Physical activity and transitioning to retirement: evidence from the China health and retirement longitudinal study.

BACKGROUND: The impact of retirement on physical activity among older individuals remains ambiguous. This study aims to investigate the influence of retirement on physical activity and delineate the trajectories of physical activity changes during the retirement transition among elderly Chinese residents. Additionally, we endeavor to examine the factors that contribute to each trajectory. METHODS: This longitudinal cohort study used data from four surveys of the China Health and Retirement Longitudinal Study and included a sample of 428 individuals who underwent formal retirement and provided information on physical activity. We employed generalized estimating equation to explore the impact of the retirement transition on physical activity among Chinese older adults. Latent class growth analysis was used to identify distinct trajectories of physical activity, and binary logistic regression was performed to identify pre-retirement factors influencing changes in physical activity. RESULTS: Our findings indicate that retirement can lead to a decline in physical activity among older Chinese residents (OR = 0.85, 95%CI 0.75 ~ 0.97). We identified three distinct trajectories of physical activity during the retirement transition: Trajectory 1 - "sustained low level of physical activity" (7.94%); Trajectory 2 - "middle level of physical activity with gradual decline" (69.16%); Trajectory 3 - "sustained high level of physical activity with significant fluctuations" (22.90%). Furthermore, we discovered that individuals in the "middle level of physical activity and gradual decline" trajectory were more likely to have an annual income exceeding 40,000 yuan (OR = 9.69, 95%CI 1.12 ~ 83.63), reside in urban areas (OR = 2.27, 95%CI 1.14 ~ 4.52), and have a fondness for playing Mahjong (OR = 2.42, 95%CI 1.18 ~ 5.00) compared to those in the "sustained high level of physical activity with significant fluctuations" trajectory. Additionally, having an annual income exceeding 40,000 yuan (OR = 19.67, 95%CI 1.30 ~ 298.61) predicted membership in the "sustained low level of physical activity" trajectory when compared to the "sustained high level of physical activity with significant fluctuations" trajectory. CONCLUSION: Retirement represents a substantial milestone in the life course and is associated with notable alterations in physical activity patterns. Among older Chinese residents, the trajectories of physical activity during the retirement transition exhibit diverse paths and are influenced by pre-retirement factors, including annual income, residential location, and hobbies. The findings of this study have important implications for the formulation of policies aimed at promoting healthy aging among individuals approaching retirement age.

The transcription factor PagLBD3 contributes to the regulation of secondary growth in Populus.

LATERAL ORGAN BOUNDARIES DOMAIN (LBD) genes encode plant-specific transcription factors that participate in regulating various developmental processes. In this study, we genetically characterized PagLBD3 encoding an important regulator of secondary growth in poplar (Populus alba × Populus glandulosa). Overexpression of PagLBD3 increased stem secondary growth in Populus with a significantly higher rate of cambial cell differentiation into phloem, while dominant repression of PagLBD3 significantly decreased the rate of cambial cell differentiation into phloem. Furthermore, we identified 1756 PagLBD3 genome-wide putative direct target genes (DTGs) through RNA sequencing (RNA-seq)-coupled DNA affinity purification followed by sequencing (DAP-seq) assays. Gene Ontology analysis revealed that genes regulated by PagLBD3 were enriched in biological pathways regulating meristem development, xylem development, and auxin transport. Several central regulator genes for vascular development, including PHLOEM INTERCALATED WITH XYLEM (PXY), WUSCHEL RELATED HOMEOBOX4 (WOX4), Secondary Wall-Associated NAC Domain 1s (SND1-B2), and Vascular-Related NAC-Domain 6s (VND6-B1), were identified as PagLBD3 DTGs. Together, our results indicate that PagLBD3 and its DTGs form a complex transcriptional network to modulate cambium activity and phloem/xylem differentiation.

Downregulation of HMGB1 is required for the protective role of Nrf2 in EMT-mediated PF.

Epithelial-mesenchymal transition (EMT) is considered to be the key event in the formation of pulmonary fibrosis (PF). High-mobility group box 1 (HMGB1) is a novel mediator of EMT. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a critical transcription factor for protecting against PF. However, it is unknown the relationship between Nrf2 and HMGB1 in EMT-mediated PF. Bleomycin (BLM)-induced PF in Nrf2-knockout (Nrf2-/- ) and wild-type (WT) mice and transforming growth factor ß1 (TGF-ß1)-induced EMT in rat type II alveolar epithelial cell line (RLE-6TN) and human alveolar epithelial cell line (A549) were established to observe the relationship among Nrf2, HMGB1, and EMT by western blot and immunohistochemistry. BLM-induced EMT was more severe and the expression of HMGB1 was more increased in Nrf2 -/- mice compared with WT mice. In vitro, Nrf2 activation attenuated TGF-ß1-induced EMT and ROS production accompanied by the downregulation of HMGB1. In contrast, silencing Nrf2 enhanced TGF-ß1-induced EMT and ROS production along with increased the protein expression and the release of HMGB1. Moreover, HMGB1 activation aggravated TGF-ß1-induced EMT and HMGB1 deficiency alleviated TGF-ß1-induced EMT. Furthermore, HMGB1 silence attenuated the protective effect of Nrf2 on EMT. These findings suggest downregulation of HMGB1, which is required for the protective role of Nrf2 in EMT-mediated PF and provide an important therapeutic target for PF.

Genome-wide transcriptional adaptation to salt stress in Populus.

BACKGROUND: Adaptation to abiotic stresses is crucial for the survival of perennial plants in a natural environment. However, very little is known about the underlying mechanisms. Here, we adopted a liquid culture system to investigate plant adaptation to repeated salt stress in Populus trees. RESULTS: We first evaluated phenotypic responses and found that plants exhibit better stress tolerance after pre-treatment of salt stress. Time-course RNA sequencing (RNA-seq) was then performed to profile changes in gene expression over 12 h of salt treatments. Analysis of differentially expressed genes (DEGs) indicated that significant transcriptional reprogramming and adaptation to repeated salt treatment occurred. Clustering analysis identified two modules of co-expressed genes that were potentially critical for repeated salt stress adaptation, and one key module for salt stress response in general. Gene Ontology (GO) enrichment analysis identified pathways including hormone signaling, cell wall biosynthesis and modification, negative regulation of growth, and epigenetic regulation to be highly enriched in these gene modules. CONCLUSIONS: This study illustrates phenotypic and transcriptional adaptation of Populus trees to salt stress, revealing novel gene modules which are potentially critical for responding and adapting to salt stress.

Nrf2 attenuates inflammatory response in COPD/emphysema: Crosstalk with Wnt3a/ß-catenin and AMPK pathways.

Chronic obstructive pulmonary disease (COPD) is characterized by persistent airflow limitation and abnormal inflammatory response. Wnt/ß-catenin and AMP-activated protein kinase (AMPK) have been shown to modulate lung inflammatory responses and injury. However, it remains elusive whether Wnt/ß-catenin and AMPK modulate nuclear factor erythroid-2 related factor-2 (Nrf2)-mediated protective responses during the development of emphysema. Here we showed that treatment with a Wnt pathway activator (LiCl) reduced elastase-induced airspace enlargement and cigarette smoke extract (CSE)-induced lung inflammatory responses in WT mice, which was associated with increased activation of Nrf2 pathway. Interestingly, these effects of LiCl were not observed in Nrf2-/- mice exposed to elastase. In normal human bronchial epithelial (NHBE) cells, Wnt3a overexpression up-regulated, whereas Wnt3a knockdown further down-regulated the levels of Nrf2 and its target proteins heme oxygenase-1 (HO-1) and NAD(P)H: quinone oxidoreductase 1 (NQO1) by CSE treatment. In contrast, Nrf2 deficiency did not have any effects on Wnt/ß-catenin pathway in mouse lungs and NHBE cells. Both elastase and CSE exposures reduced AMPK phosphorylation. A specific AMPK activator metformin increased Wnt3a, ß-catenin, Nrf2 phosphorylation and activation but reduced the levels of IL-6 and IL-8 in NHBE cells and mouse lungs exposed to CSE. Furthermore, Nrf2 deficiency abolished the protection of metformin against CSE-induced increase in IL-6 and IL-8 in NHBE cells. In conclusion, Nrf2 mediates the protective effects of both Wnt3a/ß-catenin and AMPK on lung inflammatory responses during the development of COPD/emphysema. These findings provide potential therapeutic targets for the intervention of COPD/emphysema.

Molecular pathogenesis in chronic obstructive pulmonary disease and therapeutic potential by targeting AMP-activated protein kinase.

Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide, which is characterized by a persistent airflow limitation caused by chronic inflammatory responses to noxious particles or gases. Cigarette smoke and environmental pollutions are major etiological factors for causing COPD. It has been shown that cigarette smoking causes abnormal inflammatory responses, cellular senescence, mitochondrial dysfunction and metabolic dysregulation, suggesting their involvement in the development of COPD. Although the medical care and treatment have advanced, there are no effective therapies to stop or reverse lung destruction in COPD/emphysema. AMP-activated protein kinase (AMPK) is a serine threonine kinase with α, ß, and γ subunits that are highly conserved through evolution. AMPK has been shown to regulate bioenergetics, inflammatory responses, senescence, and metabolism. This review focused on the updated understanding of molecular pathogenesis of COPD, and highlighted the crucial roles of AMPK in lung abnormalities as well as discussed the potential therapeutics of AMPK activators in preventing and halting the progression of COPD.

Activation of Wnt/ß-catenin signalling is required for TGF-ß/Smad2/3 signalling during myofibroblast proliferation.

Fibrosis in animal models and human diseases is associated with aberrant activation of the Wnt/ß-catenin pathway. Despite extensive research efforts, effective therapies are still not available. Myofibroblasts are major effectors, responsible for extracellular matrix deposition. Inhibiting the proliferation of the myofibroblast is crucial for treatment of fibrosis. Proliferation of myofibroblasts can have many triggering effects that result in fibrosis. In recent years, the Wnt pathway has been studied as an underlying factor as a primary contributor to fibrotic diseases. These efforts notwithstanding, the specific mechanisms by which Wnt-mediated promotes fibrosis reaction remain obscure. The central role of the transforming growth factor-ß (TGF-ß) and myofibroblast activity in the pathogenesis of fibrosis has become generally accepted. The details of interaction between these two processes are not obvious. The present investigation was conducted to evaluate the level of sustained expression of fibrosis iconic proteins (vimentin, α-SMA and collagen I) and the TGF-ß signalling pathway that include smad2/3 and its phosphorylated form p-smad2/3. Detailed analysis of the possible molecular mechanisms mediated by ß-catenin revealed epithelial-mesenchymal transition and additionally demonstrated transitions of fibroblasts to myofibroblast cell forms, along with increased activity of ß-catenin in regulation of the signalling network, which acts to counteract autocrine TGF-ß/smad2/3 signalling. A major outcome of this study is improved insight into the mechanisms by which epithelial and mesenchymal cells activated by TGFß1-smad2/3 signalling through Wnt/ß-catenin contribute to lung fibrosis.

Temporal variations in water quality in a brackish tidal pond: Implications for governing processes and management strategies.

Brackish tidal ponds have been constructed along coastal areas in many parts of the world for aquaculture, including some Ramsar Sites. Such ponds are considered a sustainable, wise use of wetlands if managed properly, but they can also pose serious environmental problems if mismanaged. To understand the governing processes and to promote sustainable management strategies, this study examines the different temporal variations in water quality parameters in a brackish tidal pond located within the wetland complex of the Mai Po Ramsar Site in Hong Kong, China. The variations are compared with those of the receiving bay, and the water channel that connects the pond and the bay. Equations are then developed to link the dissolved oxygen (DO) concentrations in the pond with the governing processes, and to analyze their relative contributions to DO levels. Field data show seasonal patterns in water temperature and salinity in response to the seasonal variations in solar radiation and rainfall. For the pond and the channel, DO, chlorophyll and pH exhibit fortnightly variations due to the bi-weekly water exchange between the pond and the bay. There were also diurnal variations in water temperature and DO in response to changes in solar radiation for both locations, and the tidal flushing for the water channel. Analysis of the findings indicates that water exchange influences the DO concentration more strongly than solar radiation. The DO equation links pond water quality with the time of day, and the time in a water exchange cycle, and thus provides some guidance for determining water exchange and water sampling schedules. The study sheds light on the governing processes and management strategies related to the sustainable management of a brackish tidal pond. The results are thus beneficial in elucidating and promoting the sustainable management and wise use of wetlands in other locations.

High-Mobility Group Box 1 Mediates Epithelial-to-Mesenchymal Transition in Pulmonary Fibrosis Involving Transforming Growth Factor-ß1/Smad2/3 Signaling.

Epithelial-to-mesenchymal transition (EMT) is a crucial event in the cellular origin of myofibroblasts that secrete extracellular matrix in the progression of pulmonary fibrosis (PF). High-mobility group box 1 (HMGB1) is a novel mediator of EMT. However, whether this process involves the recognized transforming growth factor-ß1 (TGF-ß1)/Smad signaling that also contributes to EMT in PF has not yet been elucidated. Here, we developed a model of PF induced by bleomycin (BLM) in rats and conducted several simulation experiments in A549 (human) and RLE-6TN (rat) alveolar epithelial cell (AEC) lines to unravel the role of TGF-ß1/Smad2/3 signaling in HMGB1-mediated EMT. We found that the levels of serum HMGB1 and lung hydroxyproline were severely elevated after BLM administration. Moreover, the protein expression of HMGB1, TGF-ß1, phosphorylated Smad2/3 (p-Smad2/3), and mesenchymal markers including α-smooth muscle actin, vimentin, and type I collagen were significantly increased with the reduced protein expression of an epithelial marker (E-cadherin) in the rat model by Western blot or immunohistochemical analysis. In addition, the uptake of both exogenous TGF-ß1 and HMGB1 by AECs could induce EMT; meanwhile, HMGB1 dramatically enhanced TGF-ß1 expression and triggered Smad2/3 phosphorylation. In contrast, TGF-ß1 deficiency evidently ameliorated HMGB1-mediated EMT with reduced p-Smad2/3 in A549 cells. It provides new insights that HMGB1 release from injured lungs promotes AEC damage through induction of the EMT process, in which TGF-ß1/Smad2/3 signaling is activated and contributes to PF. These results suggest that HMGB1 may constitute a therapeutic target for developing antifibrotic agents for abnormal lung remodeling.

Total glycosides of Yupingfeng protects against bleomycin-induced pulmonary fibrosis in rats associated with reduced high mobility group box 1 activation and epithelial-mesenchymal transition.

BACKGROUND: Pulmonary fibrosis (PF) is a fatal inflammatory disease with limited effective strategies. Epithelial-mesenchymal transition (EMT) is a pivotal origin of myofibroblasts that secrete extracellular matrix (ECM) in the development of PF. High mobility group box 1 (HMGB1), one of the mediators of inflammation, has been proved abnormal activation in the pathogenesis of PF. AIM: The present study was aimed to investigate the potential effects of total glycoside of Yupingfeng (YPF-G), the natural compound extracted from Yupingfeng san, on HMGB1 activation and EMT in bleomycin-induced PF, which was a serious disease of respiratory system. METHODS: The Sprague-Dawley (SD) rat model of PF was duplicated by intratracheal instillation of bleomycin (5 mg kg(-1)). After that, YPF-G (5, 10 mg kg(-1)) and prednisone (5 mg kg(-1)) were separately administered intragastrically, and then the rats were killed at days 14 and 28, respectively. Hematoxylin and eosin and Masson's trichrome staining were performed to assess the histopathologic level of lung tissues, western blotting and the common kits were utilized to investigate the hallmarks molecule expression of ECM and EMT, and the level of HMGB1 in lung tissues and serum. RESULTS: We found that both dose of YPF-G markedly reduced bleomycin-induced alveolitis and PF in rats. Besides, the levels of HMGB1, laminin, hyaluronic acid, and hydroxyproline were effectively reduced. Meanwhile, the increased protein expression of HMGB1 and the mesenchymal markers including vimentin and alpha-smooth muscle actin, and the decreased protein expression of epithelial marker E-cadherin were dramatically inhibited after YPF-G treatment. CONCLUSION: Our results demonstrated that YPF-G could ameliorate bleomycin-induced PF by reducing HMGB1 activation and reversing EMT.

Stromal cell-derived factor-1 enhances wound healing through recruiting bone marrow-derived mesenchymal stem cells to the wound area and promoting neovascularization.

Stromal cell-derived factor-1 (SDF-1) is a potent chemokine for bone marrow-derived stromal stem cells (BMSCs) that express CXCR4, the receptor for SDF-1. SDF-1 is considered to play an important role in the trafficking of BMSCs. We investigated the contribution of SDF-1 to the recruitment of BMSCs to the wound area and its promotion of wound repair and neovascularization. BMSCs were pretreated with or without anti-CXCR4 blocking antibody and combined with CM-DiI label, and injected via the tail vein into mice with full-thickness skin wounds on the dorsum. Simultaneously, anti-SDF-1 antibody was injected into local wounds in another group of mice. The results show that blockade of CXCR4 on either infused BMSCs or SDF-1 in the host wounds (1) dramatically impaired the number of infused BMSCs being recruited to the injured tissue, (2) reduced the expression of growth factors involved in the repair of injured tissue such as vascular endothelial growth factor, basic fibroblast growth factor and transforming growth factor beta 1, (3) decreased the resultant neovascularization, and (4) retarded wound healing. Taken together, the findings indicate that the SDF-1/CXCR4 signal pathway facilitates wound healing through augmenting BMSC recruitment to wound tissues, responsive secretion of growth factors by BMSCs and neovascularization in the wound area.

Bio-inspired switchable soft adhesion for the boost of adhesive surfaces and robotics applications: A brief review.

In nature, millions of creatures, such as geckos, tree frogs, octopuses, etc., have evolved fantastic switchable adhesion capabilities to climb swiftly on vertical even inverted surfaces or hunt for prey easily, adapting to harsh and unpredictable environments. Notably, these fascinating adhesive behaviors depend on interfacial forces (friction, van der Waals force, capillary force, vacuum suction, etc.), which primarily originate from the interactions between the soft micro/nanostructures evolved in the natural creatures and objects. Over the past few decades, these biological switchable adhesives have inspired scientists to explore and engineer desirable artificial adhesives. In this review, we summarized the state-of-the-art research on the ultra-fast adhesive motion of three types of biological organisms (gecko, tree frog, and octopus). Firstly, the basic adhesion principles in the three representative organisms, including micro/nanostructures, interfacial forces, and fundamental adhesion models, are reviewed. Then, we discussed the adhesion mechanisms of the prominent organisms from the perspective of soft contacts between micro/nanostructures and the substrates. Later, the mechanics-guided design principles of artificial adhesive surfaces, as well as the smart adhesion strategies, are summarized. The applications of these bio-inspired switchable adhesives are demonstrated, including wearable electronic devices, soft grippers, and climbing robots. The challenges and opportunities in this fast-growing field are also discussed.

Pathoclinical associations between panic disorders and the brain-derived neurotrophic factor Val66Met polymorphism: an updated meta-analysis.

Prior studies have indicated the pathological role of brain-derived neurotrophic factor (BDNF) gene polymorphism in panic disorders (PD). A functionally less active BDNF Val66Met mutant was previously detected in PD patients with different ethnic backgrounds. However, the results remain inconclusive or inconsistent. A meta-analysis was used to explore the consistency of the BDNF Val66Met mutant's association with PD irrespective of the subject's ethnicity. Relevant case-controlled full-length clinical and preclinical reports were retrieved by database searching, and 11 articles involving 2203 cases and 2554 controls were systematically selected per the standard inclusion criteria. Eleven articles were finally included that explored the relationship between the Val66Met polymorphism and PD risk susceptibility. Statistical analysis revealed a significant genetic association of the mutation, allele frequencies, and genotype distributions of BDNF with PD onset. Our findings demonstrated that the BDNF Val66Met is a susceptibility factor of PD.

Meta Transfer of Self-Supervised Knowledge: Foundation Model in Action for Post-Traumatic Epilepsy Prediction.

Despite the impressive advancements achieved using deep-learning for functional brain activity analysis, the heterogeneity of functional patterns and scarcity of imaging data still pose challenges in tasks such as prediction of future onset of Post-Traumatic Epilepsy (PTE) from data acquired shortly after traumatic brain injury (TBI). Foundation models pre-trained on separate large-scale datasets can improve the performance from scarce and heterogeneous datasets. For functional Magnetic Resonance Imaging (fMRI), while data may be abundantly available from healthy controls, clinical data is often scarce, limiting the ability of foundation models to identify clinically-relevant features. We overcome this limitation by introducing a novel training strategy for our foundation model by integrating meta-learning with self-supervised learning to improve the generalization from normal to clinical features. In this way we enable generalization to other downstream clinical tasks, in our case prediction of PTE. To achieve this, we perform self-supervised training on the control dataset to focus on inherent features that are not limited to a particular supervised task while applying meta-learning, which strongly improves the model's generalizability using bi-level optimization. Through experiments on neurological disorder classification tasks, we demonstrate that the proposed strategy significantly improves task performance on small-scale clinical datasets. To explore the generalizability of the foundation model in downstream applications, we then apply the model to an unseen TBI dataset for prediction of PTE using zero-shot learning. Results further demonstrated the enhanced generalizability of our foundation model.

Crosstalk of nervous and immune systems in pancreatic cancer.

Pancreatic cancer is a highly malignant tumor known for its extremely low survival rate. The combination of genetic disorders within pancreatic cells and the tumor microenvironment contributes to the emergence and progression of this devastating disease. Extensive research has shed light on the nature of the microenvironmental cells surrounding the pancreatic cancer, including peripheral nerves and immune cells. Peripheral nerves release neuropeptides that directly target pancreatic cancer cells in a paracrine manner, while immune cells play a crucial role in eliminating cancer cells that have not evaded the immune response. Recent studies have revealed the intricate interplay between the nervous and immune systems in homeostatic condition as well as in cancer development. In this review, we aim to summarize the function of nerves in pancreatic cancer, emphasizing the significance to investigate the neural-immune crosstalk during the advancement of this malignant cancer.

Integrated single-nucleus and spatial transcriptomics captures transitional states in soybean nodule maturation.

Legumes form symbiosis with rhizobium leading to the development of nitrogen-fixing nodules. By integrating single-nucleus and spatial transcriptomics, we established a cell atlas of soybean nodules and roots. In central infected zones of nodules, we found that uninfected cells specialize into functionally distinct subgroups during nodule development, and revealed a transitional subtype of infected cells with enriched nodulation-related genes. Overall, our results provide a single-cell perspective for understanding rhizobium-legume symbiosis.

Parasitism and Suitability of Trichogramma chilonis on Large Eggs of Two Factitious Hosts: Samia cynthia ricini and Antheraea pernyi.

Trichogramma, an effective biological control agent, demonstrates promise in environmentally sustainable pest management through its parasitic action toward insect eggs. This study evaluates the parasitism fitness and ability of T. chilonis with regard to two factitious host eggs, aiming to develop a cost-effective biological control program. While T. chilonis demonstrated the ability to parasitize both host eggs, the results indicate a preference for ES eggs over COS eggs. The parasitism and emergence rates of T. chilonis regarding ES eggs (parasitism: 89.3%; emergence: 82.6%) surpassed those for COS eggs (parasitism: 74.7%; emergence: 68.8%), with a notable increase in the number of emergence holes observed in the ES eggs compared to the COS eggs. Moreover, the developmental time of T. chilonis for ES eggs (10.8 days) was shorter than that for COS eggs (12.5 days), resulting in a lower number of dead wasps produced. Notably, no significant difference was observed in the female ratios between the two species. A comprehensive analysis was conducted, comparing the size and shell thickness of the two factitious hosts. The ES eggs exhibited smaller dimensions (length: 1721.5 µm; width: 1178.9 µm) in comparison to the COS eggs (length: 2908.8 µm; width: 2574.4 µm), with the ES eggshells being thinner (33.8 µm) compared to the COS eggshells (47.3 µm). The different host species had an effect on the body length of the reared parasitoids, with T. chilonis reared on COS hosts exhibiting a larger body length (female: 626.9 µm; male: 556.7 µm) than those reared on ES hosts (female: 578.8 µm; male: 438.4 µm). Conclusively, the results indicate that ES eggs present a viable alternative to COS eggs for the mass production of Trichogramma species in biological control programs.

Comparison of liposome-polycation-DNA(LPD) and monophosphoryl lipid A(MPL) adjuvant formulations in BALB/c mice models.

It is of fundamental importance to use an appropriate adjuvant to generate a potent immune response for immunotherapy. In this study, we had a comparative investigation on the effectiveness of two adjuvant formulations, liposome-polycation-DNA (LPD) and monophosphoryl lipid A(MPL) in combination with a truncated peptide of bFGF(tbFGF) as antigen. LPD/tbFGF induced continuously increasing antibodies expression during the whole immunization period. In contrast, the level of antibodies was variable in MPL/tbFGF-immunized mice, MPL/tbFGF elicited potent antibodies response in the early-phase of immunization (during the first 3 immunizations), but the later immunizations did not produce a significant increase in the level of antibodies. Evaluation of IFN-γ and IL-4 responses revealed that both LPD/tbFGF and MPL/tbFGF demonstrated generation of higher level of IFN-γ, whereas no significant increase in IL-4 levels was detected in the two groups. In addition, histological analysis exhibited obvious germinal centers in the spleen tissues of LPD/tbFGF mice. The data suggested that LPD would be a promising long-effective adjuvant due to its potent and persistent immunostimulation and MPL could play an appropriate role in short-acting immunization.

Measurements and simulations of energy fluxes over a high-rise and compact urban area in Hong Kong.

Measuring energy fluxes in a dense and high-rise urban area is extremely challenging, thus our knowledge in such area remains limited. This study assessed the surface energy fluxes and investigated the energy balance closure (EBC) over such complex urban surface in Hong Kong. Net radiation (QN), sensible (QH) and latent (QE) heat fluxes were measured using an eddy covariance system from September 2018 to August 2019. Anthropogenic heat flux (QF) was simulated by a large-scale urban energy model (i.e., LUCY) and validated by an anthropogenic heat database (i.e., AHE_KL). Storage heat flux (QS) was estimated by an objective hysteresis model (OHM). Among five energy terms, QF showed the largest values of around 750 Wm-2 especially in the afternoon. Whereas, QE varying within 150 Wm-2 showed the smallest values. The variation range of net radiation, sensible heat flux and storage heat was respectively from -50 to 600, 0 to 450 and -30 to 300 W m-2. EBC generally showed a negative relationship with surface heterogeneity. Best EBC was observed in the direction with a relatively constant and large aspect ratio, and with the most occurrence of unstable stratifications. The uncertainties of QH and QE fluxes were respectively estimated to be approximately 8% and 7%. The result of LUCY was consistent with that of AHE_KL. EBC was not sensitive to different coefficients estimating QS. This study helped to fill a gap in our understanding of surface energy and turbulent fluxes in compact cities with high-rise buildings and shed insights into the future installation of eddy covariance tower in similar areas. The required height of the eddy covariance tower in such urban sites might not be as restrictive as that in other urban areas with low-rise buildings or with low building density, thus making it more feasible to set up such observation towers.

Knowledge transfer between brain lesion segmentation tasks with increased model capacity.

Convolutional neural networks (CNNs) have become an increasingly popular tool for brain lesion segmentation in recent years due to its accuracy and efficiency. However, CNN-based brain lesion segmentation generally requires a large amount of annotated training data, which can be costly for medical imaging. In many scenarios, only a few annotations of brain lesions are available. One common strategy to address the issue of limited annotated data is to transfer knowledge from a different yet relevant source task, where training data is abundant, to the target task of interest. Typically, a model can be pretrained for the source task, and then fine-tuned with the scarce training data associated with the target task. However, classic fine-tuning tends to make small modifications to the pretrained model, which could hinder its adaptation to the target task. Fine-tuning with increased model capacity has been shown to alleviate this negative impact in image classification problems. In this work, we extend the strategy of fine-tuning with increased model capacity to the problem of brain lesion segmentation, and then develop an advanced version that is better suitable for segmentation problems. First, we propose a vanilla strategy of increasing the capacity, where, like in the classification problem, the width of the network is augmented during fine-tuning. Second, because unlike image classification, in segmentation problems each voxel is associated with a labeling result, we further develop a spatially adaptive augmentation strategy during fine-tuning. Specifically, in addition to the vanilla width augmentation, we incorporate a module that computes a spatial map of the contribution of the information given by width augmentation in the final segmentation. For demonstration, the proposed method was applied to ischemic stroke lesion segmentation, where a model pretrained for brain tumor segmentation was fine-tuned, and the experimental results indicate the benefit of our method.