Exudative pleural effusion caused by lung fluke infection: A practical diagnostic approach.

OBJECTIVES: Pleural effusion caused by lung fluke is a rare etiology of exudative pleural effusion (EPE), which is often misdiagnosed or delayed. We aim to summarize the diagnosis and treatment course of EPE caused by lung fluke infection and put forward a practical diagnosis approach. METHODS: We retrospectively analyzed the diagnosis and treatment of 14 cases of EPE caused by lung fluke infection diagnosed by enzyme-linked immunosorbent assay of serum antibodies or egg detection. RESULTS: All patients (100%) with an absolute count of eosinophils in peripheral blood exceeded 0.5 × 109/l, and 10 patients (71.4%) had a history of special ingestion. Eosinophilic PE occurred in 11 patients (78.6%), pleural biopsy of medical thoracoscopic demonstrated eosinophils infiltration in nine patients (64.3%), and parasite eggs in one patient. All patients showed positive intradermal tests for Paragonimus-specific antigens and enzyme-linked immunosorbent assay of serum antibodies to Paragonimus. CONCLUSION: For patients with unexplained PE, lung fluke infection should be highly suspected when pleural fluid or pleural biopsy shows eosinophilic PE or eosinophils infiltration, especially for patients with certain diet history.

Transcriptional profile of Trichomonas vaginalis in response to metronidazole.

BACKGROUND: Trichomoniasis caused by Trichomonas vaginalis, combined with its complications, has long frequently damaged millions of human health. Metronidazole (MTZ) is the first choice for therapy. Therefore, a better understanding of its trichomonacidal process to ultimately reveal the global mechanism of action is indispensable. To take a step toward this goal, electron microscopy and RNA sequencing were performed to fully reveal the early changes in T. vaginalis at the cellular and transcriptome levels after treatment with MTZ in vitro. RESULTS: The results showed that the morphology and subcellular structures of T. vaginalis underwent prominent alterations, characterized by a rough surface with bubbly protrusions, broken holes and deformed nuclei with decreased nuclear membranes, chromatin and organelles. The RNA-seq data revealed a total of 10,937 differentially expressed genes (DEGs), consisting of 4,978 upregulated and 5,959 downregulated genes. Most DEGs for the known MTZ activators, such as pyruvate:ferredoxin oxidoreductase (PFOR) and iron-sulfur binding domain, were significantly downregulated. However, genes for other possible alternative MTZ activators such as thioredoxin reductase, nitroreductase family proteins and flavodoxin-like fold family proteins, were dramatically stimulated. GO and KEGG analyses revealed that genes for basic vital activities, proteostasis, replication and repair were stimulated under MTZ stress, but those for DNA synthesis, more complicated life activities such as the cell cycle, motility, signaling and even virulence were significantly inhibited in T. vaginalis. Meanwhile, increased single nucleotide polymorphism (SNP) and insertions - deletions (indels) were stimulated by MTZ. CONCLUSIONS: The current study reveals evident nuclear and cytomembrane damage and multiple variations in T. vaginalis at the transcriptional level. These data will offer a meaningful foundation for a deeper understanding of the MTZ trichomonacidal process and the transcriptional response of T. vaginalis to MTZ-induced stress or even cell death.

Profile Autonomous Underwater Vehicle System for Offshore Surveys.

Offshore marine engineering, offshore aquaculture, and offshore environmental protection require periodic offshore surveys. At present, the main means of offshore marine surveys are mooring buoys and marine survey ships. Anchored buoys are fixed in place for a long time, which affects the navigation of ships. Therefore, mooring buoys cannot be deployed over a large area with high density. The cost of marine survey ships is high, especially when multipoint synchronous marine surveys are needed, and marine survey ships cannot perform offshore surveys under bad sea conditions. A profile autonomous underwater vehicle system is developed to meet the requirements of multipoint short-term synchronous offshore surveys. It is a small, reusable, low-cost equipment designed to move up and down at a mooring position while measuring temperature, salinity, depth, and other quantities along a vertical water section. Profile autonomous underwater vehicles can be commanded remotely and report their measurements in near real-time via wireless telemetry. The time it takes for a profile AUV to move up and down can indicate the current velocity. Tests were carried out on a wharf and in offshore areas, and the results were satisfactory.

Observation of the Gut Microbiota Profile in BALB/c Mice Induced by Plasmodium yoelii 17XL Infection.

Rodent malaria caused by Plasmodium yoelii 17XL (Py 17XL) is an ideal animal model for human malaria studies. Although the gut microbiota plays an important role in the occurrence and development of infectious diseases, the gut microbiota associated with Py 17XL infection remains unclear. In the current study, the gut microbiota composition of infected BALB/c mice was surveyed. Mouse fecal samples were collected at 0, 2, 5 days post-infection (dpi), and the gut microbiota was characterized by 16S rRNA sequencing. Operational taxonomic units (OTUs) were 634 ± 26 on average. Firmicutes and Bacteroidetes were typically predominant in the gut microbiota composition at the phylum level. Compared with the Ctrl, Firmicutes was significantly decreased after infection, while Bacteroidetes was notably increased. The most dominant family was Lactobacillaceae in all samples. The alpha diversity index showed that compared with that of the Ctrl, the observed OTU number was decreased at 2 dpi and then slightly increased at 5 dpi. LEfSe analysis revealed several bacterial taxa were notably related to Py-infected mice at the phylogenetic level. Several bacterial genera, such as Lactobacillus, were overrepresented in the Py-infected fecal microbiota at 2 dpi, while Muribaculaceae was overrepresented at 5 dpi. Moreover, Alistipes and Helicobacter were overrepresented at 5 dpi compared with 2 dpi. The results indicated Py infection could alter the gut microbiota composition of mice. Besides, biomarkers could serve as direct targets to elucidate their roles in the progression and pathogenesis of malaria and provide insights into studies of antimalarial drugs and malaria vaccines.

Vaccines as a Strategy to Control Trichinellosis.

Trichinellosis caused by Trichinella spiralis is a worldwide food-borne parasitic zoonosis. Several approaches have been performed to control T. spiralis infection, including veterinary vaccines, which contribute to improving animal health and increasing public health by preventing the transmission of trichinellosis from animals to humans. In the past several decades, many vaccine studies have been performed in effort to control T. spiralis infection by reducing the muscle larvae and adult worms burden. Various candidate antigens, selected from excretory-secretory (ES) products and different functional proteins involved in the process of establishing infection have been investigated in rodent or swine models to explore their protective effect against T. spiralis infection. Moreover, different types of vaccines have been developed to improve the protective effect against T. spiralis infection in rodent or swine models, such as live attenuated vaccines, natural antigen vaccines, recombinant protein vaccines, DNA vaccines, and synthesized epitope vaccines. However, few studies of T. spiralis vaccines have been performed in pigs, and future research should focus on exploring the protective effect of different types of vaccines in swine models. Here, we present an overview of the strategies for the development of effective T. spiralis vaccines and summarize the factors of influencing the effectiveness of vaccines. We also discuss several propositions in improving the effectiveness of vaccines and may provide a route map for future T. spiralis vaccines development.

Observation of the Gut Microbiota Profile in C57BL/6 Mice Induced by Plasmodium berghei ANKA Infection.

The genus of Plasmodium parasites can cause malaria, which is a prevalent infectious disease worldwide, especially in tropical and subtropical regions. C57BL/6 mice infected with P. berghei ANKA (PbA) will suffer from experimental cerebral malaria (ECM). However, the gut microbiota in C57BL/6 mice has rarely been investigated, especially regarding changes in the intestinal environment caused by infectious parasites. P. berghei ANKA-infected (PbA group) and uninfected C57BL/6 (Ctrl group) mice were used in this study. C57BL/6 mice were infected with PbA via intraperitoneal injection of 1 × 106 infected red blood cells. Fecal samples of two groups were collected. The microbiota of feces obtained from both uninfected and infected mice was characterized by targeting the V4 region of the 16S rRNA through the Illumina MiSeq platform. The variations in the total gut microbiota composition were determined based on alpha and beta diversity analyses of 16S rRNA sequencing. The raw sequences from all samples were generated and clustered using ≥ 97% sequence identity into many microbial operational taxonomic units (OTUs). The typical microbiota composition in the gut was dominated by Bacteroidetes, Firmicutes, Proteobacteria, and Verrucomicrobia at the phylum level. Bacteroidetes and Verrucomicrobia were considerably decreased after PbA infection compared with the control group (Ctrl), while Firmicutes and Proteobacteria were increased substantially after PbA infection compared with Ctrl. The alpha diversity index showed that the observed OTU number was increased in the PbA group compared with the Ctrl group. Moreover, the discreteness of the beta diversity revealed that the PbA group samples had a higher number of OTUs than the Ctrl group. LEfSe analysis revealed that several potential bacterial biomarkers were clearly related to the PbA-infected mice at the phylogenetic level. Several bacterial genera, such as Acinetobacter, Lactobacillus, and Lachnospiraceae_NK4A136_group, were overrepresented in the PbA-infected fecal microbiota. Meanwhile, a method similar to gene coexpression network construction was used to generate the OTU co-abundance units. These results indicated that P. berghei ANKA infection could alter the gut microbiota composition of C57BL/6 mice. In addition, potential biomarkers should offer insight into malaria pathogenesis and antimalarial drug and malaria vaccine studies.

Galectin-3 mediates high-glucose-induced cardiomyocyte injury by the NADPH oxidase/reactive oxygen species pathway.

Galectin-3 is a member of the ß-galactoside-binding lectin family taking part in the regulation of inflammation, angiogenesis, and fibrosis. This study was designed to study the improved effect of galectin-3 inhibition on diabetic cardiomyopathy (DCM). Sprague-Dawley rats were randomized into the control, DCM, and DCM + modified citrus pectin (MCP) (a galectin-3 pharmacological inhibitor) groups. After 8 weeks, streptozotocin-induced DCM led to high blood glucose level, oxidative stress, cardiac injury, and dysfunction accompanied by suppressed body mass. On the contrary, MCP (100 mg·kg-1·day-1) administration improved body mass and blood glucose level and attenuated cardiac injury and dysfunction in DCM rats. Additionally, MCP attenuated pathological changes in plasma and myocardial tissue markers of oxidative stress, such as hydrogen peroxide and malonyldialdehyde, although it did not change superoxide dismutase activities, which were decreased in the DCM group. The levels of oxidative stress associated proteins evaluated by Western blot, such as p67phox and NADPH oxidase 4, were obviously increased in the DCM group, while they were reversed by MCP treatment. Therefore, galectin-3-mediated high-glucose-induced cardiomyocyte injury and galectin-3 inhibition attenuated DCM by suppressing NADPH oxidase. These findings suggested that galectin-3 could be a potential target for treatment of patients with DCM.

Circ_RUSC2 upregulates the expression of miR-661 target gene SYK and regulates the function of vascular smooth muscle cells.

Many studies have identified circRNA as a prospective direction in the field of cardiovascular research. Detection of circRNA expression in different vascular smooth muscle cell (VSMC) phenotypes revealed that circ_RUSC2 is upregulated in proliferative VSMCs. Sequence analysis of circ_RUSC2 showed that there are multiple binding sites of miR-661 on circ_RUSC2, and that SYK is an important target gene of miR-661. MiR-661 expression is downregulated in proliferative VSMCs, whereas the expression of SYK is upregulated. Circ_RUSC2 and miR-661 do not affect each other's expression levels, but circ_RUSC2 can promote the expression of SYK and inhibit the expression of SM22-alpha, whereas miR-661 has the opposite effect. At the same time, VSMC proliferation and migration can be promoted by SYK or circ_RUSC2, but the linear sequence of circ_RUSC2 can not. MiR-661 and circ_RUSC2 siRNAs inhibit VSMC proliferation and migration, and promote cell apoptosis. When an miR-661 mimic or SYK siRNAs were co-transfected with circ_RUSC2 overexpression vector, VSMC proliferation, apoptosis, and migration were not significantly altered. Accordingly, circ_RUSC2 can promote the expression of SYK, a target gene of miR-661, and regulate VSMC proliferation, apoptosis, phenotypic modulation, and migration. These findings will supply a theoretical basis for studying circRNA function in VSMCs, and new ideas for the diagnosis and treatment of cardiovascular diseases.

Corrigendum: Alterations of the Mice Gut Microbiome via Schistosoma japonicum Ova-Induced Granuloma.

[This corrects the article DOI: 10.3389/fmicb.2019.00352.].

Alterations of the Mice Gut Microbiome via Schistosoma japonicum Ova-Induced Granuloma.

Schistosomiasis, also called bilharziasis, is a neglected tropical disease induced by Schistosoma spp. that causes hundreds of millions of infections. Although Schistosoma ova-induced granulomas commonly cause inflammation, hyperplasia, ulceration, micro abscess formation, and polyposis, the role of the egg granuloma on the gut microbiome remains unclear. To explore the role, gut microbial communities in mice infected with Schistosoma japonicum were surveyed. Female C57BL/6 and BALB/c mice were exposed to cercariae of S. japonicum for 45 and 65 days and then sacrificed. Intestinal contents and feces were collected, DNA was extracted, and high-throughput 16S rRNA gene-based pyrosequencing was used to provide a comparative analysis of gut microbial diversity. The intestinal mucosal tissues were also examined. Histopathologic analysis demonstrated that the basic structure of the colonic mucosa was damaged by ova-induced granuloma. Regarding the gut microbiome, 2,578,303 good-quality sequences were studied and assigned to 25,278 Operational Taxonomic Units (OTUs) at a threshold of 97% similarity. The average number of OTUs for C57BL/6 and BALB/c were 545 and 530, respectively. At the phylum level, intestinal microbial communities were dominated by Firmicutes, Bacteroidetes, Proteobacteria, and Verrucomicrobia. Infection with S. japonicum modified bacterial richness in the fecal associated microbiota. Exposure significantly modified bacterial community composition among different groups. At the phylogenetic levels, LEfSe analysis revealed that several bacterial taxa were significantly associated with the S. japonicum-infected mice. The present results suggest that egg granulomas in the intestine influence differentiation of the gut microbial community under pathophysiological conditions. This result suggests that intestinal microbiome-based strategies should be considered for early diagnosis, clinical treatment, and prognosis evaluation of schistosomiasis.

MicroRNA-140 attenuates myocardial ischemia-reperfusion injury through suppressing mitochondria-mediated apoptosis by targeting YES1.

Myocardial ischemia-reperfusion (I/R) injury is thought to have its detrimental role in coronary heart disease (CHD), which is considered as the foremost cause of death all over the world. However, molecular mechanism in the progression of myocardial I/R injury is still unclear. The goal of this study was to investigate the expression and function of microRNA-140 (miR-140) in the process of myocardial I/R injury. The miR-140 expression level was analyzed in the myocardium with I/R injury and control myocardium using quantitative real-time polymerase chain reaction. Then the relation between the level of miR-140 and YES proto-oncogene 1 (YES1) was also investigated via luciferase reporter assay. Assessment of myocardial infarct size measurement of serum myocardial enzymes and electron microscopy analysis were used for analyzing the effect of miR-140 on myocardial I/R injury. We also used Western blot analysis to examine the expression levels of the mitochondrial fission-related proteins, Drp1 and Fis1. miR-140 is downregulated, and YES1 is upregulated after myocardial I/R injury. Overexpression of miR-140 could reduce the increase related to myocardial I/R injury in infarct size and myocardial enzymes, and it also could inhibit the expression of proteins related to mitochondrial morphology and myocardial I/R-induced mitochondrial apoptosis by targeting YES1. Taken together, these findings may provide a novel insight into the molecular mechanism of miR-140 and YES1 in the progression of myocardial I/R injury. MiR-140 might become a promising therapeutic target for treating myocardial I/R injury.

LncRNA SRA deregulation contributes to the development of atherosclerosis by causing dysfunction of endothelial cells through repressing the expression of adipose triglyceride lipase.

It has been well established that long non­coding RNAs (lncRNAs) are crucial mediators in a diverse range of diseases, including atherosclerosis. The present study aimed to examine the molecular mechanisms underlying the association between steroid receptor RNA activator (SRA) and atherosclerosis. Reverse transcription­quantitative polymerase chain reaction analysis, western blot analysis and luciferase assays were performed to examine interactions among SRA, adipose triglyceride lipase (ATGL) and peroxisome proliferator­activated receptor (PPARγ), and the effect of resveratrol (RSV) on the levels of SRA, ATGL and PPARγ. ELISA was performed to determine the effects of SRA and RSV on the production of inflammatory­associated cytokines. The results showed that knockdown of the expression of SRA by transfecting HUVECs with short hairpin RNA­SRA inhibited the production of ATGL and PPARγ. A plasmid coding SRA RNA, but not the SRAP protein, attenuated the luciferase activity of the ATGL promoter. PPARγ had no effect on the luciferase activity driven by the ATGL promoter in the absence of rosiglitazone, whereas the luciferase activity of the ATGL promoter was elevated in the presence of rosiglitazone. This effect was eliminated by SRA. SRA enhanced the production of inflammatory­associated cytokines, including tumor necrosis factor­α, interleukin­6, monocyte chemotactic protein­1 and intercellular adhesion molecule­1; however, the promoting effect of SRA was eliminated by RSV. RSV increased the expression of ATGL and PPARγ, but not that of SRA. RSV distinctly and concentration­dependently upregulated the luciferase activity of ATGL, compared with that in the cells without RSV treatment, whereas treating with rosiglitazone inhibited the effect of RSV on the luciferase activity of ATGL. The present study examined the roles of SRA in atherosclerosis, and the effects of changes in SRA and ATGL on inflammatory cytokines and HUVEC dysfunction.

Seroprevalence of human immunodeficiency virus, hepatitis B and C viruses, and Treponema pallidum infections among blood donors at Shiyan, Central China.

BACKGROUND: Ordinary screening of transfusion-transmissible infections (TTIs) among blood donors is essential for blood transfusion. Although there is several TTIs studies focus on human immunodeficiency virus, hepatitis B and C viruses, and Treponema pallidum infections in China, it is no data to illustrate any firm conclusion from Shiyan City, Central China. It aims to verify the seroprevalence of TTIs among blood donors at Shiyan. METHODS: A retrospective analysis of blood donors' information was conducted for the presence of HIV, HBV, HCV and T. pallidum. Logistic regression analysis was used to demonstrate risk factors including age, gender and occupation associated with them. The variation tendency in seroprevalence of these TTIs over the study period was evaluated by Cochran-Armitage trend test. RESULTS: Of 211 639 blood donors, 2 858 (1.35 %) had serological evidence of TTIs. The seroprevalence of HIV, HBV, HCV and T. pallidum were 0.08 %, 0.51 %, 0.20 % and 0.57 %, respectively. However, the co-infection prevalence of TTIs has not been detected. The HIV seropositivity significantly increased among female donors (OR = 1.63, P < 0.001) and farmers (OR = 2.02, P = 0.020). Significantly increased HBV seropositivity was only observed framers (OR = 1.87, P <0.001) compared to workers. Analogously, significantly increased HCV seropositivity was observed among farmers (OR = 2.59, P < 0.001), students (OR = 2.43, P < 0.001), merchants (OR = 1.70, P = 0.014) and others (OR = 1.78, P =0.001). The T. pallidum seroprevalence was notably increased among female (OR = 1.54, P < 0.001), and farmers (OR = 1.70, P <0.001). Moreover, significantly increasing trends of HIV (Z = -6.88, P < 0.01), HBV (Z = -4.52, P < 0.01), HCV (Z = -4.16, P < 0.01) and T. pallidum (Z = -1.36, P < 0.01) seropositivity were observed over the study period. CONCLUSIONS: It originally offers a substantial prevalence of TTIs among blood donors at Shiyan, Central China. Severe blood donor selection and all-inclusive screening of blood are highly recommended. It might be helpful for developing and updating guidance for blood safety. TRIAL REGISTRATION: Retrospectively registered.

Adaptive tight frame based multiplicative noise removal.

Sparse approximation has shown to be a significant tool in improving image restoration quality, assuming that the targeted images can be approximately sparse under some transform operators. However, it is impossible for a fixed system to be always optimal for all the images. In this paper, we present an adaptive wavelet tight frame technology for sparse representation of an image with multiplicative noise. The adaptive wavelet tight frame is first learned from the logarithmic transformed given images, and then it is used to recover these images. Compared with the existing non-adaptive wavelet sparse transform methods, the numerical results demonstrate that the proposed adaptive tight frame scheme improves image restoration quality.

[Correlation between left ventricular mass index and NADPH oxidase p22phox in patients with non-valvular chronic heart failure].

OBJECTIVE: To study the correlation between the expression levels of phagocytic NADPH oxidase p22phox subunit and left ventricular mass index (LVMI) in patients with non-valvular chronic heart failure and explore the role of oxidative stress caused by NADPH oxidase p22phox subunit in left ventricular remodeling. METHODS: Semi-quantitative RT-PCR was used to examine the expression levels of phagocytic NADPH oxidase p22phox in 59 patients with non-valvular chronic heart failure and 20 control subjects. All the subjects underwent ultrasonic cardiography to record their IVST, LVPWT, LVEDd, LVEDs, and EF. Based on the calculated LVMI, the patients were divided into heart failure without LV hypertrophy (LVH) group and heart failure with LVH group. RESULTS: The patients with heart failure showed significantly higher expression of phagocytic NADPH oxidase p22phox than the control subjects (0.91∓0.37 vs 0.68∓0.33, P=0.039), and the patients with LVH had significantly higher p22phox expression than those without LVH (1.58∓0.20 vs 0.71∓0.24, P=0.026). LVMI showed a positive correlation with the expression of p22phox in these patients (r=0.508, P<0.05). CONCLUSION: NADPH oxidase p22phox expression level is positively correlated with LVMI and can be indicative of the level of left ventricular remodeling in patients with non-valvular chronic heart failure.

[Molecular and chemical mechanism of Trichomonas vaginalis-induced contact-dependent cytotoxicity].

Trichomonas vaginalis parasitizes in human genitourinary tract. The protozoon adhering to target cell plays a critical role in its contact-dependent cytotoxicity. The enzymes synthesized by T.voginalis can hurt vaginalis epithelial cells (VECs) directly. The focal immune reaction in the location parasitized by the parasite may provide an immunologic protection. Meanwhile, inflammatory factors and immune cells may aggravate the situation. In general, the T. vaginalis-induced contact-dependent cytotoxicity is a result of the involvement of some molecular and chemical factors.