[Association of TNF-α gene polymorphisms with Graves disease susceptibility and early course thyroid stimulating hormone receptor antibody level in Chinese Han population in Anhui region].

OBJECTIVE: To assess the association of tumour necrosis factor-α (TNF-α) gene polymorphisms at positions -863C/A, -857C/T, -238G/A and Graves disease (GD) susceptibility in Chinese Han population in Anhui region. METHODS: The polymorphisms of TNF-α gene were determined by polymerase chain reaction with specific primers in 254 patients affected with GD and 212 healthy controls. Allelic and genotypic frequencies in GD group and normal controls as well as in different genders were compared. The allelic and genotypic frequencies for different thyroid stimulating hormone receptor antibody (TRAb) levels (TRAb > 12 U/L; ≤12 U/L) were also compared among patients with earlier onset GD. RESULTS: (1) The A allele at -863C/A locus in GD group (16.73%) was significantly greater than that of the control group (11.79%) (P< 0.05, OR = 1.503); the frequency of AA+CA genotype of -863C/A locus in GD group (32.68%) was significantly greater than that of control group (23.58%) (P< 0.05, OR = 1.573). There was no significant difference (P> 0.05) in the allelic and genotypic frequencies of -857C/T, -238G/A loci between the two groups. (2) There was no significant difference (P> 0.05) in the allelic and genotypic frequencies of -863C/A, -857C/T, -238G/A loci between patients of different genders. (3) There was no significant difference (P>0.05) in such frequencies between patients with earlier onset GD and different TRAb levels (TRAb > 12 U/L; ≤12 U/L). CONCLUSION: (1) The -863 A allele of TNF-α gene may contribute to the development of GD in Chinese Han population in Anhui, whilst -857C/T, -238G/A alleles may not. (2) There is no association between TNF-α gene -863C/A, -857C/T, -238G/A polymorphisms and development of GD in different genders. (3) There was no association between above polymorphisms and TRAb levels in patients with earlier onset GD.

Assessment of hepatic fat content in using quantitative ultrasound measurement of hepatic/renal ratio and hepatic echo-intensity attenuation rate.

AIMS: This study aims to evaluate and validate a simple quantitative ultrasound (US) method for determining the hepatic fat content (HFC) based on the combination of quantitative US hepatic/renal ratio (US-HRR) and quantitative US hepatic echo-intensity attenuation rate (US-HAR) as compared with [1H]-magnetic resonance spectroscopy (1H-MRS). MATERIAL AND METHODS: There were a total of 242 subjects recruited in the present study. All subjects were examined for HFC by quantitative US and 1H-MRS methods. The QUS-HRR and QUS-HAR were calculated from ordinary ultrasound images of liver and kidney with a triple modality 3D abdominal phantom using the Image J software. RESULTS: The results found that US-HRR and US-HAR correlated with 1H-MRS HFC (US-HRR: r=0.946, p<0.001; US-HAR: r=0.936, p<0.001). The equation for HFC prediction by using quantitative US was: HFC (%) = 28.965 × US-HRR + 218.045 × US-HAR - 8.892. Subgroup analysis in study subjects with body mass index (BMI) ≥28 showed that quantitative US HFC was associated with 1H-MRS HFC (R2=0.953, p<0.001). Receiver operating characteristic (ROC) analysis observed that the cut-off value of fatty liver diagnosis was 6.71% in using the quantitative US model; the sensitivity and specificity for fatty liver diagnosis were 94.15% and 96.30%, respectively. Variability analysis indicated that there was a relative high degree of consistency in the measurement of HFC with different operators or ultrasonic apparatus. CONCLUSIONS: Quantitative US measurement could be regarded as a simple, sensitive tool to accurately assess HFC. It provides a valid alternative to 1H-MRS as an easy, non-invasive option for the precise estimation of HFC in clinical practice.

Emodin promoted pancreatic claudin-5 and occludin expression in experimental acute pancreatitis rats.

AIM: To investigate the effect of emodin on pancreatic claudin-5 and occludin expression, and pancreatic paracellular permeability in acute pancreatitis (AP). METHODS: Experimental pancreatitis was induced by retrograde injection of 5% sodium taurocholate into the biliopancreatic duct. Emodin was injected via the external jugular vein 0 or 6 h after induction of AP. Rats from sham operation and AP groups were injected with normal saline at the same time. Samples of pancreas were obtained 6 or 12 h after drug administration. Pancreatic morphology was examined with hematoxylin and eosin staining. Pancreatic edema was estimated by measuring tissue water content. Tumor necrosis factor (TNF)-α and interleukin (IL)-6 level were measured by enzyme-linked immunosorbent assay. Pancreatic paracellular permeability was assessed by tissue dye extravasation. Expression of pancreatic claudin-5 and occludin was examined by immunohistology, quantitative real-time reverse transcriptase polymerase chain reaction and western blotting. RESULTS: Pancreatic TNF-α and IL-6 levels, wet/dry ratio, dye extravasation, and histological score were significantly elevated at 3, 6 and 12 h following sodium taurocholate infusion; treatment with emodin prevented these changes at all time points. Immunostaining of claudin-5 and occludin was detected in rat pancreas, which was distributed in pancreatic acinar cells, ductal cells and vascular endothelial cells, respectively. Sodium taurocholate infusion significantly decreased pancreatic claudin-5 and occludin mRNA and protein levels at 3, 6 and 12 h, and that could be promoted by intravenous administration of emodin at all time points. CONCLUSION: These results demonstrate that emodin could promote pancreatic claudin-5 and occludin expression, and reduce pancreatic paracellular permeability.