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Objective: To observe the toxic effects of cockle shell-derived calcium carbonate nanoparticles (CCNPs) on the SD rats, and to preliminarily explore the safe dose and biological effects of CCNPs. Methods: A total of 40 healthy male SD rats were randomly divided into control group, low, middle and high doses of CCNPs groups (given 0, 30, 60, and 120 mg middot; kg-1 CCNPs). The injection was consecutively given through the lateral tail vein once per day for 14 d. The body weights and daily feed intakes of the rats in various groups were measured. The haematology indexes, serum biochemical indexes, relative weights of organs and histopathology of main organs of the rats in various groups were detected. Results: In the 14-day repeated dose toxicity experiment, two rats died in high dose of CCNPs group, while no rats died in low and middle doses of CCNPs groups. The body weights and daily average intakes of the rats in different doses of CCNPs groups were slightly lower than those in control group, but the differences were not statistically significant (P>0. 05). There were no significant differences in the serum indexes of the rats between different doses of CCNPs groups and control group (P>0. 05). Compared with control group, the relative weights of lung of the rats in different doses of CCNPs groups were increased significant (P0. 05). The histopathological analysis results showed that the mild inflammatory infiltration was found in some organs of the rats in low dose of CCNPs group, while no obviously pathological changes were found. The obviously histopathological changes were observed in the main organs of the rats in middle and high doses of CCNPs groups, including inflammatory cell infiltration, slight disorder of hepatocytes arrangement, increased vacuoles in hepatocytes; thickening of alveolar interstitium and formation of granulomas in the lung tissue; swelling, rupture and even necrosis of cardiac muscle fibers; atrophy and fissures of glomerulus and so on. Conclusion: Intravenous administration of low dose of CCNPs couldn' t cause sever acute toxicity reaction.
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Objective:To discuss the clinical assessment value of comprehensive echocardiographic parameters in detecting the left ventricular diastolic function in patients with hypertension. Methods: 60 hypertensive patients (30 cases without left ventricular hypertrophy (non-LVH), 30 cases with left ventricular hypertrophy(LVH) were divided into hypertension group, and 60 healthy subjects were in control group. All of the subjects were underwent M type, color ultrasound and tissue Doppler imaging (TDI). And to compare their comprehensive echocardiographic parameters.Results: Compared with the healthy control group, the IVSd, LVPWd, LVMI, LAD and LVD of hypertension group were significantly enlargement; the s', e', E peak and LVEDP of hypertension group also significantly increased, while a' and A peak were significantly reduced; compared with non-LVH, e', E peak and LVEDP of LVH group were significantly increased, and a' and A peak were significantly reduced, and these differences were statistically significant (t=-4.39,t=-4.39,t=5.47,t=-8.02, t=6.20,t=18.95, t=16.12;P<0.01).Conclusion: The comprehensive echocardiographic parameters can evaluate the extent of damage for left ventricular diastolic function of patients with hypertension, and they can be as the assessment standard of left ventricular hypertrophy. In clinical practice, TDI can be used as a new means in the evaluation of ventricular diastolic function.
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Fumonisin B1 (FB1) is a carcinogenic mycotoxin found in commodities such as corn and corn-originated products. An aptamer-based method for detection of FB1 was developed using the fluorescent dye PicoGreen, which can recognize and bind double-stranded DNA. A peak fluorescence of PicoGreen was obtained in 15 min in the presence of FB1 aptamer, which formed a double-stranded hybridizer DNA with its complementary strand. The excitation and emission wavelengths for PicoGreen detection were 480 nm and 520 nm, respectively. The sensitivity of this aptamer/PicoGreen-based method was 0.1 μg/L. This method showed a good linearity for FB1 concentration ranging from 0.1 to 1 μg/L. The entire detection procedure for FB1 could be completed within 40 min. No cross reactions were observed with any other mycotoxins against aflatoxin B1, ochratoxin A, citrinin and zearalenone, demonstrating high specificity towards FB1 aptamer. Agreement between commercial, antibody-based enzyme-linked immunosorbent assay (ELISA) kit and aptamer method was excellent with a kappa value of 0.857. Taken together, this aptamer/PicoGreen-based method is more cost-effective, time-saving and useful than ELISA for detection of FB1.
Subject(s)
Aflatoxin B1 , Enzyme-Linked Immunosorbent Assay , Fluorescence , Fluorescent Dyes , Chemistry , Fumonisins , Mycotoxins , Ochratoxins , Organic Chemicals , Chemistry , Staining and Labeling , Zea maysABSTRACT
This study examined the current changes of human ether-a-go-go-related gene (hERG) mutation derived from a LQT2 Chinese family with a highly penetrating phenotype. Mutation was identified and site-directed mutagenesis was performed to induce the mutation in wild-type (WT) hERG. WT hERG and mutated V535M were cloned and transiently expressed in HEK293 cells. At the 48th and 72nd h after transfection, membrane currents were recorded using whole cell patch-clamp procedures. An A>G transition at 1605 resulting in replacement of V535M was identified. Compared to WT, V535M mutation significantly decreased tail currents of hERG. At test potential of -40 mV after depolarizing at +50 mV, tail current densities were 83.35±7.06 pA/pF in WT and 50.38±7.74 pA/pF in V535M respectively (n=20, P<0.01). Gating kinetics of hERG revealed that V (1/2) of steady-state inactivation shifted to negative potential in the mutant (V (1/2,V535M): -61.81±1.7 mV vs. V (1/2, WT): -43.1±0.71 mV). The time constant of recovery from inactivation was markedly prolonged in the mutant compared to WT among test potentials. V535M hERG mutation demonstrated markedly decreased tail current densities, which suggests that V535M is a new loss-of-function mutation of hERG channel responsible for LQT2.