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Introduction: CXCR2, the receptor of the CXC chemokines, plays a critical role in cell migration and invasion in many types of cancer. It is unclear what impact CXCR2 may have on Preeclampsia (PE), a pregnancy-specific disease, which is related to insufficient trophoblast invasion. The aim of this study was to investigate the expression pattern of CXCR2 in the placentas of healthy and PE pregnancies, and to investigate the molecular mechanism of CXCR2 involvement in the development of PE.Methods: CXCR2 expression levels in newly delivered placentas from 38 pregnant women with PE and 21 healthy pregnant women were detected using quantitative real-time PCR, immunohistochemistry and Western blot assays. The effect of CXCR2 on trophoblast invasion and the underlying mechanisms were examined in two trophoblast cell lines (HTR-8/SVneo and TEV-1 cells).Results: CXCR2 mRNA and protein expression levels were significantly decreased in preeclamptic placentas than normal control. The invasive abilities of the two trophoblast cell lines were significantly inhibited when CXCR2 was silenced, but that CXCR2 overexpression promoted trophoblast cells invasion. In addition, silencing CXCR2 reduced the expression of matrix metalloproteinase 2 and 9 (MMP2 and MMP9) and phosphorylated Akt (p-Akt). Furthermore, an Akt inhibitor suppressed the expression of MMP-2 and MMP-9.Discussion: Our results suggest that the decreased CXCR2 may contribute to the development of preeclampsia through impairing trophoblast invasion by down-regulating MMP-2 and MMP-9 via the Akt signaling pathway. [ABSTRACT FROM AUTHOR]

Objective: To identify the association between preeclampsia (PE) and selective intrauterine growth restriction (sIUGR) in twin pregnancies.Methods: This was a retrospective cohort study of 1004 twin pregnancies from 2008 to 2014. We specifically compared the incidence, clinical characteristics and outcomes of PE between sIUGR and normal-growth twin pregnancies.Results: PE occurred more frequently in sIUGR pregnancies [29.0% (51/176)] than in normal-growth twin pregnancies [13.1% (99/756), p < 0.001, adjusted odds ratio 3.29]. Among sIUGR, the incidence of PE was significantly higher in dichorionic (DC) pregnancies (37.5%, 30/80) than in monochorionic (MC) pregnancies (21.9%, 21/96). The rates of onset at <32 weeks (p = 0.045) and of severe PE (p = 0.025) were higher in sIUGR pregnancies with PE. The systolic blood pressure was also higher in sIUGR pregnancies with PE (152.6 ± 11.8 mmHg) than in normal-growth pregnancies with PE (148.0 ± 8.2 mmHg) (p = 0.042). Additionally, more sIUGR pregnancies were delivered at 32-36 weeks (p = 0.001), and fewer were delivered at ≥36 weeks (p < 0.001). Moreover, the prevalence of severe neonatal asphyxia was higher in sIUGR pregnancies with PE than in normal-growth pregnancies with PE (8.8% versus 2.5%, p = 0.020).Conclusions: sIUGR is associated with increased odds of developing severe PE in twin pregnancies, leading to poorer perinatal outcomes. [ABSTRACT FROM AUTHOR]

The 2D-3D lifting task for Human Pose Estimation is a highly nonlinear mapping problem, which requires mutual constraints among human joints. In this paper, we mainly discuss how to represent the constraints among the joints by their global and local dependencies, and how to fuse them more effectively. Therefore, we propose a novel end-to-end neural network architecture named Double chain Networks (DCN), for monocular 2D-3D human pose lifting task. The DCN consists of two parts. One is a global constraint module based on full connection layer, which extracts the global dependency information of human body joints; the other is graph convolution based local constraint module, which represents the local dependency information of human body joints. The global and local constraint features are fused by interleaved addition to combine the global and local spatial constraint features of human joints in DCN regression, which outperforms the way of concatenating them. We perform abundant ablation experiments on Human3.6M dataset to verify the advantages of the constraint modules, and compare the performance of the single/double chain networks. Experimental results show that the DCN achieves state-of-the-art performance and exhibits strong generalization ability, and its performance is comparable to the methods based on temporal information. Finally, we apply the DCN to reconstruct 3D skeletons in 3D anime characters. The equipotential-joints connection mode to extract the constraint relationships between the human equipotential-joints; The DCN can effectively extract and combine the global and local constraints of human joints; The DCN achieves state-of-the-art performance and exhibits strong generalization ability; We apply the DCN to the posture construction of 3D virtual characters. [Display omitted] • The equipotential-joints connection mode to extract the constraint relationships between human equipotential-joints. • The DCN can effectively extract and combine the global and local constraints of human joints. • The DCN achieves state-of-the-art performance and exhibits strong generalization ability. • We apply the DCN to the posture construction of 3D virtual characters. [ABSTRACT FROM AUTHOR]

• FastNet outperforms popular lightweight networks on human pose estimation. • The asymmetric bottleneck module can extract keypoint features with multi-scale. • The waterfall module can obtain delicate local representations. Aiming at the problem of developing efficient models for human pose estimation algorithms under computation-limited resources. In this paper, we proposed an efficient high-resolution network for human pose estimation, which named FastNet. First of all, The Lite-HRNet was constructed by using four parallel subnetworks. Each subnetwork contained multiple bottleneck block for feature extraction. The Lite-HRNet can effectively learn the high-resolution representation features of key points because of maintaining high-resolution. Secondly, instead of standard convolution, the asymmetric convolution was introduced to build an asymmetric bottleneck module. The asymmetric bottleneck module has different aspect ratios, and can be used to exact image features of keypoints with multi-scale characteristics and reduce the number of parameters. Thirdly, the waterfall module composed of multiple parallel convolutions were proposed to aggregates features with the same spatial size which can efficiently obtain delicate local representations. It retains rich spatial information and results in precise keypoint localization. Finally, the bottleneck blocks were replaced with asymmetric bottleneck modules in the third subnetwork of LiteHRNet. By which, The waterfall module is embedded into the structure of FastNet. Comprehensive experiments demonstrate that the proposed method achieves superior results on two benchmark datasets, MSCOCO and MPII. Moreover, FastNet demonstrates superior results on human pose estimation over popular lightweight networks. [ABSTRACT FROM AUTHOR]

Mangroves are valuable contributors to coastal ecosystems; knowledge of the dynamics of mangrove ecosystems is important in the context of global change. To obtain this knowledge, remote sensing is an indispensable means, yet it poses challenges since the accuracy is sometimes unsatisfactory in distinguishing mangroves from other land cover types with traditional classification methods. In this letter, we proposed a modified artificial immune algorithm (AIA), in which the antibodies represent the candidate solutions and the antigens are expressed by the fitness function. Multiclass coevolution was combined with the concept of clonal selection to ensure computation of an optimal clustering center in parallel for each land cover type. A cluster-center-oriented decimal encoding method for antibodies was adopted, and the inner class variance and the between-class difference together were used to formulate the fitness function. Furthermore, a design of the antibody solubility-based selection operator and nonuniform mutation operator was undertaken. Applying this modified AIA to a Landsat Thematic Mapper multispectral remote sensing imagery in the Zhangjiang estuary in southeastern China, we found that the AIA substantially improved classification accuracy over traditional methods, showing an overall accuracy of 90% (\kappa coefficient = 0.88) and was capable to discern mangrove well (commission of 10% and omission of 22%). [ABSTRACT FROM PUBLISHER]

Discriminative correlation filters (DCFs) have been shown to perform superiorly in visual object tracking. However, visual tracking is still challenging when the target objects undergo complex scenarios such as occlusion, deformation, scale changes and illumination changes. In this paper, we utilize the hierarchical features of convolutional neural networks (CNNs) and learn a spatial-temporal context correlation filter on convolutional layers. Then, the translation is estimated by fusing the response score of the filters on the three convolutional layers. In terms of scale estimation, we learn a discriminative correlation filter to estimate scale from the best confidence results. Furthermore, we proposed a re-detection activation discrimination method to improve the robustness of visual tracking in the case of tracking failure and an adaptive model update method to reduce tracking drift caused by noisy updates. We evaluate the proposed tracker with DCFs and deep features on OTB benchmark datasets. The tracking results demonstrated that the proposed algorithm is superior to several state-of-the-art DCF methods in terms of accuracy and robustness. [ABSTRACT FROM AUTHOR]

Background: The contribution of genetic variants to congenital heart defects (CHDs) has been investigated in many postnatal cohorts but described in few prenatal fetus cohorts. Overall, specific genetic variants especially copy number variants (CNVs) leading to CHDs are somewhat diverse among different prenatal cohort studies. In this study, a total of 1118 fetuses with confirmed CHDs were recruited from three units over a 5-year period, composing 961 of singleton pregnancies and 157 of twin pregnancies. We performed chromosomal microarray analysis on all cases to detect numerical chromosomal abnormalities (NCAs) and pathogenic/likely pathogenic CNVs (P/LP CNVs) and employed whole-exome sequencing for some cases without NCAs and P/LP CNVs to detect P/LP sequence variants (P/LP SVs). Results: Overall, NCAs and P/LP CNVs were identified in 17.6% (197/1118) of cases, with NCA accounting for 9.1% (102/1118) and P/LP CNV for 8.5% (95/1118). Nonisolated CHDs showed a significantly higher frequency of NCA than isolated CHD (27.3% vs. 4.4%, p < 0.001), but there was no significant difference in the frequency of P/LP CNVs between isolated and nonisolated CHD (11.7% vs. 7.7%). A total of 109 P/LP CNVs were identified in 95 fetuses, consisting of 97 (89.0%) de novo, 6 (5.5%) parental inherited and 6 (5.5%) with unavailable parental information. The 16p11.2 proximal BP4-BP5 deletion was detected in 0.9% (10/1118) of all cases, second only to the most common 22q11.21 proximal A-D deletion (2.1%, 23/1118). Most of the 16p11.2 deletions (8/10) detected were de novo, and were enriched in CHD cases compared with a control cohort from a previous study. Additionally, SV was identified in 12.9% (8/62) of cases without NCA and P/LP CNV, most of which were de novo with autosomal dominant inheritance. Conclusions: Our cohort study provides a deep profile of the contribution of genetic variants to CHDs in both singleton and twin fetuses; NCA and P/LP CNV contribute to 9.1% and 8.5% of CHD in fetuses, respectively. We confirmed the 16p11.2 deletion as a CHD-associated hotspot CNV, second only to the 22q11.21 deletion in frequency. Most 16p11.2 deletions detected were de novo. Additionally, P/LP SV was identified in 12.9% (8/62) of fetuses without NCA or P/LP CNV. [ABSTRACT FROM AUTHOR]

Objectives: To compare the clinical outcomes of different multifetal pregnancy reduction (MFPR) programs in dichorionic (DC) triplets, and explore the association between early ultrasound characteristics and co-twin death after potassium chloride (KCl) injection into one monochorionic (MC) twin. Methods: We retrospectively reviewed the data of DC triplets who underwent MFPR at our center during 2012–2021. Patients were grouped as follows: intracardiac KCl injection into one MC twin (group A), intracardiac KCl injection into both MC twins simultaneously (group B), and reduction of the singleton fetus (group C) and pregnancy outcomes were compared. Logistic regression was used to determine whether ultrasound measurements at 11–13+6 weeks predicted co-twin death and the receiver operator characteristic (ROC) analysis was conducted to assess the predictive performance. Results: Finally, we enrolled 184 patients. 153 cases were in group A, and 18, 13 cases were in group B and C respectively. Gestational age at the time of MFPR did not differ among the 3 groups (median: 12 6 7 weeks). The survival rate was 89.6%, 88.9%, and 92.3% in group A, B, and C respectively, which was comparable among groups. Preterm birth was more common in group C (10/12, 83.3%). After KCl injection into one MC twin, co-twin death occurred in 86.3% cases (132/153) within 1 day; however, 3 patients had 2 live births each, with normal postnatal development. Intertwin nuchal translucency (NT) difference/discordance significantly predicted co-twin death within 1 day after MFPR, and the areas under the ROC curve were 0.694 and 0.689, respectively. Conclusions: For MFPR in DC triplet pregnancies, reduction of the MC twins results in less preterm birth, and women with KCl injection into either one or both MC twins had similar outcomes. Large intertwin NT difference/discordance was associated with co-twin death within 1 day after KCl injection into one of the MC twins. [ABSTRACT FROM AUTHOR]

N -methyl- d -aspartate receptor (NMDAR) has been implicated in the pathophysiology of depression. However, as the unique inhibitory subunit of NMDARs, the role of GluN3A in depression is largely unclear. Firstly, expression of GluN3A was examined in a mouse model of depression induced by chronic restraint stress (CRS). Then, rescue experiment with rAAV-Grin3a injection into hippocampus of CRS mice was carried out. Lastly, GluN3A knockout (KO) mouse was generated via CRISPR/Cas9 technique, and the molecular mechanism underlying involvement of GluN3A in depression was initially explored using RNA-seq technique, RT-PCR and western blotting. GluN3A expression in hippocampus was significantly decreased in CRS mice. Depression-like behaviors induced by CRS were ameliorated when the decrease of GluN3A expression in mice exposed to CRS was restored. GluN3A KO mice exhibited symptoms of anhedonia reported as reduced sucrose preference, and symptoms of despair assayed by a longer immobility time in FST. Transcriptome analysis revealed genetic ablation of GluN3A was associated with downregulation of genes implicated in synapse and axon development. Postsynaptic protein PSD95 was decreased in GluN3A KO mice. More importantly, reduction of PSD95 in CRS mice can be rescued by viral mediated Grin3a re-expression. The mechanism underlying GluN3A involvement in depression is not fully determined. Our data suggested that GluN3A dysfunction is involved in depression, which might be mediated by synaptic deficits. These findings will facilitate the understanding of the role of GluN3A in depression, and they might provide a new strategy for the development of subunit-selective NMDAR antagonists as antidepressant drugs. • GluN3A expressionis significantly decreased in the hippocampus of CRS mice, an animal model of depression. • Depression-like behaviors in CRS mice are reversed by viral mediated Grin3a re-expression in the hippocampus. • GluN3A KO mice exhibit depression-like behaviors but not anxiety-related behaviors. • Genetic deletion of GluN3A causes a significant decrease in synaptic proteins. [ABSTRACT FROM AUTHOR]

Decreased hippocampal synaptic plasticity is an important pathological change in stress-related mood disorders, including major depressive disorder. However, the underlying mechanism is unclear. PGC-1α, a transcriptional coactivator, is a key factor in synaptic plasticity. We investigated the relationships between changes in hippocampal PGC-1α expression and depressive-like and stress-coping behaviours, and whether they are related to hippocampal synapses. Adeno-associated virus was used to alter hippocampal PGC-1α expression in male C57BL/6 mice. The sucrose preference test and forced swimming test were used to assess their depressive-like and stress-coping behaviours, respectively. Immunohistochemistry and stereology were used to calculate the total number of excitatory synapses in each hippocampal subregion (the cornu ammonis (CA) 1, CA3, and dentate gyrus). Immunofluorescence was used to visualize the changes in dendritic structure. Western blotting was used to detect the expression of hippocampal PGC-1α and mitochondrial-associated proteins, such as UCP2, NRF1 and mtTFAs. Our results showed that mice with downregulated PGC-1α expression in the hippocampus exhibited depressive-like and passive stress-coping behaviours, while mice with upregulated PGC-1α in the hippocampus exhibited increased stress-coping behaviours. Moreover, the downregulation of hippocampal PGC-1α expression resulted in a decrease in the number of excitatory synapses in the DG and in the protein expression of UCP2 in the hippocampus. Alternatively, upregulation of hippocampal PGC-1α yielded the opposite results. This suggests that hippocampal PGC-1α is involved in regulating depressive-like and stress-coping behaviours and modulating the number of excitatory synapses in the DG. This provides new insight for the development of antidepressants. • PGC-1α in the hippocampus mediates depressive-like and stress-coping behaviours. • PGC-1α in the hippocampus is involved in regulating the number of excitatory synapses in the dentate gyrus. • The regulation of excitatory synapse numbers is the key structural basis in which hippocampal PGC-1α regulates depressive-like and stress-coping behaviours. [ABSTRACT FROM AUTHOR]

Depression is a complex psychiatric disorder. Previous studies have shown that running exercise reverses depression-like behavior faster and more effectively than fluoxetine therapy. GABAergic interneurons, including the PV+ interneuron subtype, in the medial prefrontal cortex (MPFC) are involved in pathological changes of depression. It was unknown whether running exercise and fluoxetine therapy reverse depression-like behavior via GABAergic interneurons or the PV+ interneurons subtype in MPFC. To address this issue, we subjected mice with chronic unpredictable stress (CUS) to a 4-week running exercise or fluoxetine therapy. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that running exercise enriched GABAergic synaptic pathways in the MPFC of CUS-exposed mice. However, the number of PV+ interneurons but not the total number of GABAergic interneurons in the MPFC of CUS-exposed mice reversed by running exercise, not fluoxetine therapy. Running exercise increased the relative gene expression levels of the PV gene in the MPFC of CUS-exposed mice without altering other subtypes of GABAergic interneurons. Moreover, running exercise and fluoxetine therapy both significantly improved the length, area and volume of dendrites and the spine morphology of PV+ interneurons in the MPFC of mice exposed to CUS. However, running exercise but not fluoxetine therapy improved the dendritic complexity level of PV+ interneurons in the MPFC of CUS-exposed mice. In summary, the number and dendritic complexity level of PV+ interneurons may be important therapeutic targets for the mechanism by which running exercise reverses depression-like behavior faster and more effectively than fluoxetine therapy. • Runing exercise improved depression-like behavior faster and more comprehensively in CUS-exposed mice than fluoxetine therapy. • The number of PV+ interneurons rather than the total number of GABAergic neurons in the MPFC was increased by running exercise but not fluoxetine therapy. • Runing exercise, but not fluoxetine therapy, reversed the complexity levels of PV+ interneuron dendrites in the MPFC of CUS-exposed mice. [ABSTRACT FROM AUTHOR]

Background: Running exercise effectively ameliorates depressive symptoms in humans and depression-like behaviors in animals, but the underlying mechanisms remain unclear. Microglia-mediated neuroinflammation plays a major role in the development of depression. The medial prefrontal cortex (mPFC) is a key brain region involved in depression and is sensitive to physical activity. Whether the antidepressant effect of running exercise involves changes in mPFC microglia is not understood., Methods: The animals were subjected to chronic unpredictable stress (CUS) intervention followed by treadmill running. The sucrose preference test and elevated plus maze test or tail suspension test were used for behavioral assessment of the animals. The number of microglia in the mPFC was quantified by immunohistochemistry and stereology. The density and morphology of microglia were analyzed via immunofluorescence staining combined with three-dimensional laser scanning techniques. The mRNA expressions of inflammatory cytokines in the mPFC were examined via quantitative real-time PCR., Results: Running exercise effectively alleviated depressive-like behaviors in depression model animals. Running exercise reversed the increase in the number of microglia and the density of activated microglia in the mPFC of CUS animals. Running exercise effectively reversed the changes in microglia (reduced cell body area, total branch length and branch complexity) in the mPFC of CUS animals. Furthermore, running exercise regulated the gene expressions of pro-/antiinflammatory cytokines in the mPFC of CUS animals., Conclusions: Our results suggested that the antidepressant effects of running exercise may involve decreasing the number of activated microglia, reversing morphological changes in microglia in the mPFC, and reducing inflammatory responses., Competing Interests: Declaration of competing interest The authors declared that they have no conflicts of interest in this work. We declare that we do not have any commercial or associative interest that represents a conflict of interest in connection with the work submitted., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Running exercise has been shown to alleviate depressive symptoms. However, the mechanism underlying the antidepressant effects of running exercise is not fully understood. The imbalance of M1/M2 microglia phenotype/polarization and concomitant dysregulation of neuroinflammation play crucial roles in the pathogenesis of depression. Running exercise increases circulating levels of adiponectin which is known to cross the blood‒brain barrier and suppress inflammatory responses. AdipoR1 is an adiponectin receptor that is involved in regulating microglial phenotypes and activation states. However, whether running exercise regulates hippocampal microglial phenotypes and neuroinflammation through adiponectin/AdipoR1 to exert its antidepressant effects remains unclear. In the current study, 4 weeks of running exercise significantly alleviated the depressive-like behaviors of chronic unpredictable stress (CUS)-exposed mice. Moreover, running exercise decreased the microglial numbers and altered microglial morphology in three subregions of the hippocampus to restore the M1/M2 balance; these effects were accompanied by regulation of pro-/anti-inflammatory cytokine production and secretion in CUS-exposed mice. These effects may involve elevation of peripheral tissue (adipose tissue and muscle) and plasma adiponectin levels, and hippocampal AdipoR1 levels as well as activation of the AMPK-NF-κB/STAT3 signaling pathway by running exercise. When an adeno-associated virus was used to knock down hippocampal AdipoR1, mice showed depressive-like behaviors and alterations in microglia and inflammatory factor expression in the hippocampus that were similar to those observed in CUS-exposed mice. Together, these results suggest that running exercise maintains the M1/M2 balance and inhibits neuroinflammation in the hippocampus of CUS-exposed mice. These effects might occur via adiponectin/AdipoR1-mediated activation of the AMPK-NF-κB/STAT3 signaling pathway., (© 2024. The Author(s), under exclusive licence to Springer Nature Limited.)

Although the antidepressant effects of running exercise have been widely reported, further research is still needed to determine the structural bases for these effects. Astrocyte processes physically contact many synapses and directly regulate the numbers of synapses, but it remains unclear whether running exercise can modulate astrocyte morphological complexity and astrocyte-contacted synapses in the hippocampus of the mice with depressive-like behavior. Male C57BL/6 J mice underwent four weeks of running exercise after four weeks of chronic unpredictable stress (CUS). The sucrose preference test (SPT), tail suspension test (TST) and forced swim test (FST) were used to assess anhedonia in mice. Western blotting was used to measure the expression of astrocyte- and synapse-related proteins. Immunofluorescence and 3D reconstruction were used to quantify the density and morphology of astrocytes, and astrocyte-contacted synapses in each hippocampal subregion. Four weeks of running exercise alleviated depressive-like symptoms in mice. The expression of astrocyte- and synapse-related proteins in the hippocampus; astrocyte process lengths, process numbers, and dendritic arborization; and the number of astrocyte-contacted PSD95 positive synapses in the CA2-3 and DG regions were significantly decreased in the mice with depressive-like behavior, and running exercise successfully reserved these changes. Running exercise improved the decreases in astrocyte morphological complexity and astrocyte-contacted PSD95 positive synapses in the CA2-3 and DG regions of the mice with depressive-like behavior, suggesting that the physical interactions between astrocytes and synapses can be increased by running exercise, which might be an important structural basis for the antidepressant effects of running exercise., (Copyright © 2024 Elsevier Inc. All rights reserved.)

N -Methyl-d-aspartate receptor (NMDAR) signaling pathway has been implicated in the pathogenesis and treatment of depression. However, the role of NMDAR subunits in depression is still unclear. In this study, alteration in all seven NMDAR subunits in several brain areas of rats exposed to chronic unpredictable mild stress (CUMS), an animal model of depression, was detected. Our findings demonstrated that: (1) CUMS could induce a reduction in sucrose preference, an indicator of typical depression-like behaviors; (2) CUMS significantly reduced the NMDAR subunits of GluN2B and GluN3 in the medial prefrontal cortex (mPFC), but not altered all seven NMDAR subunits in hippocampus and corpus callosum of rats; (3) subunit composition of NMDARs in corpus callosum was different from that in mPFC, PFC and hippocampus; and (4) the mRNA expressions of GluN2B, GluN3A and GluN3B in mPFC as well as mRNA expression of GluN2C in corpus callosum were correlated to sucrose preference in rats. These findings suggested that GluN2B and GluN3 in mPFC may contribute to the pathophysiology of depression., Competing Interests: Conflict of interest: We declare no conflict of interests., (© 2022 Jing Chen et al., published by De Gruyter.)

Objective: To perform molecular cytogenetic study on two fetuses with abnormal ultrasound findings and analyze their genotype-phenotype correlation., Methods: G-banded karyotyping, single nucleotide polymorphism array (SNP array) and fluorescence in situ hybridization (FISH) were performed on amniotic fluid cells from both fetuses and peripheral blood samples from their parents. Results of SNP array were analyzed with bioinformatics software., Results: G-banded karyotyping failed to detect any abnormalities in both fetuses and their parents. SNP array detected a 2.484 Mb terminal deletion at 17p13.3 [arr[hg19] 17p13.3 (83 035-2 567 405)×1] in fetus 1 and a 3.295 Mb terminal deletion at 17p13.3p13.2 [arr[hg19] 17p13.3p13.2 (83 035- 3 377 560)×1] in fetus 2. Both deletions have overlapped with the critical region of Miller-Dieker syndrome (MDS) and involved candidate genes such as PAFAH1B1, YWHAE and CRK. In addition, SNP array and FISH analyses on the parental peripheral blood samples demonstrated that both 17p13.3 and 17p13.3p13.2 deletions were of de novo origin. Metaphase FISH performed on amniotic fluid cells confirmed the presence of 17p13.3 and 17p13.3p13.2 deletions detected by the SNP array, while metaphase FISH performed on the parents excluded any potential chromosome rearrangements., Conclusion: Abnormal ultrasound features for fetuses with MDS mainly include central nervous system anomalies. SNP array can efficiently detect 17p13.3 microdeletions underlying MDS, and accurately map the breakpoints and involved genes, which may facilitate understanding of the genotype and phenotype correlations for MDS.

Objective: To analyze the correlation between atypical neurofibromatosis type 1(NF1) microdeletion and fetal phenotype., Methods: Fetal blood sampling was carried out for a woman bearing a fetus with talipes equinovarus. G-banded karyotyping and single nucleotide polymorphism array (SNP-array) were performed on the fetal blood sample. Fluorescence in situ hybridization (FISH) was used to confirm the result of SNP array analysis. FISH assay was also carried out on peripheral blood specimens from the parents to ascertain the origin of mutation., Results: The karyotype of fetus was found to be 46, XY by G-banding analysis. However, a 3.132 Mb microdeletion was detected in chromosome region 17q11.2 by SNP array, which overlaped with the region of NF1 microdeletion syndrome. Analyzing of the specimens from the fetus and its parents with FISH has confirmed it to be a de novo deletion., Conclusion: Talipes equinovarus may be an abnormal sonographic feature of fetus with atypical NF1 microdeletion which can be accurately diagnosed with SNP array.

Background: This study aimed to determine the effects of long-term running exercise on spatial learning, spatial memory, and cortical capillaries in aged rats., Material and Methods: Fourteen-month-old female and male Sprague-Dawley rats were randomly divided into an exercised group (EG) and a non-exercised group (NG). The EG rats were trained on treadmill running for 4 or 14 months. The NG rats were housed under identical conditions without running. Spatial learning and memory were assessed with the Morris water maze. The cortical capillary parameters were quantitatively investigated using immunohistochemical and stereological methods., Results: The escaped latencies of the EG were significantly different from those of the NG in 18-month-old females and 28-month-old males (p<0.05). However, 28-month-old females and 18-month-old males showed no differences in escape latency between the EG and NG (p>0.05). In 28-month-old female rats, stereological techniques showed significant differences between the EG and NG in the cortical capillary volume (median, 22.55 vs. 11.42, p<0.05) and the cortical capillary surface area (median, 7474.13 vs. 3935.90, p<0.05). In 28-month-old male rats, the EG had a significantly longer total cortical capillary length (median, 530.35 vs. 156.27, p<0.05), significantly larger cortical capillary volume (median, 16.47 vs. 3.65, p<0.01), and a significantly larger cortical capillary total surface area (median, 7885.79 vs. 1957.16, p<0.01) compared with the NG group., Conclusions: These data demonstrate that exercise improved spatial learning, memory capacity and cortical capillaries in aged rats.

Objective: To investigate perinatal outcomes of twin pregnancies conceived by assisted reproductive techniques and those conceived spontaneously., Methods: The pregnant complications, delivery situation and neonatal outcomes of 104 twin pregnancies conceived by assisted reproductive techniques were compared to 173 spontaneous ones., Results: (1) The women of twin pregnancies conceived by assisted reproductive techniques were (31.2 +/- 3.7) years old while the spontaneous ones were (27.8 +/- 3.5) years old. There was significant difference between two groups (P < 0.05). (2) There were also significant differences in the incidence of premature delivery and gestational diabetes mellitus or impaired glucose tolerance(P < 0.01) between two groups. There were 70 cases (67.3%) premature delivery in assisted reproduction group, while 78 cases (45.1%) in spontaneous group. There were 16 cases (15.4%) gestational diabetes mellitus or impaired glucose tolerance in assisted reproduction group, while 4 cases (2.3%) in spontaneous group. (3) Cesarean sections were more frequently performed in assisted reproduction group (79 cases, 76.0%) than in spontaneous group (113 cases 65.3%). (4) There were no statistically significant differences in perinatal deaths, congenital malformations, neonatal asphyxia between two groups (P < 0.05)., Conclusion: The women of twin pregnancies conceived by assisted reproductive techniques were older than those conceived spontaneously. The incidence of premature delivery, gestational diabetes mellitus or impaired glucose tolerance and cesarean section were higher in assisted reproduction group. However, no statistically significant differences in perinatal morbidity were found between the two groups.