Association between Placental Malaria and Severe Pre-Eclampsia in Two University Hospitals of Yaounde City

Context: Pre-eclampsia and placental malaria, are two diseases that share pathophysiological similarities, such as placental ischemia, endothelial dysfunction and production of pro-inflammatory cytokines. Objective: The objective of our study was to investigate the association between placental malaria lesions and severe pre-eclampsia. Methodology: We conducted a prospective analytical cross-sectional study in two University Hospitals in the city of Yaounde (Yaounde Central Hospital and the Gynaecological Obstetrics and Paediatrics Hospital), and in the laboratory of the Centre Pasteur in Yaounde over an eight-month period (1st January 2021 – 1st September 2021). All patients with pre-eclampsia diagnosed according to the criteria of the International Society for the Study of Hypertension (ISSHP) and free of chronic metabolic or infectious pathology were included in this study. The patients were divided into two groups: group 1 (mild pre-eclampsia) and group 2: severe pre-eclampsia. Socio-demographic, clinical and histopathological characteristics specific to pre-eclampsia and placental malaria were investigated. Statistical analysis was performed with SPSS 23.0 software, Chi 2 was used to compare categorical variables, Student t-test was used to compare means, and logistic regression was used to assess the association between placental malaria lesions and PES. Results: The mean age of our study population was 29.93 ± 7.36 years versus 28.28 ± 7.18 years in patients with mild and severe pre-eclampsia respectively. Pre-eclampsia placental lesions (accelerated villous maturation, infarction) were significantly greater in patients with severe pre-eclampsia (p Conclusion: Placental malaria lesions were significantly associated with severe pre-eclampsia and increased the risk of developing severe pre-eclampsia placental lesions by a factor of 10.

Selective CO_(2)Electroreduction to Multi-Carbon Products on Organic-Functionalized CuO Nanoparticles by Local Micro-Environment Modulation

Surface functionalization of Cu-based catalysts has demonstrated promising potential for enhancing the electrochemical CO_(2)reduction reaction(CO_(2)RR)toward multi-carbon(C2+)products,primarily by suppressing the parasitic hydrogen evolution reaction and facilitating a localized CO_(2)/CO concentration at the electrode.Building upon this approach,we developed surface-functionalized catalysts with exceptional activity and selectivity for electrocatalytic CO_(2)RR to C_(2+)in a neutral electrolyte.Employing CuO nanoparticles coated with hexaethynylbenzene organic molecules(HEB-CuO NPs),a remarkable C_(2+)Faradaic efficiency of nearly 90%was achieved at an unprecedented current density of 300 mA cm^(-2),and a high FE(>80%)was maintained at a wide range of current densities(100-600 mA cm^(-2))in neutral environments using a flow cell.Furthermore,in a membrane electrode assembly(MEA)electrolyzer,86.14%FEC2+was achieved at a partial current density of 387.6 mA cm^(-2)while maintaining continuous operation for over 50 h at a current density of 200 mA cm^(-2).In-situ spectroscopy studies and molecular dynamics simulations reveal that reducing the coverage of coordinated K⋅H2O water increased the probability of intermediate reactants(CO)interacting with the surface,thereby promoting efficient C-C coupling and enhancing the yield of C_(2+)products.This advancement offers significant potential for optimizing local micro-environments for sustainable and highly efficient C_(2+)production.

Transplantation of human placental chorionic plate-derived mesenchymal stem cells for repair of neurological damage in neonatal hypoxic-ischemic encephalopathy

Neonatal hypoxic-ischemic encephalopathy is often associated with permanent cerebral palsy,neurosensory impairments,and cognitive deficits,and there is no effective treatment for complications related to hypoxic-ischemic encephalopathy.The therapeutic potential of human placental chorionic plate-derived mesenchymal stem cells for various diseases has been explored.However,the potential use of human placental chorionic plate-derived mesenchymal stem cells for the treatment of neonatal hypoxic-ischemic encephalopathy has not yet been investigated.In this study,we injected human placental chorionic plate-derived mesenchymal stem cells into the lateral ventricle of a neonatal hypoxic-ischemic encephalopathy rat model and observed significant improvements in both cognitive and motor function.Protein chip analysis showed that interleukin-3 expression was significantly elevated in neonatal hypoxic-ischemic encephalopathy model rats.Following transplantation of human placental chorionic plate-derived mesenchymal stem cells,interleukin-3 expression was downregulated.To further investigate the role of interleukin-3 in neonatal hypoxic-ischemic encephalopathy,we established an in vitro SH-SY5Y cell model of hypoxic-ischemic injury through oxygen-glucose deprivation and silenced interleukin-3 expression using small interfering RNA.We found that the activity and proliferation of SH-SY5Y cells subjected to oxygen-glucose deprivation were further suppressed by interleukin-3 knockdown.Furthermore,interleukin-3 knockout exacerbated neuronal damage and cognitive and motor function impairment in rat models of hypoxic-ischemic encephalopathy.The findings suggest that transplantation of hpcMSCs ameliorated behavioral impairments in a rat model of hypoxic-ischemic encephalopathy,and this effect was mediated by interleukin-3-dependent neurological function.

Effect of hypoxia on expression of placental trophoblast cells SATB1 and β-catenin and its correlation with the pathogenesis of preeclampsia

Objective: To study the effect of hypoxia on the expression of placental trophoblast cells SATB1 and β-catenin and its correlation with the pathogenesis of preeclampsia. Methods: Trophoblastic cell lines HRT8/SVneo were cultured, SATB1 and β-catenin expression and cell biological behavior were determined after hypoxia reoxygenation treatment; cell biological behavior and the expression of related genes were determined after the transfection of SATB1 and β-catenin siR NA; preeclampsia placenta and normal placenta tissues were collected and the expression of SATB1 and β-catenin were determined. Results: OD value, cell migration rate, m RNA contents of SATB1 and β-catenin of H/R group were significantly lower than those of Nor group, cell apoptosis rate was higher than that of Nor group and the number of invasive cells was less than that of Nor group; OD value and bcl-2 mRNA content of SATB1-siRNA group were lower than those of NC group; cell apoptosis rate as well as Bax, Caspase-3, caspase-6 and caspase-9 mRNA contents were higher than those of NC group; cell migration rate as well as CTSB, CTSD, MMP2 and MMP9 mRNA contents of β-catenin-siRNA group were lower than those of NC group; the number of invasive cells was less than that of NC group; the expression levels of SATB1 and β-catenin in preeclampsia placenta tissue were significantly lower than those in normal placenta tissue. Conclusions: Hypoxia can inhibit the expression of SATB1 and β-catenin in the pathogenesis of preeclampsia, which can affect the proliferation, apoptosis, migration and invasion of cells.

Consequences of gestational and pregestational diabetes on placental function and birth weight

Maternal diabetes constitutes an unfavorable environment for embryonic and fetoplacental development. Despite current treatments, pregnant women with pregestational diabetes are at increased risk for congenital malformations, materno-fetal complications, placental abnormalities and intrauterine malprogramming. The complications during pregnancy concern the mother (gravidic hypertension and/or preeclampsia, cesarean section) and the fetus (macrosomia or intrauterine growth restriction, shoulder dystocia, hypoglycemia and respiratory distress). The fetoplacental impairment and intrauterine programming of diseases in the offspring's later life induced by gestational diabetes are similar to those induced by type 1 and type 2 diabetes mellitus. Despite the existence of several developmental and morphological differences in the placenta from rodents and women, there are similarities in the alterations induced by maternal diabetes in the placenta from diabetic patients and diabetic experimental models. From both human and rodent diabetic experimentalmodels, it has been suggested that the placenta is a compromised target that largely suffers the impact of maternal diabetes. Depending on the maternal metabolic and proin ammatory derangements, macrosomia is explained by an excessive availability of nutrients and an increase in fetal insulin release, a phenotype related to the programming of glucose intolerance. The degree of fetal damage and placental dysfunction and the availability and utilisation of fetal substrates can lead to the induction of macrosomia or intrauterine growth restriction. In maternal diabetes, both the maternal environment and the genetic background are important in the complex and multifactorial processes that induce damage to the embryo, the placenta, the fetus and the offspring. Nevertheless, further research is needed to better understand the mechanisms that govern the early embryo development, the induction of congenital anomalies and fetal overgrowth in maternal diabetes.

Construction and Analysis of Three-dimensional Graphic Model of Single-chain Fv Derived from an Anti-human Placental Acidic Isoferritin Monoclonal Antibody by Computer

Summary: A three-dimensional (3D) graphic model of a single-chain Fv (scFv) which was derived from an anti-human placental acidic isoferritin (PAF) monoclonal antibody (MAb) was construct- ed by a homologous protein-predicting computer algorithm on Silicon graphic computer station. The structure, surface static electricity and hydrophobicity of scFv were investigated. Computer graphic modelling indicated that all regions of scFv including the linker, variable regions of the heavy (VH) and light (VL) chains were suitable. The VH region and the VL region were involved in composing the 'hydrophobic pocket'. The linker was drifted away VH and VL regions. The complementarity determining regions (CDRs) of VH and VL regions surrounded the 'hydrophobic pocket'. This study provides a theory basis for improving antibody affinity, investigating antibody structure and analyzing the functions of VH and VL regions in antibody activity.

Effects of different irrigation methods on micro-environments and root distribution in winter wheat fields

The irrigation method used in winter wheat fields affects micro-environment factors, such as relative humidity（RH） within canopy, soil temperature, topsoil bulk density, soil matric potential, and soil nutrients, and these changes may affect plant root growth.An experiment was carried out to explore the effects of irrigation method on micro-environments and root distribution in a winter wheat field in the 2007–2008 and 2008–2009 growing seasons.The results showed that border irrigation（BI）, sprinkler irrigation（SI）, and surface drip irrigation（SDI） had no significant effects on soil temperature.Topsoil bulk density, RH within the canopy, soil available N distribution, and soil matric potential were significantly affected by the three treatments.The change in soil matric potential was the key reason for the altered root profile distribution patterns.Additionally, more fine roots were produced in the BI treatment when soil water content was low and topsoil bulk density was high.Root growth was most stimulated in the top soil layers and inhibited in the deep layers in the SDI treatment, followed by SI and BI, which was due to the different water application frequencies.As a result, the root profile distribution differed, depending on the irrigation method used.The root distribution pattern changes could be described by the power level variation in the exponential function.A good knowledge of root distribution patterns is important when attempting to model water and nutrient movements and when studying soil-plant interactions.

Effect of Bushen Yiqi Huoxue Recipe on Placental Vasculature in Pregnant Rats with Fetal Growth Restriction Induced by Passive Smoking

Interactions of vascular endothelial growth factor （VEGF） with receptors VEGFR1/Fltl and VEGFR2/Flk1, and those of angiopoietins （Ang-1, Ang-2） with receptor Tie2 play important roles in placental angiogenesis. This study investigated vascular morphology and expression of these angiogenic factors in rat placenta on the day 15, 18, 21 of gestation （D 15, D 18 and D21）. The rats were randomly assigned into 3 groups： normal group, model group [fetal growth restriction （FGR） model], and Bushen Tqi Huoxue （BYHR） recipe treatment group （BYHR group, the pregnant rats with FGR were treated with BYHR recipe）. Morphological analysis indicated that during initial villous formation, fetal nucle- ated erythrocytes （FNEs） appeared in maternal blood sinus （MBS）. Subsequently, FNEs were sur- rounded by endothelial cells to form fetal capillary （FC） and then by trophoblast cells to form villi. As pregnancy proceeded, FC density increased progressively with increasing endothelial identification staining （EIS） in normal and BYHR groups. Whereas, villous formation was suppressed, normal in- crease in FC density was impaired and EIS was weakened in model group. Quantitative PCR analysis showed that VEGF and Flkl mRNA increased over gestation in all groups, indicating that VEGF might play a pivotal role in FC growth during late gestation. VEGF mRNA was increased on D15, while de- creased on D21 in model group as compared with normal group and BYHR group. Immunohistochemi- cally, Ang-2 protein was highly expressed in FNEs, gradually disappeared as villi matured, and decreased over gestation in all groups, indicating that Ang-2 might play a pivotal role in villous formation, which was further supported by decreased Ang-2 mRNA and protein expression in model group on D 15. Ang-1 mRNA, Tie2 mRNA and Ang-1/Ang-2 ratio increased from D15 to D18 in all groups as placenta matured. Ang-1 mRNA, Tie2 mRNA and Ang-1/Ang-2 ratio were decreased on D18 in model group as compared with normal and BYHR groups, indicating delayed maturity of FGR placenta. Alterations in angiogenic factors may result in altered placental vasculature and cause placental insufficiency. BYHR recipe could balance the angiogenic factors to promote the formation and maturation of FGR placental vasculature.

Bile Acid Effects on Placental Damage in Intrahepatic Cholestasis of Pregnancy

Aims: The abnormal increase of bile acid is found in intrahepatic cholestasis of pregnancy (ICP). It also can be observed the damage of placental tissue in ICP. The aim of this study was to find the associations of the bile acid in umbilical vein and the damage of placental tissue. Methods: Thirty women diagnosed with ICP and fifty normal pregnant women between September 2015 and September 2017 at Nanshan District Maternity & Child Healthcare Hospital of Shenzhen were included in this study. The glycocholic acid (GA), total bile acids (TBA), total bilirubin (TB), direct bilirubin (DB) and albumin level in umbilical vein were measured by cycle enzyme method in ICP and control group. The placental damage was analyzed by morphologic study using hematoxylin dyes in two groups. The correlation between the level of the bile acid in the umbilical vein and the damage of the placenta was assessed using SPSS software. Results: The GA, TBA, TB, DB and albumin level in umbilical vein were significantly higher in ICP than those of pregnant women, respectively. The placental villis were expanded and the structure was destroyed in ICP. The vessel was damaged and the cell trophoblast hyperplasia in ICP. It also can be seen that there was obvious nodules and a typical fibrous necrotic substance in ICP but not in control group. There is a positive correlation between the level of the TBA in the umbilical vein and the damage of the placenta in ICP. Conclusion: The TBAs were significantly higher in umbilical vein and were related to the placental damage in ICP.

Plasma Nogo-A and placental growth factor levels are associated with portal hypertension in patients with liver cirrhosis

BACKGROUND Clinically significant portal hypertension(CSPH) and severe portal hypertension(SPH) increase the risk for decompensation and life-threatening complications in liver cirrhosis. Pathologic angiogenesis might contribute to the formation of these conditions. Placental growth factor(PlGF) and Nogo-A protein are biomarkers of pathological angiogenesis, but data on their role in liver cirrhosis and portal hypertension is scarce.AIM To determine plasma levels of PlGF and Nogo-A in patients with liver cirrhosis,CSPH, SPH and potential to predict portal hypertension.METHODS A cohort of 122 patients with hepatitis C virus and/or alcohol-induced liver cirrhosis with characterized hepatic venous pressure gradient(HVPG) were included in the study. Demographic data, medical history, Child-Turcotte-Pugh and Model of End Stage liver disease score, clinical chemistry, liver stiffnessvalues were recorded on the day of the procedure prior HVPG measurement. The degree of portal hypertension was determined by the invasive HVPG measurement. Nogo-A and PlGF plasma levels were evaluated using enzyme linked immunosorbent assay. The control group consisted of 30 healthy age-and sex-matched individuals.RESULTS Peripheral PlGF levels were higher and Nogo-A levels were lower in patients with liver cirrhosis(23.20 vs 9.85;P < 0.0001 and 2.19 vs 3.12;P = 0.004 respectively). There was a positive linear correlation between peripheral levels of PlGF and HVPG(r = 0.338, P = 0.001) and negative linear correlation between the peripheral Nogo-A levels and HVPG(r =-0.267, P = 0.007). PlGF levels were higher in CSPH and SPH(P = 0.006;P < 0.0001) whereas Nogo-A levels were lower(P = 0.01;P < 0.033). Area under the curve for the diagnosis of CSPH for PlGF was 0.68(P = 0.003) and for Nogo-A-0.67(P = 0.01);for SPH 0.714(P <0.0001) and 0.65(P = 0.014) respectively. PlGF levels were higher and Nogo-A levels were lower in patients with esophageal varices(P < 0.05). PlGF cut-off value of 25 pg/mL distinguished patients with CSPH at 55.7% sensitivity and76.7% specificity;whereas Nogo-A cut-off value of 1.12 ng/mL was highly specific(93.1%) for the diagnosis of CSPH.CONCLUSION Plasma PlGF levels were higher while Nogo-A levels were lower in patients with liver cirrhosis and portal hypertension. Biomarkers showed moderate predictive value in determining CSPH and SPH.

Placental Malaria and Pre-Eclampsia from the Lagos State University Teaching Hospital, Ikeja, Lagos Nigeria

Objective: To determine the relationship between placental malaria infection and pre-eclampsia in a holo-endemic zone. Design: Prospective case-control study. Materials and Methods: One hundred and twenty seven (127) pregnant women with a diagnosis of pre-eclampsia in labour or having caesarean section served as cases while controls were 127 normotensive parturient women. They were recruited from the maternity unit of Ifako Ijaiye and Isolo General Hospitals, Lagos that served as secondary care centers. At delivery, either spontaneous vaginal delivery or by caesarean section, a 2.0 cm × 2.0 cm placenta tissue was cut with scalpel and fixed in 10% formaldehyde in a specimen bottle and sent to the pathologist. Following this, 2.5 mls of Cord blood and 2.5 mls of the maternal venous blood were taken into separate EDTA bottles properly labeled at delivery, samples were sent to the haematology laboratory immediately for peripheral thick film smear for malaria parasite. Results were obtained from the laboratory and together with data from the case files, they were entered into SPSS version 16 for analysis. Independent Student t-test was used for significance for continuous variables while Chi-square was used for qualitative data. The significance was set at 0.05. Results: There were statistically significant differences between the cases and controls regarding the maternal age, number of pregnancies, p p > 0.05. There was statistically significant difference between the two groups regarding the diagnosis of placental malaria as well as past history of alcohol intake and occupation, p Conclusion: Placental malaria infection was more common in patients with preeclampsia than their matched normotensive patients in our environment. At the same time, chronic malaria was found to be an independent risk factor for preeclampsia. More concerted efforts by all stake holders should be geared towards primary prevention together with early diagnosis and treatment of malaria especially in early pregnancy. This may reduce the incidence and complication of preeclampsia in our environment.

Placental Origins of Preeclampsia:Potential Therapeutic Targets

Preeclampsia(PE)remains a leading cause of maternal and perinatal morbidity and mortality in obstetrics worldwide.No effective treatments to reduce its incidence and severity in clinical practice are currently available.A variety of hypotheses have been generated aiming to explain the origins of PE,notably being the genetic predispositions and placental dysfunction.As regard to placental dysfunction,much progress has been made in basic research and several potential therapeutic targets have been identified.This review will discuss in detail the potential therapeutic targets in PE models including uteroplacental blood flow,oxidative stress,vasoactive factors and inflammation/immune response,and introduce the evolving technologies for placental research nowadays.

Inhibitory effect on subretinal fibrosis by anti-placental growth factor treatment in a laser-induced choroidal neovascularization model in mice

AIM:To investigate whether anti-placental growth factor(PGF) can inhibit subretinal fibrosis and whether this effect is mediated by the inhibitory effect of PGF on epithelial-mesenchymal transition(EMT) of retinal pigment epithelial(RPE) cells.METHODS:Subretinal fibrosis model was established in laser induced choroidal neovascularization(CNV) mice on day 21 after laser photocoagulation.Immunofluorescence staining(IFS) of cryosections and enzyme-linked immunosorbent assay(ELISA) were used to detect the expression of PGF.IFS of whole choroidal flat-mounts was used to detect the degree of subretinal fibrosis.IFS of cryosections and ELISA were used to detect the expression of EMT related indicators in subretinal fibrosis lesions.RESULTS:The expression of PGF protein in subretinal fibrosis lesions was significantly up-regulated(P<0.05),and mainly co-stained with pan-cytokeratin labeled RPE cells.Intravitreal injection of anti-PGF neutralizing antibody reduced the area of subretinal fibrosis and the ratio of fibrotic/angiogenic area significantly at the concentrations of 0.25,0.5,1.0,and 2.0 μg/μL(all P<0.05).The expression of E-cadherin in the local RPE cells decreased,while α-SMA increased significantly in subretinal fibrosis lesions,and the application of anti-PGF neutralizing antibody could reverse these changes(P<0.05).CONCLUSION:The expression of PGF is up-regulated in the lesion site of subretinal fibrosis and mainly expressed in RPE cells.Intravitreal injection of anti-PGF neutralizing antibody can significantly inhibit the degree of subretinal fibrosis in CNV mice,and this effect may be mediated by the inhibition of PGF on EMT of RPE cells.

Complex Limb Salvage with Placental-Based Allografts: A Pilot Study

Background: Commercially available human placental amnion/chorion tissue allografts have been successfully used as protective treatment barriers for wounds and diabetic ulcers. Burn and traumatic limb injuries with exposed bone or tendon generally require surgical flaps or amputations for healing. The purpose of this study was to determine if dehydrated human amnion/ chorion membrane allografts (dHACM) with decellularized human collagen matrix (dHCM) could be used to salvage injured human extremities. Methods and Materials: dHACM/dHCM was topically applied to the wounds after debridement. Negative Pressure Wound Therapy (NPWT) was concurrently initiated, primarily to bolster the tissue with moisture and contamination control. Approximately every seven days, wounds were re-evaluated for granulation tissue growth response. As needed, patients received dHACM/ dHCM and NPWT in the outpatient or home care settings after discharge. Results: Fifteen males and two females (26 extremities) were treated for fourteen burn and three Necrotizing Soft Tissue Infections (NSTI) injuries. Closure was observed in patients after two to five dHACM/dHCM applications. The dHACM/dHCM treatment was initiated: (median) 17-days after injury;NPWT for 17-days;autograft or primary closure after 21-days;discharge 25-days after the first application. Conclusion: Treatment with human placental-derived allografts provided a protective covering that enabled the healing cascade to generate granulation tissue formation in extremity wounds with exposed tendon and/or bone. In select limb salvage cases, dHACM/dHCM treatment may be a promising alternative to amputations, tissue rearrangements, free tissue flaps or other techniques for resolution of extremity wounds with bone and tendon exposure.

Prenatal Exposure to Perfluorooctane Sulfonate impairs Placental Angiogenesis and Induces Aberrant Expression of LncRNA Xist

Perfluorooctane sulfonate （PFOS） is a class of stable organic compounds with wide industrial,commercial, and consumer applications, such as in textiles, paper, pesticides, and shampoos;. It is readily absorbed, but poorly eliminated, with the elimination half-life of approximately 5 years;.Hence, there have been concerns regarding its potential damage to human health. Some studies

Placental abruption

Placental abruption(also termed accidental haemorrhage) refers to the separation of a normally sited placenta from the uterine wall resulting in maternal haemorrhage into the interventing space. If this space communicates with the external os of the cervix, the haemorrhage will be revealed. If not,the haemorrhage may result in delay in diagnosis, and underestimation of blood loss,which in turn increases the likelihood of coagulopathy and maternal morbidity. In the presence of massive abruption, blood tracks under pressure back into the myometrium, and may be visible beneath the uterine serosa at caesarean section. This appearance is referred to as a ’Couvelaire uterus’. Fetal bleeding can occur with placental abruption , though it is rare. It can be detected by a Kleihauer test which detects fetal haemoglobin in the maternal circulation and can be a clue to retroplacental bleeding in cases of trauma.

Accessory Placental Structures—A Review

Many studies have reported on the different types of placenta in different species, but accessory or paraplacental structures are mentioned only in species that have such a nutrient-exchanging mechanism. Hystricomorph rodents possess a subplacenta, swine and equines have the placental areola, equines have the chorionic girdle, and carnivores have hemophagous organs that are equivalent to the placental hematoma in ruminants. These accessory structures are specialized tissues for specific nutrient exchanges in different species, and they are adaptive modifications exhibited by domestic and wild species to remedy the nutritional deficiencies that are related to permeability of the main placenta to important nutrients for the growth and development of the fetus during the gestation.

Effects of Placental Isoferritin on the Mouse Embryo Development in vitro

To investigate the effect of placental isoferritin （PLF） on mouse embryo development in vitro, mice 2-cell embryos were co-cultured with human first trimester decidual cells at different concentrations of PLF in vitro. The following changes of the above system were observed under an invert microscope and the number of embryos were recorded and the embryos were classified. The results showed there was no significant difference in the percentage of embryos development to 4-cell 8-cell and morula （P〉0.05）. PLF at the doses of 10 and 100 U/mL significantly enhanced more embryos development to the blastocyst and hatching blastocyst （P〈0.05）. PLF at the dose of 1000 U/mL depressed more embryos development from 2-cell to hatching blastocyst, meanwhile such phenomena as cell degeneration and irregular cleavage were observed in part of embryos, but there was no significant difference in statistics （P〉0.05）. It was concluded that PLF at the concentration of 10-- 100 U/mL had no significant effects on the early development of mice embryos, however, PLF could promote the growth, differentiation, and hatching of preimplantion blastocysts.

Analysis of Placental Growth Factor in Placentas of Normal Pregnant Women and Women with Hypertensive Disorders of Pregnancy

To investigate the expressions of placental growth factor （PLGF） in placenta with hypertensive disorders of pregnancy （ HDP）, 45 women with HDP and 20 normally pregnant women were studied. Among 45 women with HDP, there were 23 cases of severe preeclampsia and one case of eclampsia. The location and level of PLGF proteins was determined by immunohistochemistry and Western blot. The expression of PLGF mRNA in placenta was assessed by reverse transcriptionalpolymerase chain reaction （RT-PCR）. The results showed that： （1） The distribution of PLGF in placenta with HDP was similar to normal one, which was mainly in the cytoplasm of villous syncytiotrophoblast and villous stroma; （2） The expression of PLGF protein was significantly decreased in placentas with mild and severe preeclampsia compared to the normal ones （0.3±0.4 vs 0.6± 0.4, 0.2±0.5 vs 0. 6±0. 4, P〈0.01）. There were no differences between the gestational hypertension placenta and normal one （0.5±0.6 vs 0. 6±0. 4, P〉0.05） ; （3） The transcription levels of the PLGF mRNA in placentas with preeclampsia were significantly lower than in normal groups （3.33±0.39 vs 4.87±0. 60, 1.97±0.29 vs 4.87±0.60, P〈0.01）, and no differences were found between the gestational hypertension placenta and normal groups. These findings suggest that the abnormal expression of PLGF in placentas is related to the pathogenesis of HDP.

Placental Isoferritin Action in Pathogenesis of Pre-eclampsia and/or Intrauterine Growth Retardation and Its Earlier Predictive Value

In order to investigate the role of placental isoferritin (PLF) in pathogenesis of pre-eclampsia and/or intrauterine growth retardation (IUGR) and its earlier predictive value, a prospective double-blinded study was performed. In 120 initial normal pregnant women at earlier third trimester (from 24 to 34 weeks), plasma placental isoferritin and nitric oxide (NO) metabolites (nitrite/nitrate) (NO 2 -/NO 3 -) were examined by using ELISA and Criess assay respectively. The outcome of pregnancies and birth weight of their infants were followed up. The receiver operating characteristic curves (ROC) and predictive values of PLF predicting the outcome of pregnancy with IUGR, pre-eclampsia were analyzed. Results showed that in 120 initial normal pregnant women, IUGR occurred in 15 pregnant women (IUGR group) and pre-eclampsia in 19 (pre-eclampsia group), and the remaining 86 had normal pregnancy (normal group). The levels of plasma placental isoferritin were significantly decreased in IUGR group (260.01±58.95) μg/ml and pre-eclampsia group (285.31±53.73) μg/ml as compared with those in normal group (775.62±89.32) μg/ml at earlier third trimester (both P<0.01). The levels of plasma NO were significantly increased in IUGR group (61.57±46.22) μmol/L and pre-eclampsia group (58.37±30.52) μmol/L as compared with those in the normal group (35.29±24.46) μmol/L (both P<0.01). There was no significant difference in plasma placental isoferritin and NO levels between IUGR group and pre-eclampsic group (both P>0 05). The plasma placental isoferritin was negatively correlated with NO levels (r=0.329,P<0 01). The areas under ROC of PLF predicting IUGR and pre-eclampsia were 0.977 and 0.905 respectively. At the cut point of 400 μg/ml PLF level, the sensitivity, specificity, positive predictive value, negative predictive value and Kappa index of PLF levels predicting the outcome of pregnancy with pre-eclampsia were 100 %, 85.15 %, 55.88 %, 100 % and 0.645 respectively. At the cut point of 390 μg/ml PLF level, the sensitivity, specificity, positive predictive value, negative predictive value and Kappa index of PLF levels predicting the outcome of pregnancy with IUGR were 100 %, 81.9 %, 44.12 %, 100 % and 0.663 respectively. It was concluded that the decrease of plasma placental isoferritin levels at earlier third trimester was associated with IUGR and/or pre-eclampsia, and the endothelial cell damage may be one of its mechanisms. The plasma PLF level can be used as an earlier predictor for screening of IUGR and/or pre-eclampsia.