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Bronchial mucosa congestion and edema are the major performances of patients with unknown hemoptysis under bronchoscope, followed by the neoplasma, 1 hypertrophic and uneven mucosa. The main causes are bronchial lung cancer, bronchitis and tuberculosis.

不明原因咯血患者支气管镜下表现主要为支气管黏膜充血水肿,其次是管腔内新生物形成,黏膜肥厚、凹凸不平,主要病因分别是支气管肺癌、支气管炎性病变和结核。

Results The model showed serious edema, proteinuria, hypoproteinemia, and hyperlipidemia. Podocytes were swollen and mesangial cells developed mild hyperplasia at the end of the fourth week. The nephric tubule atrophied at the end of the eighth week accompanied with adhesion between glomeruli and Bowman's capsule. Glomeruli sclerosis of mild or medium degree was observed at the end of the twelfth week with obvious lymphocyte infiltration in the renal interstitium as well as the formation of collagen fibers.

结果 该模型表现为严重水肿、大量蛋白尿、低蛋白血症和高脂血症;病理学检查显示,4周末肾小球足细胞肿胀,系膜细胞轻度增生;8周末有球囊粘连,肾小管上皮细胞萎缩;12周末部分肾小球节段性轻、中度硬化,间质内有明显灶性淋巴细胞浸润,并有轻度纤维化。

Aching: Acute inflammation is apparent, because cilia state system suffers exciting and contractive be caused by,be, it is system of state of cilia of sex of a kind of convulsion neuralgic, basically be iris and hyperaemia of strut of organization of cilia state system, oedema and noxiousness material stimulation nerve ending place causes cilia state system.

疼痛:急性炎症明显,是由于睫状体受刺激收缩所致,是一种痉挛性睫状体神经痛,主要是虹膜和睫状体组织肿胀充血、水肿和毒性物质刺激睫状体神经末梢所引起。

Electron microscopic examination showed that the spinal cords were normal in group N and A, slight edema of mitochondria and endoplasmic reticulum in group B, loosened fibrous layers in medullary sheath, edema and local degeneration of neuraxis in group C,and shrinkage of nuclear membrane, serious edema of ER, vacuolus change of mitochondria and local demyelination in group D.

电镜结果显示,N组和A组脊髓超微结构正常;B组线粒体、内质网轻度水肿;C组脊髓髓鞘纤维板层结构疏松,轴索肿胀,局灶变性;D组脊髓神经元细胞核膜皱缩,线粒体空泡样变,内质网肿胀严重,局灶性脱髓鞘改变。

Naloxone can carry out its protective function to injuried neurocyte through alleviating neuronal cell apoptosis and hydrocephalus, and the effect was better as early as it used.

纳洛酮可通过减轻神经细胞的凋亡及脑水肿以实现对神经细胞损伤的保护作用,且早期使用效果更佳。

Neuromyelitis Optica ;; Aquaporin 4;; Brain Edema ;; Autoimmunity ;; Immunity, Humoral ;; Immune System ;; Osmotic Pressure ;; Cerebrospinal Fluid ;; Pathology ;; Absorption

视神经脊髓炎;;水孔蛋白4;;脑水肿;;自身免疫;;免疫,体液;;免疫系统;;渗透压;;脑脊髓液;;病理学;;吸收

In addition, since SS could evoke neuronic edema of CNS, and inhibit accumulation of cAMP and influence neuronic depolarization, it is implied that SS plays an role in the damage of CNS neurons.

这一变化规律与血肿大小的发生、发展基本一致,充分说明SS及其mRNA的表达,参与大鼠脑出血的病理生理过程,由于SS具有促发中枢NC水肿的作用,抑制cAMP积聚,影响NC去极化,从而对CNS NC具有损伤作用。

During rat's intracerebral hemorrhage processes, Glu is over released and accumulated in hypothalamus and brain tissues surrounding hematoma, which could induce the opening of 〓 and 〓 ion channels, and evoke cellular-toxic edema. Meanwhile it may also evoke 〓 influx into neurons. It is this 〓 influx that may activate phosphase and proteinase, disrupt protein and cellular skeletons, and further aggravate neuronic damage.

大鼠脑出血过程中Glu在下丘脑及血肿周边脑组织的大量释放和积聚,通过其开放〓离子通道,造成细胞毒性水肿,使〓内流激活磷酸酶和蛋白酶,破坏蛋白质和细胞骨架,加重NC的损伤过程。

It is recently reported that SS and SS mRNA may contribute to the formation of neuronic edema surrounding an intracerebral hematoma, inhibit the assembling of cAMP in neurons, promote regulatory disorders of Growth Hormone , and thus aggravated neuronic injury in intracerebral hemorrhage.

SS(Somatostatin,SS)及其mRNA在CNS及胃肠胰均有广泛分布,是传递脑与胃肠信息联系的重要递质,进年来证明,它们在CNS通过促进血肿周边NC水肿,抑制NC cAMP的积聚,并使生长激素(Growth Hormone,GH)调控失衡加重脑出血对CNS NC的损伤。

The main pathology histology change included liver denaturalization, necrosis, spleen giant cell hyperplasia, lymphocyte necrosis, lung and kidney microthrombus form, small intestine edema, microvascular hyperemia, cerebrum neuronophagia and satellitosis.

主要病理组织学变化为:肝变性、坏死,脾巨细胞增生、部分淋巴细胞坏死,肺充血,肾间质血管微血栓形成,小肠绒毛结构被破坏,固有层水肿,间质微血管充血,大脑噬神经现象和卫星化现象等。

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客人们在卡罗利娜·埃凯家里,举止就文雅一些,因为卡罗利娜的母亲治家很严厉。

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