Objective To develop an embedded system by using time-triggered system and ATmega128.Methods Making use of the minimum system structure of ATmega128,a multitask system,which could be implanted into AVR CPU,was designed based on the singlechip with 8 bits and 51series.Results Time-Triggered Embedded System kept the controlling precision on ms degree and ensured a sensitive and rapid response to keyboard input.Conclusion Software designed by Time-Triggered Embedded System has advantage in real time,so it is applicable to minitype real time control system.

This paper presents a microcontroller system for target controlled infusion according to pharmacodynamic parameters of intravenous anesthetics. It can control the depth of anesthesia by adjusting the level of plasma concentrations. The system has the advantages of high precision, extending power and easy manipulation. It has been used in the clinical anesthesia.
Anesthesia, Intravenous ; instrumentation ; methods ; Anesthetics, Intravenous ; administration & dosage ; pharmacokinetics ; Drug Delivery Systems ; methods ; Drug Therapy, Computer-Assisted ; methods ; Humans ; Monitoring, Intraoperative ; methods

Objective To investigate the effect of transplantation of bone marrow mesenchymal stem cells (MSCs) in subarachnoid space on chronic neuropathic pain in rats. Methods One hundred and forty female SD rats weighing 180-200 g were used in this study. Chronic neuropathic pain (NP) was induced by ligation and separation of tibial and common fibular nerves (SNI). Two weeks after the surgery the animals were randomly divided into4 groups (n=35 each):group Ⅰ NP; group Ⅱ NP+ MSC (MSCs); group Ⅲ NP+ phosphate buffer saline (PBS) and group Ⅳ NP+ bone marrow monocyte (BNMCs). MSCs 10 μl, PBS 10 μl and BNMCs 10 μl were injected into subaraclmoid space at 2 weeks after surgery in group Ⅱ , Ⅲ and Ⅳ respectively. Paw withdrawal threshold to yon Frey filament stimulation (PWT) was measured before surgery (T0, baseline), at 2 weeks after surgery (T1) and 1, 2, 3, 4 and 5 weeks after subarachnoid injection (T2-6). Five animals were killed at T1-6 in each group and their lumbar enlargements were removed for determination of BDNF mRNA expression. Results PWT was significantly decreased by SNI at T1 in all 4 groups, and at T2-6 in group Ⅰ , Ⅲ and Ⅳ as compared with the baseline at T0 (P ＜ 0.05). Subarachnoid MSC transplantation significantly reduced mechanical hyperalgesia at T2-6 and up-regulated BDNF mRNA expression at T2-4 as compared with that at T1 (P ＜0.05). There was no significant change in PWT and BDNF mRNA expression after subarachnoid PBS and BNMCs injection in group Ⅲ and Ⅳ (P ＞ 0.05). Compared with group Ⅰ , PWT was significantly increased and BDNF mRNA expression was up-regulated in group Ⅱ (P ＜ 0.05), but no significant change in PBS and BNMCs was found in group Ⅲ (P ＞ 0.05) .Conclusion Up-regulation of BDNF mRNA expression in the spinal cord may be involved in the amelioration of chronic neuropathic pain by subarachnoid bone marrow mesenchymal stem cell transplantation.

Descending nociceptive modulation from the supraspinal structures plays an important role in cancer-induced bone pain (CIBP). Rostral ventromedial medulla (RVM) is a critical component of descending nociceptive facilitation circuitry, but so far the mechanisms are poorly known. In this study, we investigated the role of RVM glial activation in the descending nociceptive facilitation circuitry in a CIBP rat model. CIBP rats showed significant activation of microglia and astrocytes, and also up-regulation of phosphorylated p38 mitogen-activated protein kinase (p38 MAPK) and pro-inflammatory mediators released by glial cells (IL-1β, IL-6, TNF-α and brain-derived neurotrophic factor) in the RVM. Stereotaxic microinjection of the glial inhibitors (minocycline and fluorocitrate) into CIBP rats' RVM could reverse the glial activation and significantly attenuate mechanical allodynia in a time-dependent manner. RVM microinjection of p38 MAPK inhibitor (SB203580) abolished the activation of microglia, reversed the associated up-regulation of pro-inflammatory mediators and significantly attenuated mechanical allodynia. Taken together, these results suggest that RVM glial activation is involved in the pathogenesis of CIBP. RVM microglial p38 MAPK signaling pathway is activated and leads to the release of downstream pro-inflammatory mediators, which contribute to the descending facilitation of CIBP.

Descending nociceptive modulation from the supraspinal structures plays an important role in cancer-induced bone pain (CIBP).Rostral ventromedial medulla (RVM) is a critical component of descending nociceptive facilitation circuitry,but so far the mechanisms are poorly known.In this study,we investigated the role of RVM glial activation in the descending nociceptive facilitation circuitry in a CIBP rat model.CIBP rats showed significant activation of microglia and astrocytes,and also up-regulation of phosphorylated p38 mitogen-activated protein kinase (p38 MAPK) and pro-inflammatory mediators released by glial cells (IL-1β,IL-6,TNF-a and brain-derived neurotrophic factor) in the RVM.Stereotaxic microinjection of the glial inhibitors (minocycline and fluorocitrate) into CIBP rats' RVM could reverse the glial activation and significantly attenuate mechanical allodynia in a time-dependent manner.RVM microinjection of p38 MAPK inhibitor (SB203580) abolished the activation of microglia,reversed the associated up-regulation of pro-inflammatory mediators and significantly attenuated mechanical allodynia.Taken together,these results suggest that RVM glial activation is involved in the pathogenesis of CIBP.RVM microglial p38 MAPK signaling pathway is activated and leads to the release of downstream pro-inflammatory mediators,which contribute to the descending facilitation of CIBP.

Aristolochic acid (AA), extracted from Aristolochiaceae plants, plays an essential role in traditional herbal medicines and is used for different diseases. However, AA has been found to be nephrotoxic and is known to cause aristolochic acid nephropathy (AAN).AA-induced acute kidney injury (AKI) is a syndrome in AAN with a high morbidity that manifests mitochondrial damage as a key part of its pathological progression. Melatonin primarily serves as a mitochondria-targeted antioxidant. However, its mitochondrial protective role in AA-induced AKI is barely reported. In this study, mice were administrated 2.5 mg/kg AA to induce AKI. Melatonin reduced the increase in Upro and Scr and attenuated the necrosis and atrophy of renal proximal tubules in mice exposed to AA. Melatonin suppressed ROS generation, MDA levels and iNOS expression and increased SOD activities in vivo and in vitro. Intriguingly, the in vivo study revealed that melatonin decreased mitochondrial fragmentation in renal proximal tubular cells and increased ATP levels in kidney tissues in response to AA. In vitro, melatonin restored the mitochondrial membrane potential (MMP) in NRK-52E and HK-2 cells and led to an elevation in ATP levels. Confocal immunofluorescence data showed that puncta containing Mito-tracker and GFP-LC3A/B were reduced, thereby impeding the mitophagy of tubular epithelial cells. Furthermore, melatonin decreased LC3A/B-II expression and increased p62 expression. The apoptosis of tubular epithelial cells induced by AA was decreased. Therefore, our findings revealed that melatonin could prevent AA-induced AKI by attenuating mitochondrial damage, which may provide a potential therapeutic method for renal AA toxicity.

Restorative materials such as conventional glass ionomer cement (CGIC), resin-modified glass ionomer cement (RMGIC), polyacid-modified composite resin (compomer), and giomer have the properties of fluoride release and refill, which may prevent or slow down the progression of caries. The caries resistance of these materials was evaluated according to the following criteria: fluorine-releasing ability, antibacterial activity, mechanical properties and anti-aging properties. The anti-caries effect of these materials mainly depends on the effect of fluoride ions on mineralization. However, materials with strong fluorine release ability, such as CGIC, are mainly used in pediatric dentistry and temporary restoration due to their poor mechanical properties. It is difficult to achieve both fluoride ion release potential and mechanical strength, and there are few materials that can provide ideal mechanical strength while maintaining a high standard of fluoride release. The fluoride releasing and recharging capacity of CGIC, RMGIC, compomer and giomer decrease successively. The trend of material modification, to a certain extent, tends to sacrifice the fluoride release capacity of materials to maintain the ideal mechanical strength. In recent years, scholars have tried to add a variety of fillers to further enhance the anti-cracking ability of materials and add antibacterial agents to compensate for the anti-caries effect to reduce the loss of fluoride release.