138 research outputs found

    Multimodal deep learning for mapping forest dominant height by fusing GEDI with earth observation data

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    The integration of multisource remote sensing data and deep learning models offers new possibilities for accurately mapping high spatial resolution forest height. We found that GEDI relative heights (RH) metrics exhibited strong correlation with the mean of the top 10 highest trees (dominant height) measured in situ at the corresponding footprint locations. Consequently, we proposed a novel deep learning framework termed the multi-modal attention remote sensing network (MARSNet) to estimate forest dominant height by extrapolating dominant height derived from GEDI, using Setinel-1 data, ALOS-2 PALSAR-2 data, Sentinel-2 optical data and ancillary data. MARSNet comprises separate encoders for each remote sensing data modality to extract multi-scale features, and a shared decoder to fuse the features and estimate height. Using individual encoders for each remote sensing imagery avoids interference across modalities and extracts distinct representations. To focus on the efficacious information from each dataset, we reduced the prevalent spatial and band redundancies in each remote sensing data by incorporating the extended spatial and band reconstruction convolution modules in the encoders. MARSNet achieved commendable performance in estimating dominant height, with an R2 of 0.62 and RMSE of 2.82 m, outperforming the widely used random forest approach which attained an R2 of 0.55 and RMSE of 3.05 m. Finally, we applied the trained MARSNet model to generate wall-to-wall maps at 10 m resolution for Jilin, China. Through independent validation using field measurements, MARSNet demonstrated an R2 of 0.58 and RMSE of 3.76 m, compared to 0.41 and 4.37 m for the random forest baseline. Our research demonstrates the effectiveness of a multimodal deep learning approach fusing GEDI with SAR and passive optical imagery for enhancing the accuracy of high resolution dominant height estimation

    Prenatal Diagnosis of Pulmonary Sequestration by Ultrasound and Magnetic Resonance Imaging

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    A 36-year-old multigravida, G2P1, underwent routine ultrasound scan at 22+1 weeks of gestation, which revealed a single normally growing fetus with left intrathoracic mass and left displacement of the cardiac apex. The left intrathoracic wedge-shaped hyperechogenic mass, measuring 32 × 25 mm in size, was situated at the lower portion of the left lung. A combination of color and power Doppler ultrasound allowed visualization of a vessel arising from the descending aorta, which supplied the mass. The diagnosis of extralobar pulmonary sequestration was made. Magnetic resonance imaging (MRI) was also performed and revealed a well-defined mass with homogeneous high-signal intensity when compared with normal lung tissue in the left upper lung field, which was compatible with pulmonary sequestration. The pulmonary mass was followed up by color and power Doppler every 2 weeks. The peak velocity of 11.85 cm/sec and the diameter of the feeding artery of 1.19 mm gradually decreased and disappeared 8 weeks later. The intrathoracic mass disappeared 10 weeks later at 32+1 gestational weeks. Repeat MRI also revealed spontaneous regression of the mass in favor of resorption of sequestration. The fetus was delivered at 38+1 gestational weeks. A male newborn weighing 2,520 g was spontaneously delivered with an Apgar score of 8 at 1 minute and 9 at 5 minutes. In our patient, it is suggested that progressive decreases in the peak velocity of the feeding vessel heralded the spontaneous regression of pulmonary sequestration not associated with hydrops/hydrothorax

    Role of Endogenous Sulfur Dioxide in Regulating Vascular Structural Remodeling in Hypertension

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    Sulfur dioxide (SO2), an emerging gasotransmitter, was discovered to be endogenously generated in the cardiovascular system. Recently, the physiological effects of endogenous SO2 were confirmed. Vascular structural remodeling (VSR), an important pathological change in many cardiovascular diseases, plays a crucial role in the pathogenesis of the diseases. Here, the authors reviewed the research progress of endogenous SO2 in regulating VSR by searching the relevant data from PubMed and Medline. In spontaneously hypertensive rats (SHRs) and pulmonary hypertensive rats, SO2/aspartate aminotransferase (AAT) pathway was significantly altered. SO2 inhibited vascular smooth muscle cell (VSMC) proliferation, promoted apoptosis, inhibited the synthesis of extracellular collagen but promoted its degradation, and enhanced antioxidative capacity, thereby playing a significant role in attenuating VSR. However, the detailed mechanisms needed to be further explored. Further studies in this field would be important for the better understanding of the pathogenesis of systemic hypertension and pulmonary hypertension. Also, clinical trials are needed to demonstrate if SO2 would be a potential therapeutic target in cardiovascular diseases

    Ион-парная ВЭЖХ производных пиримидина и пурина

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    ПИРИМИДИНЫГЕТЕРОЦИКЛИЧЕСКИЕ СОЕДИНЕНИЯ ОДНОКОЛЬЦЕВЫЕПУРИНЫГЕТЕРОЦИКЛИЧЕСКИЕ СОЕДИНЕНИЯ ДВУХКОЛЬЦЕВЫЕХРОМАТОГРАФИЯ ЖИДКОСТНАЯ ВЫСОКОГО ДАВЛЕНИЯХРОМАТОГРАФИЯ ИОНООБМЕННАЯДНКРНКПРОТИВООПУХОЛЕВЫЕ СРЕДСТВАПРОТИВОВИРУСНЫЕ СРЕДСТВ

    Sulfur Dioxide Activates Cl-/HCO3- Exchanger via Sulphenylating AE2 to Reduce Intracellular pH in Vascular Smooth Muscle Cells

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    Sulfur dioxide (SO2) is a colorless and irritating gas. Recent studies indicate that SO2 acts as the gas signal molecule and inhibits vascular smooth muscle cell (VSMC) proliferation. Cell proliferation depends on intracellular pH (pHi). Transmembrane cystein mutation of Na+- independent Cl-/HCO3- exchanger (anion exchanger, AE) affects pHi. However, whether SO2 inhibits VSMC proliferation by reducing pHi is still unknown. Here, we investigated whether SO2 reduced pHi to inhibit the proliferation of VSMCs and explore its molecular mechanisms. Within a range of 50–200 μM, SO2 was found to lower the pHi in VSMCs. Concurrently, NH4Cl pre-perfusion showed that SO2 significantly activated AE, whereas the AE inhibitor 4,4′-diisothiocyanatostilbene- 2,20-disulfonic acid (DIDS) significantly attenuated the effect of SO2 on pHi in VSMCs. While 200 μM SO2 sulphenylated AE2, while dithiothreitol (DTT) blocked the sulphenylation of AE2 and subsequent AE activation by SO2, thereby restoring the pHi in VSMCs. Furthermore, DIDS pretreatment eliminated SO2-induced inhibition of PDGF-BB-stimulated VSMC proliferation. We report for the first time that SO2 inhibits VSMC proliferation in part by direct activation of the AE via posttranslational sulphenylation and induction of intracellular acidification

    Value of Immediate Heart Rate Alteration From Supine to Upright in Differential Diagnosis Between Vasovagal Syncope and Postural Tachycardia Syndrome in Children

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    Objectives: To explore the predictive value of immediate heart rate alteration from supine to upright in the differential diagnosis between vasovagal syncope (VVS) and postural tachycardia syndrome (POTS) in children.Materials and Methods: A total of 76 pediatric outpatients or inpatients who visited the Peking University First Hospital from July 2016 to November 2017 were recruited in the study. Among them, 52 patients were diagnosed with VVS and 24 patients were diagnosed with POTS. The differential diagnostic value of acceleration index (AI) and 30/15 ratio was evaluated by the receiver operating characteristic (ROC) curve. An external validation test was performed in another 46 patients.Results: Compared with the cases in the VVS group, patients in the POTS group had a significantly increased AI but a decreased 30/15 ratio (33.495 ± 8.472 vs. 23.440 ± 8.693, p < 0.001; 0.962 ± 0.067 vs. 1.025 ± 0.084, p = 0.002; respectively). The ROC curves showed that AI and 30/15 ratio were useful for differentiating POTS from VVS. A cut-off value of AI set at 28.180 yielded a sensitivity of 79.2% and a specificity of 73.1%. A cut-off value of 30/15 ratio set at 1.025 yielded a sensitivity of 87.5% and a specificity of 61.5%. A combined use of these two indices improved the sensitivity to 95.8% when either AI or 30/15 was used, and specificity to 80.8% with the use of both AI and 30/15 at the same diagnosis. The external validation test showed that the positive and negative predictive values of the AI and 30/15 ratio were 77.3 and 79.2%, and 72.0 and 81.0%, respectively. The positive predictive value increased to 87.5% when both the AI and 30/15 ratio cut-off values were used together.Conclusions: The AI and 30/15 ratio, which are easy to perform and non-invasive, have proper sensitivity and specificity to differentiate patients with POTS from those with VVS. The combination of these two indices significantly improves the predictive value

    Genome assembly and gene expression in the American black bear provides new insights into the renal response to hibernation.

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    The prevalence of chronic kidney disease (CKD) is rising worldwide and 10-15% of the global population currently suffers from CKD and its complications. Given the increasing prevalence of CKD there is an urgent need to find novel treatment options. The American black bear (Ursus americanus) copes with months of lowered kidney function and metabolism during hibernation without the devastating effects on metabolism and other consequences observed in humans. In a biomimetic approach to better understand kidney adaptations and physiology in hibernating black bears, we established a high-quality genome assembly. Subsequent RNA-Seq analysis of kidneys comparing gene expression profiles in black bears entering (late fall) and emerging (early spring) from hibernation identified 169 protein-coding genes that were differentially expressed. Of these, 101 genes were downregulated and 68 genes were upregulated after hibernation. Fold changes ranged from 1.8-fold downregulation (RTN4RL2) to 2.4-fold upregulation (CISH). Most notable was the upregulation of cytokine suppression genes (SOCS2, CISH, and SERPINC1) and the lack of increased expression of cytokines and genes involved in inflammation. The identification of these differences in gene expression in the black bear kidney may provide new insights in the prevention and treatment of CKD

    Novel Urine Cell-Free DNA Methylation Markers for Hepatocellular Carcinoma

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    An optimized hepatocellular carcinoma (HCC)-targeted methylation next generation sequencing assay was developed to discover HCC-associated methylation markers directly from urine for HCC screening. Urine cell-free DNA (ucfDNA) isolated from a discovery cohort of 31 non-HCC and 30 HCC was used for biomarker discovery, identifying 29 genes with differentially methylated regions (DMRs). Methylation-specific qPCR (MSqPCR) assays were developed to verify the selected DMRs corresponding to 8 genes (GRASP, CCND2, HOXA9, BMP4, VIM, EMX1, SFRP1, and ECE). Using archived ucfDNA, methylation of GRASP, HOXA9, BMP4, and ECE1, were found to be significantly different (p \u3c 0.05) between HCC and non-HCC patients. The four markers together with previously reported GSTP1 and RASSF1A markers were assessed as a 6-marker panel in an independent training cohort of 87 non-HCC and 78 HCC using logistic regression modeling. AUROC of 0.908 (95% CI, 0.8656-0.9252) was identified for the 6-marker panel with AFP, which was significantly higher than AFP-alone (AUROC 0.841 (95% CI, 0.778-0.904), p = 0.0026). Applying backward selection method, a 4-marker panel was found to exhibit similar performance to the 6-marker panel with AFP having 80% sensitivity compared to 29.5% by AFP-alone at a specificity of 85%. This study supports the potential use of methylated transrenal ucfDNA for HCC screening

    Transcriptional profiling of the effects of 25-hydroxycholesterol on human hepatocyte metabolism and the antiviral state it conveys against the hepatitis C virus

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    <p>Abstract</p> <p>Background</p> <p>Hepatitis C virus (HCV) infection is a global health problem. A number of studies have implicated a direct role of cellular lipid metabolism in the HCV life cycle and inhibitors of the mevalonate pathway have been demonstrated to result in an antiviral state within the host cell. Transcriptome profiling was conducted on Huh-7 human hepatoma cells bearing subgenomic HCV replicons with and without treatment with 25-hydroxycholesterol (25-HC), an inhibitor of the mevalonate pathway that alters lipid metabolism, to assess metabolic determinants of pro- and antiviral states within the host cell. These data were compared with gene expression profiles from HCV-infected chimpanzees.</p> <p>Results</p> <p>Transcriptome profiling of Huh-7 cells treated with 25-HC gave 47 downregulated genes, 16 of which are clearly related to the mevalonate pathway. Fewer genes were observed to be upregulated (22) in the presence of 25-HC and 5 genes were uniquely upregulated in the HCV replicon bearing cells. Comparison of these gene expression profiles with data collected during the initial rise in viremia in 4 previously characterized HCV-infected chimpanzees yielded 54 overlapping genes, 4 of which showed interesting differential regulation at the mRNA level in both systems. These genes are PROX1, INSIG-1, NK4, and UBD. The expression of these genes was perturbed with siRNAs and with overexpression vectors in HCV replicon cells, and the effect on HCV replication and translation was assessed. Both PROX1 and NK4 regulated HCV replication in conjunction with an antiviral state induced by 25-hydroxycholesterol.</p> <p>Conclusion</p> <p>Treatment of Huh-7 cells bearing HCV replicons with 25-HC leads to the downregulation of many key genes involved in the mevalonate pathway leading to an antiviral state within the host cell. Furthermore, dysregulation of a larger subset of genes not directly related to the mevalonate pathway occurs both in 25-HC-treated HCV replicon harbouring cells as well as during the initial rise in viremia in infected chimpanzees. Functional studies of 3 of these genes demonstrates that they do not directly act as antiviral gene products but that they indirectly contribute to the antiviral state in the host cell. These genes may also represent novel biomarkers for HCV infection, since they demonstrate an outcome-specific expression profile.</p
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