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In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.
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Introduction: Accurate and timely prediction for endemic infectious diseases is vital for public health agencies to plan and carry out any control methods at an early stage of disease outbreaks. Climatic variables has been identified as important predictors in models for infectious disease forecasts. Various approaches have been proposed in the literature to produce accurate and timely predictions and potentially improve public health response. Methods: We assessed how the machine learning LASSO method may be useful in providing useful forecasts for different pathogens in countries with different climates. Separate LASSO models were constructed for different disease/country/forecast window with different model complexity by including different sets of predictors to assess the importance of different predictors under various conditions. Results: There was a more apparent cyclicity for both climatic variables and incidence in regions further away from the equator. For most diseases, predictions made beyond 4 weeks ahead were increasingly discrepant from the actual scenario. Prediction models were more accurate in capturing the outbreak but less sensitive to predict the outbreak size. In different situations, climatic variables have different levels of importance in prediction accuracy. Conclusions: For LASSO models used for prediction, including different sets of predictors has varying effect in different situations. Short term predictions generally perform better than longer term predictions, suggesting public health agencies may need the capacity to respond at short-notice to early warnings.
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The utility of LASSO-based models for real time forecasts of endemic infectious diseases: A cross country comparison


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Background: Chemokines and chemokine receptors cooperate to promote immune cell recruitment to the central nervous system (CNS). In this study, we investigated the roles of CXCR2 and CXCL1 in leukocyte recruitment to the CNS using a murine model of neuroinflammation. Methods: Wild-type (WT), CXCL1 −/− , and CXCR2 −/− mice each received an intracerebroventricular (i.c.v.) injection of lipopolysaccharide (LPS). Esterase staining and intravital microscopy were performed to examine neutrophil recruitment to the brain. To assess endothelial activation in these mice, the expression of adhesion molecules was measured via quantitative real-time polymerase chain reaction (PCR) and Western blotting. To identify the cellular source of functional CXCR2, chimeric mice were generated by transferring bone marrow cells between the WT and CXCR2 −/− mice. Results: Expression levels of the chemokines CXCL1, CXCL2, and CXCL5 were significantly increased in the brain following the i.c.v. injection of LPS. CXCR2 or CXCL1 deficiency blocked neutrophil infiltration and leukocyte recruitment in the cerebral microvessels. In the CXCR2 −/− and CXCL1 −/− mice, the cerebral endothelial expression of adhesion molecules such as P-selectin and VCAM-1 was dramatically reduced. Furthermore, the bone marrow transfer experiments demonstrated that CXCR2 expression on CNS-residing cells is essential for cerebral endothelial activation and leukocyte recruitment. Compared with microglia, cultured astrocytes secreted a much higher level of CXCL1 in vitro. Astrocyte culture conditioned medium significantly increased the expression of VCAM-1 and ICAM-1 in cerebral endothelial cells in a CXCR2-dependent manner. Additionally, CXCR2 messenger RNA (mRNA) expression in cerebral endothelial cells but not in microglia or astrocytes was increased following tumor necrosis factor-α (TNF-α) stimulation. The intravenous injection of the CXCR2 antagonist SB225002 significantly inhibited endothelial activation and leukocyte recruitment to cerebral microvessels. Conclusions: CXCL1 secreted by astrocytes and endothelial CXCR2 play essential roles in cerebral endothelial activation and subsequent leukocyte recruitment during neuroinflammation.
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CXCR2 is essential for cerebral endothelial activation and leukocyte recruitment during neuroinflammation


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We have recently identified a rare subpopulation of lung colony cells with the characteristics of pulmonary stem cells, and discovered that stem cell colonies grew preferentially on type I collagen films in a serum-free medium. In order to further optimize culture conditions and determine stem cell growth in relation to microenvironments (including the stroma, medium and nanostructures of type I collagen films), both primary and pre-sorted stem cells were cultured on the type I collagen films with controllable degree of polymerization and film thickness, as confirmed by an atomic force microscope and surface profiler. We found that in a primary culture, the spreading of stromal cells is greatly restrained and both the size and number of colonies are significantly reduced on highly polymerized collagen films. In contrast, in a pre-sorted stem cell culture without stromal cells, the intrinsic stem cell properties and cell number are independent of the degree of collagen polymerization. Our results indicate that the nanostructures of type I collagen films primarily affect stem colony formation through the collagene stroma interactions. In those cases, collagen film thickness shows no effect on colony formation.
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The influence of collagen film nanostructure on pulmonary stem cells and collagenestromal cell interactions