396 research outputs found

    Sequential Appointment Scheduling Considering Walk-In Patients

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    This paper develops a sequential appointment algorithm considering walk-in patients. In practice, the scheduler assigns an appointment time for each call-in patient before the call ends, and the appointment time cannot be changed once it is set. Each patient has a certain probability of being a no-show patient on the day of appointment. The objective is to determine the optimal booking number of patients and the optimal scheduling time for each patient to maximize the revenue of all the arriving patients minus the expenses of waiting time and overtime. Based on the assumption that the service time is exponentially distributed, this paper proves that the objective function is convex. A sufficient condition under which the profit function is unimodal is provided. The numerical results indicate that the proposed algorithm outperforms all the commonly used heuristics, lowering the instances of no-shows, and walk-in patients can improve the service efficiency and bring more profits to the clinic. It is also noted that the potential appointment is an effective alternative to mitigate no-show phenomenon

    Sequential Appointment Scheduling Considering Walk-In Patients

    Get PDF
    This paper develops a sequential appointment algorithm considering walk-in patients. In practice, the scheduler assigns an appointment time for each call-in patient before the call ends, and the appointment time cannot be changed once it is set. Each patient has a certain probability of being a no-show patient on the day of appointment. The objective is to determine the optimal booking number of patients and the optimal scheduling time for each patient to maximize the revenue of all the arriving patients minus the expenses of waiting time and overtime. Based on the assumption that the service time is exponentially distributed, this paper proves that the objective function is convex. A sufficient condition under which the profit function is unimodal is provided. The numerical results indicate that the proposed algorithm outperforms all the commonly used heuristics, lowering the instances of no-shows, and walk-in patients can improve the service efficiency and bring more profits to the clinic. It is also noted that the potential appointment is an effective alternative to mitigate no-show phenomenon

    Association of Wnt1-inducible signaling pathway protein-1 with the proliferation, migration and invasion in gastric cancer cells

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    Wnt1-inducible signaling pathway protein-1 is a cysteine-rich protein that belongs to the CCN family, which has been implicated in mediating the occurrence and progression through distinct molecular mechanisms in several tumor types. However, the association of Wnt1-inducible signaling pathway protein-1 with gastric cancer and the related molecular mechanisms remain to be elucidated. Therefore, this study aimed to clarify the biological role of Wnt1-inducible signaling pathway protein-1 in the proliferation, migration, and invasion in gastric cancer cells and further investigated the associated molecular mechanism on these biological functions. We first detected the expression level of Wnt1-inducible signaling pathway protein-1 in gastric cancer, and the reverse transcription polymerase chain reaction have shown that Wnt1-inducible signaling pathway protein-1 expression levels were upregulated in gastric cancer tissues. The expression of Wnt1-inducible signaling pathway protein-1 in gastric cancer cell lines was also detected by quantitative real-time polymerase chain reaction and Western blotting. Furthermore, two gastric cancer cell lines with high expression of Wnt1-inducible signaling pathway protein-1 were selected to explore the biological function of Wnt1-inducible signaling pathway protein-1 in gastric cancer. Function assays indicated that knockdown of Wnt1-inducible signaling pathway protein-1 suppressed cell proliferation, migration, and invasion in BGC-823 and AGS gastric cancer cells. Further investigation of mechanisms suggested that cyclinD1 was identified as one of Wnt1-inducible signaling pathway protein-1 related genes to accelerate proliferation in gastric cancer cells. In addition, one pathway of Wnt1-inducible signaling pathway protein-1 induced migration and invasion was mainly through the enhancement of epithelial-to-mesenchymal transition progression. Taken together, our findings presented the first evidence that Wnt1-inducible signaling pathway protein-1 was upregulated in gastric cancer and acted as an oncogene by promoting proliferation, migration, and invasion in gastric cancer cells

    Increased expression of Gremlin1 promotes proliferation and epithelial mesenchymal transition in gastric cancer cells and correlates with poor prognosis of patients with gastric cancer

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    Background/Aim: Gremlin1 (GREM1) plays an important role in certain malignancies by antagonising bone morphogenetic proteins and regulating angiogenesis directly/indirectly. The present study aimed to investigate the role of Gremlin1 in the development and progression of gastric cancer (GC). Materials and Methods: Expression of GREM1 in GCs was examined using quantitative real time PCR and The Cancer Genomic Atlas (TCGA) data. Influence on cellular functions was determined in both Gremlin1 knockdown and overexpression cell line models. Results: GREM1 expression was up-regulated in GCs, which was correlated with poorer survival. Increased GREM1 expression was significantly correlated with tumour growth/invasion and lymphatic metastasis. Gremlin1 promoted proliferation and tumourigenic capacity of GC cells in vitro. GREM1 expression was associated with epithelial mesenchymal transition (EMT), angiogenesis and lymphangiogenesis in GC. Conclusion: Increased GREM1 expression in GCs is associated with disease progression and poor prognosis in which EMT, angiogenesis and lymphangiogenesis are likely involved

    Differential expression of CCN family members CYR611, CTGF and NOV in gastric cancer and their association with disease progression

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    CCN is an acronym for cysteine-rich protein 61 (CYR61), connective tissue growth factor (CTGF) and nephroblastoma overexpressed (NOV). Aberrations of certain CCN members including CYR61, CTGF, Wnt1-inducible signalling pathway protein (WISP)-1 and -3 have been reported in gastric cancer. The present study aimed to examine the clinical relevance of NOV along with CYR61 and CTGF in gastric cancer by analysing their transcript levels. CYR61, CTGF and NOV transcript expression in 324 gastric cancer samples with paired adjacent normal gastric tissues were determined using real-time quantitative PCR and the results were statistically analysed against patient clinicopathological data using SPSS software. NOV mRNA levels in gastric cancer tissues were significantly elevated when compared with levels in their paired adjacent non-cancerous tissues. Local advanced tumours with invasive expansion (T3 and T4) expressed higher levels of NOV (p=0.013) compared with the less invasive tumours (T1 and T2). CYR61 transcript levels were also significantly increased in gastric cancers compared with levels in the adjacent non cancerous tissues. Kaplan-Meier survival curves revealed that patients with CYR61-low transcript levels had longer overall survival (OS) (p=0.018) and disease-free survival (DFS) (p=0.015). NOV overexpression promoted the in vitro proliferation of AGS cells while the knockdown resulted in a reduced proliferation of HGC27 cells. A similar effect was observed for the invasion of these two gastric cancer cell lines. NOV expression was increased in gastric cancer which was associated with local invasion and distant metastases. Taken together, the expression of NOV and CYR61 was increased in gastric cancer. The elevated expression of CYR61 was associated with poorer survival. NOV promoted proliferation and invasion of gastric cancer cells. Further investigations may highlight their predictive and therapeutic potential in gastric cancer.Cancer Research Wales; Chinese Medical Research Scholarship of Cardiff UniversitySCI(E)[email protected]; [email protected]

    Constructing quantum dots@flake g-C3N4 isotype heterojunctions for enhanced visible-light-driven NADH regeneration and enzymatic hydrogenation

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    The authors thank the financial support from National Natural Science Funds of China (21406163, 91534126, 21621004), Tianjin Research Program of Application Foundation and Advanced Technology (15JCQNJC10000), Open Funding Project of the National Key Laboratory of Biochemical Engineering (2015KF-03), and the Program of Introducing Talents of Discipline to Universities (B06006). X.W. also acknowledges financial support from The Carnegie Trust for the Universities of Scotland (70265) and The Royal Society (RG150001 and IE150611).Peer reviewedPostprin

    Overexpression of EPHB4 Is associated with poor survival of patients with gastric cancer

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    Background: Increased expression of erythropoietin-producing human hepatoma (EPHB4) leads to enhanced cell migration, growth and adhesion in tumor cells. However, little is known regarding the effects of EPHB4 in gastric cancer. The present study aimed to examine the clinical relevance of EPHB4 and its association with the prognosis of gastric cancer. Materials and Methods: EPHB4 transcript expression in 324 gastric cancer samples with paired adjacent normal gastric tissues was determined using quantitative polymerase chain reaction and the results were statistically analyzed against patient clinicopathological data. AGS and HGC27 cell lines were transfected with EPHB4 siRNA and the effects examined by functional analysis. Results: EPHB4 mRNA levels in gastric cancer tissues were significantly elevated when compared to non-cancerous tissues (p=0.0110). Tissue samples from male patients exhibited lower expression than those from female patients (p=0.0110). Non-cardiac gastric tumors (fundus, corpus and pylorus) expressed a higher number of EPHB4 transcripts in comparison to cardiac gastric tumors (p<0.001). Increased expression of EPHB4 was significantly associated with poorer overall (p=0.0051) and progression-free (p=0.0262) survival. EPHB4 knockdown appeared to reduce post-wound migration of AGS cells (p=0.0057) and increase migration of HGC27 cells (p=0.0337). EPHB4 knockdown significantly increased adhesive ability in HGC27 (p<0.0001). Conclusion: The expression of EPHB4 was increased in gastric cancer and increased EPHB4 expression was correlated with poor survival. Knockdown of EPHB4 promoted adhesion and exerted diverse effects on migration of gastric cancer cells. Further investigations may highlight its predictive and therapeutic potential in gastric cancer

    Spatial analysis of malaria in Anhui province, China

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    <p>Abstract</p> <p>Background</p> <p>Malaria has re-emerged in Anhui Province, China, and this province was the most seriously affected by malaria during 2005–2006. It is necessary to understand the spatial distribution of malaria cases and to identify highly endemic areas for future public health planning and resource allocation in Anhui Province.</p> <p>Methods</p> <p>The annual average incidence at the county level was calculated using malaria cases reported between 2000 and 2006 in Anhui Province. GIS-based spatial analyses were conducted to detect spatial distribution and clustering of malaria incidence at the county level.</p> <p>Results</p> <p>The spatial distribution of malaria cases in Anhui Province from 2000 to 2006 was mapped at the county level to show crude incidence, excess hazard and spatial smoothed incidence. Spatial cluster analysis suggested 10 and 24 counties were at increased risk for malaria (<it>P </it>< 0.001) with the maximum spatial cluster sizes at < 50% and < 25% of the total population, respectively.</p> <p>Conclusion</p> <p>The application of GIS, together with spatial statistical techniques, provide a means to quantify explicit malaria risks and to further identify environmental factors responsible for the re-emerged malaria risks. Future public health planning and resource allocation in Anhui Province should be focused on the maximum spatial cluster region.</p
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