MOESM3 of De Novo sphingolipid synthesis is essential for Salmonella-induced autophagy and human beta-defensin 2 expression in intestinal epithelial cells

Additional file 3: Figure S3. Effect of fumonisin B1on Salmonella-induced hBD-2 mRNA expression in Caco-2 cells. Caco-2 cells were left untreated, or treated with 25 μg/mL fumonisin B1 (FB1). They were then infected with the wild-type S. Typhimurium strain SL1344 for 1 h. Total RNA was prepared and analyzed by real-time quantitative PCR to estimate amounts of hBD-2 transcript. The amount of hBD-2 mRNA expression, normalized to the corresponding amount of GAPDH transcript, is shown as the fold increase over uninfected, control cells (CON). Results are represented as mean ± S.E.M. for at least three determinations from independent experiments. An asterisk indicates a significant difference (p < 0.005)

MOESM2 of De Novo sphingolipid synthesis is essential for Salmonella-induced autophagy and human beta-defensin 2 expression in intestinal epithelial cells

Additional file 2: Figure S2. Effect of fumonisin B1 on the membrane recruitment of NOD2 and Atg16L1 in Salmonella-infected Caco-2 cells. Caco-2 cells were untreated (CON) or treated with fumonisin B1 (FB1) and then infected by S. typhimurium wild-type strain SL1344 for indicated times. Immunoblots were performed on membrane lysates with antibody to detect Atg16L1 and NOD2expression, and E-cadherin for normalization of membrane protein. Representative immunoblots are shown

MOESM1 of De Novo sphingolipid synthesis is essential for Salmonella-induced autophagy and human beta-defensin 2 expression in intestinal epithelial cells

Additional file 1: Figure S1. Effect of myriocin on the expression of autophagy in Salmonella-infected SW480 cells. SW480 cells were untreated (CON) or treated with myriocin and then infected by S. typhimurium wild-type strain SL1344. Immunoblots were performed on whole cell lysates with antibody to detect autophagy Beclin-1 and Atg5 proteins expression, or GAPDH for normalization of proteins. Representative immunoblots (A) and densitometric quantification of immunoreactive bands are shown. The relative band intensities of Beclin-1 (B) and Atg5 (C) in untreated (white) and treated (black) SW480 cells are quantified as fold increases compared with the control cells. Each value represents the mean ± S.E.M. of 3 independent experiments. An asterisk indicates a significant difference (p < 0.05)

Room-temperature biphoton source with a spectral brightness near the ultimate limit

The biphotons, generated from a hot atomic vapor via the process of spontaneous four-wave mixing (SFWM), have the following merits: stable and tunable frequencies as well as linewidth. Such merits are very useful in the applications of long-distance quantum communication. However, the hot-atom SFWM biphoton sources previously had far lower values of generation rate per linewidth, i.e., spectral brightness, as compared with the sources of biphotons generated by the spontaneous parametric down conversion (SPDC) process. Here, we report a hot-atom SFWM source of biphotons with a linewidth of 960 kHz and a generation rate of 3.7$\times$ $10^5$ pairs/s. The high generation rate, together with the narrow linewidth, results in a spectral brightness of 3.8$\times$ $10^5$ pairs/s/MHz, which is 17 times of the previous best result with atomic vapors and also better than all known results with all kinds of media. The all-copropagating scheme together with a large optical depth (OD) of the atomic vapor is the key improvement, enabling the achieved spectral brightness to be about one quarter of the ultimate limit. Furthermore, this biphoton source had a signal-to-background ratio (SBR) of 2.7, which violated the Cauchy-Schwartz inequality for classical light by about 3.6 folds. Although an increasing spectral brightness usually leads to a decreasing SBR, our systematic study indicates that both of the present spectral brightness and SBR can be enhanced by further increasing the OD. This work demonstrates a significant advancement and provides useful knowledge in the quantum technology using photons

Infantile Hepatitis B in Immunized Children: Risk for Fulminant Hepatitis and Long-Term Outcomes

<div><p>Background</p><p>Infantile hepatitis B after neonatal immunoprophylaxis is a rare yet distinct disease. This study aimed to analyze the long-term outcomes and risk factors in immunized infants with hepatitis B.</p><p>Methods</p><p>The clinical parameters and outcomes of 41 infants born after universal immunization, and admitted for HBV-positive hepatitis were studied. All patients were followed for at least 6 months (median  = 4.4 years, range 0.6–18.1 years). Patient survival, changes of HBsAg and HBeAg status, and complications were analyzed.</p><p>Results</p><p>Among the 41 cases (32 males, 9 females), 21 presented with fulminant hepatitis (FH), and 20 with non-fulminant hepatitis (NFH). Ninety-five percent (36/38) of the mothers were positive for hepatitis B surface antigen (HBsAg). Multivariate analyses revealed younger age of onset (age <7 months) and negative maternal hepatitis B e antigen (HBeAg) were associated with FH (p = 0.03 and p = 0.01, respectively). An infantile fulminant hepatitis B risk score using maternal/infant HBeAg positivity and onset age was proposed. Among the FH cases, the rate of mortality, HBsAg clearance, and chronic HBV infection were 47.6%, 38.1%, and 14.3%, respectively. Among the NFH cases, 35% developed chronic infection. Of the 9 chronically infected children received long-term follow-up, 8 had HBeAg seroconversion before 4 years of age. One case of FH developed hepatocellular carcinoma 14 years later.</p><p>Conclusions</p><p>Maternal HBsAg + /HBeAg- and early onset age were risk factors for FH in immunized infants. A significant portion of patients with FH or NFH evolve to chronic HBV infection, with HBeAg seroconversion in young childhood. Close surveillance for hepatocellular carcinoma is warranted in patients surviving infantile hepatitis B.</p></div

Clinical course and outcomes of infants with hepatitis B; FH, fulminant hepatitis; NFH, non-fulminant hepatitis.

<p>Recovery is defined as HBsAg seroclearance. Chronic infection is defined as persistence of HBsAg for more than 6 months.</p

Top three gene ontology enrichment groups associated with susceptibility of CAA formation in KD.

<p>After gene ontology (GO) enrichment analysis, 162 over-represented GO terms were obtained and further summarized into GO clusters. The top three significant clusters were regulation of cell projection organization (<i>P</i> = 2.22 × 10⁻⁶), neuron recognition (<i>P</i> = 6.72 × 10⁻⁵), and peptidyl-threonine phosphorylation (<i>P</i> = 1.53 × 10⁻³).</p

Genome-Wide Association Study Identifies Novel Susceptibility Genes Associated with Coronary Artery Aneurysm Formation in Kawasaki Disease

<div><p>Kawasaki disease (KD) or Kawasaki syndrome is known as a vasculitis of small to medium-sized vessels, and coronary arteries are predominantly involved in childhood. Generally, 20–25% of untreated with IVIG and 3–5% of treated KD patients have been developed coronary artery lesions (CALs), such as dilatation and aneurysm. Understanding how coronary artery aneurysms (CAAs) are established and maintained in KD patients is therefore of great importance. Upon our previous genotyping data of 157 valid KD subjects, a genome-wide association study (GWAS) has been conducted among 11 (7%) CAA-developed KD patients to reveal five significant genetic variants passed pre-defined thresholds and resulted in two novel susceptibility protein-coding genes, which are NEBL (rs16921209 (P = 7.44 × 10⁻⁹; OR = 32.22) and rs7922552 (P = 8.43 × 10⁻⁹; OR = 32.0)) and TUBA3C (rs17076896 (P = 8.04 × 10⁻⁹; OR = 21.03)). Their known functions have been reported to associate with cardiac muscle and tubulin, respectively. As a result, this might imply their putative roles of establishing CAAs during KD progression. Additionally, various model analyses have been utilized to determine dominant and recessive inheritance patterns of identified susceptibility mutations. Finally, all susceptibility genes hit by significant genetic variants were further investigated and the top three representative gene-ontology (GO) clusters were regulation of cell projection organization, neuron recognition, and peptidyl-threonine phosphorylation. Our results help to depict the potential routes of the pathogenesis of CAAs in KD patients and will facilitate researchers to improve the diagnosis and prognosis of KD in personalized medicine.</p></div

Top 15 non-intergenic SNPs associated with susceptibility of CAA formation in KD.

<p>Top 15 non-intergenic SNPs associated with susceptibility of CAA formation in KD.</p

The infant fulminant hepatitis B (IFHB) Risk Score to predict fulminant hepatitis B in infancy.

<p>*The score was 0 for positive maternal HBeAg patients and 1 for negative maternal HBeAg patients.</p>#<p>The score was 0 for onset age ≥7 month-old and 2 for onset age <7 month-old.</p>$<p>The score was 0 for positive HBeAg patients and 1 for negative HBeAg patients.</p><p>The infant fulminant hepatitis B (IFHB) Risk Score to predict fulminant hepatitis B in infancy.</p