傣族的植物认知：命名－含义与分类

通过所收集的1175种(品种)植物的1390个傣名,并对生活型外的1691个含义进行分析、统计、归纳,阐明了傣族对植物的认知。他们用“宏哦宾”,即“从地上长出来的,有生命的东西”对“植物”这个抽象而综合词汇进行定义,与现代科学“从地上长出的任何东西”的“植物”定义异曲同工,这是世界上很多其它民族所没有的。他们把植物的生活型和经济类型作为“属”名,把植物的形态特征、经济用途、分布生态和故事传说等有关含义作为“种”名,在对1691个植物名字含义的统计中,它们分别占了60％、30％、8％和2％,充分体现了傣族对植物“见什么像什么就叫什么”的植物命名方法。它类似于现代植物分类学对植物命名的林奈氏“双名法”。基于傣族对植物的认知和植物傣名结构,可以建立起“植物界”、栽培植物和野生植物的两个“科”、生活型和经济类型的约20个“属”,以及具有“双名”的3000多个“种”和1000多个“品种”的5个结构层次的民间植物分类系统。     

Structure,Delimitation,Nomenclature and Classification of Stomata

The paper reviews stomatal types observed in 500 species of angiosperms besides those described in the literature and deals with the problems of their structure, delimitation, nomenclature and classification. In view of the varied definitions available in the literature for subsidiaries, stomatal types and,the definition and delimitations being variously interpreted by different workers, a modified definition for the subsidiaries and stomata is presented. In accordance with the international code of nomenclature for plants, the names of the stomata widely in use are retained (rule of priority). They have been presently classified as pericytic, desmocytic, paracytic, diacytic, anisocytic, anisotricytic, isotricytic, tetracytic,staurocytic, anomocytic, cyclocytic and a good number of varieties under each type are presented. These stomatal types are recognised on the basis of their structure rather than its ontogenetic pathways.     

Structure, Delimitation, Nomenclature and Classification of Stomata

The paper reviews stomatal types observed in 500 species of angiosperms besides those described in the literature and deals with the problems of their structure, delimitation, nomenclature and classification. In view of the varied definitions available in the literature for subsidiaries, stomatal types and, the definition and delimitations being variously interpreted by different workers, a modified definition for the subsidiaries and stomata is presented. In accordance with the international code of nomenclature for plants, the names of the stomata widely in use are retained (rule of priority). They have been presently classified as pericytic, desmocytic, paracytic, diacytic, anisocytic, anisotricytic, isotricytic, tetracytic, staurocytic, anomocytic, cyclocytic and a good number of varieties under each type are presented. These stomatal types are recognised on the basis of their structure rather than its ontogenetic pathways.     

运用傣族的传统信仰保护西双版纳植物多样性的探讨

探讨不同的途径来保护日益减少的生物多样性已成为国际社会关注的一个热点。研究证明依靠西双版纳傣族传统信仰文化而建立的龙山林与寺庙庭园 ,就象一些小保护区和小植物园一样在植物多样性的保护中发挥了重要作用。在此基础上 ,探讨了在人口增加、森林减少和生活方式发生一定改变的今天通过成立宗教植物保护协会来运用信仰的力量参与生物多样性的管理、通过多层次培训教育提高公众的保护意识与技能 ,通过示范来鼓励土著民族参与等多种方法来保护该地区生物多样性的途径 ,受到了良好的效果。     

中国西双版纳傣族与泰国泰族民间植物命名方法与土著名字的相似性探讨

通过对中国西双版纳与泰国都有分布和栽培的641种植物的傣、泰土著名字相似性比较,发现这两个民族具有基本相同的民间植物命名的"双名法"。西双版纳傣族与泰国的兰纳地区、北—东北部和其它地区泰族的植物土著名相同、相似的分别占0.69、0.57和0.37,主要包括药用植物在内的经济植物和与南传上座部佛教文化密切相关的植物。其主要成因包括他们的语言文字、宗教信仰、生活习俗等的傣、泰历史渊源及其所具有的传统文化密切程度相关。其中,兰纳地区地处泰国北部,它不仅邻近西双版纳,而且在历史上,它们曾经同属于"兰纳王国",两地的边界曾是"犬牙交错",成为"曼比勐农"(兄弟之邦)。这样,使包括土著名字在内的佛教植物、野生植物和栽培植物等的交流比泰国其它地区更加密切,相似性便最高。西双版纳傣族和兰纳泰族被视为尚存的标准"Tai"人区。因此,该研究对于中国Dai、泰国Thai、缅甸Siam和老挝Laos等国家民族的科学文化交流及其植物资源的利用和保护等具有重要的意义。     

濒危植物海南龙血树种子休眠机理及其生态学意义

通过对中国西双版纳与泰国都有分布和栽培的641种植物的傣、泰土著名字相似性比较,发现这两个民族具有基本相同的民间植物命名的“双名法”。西双版纳傣族与泰国的兰纳地区、北—东北部和其它地区泰族的植物土著名相同、相似的分别占0.69、0.57和0.37,主要包括药用植物在内的经济植物和与南传上座部佛教文化密切相关的植物。其主要成因包括他们的语言文字、宗教信仰、生活习俗等的傣、泰历史渊源及其所具有的传统文化密切程度相关。其中,兰纳地区地处泰国北部,它不仅邻近西双版纳,而且在历史上,它们曾经同属于“兰纳王国”,两地的边界曾是“犬牙交错”,成为“曼比勐农”（兄弟之邦）。这样,使包括土著名字在内的佛教植物、野生植物和栽培植物等的交流比泰国其它地区更加密切,相似性便最高。西双版纳傣族和兰纳泰族被视为尚存的标准“Tai”人区。因此,该研究对于中国Dai、泰国Thai、缅甸Siam和老挝Laos等国家民族的科学文化交流及其植物资源的利用和保护等具有重要的意义。 关键词： 民族植物学研究, 中国西双版纳傣族与泰国泰族, 相同植物的民间命名方法, 相似的植物土著名字, 相似的历史渊源成因, 科学与文化交流的意义     

Plants among Yi People’s Traditional Folk Customs and Their Cultural Significance in Liangshan Yi Autonomous Prefecture,Sichuan

The culture of plants used in Liangshan Yi people’s traditional folk customs is widespread. These plants represented rich cultural diversity, mainly existing in witchcrafts, rites and festivals. A community based study and an extensive field surveys had been carried out. The methods including Key Informant Interviews, Semi structured Interviews and Participatory Observation were adopted in the study. The plants in traditional folk customs used by the Yi people in Liangshan Yi Autonomous Prefecture and their cultural contexts were documented and inventoried. The results showed that there were 102 plant species used in Yi people’s traditional folk customs and expressed diversity and richness in terms of cultural meanings. The plants were used for witchcrafts and rites, social rituals, festive events, including 21 species used in wedding, 24 in funeral, 11 in the adult ceremony, 3 in daily life; 14 in the Torch Festival, 15 in the Yi National new year, 91 in witchcrafts and rites. The folk plants’ cultural meanings are mainly reflected in exorcism, reproductive worship and ancestor worship. The main reasons are that the Yi people advocate ghosts and believe the animism of primitive religion in Lianshan region. The cultures of folk plants are an important component of the natural primary religion and Bimo culture. It is an indispensable part of the traditional culture of the Yi people.     

Huntington’s Disease: The Past,Present, and Future Search for Disease Modifiers

Huntington’s disease (HD) is an autosomal dominant genetic disorder that specifically causes neurodegeneration of striatal neurons, resulting in a triad of symptoms that includes emotional, cognitive, and motor disturbances. The HD mutation causes a polyglutamine repeat expansion within the N-terminal of the huntingtin (Htt) protein. This expansion causes aggregate formation within the cytosol and nucleus due to the presence of misfolded mutant Htt, as well as altered interactions with Htt’s multiple binding partners, and changes in post-translational Htt modifications. The present review charts efforts toward a therapy that delays age of onset or slows symptom progression in patients affected by HD, as there is currently no effective treatment. Although silencing Htt expression appears promising as a disease modifying treatment, it should be attempted with caution in light of Htt’s essential roles in neural maintenance and development. Other therapeutic targets include those that boost aggregate dissolution, target excitotoxicity and metabolic issues, and supplement growth factors.     

Focus: Rare Disease: Differential Diagnosis of a Case of Dercum’s Disease with Possible Familial Involvement and Review of Literature

Dercum’s disease (DD), also described as adiposis dolorosa, is a poorly understood and rare adipose tissue disorder involving obesity and painful adipose tissue masses. Patients may have associated bruising and constitutional symptoms such as fatigue, difficulty concentrating, and sleep disturbance. DD was initially described in 1888 by Francis Xavier Dercum, and was classified into four subtypes, including generalized diffuse, generalized nodular, localized nodular, and juxta-articular subtypes. While this disease has been described for more than 130 years, its etiology and treatment remain elusive. We describe a case of a patient with DD who presented to Ochsner Medical Center, New Orleans, LA, for evaluation of treatment options. We review current knowledge on this rare disease and data on modern treatment methods.     

运动与阿尔茨海默病：基于Tau蛋白翻译后修饰视角的研究述评

阿尔茨海默病（Alzheimer’s disease,AD）是一种与年龄有关的神经退行性疾病,严重危害老年人的身心健康,给社会带来巨大的经济压力。但目前其发病机制尚不完全明确,临床仍无根治的有效方法。Tau蛋白是一种微管相关蛋白质,能够参与维持微管相关结构稳定,具有可溶性且不会聚集。在AD病理状态下,病人脑内Tau蛋白结构和功能异常。异常的Tau蛋白聚集成不可溶的神经纤维缠结,损害微管运输能力,导致病人认知功能障碍。Tau蛋白结构和功能的改变是由多种翻译后修饰过程来调控的,即将特定的化学修饰基团与Tau蛋白N-端或C-端结合,直接改变蛋白质的性质和功能。AD病人脑内Tau蛋白的磷酸化、糖基化、乙酰化及SUMO化等多种翻译后修饰异常,与Tau蛋白的降解和毒性物质的聚集密切相关。本文综述近年来的研究后发现,运动可以通过改善Tau蛋白翻译后的某些异常修饰来预防和改善AD,主要作用方式如下：(1）运动可通过抑制GSK 3β和MAPK等蛋白激酶活性来抑制Tau蛋白的过度磷酸化,可能通过上调PP2A活性来促进Tau蛋白去磷酸化;(2）运动可通过提高GLUT1和GLUT3蛋白质水平,可能通过调节OGA和OGT活性平衡,提高蛋白质O-GlcNAc糖基化水平;(3）运动可能通过AMPK/mTORC1途径抑制p300以及激活SIRT1,降低Tau蛋白乙酰化水平;同时运动还可能通过抑制HDAC6,改善Tau蛋白KXGS基序异常乙酰化程度;(4）运动可能通过调节磷酸化与SUMO化共定位点,改善Tau蛋白异常SUMO化水平。     

Post-translational modifications of Parkinson's disease-related proteins: Phosphorylation,SUMOylation and Ubiquitination

Parkinson's disease (PD) is a neurodegenerative disorder characterized by loss of dopaminergic neurons in the nigrostriatal pathway. The etiology of PD remains unclear and most cases are sporadic, however genetic mutations in more than 20 proteins have been shown to cause inherited forms of PD. Many of these proteins are linked to mitochondrial function, defects in which are a central characteristic of PD. Post-translational modifications (PTMs) allow rapid and reversible control over protein function. Largely focussing on mitochondrial dysfunction in PD, here we review findings on the PTMs phosphorylation, SUMOylation and ubiquitination that have been shown to affect PD-related proteins.     

Focus: Rare Disease: Behçet’s Disease and Pregnancy: A Retrospective Case-control Study

Background: Behçet’s disease (BD) is a rare chronic multisystemic vasculitis of unknown etiology. It is usually diagnosed between the 2^nd and 4^th decades of life, so its association with pregnancy is not unusual. This study aims to characterize the evolution of pregnancy in a group of pregnant women with BD and the impact of this pathology in embryo-fetal morbidity. Methods: A retrospective case-control study included 49 pregnancies in women suffering from BD, followed in our institution. Pregnancy outcomes were compared with a control group of healthy pregnant women. Two controls per case were randomly selected. Statistical analysis used SPSS 25.0, and a p-value of 0.05 was considered statistically significant. Results: Forty-nine pregnancies were included in 27 patients with BD. BD exacerbation occurred in 32.6% of the pregnancies. There were no significant statistical differences between the two groups regarding the rate of preterm delivery, gestational diabetes, and preeclampsia (p>0.05). In the BD group, we found a higher rate of miscarriage (24.5%) and fetal growth restriction (FGR, 13.3%, p<0.05). In the study group, 13 (32.5%) of the pregnant patients did not need treatment. The cesarean rate was significantly higher in the BD group (43.2% vs 20.4% in the control group, p<0.05), and there were no significant differences in median gestational age at the time of delivery (p>0.05). The birth weight of newborns did not differ significantly between the groups. There was no association of BD with maternal morbidity and neonatal complications. Conclusion: In this study, the majority of pregnant with BD did not present clinical exacerbation of their pathology. However, BD may have an adverse influence on pregnancy outcomes. FGR and miscarriage rates were significantly higher in the study group.     

Modelling the functional genomics of Parkinson’s disease in Caenorhabditis elegans: LRRK2 and beyond

For decades, Parkinson’s disease (PD) cases have been genetically categorised into familial, when caused by mutations in single genes with a clear inheritance pattern in affected families, or idiopathic, in the absence of an evident monogenic determinant. Recently, genome-wide association studies (GWAS) have revealed how common genetic variability can explain up to 36% of PD heritability and that PD manifestation is often determined by multiple variants at different genetic loci. Thus, one of the current challenges in PD research stands in modelling the complex genetic architecture of this condition and translating this into functional studies. Caenorhabditis elegans provide a profound advantage as a reductionist, economical model for PD research, with a short lifecycle, straightforward genome engineering and high conservation of PD relevant neural, cellular and molecular pathways. Functional models of PD genes utilising C. elegans show many phenotypes recapitulating pathologies observed in PD. When contrasted with mammalian in vivo and in vitro models, these are frequently validated, suggesting relevance of C. elegans in the development of novel PD functional models. This review will discuss how the nematode C. elegans PD models have contributed to the uncovering of molecular and cellular mechanisms of disease, with a focus on the genes most commonly found as causative in familial PD and risk factors in idiopathic PD. Specifically, we will examine the current knowledge on a central player in both familial and idiopathic PD, Leucine-rich repeat kinase 2 (LRRK2) and how it connects to multiple PD associated GWAS candidates and Mendelian disease-causing genes.     

北部湾涠洲岛水域发现上颌和须板异常的布氏鲸:对保护的启示

2018年初以来,北部湾涠洲岛附近出现了布氏鲸（Balaenoptera edeni）的活动。一头上颌与须板异常的小布氏鲸个体引发热议,其视频在网络上广泛流传。我们在船只调查时,目击该个体10次,其以单独活动为主（90%）,主要出现在涠洲岛到斜阳岛之间的水域,最小凸多边形家域面积为14km2,核心家域面积为166.9km²。然而,在 2019年3月30日我们发现该个体已死亡漂浮在海面,根据尸体腐烂状况来推测,该个体的死亡时间大约为3~5日,死亡原因不明。根据照片和现场解剖分析,推测该小布氏鲸的上颌和鲸须异常可能是被渔网或绳索缠绕导致的。由于无法从外形上确认属于哪一个亚种,因此我们测定了该个体的线粒体DNA D-loop（mitochondrial DNA, mtDNA）和细胞色素b（cytochrome b, Cyt b）基因,分别得到909bp和395bp的序列,经比对和系统发育重建,发现该个体属于近岸分布的小布氏鲸亚种（Eden’s whale, B. e. edeni）。由于小布氏鲸具有一定季节迁移特性,我们无法判断造成其上颌伤害的渔网或绳索是否在中国水域。尽管如此,仍然建议当地部门应加强宣传,减少渔网等海洋垃圾的丢弃和排放,为小布氏鲸营造一个安全的栖息环境。     

Acetylation as a major determinant to microtubule-dependent autophagy: Relevance to Alzheimer's and Parkinson disease pathology

Protein post-translational modifications (PTMs) that potentiate protein aggregation have been implicated in several neurological disorders, including Alzheimer's (AD) and Parkinson's disease (PD). In fact, Tau and alpha-synuclein (ASYN) undergo several PTMs potentiating their aggregation and neurotoxicity.Recent data posits a role for acetylation in Tau and ASYN aggregation. Herein we aimed to clarify the role of Sirtuin-2 (SIRT2) and HDAC6 tubulin deacetylases as well as p300 acetyltransferase in AD and PD neurodegeneration. We used transmitochondrial cybrids that recapitulate pathogenic alterations observed in sporadic PD and AD patient brains and ASYN and Tau cellular models.We confirmed that Tau protein and ASYN are microtubules (MTs)-associated proteins (MAPs). Moreover, our results suggest that α-tubulin acetylation induced by SIRT2 inhibition is functionally associated with the improvement of MT dynamic determined by decreased Tau phosphorylation and by increased Tau/tubulin and ASYN/tubulin binding. Our data provide a strong evidence for a functional role of tubulin and MAPs acetylation on autophagic vesicular traffic and cargo clearance. Additionally, we showed that an accumulation of ASYN oligomers imbalance mitochondrial dynamics, which further compromise autophagy. We also demonstrated that an increase in Tau acetylation is associated with Tau phosphorylation. We found that p300, HDAC6 and SIRT2 influences Tau phosphorylation and autophagic flux in AD. In addition, we demonstrated that p300 and HDAC6 modulate Tau and Tubulin acetylation.Overall, our data disclose the role of Tau and ASYN modifications through acetylation in AD and PD pathology, respectively. Moreover, this study indicates that MTs can be a promising therapeutic target in the field of neurodegenerative disorders in which intracellular transport is altered.     

Neuroprotection by dipeptidyl-peptidase-4 inhibitors and glucagon-like peptide-1 analogs via the modulation of AKT-signaling pathway in Alzheimer’s disease

Alzheimer’s disease (AD) is the most common reason for progressive dementia in the elderly. It has been shown that disorders of the mammalian/mechanistic target of rapamycin (mTOR) signaling pathways are related to the AD. On the other hand, diabetes mellitus (DM) is a risk factor for the cognitive dysfunction. The pathogenesis of the neuronal impairment caused by diabetic hyperglycemia is intricate, which contains neuro-inflammation and/or neurodegeneration and dementia. Glucagon-like peptide-1 (GLP1) is interesting as a possible link between metabolism and brain impairment. Modulation of GLP1 activity can influence amyloid-beta peptide aggregation via the phosphoinositide-3 kinase/AKT/mTOR signaling pathway in AD. The GLP1 receptor agonists have been shown to have favorable actions on the brain such as the improvement of neurological deficit. They might also exert a beneficial effect with refining learning and memory on the cognitive impairment induced by diabetes. Recent experimental and clinical evidence indicates that dipeptidyl-peptidase-4 (DPP4) inhibitors, being currently used for DM therapy, may also be effective for AD treatment. The DPP-4 inhibitors have demonstrated neuroprotection and cognitive improvements in animal models. Although further studies for mTOR, GLP1, and DPP4 signaling pathways in humans would be intensively required, they seem to be a promising approach for innovative AD-treatments. We would like to review the characteristics of AD pathogenesis, the key roles of mTOR in AD and the preventive and/ or therapeutic suggestions of directing the mTOR signaling pathway.     

Neuroinflammation and oxidative stress: Co-conspirators in the pathology of Parkinson’s disease

Parkinson’s disease (PD) is a complex disease, with genetics and environment contributing to the disease onset. Recent studies of causative PD genes have confirmed the involvement of cellular mechanisms engaged in mitochondrial and UPS dysfunction, oxidative stress and apoptosis in the progressive degeneration of the dopaminergic neurons in PD. In addition, clinical, epidemiological and experimental evidence has implicated neuroinflammation in the disease progression. This review will discuss neuroinflammation in PD, with particular focus on the genetic and toxin-based models of the disease. These studies have confirmed elevated oxidative stress and the pro-inflammatory response occurs early in the disease and these processes contribute to and/or exacerbate the nigro-striatal degeneration. In addition, the experimental models discussed here have also provided strong evidence that these pathways are an important link between the familial and sporadic causes of PD. The potential application of anti-inflammatory interventions in limiting the dopaminergic neuronal cell death in these models is discussed with evidence suggesting that the further investigation of their use as part of multi-targeted clinical trials is warranted.     

The use of islands and cluster-randomized trials to investigate vector control interventions: a case study on the Bijagós archipelago,Guinea-Bissau

Vector-borne diseases threaten the health of populations around the world. While key interventions continue to provide protection from vectors, there remains a need to develop and test new vector control tools. Cluster-randomized trials, in which the intervention or control is randomly allocated to clusters, are commonly selected for such evaluations, but their design must carefully consider cluster size and cluster separation, as well as the movement of people and vectors, to ensure sufficient statistical power and avoid contamination of results. Island settings present an opportunity to conduct these studies. Here, we explore the benefits and challenges of conducting intervention studies on islands and introduce the Bijagós archipelago of Guinea-Bissau as a potential study site for interventions intended to control vector-borne diseases.This article is part of the theme issue ‘Novel control strategies for mosquito-borne diseases''.     

Adenovirus 36 improves glycemic control and markers of Alzheimer's disease pathogenesis

Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder worldwide. While the causes of AD are unclear, several risk factors have been identified, including impaired glycemic control, which significantly increases the risk of cognitive decline and AD. In vitro and in vivo studies show that human adenovirus 36 (Ad36) improves glycemic control by increasing cellular glucose uptake in cells, experimental animal models and in humans who are naturally exposed to the virus. This study, tested improvement in glycemic control by Ad36 and delay in onset of cognitive decline in APPswe transgenic mice (Tg2576 line), a model of genetic predisposition to impaired glycemic control and AD. Three-month old APPswe mice were divided into Ad36 infected (Ad36) or mock infected (control) groups and baseline glycemic control measured by glucose tolerance test (GTT) prior to infection. Changes in glycemic control were determined 10- and 24-week post infection. Serum insulin was also measured during GTT. Cognition was determined by Y-maze test, while motor coordination and skill acquisition by rotarod test. Glycemic control as determined by GTT showed less deterioration in Ad36 infected mice over time, accompanied by a significant attenuation of cognitive decline. Analysis of brain tissue lysate showed significantly reduced levels of amyloid beta 42 in Ad36 mice relative to control mice. Golgi-Cox staining analysis also revealed reduced dendritic spines and synaptic gene expression in control mice compared to Ad36 infected mice. This proof of concept study shows that in a mouse model of AD, Ad36 improves glycemic control and ameliorates cognitive decline.     

SORL1 and SIRT1 mRNA expression and promoter methylation levels in aging and Alzheimer’s Disease

Alzheimer’s Disease (AD) is a neurodegenerative disorder and the most common cause of dementia among the elderly. Efforts have been made to understand the genetic and epigenetic mechanisms involved in the development of this disease. As SORL1 (sortilin-related receptor) and SIRT1 (sirtuin 1) genes have been linked to AD pathogenesis, we aimed to investigate their mRNA expression and promoter DNA methylation in post mortem brain tissues (entorhinal and auditory cortices and hippocampus) from healthy elderly subjects and AD patients. We also evaluated these levels in peripheral blood leukocytes from young, healthy elderly and AD patients, investigating whether there was an effect of age on these profiles. The comparative CT method by Real Time PCR and MALDI-TOF mass spectrometry were used to analyze gene expression and DNA methylation, respectively. SORL1 gene was differently expressed in the peripheral blood leukocytes and might act as a marker of aging in this tissue. Furthermore, we found that SORL1 promoter DNA methylation might act as one of the mechanisms responsible for the differences in expression observed between blood and brain for both healthy elderly and AD patients groups. The impact of these studied genes on AD pathogenesis remains to be better clarified.