Influence of Different Rice Cultivars on Schizotetranychus oryzae Development.

Schizotetranychus oryzae Rossi de Simons (Acari: Tetranychidae) is considered one of the most important phytophagous mite in rice cultivation in the Americas South, Central, and North. This study aimed to examine some biological aspects of S. oryzae developing on leaves of three different cultivars of rice [Oryza sativa (L.)-Poaceae] produced in the state of Rio Grande do Sul, Brasil. The plants were kept in a room at 25 ± 1°C, with natural light (photophase of approximately 14 h) and 70 ± 5% relative humidity. During the immature stages, observations were carried out daily at 7 am, 1 pm, and 7 pm. The results showed that the mean duration of the egg-adult period in days were similar between cultivars evaluated (Irga 424, 11.27 ± 0.13; Taim, 11.21 ± 0.14 and Sinuelo, 11.13 ± 0.15). Egg-adult viability on Irga 424, Sinuelo, and Taim was 61.9, 85.71, and 90.48%, respectively, being lowest on Irga 424 (χ2 = 28.62, p < 0.0001). The duration of the immature stages was not affected by cultivar, but on Irga 424, egg-adult viability and female longevity were lower. The results of this study can help select O. sativa cultivar resistant to S. oryzae. However, historically, the IRGA 424 has lower populations of S. oryzae in field conditions.

Growth of fetal lean mass and fetal fat mass in gestational diabetes.

OBJECTIVES: This study was carried out to investigate growth indicators of fetal lean mass and fat mass in the second half of the gestational period in pregnancies complicated by gestational diabetes mellitus (GDM) in comparison to normal control pregnancies. METHODS: Forty-three control and 171 GDM pregnancies were followed longitudinally by ultrasound examinations, measuring both traditional biometric parameters and six non-traditional parameters for the evaluation of lean and fat mass. A mixed linear model derived from the log-Count function was used to model fetal growth and to make comparisons between groups. Factor analysis was used to evaluate the associations between gestational diabetes and fetal size and fetal fat/lean mass ratios. RESULTS: A total of 506 scans were obtained in the 214 pregnancies, a mean of 2.4 scans per pregnancy (range 2-5). Maternal age, prepregnancy weight and body mass index were significantly higher in GDM pregnancies. Fetuses of GDM pregnancies showed greater growth, at the same gestational age, for each lean and fat non-traditional parameter, having a significantly greater amount of total tissue mass and a higher fat mass/lean mass ratio, independent of gestational age, in comparison to control pregnancies. CONCLUSIONS: A non-invasive, repeatable evaluation of fetal body composition in utero could represent a useful method for the early detection of growth abnormalities and for direct estimation of the fetal metabolic status.

Effects of gestational diabetes on fetal oxygen and glucose levels in vivo.

OBJECTIVE: Fetal hypoxia and acidemia have been reported in pregestational diabetic pregnancies in relation to poor glycaemic control, but it is still uncertain whether this is the case in apparently well-controlled gestational diabetes. POPULATION AND METHODS: Maternal arterial and umbilical venous and arterial blood samples were collected from 37 normal (N) and 38 pregnancies complicated by gestational diabetes (GDM) at the time of caesarean section. MAIN OUTCOME MEASURES: Respiratory gases, acid-base balance, lactate and glucose concentrations were measured. RESULTS: Both fetal and placental weights were significantly increased in GDM compared to N pregnancies, despite similar gestational age. Maternal biochemical parameters were similar in N and GDM but GDM fetuses were significantly more hypoxic (O2 saturation: N 63.2+/-13.9; GDM 53.8+/-14.6%, P<0.01; O2 content: N 5.5+/-1.4; GDM 4.8+/-1.2 mmol/l, P<0.05). Glucose (N 3.4+/-0.5, GDM 3.9+/-1.2 mmol/l, P<0.05) and lactate (N 1.32+/-0.49; GDM 1.64+/-0.75 mmol/l, P<0.05) concentrations were significantly increased in the umbilical vein in GDM compared to N fetuses. Placental histology was consistent with altered villous morphology. CONCLUSIONS: Our data indicate that fetuses from gestational diabetic mothers have increased umbilical glucose concentrations despite normal maternal glucose levels and a reduction in oxygen saturation and O2 content together with increased lactate concentration, reflecting altered fetal metabolism. These data suggest that 'good maternal metabolic control' achieved by currently used methods of monitoring glucose control is not sufficient to ensure a normal oxygenation status and metabolic milieu for the fetus in GDM pregnancies.

Higher mitochondrial DNA content in human IUGR placenta.

IUGR has been associated to a specific placental phenotype with reduced uptake of specific nutrients. Recently, it has been hypothesized that IUGR may be determined during early gestation. This period is characterized by decidual trophoblast invasion and by intense cellular growth, replication and differentiation. Since a huge energetic availability is required during gestation, we hypothesize that mitochondria may play a crucial role in this process being the main energetic producer in the cell. The aim of this study was to investigate the role of mitochondria in IUGR pathogenesis, evaluating the number of mitochondrial DNA copies (mtDNA) in IUGR placentae compared to controls. Placental samples were collected from 50 singleton pregnancies at the time of elective caesarean section. Twenty-six pregnancies were controls with normal intrauterine growth (AGA) and 24 were studied after the in utero diagnosis of IUGR. All samples were analyzed by real-time quantitative PCR and statistical analysis was performed by non-parametric tests. The median value of mitochondrial DNA content (IQR) in AGA and IUGR placentae was significantly different (455 and 698, respectively, p=0.004). The cell types responsible for the difference observed is unknown and it is possible that changes observed in the proportion of cell types may influence this measurement. Moreover, a significant negative relationship was observed between mtDNA and umbilical venous pO(2), with the highest levels detected in the most severe IUGR cases according to Doppler findings and to the presence of preeclampsia. These data suggest a relationship between the pathogenesis of IUGR and increased placental mtDNA copies. From our results we can speculate that increased mtDNA represents an adaptation of the metabolic placental mechanism to the calorie restriction of the fetus. Furthermore, we found that this rise was inversely related to oxygen tension in the umbilical vein. Although no specific pathogenetic role can be implied, mtDNA increases with hypoxia in placentas of IUGR.

Placental transport and metabolism in fetal overgrowth -- a workshop report.

Fetal overgrowth in pregnancies complicated by diabetes is the result of an increased substrate availability which stimulates fetal insulin secretion and fetal growth. However, despite strict glycemic control in modern clinical management of the pregnant woman with diabetes, fetal overgrowth remains an important clinical problem. Recent studies in vivo provide evidence for increased delivery of amino acids to the fetus in gestational diabetes (GDM) even when metabolic control is strict. This could be due to that truly normal maternal substrate levels cannot be achieved in diabetic pregnancies and/or caused by altered placental nutrient transport and metabolism. Studies in vitro demonstrate an up-regulation of placental transport systems for certain amino acids in GDM associated with fetal overgrowth. GDM is also characterized by changes in placental gene expression, including up-regulation of inflammatory mediators and Leptin. In type-I diabetes with fetal overgrowth the in vitro activity of placental transporters for both glucose and certain amino acids as well as placental lipoprotein lipase is increased. Furthermore, both clinical observations in type-I diabetic pregnancies and preliminary animal experimental studies suggest that even brief periods of metabolic perturbation early in pregnancy may affect placental growth and transport function for the remainder of pregnancy, thereby contributing to fetal overgrowth. Ultrasound measurements of fetal fat deposits and abdominal circumference as well as 3D ultrasound assessment of placental volume represent non-invasive techniques for in utero diagnosis of fetal and placental overgrowth. It is proposed that these methods represent valuable additions to the clinical management of the diabetic pregnancy. In conclusion, altered placental function may be a mechanism contributing to fetal overgrowth in diabetic pregnancies with apparent optimal metabolic control. It is proposed that detailed information on placental metabolism and transport functions obtained in vitro and in vivo represent a placental phenotype that provides important information and may facilitate diagnosis and improve clinical management of fetal overgrowth.

Flexible treatment of gestational diabetes modulated on ultrasound evaluation of intrauterine growth: a controlled randomized clinical trial.

OBJECTIVES: In order to prevent abnormalities of fetal growth still characterizing pregnancies complicated by Gestational Diabetes (GDM), in the present study we evaluated a therapeutic strategy for GDM based on ultrasound (US) measurement of fetal insulin-sensitive tissues. METHODS: All GDM women diagnosed before 28th week immediately started diet and self-monitoring of blood glucose; after 2 weeks they were randomized to conventional (C) or modified (M) management. In C the glycemic target (GT) was fixed at 90 fasting/120 post-prandial mg/dl; in M GT varied, according to US measurement of the Abdominal Circumference (AC) centile performed every 2 weeks: 80/100 if AC > or =75th, 100/140 if AC<75th. Therapy was tailored to mean fasting (FG) and postprandial glycemia (PPG). RESULTS: Globally, 229 women completed the study, 78 in C, 151 in M. Use of insulin was 16.7% in C, 30.4% in M (total groups), significantly more frequent in M than in C (59.7% vs 15.4%) when considering only women with AC > or =75th c. Mean metabolic data were similar in the 2 groups, but in M a tightly-optimized subgroup, resulting from the lowering of GT due to AC > or =75th, coexisted with a less-controlled one, whose higher GT was justified by AC<75th. Pregnancy outcome was better in M, with lower (p<0.05*) rate of LGA* (7.9% vs 17.9%), SGA (6.0% vs 9.0%) and Macrosomia* (3.3% vs 11.5%). CONCLUSIONS: Our data show the value of a flexible US-based approach to the treatment of GDM. This model does not necessarily involve a generalized aggressive treatment, allowing to concentrate therapeutical efforts on a small subgroup of women showing indirect US evidence of fetal hyperinsulinization. Such a selective approach allowed to obtain a near-normalization of fetal growth, with clear advantages on global pregnancy outcome.

Advanced tubal pregnancy associated with severe fetal growth restriction: a case report.

A case is described of advanced tubal pregnancy associated with severe fetal growth restriction delivered at 27 weeks. The placenta was implanted on the salpinx and on the uterotubal angle. Progressing tubal pregnancy and its placental histological characteristics could be a model of placental dysfunction typically associated with intrauterine growth restriction.

The evaluation of maternal parameters at diagnosis may predict HELLP syndrome severity.

OBJECTIVE: Hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome, a severe manifestation of pre-eclampsia and/or intrauterine growth restriction (IUGR) of the fetoplacental unit, is classified into three classes, according to the lowest platelet count observed during the course of the disease. The aim of our work was to analyze the levels of lactate dehydrogenase (LDH), aspartate transferase (AST), alanine transferase (ALT) and platelets at the time of HELLP syndrome diagnosis, to find possible cut-off values that could predict the severity of the syndrome from its early onset. METHODS: A retrospective analysis of the clinical records of 26 patients consecutively diagnosed with classes 1 and 2 HELLP syndrome was performed. Platelet count (x 1000/ml), LDH (IU/l), AST (IU/l), ALT (IU/l), hemoglobin (g/dl), hematocrit (%) and D-dimer (log of titer) were determined at admission and compared with the most severe peak values. Receiver operating characteristic (ROC) curves were used to calculate the best cut-off value at admission which correlated with the development of class 1 HELLP syndrome (the most severe condition). The post-test probability of developing class 1 severity was calculated. RESULTS: Mean gestational age at diagnosis was 33.4 weeks (range 23-40 weeks). Peak values of LDH, AST and ALT were significantly higher in class 1 HELLP syndrome patients. The platelet count at admission was not informative in differentiating patients who would later develop class 1 or class 2 HELLP syndrome. According to the best cut-off values at admission for LDH, AST and ALT, the post-test probability to predict patients with class 1 HELLP syndrome was 74%, 71% and 78%, respectively. If all the three parameters were above the cut-off value, the probability increased to 90%. CONCLUSIONS: The LDH, AST and ALT values at admission blood test, and to a greater extent the combination of all three abnormal tests, could predict the severity of HELLP syndrome.

Foetal and placental weights in relation to maternal characteristics in gestational diabetes.

An increased placental weight has been reported in pregnancies complicated with gestational diabetes (GDM). We have analysed foetal (F) and placental weight (P) and foetal length in 143 consecutive normal (N) and 132 GDM pregnancies in relation to type of treatment and to a number of maternal variables. All N pregnancies had a negative oral glucose challenge test at 24-28 weeks. GDM was diagnosed at 28-32 weeks by a 100-gm, 3-h oral glucose tolerance test (OGTT). Treatment was diet (D: n=82) or diet plus insulin (D+I: n=50) according to self-monitoring of blood glucose. A significant difference was observed between N and GDM pregnancies for maternal age (N=30.6+/-5.38 years; GDM=33.2+/-4.53 years; P< 0.001), pre-pregnancy weight (N=58.2+/-8.0 kg; GDM=63.0+/-12.9 kg; P< 0.001) and BMI (N= 21.9+/-2.63; GDM=24.4+/-4.71;P< 0.001). Foetal weight became significantly higher in the GDM group (N=3274.2+/-296.0 g; GDM=3287.1+/-474.1g; P< 0.05) once correction was made for the significant difference in gestational age between the two groups (N=39.4+/-1.17 weeks; GDM=38.8+/-1.39 weeks; P< 0.001). Significantly higher placental weights (N=561.87+/-91.0 g; GDM=592.2+/-115.8 g;P< 0.01) and significantly lower F/P weight ratios were found in GDM pregnancies (N=5.96+/-1.02; GDM=5.69+/-1.13; P< 0.05). In GDM pregnancies a significantly negative correlation was found between the OGTT response and weights of foetus and placentae at delivery, suggesting that both foetal and placental growth are affected by maternal insulin resistance.

Cationic amino acid transporter activity in the syncytiotrophoblast microvillous plasma membrane and oxygenation of the uteroplacental unit.

The purpose of this study was to determine whether there is any relationship between the activity of cationic amino acid transporters in the microvillous plasma membrane (MVM) of the syncytiotrophoblast and the oxygenation of the uteroplacental unit. Oxygenation data were obtained at the time of caesarean section from the uterine veins, the maternal radial artery and the umbilical vessels of 7 normal (AGA) and 13 intrauterine growth restricted (IUGR) pregnancies. Microvillous plasma membranes were isolated from the same placentas and the activity of the system y(+) and y(+)L cationic amino acid transporters determined by measuring (3)H- l -arginine uptake in the presence and absence of l -glutamine. In IUGR pregnancies uterine venous Po(2) was significantly higher (AGA=44.7+/-8.0 mmHg; IUGR=57.2+/-2.3 mmHg, P< 0.05) and umbilical venous Po(2) was significantly lower (AGA=33.4+/-3.0 mmHg; IUGR=25.1+/-2.0 mmHg, P< 0.05) than in AGA pregnancies. System y(+)L activity, but not system y(+) activity, was inversely correlated with uterine venous Po(2) (P< 0.01; r(2)=0.4) in AGA and IUGR pregnancies. In IUGR pregnancies without associated maternal pre-eclampsia, y(+)L activity, but not y(+) activity, was also directly related to the umbilical O(2) content difference (P< 0.01; r(2)=0.9). A significant negative correlation was found between system y(+) and the umbilical O(2) content difference in AGA pregnancies (P< 0.01; r(2)=0.9). Our data are consistent with the hypothesis that in IUGR fetuses uterine oxygenation is not reduced and can be increased. The inverse correlation between system y(+)L activity and uterine venous Po(2) and the correlations with umbilical venous-arterial O(2) content difference suggest a relationship between cationic amino acid transporter activity and oxygen tension in the uteroplacental unit.

Intrauterine growth of normal thyroid.

In this study we describe fetal thyroid growth during gestation and establish normal reference values using a simple linear ultrasound measurement of the thyroid. A total of 1180 normal singleton pregnancies, with no known risk factors for thyroid disorders, were enrolled from 12 to 39 weeks of gestation. The thyroid antero-posterior diameter was measured on a transverse axial plane through the fetal neck. The best fit regression was a power equation: thyroid diameter = 0.2412 weeks(1.0278) (r(2) = 0.55). The percentiles smoothed curves were calculated for each week. In conclusion, the results of the present study support previous findings that the fetal thyroid grows between 12 and 39 weeks of gestation with a steepest increase during the second trimester, that is when the fetal thyroid becomes functionally active. The normal ranges of this simple index of thyroid growth can be useful both as screening and for the clinical evaluation of pregnant patients with thyroid disorders.

Post-zygotic origin of complete maternal chromosome 7 isodisomy and consequent loss of placental PEG1/MEST expression.

Maternal UPD of chromosome 7 is associated with pre- and postnatal growth retardation (IUGR, PNGR) and Silver-Russell syndrome (SRS [MIM 180860]). We report a case of IUGR in a newborn with SRS stigmata. Using combined haplotyping and cytogenetic-FISH studies we characterized the lymphocytes, umbilical cord and four placental cotyledons. The results are consistent with complete maternal isodisomy 7 and trisomy 7 mosaicism of post-zygotic origin. The trisomic cell line was prevalent in trophoblast cells from two placental cotyledons. Trisomy 7 of post-zygotic origin is a frequent finding, but maternal isodisomy 7, due to trisomic rescue has never been reported. PEG1/MEST expression was evaluated on placenta cDNA and a specific transcript was revealed only in the cotyledons with a high percentage of trisomic cells and the presence of the paternal chromosome 7 contribution, but not in the placental biopsies with maternal isodisomy 7. The histological features of the four placental fragments revealed that isodisomy 7 correlates with a pattern of cotyledonary hyper-ramification due to an increase of the branching angiogenesis, which could be the result of a defect of angiogenesis caused by the absence of PEG1 product. The severe hypo-ramification of the two cotyledons, showing trisomy 7 mosaicism, may be due to the triplicate dosage of genes on chromosome 7. The delayed fetal growth could be the phenotypic effect of the imbalance between imprinted and non-imprinted genes on chromosome 7 in the fetus or the result of abnormal placental function during pregnancy.

Reduction of subcutaneous mass, but not lean mass, in normal fetuses in Denver, Colorado.

OBJECTIVE: To test the hypothesis that reduced birth weight in normal fetuses born at moderately high altitude (Denver), compared with the birth weight in normal fetuses born at sea level (Milan), is caused by a reduction in both lean mass and subcutaneous fat mass. STUDY DESIGN: Ninety-four normal singleton pregnancies (46 in Denver, 48 in Milan) had serial ultrasonographic axial images obtained to assess subcutaneous tissues of fetuses as a measure of body fat. The abdominal wall thickness and mid upper arm and mid thigh were examined. The equation was: Subcutaneous tissue equals total cross-sectional area minus bone and muscle area. Lean mass included the area of muscle and bone, head circumference, and femur length. RESULTS: Gestational age at delivery was similar between groups. Birth weight was less at Denver's altitude (2991 +/- 79 g versus 3247 +/- 96 g; P =.04). Abdominal wall thickness, mid upper arm, and mid thigh subcutaneous tissues measurements were significantly reduced at Denver's altitude and increased further in significance with advancing gestational age. Lean mass measurements were similar between groups. CONCLUSIONS: The reduced birth weight of the newborns in Denver was the result of a reduction in fetal subcutaneous fat tissue and not lean mass. Ultrasonography can be used to follow subcutaneous measurements longitudinally and to detect differences, and potentially disease processes, in study populations.

Mutations in the thrombomodulin and endothelial protein C receptor genes in women with late fetal loss.

Late fetal loss can be associated with placental insufficiency and coagulation defects. Thrombomodulin (TM) and the endothelial protein C receptor (EPCR) are glycoprotein receptors expressed mainly on the endothelial surface of blood vessels and also in the placenta; they both play a key physiological role in the protein C anticoagulant pathway. Defects in these proteins might play an important role in the pathogenesis of late fetal loss. We performed a case-control study in 95 women with unexplained late fetal loss (> 20 weeks), to elucidate whether TM or EPCR gene mutations were associated with an increased risk for this complication of pregnancy. The control group comprised 236 women who gave birth to at least one healthy baby and had no history of late fetal death or obstetrical complications. The entire TM and EPCR genes, including the promoter region, were screened. In total, five mutations were identified in the TM gene in 95 patients and three in 236 control subjects, and two mutations were identified in the EPCR gene in 95 patients and one in 236 control subjects. The relative risk for late fetal loss when having a mutation in the TM or EPCR gene was estimated by an odds ratio of 4.0 (95% CI 1.1-14.9). In conclusion, identified mutations in the TM and EPCR genes of women with unexplained fetal loss are more prevalent compared with women with no obstetrical complications.

The endocrine and metabolic profile of the growth-retarded fetus.

Intrauterine growth retardation (IUGR) is characterized by the failure of the fetus to grow at a normal rate in utero and is associated with a number of endocrine and metabolic changes. Our knowledge of the placental nutrient supply and the endocrine status of the fetal-placental unit during pregnancies involving IUGR has greatly increased over the past decade as a result of the availability of fetal blood samples obtained under relatively steady state conditions. These studies have provided evidence that the supply of glucose is impaired only under severe conditions, whereas placental transfer of amino acids is reduced even in fetuses with normal oxygenation and feto-placental blood flow. Moreover, significant in utero relationships have been reported between fetal weight and circulating levels of growth factors such as insulin-like growth factor-I and leptin. When measured per kg fetal weight, however, levels of leptin are significantly higher in growth-retarded fetuses, with abnormal feto-placental blood flow and reduced oxygen content. The metabolic and endocrine changes observed should be interpreted in relation to the severity of the disease.

Fetal plasma leptin concentrations: relationship with different intrauterine growth patterns from 19 weeks to term.

The relationship between in utero fetal growth and fetal leptin concentrations was investigated between 19 and 41 wk in 40 normal (appropriate for gestational age, AGA) fetuses, in 25 intrauterine growth-restricted (IUGR) fetuses, and in 18 fetuses from gestational diabetic mothers (GDM), representing different intrauterine growth patterns. Umbilical venous plasma leptin concentrations were determined at the time of either in utero fetal blood sampling or delivery. Plasma leptin was measurable as early as 19 wk of gestation. A significant difference was observed between umbilical venous and arterial plasma leptin concentrations (0.6+/-0.6 ng/mL; p<0.01). In AGA and in IUGR fetuses, significant positive relationships were found between fetal leptin concentrations and both gestational age (p<0.001) and fetal weight (p<0.001). Leptin concentrations were significantly higher in AGA than IUGR only after 34 wk (p<0.05), but leptin per kilogram fetal weight (leptin/kg) was not significantly different. In IUGR with abnormal umbilical arterial Doppler velocimetry and fetal heart rate, leptin/kg significantly higher than in IUGR with normal biophysical and biochemical parameters was found (p<0.05). Both circulating plasma leptin and leptin/kg were significantly higher in GDM than in normal fetuses (p<0.001) and correlated with abdominal fat mass measured by ultrasound. No gender differences were observed in any group of fetuses. These findings indicate a clear relationship between fetal leptin concentrations and fetal fat mass. Data in severe IUGR suggest the presence of increased leptin concentrations associated with in utero signs of fetal distress.

Sonographic measurements of subcutaneous fetal fat in pregnancies complicated by gestational diabetes and in normal pregnancies.

AIM: To compare sonographic measurements of fetal fat tissue in pregnancies complicated by gestational diabetes (GD), with patients undergoing either a diet only or a combined diet and insulin treatment, to those obtained in pregnancies with a normal glucose challenge test. METHODS: Forty-five singleton pregnancies complicated by GD but free of any other maternal disease known to affect fetal growth were recruited. GD was diagnosed by a 3-hour OGTT, and treatment was differentiated according to the glycemic profile. GD mothers were divided into two treatment groups: glycemic profile normalized by diet only treatment (n=16) and by combined diet and insulin treatment (n=29). Fetal biometry and subcutaneous fat tissue thickness of the anterior abdominal wall were sonographically evaluated at the time of diagnosis and every 4 weeks afterwards in both GD and normal glucose challenge test group (n=25). RESULTS: No differences were found in neonatal outcomes between combined diet and insulin treatment group and normal cases, whereas neonatal weight showed a statistically significant difference between diet only treatment group and healthy population. Abdominal circumference in fetuses from GD mothers and normal fetuses was similar, but there was a difference in the fetal fat tissue thickness at the time of diagnosis. CONCLUSION: Increased fetal fat tissue thickness in GD mothers at recruitment and its growth rate reduction during adequate treatment may be a new criterion for direct estimation of fetal metabolic status instead of the traditional indirect evaluation based on maternal glucose concentrations.