Study on the association between vitamin D receptor gene fokI (T/C) polymorphisms and the susceptibility to type 2 diabetic kidney disease of Han nationality in south of China.

AIMS: To investigate the distribution of vitamin D receptor fokI gene polymorphism in Yunnan Han population, and to explore the relationship between SNP of fokI and type 2 diabetic kidney disease. METHODS: We included 276 individuals of Han population of Yunnan in this study: 91 type 2 diabetes patients without kidney disease (DM group), their duration of diabetes is more than 10 years, 89 type 2 diabetes patients with diabetic kidney disease (DKD group), their duration of diabetes is less than 10 years and 96 healthy controls (NC group). We compared the concentration of 25 hydroxy vitamin D in different groups and used taqman probe to detect the genotype and allele of fokI, then analysed the relationship between the polymorphisms of fokI and the susceptibility of diabetic kidney disease. RESULTS: (1) NC group had a significantly higher plasma concentrations of 25 (OH) D than DKD group and DM group (P < 0.01); (2) 25 (OH) D and age, BMI, HbA1c, TG showed a weak negative correlation (P < 0.01); (3) Genotype of fokI showed no differences in DM group and DKD group, same as in DM group and NC group; FF genotype in DKD group is relatively lower than NC group (P < 0.05), and there is no difference in Ff and ff genotype (P > 0.05); In DKD group, f allele was 53.4%, higher than DM group (RR = 1.46, P < 0.05); (4) Logistic regression analysis showed that ff genotype may be a susceptible factor for DKD (P = 0.04, OR = 2.37). CONCLUSION: FokI Ff genotype accounted for a larger proportion of the Han population in Yunnan, and ff genotype may be a susceptible factor for DKD in Yunnan Han population.

Long-term streptozotocin-induced diabetes in rats leads to severe damage of brain blood vessels and neurons via enhanced oxidative stress.

The aim of this study was to investigate pathophysiological alterations and oxidative stress in various stages of streptozotocin (STZ)­induced diabetes mellitus (DM) in rats. Male Sprague-Dawley rats (120) were randomized into DM and control groups. Body mass, plasma glucose, glycated hemoglobin (HbA1c), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) levels, as well as aldose reductase (AR) activities, in brain tissue and serum were determined. Electron microscopy was used to observe neuron and vessel changes in the brain. In STZ­treated rats, blood glucose, low density lipoproteins, triglycerides and total cholesterol levels increased 1.43­3.0­fold and high density lipoprotein, HbA1c and insulin sensitivity index increased 1.1­1.23­fold compared with control. At week 16 following treatment, DM rat serum H2O2 concentration was increased, indicating oxidative stress and mRNA levels of GPx and SOD were 2­fold higher than the control. Protein GPx and SOD levels were reduced (P<0.01). DM rats were identified to exhibit early irregular glomerular capillary basement membrane thickening and vacuolization in the mitochondria and epithelial cells. Neuron cells and blood vessels in the DM rat brains became increasingly abnormal over time with altered Golgi bodies, mitochondria and endoplasmic reticulum cisterns, concurrent with SOD inactivation and AR protein accumulation. Disease progression in rats with STZ­induced DM included brain pathologies with vascular and neuron cell abnormalities, associated with the reduction of SOD, CAT and GPx activities and also AR accumulation.

Angiogenic study in Graves' disease treated with thyroid arterial embolization.

PURPOSE: To investigate angiogenesis in the thyroid of Graves' disease (GD) treated with thyroid arterial embolization through analysis of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and microvessel density (MVD). MATERIALS AND METHODS: Forty-two GD patients were treated with thyroid arterial embolization and followed up for 1-68 months after embolization. Before embolization and at 7 days, 3, 6, 12, 36 and 48 months following embolization, TT3, TT4, FT3, FT4, TSH and thyroid stimulating antibody (TSAb) were tested respectively. Thyroid biopsy was performed under the guidance of computed tomography for immunohistochemical staining of VEGF and bFGF, and MVD within the thyroid gland was marked by CD34. RESULTS: VEGF and bFGF were mostly expressed in the cytoplasm and on the cell membrane. The expression of VEGF was increased (P < 0.05) at < or = 6 months compared with before embolization and decreased (P < 0.05) at > or = 1 year compared with either at < or = 6 months or before embolization. The expression of bFGF was not statistically different at < or = 6 months compared with before embolization but was decreased (P < 0.05) at > or = 1 year compared with either at ?6 months or before embolization. Thyroid MVD marked by CD34 had similar changes to those of the VEGF expression after embolization. There was a positive correlation between VEGF and bFGF (P < 0.05) and between VEGF or bFGF and MVD (P < 0.05). Thyroid hormones mostly returned to normal and TSAb was decreased in longer follow-up. CONCLUSION: Thyroid arterial embolization can decrease the expression of VEGF, bFGF and MVD. Consequently, angiogenesis within the GD thyroid will be decreased in the long term after embolization and may serve as the basis for reduced thyroid size and function.

Long-term immunological study in Graves' disease treated with thyroid arterial embolization.

OBJECTIVE: The aim of this study was to investigate long-term immunological changes after the treatment of Graves' disease (GD) with thyroid arterial embolization and the effect of thyroid arterial embolization on the body's immunological functions. MATERIALS AND METHODS: Forty-one patients with clinically and laboratorily ascertained GD were treated with thyroid arterial embolization and followed up for 3-54 months following embolization. Prior to embolization and at 1, 3, 6, 12, and 36 months following embolization, thyroid autoimmune antibodies were tested respectively, including thyroid stimulating antibody (TSAb), thyrotropin antibody (TRAb), thyroglobulin antibody (TGAb), and thyroid microsomal antibody (TMAb), as well as subgroup lymphocytes of CD16+CD56+, CD19+, CD3+, CD3+CD4+ and CD3+CD8+. The autoimmune status of GD patients prior to embolization and the dynamic changes of the immunological function after embolization were analyzed. RESULTS: The therapy of thyroid arterial embolization could effectively decrease the activity/titer and positive rate of TRAb and the ratio of CD4+/ CD8+ to normal levels at 6 months following embolization, while the ratio of CD3+CD8+ increased gradually to normal level at 1 year following embolization. In patients with recurrence, TSAb and TRAb remained at a higher level, while the rate of CD3+CD8+ and the ratio of CD4+/CD8+ were not statistically significantly different from those before embolization. CONCLUSION: Immunological functional disorder exists in GD patients. The treatment method of thyroid arterial embolization can effectively resume the basic immunological function to normal range while patients with recurrence have no significant improvement, suggesting that thyroid arterial embolization has an effective role in adjusting the immunological function.