Data_Sheet_1_Case Report: Considerations of nocturnal ventilator support in ROHHAD syndrome in chronic care of childhood central hypoventilation with hypothalamus dysfunction.PDF

Rapid-onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation (ROHHAD) is a rare life-threatening disorder that can occur during childhood. All children with ROHHAD develop alveolar hypoventilation during wakefulness and sleep. The key treatment for these patients is the optimization of oxygenation and ventilation. Here, we report the case of a 5-year-old girl with suspected ROHHAD, with rapid weight gain, breathing cessation, decreased height, hypoventilation, central hypothyroidism, hyperprolactinemia, and absolute deficiency of growth hormone, and negative PHOX2B sequencing results. The presentation met the diagnostic criteria for ROHHAD syndrome. During the 5-year follow-up, she presented with progressive deterioration of the function of the hypothalamus and respiratory center, hypoxemia (PO2 2) > 70 mmHg] during the first two cycles of N3 sleep with a poor response to ventilatory support. Early diagnosis and application of non-invasive positive pressure ventilation during sleep can improve the quality of life and outcomes of patients with ROHHAD, and polysomnography and TcPCO2 should be repeated every 3–6 months to follow the progress and regulate ventilator support. Multidisciplinary care is crucial for the successful management of these patients.</p

A microfluidic chip designed for the study of cancer cells invasion in 3D matrix.

<p>(A) Schematic representation of the microfluidic platform. Layout of the integrated microfluidic device is composed of three units sharing a common outlet, each of which contains an inlet, three parallel main channels, three cell culture chambers and an outlet. (B) A magnified illustration of one cell culture chamber. (C) Photograph of the microfluidic system.</p

Invadopodia formation assay and quantification analysis with confocal system in A549 cells.

<p>The cells in control group (A), EGF group (B), and GM6001/EGF group (C), were cultured on a 3D microfluidic device for 12 h. The cells were stained green represented combined with cortactin, stained red represented combined with F-actin, and arrowheads in merge pictures indicated cells displaying invadopodia. (D) The percent of the cells with invadopodia formation. (E) The average number of invadopodia per cell. Error bars represented the SD of three different determinations. *Statistically significant between control group and EGF group; **statistically significant between EGF group and GM6001/EGF group, p<0.05. Magnification: ×1200.</p

Fluoresent analysis of apoptotic in A549 cells.

<p>Cells were cultured on the 3D microfluidic device for 96 h and then stained by Hoechst and PI. Live cells were stained blue and dead cells were stained red. Magnification: ×200.</p

Illustration of medium flow direction in the microfluidic device.

<p>The blue, red and green indicators represented control group, EGF group, GM6001/EGF group respectively. These three indicators were perfused into microchannels from inlet A, B, C simultaneously and separately, while these indicators could spread out to cell chambers of both sides via oval microchannels uniformly and in parallel without crossing.</p

Actual invadopodia formation of A549 cells in control group (A), EGF group (B), and GM6001/EGF group (C) in 3D extracellular matrix in the microfluidic device with confocal system.

<p>Invadopodia could be obviously induced by EGF in (B), <b>while</b> this induction could be inhibited by GM6001 in (C). White arrowheads represented invadopodia. Magnification: ×1200.</p

DataSheet_1_Lysophosphatidylcholine acyltransferase level predicts the severity and prognosis of patients with community-acquired pneumonia: a prospective multicenter study.docx

BackgroundIdentifying the diagnosis as well as prognosis for patients presented with community-acquired pneumonia (CAP) remains challenging. We aimed to identify the role of lysophosphatidylcholine acyl-transferase (LPCAT) for CAP along with assessing this protein’s effectiveness as a biomarker for severity of disease and mortality.MethodsProspective multicenter research study was carried out among hospitalized patients. A total of 299 CAP patients (including 97 severe CAP patients [SCAP]) and 20 healthy controls (HC) were included. A quantitative enzyme-linked immunosorbent test kit was employed for detecting the LPCAT level in plasma. We developed a deep-learning-based binary classification (SCAP or non-severe CAP [NSCAP]) model to process LPCAT levels and other laboratory test results.ResultsThe level of LPCAT in patients with SCAP and death outcome was significantly higher than that in other patients. LPCAT showed the highest predictive value for SCAP. LPCAT was able to predict 30-day mortality among CAP patients, combining LPCAT values with PSI scores or CURB-65 further enhance mortality prediction accuracy.ConclusionThe on admission level of LPCAT found significantly raised among SCAP patients and strongly predicted SCAP patients but with no correlation to etiology. Combining the LPCAT value with CURB-65 or PSI improved the 30-day mortality forecast significantly.Trial registrationNCT03093220 Registered on March 28th, 2017.</p

data_sheet_1_S100A4+ Macrophages Are Necessary for Pulmonary Fibrosis by Activating Lung Fibroblasts.PDF

<p>S100A4, a calcium-binding protein, can promote pulmonary fibrosis via fibroblast activation. Due partly to its various cellular origins, the exact role of S100A4 in the development of lung fibrosis remains elusive. Here, we show that in the bronchoalveolar lavage fluid, numbers of S100A4⁺ macrophages correlated well with S100A4 protein levels and occurrence of idiopathic pulmonary fibrosis (IPF) in patients. A mouse model of bleomycin-induced pulmonary fibrosis demonstrated S100A4⁺ macrophages as main source for extracellular S100A4 in the inflammatory phase. In vitro studies revealed that extracellular S100A4 could activate both mouse and human lung fibroblasts by upregulation of α-SMA and type I collagen, during which sphingosine-1-phosphate (S1P) increased. Inhibiting the S1P receptor subtypes S1P₁/S1P₃ abrogated fibroblast activation. Accordingly, absence or neutralization of S100A4 significantly attenuated bleomycin-induced lung fibrosis in vivo. Importantly, adoptive transfer of S100A4⁺ but not of S100A4⁻ macrophages installed experimental lung injury in S100A4^−/− mice that were otherwise not sensitive to fibrosis induction. Taken together, S100A4 released by macrophages promotes pulmonary fibrosis through activation of lung fibroblasts which is associated with S1P. This suggests that extracellular S100A4 or S100A4⁺ macrophages within the lung as promising targets for early clinical diagnosis or therapy of IPF.</p

Additional file 2: of Metabolic profiles in community-acquired pneumonia: developing assessment tools for disease severity

Supplemental Figures. Figure S1. Metabolite base peak chromatograms of serum samples from a patient in three groups: a non-severe CAP; b severe CAP; c controls. Figure S2. S-plots identifying putative biomarkers on the basis of OPLS-DA models: a CAP patients versus controls; b severe CAP versus non-severe CAP patients. Figure S3. Box–whisker plots of relative intensity of 15 metabolites changed in CAP patients compared to controls. Horizontal line represents median; bottom and top of the box represent 25th and the 75th percentiles; whiskers represent 5% and 95% percentiles. *FDR < 0.05, **FDR < 0.001. NSCAP non-severe CAP, SCAP severe CAP. (DOCX 7213 kb

Additional file 1 of Comparison of the prevalence of respiratory viruses in patients with acute respiratory infections at different hospital settings in North China, 2012–2015

Table S1. Hospitals that participated in the study of acute respiratory infections in North China, 2012–2015. Table S2. Respiratory viruses detected in patients with acute respiratory infections in North China, 2012–2015, by age group and hospital setting. Figure S1. Frequency of co-infected viruses in patients with ARIs in North China, 2012–2015, by age group and hospital settings. (DOCX 391 kb