SALI: A Scalable Adaptive Learned Index Framework based on Probability Models

The growth in data storage capacity and the increasing demands for high performance have created several challenges for concurrent indexing structures. One promising solution is learned indexes, which use a learning-based approach to fit the distribution of stored data and predictively locate target keys, significantly improving lookup performance. Despite their advantages, prevailing learned indexes exhibit constraints and encounter issues of scalability on multi-core data storage. This paper introduces SALI, the Scalable Adaptive Learned Index framework, which incorporates two strategies aimed at achieving high scalability, improving efficiency, and enhancing the robustness of the learned index. Firstly, a set of node-evolving strategies is defined to enable the learned index to adapt to various workload skews and enhance its concurrency performance in such scenarios. Secondly, a lightweight strategy is proposed to maintain statistical information within the learned index, with the goal of further improving the scalability of the index. Furthermore, to validate their effectiveness, SALI applied the two strategies mentioned above to the learned index structure that utilizes fine-grained write locks, known as LIPP. The experimental results have demonstrated that SALI significantly enhances the insertion throughput with 64 threads by an average of 2.04x compared to the second-best learned index. Furthermore, SALI accomplishes a lookup throughput similar to that of LIPP+.Comment: Accepted by Conference SIGMOD 24, June 09-15, 2024, Santiago, Chil

Reduction and Accumulative Characteristics of Dissolved Heavy Metals in Modified Bioretention Media

Twelve bioretention filter columns with different media were designed to study the effects of media on dissolved heavy metals in bioretention systems by changing three test conditions (inflow concentration, discharge ratio, and recurrence interval). The results showed that the average load reduction efficiency of the bioretention soil media (BSM)+10%water treatment residue, BSM+10%green zeolite, and BSM+10%medicinal stone for Cu and Zn was larger than 80%. The highest volume reduction efficiency is 39.25% by BSM+coconut bran. Among the three factors selected in tests, inflow concentration had the biggest degree of influence, followed by discharge ratio and recurrence interval. The media of the upper, middle, and lower layers of each filter column were detected before and after the treatment to study the accumulative characteristics of heavy metals in the bioretention system. The accumulation of Cu, Zn, and Cd in the media of BSM+medicinal stone, BSM+fly ash, BSM+vermiculite, and BSM+turfy soil was relatively low. The contents of the three metals were positively correlated with urease and negatively correlated with protease in the media, but no obvious rule was showed in the accumulation of dissolved heavy metals with depth

Exosome Derived From Human Umbilical Cord Mesenchymal Stem Cell Mediates MiR-181c Attenuating Burn-induced Excessive Inflammation

Mesenchymal stem cell (MSC)-derived exosomes have diverse functions in regulating wound healing and inflammation; however, the molecular mechanism of human umbilical cord MSC (hUCMSC)-derived exosomes in regulating burn-induced inflammation is not well understood. We found that burn injury significantly increased the inflammatory reaction of rats or macrophages exposed to lipopolysaccharide (LPS), increased tumor necrosis factor α (TNF-α) and interleukin-1β (IL-1β) levels and decreased IL-10 levels. hUCMSC-exosome administration successfully reversed this reaction. Further studies showed that miR-181c in the exosomes played a pivotal role in regulating inflammation. Compared to control hUCMSC-exosomes, hUCMSC-exosomes overexpressing miR-181c more effectively suppressed the TLR4 signaling pathway and alleviated inflammation in burned rats. Administration of miR-181c-expressing hUCMSC-exosomes or TLR4 knockdown significantly reduced LPS-induced TLR4 expression by macrophages and the inflammatory reaction. In summary, miR-181c expression in hUCMSC-exosomes reduces burn-induced inflammation by downregulating the TLR4 signaling pathway

Exosome Derived From Human Umbilical Cord Mesenchymal Stem Cell Mediates MiR-181c Attenuating Burn-induced Excessive Inflammation

Mesenchymal stem cell (MSC)-derived exosomes have diverse functions in regulating wound healing and inflammation, however, the molecular mechanism of human umbilical cord MSC (hUCMSC)-derived exosomes in regulating burn-induced inflammation is not well understood. We found that burn injury significantly increased the inflammatory reaction of rats or macrophages exposed to lipopolysaccharide (LPS), increased tumor necrosis factor α (TNF-α) and interleukin-1β (IL-1β) levels and decreased IL-10 levels. hUCMSC-exosome administration successfully reversed this reaction. Further studies showed that miR-181c in the exosomes played a pivotal role in regulating inflammation. Compared to control hUCMSC-exosomes, hUCMSC-exosomes overexpressing miR-181c more effectively suppressed the TLR4 signaling pathway and alleviated inflammation in burned rats. Administration of miR-181c-expressing hUCMSC-exosomes or TLR4 knockdown significantly reduced LPS-induced TLR4 expression by macrophages and the inflammatory reaction. In summary, miR-181c expression in hUCMSC-exosomes reduces burn-induced inflammation by downregulating the TLR4 signaling pathway

Human umbilical cord mesenchymal stem cells transplantation promotes cutaneous wound healing of severe burned rats.

BACKGROUND: Severe burns are a common and highly lethal trauma. The key step for severe burn therapy is to promote the wound healing as early as possible, and reports indicate that mesenchymal stem cell (MSC) therapy contributes to facilitate wound healing. In this study, we investigated effect of human umbilical cord MSCs (hUC-MSCs) could on wound healing in a rat model of severe burn and its potential mechanism. METHODS: Adult male Wistar rats were randomly divided into sham, burn, and burn transplanted hUC-MSCs. GFP labeled hUC-MSCs or PBS was intravenous injected into respective groups. The rate of wound closure was evaluated by Image Pro Plus. GFP-labeled hUC-MSCs were tracked by in vivo bioluminescence imaging (BLI), and human-specific DNA expression in wounds was detected by PCR. Inflammatory cells, neutrophils, macrophages, capillaries and collagen types I/III in wounds were evaluated by histochemical staining. Wound blood flow was evaluated by laser Doppler blood flow meter. The levels of proinflammatory and anti-inflammatory factors, VEGF, collagen types I/III in wounds were analyzed using an ELISA. RESULTS: We found that wound healing was significantly accelerated in the hUC-MSC therapy group. The hUC-MSCs migrated into wound and remarkably decreased the quantity of infiltrated inflammatory cells and levels of IL-1, IL-6, TNF-α and increased levels of IL-10 and TSG-6 in wounds. Additionally, the neovascularization and levels of VEGF in wounds in the hUC-MSC therapy group were markedly higher than those in other control groups. The ratio of collagen types I and III in the hUC-MSC therapy group were markedly higher than that in the burn group at indicated time after transplantation. CONCLUSION: The study suggests that hUC-MSCs transplantation can effectively improve wound healing in severe burned rat model. Moreover, these data might provide the theoretical foundation for the further clinical application of hUC-MSC in burn areas

ER stress and subsequent activated calpain play a pivotal role in skeletal muscle wasting after severe burn injury

<div><p>Severe burns are typically followed by hypermetabolism characterized by significant muscle wasting, which causes considerable morbidity and mortality. The aim of the present study was to explore the underlying mechanisms of skeletal muscle damage/wasting post-burn. Rats were randomized to the sham, sham+4-phenylbutyrate (4-PBA, a pharmacological chaperone promoting endoplasmic reticulum (ER) folding/trafficking, commonly considered as an inhibitor of ER), burn (30% total body surface area), and burn+4-PBA groups; and sacrificed at 1, 4, 7, 14 days after the burn injury. Tibial anterior muscle was harvested for transmission electron microscopy, calcium imaging, gene expression and protein analysis of ER stress / ubiquitin-proteasome system / autophagy, and calpain activity measurement. The results showed that ER stress markers were increased in the burn group compared with the sham group, especially at post-burn days 4 and 7, which might consequently elevate cytoplasmic calcium concentration, promote calpain production as well as activation, and cause skeletal muscle damage/wasting of TA muscle after severe burn injury. Interestingly, treatment with 4-PBA prevented burn-induced ER swelling and altered protein expression of ER stress markers and calcium release, attenuating calpain activation and skeletal muscle damage/wasting after severe burn injury. Atrogin-1 and LC3-II/LC3-I ratio were also increased in the burn group compared with the sham group, while MuRF-1 remained unchanged; 4-PBA decreased atrogin-1 in the burn group. Taken together, these findings suggested that severe burn injury induces ER stress, which in turns causes calpain activation. ER stress and subsequent activated calpain play a critical role in skeletal muscle damage/wasting in burned rats.</p></div

Exosome Derived From Human Umbilical Cord Mesenchymal Stem Cell Mediates MiR-181c Attenuating Burn-induced Excessive Inflammation

Mesenchymal stem cell (MSC)-derived exosomes have diverse functions in regulating wound healing and inflammation, however, the molecular mechanism of human umbilical cord MSC (hUCMSC)-derived exosomes in regulating burn-induced inflammation is not well understood. We found that burn injury significantly increased the inflammatory reaction of rats or macrophages exposed to lipopolysaccharide (LPS), increased tumor necrosis factor α (TNF-α) and interleukin-1β (IL-1β) levels and decreased IL-10 levels. hUCMSC-exosome administration successfully reversed this reaction. Further studies showed that miR-181c in the exosomes played a pivotal role in regulating inflammation. Compared to control hUCMSC-exosomes, hUCMSC-exosomes overexpressing miR-181c more effectively suppressed the TLR4 signaling pathway and alleviated inflammation in burned rats. Administration of miR-181c-expressing hUCMSC-exosomes or TLR4 knockdown significantly reduced LPS-induced TLR4 expression by macrophages and the inflammatory reaction. In summary, miR-181c expression in hUCMSC-exosomes reduces burn-induced inflammation by downregulating the TLR4 signaling pathway

Calpain is overexpressed and activated after severe burn injury, which could be suppressed by 4-PBA treatment.

<p>The rats were randomized to four groups: sham, sham+4-PBA, burn and burn+4-PBA. Calpain activity was measured at different time points post-burn in TAM specimens (A). Gene expression levels and protein amounts of calpain-1 and 2 in TAM specimens were respectively evaluated by real-time PCR (B) and western blot (C), with GAPDH used as an internal control; the results were normalized to sham group. At 7 days post-burn, the effects of 4-PBA on the protein amounts of calpain-1 and 2 in TAM samples were examined by western blot (D). n = 6 per group. *<i>p</i><0.05, ** <i>p</i><0.01 vs. sham group. #<i>p</i><0.05 vs. burn group.</p