Isolation and Identification of Volatile Substances with Attractive Effects on Wohlfahrtia magnifica from Vagina of Bactrian Camel.

Vaginal myiasis is one of the most serious parasitic diseases in Bactrian camels. At present, there are no reports on biological control measures of the disease. In this paper, the metabolomic analysis of vaginal secretions from susceptible and non-susceptible camels was performed by ACQUITY UPLC H-Class Ultra Performance Liquid Chromatograph. The results matched in 140 vaginal compounds. Methylheptenone, 1-octen-3-ol, and propyl butyrate and their mixtures were selected for gas chromatography-electroantennography (GC-EAD), electroantennography (EAG), behavioral experiments and trapping experiments of Wohlfahrtia magnifica (W. magnifica). Results showed that the W. magnifica had EAG responses to the three compounds, respectively. The EAG responses of female flies to different concentrations of methylheptenone were significantly different, but to the others had no significant difference, and there was no significant difference in the same compounds between the different sexes. Behavioral and trapping experiments showed that methylheptenone and 1-octen-3-ol have significant attraction to W. magnifica, but there was no significant difference to propyl butyrate. When methylheptenone and 1-octen-3-ol were mixed in different proportions, it was found that a mixture at the ratio of 1:1 and 0.5:1 had extremely significant and significant attraction, respectively, to both male and female W. magnifica. The study showed that, except for propyl butyrate, the higher the concentrations of the other two compounds, the stronger the attractivity to the W. magnifica, and a mixture at the ratio of 1:1 could enhance the attractivity to the W. magnifica.

The effects of genital myiasis on the diversity of the vaginal microbiota in female Bactrian camels.

BACKGROUND: Genital myasis is one of the most important diseases that affects the reproductive organs of Bactrian camels in which can cause serious mechanical damage to the vaginal tissue. The accumulation of bacteria in the vagina of female camels can affect their health and reproductive ability. The effect of this damage is commonly manifested in the vaginal flora and vaginal mucosal immune system. Therefore, this investigation is a study of the diversity of the vaginal flora and the differences between healthy Bactrian camels and those suffering from genital myiasis. RESULTS: Vaginal microbiota samples were collected from two groups of female Bactrian camels of the same age. An Illumina MiSeq was used to sequence the 16S rRNA V3-V4 hypervariable sequence in the samples. The results showed that the vaginal microflora of the infected camels had a significantly greater operational taxonomic unit (OTU) value. According to the assessment of the alpha diversity index and the vaginal pH, the diversity index of the infected camel flora was higher than that of the normal camel flora, and the vaginal pH was lower than that of the normal camels (p < 0.01). There were no significant differences between the two groups in the abundance of dominant genera in the Bactrian camel vagina (P > 0.05), indicating that the certain stability is maintained. CONCLUSIONS: Overall, this comparison revealed the differences and similarities between the vaginal microbiota of Bactrian camels in various health statues. In addition, these data provide a reference point for understanding the types of bacteria that cause genital myiasis affecting the healthy development of Bactrian camels.

MicroRNA-4530 promotes angiogenesis by targeting VASH1 in breast carcinoma cells.

The results of our previous study revealed that microRNA (miRNA/miR)-4530 was upregulated in the serum of patients with diabetic retinopathy. The TargetScan miRNA database was used to identify potential targets of miR-4530 and vasohibin-1 (VASH1) was predicted as one of the targets. The results of our previous study demonstrated that miR-4530 was able to promote angiogenesis in human umbilical vein endothelial cells. Therefore, suppressing miR-4530 may be a potentially novel approach towards inhibiting tumor angiogenesis. The present study aimed to investigate the function of miR-4530 and determine whether miR-4530 was able to regulate angiogenesis in breast carcinoma cells by targeting VASH1. MDA-MB-231 and MCF-7 cells were transfected with miR-4530 precursor, anti-miR-4530 and empty vector plasmids. The expression levels of miRNA and mRNA were detected using the reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The expression levels of protein were detected using western blotting. Dual-luciferase reporter assays were used to identify the target of miR-4530. Furthermore, cell proliferation, cell cycle, apoptosis and tube formation assays were used to investigate the function of miR-4530 in vitro. Nude mice were used in a subcutaneous tumor model in vivo study. The results of the present study demonstrated that miR-4530 significantly suppressed proliferation and promoted apoptosis of breast carcinoma cells. In addition, miR-4530 expression promoted angiogenesis in vitro. Results from the western blotting and RT-qPCR revealed that VASH1 was significantly downregulated by miR-4530 in breast carcinoma cells. The results of the present study suggest that miR-4530 promotes angiogenesis, inhibits proliferation and induces apoptosis in breast carcinoma cells by suppressing the expression of VASH1.

Identification of the differential expression of serum microRNA in type 2 diabetes.

The identification of disease-specific alterations in miRNA expression and the ability to detect miRNAs in serum furnish the basis for identified potential research value. This study was aimed to characterize the expression of miRNAs in the serum samples from people with type 2 diabetes mellitus (T2DM) and healthy individuals in order to detect the differential expression of miRNAs in T2DM. In total, 582 participants were recruited. Microarray-based miRNA expression profiles were screened in pooled serum samples from two groups (T2DM and healthy control). The candidates' miRNAs were validated by reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR). Five significantly different serum miRNAs were identified in T2DM patients (hsa-miR-320d, hsa-miR-4534, hsa-miR-3960, hsa-miR-451a, and hsa-miR-572) compared to those in the serum of healthy controls. This study provided evidence that serum miRNAs had differential expressions between healthy controls and T2DM patients. These five differential expression miRNAs might be of help for subsequent study in T2DM.

Glutamine synthetase plays a role in D-galactose-induced astrocyte aging in vitro and in vivo.

Astrocytes play multiple roles in physiological and pathological conditions in brain. However, little is known about the alterations of astrocytes in age-related changes, and few aging models of the astrocytes in vitro have been established. Therefore, in the present study, we used d-galactose (D-Gal) to establish astrocyte aging model to explore the alterations of astrocytes in brain aging. We also used (1)H nuclear magnetic resonance ((1)H NMR) spectra to verify the metabolic changes in the cerebral cortex of mice injected with D-gal. The results showed that D-gal (55mM) treatment for 1 week induced senescence characteristics in cultured cortical astrocytes. Real-time PCR and western blot analysis showed that the levels of glutamine synthetase (GS) mRNA and protein were strikingly decreased in the cultured senescent astrocytes, and the senescent astrocytes showed less resistance to the glutamate-induced gliotoxicity. The impairments of glutamate-glutamine cycle and astrocytes were also found in the cerebral cortex of mice treatment with D-gal (100mg/kg) for 6 weeks, and the level of GS mRNA was also found to be reduced markedly, being consistent with the result obtained from the senescent astrocytes in vitro. These results indicate that astrocyte may be the predominant contributor to the pathogenic mechanisms of D-gal-induced brain aging in mice, and GS might be one of the potential therapeutic targets of the aged brain induced by D-gal.