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\"'The Great Wenchuan Earthquake of 2008: A Photographic Atlas of Surface Rupture and Related Disaster' focuses on the main deformation characteristics of co-seismic surface rupture, including rupture length and slip distribution of co-seismic surface rupture caused by the Wenchuan Earthquake and its associated relief operation. The magnitude Ms 8.0 (Mw 7.9) Wenchuan Earthquake occurred on 12 May 2008 in the Longmen Shan region of China, the topographical boundary between the Tibetan Plateau and the Sichuan Basin, resulting in extensive damage throughout central and western China. This atlas contains distinct photographs obtained during the field investigation carried out immediately 2 days after the quake. The atlas is designed for geologists, seismologists and architecture engineers engaged in seismic mechanisms and surface rupture deformation characteristics of large intracontinental earthquakes.\"--Publisher's website.

Elevated de novo lipogenesis is considered to be a crucial factor in hepatocellular carcinoma (HCC) development. Herein, we identify ubiquitin-specific protease 22 (USP22) as a key regulator for de novo fatty acid synthesis, which directly interacts with deubiquitinates and stabilizes peroxisome proliferator-activated receptor gamma (PPARγ) through K48-linked deubiquitination, and in turn, this stabilization increases acetyl-CoA carboxylase (ACC) and ATP citrate lyase (ACLY) expressions. In addition, we find that USP22 promotes de novo fatty acid synthesis and contributes to HCC tumorigenesis, however, this tumorigenicity is suppressed by inhibiting the expression of PPARγ, ACLY, or ACC in in vivo tumorigenesis experiments. In HCC, high expression of USP22 positively correlates with PPARγ, ACLY or ACC expression, and associates with a poor prognosis. Taken together, we identify a USP22-regulated lipogenesis mechanism that involves the PPARγ-ACLY/ACC axis in HCC tumorigenesis and provide a rationale for therapeutic targeting of lipogenesis via USP22 inhibition. Different deubiquitinases are associated to cancer development. Here, the authors show that PPARgamma is stabilized by USP22-mediated deubiquitination leading to lipid accumulation and promoting hepatocellular carcinoma.

With the development of the tea industry, understanding the differences in root zone microecology among different tea varieties is of great significance for improving tea quality and yield. To investigate the microbial and metabolite foundation underlying the disparities in root zone physicochemical properties between the high-aroma new tea variety JL4 (Jinlong No.4) and its grandparent HD (Huangdan), the bacterial diversity, community structure and metabolite distinctions of HD and JL4 root zone soils were analyzed using NovaSeq 6000 high-throughput sequencing and GC-MS-derived metabolomics technologies. The analysis of soil physical and chemical properties showed that, compared with HD, the available phosphorus (AP) in JL4 was significantly decreased (28.91 ±  9.78 mg · kg −1 , P  < 0.05), and so was the available potassium (AK) at 57.67 ±  4.04 mg · kg −1 . The results from 16S rDNA sequencing indicated that, compared with HD, JL4 had a lower Shannon index and a higher abundance of Gram-negative and aerobic-related bacteria. These results indicated that there was a decrease in bacterial diversity in the root zone soil of JL4. The dominant bacterial phyla included Proteobacteria , Acidobacteriota , and Chloroflexi among others. Biomarkers in HD included Firmicutes , Rhizobiales , and Caulobacterales , and biomarkers for JL4 comprised Sphingomonadaceae bacterium URHD0088 and Halomonadaceae . GC-MS derivatization metabolomics highlighted sugars as having the most differential metabolites (8). In JL4, D-manitol 2 and scylo-inositol decreased while (-)-epicatechin, catechin, and D-pinitol increased. KEGG pathway enrichment analysis revealed substantial enrichment in metabolic pathways related to flavonoid biosynthesis. The changes in these metabolites may have a significant impact on the growth and quality of tea plants. Redundancy Analysis (RDA) along with correlation analyses indicated significant impacts on root zone bacterial community structure by factors such as AK, Soil Organic Matter (SOM), NO 3 − -N (nitrate nitrogen), and pH levels. A significant positive correlation was observed between AK and both Firmicutes and Kapabacteria individually; furthermore, AP exhibited a highly significant positive correlation with Kapabacteria but a significant negative correlation with unidentified Archaea . Catechin and (-)-Epicatechin were significantly negatively correlated with Actinobacteria phylum while showing a significant positive correlation with Verrucomicrobia and Kryptonia phyla. This study systematically compared the microbial and metabolite characteristics of the root zone soil of JL4 and HD for the first time, providing new ideas and methods for tea variety improvement and precision cultivation management, which is expected to promote the high-quality development of the tea industry in the future.

Fruity-floral black tea quality is co-determined by both cultivar and processing. Jinlong No. 1 (JL1), a newly released high-aroma cultivar, lacked identified quantitative aroma markers. To elucidate the aroma characteristics of the newly released high-aroma cultivar 'Jinlong No.1' (JL1), three black teas were analyzed through GC-MS/MS-based volatile metabolomics, sensory evaluation, and relative odor activity value analysis. These included JL1 fruity-floral black tea (JL1B), JL1 conventional black tea (JL1S), and 'Huangdan' fruity-floral black tea (HDB). JL1B achieved the highest overall aroma score (8.2 ± 0.8). Comparative analysis revealed 340 differential volatiles between the two fruity-floral teas, predominantly esters (18%) and ketones (16%). Key upregulated compounds in JL1B included hexyl butanoate and hexyl 2-methylbutanoate, while ( )-2-nonenal and 1-nonen-3-ol were notably downregulated. Further comparison between the two JL1 teas identified 536 differential volatiles, with terpenoids (20%) and esters (18%) as the most abundant classes. Seventeen metabolites were commonly altered across comparisons, including the aforementioned esters. These findings establish specific quantitative targets for the precision processing and cultivar-directed breeding of premium fruity-floral black teas.

Metabolic dysregulation is emerging as a critical factor in tumorigenesis, and reprogramming of serine metabolism has been identified as an essential factor in the progression of hepatocellular carcinoma (HCC). Studies have shown that LKB1 deficiency can activate mTOR to upregulate the serine synthesis pathway (SSP) and promote tumor progression. Our team discovered that ubiquitin‐specific protease 10 (USP10) can inhibit HCC proliferation through mTOR, but its relationship with SSP needs further investigation. The metabolite assays revealed a significant increase in serine content in HCC tissues. Through the LKB1/mTOR/activating transcription factor 4 (ATF4) axis, loss of USP10 may increase serine biosynthesis and promote the proliferation of HCC in vitro and in vivo. Furthermore, it was found that USP10 could activate LKB1 through deubiquitination. Analyzing clinical HCC tissues revealed a positive correlation between USP10 and LKB1. Additionally, those with high expression of USP10 in HCC tissues showed a better degree of tumor differentiation and longer overall survival time. Moreover, we found increased expression of both serine and its synthase in liver tumor tissues of USP10 liver‐specific KO mice. Loss of USP10 inhibits the activity of LKB1, contributing to the stimulation of the mTOR/ATF4 axis and SSP and then promoting the proliferation of HCC. This work presents a novel approach for serine‐targeted treatment in HCC. Aberrant serine synthesis plays a vital role in hepatocellular carcinoma (HCC), so finding upstream regulators that control the serine synthesis pathway (SSP) is particularly important. This study shows that ubiquitin‐specific protease 10 (USP10) plays a crucial role in regulating the expression of SSP through the LKB1/mTOR/ATF4 axis and affects the proliferation of HCC. USP10 can regulate the activity of LKB1 through deubiquitination. This study identifies new potential sites for targeting therapy in HCC.

Background/Objectives: Lenvatinib combined with anti-PD-1 therapy has shown promise in the treatment of hepatocellular carcinoma (HCC). The study evaluates changes in gut microbiota (GM) and metabolites during HCC treatment with lenvatinib combined with anti-PD-1. Methods: An HCC mouse model was established via diethylnitrosamine (DEN) injection, and the mice were then treated with lenvatinib, anti-PD-1, or their combination. GM composition and structural changes were assessed by 16S rDNA sequencing, and metabolite abundance by liquid chromatography–mass spectrometry (LC–MS). Results: Significant alterations in GM and metabolites were observed in the HCC group compared to the control group, and compared with the HCC group, both monotherapy and combination therapy resulted in varying degrees of GM and metabolites rebalancing. Specifically, compared to the HCC group, lenvatinib combined with anti-PD-1 therapy decreased the abundance of GM, including p_Patescibacteria, g_Lactobacillus, g_Clostridium_sensu_stricto_1, g_Eubacterium_siraeum_group, and g_Desulfovibrio, while the abundance of g_Prevotella_7 increased. Metabolite changes included increased 4-pyridoxic acid, deoxycholic acid, and taurochenodesoxycholic acid, and decreased myristic acid, oleic acid, riboflavin, and uric acid. Conclusions: HCC induces substantial alterations in the GM and metabolic profile of mice. Lenvatinib combined with anti-PD-1 treatment partially modulates these dysregulations. The relevant GM and metabolites may be associated with the efficacy of combined therapy and could serve as potential markers for further investigation.

Background. Pancreatic ductal adenocarcinoma (PDAC) is a devastating cancer, and the therapy options for PDAC remain restricted. The distinctive tumor immunological microenvironment (TIME) of PDAC, comprising a high number of stromal cells and a limited infiltration of cytotoxic T lymphocytes (CTLs), rendered immunotherapy ineffective. The protein level of ubiquitin-specific protease 43 (USP43) was a prognostic predictor in numerous cancers; however, its function in PDAC is limited. This article focuses on the influence of USP43 expression on PDAC prognosis and TIME alteration. Methods. Based on TCGA database and tissue microarray staining, the expression of USP43 in PDAC was evaluated. The association between USP43 and prognosis was then investigated using tissue samples and online databases. In PDAC tumor tissues, the correlation between USP43 expression and clinicopathological characteristics, immune cell infiltration, and prognosis was investigated. The expression of USP43 in PDAC cell lines was evaluated using quantitative polymerase chain reaction. Using a cell counting kit-8 (CCK-8) and a cell colony formation test, the viability of the cells was determined. On the basis of online databases and tissue samples, the link between USP43 and immune cell infiltration around PDAC was also examined. For statistical analyses, the software GraphPad, R, and SPSS 26.0 were utilized. Results. The expression of USP43 was considerably higher in PDAC compared to normal pancreatic tissue in both the TCGA database and the tissue microarrays of PDAC patients (P<0.001). High USP43 expression was associated with poor overall survival in both the TCGA database and the tissue microarray of PDAC patients (P=0.046 and 0.021, respectively). USP43 overexpression promoted PANC-1 cell proliferation (P=0.0018), but USP43 knockdown decreased PANC02 cell proliferation (P<0.001). According to the TCGA database, USP43 is associated with T cell activation and inhibits CD8+ T cell activation in PDAC, as proven by a study of cell lines. Moreover, in both TCGA and PDAC cell lines, USP43 expression was negatively linked with the chemokine signaling pathway. Conclusions. Overexpression of USP43 is a potential prognostic indicator for PDAC patients. USP43 is a potential biomarker associated with T cell activation, suppression of CD8+ T cell enrichment, and the cytokine signal pathway. Future multicenter studies are needed to confirm our findings and their potential application in the treatment of PDAC patients.

The tumour microenvironment is essential for cancer progress and metastasis. Integrin-β5 (ITGB5), a member of the integrin family, has been implicated to mediate the interactions of cells with the extracellular matrix (ECM) and promote tumorigenesis in several malignancies. However, the role of ITGB5 in hepatocellular carcinoma (HCC) is still unknown. The biological function of ITGB5 in HCC was investigated using migration, colony formation assays. The potential molecular mechanism of ITGB5 in regulating HCC tumorigenesis and β-catenin stabilization was investigated by western blotting, co-immunoprecipitation and ubiquitination assays. The expression level of ITGB5 mediated by miR-185 was confirmed by bioinformatic analysis, luciferase assay. The clinical significance of ITGB5 was based on human tissue microarray (TMA) analysis. Here, we found that the expression of ITGB5 is increased in HCC tissues. Elevated ITGB5 markedly facilitates HCC cell migration and tumorigenesis in vitro and in vivo. Further mechanistic studies revealed that ITGB5, as a partner of β-catenin, directly interacts with β-catenin and inhibits its degradation, thus leading to WNT/β-catenin activity. Subsequently, we also found that ITGB5 is a direct targeted gene of miR-185. The downregulation of miR-185 in HCC cells promotes an increase in ITGB5. An additional increase of ITGB5 is associated with β-catenin upregulation and a miR-185 decrease in HCC tissues. Our data reveal that the miR-185-ITGB5-β-catenin pathway plays an important role in HCC tumorigenesis, and ITGB5 may be a promising specific target for HCC therapy.

Probiotic-based therapies have been shown to be beneficial for chemotherapy-induced mucositis. Previous research has demonstrated that a probiotic mixture (Bifidobacterium brevis, Lactobacillus acidophilus, Lactobacillus casei, and Streptococcus thermophilus) can ameliorate chemotherapy-induced mucositis and dysbiosis in rats, but the underlying mechanism has not been completely elucidated. We aimed to determine the inhibitory effects of the probiotic mixture on cisplatin-induced mucositis and pica and the underlying mechanism, focusing on the levels of 5-hydroxytryptamine (5-HT, serotonin) regulated by the gut microbiota. A rat model of mucositis and pica was established by daily intraperitoneal injection of cisplatin (6 mg/kg) for 3 days. In the probiotic+cisplatin group, predaily intragastric injection of the probiotic mixture (1×109 CFU/kg BW) was administrated for 1 week before cisplatin injection. This was then followed by further daily probiotic injections for 6 days. Histopathology, pro-/anti-inflammatory cytokines, oxidative status, and 5-HT levels were assessed on days 3 and 6. The structure of the gut microbiota was analyzed by 16S rRNA gene sequencing and quantitative PCR. Additionally, 5-HT levels in enterochromaffin (EC) cells (RIN-14B cell line) treated with cisplatin and/or various probiotic bacteria were also determined. The probiotic mixture significantly attenuated kaolin consumption, inflammation, oxidative stress, and the increase in 5-HT concentrations in rats with cisplatin-induced intestinal mucositis and pica. Cisplatin markedly increased the relative abundances of Enterobacteriaceae_other, Blautia, Clostridiaceae_other, and members of Clostridium clusters IV and XIVa. These levels were significantly restored by the probiotic mixture. Importantly, most of the genera increased by cisplatin were significantly positively correlated with colonic 5-HT. Furthermore, in vitro, the probiotic mixture had direct inhibitory effects on the 5-HT secretion by EC cells. The probiotic mixture protects against cisplatin-induced intestine injury, exhibiting both anti-inflammatory and antiemetic properties. These results were closely related to the reestablishment of intestinal microbiota ecology and normalization of the dysbiosis-driven 5-HT overproduction.

Task allocation is a critical issue of spatial crowdsourcing. Although the batching strategy performs better than the real-time matching mode, it still has the following two drawbacks: (1) Because the granularity of the batch size set obtained by batching is too coarse, it will result in poor matching accuracy. However, roughly designing the batch size for all possible delays will result in a large computational overhead. (2) Ignoring non-stationary factors will lead to a change in optimal batch size that cannot be found as soon as possible. Therefore, this paper proposes a fine-grained, batching-based task allocation algorithm (FGBTA), considering non-stationary setting. In the batch method, the algorithm first uses variable step size to allow for fine-grained exploration within the predicted value given by the multi-armed bandit (MAB) algorithm and uses the results of pseudo-matching to calculate the batch utility. Then, the batch size with higher utility is selected, and the exact maximum weight matching algorithm is used to obtain the allocation result within the batch. In order to cope with the non-stationary changes, we use the sliding window (SW) method to retain the latest batch utility and discard the historical information that is too far away, so as to finally achieve refined batching and adapt to temporal changes. In addition, we also take into account the benefits of requesters, workers, and the platform. Experiments on real data and synthetic data show that this method can accomplish the task assignment of spatial crowdsourcing effectively and can adapt to the non-stationary setting as soon as possible. This paper mainly focuses on the spatial crowdsourcing task of ride-hailing.