Abnormal IgG galactosylation in MRL-lpr/lpr mice: pathogenic role in the development of arthritis

MRL-lpr/lpr (MRL/lpr) mice spontaneously develop arthritis by an increase in the incidence of agalactosylated oligosaccharides in serum IgG, similar to rheumatoid arthritis patients. However, whether this association has a pathogenic significance is still unknown. In this study, we analyzed the oligosaccharide structure of serum IgG in various MRL mice with or without arthritis, to clarify the relationship between the oligosaccharide abnormality and the development of arthritis. The level of agalactosylation in serum IgG was comparable in both arthritis-free MRL/lpr and MRL-+/+ (MRL/+) mice at 6 weeks of age. In contrast, the incidence of IgG lacking galactose markedly increased in MRL/lpr mice at 6 months of age (the age at which arthritis occurred), compared with that from age-matched MRL/+ mice without arthritis. However, the proportion of agalactosylated IgG increased similarly in anti-CD4 monoclonal antibody-treated MRL/lpr mice at 6 months of age, despite the absence of the development of arthritis, because of depletion of CD4+ T cells. These results suggest that the abnormality in IgG galactosylation of MRL/lpr mice developed in an age-dependent manner, but it did so independently of CD4+ T cell-dependent B-cell activation and is not a consequence of the development of arthritis.     

衰老时海马神经元树突的可塑性增生

用形态计量的方法对老年(30个月)和成年(17个月)大鼠脑(Golgi染色标本)的海马CA3区锥体细胞的树突分支进行分级计数和测量了终末支的长度。结果是CA3神经元基树突和顶树突共有9级分支,衰老时第4级和第9级分支有显著的增多(P<0.02,P<0.03)。基树突终末支的长度衰老时无明显改变,顶树突终末支长度较成年组增加(P<0.05)。提示衰老时海马神经元的树突仍具有一定的增生和分化能力。这可能是对神经元退变的一种代偿机制。     

大鼠心冠状动脉系统神经肽Y年龄变化的免疫组织化学研究

运用免疫组化ＡＢＣ法对不同月龄ＳＤ大鼠心脏冠状动脉及其分支含神经肽Ｙ神经纤维的分布及其衰老变化作了详细观察．结果表明：左、右冠状动脉及其各级分支具有丰富的神经肽Ｙ能神经分布．在冠状动脉主干及其较大分支上，神经纤维较稠密，主要呈环状或网状分布，在血管围周形成较多束、丛、网，并伸入血管壁内形成壁内的神经网络分布．部分神经纤维的游离末梢有穿过血管内膜伸向腔面的迹象．在细小的冠状动脉分支上，神经纤维密度减低，主要沿血管长袖是纵向分布．两侧冠状动脉系统神经肽Ｙ能纤维分布形式及密度没有差别．老龄组动物，左、右冠状动脉及其分支的神经肽Ｙ能纤维密度趋于下降，纤维变细，呈断续状，膨体数量减少，免疫染色变浅、此外，在心内发现了神经肽Ｙ能神经节．     

Altered structural proteins in plaques and tangles: What do they tell us about the biology of Alzheimer''s disease?

The progressive dysfunction and loss of neurons in Alzheimer's disease (AD) is accompanied by marked structural changes in innumerable neuronal cell bodies and neurites, particularly in limbic and association cortices. Qualitatively indistinguishable neuronal lesions occur in much smaller numbers during normal aging. Highly insoluble paired helical filaments (PHF) and antigenically related straight filaments accumulate in perikaryal tangles and the neurites of neuritic plaques. In addition, PHF antibodies reveal the presence of PHF antigens in many individual cortical neurites not clustered into discrete plaques. Recent studies in several laboratories indicate that altered forms of the microtubule-associated phosphoprotein, tau, are important constituents of PHF. Other neuronal cytoskeletal proteins, particularly microtuble-associated protein 2 and neurofilament, have also been associated with PHF. In contrast, the extracellular amyloid filaments found in the centers of many neuritic plaques and in cortical and meningeal vessels appear to be composed of hydrophobic low molecular weight protein(s) distinct from PHF. A major question for further study regards the cellular origin and role of microvascular amyloid in the degeneration of neurites of multiple neurotransmitter specificities in AD cortex. The widespread neuritic and perikaryal alterations in brain tissue are likely to represent, at least in part, the morphological substrate of cortical dysfunction in AD.     

3D facial morphometry in Italian patients affected by Aicardi syndrome

Aicardi syndrome (AIC) is a rare congenital neurodevelopmental disorder of unknown etiology, that affects almost exclusively females, originally characterized by corpus callosum agenesis, chorioretinal lacunae, and infantile spasms. The current diagnostic criteria also include qualitative facial features (prominent premaxilla, upturned nasal tip, decreased nasal bridge angle, sparse lateral eyebrows, and microphthalmia) that still need quantification. A three‐dimensional (3D) photogrammetric assessment of 11 Italian females, age 7–32 years, who satisfied AIC criteria, was performed. Linear distances and angles were computed from soft‐tissue facial landmarks coordinates. The z‐score values were calculated using data of 850 healthy reference females matched for age and compared by Mann–Whitney test (p < .01). Patients showed a shorter philtrum and right side orbital height (mean z‐scores: ?1.7, ?0.9), shorter superior, middle, and inferior facial depths (mean z‐scores: ?1.3, ?2.2, ?2.3), and a smaller length of mandibular ramus (mean z‐score: ?2.1); conversely, they showed larger nasal and lower facial widths, and lower facial convexity (mean z‐scores: 1.7, 1.4, 2.4). The inclinations of the orbit versus the true horizontal were increased bilaterally (mean z‐scores: 1.8, 1.1). Some common facial abnormalities were quantified in AIC patients using a noninvasive instrument. They may help clinicians in performing a definite AIC diagnosis in atypical or doubt cases.     

正常人表皮细胞老化过程中生物学特性研究

目的　研究表皮细胞体外增殖与老化规律 ,为选择合适的组织工程化皮肤种子细胞提供依据。方法　取正常年轻人表皮细胞进行传代培养 ,以不同代龄细胞为实验对象 ,采用形态学观察、群体倍增时间(PDT)、免疫细胞化学及 β 半乳糖苷酶染色等一系列方法 ,检测表皮细胞老化规律。 结果　体外单层培养 9代 ,P2 (第 2代 )的PDT最短 ,前 5代增殖能力较强 ,P5(第 5代 )以后PDT明显延长 ,P8细胞不再增殖 ;随着细胞的连续传代培养 ,SA β Gal表达呈现从弱 (在年轻细胞中占 9% )到强 (在老化细胞中占 6 5 % )的趋势。 结论　体外培养第 1～第 5代表皮细胞可作为构建组织工程化皮肤的种子细胞。     

Age-associated endocrine dysfunctions and approaches to their correction

This review discusses age-specific functional changes in different components of the endocrine system (pituitary, epiphysis, adrenals, and gonads), their role in aging and age-specific diseases, and possible approaches to correction of endocrine disorders and prevention of accelerated aging.     

Estrogen stimulates neuronal plasticity in the deafferented hypothalamic arcuate nucleus in aged female rats

The hypothalamic arcuate nucleus (ARCN) was examined ultrastructurally 3 weeks after the complete deafferentation of the medial basal hypothalamus (MBH) with the island isolation technique in ovariectomized aged female rats (720-930 days of age). The mean numbers of axodendritic and axosomatic synapses in the ARCN decreased to about one-third of those in the intact controls. However, the treatment with estradiol benzoate (2 micrograms/day) during the 3 weeks following the day of brain surgery brought about a marked increase in the numbers of these synapses. The data suggest that the ARCN neurons of aged female rats still retain plasticity to react to deafferentation under influences of estrogen.