Research progress on anticaries nanomaterials / 口腔疾病防治

@#Dental caries are the most common and widespread biofilm-dependent oral disease. Nanotechnology promises to be a useful strategy for dental caries management by combating caries-related bacteria, decreasing biofilm accumulation, inhibiting demineralization and enhancing remineralization. Many potential applications of nanotechnology in the development of anticaries materials have recently been reported, especially for anticaries adhesive nanomaterials and anticaries nanofilled composite resins. This review summarizes the current progress in the application of functional nanoparticles in the following products: antibacterial nanomaterials, remineralizing nanomaterials and nanodrug delivery systems.

Changes in the expression of c-fos & heat shock protein genes & blood flow velocity in the brain of rats undergoing myocardial ischaemia/reperfusion.

BACKGROUND & OBJECTIVE: Myocardial hypofunction could lead to the derangement of brain functions. The expression of c-fos and heat shock protein (hsp) genes was recognized as markers of neural cell injury. We under took this study to investigate the influence of myocardial ischaemia and reperfusion (I/R) on these molecular events in the rat brain tissue and changes in mean arterial blood pressure (MAP) and the cerebral blood flow velocity (CBFV), to understand the basis of cerebral pathology following cardiac ischaemia and reperfusion. METHODS: Healthy rats (n=42) were randomly allocated into seven groups: sham-operated (A); myocardial ischaemia for 15 min, followed by 0.5, 1, 2, 4 and 6 h of reperfusion respectively (B2-B6) and hypovolemia at medium level (C). I/R rat models were established by ligating the anterior branch of the left coronary artery. Expressions of the c-fos, hsp70, hsp27 and hsp90 genes in the cerebrum, cerebellum, medullaoblongata and hippocampus, were studied with immunohistochemistry and in situ hybridization. The MAP and CBFV of the rats were also measured. RESULTS: The expressions of c-fos and HSP70 in brain tissue increased after myocardial ischaemia/ reperfusion, with the strongest signal appearing in the hippocampus and cerebral cortex, while labeling for HSP27 and HSP90 alpha were not detectable in any of the experimental groups. The expressions of c-fos mRNA and hsp70 mRNA shared the similar characteristics with their encoding proteins. MAP, reflection of cardiac function and cerebral blood flow decreased following cardiac ischaemia and reperfusion. INTERPRETATION & CONCLUSION: Our findings suggested that the brain damages occurred from the early phase of myocardial I/R. The exact mechanism of cerebral tissue injuries induced by myocardial I/R is not known. Further studies need to be done to throw light on these aspects.

Effect of naloxone on aluminum-induced learning and memory impairment in rats.

BACKGROUND: Uptake of aluminum may disturb the learning and memory of humans or animals. Naloxone (NAL) has been shown to exert beneficial effects on memory deficits. AIMS: We investigated the effects of naloxone on aluminum-induced learning and memory impairment in rats. SETTINGS AND DESIGN: Aluminum-induced learning and memory impairment model was established by gavage of Aluminum chloride (600 mg/kg) for 3 months. Rats were divided into three groups viz. naloxone-treated rats (NAL 0.8 mg/kg, i.p. daily for 7 days), non-treated model rats and normal controls. MATERIALS AND METHODS: The Morris water maze test was performed to study spatial learning and memory. Long-term potentiation (LTP) of the Schaffer collateral-CA1 synapse was recorded. Aluminum and zinc contents in the hippocampus were assayed with atomic absorption spectrophotometry. STATISTICAL ANALYSIS: Parameters of the hidden and visible platform trials and data of LTP were analyzed using two-way repeated measures ANOVA. RESULTS: In the hidden platform trials, escape latencies of the NAL rats were significantly shorter than that of the non-treated rats (P=0.000, 95% confidential interval low bound 14.31, upper bound 22.68). In probe trails, the number of entries in the target area of the NAL rats (6.75+/-1.28 times/min) was more than that of non-treated model rats (4.56+/-2.16 times/min, P=0.004, 95% confidence interval low bound -3.65, upper bound -0.788). The magnitudes of LTP recorded in the CA1 pyramidal neurons of the NAL-treated rats were significantly augmented when compared to the non-treated model rats (P=0.005, 95% confidence interval low bound 0.16, upper bound 0.84). CONCLUSIONS: NAL could facilitate spatial learning and memory and enhance LTP in the CA1 region of the hippocampus in aluminum-induced learning and memory impairment in rats.