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1.
IntroductionThis study was designed to assess whether a dental caries management protocol combining a single application of 38% silver diamine fluoride (SDF) with comprehensive oral health education will successfully divert high-risk children from dental treatment under dental general anaesthesia (DGA), arrest active caries in primary teeth, and improve parent-reported child oral health–related quality of life (OHRQoL).MethodsChildren aged 2 to 10 years, who attended two public dental agencies in Victoria, Australia, and were unable to tolerate restorative treatments in the clinic setting, elected to participate in either a 38% SDF intervention protocol or, alternatively, referral for DGA. Follow-up examinations were completed at 6 months to assess caries progression, decayed missing filled tooth index, PUFA index (pulpal involvement, ulceration, fistula, abscess), DGA referral rates, and OHRQoL (Early Childhood Oral Health Impact Scale [ECOHIS]).ResultsOf the total sample, 89.5% of children (n = 102) [mean (SD) age, 4.1 (1.0) years] with 401 active carious lesions elected to participate in the 38% SDF protocol; 10.5% (n = 12) of parents opted for referral for treatment under DGA. The proportion of active caries subsequently arrested at follow-up (number of arrested lesions/number of lesions treated) was 0.78 (95% CI, 0.69 to 0.87). There was an 88% reduction in referrals for DGA in eligible children over the 6-month period. The 38% SDF intervention group showed a significant improvement in ECOHIS scores at follow-up (P < .001).DiscussionAdoption of the 38% SDF intervention protocol resulted in a significant reduction in the rate of preventable dental hospitalisations. Most parents opted against referral for DGA. Parent-reported OHRQoL for children improved significantly. 相似文献
2.
发作性睡病是致残性白天睡眠增多的最常见原因之一,其治疗旨在减少白天睡眠增多和猝倒,改善夜间睡眠紊乱、睡眠瘫痪及与睡眠有关的幻觉。2019年,组胺H3受体拮抗剂替洛利生(Pitolisant)和多巴胺及去甲肾上腺素再摄取抑制剂索利氨酯(Solriamfetol)分别在欧盟和美国上市,前者具有促醒和抗猝倒作用,后者也有促醒作用,且戒断症状和滥用的发生率更低。目前,控释型羟丁酸钠(FT218)、低钠型羟丁酸盐(JZP-258)、选择性去甲肾上腺素再摄取抑制剂(瑞波西汀,又称AXS-12)以及莫达非尼联合氟卡尼制剂(THN102)等药物仍在开发和测试中,均可作为治疗发作性睡病相关白天睡眠增多和猝倒的潜在药物。本文重点介绍这些最近研发的发作性睡病治疗药物。 相似文献
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Christiana Winkler Barbara Frick Katharina Schroecksnadel Harald Schennach Dietmar Fuchs 《Food and chemical toxicology》2006,44(12):2003-2007
Antioxidant preservatives prolong the quality of food and ensure the nutritional adequacy, palatability and safety of many processed foods and beverages. Effects of sodium sulfite (E221) and sorbic acid (E200) were investigated in human peripheral blood mononuclear cells (PBMC) which were purified from blood of healthy donors. Cells were stimulated with the mitogen phytohaemagglutinin in vitro, which induces proliferation of T-cells and the production of Th1-type cytokines like interferon-γ. The latter triggers enzyme indoleamine (2,3)-dioxygenase, which degrades tryptophan, and GTP cyclohydrolase I, which leads to increased neopterin production, in monocyte-derived macrophages. Sodium sulfite and sorbic acid suppressed both these biochemical changes in a dose-dependent way (P < 0.01 at 1 mM sodium sulfite and 50 mM sorbic acid). Data demonstrate a suppressive influence of sodium sulfite and sorbic acid on the activated Th1-type immune response. 相似文献
5.
DTF降茶氟剂降茶氟初步研究 总被引:9,自引:1,他引:8
王连方 《中国地方病防治杂志》2003,18(1):17-19
目的探讨DTF制剂降茶氟效果。方法在不同制茶方法程序中加入DTF制剂观察其降氟效果。结果在冲泡或煮沸(1.0g茶叶,200ml水量)沏茶中,0.2gDTF可使茶氟降低约60%,使茶水氟浓度由2.0~4.0mg/L降到1.0mg/L左右,茶液色、味、pH值无改变。结论DTF是1种有效的降茶氟剂。 相似文献
6.
透明质酸钠对大鼠成肌细胞增殖和分化的影响 总被引:3,自引:2,他引:1
目的 研究透明质酸钠对成肌细胞增殖和分化的影响。方法 采用酶消化法将新生SD大鼠骨骼肌组织分离、纯化、原代培养及传代培养;取第3代成肌细胞,分别加入浓度为0.05%、0.1%及0.2%的透明质酸钠溶液作为生长培养基行体外培养为实验A、B及C组,加入常规生长培养基为对照D组,观察各组成肌细胞增殖情况,并采用细胞计数及MTT法绘制生长曲线。另选择0.1%透明质酸钠融合培养基行体外成肌细胞培养,常规融合培养基作对照,观察透明质酸钠对成肌细胞分化功能的影响。结果A、B及C组成肌细胞增殖表现相似,2d时进入对数生长期,4d时均达顶峰;D组成肌细胞于3d时进入对数生长期,5d时细胞数倍增,6d时达顶峰。MTT法所测吸光度(A)值的变化反映成肌细胞的增殖情况,与细胞计数的结果一致,以B组细胞增殖作用最明显,B组A值在2~8d时均高于C、D组(P〈0.05),8d时高于A组(P〈0.05)。0.1%透明质酸钠融合培养基中的成肌细胞融合率较低且上升缓慢,7d时融合率最高,为11.7%;常规融合培养基成肌细胞融合率于6d时达到峰值,约为35.0%。结论 透明质酸钠与成肌细胞的细胞相容性较好,可以作为良好的成肌细胞培养基。 相似文献
7.
过量氟化物导致大鼠腰椎黄韧带退变与骨化 总被引:2,自引:0,他引:2
[目的]研究氟化物在黄韧带骨化中可能的作用机理。[方法]36只雄性SD大鼠,实验组饮用含NaF(质量分数为1014)蒸馏水,分别于3个月及6个月时,检测骨密度,血清、骨组织标本中Ca、P^3+、Mg、Zn、Cu、Fe、F^-含量和血清碱性磷酸酶(ALP)活性;行大鼠腰段标本X线检查后组织病理观察。[结果]3个月实验组10只大鼠中6只出现氟斑牙:6个月实验组均出现氟斑牙,且大鼠中轴骨骨密度显著增加(P〈0.05)。X线检查,6个月实验组中有4只可见黄韧带嵴状骨化影。病理观察,3个月实验组大鼠黄韧带呈退行性改变;6个月实验组部分黄韧带骨化,骨化类型以膜内骨化为主。[结论]过量氟化物可造成SD大鼠腰椎黄韧带的退变、骨化,在黄韧带的骨化中可能起重要作用。 相似文献
8.
Acupuncture analgesia (AA) caused by low frequency stimulation of the acupuncture point (AP) was abolished by hypophysectomy and adrenalectomy. Termination of the AA producing pathway from the AP to the pituitary gland was in the medial hypothalamic arcuate nucleus (M-HARN). The origin of the descending pain inhibitory system associated with AA was in the posterior HARN (P-HARN). AA in the hypophysectomized rats, and enhanced neuronal activity in the P-HARN that were abolished during acupuncture stimulation, were both restored by intraperitoneal microinjection of 0.5 mg/kg morphine or 0.1 micrograms beta-endorphin into the P-HARN during acupuncture stimulation. Of the analgesia produced by dopamine or beta-endorphin injected into the P-HARN, that caused by beta-endorphin disappeared after denervation of the M-HARN. The P-HARN neurons that responded to acupuncture stimulation also responded to iontophoretic dopamine, but not to iontophoretic morphine nor ultramicroinjected beta-endorphin. The transmission between the M-HARN and P-HARN may be dopaminergic, and beta-endorphin might presynaptically modulate this transmission. Reduction of sodium ions may have been the reason for abolition of AA after adrenalectomy. 相似文献
9.
研究亚硫酸氢钠和氯化钠配伍使用的增敏性,建立了NaHSO3—NaCl—KIO3—KI四元无机体系测定碘盐中碘含量的新方法。测定碘的最佳条件:磷酸介质,pH 3~4,最大吸收波长479 nm,ε479=1.5×105L/(mol/cm),碘含量(以KIO3中I计)在0~2.24mg/L内符合比尔定律。用于测定食盐中碘的含量,回收率为99.49%~101.3%,结果满意。 相似文献
10.
Severe myoclonic epilepsy (SMEI) or Dravet syndrome is caused by mutations of the SCN1A gene that encodes voltage-gated sodium channel alpha-1 subunit. Recently, we generated and characterized a knock-in (KI) mice with an SCN1A nonsense mutation that appeared in three independent SMEI patients. The SCN1A-KI mice well reproduced the SMEI disease phenotypes. Both homozygous and heterozygous knock-in mice developed epileptic seizures within the first postnatal month. In heterozygous knock-in mice, trains of evoked action potentials in inhibitory neurons exhibited pronounced spike amplitude decrement late in the burst but not in pyramidal neurons. We further showed that in wild-type mice the Nav1.1 protein is expressed dominantly in axons and moderately in somata of parbalbumin (PV) – positive inhibitory interneurons. Our immunohistochemical observations of the Nav1.1 are clearly distinct to the previous studies, and our findings has corrected the view of the Nav1.1 protein distribution. The data indicate that Nav1.1 plays critical roles in the spike output from PV interneurons and further, that the specifically altered function of these inhibitory circuits may contribute to epileptic seizures in the mice. These information should contribute to the understanding of molecular pathomechanism of SMEI and to develop its effective therapies. 相似文献