Early Immunomodulatory Program Triggered by Protolerogenic Bifidobacterium pseudolongum Drives Cardiac Transplant Outcomes.

BACKGROUND: Despite ongoing improvements to regimens preventing allograft rejection, most cardiac and other organ grafts eventually succumb to chronic vasculopathy, interstitial fibrosis, or endothelial changes, and eventually graft failure. The events leading to chronic rejection are still poorly understood and the gut microbiota is a known driving force in immune dysfunction. We previously showed that gut microbiota dysbiosis profoundly influences the outcome of vascularized cardiac allografts and subsequently identified biomarker species associated with these differential graft outcomes. METHODS: In this study, we further detailed the multifaceted immunomodulatory properties of protolerogenic and proinflammatory bacterial species over time, using our clinically relevant model of allogenic heart transplantation. RESULTS: In addition to tracing longitudinal changes in the recipient gut microbiome over time, we observed that Bifidobacterium pseudolongum induced an early anti-inflammatory phenotype within 7 d, whereas Desulfovibrio desulfuricans resulted in a proinflammatory phenotype, defined by alterations in leukocyte distribution and lymph node (LN) structure. Indeed, in vitro results showed that B pseudolongum and D desulfuricans acted directly on primary innate immune cells. However, by 40 d after treatment, these 2 bacterial strains were associated with mixed effects in their impact on LN architecture and immune cell composition and loss of colonization within gut microbiota, despite protection of allografts from inflammation with B pseudolongum treatment. CONCLUSIONS: These dynamic effects suggest a critical role for early microbiota-triggered immunologic events such as innate immune cell engagement, T-cell differentiation, and LN architectural changes in the subsequent modulation of protolerant versus proinflammatory immune responses in organ transplant recipients.

A Load-Adaptive Driving Method for a Quasi-Continuous-Wave Laser Diode.

A quasi-continuous-wave (QCW) laser diode (LD) driver is commonly used to drive diode bars and stacks designed specifically for QCW operations in solid-state lasers. Such drivers are optimized to deliver peak current and voltage pulses to LDs while maintaining low average power levels. As a result, they are widely used in laser processing devices and laser instruments. Traditional high-energy QCW LD drivers primarily use capacitors as energy storage components and pulsed constant-current sources with op-amps and power metal-oxide-semiconductor field-effect transistors (MOSFETs) as their core circuits for generating repeated constant-current pulses. The drawback of this type of driver is that the driver's output voltage needs to be manually adjusted according to the operating voltage of the load before use to maximize driver efficiency while providing a sufficient current. Another drawback is its inability to automatically adjust the output voltage to maintain high efficiency when the load changes during the driver operation. Drastic changes in the load can cause the driver to fail to function properly in extreme cases. Based on the above traditional circuit structure, this study designed a stability compensation circuit and realized a QCW LD driver for driving a GS20 diode stack with a maximum repetition rate of 100 Hz, a constant current of approximately 300 A, a load voltage of approximately 10 V, and a pulse width of approximately 300 µs. In particular, a high-efficiency, load-adaptive driving method was used with the MOSFETs in the critical saturation region (i.e., between the linear and saturated regions), controlling its power loss effectively while achieving maximum output current of the driver. The experiments demonstrated that the driver efficiency could be maintained at more than 80% when the load current varied from 50 to 300 A.

Metal free cross-dehydrogenative N-N coupling of primary amides with Lewis basic amines.

Hydrazides, N-N containing structural motifs, are important due to their presence in a wide variety of biologically significant compounds. While the homo N-N coupling of two NH moieties to form the hydrazide N-N bond is well developed, the cross-dehydrogenative hetero N-N coupling remains very unevolved. Here we present an efficient intermolecular N-N cross-coupling of a series of primary benzamides with broad range of Lewis basic primary and secondary amines using PhI(OAc)2 as both a terminal oxidant and a cross-coupling mediator, without the need for metal catalysts, high temperatures, and inert atmospheres, and with substantial potential for use in the late-stage functionalization of drugs.

Electro-oxidative intermolecular CSP2-H amination of heteroarenes via proton-coupled electron transfer.

A new electrochemical proton-coupled electron transfer method for the intermolecular CSP2-H amination of heteroarenes without oxidants, metal catalysts and external electrolytes has been developed. Various new N-containing heteroarenes were prepared in medium to high yields, and the indole-containing product could be converted into practical 2-oxindole by simple basic hydrolysis. Mechanistic investigation indicated that ester sulfonyl-substituted N-radicals could be formed by the combination of 2,6-lutidine and electrochemical oxidation, which is the key to achieve the desired chemoselectivity.

Exploring the Function of (+)-Naltrexone Precursors: Their Activity as TLR4 Antagonists and Potential in Treating Morphine Addiction.

Disruptions in the toll-like receptor 4 (TLR4) signaling pathway are linked to chronic inflammation, neuropathic pain, and drug addiction. (+)-Naltrexone, an opioid-derived TLR4 antagonist with a (+)-isomer configuration, does not interact with classical opioid receptors and has moderate blood-brain barrier permeability. Herein, we developed a concise 10-step synthesis for (+)-naltrexone and explored its precursors, (+)-14-hydroxycodeinone (1) and (+)-14-hydroxymorphinone (3). These precursors exhibited TLR4 antagonistic activities 100 times stronger than (+)-naltrexone, particularly inhibiting the TLR4-TRIF pathway. In vivo studies showed that these precursors effectively reduced behavioral effects of morphine, like sensitization and conditioned place preference by suppressing microglial activation and TNF-α expression in the medial prefrontal cortex and ventral tegmental area. Additionally, 3 displayed a longer half-life and higher oral bioavailability than 1. Overall, this research optimized (+)-naltrexone synthesis and identified its precursors as potent TLR4 antagonists, offering potential treatments for morphine addiction.

Toxicological effects induced by two carbamates on earthworms (Eisenia fetida): Acute toxicity, arrested regeneration and underlying mechanisms.

Eisenia fetida is recognised as advantageous model species in ecotoxicological and regeneration investigations. The intensive utilization of carbamate pesticides (CARs) imposes heavy residue burdens and grave hazards on edaphic environments as well as soil fauna therein. However, precise mechanisms whereby the specific CAR exerted toxic effects on earthworms remain largely elusive, notably from regenerative perspective. Herein, acute responses and regenerative toxicity of two carbamates (metolcarb, MEB and fenoxycarb, FEB) against E. fetida were dissected using biochemical, histological as well as molecular approaches following OECD guidelines at the cellular, tissue and organismal level. The acute toxicity data implied that MEB/FEB were very toxic/medium to extremely toxic, respectively in filter paper contact test and low to medium toxic/low toxic, respectively in artificial soil test. Chronic exposure to MEB and FEB at sublethal concentrations significantly mitigated the soluble protein content, protein abundance while enhanced the protein carbonylation level. Moreover, severely retarded posterior renewal of amputated earthworms was noticed in MEB and FEB treatments relative to the control group, with pronouncedly compromised morphology, dwindling segments and elevated cell apoptosis of blastema tissues, which were mediated by the rising Sox2 and decreasing TCTP levels. Taken together, these findings not only presented baseline toxicity cues for MEB and FEB exposure against earthworms, but also yielded mechanistic insights into regenerative toxicity upon CAR exposure, further contributing to the environmental risk assessment and benchmark formulation of agrochemical pollution in terrestrial ecosystem.

Study of AEB and active seat belt on driver injury in vehicle-vehicle frontal oblique crash.

The safety of vehicle occupants in oblique collision scenarios continues to pose challenges, even with the implementation of Automatic Emergency Braking (AEB) systems. While AEB reduces collision risks, studies indicate it may heighten injury risks for out-of-position (OOP) occupants. To counteract this issue, the integration of active seat belts in vehicles equipped with AEB systems is recommended. Firstly, this study established an oblique angle collision scenario post-AEB activation using data from the Chinese National Automobile Accident In-depth Investigation System (NAIS) database, analyzed through Prescan software. The dynamic response of the vehicle was examined. Following this, finite element (FE) models were validated to assess the effects of collision overlap rate, AEB braking strategy, and active seat belt pre-tensioning on occupant injuries and kinematics. Under specific collision conditions, the impact of the timing and amount of seat belt pre-tensioning, as well as airbag deployment timing on occupant injuries, was also explored. Findings revealed that a 75% collision overlap rate significantly increases driver injury risk. Active seat belts effectively mitigate injuries caused by OOP statuses during AEB interventions, with the lowest Weighted Injury Criterion (WIC) observed at a pre-tensioning time of 200 ms for active seat belts. The study further suggests that optimal results in reducing occupant injuries are achieved when active pre-tensioning seat belts are complemented by appropriately timed airbag deployment.

Fibromodulin overexpression drives oral squamous cell carcinoma via activating downstream EGFR signaling.

Accumulating evidence has shown that fibromodulin (FMOD) plays a pivotal role in tumorigenesis and metastasis. However, the biological function of FMOD in oral squamous cell carcinoma (OSCC) remains largely unclear to date. In this study, we confirmed that FMOD was overexpressed and showed a significant association with malignant progression and lymph node metastasis in OSCC. Depletion of FMOD inhibited OSCC proliferation and metastasis in vitro and in vivo. RNA sequencing, western blotting, and rescue assays verified that FMOD exerted oncogenic roles in OSCC via activation of EGFR signaling. In addition, FMOD was proved to be a putative target gene of miR-338-3p. Taken together, FMOD overexpression due to the reduced level of miR-338-3p promotes OSCC by activating EGFR signaling. Our findings provide direct evidence that targeting FMOD could be a promising therapeutic strategy for OSCC patients.

Expression of human thrombomodulin by GalTKO.hCD46 pigs modulates coagulation cascade activation by endothelial cells and during ex vivo lung perfusion with human blood.

Thrombomodulin is important for the production of activated protein C (APC), a molecule with significant regulatory roles in coagulation and inflammation. To address known molecular incompatibilities between pig thrombomodulin and human thrombin that affect the conversion of protein C into APC, GalTKO.hCD46 pigs have been genetically modified to express human thrombomodulin (hTBM). The aim of this study was to evaluate the impact of transgenic hTBM expression on the coagulation dysregulation that is observed in association with lung xenograft injury in an established lung perfusion model, with and without additional blockade of nonphysiologic interactions between pig vWF and human GPIb axis. Expression of hTBM was variable between pigs at the transcriptional and protein level. hTBM increased the activation of human protein C and inhibited thrombosis in an in vitro flow perfusion assay, confirming that the expressed protein was functional. Decreased platelet activation was observed during ex vivo perfusion of GalTKO.hCD46 lungs expressing hTBM and, in conjunction with transgenic hTBM, blockade of the platelet GPIb receptor further inhibited platelets and increased survival time. Altogether, our data indicate that expression of transgenic hTBM partially addresses coagulation pathway dysregulation associated with pig lung xenograft injury and, in combination with vWF-GP1b-directed strategies, is a promising approach to improve the outcomes of lung xenotransplantation.

Gallic Acid Ameliorates Cognitive Impairment Caused by Sleep Deprivation through Antioxidant Effect.

Sleep deprivation (SD) has a profound impact on the central nervous system, resulting in an array of mood disorders, including depression and anxiety. Despite this, the dynamic alterations in neuronal activity during sleep deprivation have not been extensively investigated. While some researchers propose that sleep deprivation diminishes neuronal activity, thereby leading to depression. Others argue that short-term sleep deprivation enhances neuronal activity and dendritic spine density, potentially yielding antidepressant effects. In this study, a two-photon microscope was utilized to examine the calcium transients of anterior cingulate cortex (ACC) neurons in awake SD mice in vivo at 24-hour intervals. It was observed that SD reduced the frequency and amplitude of Ca2+ transients while increasing the proportions of inactive neurons. Following the cessation of sleep deprivation, neuronal calcium transients demonstrated a gradual recovery. Moreover, whole-cell patch-clamp recordings revealed a significant decrease in the frequency of spontaneous excitatory post-synaptic current (sEPSC) after SD. The investigation also assessed several oxidative stress parameters, finding that sleep deprivation substantially elevated the level of malondialdehyde (MDA), while simultaneously decreasing the expression of Nuclear Factor erythroid 2-Related Factor 2 (Nrf2) and activities of Superoxide dismutase (SOD) in the ACC. Importantly, the administration of gallic acid (GA) notably mitigated the decline of calcium transients in ACC neurons. GA was also shown to alleviate oxidative stress in the brain and improve cognitive impairment caused by sleep deprivation. These findings indicate that the calcium transients of ACC neurons experience a continuous decline during sleep deprivation, a process that is reversible. GA may serve as a potential candidate agent for the prevention and treatment of cognitive impairment induced by sleep deprivation.

Graft dysfunction in compassionate use of genetically engineered pig-to-human cardiac xenotransplantation: a case report.

BACKGROUND: A genetically engineered pig cardiac xenotransplantation was done on Jan 7, 2022, in a non-ambulatory male patient, aged 57 years, with end-stage heart failure, and on veno-arterial extracorporeal membrane oxygenation support, who was ineligible for an allograft. This report details our current understanding of factors important to the xenotransplantation outcome. METHODS: Physiological and biochemical parameters critical for the care of all heart transplant recipients were collected in extensive clinical monitoring in an intensive care unit. To ascertain the cause of xenograft dysfunction, we did extensive immunological and histopathological studies, including electron microscopy and quantification of porcine cytomegalovirus or porcine roseolovirus (PCMV/PRV) in the xenograft, recipient cells, and tissue by DNA PCR and RNA transcription. We performed intravenous immunoglobulin (IVIG) binding to donor cells and single-cell RNA sequencing of peripheral blood mononuclear cells. FINDINGS: After successful xenotransplantation, the graft functioned well on echocardiography and sustained cardiovascular and other organ systems functions until postoperative day 47 when diastolic heart failure occurred. At postoperative day 50, the endomyocardial biopsy revealed damaged capillaries with interstitial oedema, red cell extravasation, rare thrombotic microangiopathy, and complement deposition. Increased anti-pig xenoantibodies, mainly IgG, were detected after IVIG administration for hypogammaglobulinaemia and during the first plasma exchange. Endomyocardial biopsy on postoperative day 56 showed fibrotic changes consistent with progressive myocardial stiffness. Microbial cell-free DNA testing indicated increasing titres of PCMV/PRV cell-free DNA. Post-mortem single-cell RNA sequencing showed overlapping causes. INTERPRETATION: Hyperacute rejection was avoided. We identified potential mediators of the observed endothelial injury. First, widespread endothelial injury indicates antibody-mediated rejection. Second, IVIG bound strongly to donor endothelium, possibly causing immune activation. Finally, reactivation and replication of latent PCMV/PRV in the xenograft possibly initiated a damaging inflammatory response. The findings point to specific measures to improve xenotransplant outcomes in the future. FUNDING: The University of Maryland School of Medicine, and the University of Maryland Medical Center.

Driver Injury from Vehicle Side Impacts When Automatic Emergency Braking and Active Seat Belts Are Used.

As an advanced driver assistance system, automatic emergency braking (AEB) can effectively reduce accidents by using high-precision and high-coverage sensors. In particular, it has a significant advantage in reducing front-end collisions and rear-end accidents. Unfortunately, avoiding side collisions is a challenging problem for AEB. To tackle these challenges, we propose active seat belt pretensioning on driver injury in vehicles equipped with AEB in unavoidable side crashes. Firstly, records of impact cases from China's National Automobile Accident In-Depth Investigation System were used to investigate a scenario in which a vehicle is impacted by an oncoming car after the vehicle's AEB system is triggered. The scenario was created using PreScan software. Then, the simulated vehicles in the side impact were devised using a finite element model of the Toyota Yaris and a moving barrier. These were constructed in HyperMesh software along with models of the driver's side seatbelt, side airbag, and side curtain airbag. Moreover, the models were verified, and driver out-of-position instances and injuries were evaluated in simulations with different AEB intensities up to 0.7 g for three typical side impact angles. Last but not least, the optimal combination of seatbelt pretensioning and the timing thereof for minimizing driver injury at each side impact angle was identified using orthogonal tests; immediate (at 0 ms) pretensioning at 80 N was applied. Our experiments show that our active seatbelt with the above parameters reduced the weighted injury criterion by 5.94%, 22.05%, and 20.37% at impact angles of 90°, 105°, and 120°, respectively, compared to that of a conventional seatbelt. The results of the experiment can be used as a reference to appropriately set the collision parameters of active seat belts for vehicles with AEB.

Increased human complement pathway regulatory protein gene dose is associated with increased endothelial expression and prolonged survival during ex-vivo perfusion of GTKO pig lungs with human blood.

INTRODUCTION: Expression of human complement pathway regulatory proteins (hCPRP's) such as CD46 or CD55 has been associated with improved survival of pig organ xenografts in multiple different models. Here we evaluate the hypothesis that an increased human CD46 gene dose, through homozygosity or additional expression of a second hCPRP, is associated with increased protein expression and with improved protection from injury when GTKO lung xenografts are perfused with human blood. METHODS: Twenty three GTKO lungs heterozygous for human CD46 (GTKO.heteroCD46), 10 lungs homozygous for hCD46 (GTKO.homoCD46), and six GTKO.homoCD46 lungs also heterozygous for hCD55 (GTKO.homoCD46.hCD55) were perfused with human blood for up to 4 h in an ex vivo circuit. RESULTS: Relative to GTKO.heteroCD46 (152 min, range 5-240; 6/23 surviving at 4 h), survival was significantly improved for GTKO.homoCD46 (>240 min, range 45-240, p = .034; 7/10 surviving at 4 h) or GTKO.homoCD46.hCD55 lungs (>240 min, p = .001; 6/6 surviving at 4 h). Homozygosity was associated with increased capillary expression of hCD46 (p < .0001). Increased hCD46 expression was associated with significantly prolonged lung survival (p = .048),) but surprisingly not with reduction in measured complement factor C3a. Hematocrit, monocyte count, and pulmonary vascular resistance were not significantly altered in association with increased hCD46 gene dose or protein expression. CONCLUSION: Genetic engineering approaches designed to augment hCPRP activity - increasing the expression of hCD46 through homozygosity or co-expressing hCD55 with hCD46 - were associated with prolonged GTKO lung xenograft survival. Increased expression of hCD46 was associated with reduced coagulation cascade activation, but did not further reduce complement activation relative to lungs with relatively low CD46 expression. We conclude that coagulation pathway dysregulation contributes to injury in GTKO pig lung xenografts perfused with human blood, and that the survival advantage for lungs with increased hCPRP expression is likely attributable to improved endothelial thromboregulation.

FRC transplantation restores lymph node conduit defects in laminin α4-deficient mice.

Fibroblastic reticular cells (FRCs) play important roles in tolerance by producing laminin α4 (Lama4) and altering lymph node (LN) structure and function. The present study revealed the specific roles of extracellular matrix Lama4 in regulating LN conduits using FRC-specific KO mouse strains. FRC-derived Lama4 maintained conduit fiber integrity, as its depletion altered conduit morphology and structure and reduced homeostatic conduit flow. Lama4 regulated the lymphotoxin ß receptor (LTßR) pathway, which is critical for conduit and LN integrity. Depleting LTßR in FRCs further reduced conduits and impaired reticular fibers. Lama4 was indispensable for FRC generation and survival, as FRCs lacking Lama4 displayed reduced proliferation but upregulated senescence and apoptosis. During acute immunization, FRC Lama4 deficiency increased antigen flow through conduits. Importantly, adoptive transfer of WT FRCs to FRC Lama4-deficient mice rescued conduit structure, ameliorated Treg and chemokine distribution, and restored transplant allograft acceptance, which were all impaired by FRC Lama4 depletion. Single-cell RNA sequencing analysis of LN stromal cells indicated that the laminin and collagen signaling pathways linked crosstalk among FRC subsets and endothelial cells. This study demonstrated that FRC Lama4 is responsible for maintaining conduits by FRCs and can be harnessed to potentiate FRC-based immunomodulation.

Iridium catalysed C2 site-selective methylation of indoles using a pivaloyl directing group through weak chelation-assistance.

Here we present an iridium catalysed C2-selective methylation of indoles using methyltrifluoroborate as a source of methyl group. The iridium catalyst selectively discriminates the indole C2 and C4 C-H bonds by coordination with a pivaloyl directing group.

Transport-Associated Vibrational Stress Triggers Drug-Reversible Apoptosis and Cardiac Allograft Failure in Mice.

Increasingly complex and long-range donor organ allocation routes coupled with implementation of unmanned aerial vehicles (UAVs) have prompted investigations of the conditions affecting organs once packaged for shipment. Our group has previously demonstrated that different modes of organ transport exert unique environmental stressors, in particular vibration. Using a mouse heart transplant model, we demonstrated that vibrational forces exert tangible, cellular effects in the form of cardiomyocyte apoptosis and cytoskeletal derangement. Functionally, these changes translated into accelerated allograft loss. Notably, administration of an apoptosis inhibitor, Z-VAD-FMK, helped to ameliorate the detrimental cellular and functional effects of mechanical vibration in a dose-dependent manner. These findings constitute one of the first reports of the negative impact of transit environment on transplant outcomes, a contributing mechanism underpinning this effect, and a potential agent to prophylax against this process. Given current limitations in measuring donor organ transit environments in situ, further study is required to better characterize the impact of transport environment and to potentially improve the care of donor organs during shipment. Clinical and Translational Impact Statement: We show that apoptosis inhibitor, Z-VAD-FMK, ameliorated transport-related vibrational stress in murine heart transplants, which presents a potential therapeutic or preservation solution additive for future use in transporting donor organs.

A Standardized Approach to Orthotopic (Life-supporting) Porcine Cardiac Xenotransplantation in a Nonhuman Primate Model.

Cardiac xenotransplantation from swine has been proposed to "bridge the gap" in supply for heart failure patients requiring transplantation. Recent preclinical success using genetically modified pig donors in baboon recipients has demonstrated survival greater than 6 mo, with a modern understanding of xenotransplantation immunobiology and continued experience with large animal models of cardiac xenotransplantation. As a direct result of this expertise, the Food and Drug Administration approved the first in-human transplantation of a genetically engineered cardiac xenograft through an expanded access application for a single patient. This clinical case demonstrated the feasibility of xenotransplantation. Although this human study demonstrated proof-of-principle application of cardiac xenotransplantation, further regulatory oversight by the Food and Drug Administration may be required with preclinical trials in large animal models of xenotransplantation with long-term survival before approval of a more formalized clinical trial. Here we detail our surgical approach to pig-to-primate large animal models of orthotopic cardiac xenotransplantation, and the postoperative care of the primate recipient, both in the immediate postoperative period and in the months thereafter. We also detail xenograft surveillance methods and common issues that arise in the postoperative period specific to this model and ways to overcome them. These studies require multidisciplinary teams and expertise in orthotopic transplantation (cardiac surgery, anesthesia, and cardiopulmonary bypass), immunology, genetic engineering, and experience in handling large animal donors and recipients, which are described here. This article serves to reduce the barriers to entry into a field with ever-growing enthusiasm, but demands expertise knowledge and experience to be successful.

Biomimetic Nanobomb for Synergistic Therapy with Inhibition of Cancer Stem Cells.

Cancer stem cells (CSCs), a type of cell with self-renewal, unlimited proliferation, and insensitivity to common physical and chemical factors, are the key to cancer metastasis, recurrence, and chemo-resistance. Available CSCs inhibition strategies are mainly based on small molecule drugs, yet are limited by their off-target toxicity. The link between CSCs and non-CSCs interconversion is difficult to sever. In this work, a nanotherapeutic strategy based on MnOx -loaded polydopamine (MnOx /PDA) nanobombs with chemodynamic, photodynamic, photothermal and biodegradation properties to inhibit CSCs and non-CSCs concurrently is reported. The MnOx /PDA nanobombs can directly disrupt the microenvironment and tumorigenic capacity of CSCs by generating hyperthermia, oxidative stress and alleviating hypoxia. The markers of CSCs are subsequently downregulated, leading to the clearance of CSCs. Meanwhile, the synergistic therapy mediated by MnOx /PDA nanobombs can directly ablate the bulk tumor cells, thus cutting off the supply of CSCs transformation. For tumor targeting, MnOx /PDA is coated with macrophage membrane. The final tumor inhibition rate of the synergistic therapy is 70.8% in colorectal cancer (CRC) model. Taken together, the present work may open up the exploration of nanomaterial-based synergistic therapy for the simultaneous elimination of therapeutically resistant CSCs and non-CSCs.

Retrieval of tropospheric ozone profiles using ground-based MAX-DOAS.

In recent years, surface ozone concentrations have increased in many cities in China. Ground-based multi-axis differential optical absorption spectroscopy (MAX-DOAS) is a powerful technique for retrieving the profiles of tropospheric trace gases, such as NO2, SO2, and HCHO. However, since the difficulties in deducting the effects of stratospheric ozone, there are few studies on the retrieval of tropospheric ozone profiles using MAX-DOAS measurements. Here, we developed an accurate inversion method to retrieve tropospheric ozone concentrations during the PRIDE-GBA Campaign, wherein the ozone differential slant column densities (DSCDs) were retrieved in QDOAS software using the "time-interpolated zenith spectrum" as the reference spectrum. The tropospheric DSCDs (DSCDstrop) were then calculated by subtracting the simulated stratospheric DSCDs (DSCDsstr, simulated from the SCIATRAN model) from the DSCDs. Tropospheric ozone profiles were retrieved from the DSCDstrop using the optimal estimation method (OEM). The results showed that high values of tropospheric ozone were mainly distributed below 1 km, which is consistent with lidar measurements. In addition, the observed surface ozone concentrations were highly correlated with the in-situ measurements, with correlation coefficients (R) of 0.75 and 0.81, respectively. Combined with the retrieved NO2 and HCHO profiles using the MAX-DOAS measurements, we found that the planetary boundary layer ozone pollution of HeShan Observatory during the PRIDE-GBA Campaign are controlled by the NOx-limited regime. The results of this study indicate that the MAX-DOAS technique has the potential to retrieve tropospheric ozone profiles with high temporal and spatial resolution.

Object-Occluded Human Shape and Pose Estimation With Probabilistic Latent Consistency.

Occlusions between human and objects, especially for the activities of human-object interactions, are very common in practical applications. However, most of the existing approaches for 3D human shape and pose estimation require that human bodies are well captured without occlusions or with minor self-occlusions. In this paper, we focus on the problem of directly estimating the object-occluded human shape and pose from single color images. Our key idea is to utilize a partial UV map to represent an object-occluded human body, and the full 3D human shape estimation is ultimately converted as an image inpainting problem. We propose a novel two-branch network architecture to train an end-to-end regressor via a latent distribution consistency, which also includes a novel visible feature sub-net to extract the human information from object-occluded color images. To supervise the network training, we further build a novel dataset named as 3DOH50K. Several experiments are conducted to reveal the effectiveness of the proposed method. Experimental results demonstrate that the proposed method achieves state-of-the-art compared with previous methods. The dataset and codes are publicly available at https://www.yangangwang.com/papers/ZHANG-OOH-2020-03.html.