Image_1_Case report: Different clinical manifestations of the rare Loeffler endocarditis.TIF

BackgroundLoeffler endocarditis is a rare and fatal disease, which is prone to be misdiagnosed, owing to its various clinical manifestations. Consequently, an early identification of Loeffler endocarditis and its effective treatment are crucial steps to be undertaken for good prognosis.Case presentationThis report describes two cases of Loeffler endocarditis with different etiologies and clinical manifestations. Case 1 was caused by idiopathic eosinophilia and presented with a thrombus involving the tricuspid valve and right ventricular inflow tract (RVIT). The patient suffered from recurrent syncope following activity. After the patient underwent tricuspid valve replacement and thrombectomy, he took oral prednisone and warfarin for 2 years, consequent to which he discontinued both drugs. However, the disease recurred 6 months later, this time manifesting as edema of both legs. Echocardiography showed that a thrombus had reappeared in the RVIT. Thus, oral prednisone and warfarin therapy was readministered. Three months later, the thrombus had dissolved. Low-dose prednisone maintenance therapy was provided long term. Case 2 involved a patient who presented with recurrent fever, tightness in the chest, and asthma, and whose condition could not be confirmed, despite multiple local hospitalizations. In our hospital, echocardiography revealed biventricular apical thrombi. After comprehensive examinations, the final diagnosis was eosinophilic granulomatosis polyangiitis (EGPA) involving multiple organs, including the heart (Loeffler endocarditis), lungs, and kidneys. After administration of corticosteroid, anticoagulant, and immunosuppressive agents along with drugs to improve cardiac function, the patient's symptoms improved significantly.ConclusionIn Loeffler endocarditis due to idiopathic eosinophilia, long-term corticosteroid use may be required. Diverse and non-specific symptoms cause Loeffler endocarditis to be easily misdiagnosed. So, when a patient shows a persistent elevation of the eosinophil count with non-specific myocardial damage, the possibility of this disease, should always be considered. Furthermore, even when an invasive clinical procedure such as endomyocardial biopsy (EMB) is not available or acceptable, corticosteroids should be administered promptly to bring the eosinophil count back to the normal range, thereby halting the progression of disease and reducing patient mortality.</p

Image_2_Case report: Different clinical manifestations of the rare Loeffler endocarditis.TIF

BackgroundLoeffler endocarditis is a rare and fatal disease, which is prone to be misdiagnosed, owing to its various clinical manifestations. Consequently, an early identification of Loeffler endocarditis and its effective treatment are crucial steps to be undertaken for good prognosis.Case presentationThis report describes two cases of Loeffler endocarditis with different etiologies and clinical manifestations. Case 1 was caused by idiopathic eosinophilia and presented with a thrombus involving the tricuspid valve and right ventricular inflow tract (RVIT). The patient suffered from recurrent syncope following activity. After the patient underwent tricuspid valve replacement and thrombectomy, he took oral prednisone and warfarin for 2 years, consequent to which he discontinued both drugs. However, the disease recurred 6 months later, this time manifesting as edema of both legs. Echocardiography showed that a thrombus had reappeared in the RVIT. Thus, oral prednisone and warfarin therapy was readministered. Three months later, the thrombus had dissolved. Low-dose prednisone maintenance therapy was provided long term. Case 2 involved a patient who presented with recurrent fever, tightness in the chest, and asthma, and whose condition could not be confirmed, despite multiple local hospitalizations. In our hospital, echocardiography revealed biventricular apical thrombi. After comprehensive examinations, the final diagnosis was eosinophilic granulomatosis polyangiitis (EGPA) involving multiple organs, including the heart (Loeffler endocarditis), lungs, and kidneys. After administration of corticosteroid, anticoagulant, and immunosuppressive agents along with drugs to improve cardiac function, the patient's symptoms improved significantly.ConclusionIn Loeffler endocarditis due to idiopathic eosinophilia, long-term corticosteroid use may be required. Diverse and non-specific symptoms cause Loeffler endocarditis to be easily misdiagnosed. So, when a patient shows a persistent elevation of the eosinophil count with non-specific myocardial damage, the possibility of this disease, should always be considered. Furthermore, even when an invasive clinical procedure such as endomyocardial biopsy (EMB) is not available or acceptable, corticosteroids should be administered promptly to bring the eosinophil count back to the normal range, thereby halting the progression of disease and reducing patient mortality.</p

Deciphering the miRNA transcriptome of granulosa cells from dominant and subordinate follicles at first follicular wave in goat

In goats, most follicles in the ovaries will be atresia and only a few dominant follicles (DFs) may eventually mature and ovulate at a follicular wave. To investigate the potential microRNAs (miRNAs) that regulate the expression of genes associated with follicular dominance or atresia, small RNA sequencing was performed on granulosa cells of DF and subordinate follicle at the first follicular wave in goats. A total of 108 differentially expressed miRNAs were detected in the two types of follicle granulosa cells: 16 upregulated miRNAs and 92 downregulated miRNAs. Kyoto Encyclopedia of Genes and Genomes analysis of the target genes showed that TKTL1, LOC102187810, LOC102184409 and ALDOA are closely associated with follicle dominance and are involved in the pentose phosphate pathway. Furthermore, a coexpression network of miRNAs and follicular dominance-related genes was constructed. The qPCR results well correlated with the small RNA sequencing data. Our findings provide new insight for exploring the molecular mechanism of miRNAs in regulating follicular development in goats.</p

Feasibility of Using Drinking Water Treatment Residuals as a Novel Chlorpyrifos Adsorbent

Recent efforts have increasingly focused on the development of low-cost adsorbents for pesticide retention. In this work, the novel reuse of drinking water treatment residuals (WTRs), a nonhazardous ubiquitous byproduct, as an adsorbent for chlorpyrifos was investigated. Results showed that the kinetics and isothermal processes of chlorpyrifos sorption to WTRs were better described by a pseudo-second-order model and by the Freundlich equation, respectively. Moreover, compared with paddy soil and other documented absorbents, the WTRs exhibited a greater affinity for chlorpyrifos (log <i>K</i>_oc = 4.76–4.90) and a higher chlorpyrifos sorption capacity (<i>K</i>_F = 5967 mg^1–<i>n</i>·L·kg^–1) owing to the character and high content of organic matter. Further investigation demonstrated that the pH had a slight but statistically insignificant effect on chlorpyrifos sorption to WTRs; solution ionic strength and the presence of low molecular weight organic acids both resulted in concentration-dependent inhibition effects. Overall, these results confirmed the feasibility of using WTRs as a novel chlorpyrifos adsorbent

Fullerene-Induced Increase of Glycosyl Residue on Living Plant Cell Wall

In this work, we have investigated the change of cell wall for the tobacco plant cell (<i>Nicotiana tobacum</i> L. cv. Bright Yellow) under the repression of water-soluble carboxyfullerenes (C₇₀(C­(COOH)₂)_2–4). The adsorption of C₇₀(C­(COOH)₂)_2–4 on cell wall led to the disruption of cell wall and membrane, and consequently, cell growth inhibition. Results from atomic force microscopy (AFM) force measurement and confocal imaging revealed an increase of the glycosyl residue on the cell wall of carboxyfullerene-treated cells, with a time- and dose-dependent manner, and accompanied by the elevated reactive oxygen species (ROS). Moreover, the stimulation-sensitive alteration of glycosyl residue and ROS was demonstrated, which suggested a possible protection strategy for the plant cells under fullerene repression. This study provides the first direct evidence on the change of plant cell wall composition under the repression of fullerene and is the first successful application of AFM ligand-receptor binding force measurement to the living plant cell. The new information present here would help to a better understanding and assessment of the biological effect of fullerenes on plant

COX5B Regulates MAVS-mediated Antiviral Signaling through Interaction with ATG5 and Repressing ROS Production

<div><p>Innate antiviral immunity is the first line of the host defense system that rapidly detects invading viruses. Mitochondria function as platforms for innate antiviral signal transduction in mammals through the adaptor protein, MAVS. Excessive activation of MAVS-mediated antiviral signaling leads to dysfunction of mitochondria and cell apoptosis that likely causes the pathogenesis of autoimmunity. However, the mechanism of how MAVS is regulated at mitochondria remains unknown. Here we show that the Cytochrome c Oxidase (CcO) complex subunit COX5B physically interacts with MAVS and negatively regulates the MAVS-mediated antiviral pathway. Mechanistically, we find that while activation of MAVS leads to increased ROS production and COX5B expression, COX5B down-regulated MAVS signaling by repressing ROS production. Importantly, our study reveals that COX5B coordinates with the autophagy pathway to control MAVS aggregation, thereby balancing the antiviral signaling activity. Thus, our study provides novel insights into the link between mitochondrial electron transport system and the autophagy pathway in regulating innate antiviral immunity.</p> </div

COX5B mediates MAVS signaling by repressing ROS production.

<p>(A) HEK293 cells were pretreated with 10 ug/ml antimycin A for 2 h, then transfected with the indicated plasmids. Twenty-four hours after transfection, cells were lysed to measure the IFNβ induction. (B) HEK293 cells were pretreated with 250 or 500 µM Mito-TEMPO for 4 h, and then transfected with IFNβ reporter and pRSV/LacZ vectors together with empty vector or MAVS, or infected with VSVΔM51-GFP (MOI = 0.1). Cells were lysed to measure IFNβ activity after 24 h transfection or 10 h infection. (C and D) COX5B RNAi oligos or NC were transfected into HEK293 cells, after 20 h transfection, empty vector or MAVS plasmids were transfected again, 30 h after the second transfection, cells were collected for FACS analysis to check cellular or mitochondrial ROS production by staining with DCF (C) or MitoSOX (D), respectively. Results are presented relative to the FACS mean fluorescence intensity over control cells. (E) HEK293 cells were transfected with COX5B RNAi oligo or NC, 36 h after transfection, cells were pretreated with 250 µM Mito-TEMPO for 4 h, and transfected again with indicated plasmids. Twenty-four hours after second transfection, cells were lysed to measure the IFNβ induction. (F) After first transfection and treatment as described in (E), cells were transfected with IFNβ reporter and pRSV/LacZ vectors, followed by 16 h Sendai virus infection, cells were harvested for luciferase assays. (G) The experiments were carried out as in (F) except that cells were pretreated with 100 µM PDTC. (H) HEK293 cells were transfected with the indicated plasmids for 30 h, and then stained with MitoSOX followed by FACS analysis. Cells were treated with 0.1 µM H₂O₂ for 30 min as positive control. Results are presented relative to the FACS mean fluorescence intensity in control cells. (I) HEK293 cells were transfected with increasing amounts of MAVS expression plasmids, and empty vector was used to balance the total DNA amount. Total protein was prepared and subjected to immunoblot analysis after 24 h transfection. Data from A–B, E–G are representative of at least three independent experiments, (mean and s.d. of duplicate assays), and data from C, D and H are presented as mean ± SD from at least three independent experiments. *, P<0.05; **, P<0.01; *** P<0.001 versus control groups.</p

COX5B negatively controls the virus amplification.

<p>(A–C) HEK293 cells were transfected with COX5B RNAi oligos or NC. After 48 h transfection, cells were infected by Sendai virus for 12 h, and then lysed to isolate RNA to check the transcription levels of IFNβ (A), RANTES (B) and Viperin (C) by real-time PCR. (D–F) The transfection were performed as in (A–C), except that cells were infected by VSVΔM51-GFP (MOI = 0.1) for 9 h. (G) The RNAi oligo transfection was carried out as in (A), RNAi cells were infected by Sendai virus for 16 h, and the supernatant was collected for measurement of IFNβ by ELISA. (H–J) HEK293 cells were transfected with COX5B RNAi oligos for 48 h, then cells were infected by VSV-GFP (H) or VSVΔM51-GFP (I) at the MOI of 0.01 for 12 h, subsequently the culture supernatants were collected to measure virus titer by plaque assay, or cells were imaged by fluorescence microscopy (J). Data from A–I are representative of at least three independent experiments, (A–F, mean and s.d. of triplicate assays, G–I using duplicate assays). *, P<0.05; **, P<0.01 versus the control groups.</p

The mRNA levels of the four hub genes.

(A–D) Expression of the four genes in 12 pairs of ccRCC and para-cancer tissues by qRT-PCR. (E–H) expression of the four hub genes in cancer cells and normal kidney cells by qRT-PCR (**PP<0.05).</p

Additional file 1: of Phase I/II dose-finding study of nanoparticle albumin-bound paclitaxel (nabÂŽ-Paclitaxel) plus Cisplatin as Treatment for Metastatic Nasopharyngeal Carcinoma

Raw data that supports the conclusion. (XLS 763 kb