Predictive power of high-resolution vessel wall magnetic resonance imaging in ischemic stroke.

BACKGROUND AND OBJECTIVE: Intracranial atherosclerotic disease (ICAD) is a key contributor to ischemic stroke and has a high recurrence rate. This study aimed to investigate the function of high-resolution vessel wall MRI (HR-VW-MRI) and evaluate plaque characteristics in patients with ICAD. METHODS: A consecutive series of patients with ICAD who underwent HR-VW-MRI were enrolled, and imaging measurements were acquired. Baseline clinical characteristics were identified. Telephone follow-up was conducted every three months. The endpoint events were the first onset or recurrence of ischemic stroke and new clinical vascular events. Patients were divided into groups with or without events according to whether the endpoint event occurred. RESULTS: A total of 70 patients (mean age = 57.6 years old) were enrolled. The median follow-up duration was 182 days. During the follow-up, 10 patients developed ischemic stroke, experienced endpoint events, and were found with 44 plaques in the artery area. A total of 169 plaques were further found in 70 patients. There were significant differences in EI, HST1, surface features, and WA reference between the two groups (P < 0.05). Logistic analysis showed that grade 2 enhancements, stenosis degree ≥ 50%, HST1, and surface features were independent prognostic factors of the onset of stroke, caused by ICAD. CONCLUSION: This prospective study demonstrates that HR-VW-MRI can identify atherosclerotic plaques in the cerebral artery and high-risk plaques, which may contribute to the prevention of ICAD and guide clinical treatment.

Effect of cadmium on cytogenetic toxicity in hairy roots of Wedelia trilobata L. and their alleviation by exogenous CaCl2.

Effects of cadmium (Cd) alone and in combination with calcium on mitosis and chromosomal aberration in the hairy root tips of Wedelia trilobata were investigated. The results showed that Cd concentrations below 50 µmol/L had a lesser or even a promoting effect on the mitotic index (MI) and the rate of chromosomal aberration in hairy root tips, while those higher than 100 µmol/L significantly decreased the MI and gradually stimulated the rate of chromosomal aberrations with prolonged time and increasing concentrations of Cd. Concentrations of 50 µmol/L Cd mainly induced C-mitosis, while more than 100 µmol/L Cd mainly caused chromosome breakage and chromosome adhesion in hairy root tip cells. When cultured with 300 µmol/L Cd, micronuclei were only observed in the interphase, middle, and late phase of hairy root tip cells. Compared with untreated controls, exogenous calcium had an alleviating effect on Cd-induced cytotoxicity by effectively enhancing the MI and reducing the rate of chromosomal aberration in root tip cells. The results presented here provide evidence that W. trilobata hairy roots with rapid autonomous growth could be used as a sensitive tool for monitoring and evaluation of Cd pollution in the environment.

[Inhibitory effect of a novel histone deacetylases inhibitor FK228 on human colon cancer HCT-116 cells in vitro and in vivo].

OBJECTIVE: To investigate the inhibitory effects of a novel histone deacetylases inhibitor FK228 on human colon cancer HCT-116 cells in vitro and in vivo, and evaluate its toxicity and side effects. METHODS: The in vitro growth inhibitions of HCT-116 cells by different concentrations of FK228 and 5-Fu for 24, 48 and 72 h were assessed by CCK-8 assay. BALB/c nude mouse models of tumor xenografts were prepared by subcutaneous implantation of tumor tissue, and 4 mg/kg FK228 and 50 mg/kg 5-Fu were i.p. injected, respectively. The inhibitory effects on tumor growth, hematology, and liver and kidney function were evaluated. RESULTS: CCK-8 assay indicated that FK228 had an obvious growth inhibitory effect on HCT-116 cells in a dose- and time-dependent manner. The IC50 of FK228 in HCT-116 cells was 12.05 ng/ml for 48 h, while the IC50 of 5-Fu was 18.92 µg/ml. At 20 days after FK228 and 5-Fu treatment, the tumor volume of the FK228 group was (139.71 ± 44.54)mm(3), significantly lower than that of the 5-Fu group [(282.28 ± 58.81)mm(3)] and that of the model group [(520.65 ± 39.73)mm(3), P < 0.01 for both]. The average tumor weight was (0.07 ± 0.02)g in the FK228 group, significantly lower than that of the 5-Fu group [(0.20 ± 0.08)g, P < 0.01]. The tumor growth inhibition rate of the FK228 group was 73.2%, significantly higher than that of the 5-Fu group (45.8%, P < 0.01). The ALT levels of the FK228 and 5-Fu groups were significantly higher than that of the model group (P < 0.01). The BUN of 5-Fu group was significantly higher than that of the model group (P < 0.01), but the BUN of FK228 group was not significantly different from that of the blank and control groups (P > 0.05 for both). Routine blood test showed that WBC, RBC, Hb and PLT of the 5-Fu group were significantly lower than those of the model group (P < 0.05 for all), but only WBC of the FK228 group was significantly lower than that of the model group (P < 0.05). The pathological examination using HE staining revealed that in the FK228 group, there were fibrosis and inflammatory cell infiltration in the liver tissue, and mild edema of the renal tubules in the kidney. However, in the 5-Fu group there were extensive hepatocyte edema and necrosis in the liver, and evident deformation and necrosis of glomeruli and tubules, and tubular wall thinning in the kidney. CONCLUSIONS: The results of this study indicate that FK228 can more effectively than 5-Fu inhibit the growth of HCT-116 cells in vitro and vivo, and without obvious toxic effect on the kidney and hematology. Its clinical value in colon cancer treatment deserves further investigation.

[Cloning of human migfilin N-terminal domain and preparation of anti-migfilin polyclonal antibody].

OBJECTIVE: To clone migfilin-N terminal sequence into E.coli and obtain a fusion protein for preparing rabbit polyclonal antibody against migfilin, thereby facilitating the study of the role of migfilin in the biological behavior of colon cancer. METHODS: Based on human migfilin cDNA sequence, a pair of primers was designed to amplify migfilin-N terminal sequence by PCR. The PCR product was subcloned into the bacterial expression vector pGEX-4T-1 with EcoRI/XhoI sites, and the target recombinant plasmids were identified with enzymatic cleavage followed by DNA sequence analysis. By transforming the expression vector into component E.coli BL(21) cells, the GST-migfilin-N fusion protein was expressed with IPTG induction. Glutathione-sepharose beads were used to purify the fusion protein, and anti-migfilin polyclonal antibody was produced by immunization of rabbits with the purified GST-migfilin N-terminal fusion protein. The resultant anti-migfilin polyclonal antibody was purified by protein A beads and used for Western blotting for detecting migfilin expression in different cell lines. RESULTS AND CONCLUSION: The migfilin-N terminal gene fragment was cloned successfully, and purified GST-migfilin N-terminal fusion protein and anti-rabbit migfilin polyclonal antibodies were obtained. Western blot analysis demonstrates that the antibodies specifically detected migfilin expression in the cell lines, which may facilitate further investigation of the role of migfilin in the biology of colon cancer.