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qinnanli

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[交流] 200BB求助～翻译(截至到11月15日）

发的篇幅的确比较长，但希望各位虫友能够帮帮忙
声明请您不要拿灵格斯或google翻译的东西给我
提前谢谢好心的人

SP-D. SP-D is a hydrophilic 43 kDa collectin belonging to the
superfamily of collagen containing C-type lectins, and is structurally
similar to SP-A. Produced in Type II alveolar cells, it is also
found in epithelial cells and secretory glands of the gastrointestinal
tract. SP-D plays an important role in the innate immune system by
binding to specific carbohydrate and lipid structures on the surface
of bacteria, viral particles, fungi and protozoa through a calciumdependent
interaction . It has also been thought to have a role
in the control of lung inflammation . The SP-D gene consists of
8 exons spanning >11 kb of DNA located on the long arm of human
chromosome 10 . Levels of SP-D and SP-A are potential markers
for lung maturation because studies of amniotic fluid and lung
tissue have demonstrated increasing levels of SP-D with increasing
gestational age . Transcription of SP-D is regulated by direct
interaction of nuclear factor of activated T cells (NFAT) with TTF-1 .
Metabolism of surfactant
Overview of surfactant metabolism
Pulmonary surfactant is synthesized, assembled, transported
and secreted into the alveolus where it is degraded. It is then recycled
in a highly complex and regulated mechanism. This process is
slower in newborns (especially those born prematurely) than in
adults or those with lung injury.
The rate of synthesis and the half-life of surfactant are influenced
by many factors. Surfactant synthesis and turnover in preterm
infants using stable isotopes of glucose, acetate and
palmitic acid demonstrates that synthesis from glucose to surfactant
phosphatidylcholine (PC) takes approximately 19 h and
reaches a peak at 70 h after labeling. The absolute production rate
of PC is 4.2 mg/kg/day while the half-life is 113 (±25) hours .
The fractional synthesis rate of surfactant PC from plasma palmitate
was significantly higher than that from palmitate synthesized
de novo from acetate or glucose, but only accounted for half of the
total surfactant production in preterm infants .
Surfactant secretion can be stimulated by a number of mechanisms.
Type II cells have beta-adrenergic receptors and respond
to beta-agonists with increased surfactant secretion . Purines,
such as adenosine triphosphate are potent stimulators of surfactant
secretion and may be important for its secretion at birth.
Mechanical stretch such as lung distension and hyperventilation,
have also been found to be involved in stimulating surfactant
secretion. Stretch-mediated enhancement of surfactant secretionduring exercise prevents a loss of alveolar surfactant . Hormones
also play a role in surfactant secretion. Thyroxine accelerates
Type II cell differentiation while acting synergistically with
glucocorticoids to enhance the distensibility of the lung and DPPC
synthesis. However, glucocorticoids alone are used in clinical practice
to induce lung maturity because studies have not shown that
the synergistic effect with thyroxine is greater than the effect
achieved by glucocorticoids alone .
Type II cells, macrophages and the alveolar lining play a major
role in surfactant turnover. Cyclical changes in the alveolar surface
appear to promote conversion of newly secreted, apoprotein-rich,
active surfactant aggregates into protein-poor, inactive forms that
are ready for clearance . Surfactant components are removed
from air spaces through uptake by Type II cells and alveolar macrophages,
with the bulk done by the Type II cells. The phospholipids
are taken up by endocytosis into the Type II cells where they
are recycled and re-secreted, whereas the SPs are recycled back
into the lamellar bodies for re-secretion with surfactant. Surfactant
is also transformed during the cyclic compression and expansion of
alveoli from large, highly surface-active aggregates into smaller,
less active subtypes .
Defects in surfactant metabolism
Defective surfactant metabolism leads to both morbidity and
mortality in preterm and term neonates. In general, defects in surfactant
metabolism occur due to accelerated breakdown of the surfactant
complex by oxidation, proteolytic degradation, and
inhibition . Some inherited surfactant gene defects have
also been implicated.
Respiratory distress syndrome. Respiratory distress syndrome (RDS)
is one of the most common causes of morbidity in preterm neonates.
It occurs worldwide with a slight male predominance .
Patients present shortly after birth with apnea, cyanosis, grunting,
inspiratory stridor, nasal flaring, poor feeding and tachypnea. There
may also be intercostal or subcostal retractions. Radiological findings
include a diffuse reticulogranular ‘‘ground glass” appearance
(resulting from alveolar atelectasis) with superimposed air bronchograms
. The preterm infant who has RDS has low amounts of
surfactant that contains a lower percent of disaturated phosphatidylcholine
species, less phosphatidylglycerol, and less of all the
surfactant proteins than surfactant from a mature lung. Minimal
surface tensions are also higher for surfactant from preterm than
term infants . The diagnosis can be confirmed by biochemical
evidence of surfactant deficiency or pathologically. Lungs of infants
who have died from RDS show alveolar atelectasis, alveolar and
interstitial edema and diffuse hyaline membranes in distorted
small airways . Prenatal corticosteroids and postnatal surfactant
replacement therapy significantly reduce the incidence, severity
and mortality associated with RDS, and surfactant therapy has
become the standard of care in management of preterm infants
with RDS .
Meconium aspiration syndrome. Meconium aspiration syndrome
(MAS) is an important cause of morbidity and mortality from
respiratory distress in the perinatal period and affects an estimated
25,000 neonates in the United States each year .
Meconium staining of the amniotic fluid or fetus is an indication
of fetal distress. Fetal respiration is associated with movement of
fluid from the airways out into the amniotic fluid. However, in
the presence of fetal distress, gasping may be initiated in utero
leading to aspiration of amniotic fluid and its contents, which includes
meconium, into the large airways . Acute lung injury
is characterized by airway obstruction, pneumonitis, pulmonary
hypertension, ventilation/perfusion mismatch, acidosis and hypoxemia.The mechanisms underlying surfactant inactivation by meconium
are not fully understood, but it has been shown that meconium
destroys the fibrillary structure of surfactant and decreases
its surface adsorption rate [50]. MAS is associated with an inflammatory
response characterized by the presence of elevated cell
count and pro-inflammatory cytokines IL-1b, IL-6 and IL-8 as early
as in the first 6 h and significantly decreased by 96 h of life [49].
Phospholipase-A2, (PLA2) present in meconium, has been found
to inhibit the activity of surfactant in vitro in a dose-dependent
manner, through the competitive displacement of surfactant from
the alveolar film [51]. PLA2 is also known to induce hydrolysis of
DPPC, releasing free fatty acids and lyso-PC which damage the
alveolar–capillary membrane and induce intrapulmonary sequestration
of neutrophils [52]. Exogenous surfactant replacement
either as bolus therapy or with a diluted surfactant lung lavage
have been shown to reverse the hypoxemia and reduce pneumothoraces
caused by meconium aspiration, decrease requirement
for extracorporeal membrane oxygenation (ECMO), decrease duration
of oxygen therapy and mechanical ventilation, and reduce the
duration of hospital stays [47,53]. A comparison of various surfactant
treatment regimens in MAS did not find the superiority of one
form of therapy over another, and may be related to the heterogeneous
nature of this form of lung injury [54]. In an underpowered
randomized trial comparing bolus (N = 6) versus surfactant lavage
(N = 7) followed by inhaled nitric oxide, infants receiving surfactant
lavage has significant improvements in oxygenation, decreases
in mean airway pressure, and arterial-alveolar oxygen
tension gradients; however there were no significant differences
in duration of assisted ventilation, nitric oxide therapy, or
hospitalization[55].
Pulmonary hemorrhage. Pulmonary hemorrhage may also be associated
with respiratory distress syndrome (RDS) and can be difficult
to differentiate from it by radiography [46]. It occurs
subsequent to a rise in lung capillary pressure due to the effects
of hypoxia, volume overload, congestive heart failure, or it may
be induced by trauma from mechanical suctioning of the newborn
airway. There is a strong association between significant left to
right ductal shunting and pulmonary hemorrhage in preterm babies
[45,56]. There is a build up of the capillary filtrate in the interstitial
space which can then burst through into the airspaces
through the pulmonary epithelium. Neutrophils are released following
endothelial damage and they, in turn, express proteases,
oxygen free-radicals and cytokines. These free oxygen molecules
damage the Type II cells that produce SPs, thus inhibiting production
of the proteins. Elastase, one of these proteases, damages and
degrades SP-A, thereby inhibiting SP-A mediated surfactant lipid
aggregation and adsorption in vitro [2]. Pulmonary hemorrhage is
also considered a rare adverse event associated with surfactant
replacement therapy [45,46].
Acute respiratory distress syndrome. Acute respiratory distress syndrome
(ARDS) is a significant cause of morbidity and mortality in
all age groups following sepsis, hemorrhage, or other forms of lung
injury. It is defined as a severe form of acute lung injury (ALI) and a
syndrome of acute pulmonary inflammation. ALI/ARDS is characterized
by sudden onset, impaired gas exchange, decreased static
compliance, and by a non-hydrostatic pulmonary edema [57].
Infection is the most common cause of development of ARDS in
children [58]. The lungs appear particularly vulnerable in the first
year of life. Premature neonates with chronic lung disease who develop
viral pneumonia, older children with immune deficiency
syndromes, and those with childhood malignancies are especially
at risk [58].
The hallmark in the pathophysiology of the acute event is an increase
in the permeability of the alveolar–capillary barrier as a result
of injury to the endothelium and/or alveolar lining cells.
Damage to the alveolar Type I cells leads to an influx of proteinrich
edema-fluid into the alveoli, as well as decreased fluid clearance
from the alveolar space. Neutrophils are attracted into the airways
by host bacterial and chemotactic factors and express
enzymes and cytokines which further damage the alveolar epithelial
cells [2]. Type II epithelial cell injury leads to a decrease in surfactant
production, with resultant alveolar collapse.
Four clinical criteria must be met to establish a clinical diagnosis
of ARDS: (i) acute disease onset, (ii) bilateral pulmonary infiltrates
on chest radiograph, (iii) pulmonary capillary wedge
pressure <18 mmHg or absence of clinical evidence of left atrial
hypertension and (iv), ratio between arterial oxygen partial pressure
(PaO2) and the fraction of inspired oxygen (FiO2) <200 [57].
In contrast, patients that meet the first three criteria, but exhibit
a PaO2/FiO2 ratio between 200 and 300, are defined as having ALI.
Despite the introduction of novel treatments, the mortality
from ARDS in the pediatric age group still remains high. Attempts
to treat ARDS with an SP-C surfactant, Venticute (Altana Pharma,
Germany), were ineffective [59]. However, the use of calfactant
(Infasurf) in younger children with ALI was effective in reducing
ventilator days and increasing survival [60].
Pulmonary alveolar proteinosis. Pulmonary alveolar proteinosis
(PAP) is a rare lung disease in which the alveoli fill with PL-rich
proteinaceous material. This substance stains for periodic acid-
Schiff and is nearly identical to surfactant [61]. PAP occurs in three
clinically distinct forms; congenital, secondary and acquired. Congenital
PAP is an uncommon cause of respiratory failure in fullterm
newborns known to be caused by inborn errors of surfactant
protein metabolism . Lysinuric protein intolerance has also
been implicated as a secondary cause of congenital/infantile PAP. Although the specific cellular pathogenesis is unknown, recent
observations in genetically altered mice have led to the speculation
that either absolute deficiency of alveolar cells or hyporesponsiveness
of the alveolar cells to granulocyte-macrophage
colony stimulating factor (GM-CSF) is etiologic to PAP . However,
the role of GM-CSF in congenital PAP is not clear as antibodies
against GM-CSF have not been identified in infants with this condition.
The standard of care is the use of whole lung lavage to relieve
the symptoms . The prognosis for infants with
congenital PAP has been uniformly poor and they die within the
first year of life, despite maximal medical therapy . However,
a recent report also showed successful treatment of congenital
PAP with monthly doses of intravenous Immunoglobulin with
the patient remaining free of respiratory symptoms for more than
3 years .
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qinnanli(金币+200,VIP+0):在这么短的时间内～可以翻译的这么好～这么认真～钦佩 11-15 16:08
SP-D是分子量为43000的亲水性的胶原凝集素，属于含有C类型凝集素的胶原家族，在结构上与SP-A相似。它是由Ⅱ型肺泡细胞分泌产生的，在上皮细胞以及胃肠道分泌腺中也能找到。它在先天性免疫系统中扮演重要角色，即通过依赖钙离子相互作用与细菌、真菌、病毒性颗粒、原生生物表面的特殊碳水化合物和脂质结构结合。一般认为它在肺炎控制上可以发挥一定的作用。它的基因是由于8个外显子构成，其基因大小大于位于人类10号染色体长臂上11kb的DNA。SP-D和SP-A的水平是肺成熟的标志，这是由于有关羊水和肺组织的研究已经证明了SP-D的量随着妊娠期不断增加。SP-D的转录是由激活的T细胞核因子与甲状腺转录因子1的直接相互作用来调节控制。
表面活性剂代谢概述：肺表面活性剂被合成、装配、运输，然后被分泌到肺泡，最后在肺泡里被降解。然后它在一个高度复杂的调控机制下被再利用。与此过程在成人或者肺部受伤的成人体内运行相比，这个过程在新生儿体内，尤其是早熟婴儿体内较慢些。表面活性剂的合成以及它在体内的半衰期受到多种因素的影响。通过应用带有稳定同位素标记的葡萄糖、醋酸盐、棕榈酸，表面活性剂在早熟婴儿体内的合成与更新实验证明了从葡萄糖到卵磷脂的合成过程需要大约70小时才能达到高峰。卵磷脂在体内的生成速率是4.2 mg/kg/day而其在体内的半衰期大约是113 (±25)小时。从血浆棕榈酸盐到卵磷脂的合成速率分数明显高于由葡萄糖或者醋酸盐从头合成的棕榈酸为原料的合成速率，但是前者在早产儿体内合成产物只占其体内卵磷脂总量的一半。表面活性剂的分泌能够被大量机制所刺激。Ⅱ型细胞含有β受体，随着表面活性剂的分泌物逐渐增加，β受体激动剂会得到刺激发生反应。嘌呤，比如三磷酸腺苷ATP，就是表面活性物质分泌的刺激物，可能对刚出生时表面活性物质分泌具有重要的作用。机械张力，比如肺扩张和深度呼吸，已经被发现参与刺激表面活性物质分泌的活动。依靠机械张力来提高表面活性物质分泌，在运动中，可以避免肺泡内该物质的流失。激素对表面活性物质分泌也有一定的作用。甲状腺素可加速Ⅱ型细胞分化，同时在糖皮质激素协同作用下提高肺的膨胀性以及二棕榈酰卵磷脂的含量。但是，糖皮质激素在临床实践中单独用于诱导肺成熟。目前并没有足够的实验证据可以表明糖皮质激素协同甲状腺素的作用大于其自身对肺产生的效应。II型细胞、巨噬细胞以及肺泡衬里层对表面活性物质的更新扮演着重要的角色。在肺泡表面的周期性变化可以促进新产生的富含载脂蛋白具有活性的表面活性物质向易于被清除的无活性形式。表面活性物质的主要成分由II 型细胞和巨噬细胞摄取，在大气中消失。磷脂通过内吞作用重吸收入II 型细胞，进一步在那儿被再利用，从而被重新分泌。而SP系列重吸收入可以再重新分泌此物质的具有多层结构的组织中。表面活性物质也在肺泡不断重复的扩张与收缩运动下发生转换，从高浓度有活性大聚合物到较低活性的亚型。不完全的表面活性物质的代谢会导致早产婴儿以及分娩期的婴儿的发病率和死亡率升高。一般来说，此种情况的发生是由于氧化作用、蛋白水解作用和抑制作用加速了表面活性复合物的降解。除此之外，还有可能是由于一些此种物质的遗传基因缺陷。
呼吸窘迫综合征是一种很常见的早产婴儿发病原因。这种疾病在世界范围内很常见，且以男性居多。患此病的人，从一出生开始就会表现如下症状：窒息、紫绀、打呼噜、吸气性喘鸣、鼻翼煽动、呼吸急促以及营养不足。还有可能伴随着肋间和肋下肌收缩。放射性研究包括肺膨胀下扩散性网状组织粒子的形态学观察。患有此病的早产婴儿含有少量的表面活性物质，这些物质中磷脂种类少、磷脂酰甘油也少、表面活性蛋白成分也相对变少。它体内最小表面张力也比分娩期婴儿体内的张力高。此种现象已经得到表面活性物质缺乏的生化资料的证实。死于此病的婴幼儿的肺扩张不足、肺及组织间隙也发生水肿等。产前皮质类激素以及产后表面活性物质的代替疗法可以显著减少其病的发生率、严重程度和死亡率。此种疗法已经成为了治疗带有此病症的早产婴儿的标准治疗方法。
胎便吸入综合症是产期间呼吸障碍发病的一个很重要的原因。它将导致美国每年将近25000的新生儿发病或者死亡。羊水或胎儿的胎粪变色是胎儿患此病的一种表现。胎儿呼吸与体液从气道流向羊水的过程有关。但是，由于此病症，喘气在子宫内可能就会开始，从而导致羊水和包括胎粪在内的羊水内容物进入大的气管。急性肺损伤具有以下特点：气管闭塞、局部急性肺炎、肺高血症、换气不畅、酸中毒和血氧不足等。胎粪使表面活性物质失活可能的机制还不完全清楚，但是已有资料表明胎粪会破坏其纤维结构，减小其表面吸附速率。胎粪吸入综合症与这样的炎性反应有关：在刚开始6小时细胞数目及促炎症细胞因子IL-1b, IL-6 、IL-8增多；但在随后96小时它们又显著减少。磷脂酶A2存在于胎粪之中，可以抑制体外表面活性物质活性，但此作用具有剂量依赖性，通过竞争性取代肺泡膜上的表面活性物质。它也可以减少二棕榈酰卵磷脂的水解，释放游离脂肪酸和磷脂，释放的这些物质可以破坏肺毛细血管膜并诱导肺内中性粒细胞聚集。外源性替代治疗法已被显示可以逆转肺血氧不足、减少因胎粪吸入引起的自发性胸闷、减少体外膜充氧要求、减小氧气以换气治疗的时间以及减少住院时间。不种表面活性物质的治疗方案比较并不能显示哪一种方案最优越，这可能与治疗的肺损伤形式的复杂性有关。在一个有限的随机实验中，通过吸入含氮氧化物婴幼儿接收表面活性物质的能力显著提高，进一步减少了平均气道压力以及肺动脉血氧张力梯度。但是此实验并没有明显表明使用持续肺换气、使用不断含氮氧化物治疗以及医院住院治疗的差异。肺出血可能有呼吸窘迫综合症有关，且通过放射线照相术也很难将二者区分开来。肺出血可能导致肺毛细血管压力升高，这可能由于缺氧、容积超载和充血性心力衰竭，也有可能由于新生儿气管机械吸入性损伤所致。在从左到右有效的气管分支与早产婴儿肺出血有某种直接的联系。组织间隙的肺毛细血管过滤可能会突然损坏，以致过滤物直接通过肺上皮进入肺泡腔内。中性粒细胞随后被释放，它们反过来表达蛋白酶、含氧自由基和细胞相关因子。这些游离氧分子会破坏II 型细胞，进而抑制产生SP系列化合物，从而抑制蛋白质的产生。弹性蛋白酶会损坏和降解以SP-A媒介的表面活性物质脂质聚集与吸附。肺出血可能被看作表面活性物质替代疗法的一种罕见的不良反应。
急性呼吸窘迫综合症是各种患败血症、出血症和其他形式的肺损伤疾病的不同年龄群体致死率的一个重要的原因。它是一种严重的急性肺损伤，是一种急性肺部炎症损伤综合症。急性肺损伤/急性呼吸窘迫综合症的特点是突然发病、气体交换受损害、静态顺应性减少以及通过力平衡的肺水肿。儿童急性呼吸窘迫综合症的形成的一个普遍原因就是传染。在一周岁时肺极易受伤害。带有慢性肺疾病的早产婴儿会形成病毒性肺炎，患有免疫缺乏症和带有肿瘤的较大的孩子的处境更为危险。急性症状的病理学特点是肺泡与毛细血管壁渗透性的提高，这是由于内皮损伤和（或）肺衬里层细胞损伤。肺泡内I型细胞的损害会导致水肿造成的富含蛋白体液进入肺泡，以及从肺泡腔内体液清除率减小。中性粒细胞被宿主细胞和趋化因子吸引到气管，并表达相应酶和细胞因子，进而损坏肺泡上皮细胞。II 型上皮细胞损伤会导致表面活性物质的生成率减少，最后引起肺泡的塌陷。
建立一个临床诊断急性呼吸窘迫综合症必须满足四个临床标准：1、急性疾病突发准则；2、胸X射线底片上双边肺组织渗透原则；3、肺毛细血管楔压应小于18 mmHg或不存在左心房血压过高；4、动脉血氧分压与吸入氧气分数的比例应小于200。与之相对应的是，只满足前三个条件，但第四个比例值在200与300之间时，此病症被认为是急性肺损伤。尽管引入了新的治疗方法，但是儿童群体里急性呼吸窘迫综合症的死亡率仍然很高。德国阿尔塔纳公司努力尝试用SP-C来治疗此病症，但结果却无效。尽管如此，在患有急性肺损伤的幼儿身上使用calfactant治疗，可以有效减少肺换气天数，增加存活率。
肺泡蛋白沉积症是一种极少见的疾病，患者肺泡内充满了富含蛋白质的物质。此物质用高碘酸-希夫染色法染色后发现，几乎与表面活性物质相似。它在临床上有三种不同的表现形式：先天、中等程度及后天获得性病症。先天性肺泡蛋白沉积是妊娠期满的新生儿呼吸困难的一种少见原因，这是由表面活性蛋白代谢紊乱所致。赖氨酸尿性蛋白耐受不良是导致先天性肺泡蛋白沉积症的又一个原因。尽管特殊的细胞发病机制尚未明确，但是近年来从一般变异小鼠体内实验可以推测出此病症的病因：1、完全缺乏肺泡细胞；2、肺泡细胞对粒-巨噬细胞集落刺激因子的反应应答。但是，粒-巨噬细胞集落刺激因子所扮演的角色在先天性病症中并不明显，由于此种因子的抗体此时在婴幼儿体内并未完全确定。我们所关心的标准是使用对肺完全灌洗来缓解此病症。尽管运用最先进的医疗方法，但是我们目前对患有先天性肺泡蛋白沉积症的婴幼儿预测能力较弱，以致他们会在一年内迅速死去。尽管如此，但是近年来也有证据显示每月静脉注射免疫球蛋白可以成功保持病人三年以上无呼吸困难的症状。
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闲看庭前花开花落。
19楼2009-11-15 14:36:24
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yzhang1986

铁杆木虫 (文坛精英)

优秀版主
有空再说
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4楼2009-11-12 11:04:00
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yehuijian123

铁杆木虫 (职业作家)
太长了，还是自己静下心来看看吧，又什么疑问时再发帖不迟。
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看后回帖是个好习惯!
5楼2009-11-12 13:18:04
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mysky3853

金虫 (小有名气)
人表面活性蛋白D是一种亲水的43千道尔顿胶原凝集素，属于含C型凝集素胶原质家族。它在结构上和人表面活性蛋白A类似。产生于II型齿槽细胞，在上皮细胞，胃和肠壁的分泌腺中也存在。人表面活性蛋白D通过钙的作用结合细菌，轮状细菌，真菌和原生动物表面特殊的糖和脂质结构，在先天免疫系统中起着重要的作用。它还被认为在控制肺炎方面有一定的作用。
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7楼2009-11-13 11:57:03
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