SEARCH · PubMed Health

Results for “Fetal Development”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources

PubMed1985

Erythroid progenitor cells and stimulating factors during murine embryonic and fetal development.

Murine embryonic and fetal yolk-sacs, peripheral blood, and livers were assayed for hemopoietic multipotential and progenitor cell content between days 6 and 13 of gestation. Multipotential cells (Mix-CFC), erythroid-committed progenitor cells (BFU-E), and nonerythroid progenitor cells (predominantly GM-CFC) were assayed by their ability to form hemopoietic colonies in vitro when stimulated by pokeweed-mitogen-stimulated spleen-cell-conditioned media (as a source of Multi-CSF) and either human or murine erythropoietin. Late erythroid progenitor cells (CFU-E) were stimulated to form colonies by erythropoietin. Mix-CFC, BFU-E, and nonerythroid cells were first detected on day 8 in yolk-sacs, day 9 in peripheral blood, and day 11 in liver. Maximum absolute numbers of yolk-sac Mix-CFC (182), BFU-E (331), and non-erythroid CFC (1358) occurred at 11 days of gestation. The maximum frequency of peripheral blood mix-CFC (24/10(5) cells) and BFU-E (55/10(5) cells) occurred at ten days of gestation. The absolute numbers of hepatic Mix-CFC, BFU-E, nonerythroid CFC, and CFU-E increased exponentially from 11 to 13 days' gestation. CFU-E were first detected at nine days in peripheral blood, at ten days in yolk-sac, and 11 days in liver and at all ages were equally responsive to erythropoietin. The maximum frequency (151/10(5) cells) of CFU-E in the peripheral blood and the maximum number per yolk-sac (1699) both occurred on day 11 of gestation. In confirmation of previous studies, yolk-sac fluid was found to contain a macrophage colony-stimulating activity. In addition, an activity capable of stimulating fetal liver CFU-E was also detected in yolk-sac fluid. However, no activity (Multi-CSF) capable of stimulating Mix-CFC or BFU-E was detected in either yolk-sac fluid or fetal plasma.

Animals↗

PubMed2006

Magnetic resonance imaging of embryonic and fetal development in model systems.

We give an overview of the applications and methods of high-resolution anatomical magnetic resonance imaging (MRI) in the study of embryonic and fetal development in animal models. Challenges associated with performing in utero studies are described. Recent in utero images in mouse and in nonhuman primates are presented. Results using magnetic resonance microscopy in fixed mouse embryos and in amphibian embryos in vivo are reviewed. We discuss how studies of pregnancy in animal models aid in the translation of innovative new MRI techniques to clinical applications.

Animals↗

PubMed2006

Effects of a Streptococcus equi infection--mediated nutritional insult during mid-gestation in primiparous Thoroughbred fillies. Part 1: placental and fetal development.

REASONS FOR PERFORMING STUDY: There is a paucity of information on factors that influence placental development in the horse. HYPOTHESIS: Changes in nutrition, particularly around the time of proliferative placental growth, can affect development of the placenta and fetal growth. OBJECTIVE: To investigate the effects of 2 planes of nutrition and an unforeseen infection-mediated nutritional insult on placental and fetal development in the mare. METHODS: Twenty maiden Thoroughbred fillies, age 3 or 4 years, mated to one Thoroughbred stallion, were maintained on either High or Moderate food intake throughout pregnancy. In mid-gestation all the mares unexpectedly became infected with Streptococcus equi and suffered varying degrees of weight loss as a consequence. Gross and stereological measurements of the placenta and measurements of foal birthweight, crown-rump length, ponderal index and plasma IGF-1 concentration were made at term. RESULTS: Gains in bodyweight during gestation were significantly higher in the High vs. the Moderate nutrition groups. Placental and fetal growth parameters were not influenced by the plane of nutrition. However, transient weight loss in mid-gestation from acutely reduced food intake resulted in morphological changes to the allantochorion and decreased foal birthweight. CONCLUSIONS: Excessive weight gain during gestation in maiden Thoroughbred fillies does not result in nutrient partitioning to the dam at the expense of the fetus. However, sudden weight loss in mid-gestation has detrimental effects on placental development which results in reduced fetal growth. POTENTIAL RELEVANCE: Clinicians should appreciate the likely effects of maternal infection and resulting weight loss on pregnancy outcome.

Animal Nutritional Physiological Phenomena↗

PubMed2001

Extensive tissue-specific variation of allelic methylation in the Igf2 gene during mouse fetal development: relation to expression and imprinting.

The imprinted Igf2 gene is active only on the paternal allele in most tissues. Its imprinting involves a cis-acting imprinting-control region (ICR) located upstream of the neighboring and maternally expressed H19 gene. It is thought that differential methylation of the parental alleles at the ICR is crucial for parental imprinting of both genes. Differentially methylated regions (DMRs) have also been identified within the Igf2 gene and their differential methylation is thought to be established during early development. To gain further insight into the function of these DMRs, we performed a quantitative analysis of their allelic methylation levels in different tissues during fetal development and the postnatal period in the mouse. Surprisingly, we found that the methylation levels of Igf2 DMRs vary extensively during fetal development, mostly on the expressed paternal allele. In particular, in skeletal muscle, differential allelic methylation in both DMR 1 and DMR 2 occurs only after birth, whereas correct paternal monoallelic expression is always observed, including in the embryonic stages. This suggests that differential methylation in the DMR 1 and DMR 2 of the Igf2 gene is dispensable for its imprinting in skeletal muscle. Furthermore, progressive methylation of the Igf2 paternal allele appears to be correlated with concomitant postnatal down-regulation and silencing of the gene. We discuss possible relations between Igf2 allelic methylation and expression during fetal development.

Age Factors↗

PubMed2006

In utero exposure to phthalates and fetal development.

The diesters of benzene-1,2-dicarboxylic (phthalic) acid, commonly known as phthalates, are a family of industrial compounds, primarily used as plasticizers in enormous quantities for a variety of industrial uses in the formulation of plastics. Di-(2-ethylhexyl) phthalate (DEHP) is the most commonly used plasticizer. These plasticizers are not covalently bound to the polymer and leach out into the environment, thus becoming ubiquitous environmental contaminants. Cumulating evidence points out on the adverse effects of phthalate exposure during intrauterine life. Recently, it has been documented that in utero phthalate exposure is associated with a shorter duration of pregnancy. Phthalates induce and activate a subset of peroxisome proliferator-activated receptors (PPARs) and have an intrinsic pro-inflammatory activity, while some natural PPAR agonists induce cyclooxygenase (COX)-2 expression. To this regard, COX-2 is thought to be overexpressed in chorioamnionitis (CA), a fetal systemic inflammatory response syndrome and a leading cause of preterm birth. An adequate maternal dietary intake of essential fatty acids, well known anti-inflammatory agents, is indispensable to fetal development. Recently, it has been shown that phthalates alter the placental essential fatty acids (EFAs) homeostasis so potentially leading to abnormal fetal development. Likewise, a possible down-regulation of COX-2 by omega-3 fatty acids has been suggested. As a consequence, maternal supplementation with omega 3 during pregnancy could counteract the adverse effects of phthalates exposure in the human fetus. Here, we analyze the existing evidence on the link between antenatal phthalate exposure and abnormal fetal development, as well as on possible therapeutic tools to fight the adverse effect of this exposure.

Animals↗

PubMed1998

Fetal development of Leydig cell activity in the mouse is independent of pituitary gonadotroph function.

During fetal development the testes secrete anti-Mullerian hormone and testosterone to induce formation of the male phenotype. Adult Leydig cells secrete testosterone under the control of LH, but the role of the fetal pituitary in regulating fetal Leydig cell function is unclear. To study the early relationship between pituitary and Leydig cell function, we have examined the development of fetal pituitary LH levels and Leydig cell function in normal mice and in hypogonadal (hpg) mice that lack GnRH and, thus, circulating gonadotropins. In normal and hpg mice, pituitary LH content was barely detectable until embryonic day 17 (E17), when levels began to increase significantly in both groups. Pituitary levels of LH in hpg mice were, however, only about 10% of normal at all ages. Full-length LH receptor transcripts were first detectable in fetal testes on E16 in both normal and hpg mice. In normal mice, levels of testicular messenger RNA (mRNA) encoding cytochrome P450 side-chain cleavage and 17alpha-hydroxylase increased from E13 to reach a peak around birth. In hpg mice, levels of mRNA encoding these enzymes were normal until around birth, at which time there was a significant decline. Levels of testicular mRNA encoding 3beta-hydroxysteroid dehydrogenase type I were similar in normal and hpg mice and showed little change during development. Intratesticular testosterone reached a peak on E18 in normal animals before declining again after birth. In hpg mice, intratesticular testosterone levels were normal throughout fetal development and on the day of birth, but were barely detectable by postnatal day 5. Results show 1) that fetal Leydig cell function in the mouse is normal in the absence of endogenous circulating gonadotropins; 2) that Leydig cells become dependent on gonadotropins shortly after birth; and 3) that pituitary LH synthesis can start in the absence of GnRH but is dependent on LH for a normal level of synthesis and secretion.

Animals↗

PubMed1981

Estimation of gestosis of pregnancy (EPH-gestosis), relationship between fetal development and gestosis index.

Gestosis index score at delivery was compared with factors reflecting the fetal development in a series of 95 patients with EPH-gestosis collected in Okayama University Medical School in 1975-1979. The prediction of small for date (SFD) was performed by means of multivariate analysis of 10 variables, i.e. gestosis index, maternal body weight, height, uterine fundal length, abdominal circumference, maternal age at delivery and urinary estriol within one week prior to delivery. The result was that gestosis index was as useful as uterine fundal length in predicting SFD. The more gestosis index score increased, the more markedly the fetal development ws disturbed. Especially in the cases with scoring above 4 and in those with hypertension and proteinuria, the incidence of SFD increased obviously. No correlation between gestosis index and neonatal asphyxia was noticed. From the growth pattern of uterine fundal length and BPD, intrauterine growth retardation (IUGR) in pregnancy with EPH-gestosis occurred mainly within the third trimester of pregnancy. The functional development of the fetus with EPH-gestosis was evaluated with the use of urinary estriol level and fetal heart rate (FHR) monitoring. In the cases with EPH-gestosis scoring above 4, extreme disturbance of functional development of the fetus was observed.

Female↗

PubMed1997

Cyclooxygenase-2 is expressed in bladder during fetal development and stimulated by outlet obstruction.

Studies were undertaken to assess expression of inducible cyclooxygenase (COX)-2 in bladder during fetal development and COX-1 and COX-2 expression after outlet obstruction. Bladder tissue or bladder progenitor tissue was harvested from CD-1 murine embryos at embryonic days 11.5 (E11.5), E14.5, E17.5, E20.5 (newborn), and from adult. Bladder obstruction was created in adult female mice by ligating the urethra, and bladders were harvested after 3-24 h of obstruction. Gene expression was assessed by semiquantitative reverse transcription-polymerase chain reaction and Western blotting. COX-2 was highly expressed at the early stages of bladder development and declined progressively throughout gestation. In adult bladder, both COX-1 and COX-2 were detectable at low levels under basal conditions. An approximately 30-fold increase in COX-2 mRNA was seen after 24 h of obstruction. In contrast, COX-1 did not change with obstruction. COX-2 mRNA levels peaked at 6 h of obstruction. In regional bladder-distention models, COX-2 induction was confined to the area of distention. Bladder outlet obstruction stimulates COX-2 expression dramatically, reactivating a gene that is highly expressed during fetal development.

Animals↗

PubMed1980

Measurement of euglobulin fibrinolysis time in women with retarded fetal development. The effect of the clamping and step tests on plasminogen activator activity.

The effects of two experimental stimuli, clamping of the cubital vein and exercise (step test), on the euglobulin lysis time of women with retarded fetal development (92 cases), with physiologic pregnancy (50 cases) and non-pregnant women (20 cases) were studied. Both tests resulted in a pronounced shortening of euglobulin lysis time in the non-pregnant and to a lesser extent in the physiologic pregnancy cases (statistically significant after clamping of the cubital vein, statistically insignificant after the step test). In the etiologically heterogeneous group of pregnancy with retarded fetal development the response to both stimuli was weaker in comparison with the normal pregnancy group, and in many cases (58.7%) even "paradoxical", that is, instead of a rise in fibrinolytic activity, a fall was observed. These results indicate that in women with retarded fetal development fibrinolytic activity of the blood doses not rise as readily as it does in normal pregnancies. This applies both to local response (clamping test) and systemic response (step test), and is probably due to a fall in the plasminogen activator content of the venous vessel walls. As a working hypothesis, it is presumed that insufficiency of the plasminogen activator activity system facilitates the accumulation of fibrin deposits in the uterine--placental blood circulation, and contributes to retardation of intrauterine fetal growth.

Exercise Test↗

PubMedDate not supplied

Regional myocardial glucose utilization by developing fetal and maternal hearts.

Regional glucose utilization of the developing fetal feline heart was assessed during three stages of gestation and compared with the maternal heart and non-pregnant controls. The specific aims were to determine: 1) if glucose utilization by the whole heart changes from early to late gestation; 2) if there are differences in glucose utilization by specific regions of the heart; 3) if these regional differences in glucose utilization are consistent throughout gestation. Regional myocardial glucose utilization was measured using the [14C] 2-deoxyglucose high spatial resolution autoradiographic technique. Eleven fetal and 16 adult hearts were studied. Two of the fetuses were at 49 days of gestation, three were at 35 days, and six were at 25 days of gestation. This was the first study to assess regional myocardial glucose utilization in the developing fetus. Glucose utilization by the fetal heart was greater than that seen in the normal control adult or maternal heart, and was highest during early gestation. The posterior wall of the left ventricle had glucose utilization twice that measured for the anterior wall. Other regions were not significantly different. This information indicates that availability of glucose to the fetus is important for normal cardiac metabolism and development.

Animals↗

PubMed1994

Vitamin C deficiency causes hematological and skeletal abnormalities during fetal development in swine.

The influence of maternal vitamin C deficiency on fetal development was studied in swine with a hereditary lack of ability to synthesize ascorbic acid (OD pigs). Thirteen pregnant sows homozygous (od/od) for the defect were depleted of ascorbic acid for 24 to 38 d at various stages of gestation. Six normal (OD/OD) sows were used as controls. Only a few experimental sows showed clinical symptoms of vitamin C deficiency. Nevertheless, severe pathological changes were seen in the uterus and fetuses. Characteristic findings were hemorrhages and hematomas in both fetal and maternal placenta, and general edema and subcutaneous hemorrhages in the fetuses. Similarities were noted to the abruptio placentae syndrome in women. Depletion of vitamin C resulted in a pronounced decline in ascorbic acid concentration in most maternal and fetal organs as well as in plasma and embryonic fluids. No morphological malformations were found in the fetuses, but the ossification of the skeleton was severely deranged. Macroscopically the lesions comprised swelling of the costochondral junction and separation of the epiphysial cartilage from the spongiosa in ribs and limb bones. Another characteristic finding was loosening of the periost from the cortex, often resulting in subperiosteal bleedings. Microscopically normal osteoblasts were few and the formation of osteoid defective.

Animals↗

PubMed1999

Glucose transporter expression in developing fetal lungs and lung neoplasms.

Glucose uptake and metabolism are essential for proliferation and survival of cells, and are supposed to be enhanced in actively proliferating cell systems such as embryonic and cancer tissues. Glucose uptake is usually carried out through glucose transporters. In the developing fetal lung, metabolism of glucose is thought to be an important process in cell proliferation, differentiation and maturation. Active glucose uptake could result in accumulation of glycogen in epithelial cells, and utilization of glycogen could be a critical phenomenon for lung epithelial development. In hamsters, although facilitative glucose transporter isoform 1 (GLUT1) and isoform 4 (GLUT4) are not detected in adult lungs, expression of them is detected with immunohistochemical and Western blot analyses in the developing fetal lungs. In human lung carcinomas, GLUT1 expression is seen in most cases of lung carcinoma, and is seen especially frequently in squamous cell carcinoma. GLUT1 expression in adenocarcinoma of the lung is correlated with reduced cell differentiation, larger tumor size and positive lymph node metastasis. A few cases of lung carcinoma show positive staining for GLUT3 and GLUT4. Thus, expression of some facilitative glucose transporter isoforms is detected in developing fetal epithelium and in lung carcinomas. Overexpression of them could enhance uptake of glucose into these cells, and the increased influx of glucose could be involved in active cell proliferation, which is a common character of the developing lung epithelium and carcinoma.

Animals↗

PubMed1997

[Studies on teratogenic effects of aluminum on intra uterine fetal development in mice].

Effects of oral administration of different doses of aluminum during pregnancy on intra uterine fetal development in mice were studied with experimental teratological methods. Results showed that over-intake of aluminum could lead obvious teratogenic and toxic effects on fetal development in mice. It could cause formation of encephalocele and dysostosis, intra uterine fetal growth retardation, and increase of embryo death rate, with a obvious dose-dependent relation. It suggests that excessive ingestion of aluminum may be one of the risk factors contributing to congenital neural tube defects, intra uterine fetal growth retardation and perinatal deaths.

Aluminum↗

PubMed1989

Expression of ras oncogene p21 during human fetal development as determined by monoclonal antibodies RAP-5, Y13-259, and DWP.

In this report we describe the expression of the ras proto-oncogene p21 protein in various tissues during normal fetal development. Conventional, formalin fixed and paraffin-embedded sections of normal organs were examined from fetuses ranging 9 to 42 weeks of gestation. Immunohistochemical localization of ras p21 was accomplished using the broadly reactive, mouse monoclonal antibodies RAP-5 and Y13-259. The monoclonal antibody DWP, which is specific for a mutated form of ras p21 having a valine/cysteine at amino acid position 12, was also used. Detectable expression of the p21 protein was seen at different time periods during fetal development depending on the tissue. The expression of ras p21 (as detected by RAP-5 and Y13-259) was noted in a wide range of cell types and tissues; intense immunostaining was noted in epithelial cells of the gastrointestinal tract, exocrine and endocrine pancreas, renal tubules and transitional urotheliem, as well as in other tissues. This immunostaining generally, but not invariably, corresponded with patterns previously reported in benign and/or malignant neoplasms of adult tissues. In most instances ras p21 expression, when present, occurred during periods of rapid growth in given organ systems. However, some actively proliferating fetal tissues such as thymus and spleen, failed to express detectable ras p21 suggesting that factors other than cell cycle may influence its expression. No reactivity with DWP was noted in any of the tissues, suggesting that the mutated forms detected by this monoclonal antibody are not expressed during normal human embryogenesis. These data show that there is regulated expression, and broad distribution of this gene product in normal developing human fetal tissue.

Antibodies, Monoclonal↗

PubMed2004

Secretory immune system in human embryonic and fetal development: joining chain and immunoglobulin transport (Review).

The role of joining (J) chain, one of the protein components of the secretory immune system (SIS), in the immune reactions of the human embryo and fetus was analyzed on the basis of data from the literature and our previous studies. All organs and structures, including extra-corporeal ones, of 18 embryos (4-8 weeks of development) and 45 fetuses (9-38 weeks) were studied using methods of pathomorphology, immunohistochemistry and morphometry. This approach enabled us to analyze the problem in the whole organism throughout its embryonic and fetal development. J chain, as well as polymeric immunoglobulin (Ig) receptor-secretory component (pIgR/SC) and Igs, are already widely distributed in 4-week-old embryos before the appearance of the common immune system. The whole complex of protein components of the SIS was seen in mucous layers, and in blood-tissue and tissue-tissue barrier structures. Therefore, we can consider two parts of the SIS: mucosal and barrier. Already in embryos, an increase in the functional activity of the SIS following massive antigenic attack in cases of acute chorioamnionitis reflects the increased exocrine secretion of Igs. The J chain appears to participate in the endocytosis but not exocytosis of Igs. J chain and Igs, but not pIgR/SC, were present in cells of the heart, endocrine glands, gonads and some other organs. The exocrine secretion of Igs, the main function of the SIS, is absent in these organs, and, they are therefore, not considered part of the SIS.

Embryonic Development↗

PubMed1989

Effects of eflornithine hydrochloride (DFMO) on fetal development in rats and rabbits.

Eflornithine hydrochloride (DFMO) is a highly selective, enzyme-activated, irreversible inhibitor of the enzyme L-ornithine decarboxylase (ODC). Because of its role in the biosynthetic pathway of polyamines, ODC is essential for the growth and development of newly implanted embryonic tissue. In order to assess its effect on embryonic growth and fetal development, at various stages of gestation, DFMO was administered in the drinking water to pregnant rats and rabbits at several concentrations (from 0.03% to 3.0%) and times (from days 7, 10, or 11 through days 18 or 19). Rats were killed on day 21 and rabbits on day 29 of pregnancy (day 1 = day of insemination), and the implantations and fetuses were examined. At a concentration of 1.0% (approximately 1,270 mg/kg/day) in rats and 3.0% (approximately 915 mg/kg/day) in rabbits, maternal food and water consumption and body weight gain were significantly reduced during the treatment period, and all implantations were aborted or resorbed. At lower doses (approximately 200-600 mg/kg/day) fetuses survived to term, though in reduced numbers, and a marked reduction in average fetal weight was seen. At levels of 60 mg/kg/day or lower, there were no deleterious effects to the dams or their offspring. Few malformations were detected at any dose level by gross teratologic examination; nor were any considered to have been drug induced because of their sporadic incidence. The embryotoxicity and severe growth retardation demonstrated by these studies verify that adequate polyamine levels are essential for normal embryonic and fetal development.

Abnormalities, Drug-Induced↗

PubMed2002

Fetal development of the first metatarsophalangeal joint complex with special reference to the intersesamoidal ridge.

In most individuals, plantar to the first metatarsal head, a more or less well developed crest separates the two furrows for the medial and the lateral sesamoid bones. In some instances, the absence of this crest has been observed in a previous study. This observation may be related to a pathological and/or an ontogenetic development. For the present examination, we have assumed the ontogenetic hypothesis. Twenty-two feet were examined at different developmental stages from week 12 to 38. The feet were prepared for examination using methods of plastination-histology. Sesamoids have already developed from the joint capsule by the first stage (12th week). Attachment bundles of collagenous fibers have deeply penetrated the cartilage of the sesamoids on their capsular side. Only some inner fibers of the muscular tendons join the sesamoids on their plantar side. The intersesamoid ligament is blended into the synovial tendon sheath of the flexor hallucis longus. The plantar crest has already developed in the fetal cartilage of the first metatarsal head as a strong ridge. With further growth, the surfaces become inwardly tapered on both sides of the ridge through the sesamoid bones, so that in the end the ridge results in a more or less clear crest. If the tapering of the furrows for the sesamoid bones proceeds too briskly or too far, this can result in an absence of the plantar crest. If the absence of this crest stands in relation to the formation of a Hallux valgus, this result would be a first indication of an developmentally based cause for this wide-spread disease of the foot.

Embryonic and Fetal Development↗

PubMed1999

Structure-function analyses of thrombomodulin by gene-targeting in mice: the cytoplasmic domain is not required for normal fetal development.

Thrombomodulin (TM) is a widely expressed glycoprotein receptor that plays a physiologically important role in maintaining normal hemostatic balance postnatally. Inactivation of the TM gene in mice results in embryonic lethality without thrombosis, suggesting that structures of TM not recognized to be involved in coagulation might be critical for normal fetal development. Therefore, the in vivo role of the cytoplasmic domain of TM was studied by using homologous recombination in ES cells to create mice that lack this region of TM (TMcyt/cyt). Cross-breeding of F1 TMwt/cyt mice (1 wild-type and 1 mutant allele) resulted in more than 300 healthy offspring with a normal Mendelian inheritance pattern of 25.7% TMwt/wt, 46.6% TMwt/cyt, and 27.7% TMcyt/cyt mice, indicating that the tail of TM is not necessary for normal fetal development. Phenotypic analyses showed that the TMcyt/cyt mice responded identically to their wild-type littermates after procoagulant, proinflammatory, and skin wound challenges. Plasma levels of plasminogen, plasminogen activator inhibitor 1 (PAI-1), and alpha2-antiplasmin were unaltered, but plasmin:alpha2-antiplasmin (PAP) levels were significantly lower in TMcyt/cyt mice than in TMwt/wt mice (0.46 +/- 0.2 and 1.99 +/- 0.1 ng/mL, respectively; P <.001). Tissue levels of TM antigen were also unaffected. However, functional levels of plasma TM in the TMcyt/cyt mice, as measured by thrombin-dependent activation of protein C, were significantly increased (P <.001). This supported the hypothesis that suppression in PAP levels may be due to augmented activation of thrombin-activatable fibrinolysis inhibitor (TAFI), with resultant inhibition of plasmin generation. In conclusion, these studies exclude the cytoplasmic domain of TM from playing a role in the early embryonic lethality of TM-null mice and support its function in regulating plasmin generation in plasma.

Animals↗