Effects of Supplementation with Oregano Essential Oil during Late Gestation and Lactation on Serum Metabolites, Antioxidant Capacity and Fecal Microbiota of Sows.

A total of 20 healthy white × landrace sows were evenly and randomly divided into two groups, and fed basal diets unsupplemented or supplemented with 500 g/t Meriden-Stim® from day 100 of gestation until day 21 of lactation. Serum and fecal samples were collected from the sows on the final day for subsequent analysis. Compared to the control group, there were no significant differences in the sows' performances; however, an increase was observed in the piglets' weight at weaning (p = 0.08). Moreover, oregano essential oil (OEO) significantly reduced the levels of urea (UREA) (p < 0.01), total cholesterol (TC) (p < 0.05), low-density lipoprotein (LDL-C) (p < 0.05) and alanine aminotransferase (ALT) (p < 0.05) in serum. In terms of antioxidant indexes in serum, the catalase (CAT) and glutathione (GSH) levels showed significant increases (p < 0.05) while the malondialdehyde (MDA) level exhibited a decrease tendency (p = 0.09). 16S rRNA analysis identified the specific bacteria taxa in feces. OEO significantly decreased the relative abundance of Proteobacteria and Actinobacteria at the phylum level (p < 0.05). At the genus level, OEO significantly increased the relative abundance of Lactobacillus and Prevotellaceae UCG 003 and UCG 005, while decreasing that of Escherichia-Shigella (p < 0.05). Taken together, OEO supplementation in maternal diets during late gestation and lactation improved serum metabolites, antioxidant capacity and regulated the intestinal-flora balance of sows, thereby tending to increase the piglets' weight at weaning.

Serum amyloid A and mitochondrial DNA in extracellular vesicles are novel markers for detecting traumatic brain injury in a mouse model.

This study investigates the potential use of circulating extracellular vesicles' (EVs) DNA and protein content as biomarkers for traumatic brain injury (TBI) in a mouse model. Despite an overall decrease in EVs count during the acute phase, there was an increased presence of exosomes (CD63+ EVs) during acute and an increase in microvesicles derived from microglia/macrophages (CD11b+ EVs) and astrocytes (ACSA-2+ EVs) in post-acute TBI phases, respectively. Notably, mtDNA exhibited an immediate elevation post-injury. Neuronal (NFL) and microglial (Iba1) markers increased in the acute, while the astrocyte marker (GFAP) increased in post-acute TBI phases. Novel protein biomarkers (SAA, Hp, VWF, CFD, CBG) specific to different TBI phases were also identified. Biostatistical modeling and machine learning identified mtDNA and SAA as decisive markers for TBI detection. These findings emphasize the importance of profiling EVs' content and their dynamic release as an innovative diagnostic approach for TBI in liquid biopsies.

Racial Disparities in Cataract Surgery Timeline and Intraocular Lens Selection: A Retrospective Study.

Purpose: There is a significant amount of literature focusing on racial inequities in utilization rates and intraoperative complications of cataract surgery. Unfortunately, little is known about racial disparities regarding the timeline of cataract surgery and intraocular lens (IOL) selection. This study investigated whether black patients have a different preoperative and postoperative cataract surgery timeline and IOL selection than white patients. Methods: A total of 10,235 patients (83.47% white) were retrospectively identified from a tertiary academic center who underwent cataract surgery between 2015 and 2022. Each patient's best corrected visual acuity (BCVA), slit lamp findings, and surgical timeline were recorded. IOL selection was categorized as standard or premium. Results: Black patients had significantly worse mean ± SD preoperative logMAR BCVA than white patients (0.47 ± 0.55 vs. 0.58 ± 0.70, respectively; P = 0.0117) and were significantly less likely to receive surgery within 120 days of referral (RR, 0.71 [95% confidence interval {CI}, 0.64-0.79]; P < 0.0001). White patients were 25%, 24%, and 29% less likely to follow-up than black patients at postoperative day 1, day 7, and day 30, respectively (P < 0.0001). White patients were 6.09 (95% CI, 3.49, 10.63) times more likely to receive a premium IOL compared to black patients (P < 0.0001). Conclusions: Black patients experienced more delays with receiving cataract surgery but are more adherent with postoperative follow-up. Black patients were far less likely to receive a premium IOL than white patients. Translational Relevance: Increased awareness of racial inequities in cataract surgery may improve the delivery of eye care to minority groups.

Association Between Aspirin-Exacerbated Respiratory Disease and Atherosclerotic Cardiovascular Disease: A Retrospective Review of US Claims Data.

BACKGROUND: Aspirin-exacerbated respiratory disease (AERD) consists of chronic rhinosinusitis with nasal polyps (CRSwNP), asthma, and hypersensitivity to aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs). Asthma is associated with increased risk of atherosclerotic cardiovascular diseases (ASCVD). However, there is lack of data on association between AERD and ASCVD. OBJECTIVE: To investigate the relationship between AERD and subsequent risk of ASCVD. METHODS: An algorithm to find patients with AERD was generated and validated through chart review at our home institution. This algorithm was applied to a national insurance claims database to obtain data for a retrospective cohort study. Demographic and comorbidity data were obtained for propensity matching. Several methods of analysis were performed on the data. RESULTS: A total of 571 patients met criteria for AERD; 3909 met criteria for asthma, CRSwNP, and no allergy to aspirin or NSAIDs (group 1); and 75,050 met criteria for asthma, CRS without nasal polyps, and no allergy to aspirin or NSAIDs (group 2). After covariate adjustment, AERD was significantly associated with ASCVD, including severe ASCVD, over groups 1 and 2 regardless of asthma severity. CONCLUSION: Patients with AERD are at higher risk of ASCVD than patients with asthma and CRSwNP or CRS without nasal polyps, underscoring the need for early ASCVD screening and a consideration for aspirin desensitization or use of a nonaspirin antiplatelet agent in the setting of AERD and comorbid ASCVD.

VAMP8 suppresses the metastasis via DDX5/ß-catenin signal pathway in osteosarcoma.

Osteosarcoma is a highly metastatic malignant bone tumor, necessitating the development of new treatments to target its metastasis. Recent studies have revealed the significance of VAMP8 in regulating various signaling pathways in various types of cancer. However, the specific functional role of VAMP8 in osteosarcoma progression remains unclear. In this study, we observed a significant downregulation of VAMP8 in osteosarcoma cells and tissues. Low levels of VAMP8 in osteosarcoma tissues were associated with patients' poor prognosis. VAMP8 inhibited the migration and invasion capability of osteosarcoma cells. Mechanically, we identified DDX5 as a novel interacting partner of VAMP8, and the conjunction of VAMP8 and DDX5 promoted the degradation of DDX5 via the ubiquitin-proteasome system. Moreover, reduced levels of DDX5 led to the downregulation of ß-catenin, thereby suppressing the epithelial-mesenchymal transition (EMT). Additionally, VAMP8 promoted autophagy flux, which may contribute to the suppression of osteosarcoma metastasis. In conclusion, our study anticipated that VAMP8 inhibits osteosarcoma metastasis by promoting the proteasomal degradation of DDX5, consequently inhibiting WNT/ß-catenin signaling and EMT. Dysregulation of autophagy by VAMP8 is also implicated as a potential mechanism. These findings provide new insights into the biological nature driving osteosarcoma metastasis and highlight the modulation of VAMP8 as a potential therapeutic strategy for targeting osteosarcoma metastasis.

The transcription factor XBP1 in dendritic cells promotes the TH2 cell response in airway allergy.

Dendritic cells (DCs) that express T cell immunoglobulin domain molecule-4 (TIM4), a cell surface receptor for phosphatidylserine, induce T helper 2 (TH2) cell responses and allergic reactions. We elucidated the role of the transcription factor X-box-binding protein-1 (XBP1) in the induction of the TH2 cell response through its role in generating TIM4+ DCs. We found that XBP1 was required for TIM4 mRNA and protein expression in airway DCs in response to the cytokine interleukin-2 (IL-2) and that this pathway was required for TIM4 expression on DCs in response to the allergens PM2.5 and Derf1. The IL-2-XBP1-TIM4 axis in DCs contributed to Derf1/PM2.5-induced, aberrant TH2 cell responses in vivo. An interaction between the guanine nucleotide exchange factor Son of sevenless-1 (SOS1) and the GTPase RAS promoted XBP1 and TIM4 production in DCs. Targeting the XBP1-TIM4 pathway in DCs prevented or alleviated experimental airway allergy. Together, these data suggest that XBP1 is required for TH2 cell responses by inducing the development of TIM4+ DCs, which depends on the IL-2-XBP1-SOS1 axis. This signaling pathway provides potential therapeutic targets for the treatment of TH2 cell-dependent inflammation or allergic diseases.

The Impact of Neisseria gonorrhoeae Mono- and Coinfection on Adverse Pregnancy Outcomes.

Background: Sexually transmitted infections (STIs) have recently been linked to hypertensive disorders of pregnancy (HDP). However, the impact of Neisseria gonorrhoeae on risk of HDP is not well understood. This study determined the impact of gonorrhea and gonorrhea coinfection on HDP and other adverse pregnancy outcomes in a population with a high screening rate and presumed treatment. Methods: This retrospective study included 29 821 singleton births between 2016 and 2021. The STI testing results, demographic variables, and pregnancy outcomes were identified from electronic health records. The HDP were primary outcomes of interest including gestational hypertension, preeclampsia, and superimposed preeclampsia. We further examined preeclampsia subtypes defined by severe features and gestational age of delivery (term and preterm preeclampsia). Secondary outcomes included preterm premature rupture of membranes, chorioamnionitis, and preterm delivery. Logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs). Models were adjusted for maternal age, maternal race/ethnicity, and smoking. Results: Gonorrhea screening occurred in 95% of the population. Gonorrhea increased the odds of preterm preeclampsia (adjusted OR [ORadj.], 1.95; 95% CI, 1.02-3.73) and preterm birth (ORadj., 1.78; 95% CI, 1.22-2.60). Furthermore, gonorrhea-chlamydia coinfection was associated with preterm birth (ORadj., 1.77; 95% CI, 1.03-3.04). However, results were similar when we examined gonorrhea monoinfection (ORadj., 1.76; 95% CI, 1.04-2.97). Conclusions: Among a diverse population of pregnant individuals, gonorrhea increased odds of preterm preeclampsia and preterm delivery Further research is needed to determine the burden of STIs on HDP, including investigations into biological effects during pregnancy.

First Report of Leaf Spot on Soybean Caused by Epicoccum sorghinum in Heilongjiang Province, China.

Soybean (Glycine max (Linn.) Merr.) is one of the important oil crops in China. In September 2022, a new soybean leaf spot disease was found in Zhaoyuan County, Suihua City, Heilongjiang Province, China. Symptoms of the initial formation of irregular brown lesions on the leaves, dark brown inside, the periphery is yellow, vein chlorotic yellow, severe leaf spots connected into pieces, late fall off, not the same as previously reported soybean leaf spot (Fig. 1A). The leaf samples of infected plants were collected, and the leaf tissue (5 × 5 mm) was cut from the edge of the lesion, and then surface sterilized with 3% sodium hypochlorite for 5 min, rinsed with sterile distilled water for 3 times, and inoculated on potato dextrose agar (PDA) at 28°C. Isolates growing around the tissues from samples were subcultured on PDA, and 3 isolates were obtained using the single-spore isolation method. The fungal hyphae were white or grayish white in early stage, and the hyphae with light green concentric ring appeared on the front of the colony after 3 days, appeared orange, pink or white convex, irregular shape, reddish brown on the front of the colony for 10 days and black spherical pycnidium can be produced in the hyphae layer for 15 days (Fig.1D, E). Conidia were oval, hyaline, unicellular, aseptate, and 2.3 to 3.7 × 4.1 to 6.8 µm (n=30, Fig. 1F). Chlamydospores were subglobose, light brown, unicellular or multicellular, and 7.2 to 14.7 × 12.2 to 43.9 µm (n=30, Fig. 1H, I). Pycnidia mostly spheroid, brown, and 47.1 to 114.4 × 72.6 to 167.4 µm (n=30, Fig. 1G). A cetyl trimethyl ammonium bromide method was used to extract DNA from 7-day-old. Internal transcribed spacer (ITS), RNA polymerase II (RPB2) and ß-tubulin (TUB) gene were amplified using ITS1/ITS4 (White et al. 1990), RPB2-5F/RPB2-7cR (Liu et al. 1999) and BT2a/Bt2b (O'Donnell et al. 1997) primers respectively. The sequences obtained by polymerase chain reaction (PCR) were sequenced and the results showed that the DNA sequences of the 3 isolates were identical. Therefore, the sequence of isolate DNES22-01, DNES22-02 and DNES22-03 was submitted to GenBank. According to BLAST search, the ITS (OP884646), RPB2 (OP910000) and TUB (OP909999) sequences showed 99.81% similarity to Epicoccum sorghinum strain LC12103 (MN215621.1), 99.07% to strain P-XW-9A (MW446946.1), and 98.85% with the strain UMS (OM048108.1), respectively. Phylogenetic analysis by maximum likelihood method (MEGA7.0) generated based on the ITS, RPB2 and TUB sequences indicated that the isolates formed a supported clade to the related E. sorghinum type sequences. Isolates was found to be most closely related to E. sorghinum and far from other species. Based on morphological and phylogenetic characteristics, isolates DNES22-01, DNES22-02 and DNES22-03 was identified as E. sorghinum (Bao et al. 2019; Chen et al. 2021; Zhang et al. 2022). At the 4-leaf-stage, 10 soybean plants were inoculated by spraying with a conidial suspension (1 × 106 spores·ml-1). Sterile water served as a control. The test was repeated 3 times. All samples were incubated in a growth chamber at 27°C. Symptoms typical developed on the leaves after 7 days, but control samples remained healthy (Fig.1B, C). The fungus was reisolated from symptomatic tissues and identified as E. sorghinum by morphology characteristics and molecular characterization. To our knowledge, this is the first report of E. sorghinum causing leaf spot on soybean in Heilongjiang, China. The results can provide the basis for future studies on the occurrence, prevention, and management of this disease.

Knockdown of CENPU inhibits cervical cancer cell migration and stemness through the FOXM1/Wnt/ß-catenin pathway.

Currently, the clinical outcome of cervical cancer (CC) is still undesirable, and it is urgent to explore more treatment strategies for CC. In this study, the effects of CENPU on migration and stemness of CC was studied. The CENPU expression were retrieved from The Cancer Genome Atlas (TCGA). The effects of CENPU on the viability and proliferation of cells were evaluated by CCK-8 assay and colony formation assay. Wound healing assay and invasion assay were chosen to assess migration and invasion of cells. Tumorsphere-forming assay was applied for testing the stemness. Western blot analysis was applied for assessing the level of CENPU, Nanog, Oct4, FOXM1, ß-catenin, c-myc and MMP-7. The tumor sizes and volumes were also measured. The TCGA data and WB assay suggested that CENPU was upregulated in CC. CENPU knockdown would inhibit the viability of CC cells and prohibit the migration and invasion of cells. Tumorsphere-forming assay and WB results suggested that CENPU silencing decreased the sphere formation rate and the expression of Nanog and Oct4. Moreover, CENPU knockdown suppressed the expression of FOXM1, ß-catenin, c-myc and MMP-7 by WB. In vivo study demonstrated that CENPU knockdown inhibited the growth of CC, indicated by reduced sizes and volumes of CC. In summary, our results suggested that knockdown of CENPU inhibited CC migration and stemness through the FOXM1/Wnt/ß-catenin pathway.

A comparison of Atrial Fibrillation Detection Strategies After Ischemic Stroke-A Retrospective Study.

Objective of this retrospective study was to determine if long-term continuous cardiac monitoring with Implantable loop recorder (ILR) in patients with Cryptogenic strokes or TIA is superior at detecting Atrial Fibrillation (AF) than 30-day Event Monitor (EM) and 48-hour Holter Monitor (HM). Furthermore, we aimed to deduce if uncovering AF leads to lower risk of future ischemic strokes, or reduction in mortality. In 20%-30% cases, the cause of stroke remained unexplained after diagnostic workup which has led to coining of the term, Cryptogenic Stroke (CS). Undiagnosed AF is a prime suspect in CS, but guidelines do not recommend initiation of anticoagulation unless AF has formally been detected. IRB approved retrospective study included patients with at least 1 episode of ischemic stroke or TIA without identifiable cause and was monitored with either HM, EM or ILR to diagnose any undiscovered AF. All patients (n = 531) had at least 1 year, and up to 3 years, of follow-up after device placement. Chi-Squared analysis and Multivariable logistic regression demonstrated no statistically significant difference among 3 devices for detection of AF within 1 month of index stroke but a significant difference in AF detection was observed at 6, 12 and 24 months. Cox proportional hazard model showed device type had no significant impact on secondary outcomes: Subsequent ischemic stroke or TIA, Initiation of anticoagulation, Mortality and Incidence of major bleeding. Despite the superiority of AF detection by ILR, it is not superior to HM or EM in lowering the risk of subsequent stroke or TIA, or in reducing mortality.

Obtaining acidic and basic charge variants using a twin-column continuous chromatography system.

For recombinantly produced monoclonal antibody (mAb), charge variants including acidic and basic species are common heterogeneities. For characterization purpose, sufficient amount of acidic and basic species with high purity is needed. In this work, we developed an approach that allows for continuous separating and collecting of acidic and basic charge variants. First, with batch-mode cation exchange (CEX) chromatography, the load density and linear salt gradient elution conditions under which good separation of both charge variants can be achieved were determined. Next, a stepwise elution protocol was developed based on the linear gradient elution. Finally, acidic and basic charge variants were persistently produced under stepwise elution using a customized twin-column continuous chromatography system. This approach allows acidic and basic charge variants with high purity (i.e., >90%) to be efficiently generated in sufficient amount, which greatly facilitates the necessary characterization of these mAb variants.

COL8A1 Promotes NSCLC Progression Through IFIT1/IFIT3-Mediated EGFR Activation.

Activation of EGFR is a major risk factor for non-small cell lung cancer (NSCLC). Understanding the molecular events promoting EGFR activation can help us gain more insights into the progression of NSCLC. In this study, we demonstrate that collagen type VIII alpha 1 chain (COL8A1), an extracellular matrix component, was overexpressed in NSCLC. In NSCLC cells, knockdown of COL8A1 suppressed cell growth, cycle progression, and migration, and induced cell apoptosis. While COL8A1 overexpression promoted cell proliferation and inhibited cell apoptosis. In addition, we found that COL8A1 depletion reduced interferon response signaling and downregulated (IFIT1) and interferon-induced proteins with tetratricopeptide repeats 3 (IFIT3). Moreover, we indicated that COL8A1 could upregulate IFIT1 and IFIT3 mediated EGFR activation in vitro and in vivo. Lastly, there was a positive correlation among COL8A1, IFIT1, and IFIT3 expression, and EGFR activity in patients with NSCLC. Overall, our data demonstrate that COL8A1 contributes to NSCLC proliferation and invasion through EGFR activation, dependent on IFIT1 and IFIT3 expression.

Flow-Induced Concentration Nonuniformity and Shear Banding in Entangled Polymer Solutions.

Recent models have predicted entangled polymer solutions could shear band due to unstable flow-induced demixing. This work provides the first experimental probe of the in situ concentration profile of entangled polymer solutions under shear. At shear rates above a critical value, we show that the concentration and velocity profiles can develop bands, in quantitative agreement with steady-state model predictions. These findings highlight the critical importance of flow-concentration coupling in entangled polymer solutions.

Modulating oxidative stress counteracts specific antigen-induced regulatory T-cell apoptosis in mice.

Treg are known to have a central role in orchestrating immune responses, but less is known about the destiny of Treg after being activated by specific Ags. This study aimed to investigate the role of superoxide dismutase, an active molecule in the regulation of oxidative stress in the body, in the prevention of Treg apoptosis induced by specific Ags. Ag-specific Tregs were isolated from the DO11.10 mouse intestine. A food allergy mouse model was developed with ovalbumin as the specific Ag and here, we observed that exposure to specific Ag induced Treg apoptosis through converting the precursor of TGF-ß to its mature form inside the Tregs. Oxidative stress was induced in Tregs upon exposure to specific Ags, in which Smad3 bound the latency-associated peptide to induce its degradation, converting the TGF-ß precursor to its mature form, TGF-ß. Suppressing oxidative stress in Tregs alleviated the specific Ag-induced Treg apoptosis in in vitro experiments and suppressed experimental food allergy by preventing the specific Ag-induced Treg apoptosis in the intestine. In conclusion, exposure to specific Ags induces Treg apoptosis and it can be prevented by upregulating superoxide dismutase or suppressing reactive oxidative species in Tregs.

Chimeric antigen-guiding extracellular vesicles eliminate antigen-specific Th2 cells in subjects with food allergy.

BACKGROUND: Antigen (Ag)-specific T helper (Th)2 cells play a central role in food allergy (FA) pathogenesis. Methods can be used to eliminate Ag-specific Th2 cells that are currently lacking. This study aims to eliminate the Ag-specific Th2 cells with a novel nanoparticle, the mEV (modified extracellular vesicles, that carry a chimeric antigen peptide, MHC II and caspase 3) in a murine FA model. METHODS: mEVs were generated by exposing dendritic cells (DC) to ovalbumin (OVA, a specific Ag) and recombinant caspase 3 (Casp3) in the culture overnight. Exosomes were purified from culture supernatant by the magnetic antibody approach. A murine FA model was developed with OVA as the specific Ag. RESULTS: Purified mEVs had the molecular markers of extracellular vesicle, CD81, CD63, and CD9, cleaved Casp3 and MHC II/OVA complexes. mEVs specifically bound to the surface of Ag-specific CD4+ T cells, induced Ag-specific CD4+ T cell apoptosis both in vitro and in vivo as well as increased regulatory T cells in the intestinal tissues. Administration of mEV efficiently suppressed experimental FA. CONCLUSIONS: mEVs carry Ag/MHC II complexes and Casp3, that can induce Ag-specific Th2 cell apoptosis. Administration of mEV can efficiently suppress experimental FA. The results suggest that the mEVs have the translational potential to be used in the treatment of FA and other allergic diseases.

Integrin αvß6 cooperates with resiquimod to restore antigen-specific immune tolerance in airway allergy.

BACKGROUND: Integrin αvß6 can convert the transforming growth factor (TGF)-ß precursor to the mature form. Resiquimod (R848) can generate TGF-ß-producing regulatory T cells (Treg). Thus, to concurrent administration of specific antigen and R848 may generate antigen-specific Tregs, that is expected to restore immune tolerance in subjects with airway allergic diseases (AAD). METHODS: A bio-nanoparticle, designated Rexo, containing an antigen/MHC II complex and R848, was naturally assembled in dendritic cells, that was released as an exosome. An AAD mouse model was developed used to test the effects of Rexo on restoring the immune tolerance in the airways. RESULTS: Exposure to R848 failed to induce Tregs in the ß6-deficient mouse airway tissues, that were successfully induced in wild type mice. The results were validated inin vitro experiments. R848 activated the TLR7/MyD88/p38 signal pathway to increase the αvß6 levels in CD4+ T cells, the αvß6 then converted the TGF-ß precursor to its mature form, and thus, induced Treg generation. Administration of Rexo restored the antigen-specific immune tolerance in the airways manifesting efficiently suppressing experimental AAD by inducing antigen-specific Tregs in the airways and inhibiting antigen-specific Th2 response. CONCLUSIONS: Rexos can inhibit experimental AAD via inducing antigen-specific Tregs to restore immune tolerance in the airway tissues, suggesting that Rexos have the translational potential to be used in the treatment of AAD.

FcγRI plays a critical role in patients with ulcerative colitis relapse.

Ulcerative colitis (UC) is a disease that frequently relapses and affects more than 0.1% general population; the underlying mechanism is poorly understood. Published data show that polymorphonuclear neutrophils (PMN) contribute to the pathogenesis of UC. This study aims to identify antigen (Ag)-specific PMNs and investigate their role in UC relapse. In this study, the correlation between PMN activities and UC relapse was assessed in a group of UC patients. A UC mouse model was developed to expand the findings of UC patient study. The results showed that a positive correlation was detected between the high PMN activities and the food Ag-specific IgG amounts in colon biopsies of UC patients. UC patient-derived Ag-specific PMNs could be activated upon exposure to food specific Ag. The Ag/FcγRI complexes were detected on the surface of PMNs in UC patients. Re-exposure of sensitized PMNs to specific Ag triggered PMN activation and induced UC-like inflammation in the mouse colon. We conclude that FcγRI plays a critical role in UC relapse. Inhibition of FcγRI can efficiently inhibits experimental UC.

Extracting Rectified Building Footprints from Traditional Orthophotos: A New Workflow.

Deep learning techniques such as convolutional neural networks have largely improved the performance of building segmentation from remote sensing images. However, the images for building segmentation are often in the form of traditional orthophotos, where the relief displacement would cause non-negligible misalignment between the roof outline and the footprint of a building; such misalignment poses considerable challenges for extracting accurate building footprints, especially for high-rise buildings. Aiming at alleviating this problem, a new workflow is proposed for generating rectified building footprints from traditional orthophotos. We first use the facade labels, which are prepared efficiently at low cost, along with the roof labels to train a semantic segmentation network. Then, the well-trained network, which employs the state-of-the-art version of EfficientNet as backbone, extracts the roof segments and the facade segments of buildings from the input image. Finally, after clustering the classified pixels into instance-level building objects and tracing out the roof outlines, an energy function is proposed to drive the roof outline to maximally align with the building footprint; thus, the rectified footprints can be generated. The experiments on the aerial orthophotos covering a high-density residential area in Shanghai demonstrate that the proposed workflow can generate obviously more accurate building footprints than the baseline methods, especially for high-rise buildings.

House Dust Mite Specific Antibodies induce Neutrophilic Inflammation in the Heart.

Rationale: Inflammatory heart disorders are among the causes of human death. The causative factors of heart inflammation are to be further elucidated. House dust mite (HDM)-derived protein antigens are involved in the pathogenesis of many human diseases. This study aims to investigate the role of HDM-specific autoantibodies in the pathogenesis of heart inflammation. Methods: Human heart tissue samples were obtained from surgically removed hearts in heart transplantation. The interaction of the heart tissues with HDM-specific antibodies was assessed by pertinent immune analysis. The role of HDM-specific autoantibodies in the induction of heart inflammation was assessed with a murine model. Results: HDM-specific IgG (mIgG) was detected in the serum of patients with myocarditis (Mcd); the mIgG titers were positively correlated with the neutrophil counts in the heart tissues. The mIgG specifically bound to keratin-10 (KRT10) in heart vascular endothelial cells and the heart tissue protein extracts. The amounts of C3a, C5a and C5b-9 were increased in the mouse heart tissues after exposing to mIgG. In the presence of the complement-containing serum, mIgG bound cardiovascular epithelial monolayers to impair the barrier functions. Administration of mIgG or HDM induced the Mcd-like inflammation in the heart, in which neutrophils were the dominant cellular components in the infiltration of inflammatory cells. Conclusions: Mcd patients with neutrophilic inflammation in the heart had higher serum levels of mIgG. The mIgG bound heart endothelial cells to impair the endothelial barrier functions and induce neutrophilic inflammation in the heart.