Quercetin attenuates domoic acid-induced cognitive deficits in mice

Domoic acid (DA) is one of the best known marine toxins, causative of important neurotoxic alterations. DA effects are documented both in wildlife and experimental assays, showing that this toxin causes severe injuries principally in the hippocampal area. Accumulating evidence indicates that mitochondrial dysfunction and oxidative stress are involved in DA-induced cognitive functional impairment. Therefore, therapeutics targeted to improve mitochondrial function and increase oxidative stress defence could be bene?cial. Quercetin, a bio?avanoid, has been reported to have potent neuroprotective effects and anti-oxidative ability, but its preventive effects on DA-induced mitochondrial dysfunction and cognitive impairment have not been well characterised. In this study, we evaluated the effects of quercetin on DA-induced cognitive deficits in mice and explored its potential mechanism. Our results showed that the oral administration of quercetin to DA-treated mice significantly improved their behavioural performance in a novel objective recognition task and a Morris water maze task. These improvements were mediated, at least in part, by a stimulation of PPARγ coactivator 1α-mediated mitochondrial biogenesis signalling and an amelioration of mitochondrial dysfunction. Moreover, quercetin activated nuclear factorerythroid-2-related factor-2 (Nrf2)-mediated phase II enzymes and decreased reactive oxygen species and protein carbonylation. Furthermore, the AMP-activated protein kinase (AMPK) activity significantly increased in the quercetin-treated group. Taken together, these findings suggest that a reduction in mitochondrial dysfunction through the increase of AMPK activity, coupled with an increase in Nrf2 pathway mediated oxidative defence, may be one of the mechanisms by which quercetin improves cognitive impairment induced by DA in mice.     

中药材产业扶贫重点优先区域划分和推荐种植中药材名录整理

推进中药材产业扶贫,是贯彻落实中央重大战略部署的重要举措。我国的贫困县绝大部分都是分布在14个集中连片贫困地区,这些地区由于生产生活条件恶劣,农林牧业的生产效益非常低下,仅靠生态补偿或传统农业难以脱贫致富,中药材产业是我国农村贫困人口脱贫增收的重要途径。为推进国家中医药管理局和国务院扶贫办等5部门联合印发《中药材产业扶贫行动计划(2017—2020年)》的实施,因地制宜的指导和规划中药材生产实践,促进中药材产业扶贫相关工作向最佳生产区域集中,该文基于贫困地区的相关数据资料,对具有优先开展中药材产业扶贫条件的区域进行划分,并在宏观层面对贫困地区可种植的中药材名录进行分析整理。结果显示:国家级贫困县和集中连片贫困地区涉及的县中至少有10%以上的贫困县,已经有很好的中药材产业基础,是中药材产业扶贫的重点优先区域;有53%的贫困县,具有一定的发展中药材产业扶贫条件,需要加强相关工作拓展中药材产业扶贫的基础和能力;有37%的贫困县发展中药材产业扶贫的基础条件较弱。建议:先期重点优先考虑,已经有很好中药材产业基础的县,通过近百个重点优先发展的县,带动其他有条件的贫困县,实施好《中药材产业扶贫行动计划》。     

Treatment of Class II, division 2 in the late growth period

The Deckbiss with skeletal Class II jaw relationship sometimes presents a considerable therapeutic problem, particularly in the late growth period (DP3U), as regards the coordination of dental and skeletal treatment objectives. An effective treatment approach was demonstrated: a modified Herbst appliance used simultaneously with fixed appliances in the maxilla. The sample comprised 12 male (14.0±0.9 years old) and 10 female (12.3±0.4 years old) patients. Correction of the distal occlusion was achieved in all patients by means of the Herbst appliance, which was removed after an average time period of 6.4±0.2 months. In the mandible the multibracket appliances were then immediately inserted, and Class II elastics were used for retention. Maximum anchorage was required in the maxilla as well as in the mandible. Complete diagnostic records were made at the begnning of the treatment as well as 6 and 12 months later, in order to document skeletal and dental changes.A dental and skeletal Class I relationship was achieved in all cases. A significant improvement was recorded in the vertical jaw base relationship; this was still stable after a period of 12 months. In the dental area in particular, a so-called high-pull headgear effect (intrusion and distalization 16, 26) and intrusion of teeth 34, 44 were registered. Only a minor protrusion of the mandibular incisors was observed. Reinforcement of the bands reduced the failure rate significantly.The Herbst appliance does not represent a standard treatment for Class II. Its indication range is limited.     

伴口呼吸安氏Ⅱ类1分类错患者的牙颌面横向结构特征

目的　比较伴口呼吸安氏Ⅱ类1分类错患儿与正常儿童的牙颌颅面硬组织横向结构的差异,为临床 诊断及选择合理的治疗方案提供理论依据。方法　借助头颅后前位X线头影测量,对12例伴口呼吸的安氏Ⅱ类1 分类错患儿的牙颌颅面硬组织结构进行测量分析,并与15例正常儿童相应结构进行分析比较。结果　伴口 呼吸安氏Ⅱ类1分类错患儿的上颌基骨宽度、上磨牙间距、下尖牙间距及骨性鼻腔宽度明显低于正常儿童 (P<0·01);与正常相比,错患儿的下颌骨宽度、下磨牙间距的测量值也低于正常儿童(P<0·05)。结论　口呼 吸可引起儿童牙颌面横向结构上发育的异常,临床诊治时应对此异常给予考虑。     

Timing the early treatment of Class II,division 1 malocclusion — Clinical and research considerations

The aim of this study was to evaluate the correlation between timing of emergence of the permanent teeth and sagittal occlusal changes in children enrolled in a prospective clinical trial of Class II, division 1 treatment. The children, ages 7.2–13.3 years, met strict inclusion criteria and were assigned at random to treatment with either a headgear or a Fränkel functional appliance. Relationships between maxillary and mandibular first molars and canines, as well as overjet, were measured with digital calipers on casts made every 2 months and mounted on a SAM II articulator. The emergence of a permanent tooth was scored on a scale from 1 to 3, depending on the eruptive level of the tooth from cutting through the gingiva (1) to reaching the occlusal table (3). Specifically, emergence of the second premolars (PM2) and permanent second molars (M2), the most adjacent teeth to the first molars, was evaluated as it interacted with the development of the sagittal occlusion. Treatment of the distocclusion was as effective in late childhood as in mid-childhood. Within each appliance group, the emergence of PM2 and M2 did not affect the amount of progress toward Class I significantly (p> 0.05), indicating that improvement from distocclusion to neutrocclusion with each appliance is not influenced by the timing of emergence of these teeth. Although these findings support a one-phase treatment starting in the late mixed dentition, earlier intervention in mid-childhood may be required in the presence of several developmental conditions, or when the dental and skeletal development deviate significantly in the individual patient.     

恒牙初期安氏Ⅱ~1错不同骨面型颅底形态变化的头影测量分析

目的:探讨安氏Ⅱ1错牙合不同骨面型的颅底形态特征。方法:选取恒牙初期的正常牙合和Ⅱ1错牙合均角型、高角型、低角型的X线头颅侧位片各30张,男女各半,通过X线头影测量分析,比较Ⅱ1错牙合3种骨面型和正常牙合的颅底形态变化。结果:Ⅱ1错牙合3种骨面型均表现为颅基底角(Ba-SE-FMS)增大,高角组尤其表现在颅前基底角(FMS-SE-PM)增大,均角组、低角组颅中基底角(Ba-SE-PM)增加更为明显。Ⅱ1错牙合颅底的有效垂直高度从低角组、均角组、高角组依次减小。结论:颅基底角可能更准确反映颅底的曲度,体现Ⅱ1错牙合不同骨面型形成的机制。     

功能和固定矫治器联合矫治安氏Ⅱ类1分类骨性错畸形

目的 通过对功能和固定矫治器联合矫治恒牙列早期安氏Ⅱ类1分类骨性错(牙合)畸形的研究,探讨发育期骨性错(牙合)畸形一期矫治的优越性。方法 应用双(牙合)垫矫治器或斜面导板结合方丝弓矫治器对12例恒牙列早期安氏Ⅱ类1分类骨性错(牙合)联合矫治,对治疗前后头颅侧位定位片进行分析。结果 SNB角增加1.28°,FMA角无明显改变,OP-SN值变大,Go-Pog、Go-Ar都呈显著性增大,前牙覆盖减少7.26mm,上下唇至审美平面距离显著减小。结论 利用功能矫治器和固定矫治器联合一期矫治恒牙列早期安氏Ⅱ类1分类骨性错(牙合),,同样可收到双期矫治的效果。     

CDK1、CCNB1和NDC80与乙型肝炎相关肝细胞癌的预后和进展相关:基于生物信息学方法

目的 探讨 HBV 转化为 HCC 相关的关键基因,并探索相关的分子机制。方法 分析基因表达综合（GEO）数据库中GSE55092、GSE84044和GSE121248的mRNA微阵列数据,其中包括119个HBV相关的HCC组织和252个HBV相关的非肿瘤组织。“sva”R包用于去除批间差。进行整合分析,获取HBV相关肝癌和HBV组织中的差异表达基因（DEGs）,通过基因本体论（GO）和京都基因与基因组百科全书（KEGG）分析对差异表达基因进行功能注释。使用相互作用基因搜索工具（STRING）构建蛋白质-蛋白质相互作用网络,挖掘最重要的模块和关键基因。cBioportal用于分析hub基因的相关性。利用Kaplan-Meier和Oncomine数据库对TCGA数据库中肝癌基因表达数据进行验证,探讨hub基因与肝癌发生、发展和预后的关系。通过逆转录定量PCR（RT-qPCR）实验验证17对临床肝细胞癌样本与邻近非肿瘤组织中hub基因的表达。结果 共获得121个DEGs（P< 0.01）,鉴定出3个遗传标记,细胞周期素依赖性激酶1（CDK1）、细胞周期蛋白B1（CCNB1）和核分裂周期蛋白80（NDC80）,与细胞周期、嘧啶代谢和DNA复制有关,这3个基因高度相关（P<0.05）。UALCAN数据库证实这些基因在肝癌组织中高表达并获得相关预后信息。Kaplan-Meier表明,它们与HCC患者的低存活率相关。CDK1、CCNB1和NDC80与肝癌分级相关（P< 0.05）,RT-qPCR实验证实CDK1、CCNB1和NDC80的mRNA在肝细胞癌中的表达明显高于癌旁组织。结论 CDK1、CCNB1 和NDC80基因可作为HBV相关肝细胞癌的预后标志物,在肝癌的基础研究和临床治疗方面有一定的应用价值。     

Mitochondrial transfer from bone-marrow-derived mesenchymal stromal cells to chondrocytes protects against cartilage degenerative mitochondrial dysfunction in rats chondrocytes

BackgroundPrevious studies have reported that mitochondrial dysfunction participates in the pathological process of osteoarthritis (OA). However, studies that improve mitochondrial function are rare in OA. Mitochondrial transfer from mesenchymal stem cells (MSCs) to OA chondrocytes might be a cell-based therapy for the improvement of mitochondrial function to prevent cartilage degeneration. This study aimed to determine whether MSCs can donate mitochondria and protect the mitochondrial function and therefore reduce cartilage degeneration.MethodsBone-marrow-derived mesenchymal stromal cells (BM-MSCs) were harvested from the marrow cavities of femurs and tibia in young rats. OA chondrocytes were gathered from the femoral and tibial plateau in old OA model rats. BM-MSCs and OA chondrocytes were co-cultured and mitochondrial transfer from BM-MSCs to chondrocytes was identified. Chondrocytes with mitochondria transferred from BM-MSCs were selected by fluorescence-activated cell sorting. Mitochondrial function of these cells, including mitochondrial membrane potential (Δψm), the activity of mitochondrial respiratory chain (MRC) enzymes, and adenosine triphosphate (ATP) content were quantified and compared to OA chondrocytes without mitochondrial transfer. Chondrocytes proliferation, apoptosis, and secretion ability were also analyzed between the two groups.ResultsMitochondrial transfer was found from BM-MSCs to OA chondrocytes. Chondrocytes with mitochondrial from MSCs (MSCs + OA group) showed increased mitochondrial membrane potential compared with OA chondrocytes without mitochondria transfer (OA group) (1.79 ± 0.19 vs. 0.71 ± 0.12, t = 10.42, P < 0.0001). The activity of MRC enzymes, including MRC complex I, II, III, and citrate synthase was also improved (P < 0.05). The content of ATP in MSCs + OA group was significantly higher than that in OA group (161.90 ± 13.49 vs. 87.62 ± 11.07 nmol/mg, t = 8.515, P < 0.0001). Meanwhile, we observed decreased cell apoptosis (7.09% ± 0.68% vs.15.89% ± 1.30%, t = 13.39, P < 0.0001) and increased relative secretion of type II collagen (2.01 ± 0.14 vs.1.06 ± 0.11, t = 9.141, P = 0.0008) and proteoglycan protein (2.08 ± 0.20 vs. 0.97 ± 0.12, t = 8.227, P = 0.0012) in MSCs + OA group, contrasted with OA group.ConclusionsMitochondrial transfer from BM-MSCs provided protection for OA chondrocytes against mitochondrial dysfunction and degeneration through improving mitochondrial function, cell proliferation, and inhibiting apoptosis in chondrocytes. This finding may offer a new therapeutic direction for OA.