The Association of Phytoplasma with Stunting, Leaf Necrosis and Witches' Broom Symptoms in Magnolia Plants

In 1999–2000 a severe disease was observed on plants of four Magnolia spp. cultivated in a commercial nursery in Poland. Affected plants showed a progressive loss of vigour, were stunted, and had severely malformed leaves, leaf necrosis and witches' broom. Phytoplasma was detected in magnolias with severe symptoms and in dodder-inoculated Catharanthus roseus seedlings by nested polymerase chain reaction (PCR) assay with primer pair R16F1/R0 followed by universal (rA/fA) and group specific (R16(I)F1/R1) primer pairs which amplified a fragment of phytoplasma 16S rDNA. The PCR products (560 bp or 1.1 kb) of all samples used for restriction fragment length polymorphism analysis after digestion with endonuclease enzymes Alu I and Mse I produced the same profile which corresponded to that of an aster yellows phytoplasma reference strain. Phytoplasma DNA was detected throughout the growing season in roots, stems and young but not mature leaves. Electron microscope examination of the ultra-thin sections of the leaf and stem of diseased magnolias showed collapsed and degenerated sieve tube elements with wall thickening. The reduced lumen of these sieve elements contained numerous vesicles and membrane-bound structures, but no typical phytoplasma cells. This is the first report of aster yellows phytoplasma in magnolia identified by molecular assays.     

陆地棉品种抗黄萎病反应规律的研究

对我国自育的108个陆地棉品种的抗黄萎病性进行了研究。在黄萎病发病期内,对黄萎病发病情况进行连续调查,测定产量、考查产量因素并检测纤维品质。利用因子分析法对陆地棉抗黄萎病反应规律进行分析,得出不同时期的黄萎病病指主要与前后3～5个阶段抗病性有关。病情发展主要由4个主因子决定,且第1、2主因子具有较大的方差贡献率。第1主因子(F1)主要与品种7月26日至8月9日的黄萎病病指有关,第2主因子(F2)主要与品种8月20日至9月4日的黄萎病病指有关。利用因子分析结果将108个品种划分为4个类型,前期抗病性较好而后期发病较快的第Ⅰ类品种,其产量较低,单株结铃数、单铃重、衣分均低于其他3类;纤维品质均较差,纤维长度、整齐度、比强度和马克隆值均较其他3类差。前期和后期病指均较低、发病缓慢的第Ⅱ类则小区产量最高,纤维品质处于平均水平。第Ⅲ类品种前期发病较慢,中期发病较快,具有较高的小区产量,单铃重最高;纤维整齐度、比强度和伸长率好于其他3类品种;前期发病较快,中期发病平缓,后期仍具有较高病指的为第Ⅳ类品种,小区产量较低,单株产量、单株结铃数和衣分较高;其他性状处于中等水平。但研究表明,某一阶段具有的抗病性并不能完全代表品种的抗病性。     

Secretases as therapeutic targets for Alzheimer's disease

Accumulation of amyloid-β (Aβ) is widely accepted as the key instigator of Alzheimer’s disease (AD). The proposed mechanism is that accumulation of Aβ results in inflammatory responses, oxidative damages, neurofibrillary tangles and, subsequently, neuronal/synaptic dysfunction and neuronal loss. Given the critical role of Aβ in the disease process, the proteases that produce this peptide are obvious targets. The goal would be to develop drugs that can inhibit the activity of these targets. Protease inhibitors have proved very effective for treating other disorders such as AIDS and hypertension. Mutations in APP (amyloid-β precursor protein), which flanks the Aβ sequence, cause early-onset familial AD, and evidence has pointed to the APP-to-Aβ conversion as a possible therapeutic target. Therapies aimed at modifying Aβ-related processes aim higher up the cascade and are therefore more likely to be able to alter the progression of the disease. However, it is not yet fully known whether the increases in Aβ levels are merely a result of earlier events that were already causing the disease.     

Mitogenomic phylogeny of the Percichthyidae and Centrarchiformes (Percomorphaceae): comparison with recent nuclear gene-based studies and simultaneous analysis

Delineation of the fish family Percichthyidae (Percomorphaceae) has a long and convoluted history, with recent morphological-based studies restricting species members to South American and Australian freshwater and catadromous temperate perches. Four recent nuclear gene-based phylogenetic studies, however, found that the Percichthyidae was not monophyletic and was nested within a newly discovered inter-familial clade of Percomorphaceae, the Centrarchiformes, which comprises the Centrarchidae and 12 other families. Here, we reexamined the systematics of the Percichthyidae and Centrarchiformes based on new mitogenomic information. Our mitogenomic results are globally congruent with the recent nuclear gene-based studies although the overall amount of phylogenetic signal of the mitogenome is lower. They do not support the monophyly of the Percichthyidae, because the catadromous genus Percalates is not exclusively related to the freshwater percichthyids. The Percichthyidae (minus Percalates) and Percalates belong to a larger clade, equivalent to the Centrarchiformes, but their respective sister groups are unresolved. Because all recent analyses recover a monophyletic Centrarchiformes but with substantially different intra-relationships, we performed a simultaneous analysis for a character set combining the mitogenome and 19 nuclear genes previously published, for 22 centrarchiform taxa. This analysis furthermore indicates that the Centrarchiformes are divided into three lineages and the superfamily Cirrhitoidea is monophyletic as well as the temperate and freshwater centrarchiform perch-like fishes. It also clarifies some of the relationships within the freshwater Percichthyidae.     

龈沟液炎性因子及TSP-1在拔牙正畸患者中的表达情况及发生牙周疾病的影响因素分析

摘要 目的：探讨龈沟液炎性因子及TSP-1在拔牙正畸患者中的表达情况及发生牙周疾病的影响因素。方法：选取我院2020年8月到2023年8月收治的80例拔牙正畸治疗患者进行回顾性分析,分别取所有患者正畸前、正畸后1个月、3个月及正畸结束时的龈沟液样本检测肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）、血小板反应蛋白-1（TSP-1）表达水平。随后依照患者正畸治疗过程中是否患有牙周疾病将其分为牙周疾病组（n=36）及非牙周疾病组（n=44）,对比两组患者正畸前及正畸结束时的TNF-α、IL-1β、IL-6、TSP-1表达水平,对比两组患者一般情况,采用logistics回归模型分析拔牙正畸患者牙周疾病的影响因素。结果：80例拔牙正畸患者中正畸后1个月、3个月 TNF-α、IL-1α、IL-6、TSP-1水平升高,正畸后3个月到正畸结束时TNF-α、IL-1β、IL-6、TSP-1水平趋于平稳,但正畸后1个月、3个月及结束时明显高于正畸前（P＜0.05）;牙周疾病组与非牙周疾病组患者正畸前、正畸后TNF-α、IL-1β、IL-6、TSP-1表达水平对比差异显著,牙周疾病组明显高于非牙周疾病组（P＜0.05）;牙周疾病组及非牙周疾病组患者性别、年龄、BMI对比无明显差异（P＞0.05）,牙周疾病组及非牙周疾病组患者正畸治疗时间、拔牙数量、正畸方式、口腔清洁度对比差异显著（P＜0.05）;logistic回归分析结果表明：TNF-α、IL-1β、IL-6、TSP-1、正畸方式、口腔清洁度为拔牙正畸患者牙周疾病的独立危险因素（P＜0.05）。结论：拔牙正畸患者随着正畸时间延长龈沟液炎性因子及TSP-1水平明显升高,且TNF-α、IL-1β、IL-6、TSP-1、正畸方式、口腔清洁度为拔牙正畸患者牙周疾病的独立危险因素。     

Molecular bases for human complement C7 polymorphisms,C7*3 and C7*4

Complement C7 is one of the components of membrane attack complex (MAC) generated by the terminal complement cascade. C7 protein is polymorphic and most of its polymorphisms have been identified using isoelectric focusing (IEF), which detects protein charge differences. To date, the molecular bases of the polymorphisms detected by IEF have not been determined. In this paper, we describe the structural bases of two C7 IEF-detected polymorphisms, C7*3 and C7*4, both of which are common in Asian populations. C7*3 resulted from substitution of cysteine (Cys) at amino acid residue 106 by charged arginine (Arg; C106R), while charged lysine (Lys) at amino acid residue 398 was replaced by neutral glutamine (Gln; K398Q) in C7*4. As C7*3 is hypomorphic, it is important to study its possible associations with diseases such as immunological disorders and infections. We present genetic bases for this C7 polymorphism, which we determined using polymerase chain reaction (PCR)-based genotyping, a simple and accurate method suitable for large-scale studies.     

Preparation of pure populations of covalently stabilized amyloid β-protein oligomers of specific sizes

Evidence suggests that amyloid β-protein (Aβ) oligomers may be seminal pathogenic agents in Alzheimer's disease (AD). If so, developing oligomer-targeted therapeutics requires an understanding of oligomer structure. This has been difficult due to the instability of these non-covalently associated Aβ assemblies. We previously used rapid, zero-length, in situ chemical cross-linking to stabilize oligomers of Aβ40. These enabled us to isolate pure, stable populations of dimers, trimers, and tetramers and to determine their structure-activity relationships. However, equivalent methods applied to Aβ42 did not produce stable oligomers. We report here that the use of an Aβ42 homologue, [F10, Y42]Aβ42, coupled with sequential denaturation/dissociation and gel electrophoresis procedures, provides the means to produce highly pure, stable populations of oligomers of sizes ranging from dimer through dodecamer that are suitable for structure-activity relationship determination.     

COMPETENCE,PRACTICAL RATIONALITY AND WHAT A PATIENT VALUES

According to the principle of patient autonomy, patients have the right to be self‐determining in decisions about their own medical care, which includes the right to refuse treatment. However, a treatment refusal may legitimately be overridden in cases where the decision is judged to be incompetent. It has recently been proposed that in assessments of competence, attention should be paid to the evaluative judgments that guide patients' treatment decisions. In this paper I examine this claim in light of theories of practical rationality, focusing on the difficult case of an anorexic person who is judged to be competent and refuses treatment, thereby putting themselves at risk of serious harm. I argue that the standard criteria for competence assess whether a treatment decision satisfies the goals of practical decision‐making, and that this same criterion can be applied to a patient's decision‐guiding commitments. As a consequence I propose that a particular understanding of practical rationality offers a theoretical framework for justifying involuntary treatment in the anorexia case.