柱前衍生化HPLC法测定黄河滩枣多糖的单糖组成

目的建立PMP(1-苯基-3-甲基-5-吡唑啉酮)柱前衍生化HPLC法测定黄河滩枣多糖的单糖组成。方法采用水提醇沉法提取黄河滩枣多糖,多糖水解后进行PMP衍生化,HPLC法测定黄河滩枣多糖的单糖组成及摩尔比,并对等度和梯度洗脱两种模式的测定结果进行分析比较。结果黄河滩枣多糖由D-甘露糖、L-鼠李糖、D-半乳糖醛酸、D-葡萄糖、D-半乳糖、L-阿拉伯糖等六种单糖组成,它们的摩尔比约为0.54∶0.50∶0.27∶2.03∶5.40∶1.00,等度和梯度洗脱测定结果基本一致。结论本实验改进的等度洗脱方式更加简便易行,快速准确,适用于黄河滩枣多糖的单糖组成分析。     

Thalamic cholinergic innervation is spared in Alzheimer disease compared to parkinsonian disorders

There are two major sources of cholinergic projections in the brain. The nucleus basalis of Meynert provides the principal cholinergic input of the cortical mantle and the pedunculopontine nucleus–laterodorsal tegmental complex (PPN–LDTC; hereafter referred to as PPN) provides the major cholinergic input to the thalamus. Cortical cholinergic denervation has previously been shown to be part of Alzheimer and parkinsonian dementia but there is less information about subcortical thalamic cholinergic denervation. We investigated thalamic cholinergic afferent integrity by measuring PPN–Thalamic (PPN–Thal) acetylcholinesterase (AChE) activity via PET imaging in Alzheimer (AD), Parkinson disease without dementia (PD), Parkinson disease with dementia (PDD) and dementia with Lewy bodies (DLB). AD (n = 13; mean age 75.4 ± 5.5), PD (n = 11; age 71.4 ± 6.4), PDD (n = 6; age 70.8 ± 4.7), DLB (n = 6; age 68.0 ± 8.6) and normal controls (NC; n = 14; age 69.0 ± 7.5) subjects underwent AChE [¹¹C]-methyl-4-piperidinyl propionate (PMP) PET imaging. PPN–Thal PET data were analyzed using the Nagatsuka method. There were no significant differences in mean age between the groups (F = 1.86, p = 0.134). Kruskal–Wallis testing demonstrated a significant group effect for PPN–Thal AChE hydrolysis rates (F = 9.62, p < 0.0001). Compared to NC, reduced thalamic k3 hydrolysis rate was noted in subjects with PDD (−19.8%; AChE k3 hydrolysis rates 0.1072 ± 0.0143 min⁻¹), DLB (−17.4%; 0.1103 ± 0.0112 min⁻¹) and PD (−12.8%; 0.1165 ± 0.0114 min⁻¹). Each of these 3 subgroups was statistically different from AD subjects (−0.7%; 0.1326 ± 0.0095 min⁻¹) who showed relatively spared thalamic k3 hydrolysis rates which were comparable to NC (0.1336 ± 0.0142 min⁻¹). Thalamic cholinergic denervation is present in PD, PDD, and DLB but not in AD. Neurodegenerative involvement of thalamic cholinergic afferent projections may contribute to disease-specific motor and cognitive abnormalities.     

Comparison of polysaccharides from different Dendrobium using saccharide mapping

Multiple species of Dendrobium are widely used as Shihu, a well known Chinese herb, for medicinal purpose in China. Small molecules such as phenols, alkaloids and coumarins are obviously varied in different species of Dendrobium. But there are few reports on polysaccharides, one of major active components, from Dendrobium. In this study, polysaccharides from different species or locations of Dendrobium were compared using saccharide mapping. The results showed that polysaccharides of Dendrobium from different species or locations were obviously varied in spite of they had some similar characters, which is helpful to control the quality of Dendrobium.     

IL-11调控 gp130/JAK2/STAT3信号通路促进Wistar大鼠雪旺细胞中PMP22的表达

目的:探索白介素-11对大鼠雪旺细胞分泌髓鞘蛋白的调节作用及相关机制。方法:取成年Wistar大鼠坐骨神经,分离纯化培养雪旺细胞。加入重组大鼠白介素-11,分别采用realtime RT-qPCR和Western boltting检测雪旺细胞髓鞘蛋白的表达情况,进一步检测IL-11调控髓鞘蛋白表达的相关通路的激活情况。结果:Realtime RT-qPCR和Western boltting结果均提示白介素-11可以显著提高雪旺细胞中周围神经髓鞘蛋白22的表达水平,而对雪旺细胞中髓鞘碱性蛋白和髓鞘蛋白零的表达水平则没无明显影响,该生理作用可被JAK特异性抑制剂AG490所抑制。在经过IL-11处理的SCs 细胞中可以观察到pJAK2（Y1007＋Y1008）和pSTAT3（Y705）含量明显高于对照组且伴随着SCs中gp130表达的上调。结论:白介素-11可通过调剂gp30/JAK2/STAT3信号通路以促进雪旺细胞中周围神经髓鞘蛋白22的表达。     

Recent advances in understanding the roles of blood platelets in the pathogenesis of allergic inflammation and bronchial asthma

Platelets play an essential role in hemostasis to minimize blood loss due to traumatic injury. In addition, they contain various immune-associated molecules and contribute to immunological barrier formation at sites of vascular injury, thereby protecting against invading pathogens. Platelets are also crucially involved in development of allergic diseases, including bronchial asthma. Platelets in asthmatics are more activated than those in healthy individuals. By using a murine asthma model, platelets were shown to be actively involved in progression of the disease, including in airway eosinophilia and airway remodeling. In the asthmatic airway, pathological microvascular angiogenesis, a component of airway remodeling, is commonly observed, and the degree of abnormality is significantly associated with disease severity. Therefore, in order to repair the newly formed and structurally fragile blood vessels under inflammatory conditions, platelets may be continuously activated in asthmatics. Importantly, platelets constitutively express IL-33 protein, an alarmin cytokine that is essential for development of bronchial asthma. Meanwhile, the concept of development of allergic diseases has recently changed dramatically, and allergy researchers now share a belief in the centrality of epithelial barrier functions. In particular, IL-33 released from epithelial barrier tissue at sites of eczema can activate the antigen-non-specific innate immune system as an alarmin that is believed to be necessary for subsequent antigen-specific acquired immunological responses. From this perspective, we propose in this review a possible mechanism for how activated platelets act as an alarmin in development of bronchial asthma.     

Wrist drop in an arcade dancing game: Unusual sudden bilateral radial palsy

Bilateral simultaneous radial palsy is uncommon, and the few cases reported in the literature are due to compressive injuries, such as in the use of axillary crutch or birthing bar during labor. We present a patient who developed a severe bilateral palsy after playing in a dancing simulator machine. The patient's position during the game was a combination of wrist extension, elbow flexion, retroversion of arms and a degree of minor torsion of both upper limbs. This mechanism has not been reported as a cause of neuropathic damage. An underlying neuropathy was suspected, and most acquired causes of neuropathy were excluded. A sequence analysis showed a novel point mutation in NM_000304.3(PMP22):c.83G>A (p.Trp28Ter), an heterozygous pathogenic variant. Hereditary neuropathy with liability to pressure palsies is an autosomal dominant disorder characterized by recurrent painless entrapment neuropathies; no case of bilateral simultaneous radial paralysis has been reported previously.     

Review: Pathology and Its Clinical Relevance of Mucinous Appendiceal Neoplasms and Pseudomyxoma Peritonei

Until recently, many classifications existed for the terminology and histopathologic classification of appendiceal mucinous neoplasms, mucinous appendiceal adenocarcinomas, and pseudomyxoma peritonei (PMP). A major accomplishment was achieved by consensus-based histopathologic classifications on behalf of the Peritoneal Surface Oncology Group International regarding mucinous appendiceal tumours and PMP. As different classifications were used over the years and also owing to the rare nature of these tumors, many clinicians are not familiar with the terminology and the impact on patient management. Hence, an overview concerning mucinous appendiceal neoplasms, mucinous appendiceal adenocarcinomas, and PMP is provided to serve as an introduction into the basic morphology of these tumors with tentative recommendations for management.     

Detection of hereditary neuropathy with liability to pressure palsies among patients with acute painless mononeuropathy or plexopathy

Hereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal dominant disorder characterized by recurrent mononeuropathies or brachial plexopathies, commonly associated with a chromosome 17p11.2-12 deletion encompassing the peripheral myelin protein-22 (PMP22) gene. We tried to identify criteria distinguishing HNPP among patients with acute painless mononeuropathy/plexopathy. We investigated by pulsed-field gel electrophoresis the presence of the deletion in 27 patients with isolated or recurrent acute painless mononeuropathy or brachial plexopathy, and no obvious cause of neuropathy. Eight patients carried the deletion, whereas 19 had neither the deletion nor mutations in the PMP22 gene. Age at onset, presenting modality, precipitating events, and rate of recovery did not significantly differ in the two groups. Family history was informative for HNPP diagnosis in 3 cases only. HNPP patients more often showed recurrent episodes, brachial plexopathy, and clinical or electrophysiologic involvement of other nerves. Non-HNPP patients more frequently had peroneal palsy, recent weight loss, and normal electrophysiologic examination in other nerves. Signs of generalized neuropathy and evidence of disease in other family member are often subtle in HNPP and must be thoroughly investigated in patients with acute painless mononeuropathy/plexopathy. © 1998 John Wiley & Sons, Inc. Muscle Nerve 21: 1686–1691, 1998.     

Improved culture methods to expand schwann cells with altered growth behaviour from CMT1A patients

A duplication of the gene for myelin protein PMP22 is by far the most common cause of the hereditary demyelinating neuropathy CMT1A. A role for PMP22 in cell growth in addition to its function as a myelin protein has been suggested because PMP22 is homologous to a gene specifically upregulated during growth arrest. Furthermore, transfected rat Schwann cells overexpressing PMP22 show reduced growth. In addition, abnormal Schwann cell differentiation has been described in nerve biopsies from CMT1A patients. To analyse whether the duplication of the PMP22 gene in CMT1A neuropathy primarily alters Schwann cell differentiation and to exclude nonspecific secondary responses, we improved human Schwann cell culturing. This allowed us long-term passaging of human Schwann cells with unchanged phenotype, assessed by expression of different Schwann cell markers. Subsequently we established Schwann cell cultures from CMT1A nerve biopsies. We find decreased proliferation of Schwann cells from different CMT1A patients in all passages. We also demonstrate PMP22 mRNA overexpression in cultured CMT1A Schwann cells. We conclude that decreased proliferation in cultured Schwann cells that carry the CMT1A duplication indicates abnormal differentiation of CMT1A Schwann cells. The identification of an abnormal phenotype of CMT1A Schwann cells in culture could possibly lead to an in vitro disease model. GLIA 23:89–98, 1998. © 1998 Wiley-Liss, Inc.