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小木虫论坛-学术科研互动平台» 学术交流区» 论文翻译 » 论文翻译求助完结子版 » 200BB求助～翻译(截至到11月15日）
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qinnanli

金虫 (初入文坛)

[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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1楼 2009-11-12 09:38:10
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rumin20

木虫 (正式写手)

http://t.sina.com.cn/i/17 .
虽然由血浆棕榈酸酯合成PC的分级合成速率要显著高于由醋酸盐或是葡萄糖重头合成途径，但是由血浆棕榈酸酯合成PC在新生儿中只占到一半。

许多的机制都能刺激肺的表面活性物质的分泌。II型肺泡细胞有β-肾上腺素能受体、能应答β-激动剂增加表面活性物质的分泌。嘌呤类物质，如三磷酸腺苷等是表面活性剂分泌的有效刺激因子，并且可能对出生时其分泌非常重要。机械牵张如肺扩张和过度通气，也与表面活性剂的分泌有关。拉伸运动介导的表面活性物质的分泌增强，阻止了肺泡表面活性物质损失。

激素也在其分泌过程中起重要作用。甲状腺素加速了II型肺泡细胞的分化，并且同时协同合成糖皮质激素，以促进肺的扩张和酰胆碱的合成。不过，在临床实践中一般单独使用糖皮质激素来促使肺细胞的成熟，因为没有研究表明与甲状腺素协同作用时要比单独使用糖皮质激素效果好。
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宠辱不惊，看庭前花开花落；去留无意，观天上云卷云舒！
12楼2009-11-13 19:16:01
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yzhang1986

铁杆木虫 (文坛精英)

优秀版主
有空再说
现在没空
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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。
有空继续。
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7楼2009-11-13 11:57:03
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