Additional file 4 of Genome-wide analysis of the P450 gene family in tea plant (Camellia sinensis) reveals functional diversity in abiotic stress

Additional file 4

Additional file 6 of Genome-wide analysis of the P450 gene family in tea plant (Camellia sinensis) reveals functional diversity in abiotic stress

Additional file 6

Additional file 3 of Genome-wide analysis of the P450 gene family in tea plant (Camellia sinensis) reveals functional diversity in abiotic stress

Additional file 3

CK-18 fragments are significantly higher in the serum with NASH compared to patients with non-NASH.

<p>The vertical axis represents serum CK-18 levels in U/L, whereas the horizontal axis refers to patient groups. The box and bars represent the interquartile range (the 25^th and 75^th percentiles) from the median (the horizontal line) and the 95% confidence interval, respectively. CK-18 fragments levels significantly increased in patients with NASH compared to non-NASH patients (median (Q25, Q75): 372.9 U/L (319.6, 431.4), 248.1 U/L (237.5, 266.6), respectively; <i>P</i> < 0.001).</p

Representative graphs and bar charts of the mRNA and protein expressions of iNOS, eNOS, α-SMA, and Collagen І in LX-2 cells cultured with L-NAME and simvastatin.

<p>L-NAME served as a NOS inhibitor, it inhibited both iNOS and eNOS expression (A~E) and induced more α-SMA, and Collagen І expressions (F~I). Simvastatin had antagonistic effect on the activation of LX-2 cells induced by L-NAME via increasing the eNOS expression (D, E). (^#<i>P</i><0.05, compared with the control group; * <i>P</i><0.05, compared with LX-2 cells treated with L-NAME; ^ <i>P</i><0.05, compared with LX-2 cells treated with simvastatin.).</p

Masson staining of hepatic tissues in each group of rats.

<p>Slightly sinusoidal fibrosis appeared only in part of model rats until 16^th week (B). At the end of 24^th week, all model rats showed hepatic fibrosis in sinusoids, partly in portal area (C). These changes were improved in the liver of simvastatin-treated rats (D). A: Control ×200; B: 16^th week ×200; C: 24^th week ×200; D: Simvastatin-treated group ×200.</p

Representative graphs and bar charts of hepatic mRNA and protein expressions of iNOS, eNOS, and Collagen І in each group of rats.

<p>The hepatic protein expression of iNOS and eNOS were detected in the control group of rats, with little collagen I expression (A). With the consumption of high-fat diet, the iNOS and collagen I expressions were gradually increased (B, C, F, G), while eNOS expression was gradually decreased (D, E). Compared with rats in the 24^th week group, simvastatin treatment could up-regulate eNOS expression (A, D, E) and down-regulate iNOS expression (B, C), followed by improved hepatic fibrosis, which represented by decreased collagen I expression (F, G). (^#<i>P</i><0.05, compared with the control group; * <i>P</i><0.05, compared with 24^th week group.).</p

Meta-analysis of total LT-free survival in patients with AE of CHB.

<p>At 3 months, 84% of the 215 LAM-treated patients with AE of CHB survived without liver transplantation as compared to 85% of the 126 untreated controls with odds ratio of 0.981 (95% CI, 0.501–1.918, P = 0.956).</p

Flow-chart identifying eligible studies.

<p>Flow-chart identifying eligible studies.</p

Baseline characteristics of patients receiving NAs for AE of CHB.

<p>AIH, autoimmune hepatitis; ALD, alcoholic liver disease; ALT, alanine aminotransferase; DM, diabetes mellitus; ETV, entecavir; HAV, hepatitis A virus; HBV, hepatitis B virus; HCC, hepatocellular carcinoma; HCV, hepatitis C virus; HDV, hepatitis D virus; HE, hepatic encephalopathy; HEV, hepatitis E virus; HIV, Human immunoddficiency virus; LAM, lamivudine; LDT, telbivudine; NA, not available; NAs, nucleos(t)ide analogues; PT, prothrombin time; TB, serum total biliruin; ULN, upper limit of normal.</p>†<p>Of 10 enrolled, 6 patients with dose of LAM 300 mg/day, 4 had undergone interferon or corticosteroid treatment for liver disease.</p>††<p>Patients had comorbid illnesses in both groups.</p>*<p>Dose of LAM 150 mg/day; otherwise the doses of drugs were as follows: LAM 100 mg/day, ETV 0.5 mg/day, LDT 600 mg/day.</p>**<p>IgM anti-HBc seronegative patients were recruited as control group.</p>‡<p>Patients without AE were recruited as control group, and subset data on 45 patients with AE were abstracted.</p><p>♂15 patients with SAE were treated with LAM 300 mg/day for only a short term at the start of therapy.</p><p>♂♂ 38.3% and 4.8% of patients had exposed to LAM and had definitely LAM resistance before enrolment, 104 were examined for HBV genotypes.</p><p>○ Detection limit for HBV DNA was 100 copies/ml for calculation.</p