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OBJECTIVE: Network pharmacology is a bioinformatics-based research strategy for identifying the mechanisms of drugs and promoting drug development. This study used network pharmacology to investigate the mechanism of the Loulu-Cremastrae Pseudobulbus drug pair treating breast cancer (BC). MATERIALS AND METHODS: The ingredients and potential targets of the drug pair were searched with Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCSMP). National Center for Biotechnology Information (NCBI) and gene cards were used to search the targets of BC. Networks of "drugs-components-targets" and protein-protein interaction were constructed through Cytoscape. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were carried out through common targets. Using AutoDock tool, molecular docking was performed to verify the binding between key targets and compounds. RESULTS: Finally, we selected 6 active compounds from the drug pair. A total of 61 targets were associated with the drug pair, and 15,295 targets were related to BC. 55 common targets were obtained after the intersection. The key targets included Transcription factor Jun (JUN), Heat shock protein HSP 90-alpha (HSP90AA1), and Caspase-3(CASP3). 327 terms were obtained by GO analysis. 78 pathways (p < 0.05) were identified through KEGG analysis. Molecular docking indicated that important compounds combined well with key targets. CONCLUSIONS: Various active compounds, including beta-sitosterol, 2-methoxy-9,10-dihydrophenanthrene-4,5-diol, and stigmasterol, can regulate multiple signaling pathways related to BC, such as the estrogen and prolactin signaling pathways, playing therapeutic roles in BC. [ABSTRACT FROM AUTHOR]

The aim of this study was to analyse the impact of postoperative positron emission tomography–computed tomography (PET–CT) before adjuvant treatment in oral squamous cell carcinoma (OSCC) patients. Patients with OSCC requiring adjuvant treatment following surgery were divided retrospectively into two groups based on the implementation of PET–CT. The study endpoints were disease-specific survival (DSS) and overall survival (OS). A total of 123 patients underwent PET–CT examination; 28 had abnormal images, but only seven were confirmed to be pathologically positive. A total of 145 patients underwent computed tomography/magnetic resonance imaging (CT/MRI) examination; 20 had abnormal images, but only one was confirmed to be pathologically positive. The median OS time was 5.4 years in the PET–CT group and 4.3 years in the CT/MRI group, demonstrating a significant difference (P = 0.024). Findings were similar for the median DSS time. In patients with positive PET–CT results, the median DSS was 4.3 years and median OS was 3.5 years, and in those with negative PET–CT results, the median survival time could not be calculated as fewer than 50% of patients reached these endpoints; both differences were significant (P = 0.007 and P < 0.001). Although the false-positive rate of postoperative PET–CT is high, it improves the chance of survival through early and more frequent detection of recurrence. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Stomach adenocarcinoma (STAD) is the major cancer worldwide with high morbidity and mortality rate. Late diagnosis and limited treatment options of STAD lead to disease progression, spread, and metastasis. Therefore, finding a new biomarker to diagnosis and treatment is very important for STAD in clinical practice. MATERIALS AND METHODS: The clinical data, transcriptome data and CCLE data were downloaded from TCGA database and CCLE database, respectively. TIMER website, TISIDB website and CIBERSORT methodology were used to analyse immune infiltration. R software and R package were used to analyse gene difference expression, determine co-expression genes, conduct gene enrichment analyses, construct a prognostic signature and establish nomogram. RESULTS: MASP1 was decreased in STAD compared with normal tissue at the mRNA level (p < 0.001). The enrichment analysis showed that mismatch repair (MMR) was related to the MASP1 gene. Up-regulation of MAPS1 expression was positively associated with dendritic cells (p < 0.01), neutrophils (p < 0.05), macrophages (p < 0.001), CD4+ T cells (p < 0.001) and B cells (p < 0.05). A four-gene prognostic signature was determined based on MASP1-related immunomodulators. The prognostic signature was an independent prognostic predictor in STAD. Finally, we established a nomogram to forecast survival and the nomogram has a good prediction accuracy. CONCLUSIONS: In STAD, MASP1 is closely related to immunity. MASP1 has the potential to positively regulate the abundance of immune cells. The MASP1-related prognosis signature and nomogram can accurately predict the survival of patients with STAD. Therefore, MASP1 is likely to be a diagnosis and promising immunotherapy target spot in STAD clinical practice. [ABSTRACT FROM AUTHOR]

The feasibility of submandibular gland (SMG) preservation during neck dissection has been described. The aim of this study was to analyse the functional outcomes in patients undergoing SMG preservation during neck dissection for cT1–2N0 oral squamous cell carcinoma. Consecutive patients were divided into two groups based on the management of the SMG, and underwent a saliva flow test before surgery, 7 days after surgery, and at 3, 6, 9, and 12 months after surgery. All enrolled patients completed the fourth version of the University of Washington Quality of Life (UWQOL) questionnaire at 12 months after surgery. In patients who underwent SMG preservation during neck dissection, the flow rate at 7 days after surgery was significantly lower than that preoperative; however, it gradually returned to baseline at 9 months after surgery. The saliva flow rate at 9 months after surgery was similar to that at 12 months after surgery. Further, patients with SMG preservation had higher scores for the activity, swallowing, chewing, and saliva domains than patients without SMG preservation. The results of the study suggest that saliva secretion ability can be preserved following SMG-sparing neck dissection, and that SMG preservation improves postoperative quality of life. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Our review aims at comparing the morbidity and mortality-related risks associated with the pre-injury administration of VK-antagonists or DOACs in elderly patients with TBI. MATERIALS AND METHODS: We performed a systematic search of the academic literature across five databases (Web of Science, EMBASE, CENTRAL, Scopus, and MEDLINE), following PRISMA guidelines. We conducted a random-effect meta-analysis to compare the influence of pre-injury VK-antagonists or DOACs administration on the overall intensive care unit and hospital stays of patients with TBI. We also evaluated the overall risks associated with VK-antagonists and with DOACs for intracranial hemorrhage progression, surgical intervention, and overall mortality in patients with TBI. RESULTS: From 973 studies, we found 11 eligible with 4,991 patients with traumatic brain injury (mean age, 77.82 ± 6.76 years). Our meta-analysis revealed insignificantly higher odds of surgical intervention (OR=1.72) and mortality (OR=1.07) associated with VK-antagonists administration than with DOACs administration. Similarly, we found that the intensive care unit (Hedge's g, 0.13) and hospital (g, 0.26) stays were insignificantly longer for individuals on VK-antagonists than for those on DOAC. Moreover, we observed insignificantly higher intracranial hemorrhage progression risks (OR=1.22) for individuals receiving DOACs than for those receiving VK-antagonists. CONCLUSIONS: This study provides evidence on the morbidity and mortality-related outcomes associated with the pre-injury administration of VK-antagonists or DOACs in patients with TBI. We found no significant differences between VK-antagonists and DOACs on the overall morbidity (hospital and intensive care unit stays, intracranial hemorrhage, and surgical intervention frequency) and mortality outcomes in elderly patients with TBI. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Hepatopulmonary syndrome (HPS) is a kind of pulmonary microvascular disease and occurs in 15%-30% cirrhosis. This study aimed to investigate the effects of pulmonary CX3CR1 on angiogenesis and associated mechanisms in HPS animal models. MATERIALS AND METHODS: CX3CR1GFP/ GFP mice were constructed by replacing CX-3CR1 with GFP. Common bile duct ligation (CBDL) mouse model was established with surgery. Release of nitric oxide (NO) was evaluated. Hematoxylin-eosin (HE) staining was employed to examine the inflammation of lung tissues. CD31 expression was detected with immunohistochemistry assay. Western blotting was used to evaluate the expression of CX3CL1, CX3CR1, phosphorylated-AKT (p-AKT), phosphorylated-ERK (p-ERK). Quantitative Real Time-PCR (qRT-PCR) assay was used to examine VEGF, PDGF, iNOS, eNOS, and HO-1 expression. RESULTS: CX3CR1-deficiency (CX3CR1GFP/ GFP-sham or CX3CR1GFP/GFP-CBDL mice) significantly reduced NO release compared to wide type (WT)-mice or WT-CBDL mice (p<0.05). CX3CR1-deficiency significantly alleviated inflammation compared to wide type (WT)-mice or WT-CBDL mice (p<0.05). CX3CR1-deficiency significantly reduced CD31 expression compared to WT-sham and WT-CBDL mice, respectively (p<0.05). CX3CR1 also participated in anti-angiogenesis efficacy of Bevacizumab. CX-3CR1-deficiency significantly down-regulated the ratio of p-AKT/AKT and p-ERK/ERK and inhibited the secretion of VEGF and PDGF compared to WT-mice (p<0.05). CX3CR1-deficiency significantly reduced iNOS, eNOS, and HO-1 expression compared to WT-mice (p<0.05). CONCLUSIONS: CX3CR1 deficiency reduced VEGF and PDGF production, inhibited p-AKT, and p-ERK activation and down-regulated iNOS, eNOS, and HO-1 expression. Therefore, CX-3CR1 participates in pulmonary angiogenesis in the experimental HPS mice via inhibiting AKT/ ERK signaling pathway and regulating NO/NOS release. These findings would provide a potential insight for clarifying the pathological mechanisms of HPS. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of this study was to explore the effect of long non-coding ribonucleic acid (lncRNA) KCNQ1 overlapping transcript 1 (KCNQ1OT1) on fracture healing and its possible mechanism. PATIENTS AND METHODS: Abnormal lncRNAs were compared between patients with delayed fracture healing and those with normal fracture healing using gene expression profiling method. LncRNA expression in patients was verified by quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). Subsequently, the model of tibial fracture was successfully established in rabbits. The effect of lncRNA KCNQ1OT1 expression on tibial fracture healing in rabbits was explored. Meanwhile, the effects of lncRNA KCNQ1OT1 on cell proliferation and apoptosis were investigated by knockdown and overexpression experiments with HC-a as a cell model. Furthermore, Western blotting was used to explore the expressions of proteins in signaling pathway affected by lncRNA KCNQ1OT1. RESULTS: Gene expression profiling and qRT-PCR revealed that lncRNA KCNQ1OT1 was significantly down-regulated in bone tissues of patients with delayed fracture healing. Compared with the control group, knocking down lncRNA KCNQ1OT1 remarkably reduced the serum levels of alkaline phosphatase (ALP) and osteoprotegerin (OPG) in rabbits, and markedly decreased bone trabecular growth index (p<0.05). In HC-a cells, overexpression of lncRNA KCNQ1OT1 activated the Wnt/β-catenin signaling pathway, which could be suppressed by knocking down lncRNA KCNQ1OT1. Cell Counting Kit-8 (CCK-8) assay and 5(6)-carboxyfluorescein diacetate, succinimidyl ester (CFSE) results manifested that lncRNA KCNQ1OT1 remarkably promoted the proliferation and inhibited apoptosis of HC-a cells by activating the Wnt/β-catenin signaling pathway. CONCLUSIONS: LncRNA KCNQ1OT1 plays a vital role in delayed fracture healing. Moreover, it can induce cell proliferation and inhibit cell apoptosis by activating the Wnt/β-catenin signaling pathway. Therefore, KCNQ1OT1 may be used as a biomarker to predict the occurrence of delayed fracture healing. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Hepatocellular carcinoma (HCC) is a common malignant tumor that poses a serious threat to human health and life. Metastasis is one of the reasons for high rate of relapse. Due to the lack of effective treatment, the prognosis of HCC patients is far from satisfactory. The aim of this study was to investigate the role of long non-coding RNA (lncRNA)- TPTE2P1 in HCC development. Moreover, we aimed to search for new biomarkers which could predict the metastasis and provide novel therapeutic strategies for HCC. PATIENTS AND METHODS: Quantitative real- time polymerase chain reaction (qRT-PCR) was used to evaluate the expression level of lncRNA- TPTE2P1 in both HCC tissues and cell lines. Wound-healing assay and transwell assay were applied to determine the ability of cell migration. Meanwhile, transwell matrigel assay was applied to detect the invasion of HCC cells. The protein expressions of E-cadherin, Vimentin and N-cadherin in chosen cell lines were detected by Western blotting. RESULTS: Results found that lncRNA-TPTE2P1 was overexpressed in both HCC tissues and cell lines. Further analysis revealed that overexpression of lncRNA-TPTE2P1 was correlated with tumor size, distant metastasis, differentiation degree, as well as tumor node metastasis (TNM) stage of HCC patients. Subsequent wound-healing assay, transwell assay and Matrigel assay confirmed that down-regulated lncRNA-TPTE2P1 could significantly suppress the invasion and migration of cells. However, up-regulation of lncRNA- TPTE2P1 showed the opposite results. Moreover, lowly expressed lncRNA-TPTE2P1 significantly decreased the protein levels of E-cadherin, Vimentin and N-cadherin. These results indicated that lncRNA-TPTE2P1 might stimulate the migration and invasion of HCC cells by promoting epithelial-mesenchymal transition (EMT). CONCLUSIONS: In summary, our results suggested that lncRNA-TPTE2P1 functioned as an oncogene in HCC. Meanwhile, lncRNA-TPTE2P1 stimulated HCC cell migration and invasion by promoting EMT. LncRNA-TPTE2P1 might play a vital role in the development and progression of HCC. Our findings demonstrated that lncRNA- TPTE2P1 could serve as an early biomarker of metastasis and therapeutic target for HCC. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of this study was to investigate the protective effect of sitagliptin on cardiac function in mice with diabetes and myocardial infarction (MI), and to explore its possible mechanism using the mouse models of diabetes and MI. MATERIALS AND METHODS: The models of diabetes and MI were established using C57BL/6 mice. All mice were randomly divided into 5 groups, including the control sham (CS) group, the control MI (CMI) group, the diabetes sham (DS) group, diabetes + MI (DMI) group and the DMI + sitagliptin (DMI+SGL) group. After modeling, mice in the DMI+SGL group were intragastrically administrated with sitagliptin (10 mg/kg/ day) for 21 d and the survival rate of mice was recorded. Before and 7, 14, 21 days after MI, the cardiac function of mice in each group was detected via ultrasound. 21 days after MI, the area of MI was measured via 2,3,5-triphenyl tetrazolium chloride (TTC). Meanwhile, the degree of fibrosis in the peripheral region of MI was determined via Masson staining. Moreover, myocardial autophagosomes of mice in each group were observed by transmission electron microscope (TEM). 7 days after MI, the expressions of autophagy- related proteins LC3II and P65 were detected via Western blotting. The expressions of myocardial inflammatory factors, interleukin-1β (IL-1β), IL-6 and tumor necrosis factor-α (TNF-α) were detected via enzyme-linked immunosorbent assay (ELISA). In addition, the expression of nuclear factor-κB (NF-κB) was also detected via Western blotting. RESULTS: Sitagliptin increased survival rate, improved cardiac function, reduced infarction area, alleviated myocardial fibrosis, enhanced autophagy in the peripheral region and inhibited inflammation in the peripheral region in mice with diabetes after MI. CONCLUSIONS: Sitagliptin can improve cardiac function and reduce the mortality rate in diabetic rats after MI. The possible underlying mechanism may be related to the fact that sitagliptin activates autophagy and inhibits inflammatory response in diabetes after MI. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To explore whether microRNA-377 could participate in the development of Alzheimer's disease (AD) by regulating CDH13. MATERIALS AND METHODS: In this research, AD model was constructed by the SH-SY5Y cells. The expression levels of microRNA-377 and CDH13 in the AD model were detected by quantitative Real-time polymerase chain reaction (qRT-PCR). The cell viability and apoptosis after knockdown of microRNA-377 and CDH13 were measured by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. The regulatory mechanism of microRNA-377 on CDH13 was confirmed by dual-luciferase reporter gene assay, qRT-PCR and Western blot. RESULTS: Downregulated microRNA-377 and upregulated CDH13 were observed after successful construction of the AD model. Cell viability in the AD model group was significantly reduced compared with that of the control group. Moreover, downregulated microRNA-377 could further inhibit the cell viability, which was reversed by CDH13 knockdown. Cell apoptosis in the AD model group was enhanced after microRNA-377 knockdown, which was rescued by decreasing the expression level of CDH13. MicroRNA-377 was confirmed to regulate the expression level of CDH13 by dual-luciferase reporter gene assay, qRT-PCR and Western blot. CONCLUSIONS: MicroRNA-377 could regulate the expression level of CDH13 by promoting cell proliferation and inhibiting cell apoptosis, thus participating in the occurrence of the Alzheimer's disease. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Previous study has reported that miR-330-3p was highly expressed in breast cancer (BC) patients. However, the effect of miR-330-3p in BC progression remains largely unclear. The purpose of this study was to investigate the clinical significance of miR-330- 3p expression in BC. PATIENTS AND METHODS: The expression of miR-330-3p was detected by quantitative Real- time PCR in BC tissues and matched normal breast tissues. The association of miR-330-3p expression with clinicopathological factors of BC patients was also analyzed by x2-test. Prognosis value of patients with BC was assessed by Kaplan-Meier method and Cox proportional hazards model, respectively. RESULTS: Quantitative real-time PCR analysis showed that the expression level of miR- 330-3p was significantly higher in BC specimens than that in corresponding noncancerous tissues (p < 0.01). The levels of miR-330- 3p were positively correlated with the status of TNM stage (p = 0.011) and lymph node metastasis (p = 0.006). Kaplan-Meier analysis revealed that 5-year overall survival of BC patients with high miR-330-3p expression was shorter compared to those patients with low miR-330-3p expression (p < 0.0001). Moreover, univariate and multivariate regression analysis demonstrated that miR-330-3p was an independent prognostic factor in BC. CONCLUSIONS: Our data suggest that miR- 330-3p upregulation maybe concurrently associated with prognosis in patients with BC, suggesting that miR-330-3p may be a potential prognostic biomarker and therapeutic target for patients with BC. [ABSTRACT FROM AUTHOR]

Background Primary adenosquamous carcinoma (ASC) of the lung is rare and its biological behavior has not yet been thoroughly described. The aim of this study was to analyze the clinicopathological characteristics and prognostic factors associated with ASC. Materials Clinical records of patients with ASC of the lung who underwent surgery between October 2008 and December 2014 in a single institution were retrospectively reviewed. Results A total of 205 patients were identified. Patients with balanced structural components had significantly better prognosis than those with squamous ( p = 0.014) or adenomatous ( p < 0.001) predominance, and those with N0, N1, and N2 ASC (N0 vs. N1 [ p = 0.031] and N1 vs. N2 [ p = 0.037], respectively), or stage I, II and IIIA ASC (stage I vs. II [ p = 0.021] and stage II vs. IIIA [ p = 0.007], respectively) had significant differences with respect to overall survival (OS). Multivariate analysis identified structural components ( p = 0.011), tumor, node and metastasis (TNM) status ( p < 0.001), and adjuvant chemotherapy ( p = 0.008) as significantly prognostic factors for OS, and structural components ( p = 0.030), TNM stage ( p < 0.001) and adjuvant chemotherapy ( p = 0.005) as the corresponding variables for disease-free survival. Conclusions A balanced structure between adenomatous and squamous components in patients with primary ASC of the lung was associated with better prognosis. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The incidence of missed miscarriage has been increasing during the past decade in China and the etiology of about half of the cases remains unclear. Exposure to phthalates has been considered as a risk factor. The aim of this paper is to assess the association between exposure to phthalates and missed miscarriage. PATIENTS AND METHODS: A case-control study was performed including 150 cases of missed miscarriage and 150 matched controls with normal pregnancies. The levels of phthalate exposure were compared between the two groups by measuring 13 phthalate metabolites in urine samples. Blood samples were collected for serum hormone measurement to assess the relationship between serum hormone level and phthalate exposure. RESULTS: The urinary levels of metabolites of di-(2-ethylhexyl) phthalate (DEHP) and dimethyl phthalate (DMP) were significantly higher in the cases than in the controls. A strong dose-response relationship was observed between urinary metabolite levels and the odds of missed miscarriage. Monomethyl phthalate (MMP), a metabolite of DMP, and mono-2-ethylhexyl phthalate (MEHP), a metabolite of DEHP, each had significant negative correlation with maternal serum hormone levels. CONCLUSIONS: In the current study, exposure to DEHP and DMP was found to be associated with missed miscarriage. Interruption of hormone synthesis by DMP and DEHP metabolites represents a plausible mechanism of phthalate reproductive toxicity. [ABSTRACT FROM AUTHOR]

Placental soluble fms-like tyrosine kinase 1 (sFlt1) release is increased in preeclampsia, which might be associated with increased shedding of Flt-1 through a disintegrin and metalloproteinase 10 (ADAM10). Here, we explored whether ADAM10 expression is regulated by hydrogen sulfide (H 2 S) in placenta. Pro- and active-ADAM10 expression were significantly increased in preeclamptic placentas and inversely correlated to H 2 S production enzymes cystathionine β-synthase and cystathionine γ-lyase expression. H 2 S significantly suppressed pro- and active-ADAM10 expression whilst inhibited sFlt-1 release. Knockdown of ADAM10 caused a decrease in sFlt-1 release. Our data suggest that dysregulation of H 2 S production may contribute to excessive Flt-1shedding in preeclampsia. [ABSTRACT FROM AUTHOR]

A novel volatile organic compound (VOC) detection system based on colorimetric sensor array was developed for the quality assurance and quality control of food and beverages. Time-dependent density functional theory and density functional theory were performed on models of metalloporphyrins and their complexes. The ground state for metalloporphyrins and their complexes is obtained from the relative energies at different spin states. The changes in binding energies, excitation energies, and oscillator strength were obtained by differentiating the parameters of the metalloporphyrins before and after binding to VOCs. The above data representing the colour change profiles for VOCs were analysed for the further design of CSA sensor. The sensitive of CSA were classified into three groups by the comprehensive consideration of binding energies, excitation energies, and oscillator strength. The calculation results are consistent with other studies. This theoretical result can be used to optimise the sensor to increase the detection ability of colorimetric sensor array. [ABSTRACT FROM AUTHOR]

Cobalt porphyrin and similar metalloporphyrins (MPs) were initially used in the colorimetric sensor array (CSA) system for quality assurance and quality control in beverage and food. In order to design a proper CSA sensor, density functional theory method with B3LYP/LANL2DZ basis set was performed to investigate the influences of axial ligand, substituent group and volatile organic compounds (VOCs) on the binding process. Ground state structure was determined at three spin states: low, intermediate and high spin states, based on the relative energy. The binding energy (BE) for each MP model was obtained by differentiating the energy of MP before and after binding with VOCs. The binding ability of MPs and their complexes can be divided into three classes based on the BE. This theoretical research would be used for the further design of CSA sensor to extend the application of CSA. [ABSTRACT FROM AUTHOR]

Self-incompatibility (SI) in broccoli (Brassica oleracea L. var. italica) is common, and controlled by the 5-locus which contains at least three genes: SLG (the 5-locus glycoprotein), SRK (the 5-locus receptor kinase), and SCR (the 5-locus cysteine-rich protein) also named SP11 (the 5-locus protein 11). As the 5-locus is complex, the classical term '5-allele' was changed to '5-haplotype'. Information on 5-alleles in breeding lines is important for breeders to ensure cross-compatibility between lines. In this work, the 5-haplotypes of 18 dihaploid (DH) broccoli lines were examined. For each line, fragments of the SRK and SCR/SP11 genes were amplified by PCR and their sequences were determined. The results showed that: (i) out of the 18 DH broccoli lines, 15 belonged to Class II 5-haplotypes, while the other three lines were Class I, based on the amplification patterns of SRK and SCR/SP11; (ii) the sequences of Class II 5-haplotype SRK and SCRISP11 fragments of 15 of the DH lines were identical; (iii) the Class I S-haplotypes of three DH lines were different from each other, based on the DNA sequences of their SRK genes; and (iv) one Class II and three Class I S-haplotypes were present in the broccoli DH lines. [ABSTRACT FROM AUTHOR]

Mesoporous silica materials have been increasingly used as immobilising and adsorptive carriers of proteins in the biochemical analysis field. The sustained requirements on protein adsorption carriers keep motivating chemists to seek new modified mesoporous silica materials to improve their protein adsorption capacity. With the aim to improve the material's capacity of absorbing protein, in this paper, we proposed a new approach to synthesise a modified mesoporous silica material sharing an external hydrophobic and internal hydrophilic surface (methyl-amino-SiO2). This was followed by the measurement of both the pore structure of the material and its capacity in absorbing hemoglobin. The experiment demonstrated that the new material maintained the original physical properties and showed a better absorptive capacity in protein. The better absorbability of the material comes from the novel synthesis method that chose the different chemical substitutes for replacing the exterior and inner surface of the material respectively. As the experimental results demonstrated, the modified mesoporous material supplied a better absorptive capacity in protein. As a result, it increased the applicability of the mesoporous material as adsorptive carriers of proteins in the biochemical analysis field [ABSTRACT FROM AUTHOR]

Mango (Magnifera indica L.) is a popular fruit, but it is susceptible to post-harvest diseases. To study the resistance of mango fruit to anthracnose disease and the possible defence mechanisms involved, the resistance of two mango cultivars ('Zill' and 'Keitt') was examined in relation to their defence enzyme systems. The results showed that in both young or commercially mature fruit inoculated with Colletotrichum gloeosporioides, lesion sizes on 'Keitt' fruit were smaller than on 'Zill' fruit. For non-inoculated fruit harvested at commercial maturity, the disease index of 'Keitt' was lower than that of 'Zill'. This indicates that 'Keitt' was more disease resistant than 'Zill'. Compared with 'Zill', 'Keitt' fruit showed higher phenylalanine ammonia lyase (PAL), peroxidase (POD), and polyphenol oxidase (PPO) activities during development and storage, as well as elevated levels of H2O2, total phenolic compounds and lignin during development, and higher contents of H2O2 and lignin in harvested fruit early during storage. These results suggest that defence enzymes and compounds plays important roles in the resistance of mango fruit to anthracnose disease and could be used as indicators to screen for mango cultivars that are more resistant to post-harvest diseases. [ABSTRACT FROM AUTHOR]

Guava (Psidium guajava L. 'Pearl') fruit were harvested at approx, the 80% mature stage. Fruit were exposed to 1.0 µl 1-1 1-methylcyclopropene (1-MCP) gaseous vapour for 12 h in a closed chamber maintained at 25°C, stored at 28°C and 60-65% relative humidity (RH) for 15 d, then assessed for their physiological and quality characteristics. The results showed that 1-MCP treatment delayed any increase in the incidence of decay, weight loss, and malondialdehyde (MDA) content. 1-MCP treatment had a positive effect on the retention of skin colour and on the firmness of guava fruit. Meanwhile, 1-MCP treatment maintained a higher vitamin C content and a lower soluble solids content, but titratable acidity was not affected by 1-MCP treatment. Moreover, 1-MCP treatment increased the activities of superoxide dismutase, catalase, and peroxidase, while reducing the activity of polyphenol oxidase. These results suggest that 1-MCP could delay the ripening process, maintain quality, and increase the anti-oxidant capacity of guava fruit stored at 28°C. [ABSTRACT FROM AUTHOR]

Hydraulic-fracturing treatments have become an indispensable part of well completion in shale gasfield development. Shale formations often contain natural fractures, and complex hydraulic-fracture networks may form during a treatment. The complex fracture network is strongly influenced by the interaction between the hydraulic fracture and the pre-existing natural fractures. A criterion has been developed to determine whether a fracture crosses a frictional interface (pre-existing fracture) at nonorthogonal angles. This criterion is an extension of the one for orthogonal crossing originally developed by Renshaw and Pollard (1995). The dependence of crossing on the intersection angle is shown quantitatively using the extended criterion. The fracture is more likely to turn and propagate along the interface than to cross it when the angle is less than 90°. The validation of the criterion using laboratory experiments for various angles is described and discussed. When applied to laboratory experiments, good agreement between the criterion and experiments is observed for a wide range of angles. The criterion can be used to determine whether hydraulic fractures cross natural fractures under particular field conditions, and it has been incorporated in a hydraulic-fracture model that simulates hydraulic-fracture propagation in a naturally fractured formation. [ABSTRACT FROM AUTHOR]

The article discusses a study which explained a hydraulic-fracture model that assumes propagation of complex fractures in a naturally fractured formation. According to the researchers, this model can determine whether a hydraulic-fracture front crosses or stopped by a natural fracture it encounters complexity. They concluded that this model can be a vital tool for engineers working on shale-gas stimulation to attain maximum benefits.

Abstract: Aims: To examine the effect of the TIMP-2 G-418C polymorphism on gastric cancer risk. Methods: We conducted a hospital-based, case–control study using polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) method in 412 individuals (206 gastric cancer patients and 206 age, sex matched cancer-free controls). Results: The genotype and allele frequencies were significantly different (P =0.007 and 0.005, respectively) between cases and controls. Further analysis showed that the variant TIMP-2 genotypes (CC+GC) had a 51% increased risk of gastric cancer compared with GG [adjusted odds ratio (OR) 1.51, 95% confidence interval (CI) 1.00–2.26, P =0.049]. The elevated gastric cancer risk was especially evident in younger individuals (age<58 years old) (adjusted OR 2.21, 95% CI 1.18–4.16) and smokers (adjusted OR 2.61, 95% CI 1.01–6.72). However, no significant association was observed between the variant genotypes and clinicopathological features of gastric cancer. Conclusions: These findings suggest that the TIMP-2 G-418C polymorphism is a genetic predisposing factor for gastric cancer. [Copyright &y& Elsevier]