Effect of different time windows and interventions on skin pressure ulcers and ischemia-reperfusion injury in rats / 南方医科大学学报

<p><b>OBJECTIVE</b>To observe the effect of different time windows and interventions on skin pressure ulcers and ischemia-reperfusion (I/R) injury in rats.</p><p><b>METHODS</b>Sixty?eight SD rats were randomly divided into blank control group (n=4) and model group (n=64). The rats in the model group were randomly divided into group A (n=32) without intervention and group B (n=32) with post?conditioning. The degree of skin compression, neutrophil infiltration and serum levels of free radicals were observed in the rats after compression for 2, 4, 6, and 8 h (8 rats at each time point).</p><p><b>RESULTS</b>A significant difference was found in the severity of skin damage among the control group, group A, and group B (P=0.001), and the injury was milder in group B than in group A. Severe skin lesions occurred in 2 rats after skin compression for 6 h, as compared with 6 after compression for 8 h (P=0.043), but in none of the rats after compression for 2 or 4. Seventeen rats in group B and 15 in group A showed grade 1 neutrophil infiltration in the skin lesions, and 8 rats in group B and 10 in group A showed grade II neutrophil infiltration (P=0.002). Neutrophil infiltration was the mildest in rats with a 2?h compression, and exacerbated progressively and significantly as the compression time extended (P=0.027). With the prolongation of the intervention time, the rats in both groups A and B showed decreased SOD and increased MDA and NO levels, and overall the I/R injury was milder in 2? and 4?h compression groups than in 6? and 8?h compression groups. The level of serum SOD was significantly higher and MDA and NO levels were significantly higher in group B than in group A (P<0.05).</p><p><b>CONCLUSION</b>Ischemic post?conditioning can relieve I/R injury in acute pressure ulcer in rats. The effective time window for intervention is within 6 h of ischemia, and the effect of ischemic post-conditioning is optimal within 2 h. Ischemic post?conditioning can alleviate free radical injury and inflammation caused by I/R injury.</p>

The Correlation between NK Cell and Liver Function in Patients with Primary Hepatocellular Carcinoma

BACKGROUND/AIMS: This study aimed to detect the expression of natural killer (NK) cell receptor natural killer group 2D (NKG2D) in the peripheral blood of patients with primary hepatocellular carcinoma and to discuss the correlation between NK cell cytotoxicity and liver function. METHODS: The number of NK cells and the expression of NK cell receptor NKG2D in peripheral blood were determined by flow cytometry in patients with primary hepatocellular carcinoma, hepatitis B cirrhosis, chronic hepatitis B, and healthy controls. RESULTS: When compared with patients in the healthy and the chronic hepatitis B groups, the primary hepatocellular carcinoma group showed significant decreases in all parameters, including the cytotoxicity of NK cells on K562 cells, expression rate of NKG2D in NK cells, number of NKG2D+ NK cells, expression level of NKG2D, and number of NK cells (p<0.05). The activity of NK cells showed a positive correlation, whereas the Child-Pugh scores in the primary hepatocellular carcinoma and the hepatitis B cirrhosis groups showed a negative correlation with all parameters detected above. CONCLUSIONS: The decrease of NK cell activity in patients with primary hepatocellular carcinoma is closely related to their lower expression of NKG2D. Liver function affects the expression of NKG2D and the activity of NK cells.

Association of hepatic lipase gene promoter polymorphism -514C/T with nonalcoholic fatty liver disease / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To study the prevalence of the hepatic lipase gene (LIPC) promoter polymorphism (at position -514) in patients with nonalcoholic fatty liver disease (NAFLD), and its relationship with the susceptibility to NAFLD.</p><p><b>METHODS</b>Genotype of LIPC promoter was detected with PCR-RFLP in 106 patients with NAFLD. Body mass index, waist-to-hip ratio (WHR), blood pressure, CHOL, HDL, LDL, TG, FPG and FINS of the patients were measured. Index of insulin resistance was determined using the homeostasis model assessment (HOMA) method. One hundred six healthy subjects matched for age and sex served as controls.</p><p><b>RESULTS</b>The frequency of CC genotype and C allele in the NAFLD group were significantly higher than those in the control group (31.1% vs 26.4%, 62.7% vs 54.2%, P<0.05). Compared with TT genotype, both CC genotype and CT genotypes had higher relative risk of NAFLD (OR: 3.73, 95% CI: 1.31, 10.63; OR: 3.60, 95% CI: 1.35, 9.60). At the same time, the non-carriers of T allele in -514 had higher WHR than the T carriers (0.877+/-0.06 vs 0.848+/-0.06, t=2.072, P<0.05)). Logistic regression analysis showed that T substitution in LIPC-514 position (OR: 1.28, 95% CI 0.10-0.74) had a lower susceptibility to NAFLD.</p><p><b>CONCLUSION</b>The LIPC-514C/T polymorphism is associated with WHR, and the T substitution of LIPC-514 may lower the susceptibility to NAFLD.</p>

The relationship between insulin resistance and adiponectin gene expression in nonalcoholic fatty liver disease / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate the relationship between insulin resistance (IR) and adiponectin gene expression in patients with nonalcoholic fatty liver disease (NAFLD).</p><p><b>METHODS</b>Subcutaneous (SC) and omental (OM) adipose tissues were obtained from 21 NAFLD patients with obesity (n=10) and nonobesity (n=11) and also from 24 subjects (without NAFLD) with obesity (n=11) and nonobesity (n=13) who served as controls. Adiponectin mRNA expression levels in subcutaneous and omental adipose tissues were measured using SYBR Green I quantitative real-time PCR. The levels of plasma adiponectin and insulin were measured with ELISA. IR was estimated using the homeostasis assessment (HOMA).</p><p><b>RESULTS</b>The scores of HOMA-IR levels of the NAFLD patients and the controls with obesity and nonobesity were: 3.0+/-0.8, 2.8+/-0.9, 2.0+/-0.6, 1.2+/-0.5 respectively. The relative mRNA expression of adiponectin and blood adiponectin levels in NAFLD patients differed significantly from those of the controls. The HOMA-IR negatively correlated with the adiponectin mRNA expression levels of adipose tissues (r = -0.5) and blood adiponectin; it positively correlated with body mass index (r = 0.4), waist-hip-ratio (r = 0.4) and serum triglyceride (r = 0.3), but did not correlate with serum total cholesterol (r = 0.2).</p><p><b>CONCLUSION</b>IR of NAFLD patients was linked to low adiponectin gene expression in their adipose tissues. This finding suggests that low adiponectin gene expression may play a role in the pathogenesis of insulin resistance and NAFLD.</p>

Relationship between leptin gene of adipose tissues and nonalcoholic fatty liver disease / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate leptin mRNA expressions in subcutaneous (SC) and omental (OM) adipose tissues of patients with nonalcoholic fatty liver disease (NAFLD), and their relationships with insulin resistance (IR), blood leptin, blood triglyceride, total blood cholesterol, blood glucose, body weight index and waist-hip ratio.</p><p><b>METHODS</b>SC and OM adipose tissues were obtained from 10 obese and 11 nonobese NAFLD patients and from 11 obese and 13 nonobese patients without NAFLD, who served as controls. Leptin mRNA expression levels in the subcutaneous and omental adipose tissues were measured using SYBR Green I quantitative real-time PCR. IR was estimated using homeostasis assessment (HOMA). The levels of plasma leptin and insulin were measured using ELISA.</p><p><b>RESULTS</b>The relative mRNA expression of leptin, HOMA-IR and blood leptin levels in NAFLD differed significantly from those of the controls (P < 0.05). The leptin/GAPDH ratio of the obese and nonobese NAFLD and control cases were 1.32 +/- 0.12, 0.99 +/- 0.05, 1.10 +/- 0.09, 0.87 +/- 0.13 respectively. The expression levels of SC and OM adipose leptin mRNA in NAFLD patients were positively correlated with HOMA-IR (r=0.72, P < 0.05), blood leptin (r=0.69, P < 0.05), blood triglyceride (r=0.32, P < 0.05), body weight index (r=0.57, P < 0.05) and waist-hip ratio (r=0.50, P <0.05).</p><p><b>CONCLUSION</b>The primary reason for high levels of blood leptin is high leptin mRNA expression in adipose tissues; in both obese and nonobese patients with NAFLD; high levels of blood leptin and the leptin mRNA expression in adipose tissues and IR exist. These findings suggest that leptin resistance exists in patients with NAFLD and leptin resistance is positively correlated with NAFLD, the same as in insulin resistance.</p>