促血小板生成素对预测脑瘫高危儿的意义

目的探讨缺氧缺血性脑病(hypoxia-ischem ia encephalopathy,H IE)胎儿和H IE新生儿血清中促血小板生成素(Thrombopoietin,TPO)水平与脑损伤的关系,为脑瘫(cerebral palsy,CP)高危儿人群进行早期干预提供监测手段。方法收集23例H IE胎儿和34例H IE新生儿血清以及25例正常胎儿和30例正常新生儿血清,34例H IE新生儿包括11例轻度H IE,8例中度H IE和15例重度H IE。采用双抗体夹心ABC-ELISA法检测H IE胎儿组和轻、中、重H IE新生儿组血清中TPO的水平,并与正常胎儿组和正常新生儿组比较。结果H IE胎儿组和H IE新生儿组TPO分别高于正常胎儿组和正常新生儿组(分别P<0.01,P<0.01),重度H IE组TPO低于轻度H IE组(P<0.05)。结论血清TPO水平与H IE所致脑损伤严重程度有关。脐血TPO检测可为脑瘫高危儿人群进行早期干预提供监测手段。     

Glycogen synthase kinase-3beta is involved in the process of myocardial hypertrophy stimulated by insulin-like growth factor-1.

BACKGROUND: Glycogen synthase kinase-3 beta (GSK-3beta) is involved in many cellular processes, such as metabolism, apoptosis, differentiation and proliferation. Insulin-like growth factor-1 (IGF-1), which is well known to have a hypertrophic effect on cardiomyocytes, inactivates (phosphorylates) GSK-3beta in some cell types. The role of GSK-3beta in cardiomyocytes as a negative regulator of cardiac hypertrophy has been recently reported and the present study investigated the role of GSK-3beta in the cardiac hypertrophy of cultivated neonatal rat cardiomyocytes induced by IGF-1. METHODS AND RESULTS: First, the IGF-1 induced signal transduction leading to GSK-3beta in neonatal rat cardiomyocytes was examined. The phosphatidylinositol (PI) 3-kinase/Akt/GSK-3 beta signaling induced by IGF-1 was investigated using inhibitors of PI 3-kinase and Ad AktAA, a dominant negative form of Akt. Furthermore, using Ad MEK DN, a dominant negative form of MEK, it was found that MEK negatively regulates Akt phosphorylation upon IGF-1 stimulation. Next, it was examined whether GSK-3beta acts as a negative regulator in the cardiac hypertrophy induced by IGF-1. Sustained stimulation by IGF-1 caused cardiac hypertrophy in protein synthesis and cellular morphology, and overexpression of unphosphorylatable GSK-3beta (Ad GSK-3beta S9A) repressed these hypertrophic effects of IGF-1. CONCLUSIONS: GSK-3beta may play an important role as a negative regulator of cardiac hypertrophy induced by IGF-1.     

Effect of amyloid peptides on the increase in TrkA receptor expression induced by nicotine in vitro and in vivo

The ability of nicotine to induce a cytoprotective or neuroprotective action occurs through several down-stream mechanisms. One possibility is that the drug increases the expression of tyrosine kinase A (TrkA) nerve growth factor (NGF) receptors. Certain β-amyloid peptides (e.g., Aβ1–42) have been shown to bind with high affinity to α7 nicotinic receptors and thus interfere with a potentially neurotrophic influence. Treatment of differentiated PC-12 cells with nicotine produced a concentration-dependent increase in cell-surface TrkA receptors that occurred concomitantly with cytoprotection. The effect of nicotine was blocked by either of the α7 receptor antagonists α-bungarotoxin (α-BTX) or methyllycaconatine. The cytoprotective action of nicotine also was inhibited by pretreatment with 10–100 nM Aβ1–42. Nicotine also was administered (four injections of 30 μg, spaced evenly over 24 h) to rats by direct injection into a lateral cerebral ventricle. Brain TrkA expression was increased significantly in hippocampus and entorhinal cortex (up to 32% above control), with no changes found in cerebral cortex or hypothalamus. The nicotine-induced increases in TrKA expression in hippocampus and entorhinal cortex were significantly inhibited by 10 μg α-BTX or by 10 nmol Aβ1–42. Therefore, physiologically relevant concentrations of Aβ1–42 can prevent nicotine-induced TrkA receptor expression in brain regions containing cholinergic neurons susceptible to the neurotoxicity associated with Alzheimer’s disease.     

Possible role of cytomegalovirus in the pathogenesis of inflammatory aortic diseases: a preliminary report.

To search for possible evidence of a relationship between human cytomegalovirus and aortic diseases, we examined 41 aortic lesions excised at surgery and 16 aortic tissues obtained at autopsy for the presence of cytomegalovirus DNA, by use of polymerase chain reaction. Cytomegalovirus DNA was present in seven (88%) of eight lesions of inflammatory aortic diseases with periaortic fibrosis, five of six inflammatory aneurysms, and all of two aortic occlusive lesions with inflammation. Cytomegalovirus DNA was detected in 20 (61%) of 33 atherosclerotic aneurysms, whereas it was detected in only five (31%) of 16 autopsy samples that showed neither inflammation nor atherosclerosis. Thus the possibility that cytomegalovirus may play a role in the pathogenesis of inflammatory aortic diseases warrants further attention.     

颈椎肿瘤单侧关节突关节切除后的稳定性重建

目的：探讨颈椎肿瘤单侧关节突关节切除后稳定性重建的方法及效果。方法：对1999—2005年存我院骨科手术治疗且得到随访的18例切除单侧关节突关节的颈椎肿瘤患者的资料进行分析，男10例，女8例；年龄16～72岁，平均46岁。神经根受压表现为主者10例，VAS评分2～8分，平均4．2分；脊髓压迫表现为主者8例．ASIA分级C级5例．D级3例。均采用颈后路患侧关节突关节、侧块切除，完整切除肿瘤组织，其中10例行单侧侧块钢板固定植骨融合，8例行双侧侧块钢板固定植骨融合。结果：随访3—60个月，平均20个月，1例透明细胞癌肺转移患者死亡．余存活无复发。10例神经根受压表现为主者术后疼痛VAS评分0—4分，平均1．6分。8例脊髓压迫表现为主者，5例术前C级者术后C级2例、E级3例，3例术前D级者术后D级2例．E级l例。双侧侧块钢板固定植骨融合者术后3个月4例m现骨性融合（其中1例3个月后失访），6个月7例达到骨性融合，内固定无断裂、松动、移位。无颈椎不稳。单侧侧块钢板固定植骨融合者．1例术后5个月出现颈部疼痛；9例在术后9个月骨性融合；1例12个月时仍未能骨性融合，螺钉松动。结论：颈后路侧块钢板同定植骨融合可以实现颈椎肿瘤单侧关节突关节切除后的颈椎稳定性重建。     

莱菔硫烷对ox-LDL诱导血小板活化的抑制作用

目的：探讨莱菔硫烷（sulforaphane,SFN）对氧化低密度脂蛋白（oxidized low-density lipoprotein,ox-LDL）诱导血小板活化的影响及其可能的分子机制。方法：在体外实验中,将健康人纯化血小板与不同浓度的SFN(1.0、2.5、5.0μmol/L)共同孵育40 min,然后用ox-LDL激活血小板20 min,并检测血小板活化的指标,包括CD62P的表达、胞内血小板因子4(platelet factor4,PF4)和趋化因子配体5(chemokine ligand 5,CCL5)的释放水平。机制上,用Western blot蛋白免疫印迹法检测血小板肉瘤酪氨酸激酶（sarcoma tyrosine kinase,Src）及其下游的脾酪氨酸激酶（spleen tyrosine kinase,Syk）磷酸化水平;用活性氧（reactive oxygen species,ROS）检测试剂盒测定胞内总ROS水平。结果：ox-LDL诱导的血小板CD62P的表达以及PF4和CCL5的释放水平均可被SFN显著抑制（P <0.05）;SFN显著下调ox-LD...     

等速离心训练对肩关节内外旋肌的肌力平衡及神经肌肉控制能力的影响

背景 肩关节内外旋肌肌力失衡会增加肩部运动损伤的风险,研究等速离心训练(IET)能否提高肌力平衡并改善神经肌肉控制能力具有重要的损伤预防意义。目的 探讨IET对健康青年人肩关节内外旋肌的肌力平衡及神经肌肉控制能力的影响。方法 2020年12月至2021年11月在复旦大学附属中山医院招募32例健康青年志愿者为研究对象,随机将其分为试验组(n=16)和对照组(n=16)。试验组接受4周IET,对照组接受4周连续被动运动训练(2次/周)。采用Biodex System 4 Pro多关节等速肌力测试与训练系统(美国Biodex公司)对两组研究对象的优势侧肩关节内、外旋肌群进行训练干预,分别在60(°)/s、120(°)/s速度下进行,干预前1周、干预结束后1周对两组肩关节内外旋肌的功能性比率(FR)、加速时间(AT)和达峰力矩时间(TPT)进行评估并比较。结果 试验组全部完成了4周的训练干预和评估,对照组2例中途退出。最终共30例研究对象数据纳入统计学分析。在60(°)/s和120(°)/s速度下,试验组干预后FR高于对照组(P<0.001),试验组干预后FR高于干预前(配对t检验：t<...     

Major immunoreactive domains of human ribosomal P proteins lie N-terminal to a homologous C-22 sequence: application to a novel ELISA for systemic lupus erythematosus

The aim of this study was to identify immunoreactive domains on human ribosomal P0, P1 and P2 proteins, other than the C-22 peptide, to develop a novel ELISA using a combination of these proteins and to compare this ELISA with one using the C-22 peptide. Human recombinant P0, P1, P2 and mutant P0 lacking the homologous C-22 peptide (N-P0) were produced in bacteria and tested by ELISA and immunoblotting using sera from 48 patients with systemic lupus erythematosus (SLE), 48 with an unrelated inflammatory disorder (Crohn's disease) and 47 healthy controls. ELISA with P0, P1 and P2, premixed at equimolar concentrations, gave higher OD readings than each protein tested individually. Eighteen SLE sera tested positive by ELISA with premixed P0, P1, P2 but only 3 tested positive with the C-22 peptide. Twenty-two SLE sera reacted positively, as determined by immunoblotting, with 5 different P protein combinations: P1P2, P0P1P2, P1, P0P1, P0 and P1. Only sera reactive with all three P proteins reacted with the C-22 peptide, with absent or minimal reactivity with N-P0. Native antigens yielded sensitivity (6/48, 13%) similar to the C-22 peptide assay. An ELISA with premixed P1 and P2 gave higher OD values than the arithmetic means with P1 or P2. Fifteen SLE patients had antibodies to double stranded (ds)-DNA, of which 6 also had antibodies to P0P1P2 by ELISA but 12 reactive with P0P1P2 did not have discernable ds-DNA antibodies. Ribosomal P autoantibodies react mainly with epitopes N-terminal to a homologous C-22 peptide. An ELISA with premixed P0, P1 and P2 has 5-fold greater sensitivity (38%) for SLE than an assay with the conventional C-22 peptide (7%). The combined sensitivity for SLE for antibodies to P0P1P2 and ds-DNA is 56%, higher than C-22 and ds-DNA, 38%. Only one of the SLE patients had neuropsychiatric lupus.