114 research outputs found
STROBE-GnRHa pretreatment in frozen-embryo transfer cycles improves clinical outcomes for patients with persistent thin endometrium: A case-control study.
The well-prepared endometrium with appropriate thickness plays a critical role in successful embryo implantation. The thin endometrium is the main factor of frozen-embryo transfer (FET), resulting in the failure of implantation undergoing FET. Hormone treatment is suggested to improve endometrium thickness; however, among the larger numbers of cases, it cannot reach the sufficient thickness, which leads to a high cancelation rate of embryo transfer as well as waste high-quality embryos. Thus, it increases the burden to patients in both economic and psychological perspectives. We performed a retrospective observational study, which was composed with 2 cohorts, either with the conventional hormone replacement therapy (HRT) protocol or HRT with gonadotrophin-releasing hormone agonist (GnRHa) pretreatment to prepare the endometrium before FET. The measurements of endometrium thickness, hormone level, transfer cycle cancelation rate, pregnancy rate, and implantation rate were retrieved from the medical records during the routine clinic visits until 1 month after embryo transfer. The comparisons between 2 cohorts were performed by t-test or Mann-Whitney U test depending on the different attributions of data. In total, 49 cycles were under HRT with GnRHa pretreatment and 84 cycles were under the conventional HRT protocol. HRT with GnRHa pretreatment group improved the endometrial thickness (8.13 ± 1.79 vs 7.51 ± 1.45, P = .031), decreased the transfer cancelation rate (P = .003), and increased clinical pregnancy rate and implantation rate significantly (both P = .001). Additionally, luteinizing hormone level in pretreatment group was consistently lower than conventional HRT group (P < .05). Our study revealed HRT with GnRHa pretreatment efficiently improved the endometrial thickness, therefore, decreased the FET cycle cancelation. It also elevated the embryo implantation rate and clinical pregnancy rate by improving endometrial receptivity
OmniSeg3D: Omniversal 3D Segmentation via Hierarchical Contrastive Learning
Towards holistic understanding of 3D scenes, a general 3D segmentation method
is needed that can segment diverse objects without restrictions on object
quantity or categories, while also reflecting the inherent hierarchical
structure. To achieve this, we propose OmniSeg3D, an omniversal segmentation
method aims for segmenting anything in 3D all at once. The key insight is to
lift multi-view inconsistent 2D segmentations into a consistent 3D feature
field through a hierarchical contrastive learning framework, which is
accomplished by two steps. Firstly, we design a novel hierarchical
representation based on category-agnostic 2D segmentations to model the
multi-level relationship among pixels. Secondly, image features rendered from
the 3D feature field are clustered at different levels, which can be further
drawn closer or pushed apart according to the hierarchical relationship between
different levels. In tackling the challenges posed by inconsistent 2D
segmentations, this framework yields a global consistent 3D feature field,
which further enables hierarchical segmentation, multi-object selection, and
global discretization. Extensive experiments demonstrate the effectiveness of
our method on high-quality 3D segmentation and accurate hierarchical structure
understanding. A graphical user interface further facilitates flexible
interaction for omniversal 3D segmentation
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Increased gene copy number of DEFA1/DEFA3 worsens sepsis by inducing endothelial pyroptosis.
Sepsis claims an estimated 30 million episodes and 6 million deaths per year, and treatment options are rather limited. Human neutrophil peptides 1-3 (HNP1-3) are the most abundant neutrophil granule proteins but their neutrophil content varies because of unusually extensive gene copy number polymorphism. A genetic association study found that increased copy number of the HNP-encoding gene DEFA1/DEFA3 is a risk factor for organ dysfunction during sepsis development. However, direct experimental evidence demonstrating that these risk alleles are pathogenic for sepsis is lacking because the genes are present only in some primates and humans. Here, we generate DEFA1/DEFA3 transgenic mice with neutrophil-specific expression of the peptides. We show that mice with high copy number of DEFA1/DEFA3 genes have more severe sepsis-related vital organ damage and mortality than mice with low copy number of DEFA1/DEFA3 or wild-type mice, resulting from more severe endothelial barrier dysfunction and endothelial cell pyroptosis after sepsis challenge. Mechanistically, HNP-1 induces endothelial cell pyroptosis via P2X7 receptor-mediating canonical caspase-1 activation in a NLRP3 inflammasome-dependent manner. Based on these findings, we engineered a monoclonal antibody against HNP-1 to block the interaction with P2X7 and found that the blocking antibody protected mice carrying high copy number of DEFA1/DEFA3 from lethal sepsis. We thus demonstrate that DEFA1/DEFA3 copy number variation strongly modulates sepsis development in vivo and explore a paradigm for the precision treatment of sepsis tailored by individual genetic information
Influence of temperature on the transmission performance of track circuit in high-speed railway
In order to explore the influence of temperature on track circuit, a mathematical simulation model of track circuit is established. Then, the influence mechanism of temperature on the key equipment of track circuit is analysed. Finally, the influence on the receiver voltage and the locomotive signal current are computed based on the simulation model
Using Left and Right Brains Together: Towards Vision and Language Planning
Large Language Models (LLMs) and Large Multi-modality Models (LMMs) have
demonstrated remarkable decision masking capabilities on a variety of tasks.
However, they inherently operate planning within the language space, lacking
the vision and spatial imagination ability. In contrast, humans utilize both
left and right hemispheres of the brain for language and visual planning during
the thinking process. Therefore, we introduce a novel vision-language planning
framework in this work to perform concurrent visual and language planning for
tasks with inputs of any form. Our framework incorporates visual planning to
capture intricate environmental details, while language planning enhances the
logical coherence of the overall system. We evaluate the effectiveness of our
framework across vision-language tasks, vision-only tasks, and language-only
tasks. The results demonstrate the superior performance of our approach,
indicating that the integration of visual and language planning yields better
contextually aware task execution.Comment: 19 pages, 13 figure
Attentive Mask CLIP
Image token removal is an efficient augmentation strategy for reducing the
cost of computing image features. However, this efficient augmentation strategy
has been found to adversely affect the accuracy of CLIP-based training. We
hypothesize that removing a large portion of image tokens may improperly
discard the semantic content associated with a given text description, thus
constituting an incorrect pairing target in CLIP training. To address this
issue, we propose an attentive token removal approach for CLIP training, which
retains tokens with a high semantic correlation to the text description. The
correlation scores are computed in an online fashion using the EMA version of
the visual encoder. Our experiments show that the proposed attentive masking
approach performs better than the previous method of random token removal for
CLIP training. The approach also makes it efficient to apply multiple
augmentation views to the image, as well as introducing instance contrastive
learning tasks between these views into the CLIP framework. Compared to other
CLIP improvements that combine different pre-training targets such as SLIP and
MaskCLIP, our method is not only more effective, but also much more efficient.
Specifically, using ViT-B and YFCC-15M dataset, our approach achieves
top-1 accuracy on ImageNet-1K zero-shot classification, as well as
and I2T/T2I retrieval accuracy on Flickr30K and MS COCO, which are
, , and higher than the SLIP method, while being
faster. An efficient version of our approach running
faster than the plain CLIP model achieves significant gains of ,
, and on these benchmarks
Methylation-mediated silencing of PTPRD induces pulmonary hypertension by promoting pulmonary arterial smooth muscle cell migration via the PDGFRB/PLCγ1 axis
OBJECTIVE: Pulmonary hypertension is a lethal disease characterized by pulmonary vascular remodeling and is mediated by abnormal proliferation and migration of pulmonary arterial smooth muscle cells (PASMCs). Platelet-derived growth factor BB (PDGF-BB) is the most potent mitogen for PASMCs and is involved in vascular remodeling in pulmonary hypertension development. Therefore, the objective of our study is to identify novel mechanisms underlying vascular remodeling in pulmonary hypertension.
METHODS: We explored the effects and mechanisms of PTPRD downregulation in PASMCs and PTPRD knockdown rats in pulmonary hypertension induced by hypoxia.
RESULTS: We demonstrated that PTPRD is dramatically downregulated in PDGF-BB-treated PASMCs, pulmonary arteries from pulmonary hypertension rats, and blood and pulmonary arteries from lung specimens of patients with hypoxic pulmonary arterial hypertension (HPAH) and idiopathic PAH (iPAH). Subsequently, we found that PTPRD was downregulated by promoter methylation via DNMT1. Moreover, we found that PTPRD knockdown altered cell morphology and migration in PASMCs via modulating focal adhesion and cell cytoskeleton. We have demonstrated that the increase in cell migration is mediated by the PDGFRB/PLCγ1 pathway. Furthermore, under hypoxic condition, we observed significant pulmonary arterial remodeling and exacerbation of pulmonary hypertension in heterozygous PTPRD knock-out rats compared with the wild-type group. We also demonstrated that HET group treated with chronic hypoxia have higher expression and activity of PLCγ1 in the pulmonary arteries compared with wild-type group.
CONCLUSION: We propose that PTPRD likely plays an important role in the process of pulmonary vascular remodeling and development of pulmonary hypertension in vivo
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