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??Abstract??Objective??To investigate alterations of circulating levels of the inflammatory markers— reflecting brain and adipose tissue inflammation—in the fetal growth restriction??FGR??fetuses and newborns??and explore its possible relation ship with adverse intrauterine development. Methods??Sixty parturients??hospitalized in Shengjing hospital of China Medical University??giving consecutively birth either to 30 appropriate for gestational-age??AGA?? singleton infants ??AGA group ?? or 30 FGR full-term singleton infants ??FGR group????were recruited.Plasm hs-CRP??PAI-1??S100B and leptin levels were determined by enzyme link immune assay??ELISA??in the umbilical cords blood ??UC ?? and venous blood from neonates on postnatal day 1 ??D1?? and day 4??D4??. Results??The birth weight??body length and the body mass index ??BMI?? of the FGR neonates were significantly lower compared with those of AGA group ??P < 0.05??.The leptin levels of UC in the FGR neonates were lower than that in the AGA groups??P < 0.05????and correlated positively with the birth weights and the BMI??P < 0.05??.Plasma hs-CRP levels did not differ significantly at all time points between AGA and FGR groups??P > 0.05??.hs-CRP levels in Umbilical cords blood were significantly decreased when compared with D1 hs-CRP in both AGA and FGR groups ??P < 0.05????and D1 hs-CRP was significantly increasedwhen compared with respective D4 hs-CRP??P < 0.05??.Plasma PAI-1 and S100B levels did not differ significantly at all time points between AGA and FGR groups??P > 0.05????and did not correlated with the birth weights and the BMI. Conclusion??Despite the lower birth weight??BMI and leptin levels in FGRs?? there was no difference for the levels of inflammatory markers hs-CRP and PAI-1 between IUGR and AGA fetuses/neonates.The CRP level in both studied groups fluctuated from fetus to neonate stage might attribute to parturition stress and adaptation recovery.     

Impact of chronic pre-treatment of statins on the level of systemic inflammation and myocardial perfusion in patients undergoing primary angioplasty

Statins have many favorable pleiotropic effects beyond their lipid-lowering properties. The aim of this study was to evaluate the impact of long-term statin pretreatment on the level of systemic inflammation and myocardial perfusion in patients with acute myocardial infarctions. This was a retrospective study of 1,617 patients with acute ST-segment elevation myocardial infarctions who underwent primary percutaneous coronary intervention <12 hours after the onset of symptoms. Angiographic no-reflow was defined as postprocedural Thrombolysis In Myocardial Infarction (TIMI) flow grade ≤2. Long-term statin pretreatment was significantly less common in the no-reflow group (6.2% vs 21%, p <0.001). The serum lipid profiles of the groups were similar (p >0.05 for all parameters). Baseline C-reactive protein levels (10 ± 8.2 vs 15 ± 14 mg/L, p <0.001) and the frequency of angiographic no-reflow (3.9% vs 14%, p <0.001) were significantly lower, and myocardial blush grade 3 was more common (50% vs 40%, p = 0.006) in the statin pretreatment group (n = 306). Moreover, the frequency of complete ST-segment resolution (>70%) (70% vs 59%, p <0.001) and the left ventricular ejection fraction were higher (49 ± 7.5% vs 46 ± 8.3%, p <0.001) and peak creatine kinase-MB was lower (186 ± 134 vs 241 ± 187 IU/L, p <0.001) in the statin-treated group. In conclusion, long-term statin pretreatment is associated with lower C-reactive protein levels on admission and better myocardial perfusion after primary percutaneous coronary intervention, leading to lower enzymatic infarct area and a more preserved left ventricular ejection fraction. This is a group effect independent of lipid-lowering properties.     

家兔颈动脉粥样硬化狭窄简捷模型建立

目的探讨建立简捷、经济实用、稳定可靠的适于颈动脉粥样硬化性狭窄(CASS)的外科治疗研究的家兔CASS动物模型条件。方法新西兰白兔21只,采用3％过氧化氢液灌注动物的双侧颈总动脉,造成氧化应激损伤,然后以特定高脂饲料喂养动物不同时间。评价各组动物血管狭窄程度和病理改变特点。结果8周组和12周组中重度狭窄达到80％,个别血管出现闭塞。4周组轻度狭窄亦达到60％。病理检查证实高脂饲料喂养8周时,动脉的粥样硬化病理改变已属于纤维班快期。结论 按本实验方法,氧化应激损伤后喂养8周的动物颈动脉狭窄程度和病理改变程度已符合CASS外科治疗实验研究需要。     

半枝莲多糖的纯化及对S180荷瘤小鼠的抑瘤作用

目的将半枝莲粗多糖纯化后测定多糖含量,并比较粗多糖与精多糖的抑瘤率,为半枝莲化学及药理研究提供有益的参考。方法采用分光光度法、苯酚-硫酸显色法,在490nm处测定其含量;并利用体内实验测定多糖的抑瘤效果。结果精多糖的多糖含量为54．12％,平均加样回收率为99．66％,粗多糖的抑瘤率为45．96％,精多糖的抑瘤率为22．14％。结论测定多糖含量的方法操作简便,准确可靠,精多糖的抑瘤效果没有粗多糖抑瘤效果明显。     

New insights into the pathoanatomy of spinocerebellar ataxia type 3 (Machado-Joseph disease)

PURPOSE OF REVIEW: This review summarizes recent neuropathological findings in spinocerebellar ataxia type 3 and discusses their relevance for clinical neurology. RECENT FINDINGS: The extent of the spinocerebellar ataxia type 3 related central nervous neurodegenerative changes has been recently systematically investigated in a series of pathoanatomical studies. These studies showed that the extent of the central nervous degenerative changes of spinocerebellar ataxia type 3 has been underestimated so far. The newly described pattern of central nervous neurodegeneration includes the visual, auditory, vestibular, somatosensory, ingestion-related, dopaminergic and cholinergic systems. These pathological findings were correlated with clinical findings and explain a variety of the spinocerebellar ataxia type 3 symptoms observed in clinical practice. SUMMARY: Systematic pathoanatomical analysis of spinocerebellar ataxia type 3 brains helps to understand the structural basis of this neurodegenerative disease and offers explanations for a variety of disease symptoms. This better understanding of the neuropathology of the condition has implications for the treatment of spinocerebellar ataxia type 3 patients and represents a basis for further biochemical and molecular biological studies aimed at deciphering the pathomechanisms of this progressive ataxic disorder.     

Spinocerebellar ataxia 2 (SCA2)

Spinocerebellar ataxia type 2 (SCA2) is an autosomal dominantly inherited, neurodegenerative disease. It can manifest either with a cerebellar syndrome or as Parkinson’s syndrome, while later stages involve mainly brainstem, spinal cord and thalamus. This particular atrophy pattern resembles sporadic multi-system-atrophy (MSA) and results in some clinical features indicative of SCA2, such as early saccade slowing, early hyporeflexia, severe tremor of postural or action type, and early myoclonus. For treatment, levodopa is temporarily useful for rigidity/bradykinesia and for tremor, magnesium for muscle cramps, but neuroprotective therapy will depend on the elucidation of pathogenesis. The disease cause lies in the polyglutamine domain of the protein ataxin-2, which can expand in families over successive generations resulting in earlier onset age and faster progression. Genetic testing in SCA2 and other polyglutamine disorders like the well-studied Huntington’s disease is now readily available for family planning. Although these disorders differ clinically and in the affected neuron populations, it is not understood how the different polyglutamine proteins mediate such tissue specificity. The neuronal intranuclear inclusion bodies described in other polyglutamine disorders are not frequent in SCA2. For the quite ubiquitously expressed ataxin-2, a subcellular localization at the Golgi, the endoplasmic reticulum and the plasma membrane, in interaction with proteins of mRNA translation and of endocytosis have been observed. As a first victim of SCA2 degeneration, cerebellar Purkinje neurons may be preferentially susceptible to alterations of these subcellular pathways, and therefore our review aims to portray the particular profile of the SCA2 disease process and correlate it to the specific features of ataxin-2.