Suppression of Laccase 2 severely impairs cuticle tanning and pathogen resistance during the pupal metamorphosis of Anopheles sinensis (Diptera: Culicidae)

Amino acid sequence identity of Cu-oxidase domains of LAC2 orthologs. (PDF 109 kb

Reduced expression of cenp-e in human hepatocellular carcinoma

© 2009 Liu et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens

Cost-effectiveness analysis of malaria rapid diagnostic test in the elimination setting

BACKGROUND: As more and more countries approaching the goal of malaria elimination, malaria rapid diagnostic tests (RDT) was recomendated to be a diagnostic strategy to achieve and maintain the statute of malaria free, as it’s less requirments on equipment and experitise than microscopic examination. But there are very few economic evaluations to confirm whether RDT was cost-effective in the setting of malaria elimination. This research aimed to offer evidence for helping decision making on malaria diagnosis strategy. METHODS: A cost-effectiveness analysis was conducted to compare RDT with microscopy examination for malaria diagnosis, by using a decision tree model. There were three strategies of malaria diagnostic testing evaluated in the model, 1) microscopy, 2) RDT, 3) RDT followed by microscopy. The effect indicator was defined as the number of malaria cases treated appropriately. Based on the joint perspective of health sector and patient, costs data were collected from hospital information systems, key informant interviews, and patient surveys. Data collection was conducted in Jiangsu from September 2018 to January 2019. Epidemiological data were obtained from local malaria surveillance reports. A hypothetical cohort of 300 000 febrile patients were simulated to calculate the total cost and effect of each strategy. One-way, two-way, and probabilistic sensitivity analysis were performed to test the robustness of the result. RESULTS: The results showed that RDT strategy was the most effective (245 cases) but also the most costly (United States Dollar [USD] 4.47 million) compared to using microscopy alone (238 cases, USD 3.63 million), and RDT followed by microscopy (221 cases, USD 2.75 million). There was no strategy dominated. One-way sensitivity analysis reflected that the result was sensitive to the change in labor cost and two-way sensitivity analysis indicated that the result was not sensitive to the proportion of falciparum malaria. The result of Monte Carlo simulation showed that RDT strategy had higher effects and higher cost than other strategies with a high probability. CONCLUSIONS: Compared to microscopy and RDT followed by microscopy, RDT strategy had higher effects and higher cost in the setting of malaria elimination

Effects of dietary guava leaf aqueous extract supplementation on growth, antioxidant capacity, and non-specific immunity in mud crab <em>Scylla paramamosain</em>

Mud crab (*Scylla paramamosain*) fed five different diets with varying concentrations of guava leaf aqueous extract (0 mg·kg^--1^, 80 mg·kg^--1^, 160 mg·kg^--1^, 320 mg·kg^--1^, and 640 mg·kg^--1^) for 30 days. Mud crabs in the 320 mg·kg^--1^ guava-leaf extract groups outperformed the control group in terms of survival rates (SR), weight gain rates (WGR), and specific growth rates (SGR). When compared to the control group, mud crabs in the 320 mg·kg^--1^ guava-leaf extract groups had significantly higher levels of lipase (LPS), pepsin, lysozyme (LZM), superoxide dismutase (SOD), acid phosphatase (ACP), and glutathione (GSH) (*P \< 0.05*). The amylase (AMS) activity was significantly decreased in all experimental groups (*P \< 0.05*). Malondialdehyde (MDA) content in the hepatopancreas of mud crabs in the 160 mg·kg^--1^, 320 mg·kg^--1^, and 640 mg·kg^--1^ guava-leaf extract groups were significantly reduced compared to the control group (*P \< 0.05*). Additionally, real-time PCR results illustrated that the expression levels of *GPx3*, *CAT*, and *JNK* were all considerably increased in the 80 mg·kg^--1^ guava-leaf extract groups compared to the control group (*P \< 0.05*). In the 160 mg·kg^--1^, 320 mg·kg^--1^, and 320 mg·kg^--1^ guava-leaf extract groups, the expression levels of *SOD* genes were considerably greater than the control (*P \< 0.05*), which was consistent with the level of SOD activity. *GST* and *P53* gene expression levels were significantly up-regulated in the 80 mg·kg^--1^, 160 mg·kg^--1^, 320 mg·kg^--1^, and 640 mg·kg^--1^ guava-leaf extract groups compared to the control group (*P \< 0.05*). Overall, the addition of 160 mg·kg^--1^-320 mg·kg^--1^ guava-leaf extract to the feed of *Scylla paramamosain* promoted growth, enhanced the activities of digestive and antioxidant enzymes, and strengthened immunity

Changes and Relationship of PAF and TNF in Rats with Myocardial Ischaemia and Reperfusion Injury

In this study it is reported that: (1) the levels of blood platelet-activating factor and serum tumour necrosis factor significantly increased after coronary ligation and reperfusion, compared with sham-ligated controls, in an anaesthetized rat model; (2) compared with vehicle controls, pretreatment with the PAF antagonist BN 50739 (10 mg/kg, i.v.) produced significant decreases in infarct size (from 29.6 ± 4.0% to 22.4 ± 2.1%, p < 0.05 after 3 h ligation, and from 28.5 ± 9.5% to 10.5 ± 4.5%, p < 0.01 after 4 h reperfusion) and the level of serum TNF (from 10.4 ± 7.7 U/ml to 3.9 ± 4.8 U/ml, p < 0.05); and (3) a significan positive correlation was found between the level of blood PAF or serum TNF and infarct size. The present results indicate that PAF and TNF may be important mediators involved in myocardial ischaemia and reperfusion injury, and that PAF antagonists may exert a protective effect on ischaemic or reperfused myocardium by inhibiting the interaction of PAF and TNF

Regulatory role of Mss11 in Candida glabrata virulence: adhesion and biofilm formation

IntroductionCandida glabrata has emerged as a fungal pathogen with high infection and mortality rates, and its primary virulence factors are related to adhesion and biofilm formation. These virulence factors in C.glabrata are primarily mediated by epithelial adhesins (Epas), most of which are encoded in subtelomeric regions and regulated by subtelomeric silencing mechanisms. The transcription factor Mss11, known for its regulatory role in adhesion, biofilm formation, and filamentous growth in Saccharomyces cerevisiae and Candida albicans, has also been implicated in the expression of EPA6, suggesting its potential influence on C.glabrata virulence. The present study aims to determine the regulatory role of Mss11 in the virulence of C. glabrata.MethodsIn this work, a Δmss11 null mutant and its complemented strain were constructed from a C.glabrata standard strain. The impact of the transcription factor Mss11 on the virulence of C.glabrata was investigated through a series of phenotypic experiments, including the microbial adhesion to hydrocarbons (MATH) test, adherence assay, biofilm assay, scanning electron microscopy and Galleria mellonella virulence assay. Furthermore, transcriptome sequencing, quantitative reverse transcription polymerase chain reaction (RT-qPCR), and chromatin immunoprecipitation sequencing (ChIP-seq) were employed to investigate the molecular mechanisms behind the regulation of Mss11.ResultsIn C.glabrata, the loss of MSS11 led to a significant reduction in several virulence factors including cell surface hydrophobicity, epithelial cell adhesion, and biofilm formation. These observations were consistent with the decreased virulence of the Δmss11 mutant observed in the Galleria mellonella infection model. Further exploration demonstrated that Mss11 modulates C. glabrata virulence by regulating EPA1 and EPA6 expression. It binds to the upstream regions of EPA1 and EPA6, as well as the promoter regions of the subtelomeric silencing-related genes SIR4, RIF1, and RAP1, indicating the dual regulatory role of Mss11.ConclusionMss11 plays a crucial role in C. glabrata adhesion and biofilm formation, and thus has a broad influence on virulence. This regulation is achieved by regulating the expression of EPA1 and EPA6 through both promoter-specific regulation and subtelomeric silencing