (95% CI, 16.2-32.1 months) vs. 11.8 months (95% CI, 9.2-14.4 months); P = 0.024). Our results indicated that the combination of HFR and chemotherapy improved the prognosis of EC patients with TGLN metastasis with no increased adverse events.

Identification of MTHFD2 as a novel prognosis biomarker in esophageal carcinoma patients based on transcriptomic data and methylation profiling.

DNA methylation is an important epigenetic regulatory mechanism in esophageal carcinoma (EC) and is associated with genomic instability and carcinogenesis. In the present study, we aimed to identify tumor biomarkers for predicting prognosis of EC patients.We downloaded mRNA expression profiles and DNA methylation profiles associated with EC from the Gene Expression Omnibus database. Differentially expressed and differentially methylated genes between tumor tissues and adjacent normal tissue samples were identified. Functional enrichment analyses were performed, followed by the construction of protein-protein interaction networks. Data were validated based on methylation profiles from The Cancer Genome Atlas. Candidate genes were further verified according to survival analysis and Cox regression analysis.We uncovered multiple genes with differential expression or methylation in tumor samples compared with normal samples. After taking the intersection of 3 differential gene sets, we obtained a total of 232 overlapping genes. Functional enrichment analysis revealed that these genes are related to pathways such as "glutathione metabolism," "p53 signaling pathway," and "focal adhesion." Furthermore, 8 hub genes with inversed expression and methylation correlation were identified as candidate genes. The abnormal expression levels of MSN, PELI1, and MTHFD2 were correlated with overall survival times in EC patients (P < .05). Only MTHFD2 was significantly associated with a pathologic stage according to univariate analysis (P = .037) and multivariate analysis (P = .043).Our study identified several novel EC biomarkers with prognostic value by integrated analysis of transcriptomic data and methylation profiles. MTHFD2 could serve as an independent biomarker for predicting prognosis and pathological stages of EC.

RAI14 silencing suppresses progression of esophageal cancer via the STAT3 pathway.

Esophageal cancer (EC) is an aggressive malignancy that has an unclear molecular pathogenesis. Although retinoic acid induced 14 (RAI14) is involved in various cancer processes, the relationship between EC and RAI14 has not been elucidated. Our study reported the oncogenic function of RAI14 and its underlying mechanisms in EC. The Cancer Genome Atlas (TCGA) database revealed that RAI14 was upregulated in EC, and this upregulation correlated with T stage, histologic grade, and poor clinical prognosis. RAI14 was evaluated in EC cell lines, and the overexpression of RAI14 promoted cell proliferation, migration, and invasion in vitro. Conversely, RAI14 knockdown induced apoptosis and cell cycle arrest. RAI14 activated STAT3, upregulated Mcl-1 and cyclin D1, and inhibited cleaved caspase-3. Inhibition of STAT3 restored the oncogenic effect of RAI14, and RAI14 silencing restrained tumor growth and the protein level of Ki67 in vivo. Our results suggest that RAI14 regulates the STAT3 pathway and acts as an oncogene during EC progression.