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排序方式: 共有251条查询结果,搜索用时 15 毫秒
1.
Michael J. Soares Belinda M. Chapman Takayuki Kamei Toshiya Yamamoto 《Development, growth & differentiation》1995,37(4):355-364
Trophoblast cell differentiation is crucial to the morphogenesis of the placenta and thus the establishment of pregnancy and the growth and development of the embryo/fetus. In the present review, we discuss current evidence for the existence of regulatory genes crucial to trophoblast cell differentiation and placental morphogenesis. The elucidation of regulatory pathways controlling normal differentiation of trophoblast cells will facilitate the identification of sensitive junctures in the regulatory pathways leading to various developmental disorders, including those associated with the initiation of pregnancy, fetal growth retardation and gestational trophoblast disease. 相似文献
2.
Linda Munson Joanna E. Ellington Donald H. Schlafer 《In vitro cellular & developmental biology. Animal》1991,27(1):31-38
Summary Interactions between bovine trophoblastic cell vesicles and bovine endometrial epithelial cells were investigated by light
and electron microscopy and lectin histochemistry in a cell culture model of early blastocyst attachment. Primary lines of
bovine endometrial epithelial cells were polarized by subculturing on substrata and maintaining cultures at the air-medium
interface. Trophoblastic cell vesicles were obtained from elongated Day 14 blastocysts. In co-cultures, trophoblastic cell
vesicles adhered to endometrial epithelial cells through microvillus interdigitation and formation of primitive membrane junctional
complexes. After 3 d in co-culture, a multilayered cellular plaque formed at the trophoblastic cell-endometrial epithelial
cell interface. The type of cells contributing to this local proliferative response could not be identified specifically as
trophoblastic or endometrial cells, and areas of membrane fusion between cells were noted. Ultrastructural features of vesicle
adhesion in cultures were similar to features of conceptus attachment in vivo. Lectins bound to apical membranes of trophoblastic
cells and endometrial epithelial cells in all locations except contact sites between vesicles and endometrial cells. These
findings suggest that local cellular proliferation and membrane fusion between trophoblastic and endometrial epithelial cells
may be early events in conceptus implantation in the cow and these events can be reproduced in culture.
This work was supported by a grant from U.S. Department of Agriculture Animal Health and Disease Program, Washington, DC. 相似文献
3.
J. S. Starreveld A. M. Abdoel J. P. v. Dijk M. J. Kroos H. G. v. Eijk 《Biological trace element research》1992,35(1):55-63
During pregnancy, the mother is faced with an increased food demand. A good example of this increased demand is iron (Fe).
Fe is needed in all growing cells. During pregnancy, the Fe transport to the fetus increases enormously. This amount can easily
induce an Fe deficiency in the mother. Fe suppletion is very important for her, but not for the Fe status of the fetus, which
is protected against Fe toxicity as well as deficiency. The placenta seems to be autonomous in Fe uptake. Likely there is
a regulation mechanism. The human placenta is hemomonochorial. The cell layer of the fetus in contact with the maternal blood
is formed by syncytiotrophoblasts. Fe is transported to the placenta by transferrin. Transferrin binds to a transferrin receptor
on the trophoblast membrane and is internalized via an endocytic pathway. During this cycle, Fe is released from transferrin
and the transferrin-transferrin receptor complex is recycled to the membrane. Isolated trophoblast cells from term placentas
form a syncytium in vitro, and transferrin receptors are expressed. Expression depends on the number of cells in culture,
culture time, the amount of Fe available, and the Fe compound. By regulation of the number of transferrin receptors, trophoblasts
are able to control their Fe uptake. 相似文献
4.
5.
Yuan Lu Yan Dong Yan Zhang Di Shen Xiyao Wang Ruxiu Ge Meihua Zhang Yu Xia Xietong Wang 《Journal of cellular and molecular medicine》2020,24(12):6690-6703
Despite the widespread use of antiplatelets and anticoagulants, women with antiphospholipid syndrome (APS) may face pregnancy complications associated with placental dysplasia. Neutrophil extracellular traps (NETs) are involved in the pathogenesis of many autoimmune diseases, including vascular APS; however, their role in obstetric APS is unclear. Herein, we investigated the role of NETs by quantifying cell‐free DNA and NET marker levels. Live‐cell imaging was used to visualize NET formation, and MAPK signalling pathway proteins were analysed. Cell migration, invasion and tube formation assays were performed to observe the effects of NETs on trophoblasts and human umbilical vein endothelial cells (HUVECs). The concentrations of cell‐free DNA and NETs in sera of pregnant patients with APS were elevated compared with that of healthy controls (HCs) matched to gestational week. APS neutrophils were predisposed to spontaneous NET release and IgG purified from the patients (APS‐IgG) induced neutrophils from HCs to release NETs. Additionally, APS‐IgG NET induction was abolished with inhibitors of reactive oxygen species, AKT, p38 MAPK and ERK1/2. Moreover, NETs were detrimental to trophoblasts and HUVECs. In summary, APS‐IgG‐induced NET formation deserves further investigation as a potential novel therapeutic target in obstetrical APS. 相似文献
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8.
Jean-Jacques Candelier 《Cell Adhesion & Migration》2016,10(1-2):226-235
ABSTRACTThe hydatidiform mole (HM) is a placental pathology of androgenetic origin. Placental villi have an abnormal hyperproliferation event and hydropic degeneration. Three situations can be envisaged at its origin: 1. The destruction/expulsion of the female pronucleus at the time of fertilization by 1 or 2 spermatozoa with the former being followed by an endoreplication of the male pronucleus leading to a complete hydatidiform mole (CHM) 2. A triploid zygote (fertilization by 2 spermatozoa) leading to a partial hydatidiform mole (PHM) but can also lead to haploid and diploid clones. The diploid clone may produce a normal fetus while the haploid clone after endoreplication generates a CHM 3. A nutritional defect during the differentiation of the oocytes or the deterioration of the limited oxygen pressure during the first trimester of gestation may lead to the formation of a HM.In countries with poor medical health care system, moles (mainly the CHM) can become invasive or, in rare cases, lead to gestational choriocarcinomas. 相似文献
9.
ABSTRACTThe establishment of a functional placenta is pivotal for normal fetal development and the maintenance of pregnancy. In the course of early placentation, trophoblast precursors differentiate into highly invasive trophoblast subtypes. These cells, referred to as extravillous trophoblasts (EVTs), penetrate the maternal uterus reaching as far as the inner third of the myometrium. One of the most fundamental functions of EVTs is the transformation of spiral arteries to establish the uteroplacental blood circulation assuring an adequate nutrient and gas supply to the developing fetus. To achieve this, specialized EVT subpopulations interact with maternal immune cells, provoke elastolysis in the arterial wall and replace the endothelial cells lining the spiral arteries to induce intraluminal vascular remodeling. These and other trophoblast-mediated processes are tightly controlled by paracrine signals from the maternal decidua and furthermore underlie an intrinsic cell-type specific program. Various severe pregnancy complications such as preeclampsia or intrauterine growth retardation are associated with abnormal EVT function, shallow invasion, and decreased blood flow to the placenta. Hence a better understanding of human trophoblast invasion seems mandatory to improve therapeutic intervention. This approach, however, requires a profound knowledge of the human placenta, its various trophoblast subtypes and in particular a better understanding of the regulatory network that controls the invasive phenotype of EVTs. 相似文献
10.
Brucella melitensis infection causes acute necrotizing inflammation in pregnant animals; however, the pathophysiological mechanisms leading to placentitis are unknown. Here, we demonstrate that high‐mobility group box 1 (HMGB1) acts as a mediator of placenta inflammation in B. melitensis‐infected pregnant mice model. HMGB1 levels were increased in trophoblasts or placental explant during B. melitensis infection. Inhibition of HMGB1 activity with neutralising antibody significantly reduced the secretion of inflammatory cytokines in B. melitensis‐infected trophoblasts or placenta, whereas administration of recombinant HMGB1 (rHMGB1) increased the inflammatory response. Mechanistically, this decreased inflammatory response results from inhibition of HMGB1 activity, which cause the suppression of both mitogen‐activated protein kinases and nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB) activation. Moreover, neutralising antibody to HMGB1 prevented B. melitensis infection‐induced activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in trophoblasts. In contrast, in vitro stimulation of trophoblasts with rHMGB1 caused activation of NADPH oxidase and increased the production of ROS, which contributes to high bacterial burden within trophoblasts or placenta. In vivo, treatment with anti‐HMGB1 antibody increases the number of Brucella survival within placenta in B. melitensis‐infected pregnant mice but successfully reduced the severity of placentitis and abortion. 相似文献