The association between dietary branched-chain amino acids and the risk of cardiovascular diseases in Chinese patients with type 2 diabetes: A hospital-based case-control study.

Background: Previous studies showed conflicting evidence on the association between the intake of dietary branched-chain amino acid (BCAA) and the risk of cardiovascular disease (CVD). However, this relationship has not been studied in patients with type 2 diabetes. Therefore, we evaluated the effects of total and individual dietary BCAA (leucine, isoleucine, and valine) intake on CVD risk among individuals with type 2 diabetes in China. Materials and methods: A total of 419 patients with type 2 diabetes who have been diagnosed with CVD (within 2 weeks) were recruited between March 2013 and September 2015 in China. Cases with CVD were 1:1 matched to controls with type 2 diabetes but without CVD by age (±5 years) and sex. A validated 79-item semiquantitative food frequency questionnaire (FFQ) was administered to assess the participants' dietary data. Total dietary BCAA per individual was the summation of the daily intake of isoleucine, leucine, and valine. OR and corresponding CIs were computed by conditional logistic regression models adjusted for potential confounders. Results: Median values of the daily intake of total BCAA were 11.87 g, with an interquartile range of 10.46-13.15 g for cases, and 12.47 g, with an interquartile range of 11.08-13.79 g for controls (P = 0.001). Dietary BCAA was inversely related to CVD risk after multivariable adjustment (OR Q4-Q1 = 0.23, 95%CI = 0.10, 0.51, P trend <0.001 for total BCAA; OR Q4-Q1 = 0.20, 95%CI = 0.07, 0.53, P trend = 0.001 for leucine). For each 1-S.D. increase in total dietary BCAA, leucine or valine intake was associated with 54% (95%CI = 29%, 70%, P = 0.001), 64% (95%CI = 29%, 82%, P = 0.003), or 54% (95%CI = 1%, 79%, P = 0.049) decrease in the risk of CVD, respectively. Whole grains, starchy vegetables, mushrooms, fruit, eggs, and dairy and dairy product-derived BCAA were found to attenuate CVD risk (P ranged: = 0.002-0.027). Conclusion: Higher BCAA intake, in particular leucine and valine, might be associated with a lower risk of CVD.

Development and comparison of qPCR and qLAMP for rapid detection of the decapod iridescent virus 1 (DIV1).

Decapod iridescent virus 1 (DIV1) is a new virus discovered in recent years that infects farmed shrimp. DIV1 is highly infectious and causes substantial economic loss to the aquaculture industry of China. To prevent and control the spread and outbreak of DIV1 in a timely manner, it is necessary to establish an efficient method for DIV1 diagnosis. In this study, quantitative real-time polymerase chain reaction (qPCR) and quantitative real-time loop-mediated isothermal amplification (qLAMP) detection methods were established based on the specific sequence of the viral ATPase gene. The results indicated that the minimum detection limits of qPCR and qLAMP were 1.9 × 101 copies/µL and 1.9 × 102 copies/µL, respectively; the designed primer had good specificity for DIV1 and did not react with 13 other viruses, including white spot syndrome virus (WSSV), Enterocytozoon hepatopenaei (EHP), acute hepatopancreatic necrosis disease (AHPND), infectious hypodermal and haematopoietic necrosis virus (IHHNV), etc. A total of 43 clinical samples suspected of DIV1 infection were diagnosed by qPCR and qLAMP. Our qPCR demonstrated results consistent with a qPCR assay published previously, and the diagnostic sensitivity (DSe) and diagnostic specificity (DSp) of qLAMP were 85.71% and 100%, respectively. This result indicates that qPCR and qLAMP have good accuracy in the detection of DIVI in clinical samples. As established in this study, qPCR and qLAMP combined with a comprehensive comparative analysis can provide effective new solutions for the detection of DIV1.

Acyclovir inhibits channel catfish virus replication and protects channel catfish ovary cells from apoptosis.

The channel catfish virus (CCV) can cause lethal hemorrhagic infection in channel catfish, resulting in significant economic losses in the fish industry. Effective drugs for the virus are still lacking. Acyclovir is known as a potent antiviral agent against human herpes viruses and some animal DNA viruses. The present study was undertaken to explore the antiviral response and mechanism of acyclovir against CCV in channel catfish ovary (CCO) cells. Acyclovir was able to significantly inhibit the expression of viral genes related to CCV viral DNA synthesis and suppress viral replication at a safe concentration. Furthermore, acyclovir blocked the cytopathic effects and apoptosis induced by CCV, thereby maintaining the normal cellular morphological structure, as shown by the protection of CCO cells from the formation of apoptotic bodies or nuclear fragmentation. Moreover, reverse transcript quantitative polymerase chain reaction (RT-qPCR) demonstrated that acyclovir suppressed the expression of caspase 3, caspase 8 and caspase 9, while there was no significant impact on the expression of the apoptosis-inhibiting gene bcl-2 in CCV-infected cells. In addition, acyclovir did not promote the expression of immune-related genes such as MyD88, Mx1, IRF3, IRF7, IFN-I, NF-kB and IL-1ß, suggesting that the antiviral activity of acyclovir to CCV infection is not achieved by facilitating the expression of immune-related genes in CCO cells. Taken together, the results from this study suggest that acyclovir could effectively regulate CCV-induced infection, and thus is a promising therapeutic agent against CCV. Our results will aid our understanding of the pharmacological mechanisms of antiviral agents.

Toxic effects of waterborne lead (Pb) on bioaccumulation, serum biochemistry, oxidative stress and heat shock protein-related genes expression in Channa argus.

Lead (Pb) is a harmful metal element for aquatic animals. The aim of this study was to determine waterborne Pb exposure on oxidative stress, serum biochemistry and heat shock proteins (HSPs) genes expression in Channa argus. Fish were randomly divided into four groups and the Pb concentrations were 0, 50, 200, and 800 µg/L, respectively. The results showed that the accumulation of Pb was detected in the gill, intestine, liver and muscle following exposure to Pb. Pb accumulation content in tissues was gill > intestinal > liver > muscle. With the increased of Pb exposure concentrations, the levels of catalase (CAT), glutathione peroxidase (GPx), lysozyme (LZM) and immunoglobulin M (IgM) significantly decreased. Serum biochemistry, oxidative stress parameters and HSPs gene expression were all enhanced with the increase following Pb expose concentration. Our results suggest that waterborne Pb exposure can induce Pb accumulation, oxidative stress and immune response in C. argus.

Artemisinin enhances the anti-tumor immune response in 4T1 breast cancer cells in vitro and in vivo.

BACKGROUND: Breast cancer is a prominent cause of death among women worldwide. Recent studies have demonstrated that artemisinin (ART) displays anti-tumor activity. Using a mouse breast cancer model, we investigated the effects of ART in vitro and in vivo to determine how it influences the anti-tumor immune response. METHODS: We measured the proliferation and apoptosis of 4T1 cells in vitro after ART treatment by MTT assay and FACS. To examine the effects of ART in vivo, tumor volumes and survival rates were measured in 4T1 tumor-bearing mice. FACS was used to determine the frequencies of Tregs, MDSCs, CD4+ IFN-γ+ T cells, and CTLs in the tumors and spleens of the mice. mRNA levels of the transcription factors T-bet and FOXP3 and cytokines IFN-γ, TNF-α, TGF-ß, and IL-10 were also determined by real-time RT-PCR. ELISA was used to measure TGF-ß protein levels in the cell culture supernatants. RESULTS: ART supplementation significantly increased 4T1 cell apoptosis and decreased TGF-ß levels in vitro. ART also impeded tumor growth in 4T1 TB mice and extended their survival. MDSC and Treg frequencies significantly decreased in the 4T1 TB mice after ART treatment while CD4+ IFN-γ+ T cells and CTLs significantly increased. ART significantly increased T-bet, IFN-γ, and TNF-α mRNA levels within the tumor and significantly decreased TGF-ß mRNA levels. CONCLUSION: ART supplementation hindered 4T1 tumor growth in vivo by promoting T cell activation and quelling immunosuppression from Tregs and MDSCs in the tumor.

Comparison of high- and low-viscosity cement in the treatment of vertebral compression fractures: A systematic review and meta-analysis.

BACKGROUND: High-viscosity cement (HVC) has been gradually applied in percutaneous vertebroplasty (PVP) and percutaneous kyphoplasty (PKP). Although HVC has been reported to reduce cement leakage, different opinions exist. To assess the complications of HVC in cement leakage in the treatment of vertebral compression fractures and to evaluate the clinical effect of HVC compared with low-viscosity cement (LVC). METHODS: EMBASE, PubMed, Science Direct, Google Scholar and Cochrane Library databases were comprehensively searched from their inception to August 2017. Two researchers independently searched for articles and reviewed all retrieved studies. Forest plots were used to illustrate the results. The Q-test and I statistic were employed to evaluate between-study heterogeneity. Potential publication bias was assessed by funnel plot. RESULTS: HVC reduced the occurrence of cement leakage (risk ratio (RR) = 0.38, 95% confidence interval (CI) = 0.29 to 0.51, P < 0.00001), especially in the disc space (RR = 0.45, 95% CI = 0.45 to 0.80, P = 0.007) and the vein (RR = 0.54, 95% CI = 0.35 to 0.85, P = 0.008) but not in the intraspinal space (RR = 0.48, 95% CI = 0.19 to 1.23, P = 0.13) or the paravertebral area (RR = 0.63, 95% CI = 0.32 to 1.22, P = 0.17). No significant differences in the visual analogue scale (VAS), Oswestry Disability Index (ODI), injected cement volume or adjacent vertebral fracture were noted between HVC and LVC (P > 0.05). CONCLUSION: Compared with LVC, HVC results in a reduced incidence of cement leakage for the treatment of vertebral compression fractures, especially in the disc space and vein but not in the intraspinal space or the paravertebral area. In addition, HVC yields the same satisfactory clinical effect as LVC.

Parasite densities modulate susceptibility of mice to cerebral malaria during co-infection with Schistosoma japonicum and Plasmodium berghei.

BACKGROUND: Malaria and schistosomiasis are endemic and co-exist in the same geographic areas, even co-infecting the same host. Previous studies have reported that concomitant infection with Schistosoma japonicum could offer protection against experimental cerebral malaria (ECM) in mice. This study was performed to evaluate whether alterations in parasite density could alter this protective effect. METHODS: Mice were inoculated with 100 or 200 S. japonicum cercariae followed by infection with high or low density of Plasmodium berghei ANKA strain eight weeks after the first infection. Then, parasitaemia, survival rate and blood-brain-barrier (BBB) damage were assessed. Interferon-gamma (IFN-γ), interleukin (IL)-4, IL-5, IL-13, IL-10, and TGF-ß levels were determined in splenocyte supernatants using enzyme-linked immunosorbent assay (ELISA). Cell surface/intracellular staining and flow cytometry were used to analyse the level of CD4(+)/CD8(+) T cells, CD4(+)CD25(+)Foxp3(+) Tregs, IL-10-secreting Tregs, and IL-10(+)Foxp3-CD4(+) T cells in the spleen, and CD4(+)/CD8(+) T cells infiltrating the brain. RESULTS: Co-infection with low density P. berghei and increased S. japonicum cercariae significantly increased the levels of IL-4, IL-5, IL-13, TGF-ß and Tregs, but significantly decreased the levels of IFN-γ and the percentage of CD4(+) T cells and CD8(+) T cells in the spleen and CD8(+) T cell infiltration in the brain. Increased worm loads also significantly decreased mortality and BBB impairment during ECM. When challenged with higher numbers of P. berghei and increased cercariae, the observed cytokine changes were not statistically significant. The corresponding ECM mortality and BBB impairment also remained unchanged. CONCLUSIONS: This study demonstrates that protection for ECM depends on the numbers of the parasites, S. japonicum and P. berghei, during co-infection. Alterations in the regulatory response appear to play a key role in this adaptation.