11 research outputs found
Additional file 1: Figure S1. of Lactobacillus acidophilus attenuates Salmonella-induced intestinal inflammation via TGF-β signaling
Time required for S. typhimurium to enter host cells. Human intestinal Caco-2 cells were incubated with S. typhimurium (sal, 1×107 CFU per well) for 1, 2, or 3 h in a six-well plate. The cells were subsequently washed with PBS, and the medium was replaced with medium containing with antibiotics for 6 h. The cells were then lysed with 1 % Triton X-100 (in PBS) to obtain the intracellular S. typhimurium. Then, the lysates were incubated overnight on LB agar to determine the time required for S. typhimurium to enter cells. (TIFF 234 kb
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
Additional file 2: Figure S2. of Lactobacillus acidophilus attenuates Salmonella-induced intestinal inflammation via TGF-β signaling
Effect of L. acidophilus on SMAD3/4 transcriptional activity with active or inactive S. typhimurium. Human intestinal Caco-2 cells were transfected with luciferase reporter plasmid containing the promoter of the SMAD-binding site or CMV promoter overnight. The cells were then pretreated with L. acidophilus (MOI: 20) 1 h prior to infection with S. typhimurium (MOI: 10) or UV-inactivated S. typhimurium (MOI: 10) in antibiotic-free DMEM for 1 h at 37 °C. Then, the cells were washed twice with PBS and added to medium containing D-luciferin to monitor SMAD activity. The cells were washed twice with PBS, added to DMEM medium containing D-luciferin and antibiotics for signal measurement with a Luminometer. Data were analyzed with Prism 5, and the results are shown as the means ± SEM from three independent experiments. (TIFF 100 kb
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
Additional file 1: of Fecal carriage of multidrug-resistant Escherichia coli by community children in southern Taiwan
Table S1. Minimal inhibitory concentration breakpoints for Enterobacteriaceae. (DOCX 16 kb
Clinical characteristics of 41 infants with acute or fulminant hepatitis B.
<p>FH: fulminant hepatitis, NFH: non-fulminant hepatitis, HBsAg, hepatitis B surface antigen; HBeAg, hepatitis B e antigen, HBV, hepatitis B virus; HBIG, hepatitis B immunoglobulin; ALT, alanine aminotransferase; INR, international normalized ratio.</p><p>Clinical characteristics of 41 infants with acute or fulminant hepatitis B.</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
Serial data of a case of infantile fulminant hepatitis that became a chronic HBV carrier.
<p>HBsAg: hepatitis B surface antigen; anti-HBs: hepatitis B surface antibody, HBeAg: hepatitis B e antigen, anti-HBe: antibody to HBeAg, ALT: alanine aminotransferase level (dotted line), T-bil: total bilirubin(straight line); N: negative; P: positive.</p
The IFHB Risk Scores in the infantile cases of hepatitis B.
<p>FH, fulminant hepatitis; NFH, non-fulminant hepatitis.</p><p>The IFHB Risk Scores in the infantile cases of hepatitis B.</p
Cumulative HBeAg seroconversion rates in survivors of infantile fulminant/non-fulminant hepatitis B (N = 9).
<p>Cumulative HBeAg seroconversion rates in survivors of infantile fulminant/non-fulminant hepatitis B (N = 9).</p
