产舒康颗粒预防产后恶露不绝的临床研究

目的　探讨产舒康颗粒对产后恶露不绝的预防作用。方法　 12 0例产妇随机分为预防组和对照组 (各6 0例 ) ,分别用产舒康颗粒和益母草片治疗 5d,观察产后子宫复旧情况。结果　两组产妇第 1d、第 2d子宫高度间差别均有显著性意义 (P <0 0 5 ) ;两组生理产产妇产后恶露干净的平均时间间差别有显著性意义 (P <0 0 5 ) ,而剖宫产产妇产后恶露干净的平均时间间差别无显著性意义 (P >0 0 5 ) ;两组产妇产后恶露不绝发生率间差别有显著性意义(P <0 0 5 )。结论　产舒康颗粒可促进子宫复旧 ,减少产后恶露 ,加速产妇产后恢复 ,对产后恶露不绝确有预防作用。     

Neuroprotective Properties of Nootropic Dipeptide GVS-111 in in Vitro Oxygen-Glucose Deprivation, Glutamate Toxicity and Oxidative Stress

Argon anoxia and glucose deprivation were used for modeling of ischemic damage in the cultures of cerebellar granule cells. Protective effect of peptide piracetam analogue GVS-111 was demonstrated. GVS-111 prevented neurodegeneration induced by glutamate and oxidative stress. In contrast to GVS-111, piracetam did not attenuate neurocytotoxic effect of glutamate.     

磨积散颗粒冲剂联合FLO方案治疗晚期胃癌临床随机对照研究

[目的]探讨晚期胃癌有效治疗途径.[方法]晚期胃癌49例,对照组23例采用选择常用的FLO方案联合化疗.治疗组24例采用选择常用的FLO方案联合化疗同时加用磨积散颗粒冲剂.[结果]近期疗效治疗组有效率54.17%;对照组好转率47.83%.arnofsky评分比较,治疗组Karnofsky评分好转率62.50%,对照组为52.17%(P<0.05).体力、体重、食欲和癌痛变化变化情况,治疗组好转率、稳定率、进展率均好于对照组(P<0.05).血细胞学主要指标,治疗后两组患者血细胞学主要指标均有不同程度改变,其中WBC、Hb下降明显,尤其在治疗后3月后,单纯化疗的患者各项指标的下降更为显著,两组积分比较(P<0.05).[结论]磨积散颗粒剂能够提高化疗疗效,降低化疗毒副作用,提高生活质量、延长生存期.     

Mastoparan-induced apoptosis of cultured cerebellar granule neurons is initiated by calcium release from intracellular stores

We have recently reported that mastoparan, a peptide toxin isolated from wasp venom, induces apoptosis in cultured cerebellar granule neurons that can be blocked by cholera toxin, an activator of G_s. Measurements of intracellular free calcium concentration ([Ca²⁺]_i) reveal that mastoparan induces a dramatic elevation of [Ca²⁺]_i that is frequently followed by enhanced leakage of fura-2 out of the neurons, suggesting that this rise in [Ca²⁺]_i may be due to a more generalized change in membrane permeability. However, the mastoparan-induced initial elevation of [Ca²⁺]_i is maintained in the absence of extracellular Ca²⁺, suggesting that the rise of [Ca²⁺]_i is from intracellular stores. This conclusion is supported by the observation that depletion of [Ca²⁺]_i stores by pretreatment with either caffeine or thapsigargin attenuates both the rise in [Ca²⁺]_i and cell death induced by mastoparan. Phospholipase C (PLC) inhibitors, neomycin and U73122 block mastoparan-induced increases of [Ca²⁺]_i and protect against neuronal death. Pretreatment with cholera toxin, but not pertussis toxin, reduced the mastoparan-induced rise in [Ca²⁺]_i. Taken together, our data suggest that mastoparan initiates cell death in cerebellar granule neurons by inducing Ca²⁺ release from intracellular stores, probably via activation of PLC and IP₃. A secondary or parallel process results in disruption of plasma membrane integrity and may be ultimately responsible for the death of these neurons by mastoparan.     

Cellular changes in the cerebellar granular layer in AIDS-associated PML*

Six cases of AIDS-associated progressive multifocal leukoencephalopathy (PML) exhibited peculiar cellular changes in the cerebellar granular layer. These cells without discernible cytoplasm showed hypochromatic nuclei about twice as large as those of normal granule cells. They were restricted exclusively to the granular layer and always surrounded PML foci. An astrocytic, leukocytic or macrophage/microglial nature was largely excluded by immunocytochemistry. Human immunodeficiency virus (HIV) antigen p 24 could not be found in these cells and there was no unequivocal detection of JC virus (JCV) DNA and no ultrastructural evidence of papovavirus particles in them. They possibly represent altered cerebellar granule cells abortively or latently infected with JCV.     

The role of matrix metalloproteinases in the morphogenesis of the cerebellar cortex

The morphogenesis of the cerebellar cortex depends on intrinsic genetic programs as well as orchestrated cell-cell/cell-extracellular matrix (ECM) interactions. The matrix metalloproteinase (MMP) family comprises of more than 20 members that catalyze the degradation of all the protein constituents of the ECM. These proteolytic endopeptidases mediate cell-cell/cell-ECM interactions by remodeling the ECM and modulating the activity of membrane-associated receptors. The activity of MMPs is negatively controlled by the tissue inhibitors of metalloproteinases (TIMPs). The MMPs and TIMPs regulate diverse neuronal functions including migration, process extension and synaptic plasticity. MMP-2, -3, -9, membrane type 5-MMP (MT5-MMP), TIMP-1, -2 and -3 are expressed in the developing cerebellum. The spatiotemporal pattern of expression/activity of these enzymes suggests that they play a role in the development of the cerebellar cortex. Blockage of MMP-2/-9 activity by specific inhibitors or blocking antibody, as well as using MMP-9 knock-out mice, clearly establishes that MMP-2/-9 participates in the regulation of morphogenesis of the cerebellum. The potential contributions of these enzymes to granule neuron migration, Purkinje cell dendritogenesis and synaptogenesis are discussed.     

Effects of sleep disruption on rat dentate granule cell LTP in vivo

Sleep frequently fragmented or disrupted for prolonged periods can result in mood changes and impaired mental ability and performance. Sleep deprivation is defined as depriving a person or organism of sleep for various periods of fixed durations. Sleep disruption (SD) occurs when a person is awakened at any time when they would normally be sleeping; sometimes on a schedule but usually unexpectedly. It seems as if any disruption of an entrained sleep pattern can induce learning and memory impairment; and mood changes including irritability and aggression. Because memory is impaired under these conditions several studies have been conducted recently to examine changes in long term potentiation (LTP) in hippocampal brain slices following various periods of sleep deprivation in rats. Results of the present study show clearly that LTP is also decreased following SD but to a greater extent than that observed following sleep deprivation. The purpose of the present study was to measure dentate granule cell LTP in anesthetized rats following 1-, 2-, or 3-day schedules of SD using a modified flower pot procedure. Results showed that a single disruption of 3 h reduced LTP from a normal 38.7-7.6%; that endured for at least 14 h; and 9 h reduced it completely. Easy to handle animals become irritable, hyperactive, and aggressive following SD. Results are discussed in terms of stress related effects of SD and changes in synaptic plasticity.     

Postsynaptic Targets of Type II Auditory Nerve Fibers in the Cochlear Nucleus.

Type II auditory nerve fibers, which provide the primary afferent innervation of outer hair cells of the cochlea, project thin fibers centrally and form synapses in the cochlear nucleus. We investigated the postsynaptic targets of these synapses, which are unknown. Using serial-section electron microscopy of fibers labeled with horseradish peroxidase, we examined the border of the granule-cell lamina in mice, an area of type II termination that receives branches having swellings with complex shapes. About 70% of the swellings examined with the electron microscope formed morphological synapses, which is a much higher value than found in previous studies of type II swellings in other parts of the cochlear nucleus. The high percentage of synapses enabled a number of postsynaptic targets to be identified. Most of the targets were small dendrites. Two of these dendrites were traced to their somata of origin, which were cochlear-nucleus small cells situated at the border of the granule-cell lamina. These cells did not appear to receive any terminals containing synaptic vesicles that were large and round, indicating a lack of input from type I auditory nerve fibers. Nor did type II swellings or targets participate in the synaptic glomeruli formed by mossy terminals and the dendrites of granule cells. Other type II synapses were axosomatic and their targets were large cells, which were presumed multipolar cells and one cell with characteristics of a globular bushy cell. These large cells almost certainly receive additional input from type I auditory nerve fibers, which provide the afferent innervation of the cochlear inner hair cells. A few type II postsynaptic targets—the two small cells as well as a large dendrite—received synapses that had accompanying postsynaptic bodies, a likely marker for synapses of medial olivocochlear branches. These targets thus probably receive convergent input from type II fibers and medial olivocochlear branches. The diverse nature of the type II targets and the examples of segregated convergence of other inputs illustrates the synaptic complexity of type II input to the cochlear nucleus.     

Thiophene is toxic to cerebellar granule cells in culture after bioactivation by rat liver enzymes

Several compounds that are not neurotoxic by themselves can cause toxic effects in vivo after enzymatic bioactivation. Thiophene is an industrial solvent known to produce degeneration primarily of the granule cells in the cerebellum when administered to animals in vivo. The mechanism for thiophene toxicity is not known, although it has been suggested that thiophene metabolism may lead to formation of oxidative intermediates that could function as the ultimate toxicants. In the present work we have used rat cerebellar granule cells (CGCs) in culture combined with rat liver postmitochondrial (S9) fraction as a source of biotransformation enzymes to test the toxicity of thiophene in vitro. The results demonstrate that thiophene is toxic to rat cerebellar granule cells in culture only after biotransformation. Furthermore, the toxic effects were reduced by cytochrome P450 (CYP) inhibitors and by scavengers of reactive molecules (alpha-tocopherol, reduced glutathione, and phenyl-N-tert-butylnitrone). These findings support the hypothesis that thiophene requires metabolism to produce the ultimate toxicant, and that the cytochrome P450 enzyme system is involved in the metabolism.