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In this paper, we introduce the concept of an S-asymptotically $ \omega $-periodic process in distribution for the first time, and by means of the successive approximation and the Banach contraction mapping principle, respectively, we obtain sufficient conditions for the existence and uniqueness of the S-asymptotically $ \omega $-periodic solutions in distribution for a class of stochastic fractional functional differential equations.

Cephalanthine (CEP), a bioactive compound derived from Stephania Cephalantha Hayata, is cytotoxic to various malignancies. However, the underlying mechanism of gastric cancer is unknown. CEP inhibited the cellular activity of gastric cancer AGS and HGC27 cell lines in this study. CEP induced apoptosis, reduced Bcl-2 expression, and increased cleaved caspase 3, cleaved caspase 9, Bax, and Bad expression. CEP caused a G2 cell cycle arrest and reduced cyclin D1 and cyclin-dependent kinases 2 (CDK2) expression. Meanwhile, it increased oxidative stress, decreased mitochondrial membrane potential, and enhanced reactive oxygen species (ROS) accumulation in AGS and HGC27 cells. Mechanistically, CEP inhibited Kelch-like ECH-associated protein (Keap1) expression while activating NF-E2 related factor 2 (Nrf2) expression, increasing transcription of Nrf2 target genes quinone oxidoreductase 1 (NQO1), heme oxygenase 1 (HMOX1), and glutamate-cysteine ligase modifier subunit (GCLM). Furthermore, a combined analysis of targeted energy metabolism and RNA sequencing revealed that CEP could alter the levels of metabolic substances such as D (+) - Glucose, D-Fructose 6-phosphate, citric acid, succinic acid, and pyruvic acid, thereby altering energy metabolism in AGS cells. In addition, CEP significantly inhibited tumor growth in MFC BALB/c nude mice in vivo, consistent with the in vitrofindings. Overall, CEP can induce oxidative stress by regulating Nrf2/Keap1 and alter energy metabolism, resulting in anti-ovarian tumor effects. Our findings suggest a potential application of CEP in gastric cancer treatment.

This paper objectively analyzes the challenges faced by the teaching of engineering mathematical analysis, analyzes the connotation and essence of problem-oriented learning and teaching, puts forward the problem-oriented learning and teaching mode, and tries to improve the teaching quality of engineering mathematical analysis.

Ferroptosis is a regulated cell death nexus linking metabolism, redox biology and diseases including cancer. The aim of the present study was to identify a ferroptosis-related gene prognostic signature for stomach adenocarcinoma (STAD) by systematic analysis of transcriptional profiles from The Cancer Genome Atlas (TCGA), GEO and a clinical cohort from our centre. We developed a predictive model based on three ferroptosis-related genes (CHAC1, NOX4 and HIF1A), gene expression data and corresponding clinical outcomes were obtained from the TCGA database, and the reliability of this model was verified with GSE15459 and 51 queues in our centre. ROC curve showed better predictive ability using the risk score. Immune cell enrichment analysis demonstrated that the types of immune cells and their expression levels in the high-risk group were significantly different from those in the low-risk group. The experimental results confirmed that NOX4 was upregulated and CHAC1 was downregulated in the STAD tissues compared with the normal stomach mucosal tissues (p 0.05). In sum, the ferroptosis-related gene signature can accurately predict the outcomes of patients with STAD, providing valuable insights for personalized treatment. As the signature also has relevance to the immune characteristics, it may help improve the efficacy of personalized immunotherapy.

This study aimed to investigate the key role and mechanism of GADD45B in the radiation resistance of nasopharyngeal carcinoma (NPC) cell lines. Radiotherapy-resistant HONE1 (HONE1-R) cells with stable genetic radioresistance were cultured under continuous radiation stimulation. CCK-8 and clone formation assays were used to verify the radioresistance of the cell line. Transcriptome sequencing was used to identify the most important differential signaling pathway in the cell line. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot analysis were used to verify the sequencing results. GADD45B-siRNA was used to knock down the key gene so as to verify the downstream gene expression and analyze its mechanism. The transcriptome analysis showed that 702 genes were upregulated and 772 genes were downregulated in the HONE1-R cell lines. The core differential signaling pathway was mitogen-activated protein kinase (MAPK) signaling pathway, and the core differential gene was GADD45B. After GADD45B was knocked down, the cell viability and proliferation ability of HONE1-R cell lines significantly decreased under radiation, and the expression of cyclin B1 and p-CDK1 decreased significantly. MAPK is the core signaling pathway in radioresistance of NPC. GADD45B plays an important role by affecting cell viability and proliferation in NPC radioresistance. GADD45B is a potential target of radioresistance in NPC.

According to the characteristics of engineering mathematics analysis course, this paper discuss the problem-based teaching design of engineering mathematics analysis from the perspectives of problem raising, problem analysis, problem solving and problem feedback during the whole teaching process.

Shufen Zhao,1 Baiyao Wang,2 Yanning Ma,3 Junjie Kuang,1 Jiyun Liang,3 Yawei Yuan1,2 1Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou City, Guangdong Province 510515, People’s Republic of China; 2Department of Radiation Oncology, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou City, Guangdong Province 510095, People’s Republic of China; 3Shunde Hospital, Southern Medical University, Foshan City, Guangdong Province 528308, People’s Republic of ChinaCorrespondence: Yawei YuanNanfang Hospital, Southern Medical University, 1838 Guangzhou Dadao North, Guangzhou City, Guangdong Province 510515, People’s Republic of ChinaEmail yuanyawei33@163.comBackground: Non-small cell lung cancer (NSCLC) is a predominant type of lung cancer with a high mortality rate.Objective: The aim of this study is to investigate the roles of nuclear casein kinase and cyclin-dependent kinase substrate 1 (NUCKS1) in NSCLC and to identify the potential mechanisms.Materials and Methods: The expression of NUCKS1 in several NSCLC cells was detected firstly. Then, NUCKS1 was overexpressed or silenced in both A549 and NCI-H460 cells, where cell proliferation, invasion and migration were, respectively, determined, using CCK-8, colony formation assay, transwell and wound healing assays. Cell cycle analysis was performed, and the expression-associated proteins were detected by Western blotting. Subsequently, NCI-H460 cells with NUCKS1 overexpression for the subsequent tumor-bearing experiment. And the NUCKS1 expression in tumor tissues was measured by means of immunohistochemistry and Western blotting. Additionally, the STRING database predicted that Cyclin-Dependent Kinase 1 (CDK1) would bind to NUSK1, which was verified by the co-immunoprecipitation assay. Then, CDK1 was silenced by transfection with short hairpin RNA (shRNA)-CDK-1 or by exposure to CDK1 inhibitor p2767-00. And the biological characteristics of proliferation, invasion and migration were examined.Results: Results indicated that NUCKS1 was overly expressed in NSCLC cells, and its overexpression promoted proliferation, invasion and migration of both A549 and NCI-H460 cells while NUCKS1 knockdown displayed the opposite effects. Moreover, the results of the xenograft experiments revealed that NUCKS1-upregulation promoted the tumor growth. Furthermore, the immunoprecipitation assay verified CDK1’s interaction with NUCKS1, and CDK1 knockdown alleviates the impact of NUCKS1 overexpression on NSCLC cell proliferation, invasion and migration.Conclusion: Taken together, these findings demonstrated that NUCKS1 promotes proliferation, invasion and migration of NSCLC by upregulating CDK1, providing a novel putative target for the clinical treatment of NSCLC.Keywords: non-small cell lung cancer, NUCKS1, proliferation, migration, CDK1

Background Gastric cancer (GC) is a common malignancy of the digestive system. Antioxidant activity is regarded as a possible mechanism in ectopic cancer. Hence, oxidative stress regulation is being evaluated for cancer treatment. Previous research has demonstrated that Nestin is associated with antioxidative resistance via its modulation of the Kelch-like ECH-associated protein 1 (Keap1)–nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Methods We determined the role of Nestin-mediated redox homeostasis and tumor phenotypes in GC cells. Results We found that the Nestin expression level was high in GC tissues and cell lines. Nestin knockdown in the GC cell lines SGC-7901 and MKN-45 reduced viability, induced apoptosis, decreased antioxidant enzyme generation, and repressed GC metastasis. Nestin binds to Keap1, resulting in Nrf2 degradation and influencing downstream gene expression. Nestin knockdown resulted in the downregulation of Nrf2 expression in GC cells. The restoration of Nrf2 expression or treatment with the Nrf2 activator sulforaphane counteracted the inhibitory effect of Nestin knockdown on the proliferation, migration, invasion, and antioxidant enzyme production in GC cells. Moreover, xenograft GC tumors exhibited a slower growth rate than those of the control group in vivo. Conclusions Taken together, these findings suggest that the Nestin–Keap1–Nrf2 axis confers oxidative stress resistance and plays an important role in the proliferation, migration, and invasion of GC cells.

Plasma levels of Epstein–Barr virus (EBV) DNA have been employed to predict survival outcomes of patients with nasopharyngeal carcinoma (NPC). However, the prognostic value of subsequent EBV DNA levels (mid or post treatment) for NPC is needed to identify by a large cohort of patients. We performed a meta-analysis of studies including data from 8128 patients to evaluate the prognostic value of EBV DNA in NPC patients. We searched PubMed, Web of Science, and the Cochrane library for prospective and retrospective studies. Hazard ratios (HRs) and confidence intervals (CIs) were extracted from the studies or calculated and pooled to assess the association between EBV DNA levels pre-treatment (pre-DNA), mid-treatment (mid-DNA), and post-treatment (post-DNA) on clinical outcomes. A total of 22 studies with 8128 patients was included for analysis. Pre-DNA levels predicted overall survival, progression-free survival, distant metastasis-free survival, and local–regional failure survival with HRs (95% CIs) of 2.70 (2.06, 3.54), 2.70 (2.12, 3.44), 3.49 (2.35, 5.17), and 2.00 (1.45, 2.76), respectively, and the corresponding HRs for post-DNA levels were 4.86 (3.30, 7.17), 6.29 (3.41, 11.60), 5.68 (2.71,11.93), respectively. Mid-DNA levels predicted overall survival and progression-free survival with an HR (95% CI) of 3.02 (1.54, 5.29) and 3.15 (2.05, 4.83). Subgroup analysis showed that the HR of post-DNA wasn’t influenced by different detection time of post-DNA (P = 0.22, I2 = 33.2%). The EBV DNA levels have a significant prognostic impact in patients with NPC. The effect of post-treatment EBV DNA level dominated that of pre-DNA and mid-DNA levels.

e16044 Background: Docetaxel-based neoadjuvant chemotherapy has been suggested to be beneficial in patients with locally advanced gastric and gastro-oesophageal junction cancer (GC/GEJC). And immunotherapy also show promising treatment efficacy for advanced GC/GEJC. Here we compared the safety and efficacy of camrelizumab combined with chemotherapy versus chemotherapy alone as the neoadjuvant therapy for patients with resectable locally advanced GC/GEJC. Methods: Eligible patients diagnosed as resectable locally advanced GC/GEJC were randomized to receive neoadjuvant treatment, in arm A, the patients received FLOT alone, in arm B, the patients received FLOT combined with camrelizumab(camrelizumab 200mg intravenously every 3 weeks). Eligible patients underwent gastrectomy with D2 lymph node dissection. The primary end point of this trial was pCR rate and R0 resection rate, and the secondary end points were ORR,PFS, OS and safety profile. Results: From January 15 2020 to January 15 2022, 61 patients were recruited (28 patients in arm A and 33 patients in arm B). 51 patients had completed planned neoadjuvant treatment for 4 cycles (25 pts in the arm A, 26 ptsin the arm B). Four patients in the arm A were failure to complete surgical treatment. This analysis was based on the 47 pts. In the arm A, the median age was 63 years (45-74 years) and a total of 16 males and 4 females, ECOG PS 0 (n = 3), ECOG PS 1 (n = 18). In the arm B, the median age was 63 years (28-72 years) and a total of 20 males and 6 females, ECOG PS 0 (n = 5), ECOG PS 1 (n = 21). The R0 resection rate was high in arm B compared with arm A (26/26,100% vs. 19/21, 90.5%). The same results are also reflected in pCR:arm B compared with arm A (3/26,11.5% vs. 1/21, 4.8%). Tumour regression grade were as follows:TRG0 [arm A 5% (1/21), arm B 15% (4/26)], TRG1 [arm A 10% (2/21), arm B 4% (1/26)], TRG2 [arm A 33% (7/21), arm B 54% (14/26)], TRG3 [arm A 52% (11/21), arm B 27% (7/26)].There was a greater proportion of postoperative stage ypN0 in arm B [arm A 24% (5/21); arm B 46% (12/26)]. Postoperative pathologic staging was as follows: ypT0 [arm A 5% (1/21); armB 15% (4/26)].ypT1 [arm A 14% (3/21); armB 8% (2/26)]. ypT2 [armA 0% (0/21); armB 27% (7/21)]. ypT3 [arm A 57% (12/21); arm B 38% (10/26)]. ypT4 [armA 24% (5/21); armB 12% (3/26)]. Neither serious intraoperative complications nor immune-related adverse events were observed during perioperation. Treatment-related AEs neutropenia and leukopenia were manageable and there was no treatment-related death. Conclusions: Camrelizumab combined with FLOT showed promising efficacy as neoadjuvant treatment for patients with locally advanced gastric or GEJ adenocarcinoma, with low complications and acceptable toxicity. Clinical trial information: ChiCTR2000030610.

Background: E2F2 is a member of the E2F family of transcription factors with important yet incompletely understood biological functions in cancer. In some cancer types, controversial tumor-promoting and tumor-suppressive roles of E2F2 have been reported. However, the biological role of E2F2 in gastric cancer (GC) remains to be determined. Methods: We analyzed E2F2 expression via multiple gene expression databases. The prognostic value of the E2F2 was determined by Kaplan-Meier Plotter and Cox regression. The correlations between E2F2 and cancer immune infiltrates were investigated via Tumor Immune Estimation Resource (TIMER). The functions and pathways of E2F2 and its 50 frequently changed genes closely associated with the family members were analyzed using Database for Annotation, Visualization, and Integrated Discovery (DAVID) software. We used immunohistochemistry (IHC), quantitative real-time PCR (qPCR) and western blot to verify the expression level of E2F2 in GC and further studied the effects of E2F2 on PI3K/Akt/mTOR activity; GC cell autophagy, migration, and invasion through wound healing assays, transwell assays, Western blotting, and transmission electron microscopy.Results: We observed that compared with normal gastric tissues/cells, E2F2 is highly expressed in gastric cancer tissues and cells in both the public datasets and in our experimental verification. High E2F2 expression was associated with poorer overall survival (OS). Moreover, E2F2 expression showed strong correlations with diverse immune marker sets in GC. Moreover, E2F2 overexpression promoted GC cell migration and invasion in vitro by inactivating PI3K/Akt/mTOR-mediated autophagy. Conversely, E2F2 inhibition suppressed GC cell migration and invasion in vitro by activating PI3K/Akt/mTOR-mediated autophagy.Conclusions: In conclusion, this study provides multi-level evidence for the importance of E2F2 in gastric carcinogenesis and its potential as a biomarker in GC. We demonstrated that E2F2 is overexpressed in GC and that high E2F2 expression is associated with aggressive tumor features and poorer patient prognosis. Further, our results suggest a potential novel immune regulatory role of E2F2 in tumor immunity. Functionally, we discovered a new role of E2F2 in regulating PI3K/Akt/mTOR-mediated autophagy and the downstream processes of cell migration and invasion. Our results could potentially reveal new targets and strategies for GC diagnosis and treatment.

Background E2F2 is a member of the E2F transcription factor family and has important but not fully understood biological functions in cancers. The biological role of E2F2 in gastric cancer (GC) also remains unclear. Methods We examined the expression levels of E2F2 in GC using publicly available datasets such as TIMER, Oncomine, GEPIA, UALCAN, etc., and in our patient cohort, using quantitative real-time PCR, western blotting, and immunohistochemistry. We further investigated the effects of E2F2 on phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling, autophagy, and the migration and invasion of GC cells by the wound healing assay, Transwell assay and transmission electron microscopy. Results E2F2 was highly expressed in both GC tissues and cells compared with normal gastric tissues/cells. High E2F2 expression was associated with poor overall survival (OS). In addition, the expression of E2F2 in GC was strongly correlated with a variety of immune markers. E2F2 overexpression promoted the migration and invasiveness of GC cells in vitro through inhibition of PI3K/Akt/mTOR-mediated autophagy. Conclusion High E2F2 expression was associated with the characteristics of invasive tumors and poor prognosis. E2F2 also had potential modulatory effects on tumor immunity. We discovered a novel function of E2F2 in the regulation of PI3K/Akt/mTOR-mediated autophagy and the downstream processes of cell migration and invasion.

Landslide exposes the previously blocked groundwater discharge. High concentrations of soluble salt form salt sinters that can be observed near discharge passages. Based on existing laboratory investigation results of soil leaching and shearing reported in the literature, the effect of the soluble salt loss via spring water on irrigation-induced landslide deformation was studied under large-scale conditions. During our field investigation of landslides in the Heitai terrace of the Yellow River&rsquo, s upper reaches in Gansu Province, China, 35 spring outlets were found, and the Heitai terrace was divided into five subareas, based on the difference in spring flow. Deformation data for the terrace were obtained by small baseline subset technology (SBAS-InSAR). These data were analyzed in combination with the amount of soluble salt loss, to explore the correlation between the deformation of the landslide and the soluble salt loss in the loess irrigation area. The results showed that the cumulative deformation and the loss of soluble salt were increasing continuously in the terrace. Although the increasing intensity of each subarea was different, the changing intensity of the two during the corresponding monitoring period was highly consistent. The statistical analysis revealed a strong positive correlation between the accumulated loss of soluble salt via spring water and the accumulated displacement of the terrace edge (p &lt, 0.01). After the slope k between the two was tested by the Grubbs test and t-test, the k was no abnormality (&alpha, = 0.05) and difference (Sig &gt, 0.05), further providing the basis for confirming the existence of this positive correlation. When the loss of soluble salt in rock and soil increased gradually, the accumulated deformation of the terrace edge also increased continuously. The findings of this study are of great significance for understanding the formation mechanism of landslides and the identifying landslide revival in irrigation areas of the Loess Plateau.

The tradeoff between cost and efficiency is omnipresent in organisms. Specifically, how the evolutionary force shapes the tradeoff between biosynthetic cost and translation efficiency remains unclear. In the cancer community, whether the adjustment of cost-efficiency tradeoff acts as a strategy to facilitate tumor proliferation and contributes to oncogenesis is uninvestigated. To address this issue, we retrieved the gene expression profile in various cancer types and the matched normal samples from The Cancer Genome Atlas (TCGA). We found that the highly expressed genes in cancers generally have higher tAI/nitro ratios than those in normal samples. This is possibly caused by the higher tAI/nitro ratios observed in oncogenes than tumor suppressor genes (TSG). Furthermore, in the cancer samples, derived mutations in oncogenes usually lead to higher tAI/nitro ratios, while those mutations in TSG lead to lower tAI/nitro. For a special case of kidney cancer, we investigated several crucial genes in tumor samples versus normal samples, and discovered that the changes in tAI/nitro ratios are correlated with the changes in translation level. Our study for the first time revealed the optimization of cost-efficiency tradeoff in cancers. The cost-efficiency dilemma is optimized by the tumor cells, and is possibly beneficial for the translation and production of oncogenes, and eventually contributes to proliferation and oncogenesis. Our findings could provide novel perspectives in depicting the cancer genomes and might help unravel the cancer evolution.

Background E2F is a family of transcription factor proteins involved in multiple processes, including cell cycle regulation, cell differentiation, the DNA damage response and cell death. Studies have shown that E2Fs have prognostic significance in many cancers, but the expression patterns and prognostic values of E2Fs in gastric cancer have not been systematically elucidated. Methods In this study, we used the ONCOMINE database and UALCAN online analysis to compare the transcriptional levels and expression of eight E2F family members between gastric cancer and normal samples. UALCAN was also used to analyze the relationship between the expression of 8 E2F members and clinicopathological parameters. A protein-protein interaction (PPI) network was constructed using the STRING database. The functions and pathways of the E2F family and 50 frequently changed genes closely associated with the family members were analyzed using Database for Annotation, Visualization, and Integrated Discovery (DAVID) software. The prognostic value of the E2Fs was determined by Kaplan-Meier Plotter and Cox regression. Western blot and qPCR were used to analyze the expression of E2F2 in gastric cancer. CCK8 and EdU analyses were conducted to assess cell proliferation, and wound-healing and Transwell assays were used to analyze cell migration and invasion. Results The expression patterns of 8 E2F members were significantly related to the clinical cancer stage and tumor grade of gastric cancer patients. A high mutation rate (51%) for E2Fs was observed in patients with gastric cancer. In addition, high mRNA expression of E2F1/2/3/4/5 was a prognostic factor for poor overall survival (OS) in gastric cancer patients, while high expression of E2F6/7/8 was associated with better OS. Cox regression analysis found that E2F2 can be used as an independent prognostic factor for gastric cancer, and compared with normal cells, the expression of E2F2 in gastric cancer cells was significantly increased. In addition, we found that E2F2 silencing inhibits the proliferation, invasion and metastasis of gastric cancer cells. Conclusions Our study evaluated the expression and prognosis of the E2F family in gastric cancer and discussed the role of E2F2 in gastric cancer in detail. We found that members of the E2F family show differences in expression between cancer and normal tissues and may be closely related to the prognosis of gastric cancer. Among them, E2F2 can serve as an independent prognostic factor for gastric cancer and promote the proliferation, invasion and metastasis of gastric cancer cells. These data indicate that E2F2 could be a potential biomarker for gastric cancer.

Background E2F is a family of transcription factor proteins with multiple functions; E2F proteins are involved in cell cycle regulation, cell differentiation, the DNA damage response and cell death. Studies have shown that E2Fs have prognostic significance in many cancers, but the expression patterns and prognostic values of E2Fs in gastric cancer have not been systematically elucidated. Methods In this study, we used the ONCOMINE database and UALCAN online analysis website to compare the transcriptional levels and expression of eight E2F family members between gastric cancer and normal samples. UALCAN was also used to analyze the relationship between the expression of 8 E2F members and clinicopathological parameters. The prognostic value of the E2Fs were determined by Kaplan-Meier Plotter. A protein-protein interaction (PPI) network was constructed using the STRING database. The functions and pathways of E2F family and its neighboring 50 frequently changed genes were analyzed using the Database for Annotation, Visualization, and Integrated Discovery (DAVID) software. Finally, quantitative PCR was used to verify the expression of E2Fs in gastric cancer cells. Results The expression patterns of 8 E2F members were significantly related to the clinical cancer stage and tumor grade of gastric cancer patients. High mRNA expression of E2F1/2/3/4/5 was a prognostic factor for poor OS in gastric cancer patients, while high expression of E2F6/7/8 was associated with better OS. In addition, a high mutation rate (46%) for E2Fs was observed in patients with gastric cancer. The expression levels of E2F1/2/3/5/8 in AGS and HGC27 cell lines were higher than those in normal cells, while E2F7 showed the opposite trend. Conclusions In summary, these results indicate that E2F1/2/3/4/5 can be used as potential therapeutic targets in gastric cancer, and E2F6/7/8 can be used as new prognostic markers to improve the survival rate and prognostic accuracy in gastric cancer.

Hybrid-drugs chemotherapy is now one of the widely adopted treatments for cancer prevention with favorable diagnoses. This work has proposed compostable paclitaxel (PTX) and biotin (BT) PCEC nanomaterials (NMs) for the codelivery and to investigate the drug delivery mechanism's efficacy (PTX@BT-NMs) against gastric cancer cells in vitro and in vivo. The fabricated PTX@BT-NMs were 27.97 ± 1.87 nm in size and had a less polydispersity index (0.156 ± 0.030). PTX and BT were released slowly from the drug delivery without any burst impact. In addition, dose-responsive cytotoxic effects were observed for PTX@BT-NMs on SGC-791 cells with a higher mortality ratio than free drugs. According to a cellular uptake investigation, drug-loaded PCECs of polymeric liquid nanoparticles were considered better by cancer cells in vitro. To assess the in vivo antitumor activity, PTX@BT-NMs were administered intravenously injected to xenografted with SGC-791 cells. Substantial inhibition of tumor development was observed with extended survival time and decreased side effects with PTX@BT-NMs compared to free drugs (PTX + BT). Furthermore, compared to other therapy classes, PTX@BT-NMS care resulted in lower H&E and Ki67 expressions and improved TUNEL positive in cancer cells, indicating the chemotherapeutic efficiency of drug delivery system. Overall, the current investigation confirmed that DDS PTX@BT-NMs could be used to successfully combat gastric cancers in the immediate future.

Part of the gravitational potential energy of a landslide is converted into heat or other forms of energy via irreversible processes such as inelastic collisions and fragmentation between particles. In this study, we define the gravitational potential energy component as additional work W, which is numerically equivalent to Mgc. Based on the model proposed by Heim (1932), we conceptualize landslide movement as the movement of particles, and the concept of extra work is used to establish a model to estimate landslide sliding distance. Twenty-seven irrigation-induced loess landslides were used to build a model for the Heitai terrace in the upper reaches of the Yellow River in Gansu Province, China. Considering the additional work W, the average relative error and average error between the estimated value and the measured value were significantly reduced (the average relative error was reduced from 11.21% to 6.27%, and the average error was reduced from 20.4 m to 9.6 m). Ten landslides in the Heitai terrace and 13 landslides on the south bank of the Jing River in northwest China were used to verify the model. The average relative errors between the estimated and observed values are 5.55% and 7.78%, respectively. In addition, based on data from earthquake-induced loess landslides, we use the model to further explore the significance of additional work in the construction of a sliding distance prediction model. The results of the model show that the introduction of additional work improved the accuracy of the predicted sliding distance. The model has a good applicability to loess landslides with volumes

Small molecule tyrosine kinase inhibitors (TKIs) have transformed the management of advanced non-small-cell lung cancer (NSCLC) harboring activating epithelial growth factor receptor (EGFR) mutations, while the efficacy of TKIs in the adjuvant setting remains unclear. We collected the data of 209 EGFR-mutant NSCLC patients receiving complete resection from 2010 to 2013. Study end points were disease-free survival (DFS) and overall survival (OS). Among the eligible patients, 41 (19.6%) received EGFR TKIs in the adjuvant treatment. The 3-year DFS of adjuvant EGFR TKIs treatment group (70.5%, 95% CI, 54.6–86.4%) was significantly superior that control group (50.2%, 95% CI, 40–60.4%; log-rank P = 0.014). TKIs treatment (HR, 0.51; 95% CI, 0.29–0.97; P = 0.04) was significantly associated with improved DFS in multivariate Cox analysis. No significant difference was observed in 3-year OS between two groups (73.1% [58.0–88.2%] vs 61.8% [52.2–71.4%], log-rank P = 0.21). Propensity-score matching further confirmed that adjuvant TKIs treatment extended the DFS (log-rank P = 0.024), but did not improve OS (log-rank P = 0.40). Our analysis revealed that adjuvant EGFR TKIs treatment was beneficial for early-stage NSCLC patients harboring activating EGFR mutations after complete resection.

Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. The aim of the present study was to reveal the prognostic significance of CD147 and to preliminarily explore the molecular mechanisms involved. Blood and tumor tissue specimens were obtained from 133 HCC patients. All patients were followed up for 4 years. The serum and tissue levels of CD147 were analyzed using ELISA and immunohistochemistry, respectively. The SMMC-7721 hepatoma carcinoma cell line was transfected with CD147 overexpression vector and cell migration was evaluated using a wound healing assay. Extracellular signal-regulated kinase (ERK) inhibitor UO126 was applied to study the role of the ERK pathway in cell migration. CD147 expression in HCC tissue was associated with poor prognosis of patients [odds ratio (OR): 3.13, 95% confidence interval (CI): 1.52–6.43], and patients with no CD147 expression had a significantly survival advantage (P=0.016). However, serum CD147 levels had no such prognostic significance (OR: 1.94, 95% CI: 0.96–3.91; P=0.097). In the wound healing assay, the wound distance in the non-transfected cell group was wider than that in the transfected cell group without UO126 treatment (178.0±31.1 vs. 106.0±20.7 µm; P=0.003), but similar to that in the transfected cell group with 10 µM UO126 treatment (170.4±13.2 µm; P=0.629). The present study revealed that the expression of CD147 in HCC tissue is an independent prognostic indicator. In addition CD147 overexpression may be associated with tumor cell migration and ERK signaling pathway activation.

Squamous cell carcinoma (SCC) originating from the colon is rare. In terms of its clinicopathological characteristics, this type of cancer has been reported to be more aggressive and have a worse prognosis compared with adenocarcinoma. We herein present a successful therapeutic approach applying neoadjuvant and adjuvant gemcitabine-based chemotherapy in a patient with colon SCC. A 58-year-old male patient received two cycles of neoadjuvant chemotherapy with a regimen including gemcitabine, oxaliplatin and capecitabine, followed by radical excision and six cycles of adjuvant chemotherapy. Contrast-enhanced computed tomography and serum tumor markers were used for reassessment and evaluation was based on the World Health Organization criteria. Following neoadjuvant chemotherapy, the mass had shrunk and the patient was classed as having stable disease. Surgery and adjuvant chemotherapy were then performed and the patient had achieved a progression-free survival of 10 months when this report was submitted. Therefore, gemcitabine may be a treatment option for colon SCC in the neoadjuvant and/or adjuvant chemotherapy setting.

The discharge mechanism of the supercritical nitrogen (SCN2) at the critical point 127 K and 3.4 MPa were discussed, and the key parameters showing the discharge behaviors of the SCN2 were calculated numerically by the BOLSIG+. Furthermore, the dynamical behaviors of the SCN2 clustering are carefully demonstrated by the molecule dynamics theory and some distinctively phenomena are discovered by the simulating calculation under the 50, 100, 150, 200, 250, 300, 350, 400, 450 and 500 Td. The results show that SCN2 is a promising new dielectric in the future.

Objective: To evaluate the clinical efficacy of intensity modulated radiation therapy and endocrinotherapy for middle and advanced prostate cancer. Methods: Total 104 elderly patients with middle and advanced prostate cancer who were admitted to our hospital from November 2014 to August 2015 were selected using random number table method. They were divided into intensity-modulated radiotherapy combined with endocrinotherapy group (observation group) and conventional radiotherapy combined with endocrinotherapy group (control group), 52 each. The serum levels of prostate specific antigen (PSA) and free prostate antigen (f PSA) were measured three months after treatment. The short-term efficacy and toxic and side effects of the patients were observed, and the survival rate was recorded through three-year follow up. Results: The clinical effective rate of the observation group was 92.68%, and that of the control group was 70.73%; there was a significant difference between the two groups (P0.05). The serum PSA and f PSA levels after treatment were significantly lower than before treatment. The incidence of adverse reactions in the observation group was lower than that in the control group (P0.05). Conclusion: Intensity modulated radiotherapy combined with endocrinotherapy was safe and well tolerated in the treatment of middle and advanced prostate cancer. It can improve the short-term efficacy and effectively reduce the serum oncological index concentration of patients. It can be promoted in clinics. doi: https://doi.org/10.12669/pjms.35.5.591 How to cite this:Zhang S, Zhao S, Fu X. Intensity modulated radiotherapy in combination with endocrinotherapy in the treatment of middle and advanced Prostatic Cancer. Pak J Med Sci. 2019;35(5):1264-1269. doi: https://doi.org/10.12669/pjms.35.5.591 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

In this paper, stochastic dynamics with Lévy noise of two-consumers-one-resource competing systems with Beddington–DeAngelis functional response are considered. We first show the existence of the global positive solution, then discuss the effects of noises on the extinction of the species and the stochastic persistence of the species. In the meanwhile, numerical simulations are carried to support results. Finally, we show the existence of the stationary distribution for a special case.

The present study identified that fibroblast growth factor receptor 3 (FGFR3) was significantly upregulated in bone metastasis of lung adenocarcinoma. RNA interference (RNAi) is a powerful approach for treating a wide range of human diseases, including cancer, through downregulating the expression of selected genes. In the present study, the invasiveness of A549 cells cultured in vitro was altered by small interfering (si)RNA targeting FGFR3, and the regulatory effect of silencing FGFR3 on the expression levels of E-cadherin and matrix metalloproteinase (MMP)9 was investigated. Human lung adenocarcinoma A549 cells were transfected with synthetic specific siRNAs targeting a fragment of the FGFR3 gene (namely, siRNA-855, siRNA-1447 and siRNA-2076) or with negative control (NC) siRNA. Cells were divided into five groups (A, siRNA-855 group; B, siRNA-1447 group; C, siRNA-2076 group; D, NC-siRNA group; and E, blank control group). The effect of the above siRNAs targeting FGFR3 on the invasion capacity of A549 cells was detected by Transwell assay. siRNAs against FGFR3 were transfected into A549 cells with by Lipofectamine® 2000, and the expression levels of FGFR3, E-cadherin and MMP9 were measured by reverse transcription-quantitative polymerase chain reaction and western blot assay. The experimental findings indicated that the expression levels of FGFR3 and MMP9 were significantly reduced in the siRNA-FGFR3-transfected groups (A-C groups), compared with those in the D and E groups (P0.05). These results indicated that siRNA-FGFR3 was able to decrease the invasiveness of A549 cells, inhibit the expression of MMP9 and increase the expression of E-cadherin by downregulating the expression of FGFR3. Taken together, the results of the present study indicated that the upregulation of E-cadherin expression and the downregulation of MMP9 expression are able to inhibit the migration of A549 cells, and siRNA silencing FGFR3 acts as a tumor suppressor in these cells.

Tetraspanins are a large superfamily of glycoproteins, which are engaged in a wide range of specific molecular interactions by forming tetraspanin-enriched microdomains. Tetraspanin 9 (Tspan9) is a previously poorly studied tetraspanin gene, which was predominantly identified as an amplified gene in serous Fallopian tube carcinoma. However, the expression and role of Tspan9 in gastric cancer have yet to be fully elucidated. The aim of the present study was to evaluate the expression and clinical significance of Tspan9 in gastric cancer. In the present study, 105 gastric cancer tissue samples and corresponding adjacent normal samples were detected for Tspan9 expression using immunohistochemistry; furthermore, the association between clinical characteristics and Tspan9 expression was also analyzed. Tspan9 expression was determined to be significantly lower in cancer samples compared with those in corresponding adjacent normal samples (P