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Currently, exosome-enclosed microRNAs (miRs) in exhaled breath have potential for biomarker discovery in patients with pulmonary diseases. This study was performed to investigate the roles of M2 macrophage-derived exosomes expressing miR-328 in pulmonary fibrosis (PF). Microarray-based analysis was used to screen differentially expressed genes (DEGs) and regulatory miRs in PF. The miR-target relationship between FAM13A and miR-328 was confirmed. The expression of FAM13A and miR-328 was measured in PF rats, and gain- and loss-of-function assays were conducted to determine the regulatory effects of FAM13A and miR-328 on PF. In addition, exosomes derived from M2 macrophages were isolated and then cocultured with pulmonary interstitial fibroblasts to identify the role of these exosomes in PF. Furthermore, the effects of M2 macrophage-derived exosomes overexpressing miR-328 on pulmonary fibroblast proliferation and the progression of PF were assessed in vivo. miR-328 might perform a vital function in PF by regulating FAM13A. FAM13A expression was downregulated while miR-328 expression was upregulated in rats with PF, and a miR-target relationship between miR-328 and FAM13A was observed. Additionally, miR-328 overexpression and FAM13A silencing each were suggested to promote pulmonary interstitial fibroblast proliferation and the expression of Collagen 1A, Collagen 3A and α-SMA. Then, in vitro experiments demonstrated that M2 macrophage-derived exosomes overexpressing miR-328 contributed to enhanced pulmonary interstitial fibroblast proliferation and promoted PF. Furthermore, in vivo experiments confirmed the promotive effects of M2 macrophage-derived exosomes overexpressing miR-328 on the progression of PF. Collectively, the results showed that M2 macrophage-derived exosomes overexpressing miR-328 aggravate PF through the regulation of FAM13A. Lung disease: Small RNAs promoting pulmonary fibrosis Studies in rats suggest that microRNAs, small molecules of ribonucleic acid, released by macrophage cells of the immune system can promote pulmonary fibrosis (PF), the formation of scar tissue in lungs. Gao-Feng Zhao, Li-Hua Xing and colleagues at The First Affiliated Hospital of Zhengzhou University in China investigated the role of microRNAs in rats with a form of PF that serves as a model for the disease in humans. Their findings confirm that specific microRNAs released in tiny membrane-bound sacs called exosomes interact with and inhibit a gene whose activity is known to be disrupted in PF. The protein encoded by this gene mediates crucial molecular signaling events in lung cells. Developing drugs that interfere with the activity of the microRNAs is a potential new treatment approach for PF.

Background: Uveitis refers to inflammation in the uvea, retina, retinal blood vessels, and vitreous, which can lead to irreversible eye damage and permanent vision loss. Glucocorticoid drugs are the first-line treatment, but side effects, such as obesity and hyperglycemia, can occur. Therefore, biologics have become a new treatment choice. Case Presentation: A 18-year-old girl developed eye pain and was diagnosed with binocular uveitis. Prednisone 50 mg was administered once a day, and the redness and pain in both eyes improved. Later, the prednisone dose was gradually reduced, and treatment was discontinued 3 years ago. Two years ago, the patient’s condition relapsed, with both eyes becoming red and painful. She was administered prednisone 20 mg once daily and adalimumab. Visual acuity in both eyes continued to progressively decrease, accompanied by cataracts. At the same time, the patient experienced complications, including obesity and hyperglycemia. Subsequently, a new treatment regimen, oral prednisone 20 mg once a day, tofacitinib 5 mg twice a day, and methotrexate 10 mg once a week, as well as the use of insulin to control blood sugar, was initiated. One month later, the patient’s redness and eye pain eased, and her vision gradually improved. The dosage of prednisone was gradually reduced to 5 mg once daily. At the same time, her blood sugar returned to normal, and insulin was stopped. Outcomes: The patient was treated with tofacitinib for 10 months. Subsequently, her best-corrected visual acuity of the right eye rose from 0.06 to 0.075, and the best-corrected visual acuity of the left eye rose from CF/30 cm to CF/100 cm. Redness and eye pain were relieved, her glucocorticoid consumption reduced from 15 to 2.5 mg, and her blood sugar gradually normalized. Conclusion: This case study shows that tofacitinib relieves ocular inflammation in patients with uveitis and improves eyesight. We believe that JAK inhibitors could be another treatment option for noninfectious uveitis in patients who do not respond to conventional anti-TNF-α inhibitors (such as adalimumab).

A 28-year-old female patient was hospitalized primarily because of “intermittent fever for 28 days aggravated by systemic rashes, oral ulcer, and edema in both eyelids for 5 days.” During treatment, convulsions and loss of consciousness occurred. Magnetic resonance imaging (MRI) of the head revealed an abnormal signal with shadows in the bilateral frontal, parietal, temporal, and occipital lobes; cerebellar hemispheres; and basal nodes, with high signal intensity on T2 weighted imaging (T2WI), on fluid-attenuated inversion-recovery, and of the apparent diffusion coefficient and low signal intensity on T1WI and diffusion weighted imaging. Therefore, the patient was diagnosed with systemic lupus erythematosus (SLE) with reversible posterior encephalopathy syndrome (RPES). Intravenous high-dose methylprednisolone and cyclophosphamide were administered for blood pressure control, which effectively controlled the disease. Therefore, when patients with SLE and hypertension or renal insufficiency or those receiving high-dose methylprednisolone or immunosuppressants suddenly present with neurologic abnormalities, a diagnosis of RPES must be considered, and head MRI is the first choice for diagnosis of this disease. In terms of treatment, the blood pressure should be quickly controlled, and the primary disease should be aggressively treated.

Lung cancer poses a severe threat to human life. Biomarkers of cancers are helpful in the diagnosis and treatment of patients with cancers. Biomarkers of lung cancers are rare, and thus deserve further research. The objective of the present study was to explore the expression of Fascin-1 in human lung cancer and paracarcinoma tissue, its correlation with clinicopathological characteristics in patients with lung cancer, and study the possible relationship between Fascin-1 expression and clinical-biological behavior of lung cancer. This study used the MaxVision two-step immunohistochemical detection method to detect Fascin-1 expression in 84 of lung cancer and paracarcinoma tissues. This study set the expression of Fascin-1 in vascular endothelial cells as the positive control, and used phosphate buffered saline (replacing the primary antibodies) as negative control. Of all the 84 lung cancer tissues and paracarcinoma tissues, positive expression of the Fascin-1 protein were detected in 78 cases (92.9%) and 27 cases (32.1%), respectively, and the difference was statistically significant (P<0.05). Differences in Fascin-1 expression between different age groups, clinical stages, and lymph node metastases were statistically significant (P<0.05), while differences in Fascin-1 expression between sexes, tumor stages, and pathological types demonstrated no statistical significance (P>0.05). The survival times of the patients with different Fascin-1 protein-positive expressions in lung cancer tissues were statistically significant (P>0.05), while the survival times of the patients with different Fascin-1 protein-positive expressions in paracarcinoma tissues were not statistically significant (P>0.05). In lung cancer, Fascin-1 expression was closely related to tumor invasion and metastasis, and the difference in expression of Fascin-1 had a significant effect on the survival time of the lung cancer patients. Therefore, Fascin-1 might be expected to serve as a possible potential biomarker of lung cancer.

A computational method is presented to evaluate non-compact noise produced by compressible flow interacting with arbitrarily shaped solid objects. In conjunction with compressible calculation, hybrid computational aeroacoustics method is used to develop noise calculation. Scattering effect induced by non-compact surfaces is the prime objective to study in the present research, the fluctuations of flow variables are decomposed into hydrodynamic component mainly produced by fluid flow and acoustic component mainly produced by noise propagation. Non-compact integral surface is divided into enough fine elements, and scattered pressure on body surface is firstly captured by acoustic calculation. The acoustic noise of two dimensional stationary circular cylinders at low Mach number is considered with diameter D=0.019m (Re=90000) and D=1m (Re=100). Numerical results indicate that the noise predicated by the present method is as accurate as noise directly computed by Curles equations at low frequency, the total noise of cylinder model has a dipole-like directivity, but a petal-like pattern at high frequency when scattering effects gradually strengthen. This method exactly captures scattered noise produced by noncompact bodies, and the influence of scattered noise with increased frequency is evaluated simultaneously in this paper.

Aberrant activity of enhancer of zeste homolog 2 （EZH2） is associated with a wide range of human cancers. The interaction of EZH2 with embryonic ectoderm development （EED） is required for EZH2＇s catalytic activity. Inhibition of the EZH2-EED complex thus represents a novel strategy for interfering with the oncogenic potentials of EZH2 by targeting both its catalytic and non-catalytic functions. To date, there have been no reported high-throughput screening （HTS） assays for inhibitors acting at the EZH2-EED interface In this study, we developed a fluorescence polarization （FP）-based HTS system for the discovery of EZH2-EED interaction inhibitors. The tracer peptide sequences, positions of fluorescein labeling, and a variety of physicochemical conditions were optimized. The high Z＇ factors （〉0.9） at a variety of DMSO concentrations suggested that this system is robust and suitable for HTS. The minimal sequence requirement for the EZH2-EED interaction was determined by using this system. A pilot screening of an in-house compound library containing 1600 FDA-approved drugs identified four compounds （apomorphine hydrochloride, oxyphenbutazone, nifedipine and ergonovine maleate） as potential EZH2-EED interaction inhibitors.

With the development of computational power and numerical algorithms, computational fluid dynamics （CFD） has become an important strategy for the design of aircraft, which significantly reduces the reliance on wind-tunnel and flight tests. In this paper, we conducted a numerical investigation on the flow past a full commercial aircraft at Mach number 0.2 and 14 degrees angle of attack by means of Reynolds-averaged Navier-Stokes （RANS）, detached-eddy simulation （DES） and our newly developed constrained large-eddy simulation （CLES）. The objective of this paper is to study the capability of these models in simulating turbulent flows. To our knowledge, this is the first large-eddy simulation method for full commercial aircraft simulation. The results show that the CLES can predict the mean statistical quantities well, qualitatively consistent with traditional methods, and can capture more small-scale structures near the surface of the aircraft with massive separations. Our study demonstrates that CLES is a promising alternative for simulating real engineering turbulent flows.

Based on the investigation and analysis on the articles on collaborative digital reference service published at home in recent three years, the paper clarified the latest development on exploring theories, constructing system, applying technology, opening up service, enhancing management, integrating resources and controlling quality on collaborative digital reference service at home.

Curcumin has been shown to significantly improve spatial memory impairment induced by HIV-1 gp 120 V3 in rats, but the electrophysiological mechanism remains unknown. Using extracellular microelectrode recording techniques, this study confirmed that the gp120 V3 loop could suppress long-term potentiation in the rat hippocampal CA1 region and synaptic plasticity, and that curcumin could antagonize these inhibitory effects. Using a Fura-2/AM calcium ion probe, we found that curcumin resisted the effects of the gp120 V3 loop on hippocampal synaptosomes and decreased Ca2＋ concentration in synaptosomes. This effect of curcumin was identical to nimodipine, suggesting that curcumin improved the inhibitory effects of gpl20 on synaptic plasticity, ameliorated damage caused to the central nervous system, and might be a potential neuroprotective drug.

Severe influenza remains unusual in its virulence for humans. Complications or ultimately death arising from these infections are often associated with hyperinduction of proinflammatory cytokine production, which is also known as ＇cytokine storm＇. For this disease, it has been proposed that immunomodulatory therapy may improve the outcome, with or without the combination of antiviral agents. Here, we review the current literature on how various effectors of the immune system initiate the cytokine storm and exacerbate pathological damage in hosts. We also review some of the current immunomodulatory strategies for the treatment of cytokine storms in severe influenza, including corticosteroids, peroxisome proliferator-activated receptor agonists, sphingosine-l-phosphate receptor 1 agonists, cyclooxygenase-2 inhibitors, antioxidants, anti-tumour-necrosis factor therapy, intravenous immunoglobulin therapy, statins, arbidol, herbs, and other potential therapeutic strategies.