[Left posterior auricular Kimura's disease and related literature review: a case report].

SummaryA 43-year-old middle-aged woman admitted by our department was mainly featured by the discovery of the left posterior auricular mass for more than 1 week, and the physical examination was a painless subcutaneous mass. Peripheral eosinophil count was higher than normal, ultrasonic exceed examination showed slightly lower back after the left ear acoustic area with surrounding lymph node enlargement, CT indicated the subcutaneous tumor on the lateral side of the left parotid gland, and the enlarged lymph nodes in the bilateral carotid space, submaxillary space, the left parotid gland space and the posterior cervical space. The pathologic examination indicated lymphoid tissue nodular hyperplasia with lymphoid follicular formation, visible thin-walled blood vessels and the increase in the number of eosinophils in accordance with kimura's disease. Immunohistochemistry results showed: CD3（+）, CD20（+）, CD21 FDC network（+）, CD10 germinal center（+）, bcl-2（-）, bcl-6（-）, CD79a（+）, Lamda（+）, Kappa（+）, ki-67 germinal center（+）. After 4 weeks of operation, part of the scab skin of the incision was detached, with a small incision in the middle segment, about 0.5 cm long. Considering delayed healing of the incision, the patient's incision was restored after 2 weeks of intensive dressing change. No recurrence signs and complications of Kimura's disease were found during the 10-months follow-up.

Associations between CD36 gene polymorphisms and susceptibility to coronary artery heart disease

Associations between polymorphisms of the CD36 gene and susceptibility to coronary artery heart disease (CHD) are not clear. We assessed allele frequencies and genotype distributions of CD36 gene polymorphisms in 112 CHD patients and 129 control patients using semi-quantitative polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) analysis. Additionally, we detected CD36 mRNA expression by real-time quantitative PCR, and we quantified plasma levels of oxidized low-density lipoprotein (ox-LDL) using an enzyme-linked immunosorbent assay (ELISA). There were no significant differences between the two groups (P>0.05) in allele frequencies of rs1761667 or in genotype distribution and allele frequencies of rs3173798. The genotype distribution of rs1761667 significantly differed between CHD patients and controls (P=0.034), with a significantly higher frequency of the AG genotype in the CHD group compared to the control group (P=0.011). The plasma levels of ox-LDL in patients with the AG genotype were remarkably higher than those with the GG and AA genotypes (P=0.010). In a randomized sample taken from patients in the two groups, the CD36 mRNA expression of the CHD patients was higher than that of the controls. In CHD patients, the CD36 mRNA expression in AG genotype patients was remarkably higher than in those with an AA genotype (P=0.005). After adjusted logistic regression analysis, the AG genotype of rs1761667 was associated with an increased risk of CHD (OR=2.337, 95% CI=1.336-4.087, P=0.003). In conclusion, the rs1761667 polymorphism may be closely associated with developing CHD in the Chongqing Han population of China, and an AG genotype may be a genetic susceptibility factor for CHD.

Associations between CD36 gene polymorphisms and susceptibility to coronary artery heart disease.

Associations between polymorphisms of the CD36 gene and susceptibility to coronary artery heart disease (CHD) are not clear. We assessed allele frequencies and genotype distributions of CD36 gene polymorphisms in 112 CHD patients and 129 control patients using semi-quantitative polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) analysis. Additionally, we detected CD36 mRNA expression by real-time quantitative PCR, and we quantified plasma levels of oxidized low-density lipoprotein (ox-LDL) using an enzyme-linked immunosorbent assay (ELISA). There were no significant differences between the two groups (P>0.05) in allele frequencies of rs1761667 or in genotype distribution and allele frequencies of rs3173798. The genotype distribution of rs1761667 significantly differed between CHD patients and controls (P=0.034), with a significantly higher frequency of the AG genotype in the CHD group compared to the control group (P=0.011). The plasma levels of ox-LDL in patients with the AG genotype were remarkably higher than those with the GG and AA genotypes (P=0.010). In a randomized sample taken from patients in the two groups, the CD36 mRNA expression of the CHD patients was higher than that of the controls. In CHD patients, the CD36 mRNA expression in AG genotype patients was remarkably higher than in those with an AA genotype (P=0.005). After adjusted logistic regression analysis, the AG genotype of rs1761667 was associated with an increased risk of CHD (OR=2.337, 95% CI=1.336-4.087, P=0.003). In conclusion, the rs1761667 polymorphism may be closely associated with developing CHD in the Chongqing Han population of China, and an AG genotype may be a genetic susceptibility factor for CHD.

Significance of white blood cell count and its subtypes in patients with acute coronary syndrome.

BACKGROUND: Inflammation plays a role in the pathogenesis of coronary atherosclerosis. MATERIALS AND METHODS: Six hundred twenty-three patients with acute coronary syndrome (ACS) referred for coronary angiography for the first time in our hospital were enrolled in this study. White blood cell and its subtypes were measured on admission. The study population was divided into three groups based on total white blood cell count and followed up. Clinical end points were major adverse cardiac events (MACEs), including cardiogenic death, stroke, heart failure, non-fatal myocardial infarction, rehospitalization for angina pectoris. RESULTS: The median age was 68 years (range 31-92) and 64.2% of the patients were men. The median white blood cell count was 6.48 x 10(9 )L(-1) (range 2.34-27.10 x 10(9 )L(-1)). The median follow-up duration was 21 months (range 1-116) and MACEs occurred in 167 patients. The multivariable Cox proportional hazards regression model revealed that neutrophil count [Relative risk = 1.098, 95% Confidence interval (CI): 1.010-1.193, P = 0.029) was a risk factor for MACEs. The logistic regression model revealed that lymphocyte count [Odds ratio (OR) = 1.075, 95% CI: 1.012-1.142, P = 0.018] and monocyte count (OR = 8.578, 95% CI: 2.687-27.381, P < 0.001) were predictive of stenosis >or= 75%; Neutrophil proportion (OR = 1.060, 95% CI: 1.007-1.115, P = 0.026), monocyte count (OR = 12.370, 95% CI: 1.298-118.761, P = 0.029) were predictive of the presence of multivessel disease. Kaplan-Meier analysis of short-term and long-term cumulative survival showed no significant statistical differences among three groups. CONCLUSIONS: Neutrophil count adds prognostic information to MACEs in ACS. Monocyte count and lymphocyte count are predictive of severity of coronary atherosclerosis.

Fabrication of novel porous anodic alumina membranes by two-step hard anodization.

Porous anodic alumina (PAA) membranes with highly ordered hexagonal cells and a novel pore structure have been fabricated by two-step hard anodization in a H(2)SO(4)-Al(2)(SO(4))(3)-H(2)O system at 40 and 50 V, giving average cell diameters of 77 and 96 nm, respectively. There are several tiny pores embedded in each big shallow pore on the top of the membranes, and there is only one pore in one cell at their bottom. The cells on both sides of the membranes present almost the same periodic arrangement. In order to explore the formation of the novel pore structure, PAA membranes fabricated at different current densities (30-200 mA cm(-2)) are obtained by maintaining a constant voltage at 40 V. The experimental results show that the interpore distance is not only dependent on the anodization voltage, but is also influenced by the current density, which means that the pore structure of PAA membranes fabricated by hard anodization can be accurately designed and controlled by adjusting the anodization voltage and current density simultaneously.

The abundance of NM23-H1 mRNA is related with in situ microenvironment and intrahepatic metastasis in hepato-cellular carcinoma.

In HCC specimens from 25 patients, the levels of nm23-H1 and H-ras mRNA were analyzed by quantitative reverse transcription-polymerase-chain reaction (RT-PCR). Tumor microvessel density (MDV), the essential factor of microenvironment and proliferating cell nucleus antigen (PCNA), indexes as tumor cell proliferating in its microenvironment are also analyzed by immunohistochemical methods using antibodies against endothelial protein factor VIII related antigen (F8RA) and antibody PC-10. Results show that The MDV and PCNA index in the group with intrahepatic metastasis is remarkably higher than that in without one (p<0.01), but the abundance of nm23-H mRNA is opposite (p<0.01). The abundance of H-ras mRNA shows little difference (p>0.05). MDV index shows directly relationship with PCNA index (p<0.01), the abundance of nm23-H1 mRNA show an inverse one with PCNA index (p<0.05). We conclude that in HCC, tumor in situ microenvironment, especially a deteriorative one, plays an important selective role. The decline of nm23-H1 mRNA abundance implies the increase of highly potential metastatic cancer cells which adapt to their microenvironment.