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SAMHD1 was reported to be related with the development of tumors, while its function in gastric cancer (GC) has not been elucidated yet. Here, we investigated the role and mechanism of SAMHD1 in regulating the proliferation of GC, as well as the mechanism of its expression regulation. Our results revealed that SAMHD1 was downregulated in GC tissues and cell lines, which was correlated with tumor size, depth of invasion and TNM stage. Overexpression of SAMHD1 inhibited the proliferation, clone formation, DNA synthesis and cell cycle progression, while knockdown of SAMHD1 promoted the proliferation of GC cells in vitro and vivo. Meanwhile, SAMHD1 inhibited the activation of MAPK p38 signaling pathway. Moreover, SB203580, as a MAPK p38 inhibitor, could reverse the proliferation and activation of MAPK p38 signaling pathway caused by knockdown of SAMHD1 in GC cells. Additionally, transcription factor Krüppel-like factor 4 (KLF4) bound to the core promoter of SAMHD1, increasing its transcriptional expression in GC cells. In conclusion, SAMHD1 suppressed the proliferation of GC through negatively regulating the activation of MAPK p38 signaling pathway and was upregulated by KLF4 in GC cells.

Recent studies have shown no significant improvement in the high incidence and low cure rates of hepatocellular carcinoma (HCC). Surgery and liver transplantation are the primary means of prolonging survival in patients with HCC. however, patients with HCC have low surgical resection rates, and even when radical surgical resection is obtained, the 5-year postoperative recurrence rate remains high, the prognosis is poor, and additional therapeutic options are urgently needed. There is increasing evidence that cellular senescence is associated with human cancers. The purpose of this study was to develop a risk model associated with cellular senescence to predict the prognosis of HCC and to search for potential strategies to treat HCC. The genome associated with cellular senescence was obtained from the CellAge website. transcriptomic data and clinical data for HCC were obtained from the Cancer Genome Atlas database (TCGA).

This meta-analysis was conducted to compare the effect and safety of oral contraceptive pills (OCP) plus orlistat with OCP alone in clinical, hormonal, and lipid metabolism outcomes in patients with polycystic ovary syndrome (PCOS) and overweight/obesity.Pubmed, Embase, Web of Science, Chinese National Knowledge Infrastructure (CNKI), and SinoMed were systematically reviewed. A random-effects or fixed-effects model was used to pool the estimate.Eight studies were included in this meta-analysis. Significant reductions in BMI, WHR, and waist circumference were observed in combination group as compared with OCP alone group. Regarding the hormonal outcome, T, SHBG, FAI, LH, DHEAS, FSH, and E2 levels were significantly improved in combination group compared with OCP alone group. However, the TT and FT did not change significantly between the two groups. Regarding the lipid metabolism outcomes, TC, LDL-C, and TG levels were reduced and HDL-C level was increased in the combination group. Regarding the insulin metabolism outcomes, FINS and HOMA-IR levels were reduced in combination group than in OCP group. The ovulation rate, pregnancy rate, and overall effective rate were significantly higher in combination group than in OCP alone group. Fewer complications were observed in the combination group than in OCP group, and the difference between them was significant.This combination treatment of OCP and orlistat was more effective than OCP alone in reducing the weight, hormonal, lipid, and insulin metabolism profiles, as well as improving the ovulation rate, pregnancy rate, and overall effective rate, as compared with OCP alone.

Gastric cancer (GC) is common in East Asia, yet its molecular and pathogenic mechanisms remain unclear. Circular RNAs (circRNAs) are differentially expressed in GC and may be promising biomarkers. Here, we investigated the role and regulatory mechanism of circTMC5 in GC. CircTMC5 expression was detected in human GC and adjacent tissues using microarray assays and qRT-PCR, while the clinicopathological characteristics of patients with GC were used to assess its diagnostic and prognostic value. The circTMC5/miR-361-3p/RABL6 axis was examined in vitro and vivo, and the immune roles of RABL6 were evaluated using bioinformatics analyses and immunohistochemistry (IHC). CircTMC5 was highly expressed in GC tissues, plasma, and cell lines, and was closely related to histological grade, pathological stage, and T classification in patients with GC. CircTMC5 expression was also an independent prognostic factor for GC and its combined detection with carcinoembryonic antigen may improve GC diagnosis. Low circTMC5 expression correlated with good prognosis, inhibited GC cell proliferation, and promoted apoptosis. Mechanistically, circTMC5 overexpression promoted GC cell proliferation, invasion, and metastasis but inhibited apoptosis by sponging miR-361-3p and up-regulating RABL6 in vitro and vivo, whereas miR-361-3p up-regulation had the opposite effects. RABL6 was highly expressed in GC and was involved in immune regulation and infiltration in GC. CircTMC5 promotes GC and sponges miR-361-3p to up-regulate RABL6 expression, thus may have diagnostic and prognostic value in GC. RABL6 also displays therapeutic promise due to its role in the immune regulation of GC.

BACKGROUND Approximately 90% of new cases of noncardiac gastric cancer (GC) are related to Helicobacter pylori (H. pylori), and cytotoxin-associated gene A (CagA) is one of the main pathogenic factors. Recent studies have shown that the pharmacological effects of cryptotanshinone (CTS) can be used to treat a variety of tumors. However, the effects of CTS on H. pylori, especially CagA+ strain-induced gastric mucosal lesions, on the development of GC is unknown. AIM To assess the role of CTS in CagA-induced proliferation and metastasis of GC cells, and determine if CagA+ H. pylori strains causes pathological changes in the gastric mucosa of mice. METHODS The effects of CTS on the proliferation of GC cells were assessed using the Cell Counting Kit-8 (CCK-8) assay, and the abnormal growth, migration and invasion caused by CagA were detected by CCK-8 and transwell assays. After transfection with pSR-HA-CagA and treatment with CTS, proliferation and metastasis were evaluated by CCK-8 and transwell assays, respectively, and the expression of Src homology 2 (SH2) domain–containing phosphatase 2 (SHP2) and phosphorylated SHP2 (p-SHP2) was detected using western blotting in AGS cells. The enzyme-linked immunosorbent assay was used to determine the immunoglobulin G (IgG) level against CagA in patient serum. Mice were divided into four groups and administered H. pylori strains (CagA+ or CagA-) and CTS (or PBS) intragastrically, and establishment of the chronic infection model was verified using polymerase chain reaction and sequencing of isolated strains. Hematoxylin and eosin staining was used to assess mucosal erosion in the stomach and toxicity to the liver and kidney. RESULTS CTS inhibited the growth of GC cells in dose- and time-dependent manners. Overexpression of CagA promoted the growth, migration, and invasion of GC cells. Importantly, we demonstrated that CTS significantly inhibited the CagA-induced abnormal proliferation, migration, and invasion of GC cells. Moreover, the expression of p-SHP2 protein in tumor tissue was related to the expression of IgG against CagA in the serum of GC patients. Additionally, CTS suppressed the protein expression levels of both SHP2 and p-SHP2 in GC cells. CTS suppressed CagA+ H. pylori strain-induced mucosal erosion in the stomach of mice but had no obvious effects on the CagA- H. pylori strain group. CONCLUSION CTS inhibited CagA-induced proliferation and the epithelial-mesenchymal transition of GC cells in vitro, and CagA+ H. pylori strains caused mucosal erosions of the stomach in vivo by decreasing the protein expression of SHP2.

Globally, gastric cancer (GC) is a common and lethal solid malignant tumor. Identifying the molecular signature and its functions can provide mechanistic insights into GC development and new methods for targeted therapy.Differentially expressed genes (DEGs) and prognostic genes (from univariate Cox regression analysis) were overlapped to obtain prognostic DEGs. Subsequently, molecular modules and the functions of these prognostic DEGs were identified by Metascape and Gene Ontology (GO)/Kyoto Encyclopedia of Genes and Genomes (KEGG)/Gene Set Enrichment Analysis (GSEA) enrichment analyses, respectively. Protein-protein interaction (PPI) networks of up- and down-regulated prognostic DEGs in GC were analyzed using the MCC algorithm of the Cytohubba plug-in in Cytoscape. The prognostic gene signature was defined on hub genes of the PPI networks by least absolute shrinkage and selection operator (LASSO)-Cox regression analysis. Furthermore, the expressional level of PLG in our clinical GC samples was validated by quantitative PCR (qPCR), western blotting, and immunohistochemistry (IHC). Subsequently, the PLG expression-correlation analysis was performed to assess the role of PLG in GC progression. Immune infiltration analysis was performed by single-sample gene set enrichment analysis (ssGSEA) to assess the inhibitory effect of PLG on immune infiltration.Firstly, Up- and down-regulated prognostic DEGs and hub genes in protein-protein interaction (PPI) networks in GC were identified. A prognostic five-gene signature (i.e., PLG, SPARC, FGB, SERPINE1, and KLHL41) was identified. Among the five genes, the relationship between plasminogen (PLG) and GC remains largely unclear. Moreover, the functions of PLG-correlated genes in GC, like 'fibrinolysis', 'hemostasis', 'ion channel complex', and 'transporter complex' were identified. In addition, PLG expression correlated negatively with the infiltration of almost all immune cell types. Interestingly, the expression of PLG was significantly and highly correlated with that of CD160, an immune checkpoint inhibitor.Our findings defined a new five-gene signature for predicting GC prognosis, but more validation is required to assess the effects and mechanism of the five genes, especially PLG, for the development of new GC therapies.

Background:Members of the integrin β superfamily(ITGBs) have been shown to be aberrantly expressed in various human cancers and involved in tumorigenesis and progression. However, the diverse expression patterns and prognostic values of the entire ITGB family members in gastric cancer(GC) has not been systematically investigated.Methods:In the current study, Oncomine, GEPIA, Kaplan Meier plotter, TIMER, GeneMANIA, STRING and Metascape database were employed to explore the transcriptional and survival data of ITGB superfamily members in GC. Moreover, we confirmed the mRNA expression levels of ITGB superfamily members in GC cell lines by qRT-PCR.Results:The mRNA expression level of ITGB1/2/4/5/8 was upregulated in GC, while the expression level of ITGB7 was downregulated. Higher expression of ITGB2/7 was significantly associated with the tumor stage of patients with GC. However, we found that the expression level of ITGB1/2/4/5/6/7/8 was remarkably increased in GC cell lines compared to stomach normal cell lines, while ITGB3 expression was decreased in the former than in the latter. Meanwhile,higher expression levels of ITGB2/6/7 were closely correlated with better overall clinical survival (OS) and recurrence-free survival (RFS) in GC patients, while higher ITGB3/4/5 expression were strongly associated with poorer OS and RFS.We also discovered that the functions of ITGBs and their adjacent genes are mainly related to protein complexes involved in cell adhesion. the functions of ITGBs and their adjacent proteins are mainly related to focal adhesion, cell adhesion molecules, proteoglycans in cancer, small cell lung cancer, rap1 signaling pathway, IgA production by intestinal immune network, and microRNAs in cancer.In addition, the expression of ITGBs was significantly correlated with the infiltration of multiple immune cells, including B cells, CD8+ T cells, CD4+ T cells, neutrophils, macrophages, and dendritic cells.Conclusions:Our results suggested that abnormal expression of ITGBs plays a key role in the progression of GC and that ITGBs may be potential prognostic biomarkers and therapeutic targets for GC.

Gastric cancer (GC) is common in East Asia, yet its molecular and pathogenic mechanisms remain unclear. Circular RNAs (circRNAs) are differentially expressed in GC and may be promising biomarkers. Here, we investigated the role and regulatory mechanism of circTMC5 in GC.CircTMC5 expression was detected in human GC and adjacent tissues using microarray assays and qRT-PCR, while the clinicopathological characteristics of patients with GC were used to assess its diagnostic and prognostic value. The circTMC5/miR-361-3p/RABL6 axis was examined in vitro and vivo, and the immune roles of RABL6 were evaluated using bioinformatics analyses and immunohistochemistry (IHC).CircTMC5 was highly expressed in GC tissues, plasma, and cell lines, and was closely related to histological grade, pathological stage, and T classification in patients with GC. CircTMC5 expression was also an independent prognostic factor for GC and its combined detection with carcinoembryonic antigen may improve GC diagnosis. Low circTMC5 expression correlated with good prognosis, inhibited GC cell proliferation, and promoted apoptosis. Mechanistically, circTMC5 overexpression promoted GC cell proliferation, invasion, and metastasis but inhibited apoptosis by sponging miR-361-3p and up-regulating RABL6 in vitro and vivo, whereas miR-361-3p up-regulation had the opposite effects. RABL6 was highly expressed in GC and was involved in immune regulation and infiltration in GC.CircTMC5 promotes GC and sponges miR-361-3p to up-regulate RABL6 expression, thus may have diagnostic and prognostic value in GC. RABL6 also displays therapeutic promise due to its role in the immune regulation of GC.

Human sterile alpha motif and HD-domain-containing protein 1 (SAMHD1) has been identified as a GTP or dGTP-dependent deoxynucleotide triphosphohydrolase (dNTPase) and acts as an antiviral factor against certain retroviruses and DNA viruses. Genetic mutation in SAMHD1 causes the inflammatory Aicardi-Goutières Syndrome and abnormal intracellular deoxyribonucleoside triphosphates (dNTPs) pool. At present, the role of SAMHD1 in numerous types of cancer, such as chronic lymphocytic leukemia, lung cancer and colorectal cancer, is highly studied. Furthermore, it has been found that methylation, acetylation and phosphorylation are involved in the regulation of SAMHD1 expression, and that genetic mutations can cause changes in its activities, including dNTPase activity, long interspersed element type 1 (LINE-1) suppression and DNA damage repair, which could lead to uncontrolled cell cycle progression and cancer development. In addition, SAMHD1 has been reported to have a negative regulatory role in the chemosensitivity to anticancer drugs through its dNTPase activity. The present review aimed to summarize the regulation of SAMHD1 expression in cancer and its function in tumor growth and chemotherapy sensitivity, and discussed controversial points and future directions.

Gastric cancer (GC) is one of malignant tumors with high mortality and morbidity in the world. MicroRNA-122 (miR-122) acts as a tumor suppressor in a variety of cancers and has been found to be dominant in gastric adenocarcinoma. However, the specific biological function of miR-122-5p in GC is not completely clear. In this study, we found that miR-122-5p was low-expressed in GC tissues and cell lines by using qRT-PCR. Overexpression of miR-122-5p inhibited the proliferation, migration, and invasion of GC cells by using CCK-8 and transwell assays. On the contrary, downregulation of miR-122-5p promoted the proliferation, migration, and invasion of GC cells. In addition, we found that the expression of LYN, an Src family tyrosine kinase, was inversely correlated with miR-122-5p expression in GC tissues by using western blot analysis, immunohistochemistry, and qRT-PCR assays. Meanwhile, luciferase assay results indicated that LYN is a direct target of miR-122-5p in GC cells. Moreover, silencing LYN expression by its siRNA inhibited the proliferation, migration, and invasion of GC cells. Importantly, overexpression of LYN restored miR-122-5p-mediated inhibition of the proliferation, migration, and invasion of GC cells. Taken together, our results indicated miR-122-5p inhibited the proliferation, migration, and invasion by targeting LYN in GC.

Interleukin-34 (IL-34) is a recently discovered cytokine that promotes tissue macrophage maturation and differentiation. We previously found that 1α,25-Dihydroxyvitamin D3 up-regulated IL-34 expression in SH-SY5Y neural cells. However, whether microRNA regulates IL-34 expression is not completely clear. By using on-line TargetScan and MiRanda software, we found that there was only one conserved microRNA-31 (miR-31) binding site in the 3' untranslated region (3'UTR) of IL-34 mRNA. Intriguingly, using qPCR we demonstrated that miR-31 levels were negatively correlated to IL-34 mRNA levels in different cell lines. By examining the effect of miR-31 on IL-34 3' UTR reporter luciferase activity and on IL-34 mRNA and argonaute RISC catalytic component 2 (AGO2) binding, it was found that miR-31 bound directly to IL-34 3'UTR and regulated the post-transcriptional expression of IL-34 in MGC-803 cells. Moreover, a miR-31 mimic significantly reduced IL-34 expression levels while a miR-31 inhibitor up-regulated IL-34 expression in KYSE-45 and HT-29 cells. Taken together, these results show that miR-31 negatively regulates IL-34 expression by directly binding to the IL-34 3' UTR in vitro.

The protein voltage-gated sodium channel Nav1.5 is highly upregulated in various types of cancer and, in general, promotes cancer cell invasiveness and metastatic progression. A previous study found that Nav1.5 was highly expressed in poorly differentiated oral squamous cell carcinoma (OSCC). However, whether Nav1.5 enhances invasiveness and metastasis of OSCC are still unknown. In this study, we found that Nav1.5 was highly expressed in OSCC cell lines compared with normal oral keratinocyte HOK cell line by using western blot analysis. CCK-8 assay results revealed that downregulation of Nav1.5 expression by its specific siRNA reduced proliferation of OSCC HSC-3 cells. Moreover, transwell assay results showed Nav1.5 knockdown significantly inhibited migration and invasion of HSC-3 cells. Meanwhile, qRT-PCR and western blot analysis results showed that epidermal growth factor (EGF) induced Nav1.5 expression in a time- and dose-dependent manner. In addition, EGF promoted proliferation, migration and invasion of HSC-3 cells. Importantly, the Nav1.5 inhibitor tetrodotoxin significantly inhibited the proliferation of HSC-3 cells and impeded the migration and invasion of HSC-3 cells. Furthermore, it was found that siRNA-mediated knockdown of Nav1.5 also lessened the proliferation of HSC-3 cells and blocked the migration and invasion of HSC-3 cells. Taken together, these results indicate that Nav1.5 is involved in the progression of OSCC and Nav1.5 promotes the proliferation, migration and invasion of OSCC cells.

To explore the risk factors of vascular invasion in patients with early gastric cancer (EGC), and to investigate the influence of vascular invasion on the prognosis of EGC patients.From January 2014 to December 2015, 449 EGC patients underwent curative gastrectomy at the First Affiliated Hospital of Anhui Medical University, of whom 27 cases (6.0%) developed vascular invasion. Clinicopathological and follow-up data of EGC cases were analyzed retrospectively. The association between clinicopathological features and vascular invasion was analyzed by using the Chi-square test or Fisher exact test, and the independent risk factors influencing vascular invasion were identified with logistic regression. The influence of vascular invasion on overall survival was investigated with Kaplan-Meier curve. This study was approved by Ethics Committee of The First Affiliated Hospital of Anhui Medical University (No. 2018-03-12).Of 449 EGC patients, 325 were males and 124 were females (ratio 2.6:1.0) with the mean age of (60.8±10.5) (27 to 87) years; 228 were diagnosed as T1a stage and 221 were diagnosed as T1b. Univariate analysis showed that incidence of vascular invasion in EGC patients with ulceration or scar was 8.4%(18/225), which was higher than 3.8%(9/234) in those without ulceration, and the difference was statistically significant (χ²=4.061, P=0.044). The incidence of vascular invasion in patients with low differentiated tumor was 8.8% (20/226), which was significantly higher than 3.1%(7/223) in those with middle-high differentiated tumor(χ²= 8.363, P=0.012). The incidence of vascular invasion in patients staging T1b was 10.9% (24/221), which was significantly higher than 1.3% (3/228) in those staging T1a (P=0.000); The incidence of vascular invasion in patients with lymph node metastasis was 27.3% (15/55), which was significantly higher than 3.0%(12/394) in those without lymph node metastasis (χ²=50.122, P=0.000). However, there were no significant associations of vascular invasion with gender, age, surgical type, multiple tumor, tumor deposit, tumor location and tumor size (all P0.05). Multivariate analysis showed that T1b stage (RR=4.653, 95%CI:1.293-16.747, P=0.019) and lymph node metastasis(RR=7.302, 95%CI: 3.063-17.408, P=0.000) were independent risk factors for vascular invasion in EGC patients. Among 449 EGC patients, 444 received complete follow-up(98.9%), including 26 cases with vascular invasion and 418 cases without vascular invasion. The overall survival in vascular invasion group was significantly lower than that in non-vascular invasion group (χ²=60.463, P=0.000). Besides, 198 EGC patients gained follow-up for 3 years, and the 3-year survival rates of 11 vascular invasion cases and 187 non-vascular invasion cases were 54.5% and 96.8% respectively.The risk of vascular invasion is higher in EGC patients with lymph node metastasis and tumor infiltrating the submucosa. The prognosis of EGC patients with vascular invasion is poor.

Sterile α motif and HD domain-containing protein 1 (SAMHD1) is a novel intrinsic restriction factor that inhibits the replication of certain retroviruses and DNA viruses through its deoxynucleoside triphosphate triphosphohydrolase activity. A previous study by our group showed that SAMHD1 restrained hepatitis B virus replication and interferon (IFN)‑α induced SAMHD1 expression in liver cells. However the mechanisms of SAMHD1 upregulation by IFN‑α in liver cells have remained elusive. The present study demonstrated that IFN‑α treatment increased SAMHD1 mRNA levels in SMMC‑7721 cells in a time‑dependent manner. Knockdown of STAT1 inhibited the induction of SAMHD1 expression by IFN‑α in SMMC‑7721 cells. STAT2 silencing also suppressed the induction of SAMHD1 expression by IFN‑α in SMMC‑7721 cells. Furthermore, the induction of SAMHD1 expression in SMMC‑7721 cells by IFN‑α was found to be dependent on IFN‑regulatory factor 9 (IRF9). In conclusion, these results suggested that the interferon‑stimulated gene factor 3 complex, which consists of STAT1, STAT2 and IRF9, is required for the induction of SAMHD1 expression by IFN-α in SMMC-7721 cells.

Vitamin D supplementation is regarded as a novel approach to treat Alzheimer’s disease, but the underlying mechanism remains elusive. The cytokine IL-34 provides strong neuroprotective and survival signals in brain injury and neurodegeneration and could be an immunological mediator for the vitamin D-induced protection. The aim of this study was to investigate whether human IL-34 is up-regulated in neuronal cells by the hormonally active form of vitamin D, 1α,25-dihydroxyvitamin D3 [1α,25(OH)2D3]. We found that IL-34 was detectable in a variety of cell lines and its expression was strongly induced in SH-SY5Y neural cells in a dose- and time-dependent manner by 1α,25(OH)2D3 through the vitamin D receptor (VDR). Furthermore, we identified the core promoter of IL-34 gene and a VDR binding site (CGCCCT) that was required for 1α,25(OH)2D3-induced IL-34 expression. These findings suggest that the induction of IL-34 expression by 1α,25(OH)2D3 may constitute a mechanism that explains the protective function of vitamin D in Alzheimer’s disease.

Background: Ferritin light chain (FTL) is a functionally distinct composition of ferritin, which is over-expressed and play an important role in multiple human malignancies. Methods: Matched normal and cancerous tissues in 60 gastric cancer (GC) patients were detected for FTL expression using immunohistochemistry staining. The relationship betweent FTL expression and clinicopathological features was analyzed by chi-square test, and the Kaplan-Meier curves and Cox regression analyses were used to calculate the overall survival (OS) characteristics and recurrence-free survival (RFS). Results: FTL protein was significantly higher in GC tissues than adjacent tissues. Further, FTL expression was not correlative with gender, age, tumor size, tumor location, CEA and AFP level (P>0.05). However, the associations between FTL expression and depth of tumor invasion (P=0.014), differentiation grade (P=0.001), lymph node metastasis (P

Sterile alpha motif and HD-domain containing protein 1 (SAMHD1) is a newly identified intracellular antiviral factor. By depleting the dNTPs pool of host cells to a low level that cannot support the efficient synthesis of viral cDNA, it restricts replication of some retroviruses. As a DNA virus, Hepatitis B virus (HBV) experiences a process of reverse transcription in its life cycle akin to that of retroviruses. However, whether SAMHD1 can restrict HBV replication in liver cells is unknown. Here, we reported that SAMHD1 expression was detectable in four liver cell lines. Exogenous expression of SAMHD1 in SMMC-7721 cells restrained HBV replication. Similarly, SAMHD1 impeded HBV replication in another liver cell line, BEL-7402. Remarkably, the catalytically inactive mutant, SAMHD1 HD/AA also hampered HBV replication. Additionally, HBV replication reduced SAMHD1 expression in HepG2 cells. Moreover, it was found that IFN-α induced expression of SAMHD1 in liver cells. Together, these findings suggested that IFN-α-inducible SAMHD1 inhibited HBV replication in liver cells.

Background Adenocarcinoma of esophagogastric junction (AEG) was initially proposed in 1999 by Siewert. During recent decades, the incidence and prevalence of AEG were arising globally whereas the incidence of gastric cancer is gradually declining. Complete blood counting and liver function tests, as the routine examination of immune and nutritional status, were reported to be the predictors of overall survival (OS) in some tumors. However, little is known about the prognostic significance of these indexes in AEG patients. The purpose of this study was to assess the prediction of preoperative pre-albumin, hemoglobin, and prognostic nutritional index (PNI) for survival outcomes in AEG patients. Methods A retrospective cohort of 101 AEG patients followed by radical surgery was recruited between January and July 2010. Clinical and laboratory data were obtained and used to evaluate the predictive value through survival analysis. Receiver operating characteristic (ROC) curve analysis determined 200 mg/L, 120 g/L, 5 cm, and 51 as the cutoff values of pre-albumin, hemoglobin, tumor size, and PNI, respectively. Results Univariate analysis revealed that AEG patients with hemoglobin ≥120 g/L, albumin ≥40 g/L, pre-albumin ≥200 g/L, PNI ≥51, and tumor size

Source rock evaluation is a critical factor in resource assessment of oil and gas. Models for evaluating source rocks are dependent on established geomathematical principles, the calculation of source-rock parameters, and geological data. The sensitivities and uncertainties associated with these models are a matter of concern. In this paper, the effects and relative contributions of 13 major geological factors, as well as their variations and distribution probabilities, have been analyzed for the source rocks in the North Songliao Basin in northeastern China. The geological factors include the time of formation of the regional caprock, composition of the regional caprock, the phases of hydrocarbons in migration, and those factors associated with the generation, retention, and expulsion of hydrocarbons and their effects on source-rock efficiency. Of the 13 factors analyzed, the most important are the source-rock depth, sedimentation rate, total organic content, and kerogen-type index; the relative contributions to the uncertainty of efficient gas/oil migration amounts for the most important factors are 37, 25, 19, and 1% for oil and 32, 17, 20, and 15% for gas, respectively. These most reflect the changes that have occurred in the Qingshankou source rocks.

A probabilistic method that is based upon conditional probability theory and the laws of expectation has been developed for estimating the undiscovered oil and gas resources in a petroleum play. It takes into account the favorable geological conditions that influence the accumulation of oil and gas and those factors which influence the distribution and the quantity of undiscovered oil and gas. Information about the number and size of undiscovered resources is provided. A practical application in the Turpan-Hami Basin in northwestern China is described.

Gas generated and expelled from coals often results in economic gas accumulations. As a consequence, it is important to consider the theoretical aspects of these processes and to develop methods that can be used to assess coal as a potential source rock. On the basis of results of modeling hydrocarbon generation, expulsion, and retention in coals, two comprehensive indexes are proposed for assessing the quality and the nature of coal as a potential source rock. Theoretical charts of the two indexes are used to assess coals as potential source rocks in the Turpan-Hami Basin in northwestern China.

Hydrocarbon expulsion from a source rock is the basis of resource assessment of oil and gas. Model results for hydrocarbon expulsion from a source rock are dependent on the geomathematical models used, selected calculation parameters and available geological data; the sensitivity and uncertainty of the assessments are of greater and greater concern. This paper, applying basin modelling and uncertainty analysis methods to the SHONGLIAO basin, studied the effects and relative contributions of thirteen major geological factors to the uncertainty of model results for hydrocarbon expulsion, as well as examining the variations and distribution probabilities. Formation time of a regional caprock, composition conditions of source-reservoir-caprock, phases of hydrocarbons in migration, and all other geological factors associating with hydrocarbon generation, retention, have effects on the efficiency of hydrocarbon expulsion. The most important factors which result in the largest change of expulsion from the Qingshahou source rock in the North Shongliao basin are: depth of source rock (ZM), sedimentation rate (SR), total organic carbon (TOC %), and kerogen type index (KTI), with relative contributions (%) to the uncertainty of efficient gas/oil migration amounts at 37/32, 25/17, 19/20, and 1/15, respectively. Of these factors, KTI has a greater effect on oil migration than on gas, while SR and ZM have more effect on gas. Within the variation ranges of the thirteen major geological factors, the above four factors collectively contribute to efficient gas/oil migration amounts (m3/kg) from the Qingshahou source rock on a square (or cubic) meter basis as: 1010/1100 (3.0/3.26), 1300/1370 (3.86/4.07), 1460/1525 (4.33/4.53) and 2150/2200 (6.38/6.53), respectively, with corresponding cumulative probabilities of 16%, 50%, 68% and 84%, respectively.