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.

[Q]: Objectives: This study was conducted to investigate the correlation between antibiotic consumption and the incidence of health-care-associated infections (HCAIs) caused by methicillin-resistant Staphylococcus aureus (MRSA) (HCAI-MRSA) and vancomycin-resistant enterococci (VREs) (HCAI-VREs) at a university hospital in Taiwan during the period from 2000 to 2010. Methods: Data on annual patient-days and annual consumption (defined daily dose/1000 patient-days) of glycopeptides (vancomycin and teicoplanin), linezolid, fusidic acid, tigecycline, and daptomycin were analyzed. Yearly aggregated data on the number of nonduplicate clinical MRSA and VRE isolates causing HCAI were collected. Journal of Microbiology, Immunology and Infection (2015) 48, 431e436 aureus; Results: Overall, the consumption of teicoplanin and linezolid significantly increased during the study period. A significant decrease in the incidence of HCAI-MRSA and a significant increase in the incidence of HCAI-VRE were found during the study period. A significant correlation was found between the increased use of teicoplanin and linezolid and the decreased incidence of HCAI-MRSA. By contrast, positive correlations were found between the consumption of teicoplanin and tigecycline and the incidence of HCAI-VRE. Conclusion: This study identified various correlations between the consumption of antibiotics and the incidence of HCAI-MRSA and HCAI-VRE. Strict implementation of infection-control guidelines and reinforcement of administering appropriate antibiotic agents would be helpful in decreasing the incidence of MRSA and VRE in hospitals.
[A]: Correlation between antimicrobial consumption and incidence of health-care- associated infections due to methicillin- resistant Staphylococcus aureus and vancomycin-resistant enterococci at a university hospital in Taiwan from 2000 to 2010


[Q]: Influenza has been well documented to significantly contribute to winter increase of mortality in the temperate countries, but its severity in the subtropics and tropics was not recognized until recently and geographical variations of disease burden in these regions remain poorly understood. In this study, we applied a standardized modeling strategy to the mortality and virology data from three Asian cities: subtropical Guangzhou and Hong Kong, and tropical Singapore, to estimate the disease burden of influenza in these cities. We found that influenza was associated with 10.6, 13.4 and 8.3 deaths per 100,000 population in Guangzhou, Hong Kong and Singapore, respectively. The annual rates of excess deaths in the elders were estimated highest in Guangzhou and lowest in Singapore. The excess death rate attributable to A/H1N1 subtype was found slightly higher than the rates attributable to A/H3N2 during the study period of 2004-2006 based on the data from Hong Kong and Guangzhou. Our study revealed a geographical variation in the disease burden of influenza in these subtropical and tropical cities. These results highlight a need to explore the determinants for severity of seasonal influenza.
[A]: Influenza associated mortality in the subtropics and tropics: Results from three Asian cities


[Q]: a b s t r a c t background and purpose: Celastrol, a quinone methide triterpene isolated from the root extracts of Tripterygium wilfordii, can greatly induce the gene expression activity of heme oxygenase-1 (HO-1) to achieve disease prevention and control. HO-1 induction was recently shown to result in anti-HCV activity by inducing type I interferon and inhibiting hepatitis C virus (HCV) NS3/4A protease activity. The aim of the present study is to evaluate the anti-HCV activity of celastrol and characterize its mechanism of inhibition. Methods: The anti-HCV activity of celastrol was evaluated using the HCV subgenomic replicon and HCVcc infection systems. The anti-HCV mechanism of celastrol targeting HO-1 expression was clarified using specific inhibitors against several signaling pathways. The transcriptional regulation of celastrol on target gene expression was determined using promoter-based reporter activity assay. The synergistic effect of celastrol and a numbers of clinically used anti-HCV drugs was determined via a drug combination assay. Results: Celastrol inhibited HCV replication in both the HCV subgenomic and HCVcc infection systems with EC50 values of 0.37 ± 0.022 and 0.43 ± 0.019 mM, respectively. Celastrol-induced heme oxygenase 1 (HO-1) expression promoted antiviral interferon responses and inhibition of NS3/4A protease activity, thereby blocking HCV replication. These antiviral effects were abrogated by treatment with the HO-1specific inhibitor SnMP or silencing of HO-1 expression by transfection of shRNA, which indicates that HO-1 induction contributes to the anti-HCV activity of celastrol. JNK mitogen-activated protein kinase and nuclear factor erythroid 2-related factor 2 (Nrf2) were confirmed to be involved in the inductive effect of celastrol on HO-1 expression. Celastrol exhibited synergistic effects in combination with interferon-alpha, the NS5A inhibitor daclatasvir, and the NS5B inhibitor sofosbuvir. Conclusion: Celastrol can serve as a potential supplement for blocking HCV replication. Targeting the JNK/Nrf2/HO-1 axis presents a promising strategy against HCV infection.
[A]:
Celastrol inhibits hepatitis C virus replication by upregulating heme oxygenase-1 via the JNK MAPK/Nrf2 pathway in human hepatoma cells