Fat and water separation in balanced steady-state free precession using the Dixon method.

In this work the feasibility of separating fat and water signals using the balanced steady-state free precession (SSFP) technique is demonstrated. The technique is based on the observation (Scheffler and Hennig, Magnetic Resonance in Medicine 2003;49:395-397) that at the nominal values of TE = TR/2 in SSFP imaging, phase coherence can be achieved at essentially only two orientations (0 degrees and 180 degrees ) relative to the RF pulses in the rotating frame, under the assumption of TR < T2, and independently of the SSFP angle. This property allows in-phase and out-of-phase SSFP images to be obtained by proper choices of the center frequency offset, and thus allows the Dixon subtraction method to be utilized for effective fat-water separation. The TR and frequency offset for optimal fat-water separation are derived from theories. Experimental results from healthy subjects, using a 3.0 Tesla system, show that nearly complete fat suppression can be accomplished.     

实习护生护理程序应用能力的培养

我科开展整体护理以来，将护理程序应用能力作为基础护理技能纳入临床护理教学计划中，提高了实习质量。现将具体做法介绍如下。     

~(125)Ⅰ眼镜蛇毒及抗眼镜蛇毒血清在小白鼠体内分布的比较观察

用氯胺-T法125I标记眼镜蛇毒示踪液及抗眼镜蛇毒血清。小白鼠分二组，用125I-眼镜蛇毒、125I-抗眼镜蛇毒血清分别给小白鼠尾静脉注射，于注射后的不同时间测定血、颈部肌肉、肝、肺、肾、心等脏器放射性分布。结果发现：125I-眼镜蛇毒在肌肉及肝、肺等器官中于注射后2小时过高峰，在肾脏中浓度高，在脑未见放射性分布，抗眼镜蛇毒血清与眼镜蛇毒分布相似但在肌肉及肺脏有更高的分布。证明抗眼镜蛇毒血清能跟踪分布眼镜蛇毒。     

多囊卵巢综合征患者卵巢间质胰岛素样生长因子受体的表达

目的：探讨肥胖及非肥胖多囊卵巢综合征（ＰＣＯＳ）患者卵巢间质胰岛素样生长因子（ＩＧＦ－Ⅰ）受体基因的定量表达。方法：用逆转录基因扩增技术（ＲＴ－ＰＣＲ），检测３５例ＰＣＯＳ患者（肥胖组１５例，非肥胖组２０例）及２０例正常妇女（对照组）卵巢间质细胞ＩＧＦ－Ⅰ受体ｍＲＮＡ的表达量（灰度比值）。并对ＩＧＦ－Ⅰ受体基因ｍＲＮＡ逆转录的ｃＤＮＡ产物进行限制性内切酶酶切分析。结果：ＰＣＯＳ两组ＩＧＦ－Ⅰ受体基因的表达量显著高于对照组，ＰＣＯＳ两组灰度比值为１．１８４±０．２４０，对照组灰度比值为０．９９９±０．０８６（Ｐ＜０．００１）。非肥胖组（１．２３８±０．３８７）明显大于肥胖组（１．０５８±０．１０９，Ｐ＜０．１）。酶切分析证实，３组ＩＧＦ－Ⅰ受体基因扩增片段相同，ＰＣＯＳ两组未发现明显的碱基突变存在。结论：ＰＣＯＳ患者卵巢间质ＩＧＦ－Ⅰ受体基因呈过度表达。且ＰＣＯＳ非肥胖患者局部ＩＧＦ－Ｉ受体表达高于ＰＣＯＳ肥胖患者。     

核桃仁泥外敷治疗肌肉注射后皮下硬结的疗效观察

采用核桃仁泥外敷治疗１３８例（实验组）肌肉注射后皮下硬结，并与４０例（对照组）采用新鲜土豆片外敷硬结法比较。结果表明：实验组患者治疗１５天后Ⅰ度和Ⅱ度硬结治愈率分别为８１．１３％和４２．２５％，总有效率达９２．０３％，明显优于对照组（Ｐ＜０．００１）。     

Distribution of glutathione and glutathione-related enzyme systems in mitochondria and cytosol of cultured cerebellar astrocytes and granule cells

The cellular and regional distribution of glutathione (GSH) and GSH-related enzyme systems involved in cellular defense against reactive oxygen species and electrophilic xenobiotics in the nervous system has been extensively studied. However, little is known about the subcellular distribution of GSH systems in brain tissue and cultured neural cells. The present study investigates the distribution of mitochondrial and cytosolic GSH and GSH-related enzymes in cultured cerebellar astrocytes and granule cells, and compares them with levels in the adult rat cerebellum. Cytosolic GSH levels and cytosolic activities of glutathione reductase (GR), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) in astrocytes were 57, 153, 245, and 92% higher than those found in granule cells, respectively. In contrast, granule cells contained significantly higher mitochondrial GSH levels than astrocytes. Granule cells also demonstrated comparable mitochondria/cytosolic concentrations of GSH and GR, GPX and GST activities to those observed in the cerebellar tissue, whereas ratios in astrocytes were markedly lower. Although in vitro treatments with 100 μM ethacrynic acid depleted both cytosolic and mitochondrial GSH in cultured astrocytes and granule cells in a time-dependent fashion, cellular GSH in granule cells was more resistant to the GSH-depleting agent than astrocytes. These results suggest that although GSH and GSH-related enzymes are abundant in cytosolic compartments of astrocytes, mitochondrial pools are relatively small. Since brain mitochondria are sites of significant hydrogen peroxide generation, the mitochondrial localization of GSH and its associated enzymes in neural cells provide important defenses against toxic oxygen species in the nervous system. Differences in subcellular distribution of GSH systems in individual neural cell types may provide a basis for selective cellular and/or subcellular expression of neurotoxicity.     

Role of granulocyte colony-stimulating factor as adjunct therapy for septicemia in children with acute leukemia

The granulocyte colony-stimulating factor (G-CSF) has been shown to accelerate recovery from severe neutropenia and to decrease the incidence of documented infections after intensive chemotherapy in cancer patients. However, the routine prophylactic use of G-CSF is expensive. This study was conducted to determine the role of G-CSF as adjunct therapy for septicemia following neutropenia caused by chemotherapy in children with acute leukemia. Fifty consecutive episodes of septicemia were studied involving 34 episodes of Gram-negative, 7 episodes of Gram-positive, 5 episodes of polymicrobial bacterial septicemia, one episode of fungemia, and 3 episodes of disseminated fungal infection. In the first 25 episodes, G-CSF was not used (group A). For the next 16 episodes, G-CSF 200 μg per square meter per day subcutaneously was given immediately after the septicemia was documented until the absolute neutrophil count was maintained at more than 1,500 per cubic millimeter (group B). Thereafter, G-CSF at the same dose as that of group B was prophylactically used in all the children who received high-dose cytosine arablnc-side-containing regimens. Nine episodes of septicemia occurred (group C). The incidences of mortality per episode of septicemia in groups A, B, and C were 12.0% (3/25), 12.5% (2/16) and 0% (0/9), respectively. Statistically, there was no difference between the three groups overall and in pair-wise comparisons (all P > 0.5). The durations of G-CSF administration in group B ranged from 6 to 26 days with a median of 12 days and the durations of G-CSF administration in group C ranged from 10 to 23 days with a median of 19 days. With or without G-CSF, there may be no significant difference in the mortality of septicemia following neutropenia caused by chemotherapy in children with acute leukemia.