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The shallow, thin super-heavy oil reservoir demonstrates certain characteristics, such as shallow reservoir depths, low-formation temperature, and high crude oil viscosity at reservoir temperatures. In the current production process, the central area of P601 is undergoing high-frequency huff and puff operations, facing certain problems such as decreasing production, low recovery rates, and rapid depletion of formation pressure. Through physical simulation experiments, the various elements of HDNS-enhanced oil recovery technology were analyzed. Nitrogen plus an oil-soluble viscosity reducer can improve the thermal recovery and development effect of super-heavy oil. With the addition of the viscosity-reducing slug, the recovery rate of steam flooding was 58.61%, which was 23.32% higher than that of pure steam flooding; after adding the 0.8 PV nitrogen slug, the recovery rate increased to 76.48%. With the increased nitrogen injection dosage, the water breakthrough time was extended, the water cut decreased, and the recovery rate increased. Nitrogen also plays a role in profile control and plugging within the reservoir; this function can effectively increase the heating range, increase steam sweep efficiency, and reduce water cut. So, the synergistic effects of steam, nitrogen, and viscosity-reducing agents are good. This technology enhances the development of shallow-layer heavy oil reservoirs, and subsequent development technologies are being compared and studied to ensure the sustainable development of super-heavy oil reservoirs.

In January 2013, a long-lasting episode of severe haze occurred in central and eastern China, and it attracted attention from all sectors of society. The process and evolution of haze pollution episodes were observed by the ＂Forming Mechanism and Con- trol Strategies of Haze in China＂ group using an intensive aerosol and trace gases campaign that simultaneously obtained data at 11 ground-based observing sites in the CARE-China network. The characteristics and formation mechanism of haze pollu- tion episodes were discussed. Five haze pollution episodes were identified in the Beijing-Tianjin-Hebei （Jing-Jin-Ji） area; the two most severe episodes occurred during 9-15 January and 25-31 January. During these two haze pollution episodes, the maximum hourly PMz5 mass concentrations in Beijing were 680 and 530 ~tg m-3, respectively. The process and evolution of haze pollution episodes in other major cities in the Jing-Jin-Ji area, such as Shijiazhuang and Tianjin were almost the same as those observed in Beijing. The external cause of the severe haze episodes was the unusual atmospheric circulation, the depres- sion of strong cold air activities and the very unfavorable dispersion due to geographical and meteorological conditions. How- ever, the internal cause was the quick secondary transformation of primary gaseous pollutants to secondary aerosols, which contributed to the ＂explosive growth＂ and ＂sustained growth＂ of PM2.5. Particularly, the abnormally high amount of nitric ox- ide （NOx） in the haze episodes, produced by fossil fuel combustion and vehicle emissions, played a direct or indirect role in the quick secondary transformation of coal-burning sulphur dioxide （SO2） to sulphate aerosols. Furthermore, gaseous pollutants were transformed into secondary aerosols through heterogeneous reactions on the surface of fine particles, which can change the particle＇s size and chemical composition. Consequently, the proportion of secondary inorganic ions, such as sulphate and nitrate, gradually increased, which enhances particle hygroscopicity and thereby accelerating formation of the haze pollution.

Fine particle of organic aerosol （OA）, mostly arising from pollution, are abundant in Beijing. To achieve a better un- derstanding of the difference in OA in summer and autumn, a high-resolution time-of-flight aerosol mass spectrometer （HR- ToF-AMS, Aerodyne Research Inc., USA） was deployed in urban Beijing in August and October 2012. The mean OA mass concentration in autumn was 30 4-30 μg m-3, which was higher than in summer （13 4-6.9 μg m-3）. The elemental anal- ysis found that OA was more aged in summer （oxygen-to-carbon （O/C） ratios were 0.41 and 0.32 for summer and autumn, respectively）. Positive matrix factorization （PMF） analysis identified three and five components in summer and autumn, re- spectively. In summer, an oxygenated OA （OOA）, a cooking-emission-related OA （COA）, and a hydrocarbon-like OA （HOA） were indentified. Meanwhile, the OOA was separated into LV-OOA （low-volatility OOA） and SV-OOA （semi-volatile OOA）; and in autumn, a nitrogen-containing OA （NOA） was also found. The SOA （secondary OA） was always the most important OA component, accounting for 55% of the OA in the two seasons. Back trajectory clustering analysis found that the origin of the air masses was more complex in summer. Southerly air masses in both seasons were associated with the highest OA loading, while northerly air masses were associated with the lowest OA loading. A preliminary study of OA components, especially the POA （primary OA）, in different periods found that the HOA and COA all decreased during the National Day holiday period, and HOA decreased at weekends compared with weekdays.

Oxaliplatin resistance undermines its curative effects on cancer and usually leads to local recurrence. The oxidative stress induced DNA damage repair response is an important mechanism for inducing oxaliplatin resistance by activating autophagy. ELISA is used to detect target genes expression. TMT-based quantitative proteomic analysis was used to investigate the potential mechanisms involved in NORAD interactions based on GO analysis. Transwell assays and apoptosis flow cytometry were used for biological function analysis. CCK-8 was used to calculate IC50 and resistance index (RI) values. Dual-luciferase reporter gene assay, RIP and ChIP assays, and RNA pull-down were used to detect the interaction. Autophagy flux was evaluated using electron microscope and western blotting. Oxidative stress was enhanced by oxaliplatin; and oxaliplatin resistance gastric cancer cell showed lower oxidative stress. TMT labeling showed that NORAD may regulate autophagy flux. NORAD was highly expressed in oxaliplatin-resistant tissues. In vitro experiments indicate that NORAD knockdown decreases the RI (Resistance Index). Oxaliplatin induces oxidative stress and upregulates the expression of NORAD. SGC-7901 shows enhanced oxidative stress than oxaliplatin-resistant cells (SGC-7901-R). NORAD, activated by H3K27ac and CREBBP, enhanced the autophagy flux in SGC-7901-R to suppress the oxidative stress. NORAD binds to miR-433-3p and thereby stabilize the ATG5- ATG12 complex. Our findings illustrate that NORAD, activated by the oxidative stress, can positively regulate ATG5 and ATG12 and enhance the autophagy flux by sponging miR-433-3p. NORAD may be a potential biomarker for predicting oxaliplatin resistance and mediating oxidative stress, and provides therapeutic targets for reversing oxaliplatin resistance.

Hematopoietic stem cells, regulated by their microenvironment (or \"niche\"), sustain the production of mature blood and immune cells. Leukemia cells remodel the microenvironment to enhance their survival, which is accompanied by the loss of support for normal hematopoiesis in hematologic malignancies. Extracellular vesicles (EVs) mediate intercellular communication in physiological and pathological conditions, and deciphering their functions in cell-cell interactions in the ecosystem can highlight potential therapeutic targets. In this Review, we illustrate the utility of EVs derived from various cell types, focusing on the biological molecules they contain and the behavioral alterations they can induce in recipient cells. We also discuss the potential for clinical application in hematologic malignancies, including EV-based therapeutic regimens, drug delivery via EVs, and the use of EVs (or their cargoes) as biomarkers.

miR-150 was found to target the 3′-untranslated regions of AKT3, and the AKT pathway was affected by SR protein kinase 1 (SRPK1). However, the expression and significance of miR-150, AKT3 and SRPK1 in acute lung injury (ALI) were not clear. Here, we found that the expression of miR-150 was significantly reduced, while the expression of AKT3 and SRPK1 were markedly increased in LPS-treated A549, THP-1 and RAW 264.7 cells. miR-150 significantly decreased levels of pro-inflammatory cytokines IL-1β, IL-6 and TNF-α, reduced the expression of AKT3, but had no impact on SRPK1 expression compared with the control group in LPS-treated A549, THP-1 and RAW 264.7 cells. AKT3 silencing only reduced the production of pro-inflammatory cytokines and showed no effect on miR-150 and SRPK1 expression. Finally, we observed that miR-150 mimics and/or silencing of SRPK1 decreased the expression of AKT3 mRNA. Besides, over-expression of miR-150 or silencing of SRPK1 also reduced the expression of AKT3 protein, which exhibited the lowest level in the miR-150 mimics plus si-SRPK1 group. However, si-SRPK1 had no effect on miR-150 level. In conclusion, miR-150 and SRPK1 separately and cooperatively participate into inflammatory responses in ALI through regulating AKT3 pathway. Increased miR-150 and silenced SRPK1 may be a novel potential factor for preventing and treating more inflammatory lung diseases.

The aberrant expression of microRNAs (miRNAs) is associated with the pathogenesis of inflammation-related diseases. However, the biological functions of miR-21 in acute lung injury (ALI) remain largely unknown. In this study, the level of miR-21 was obviously increased, but B cell lymphoma-2 (Bcl-2) expression was markedly decreased in LPS-treated human pulmonary alveolar epithelial cells (HPAEpiC). Suppression of miR-21 attenuated LPS-induced apoptosis and inflammation in HPAEpiC and promoted the survival of mice with ALI by decreasing the inflammatory cell count, release of cytokines and permeability in lung tissues. Importantly, Bcl-2 was a direct target of miR-21, and its expression was significantly inhibited by miR-21 mimics at a post-transcriptional level. Besides, Bcl-2 over-expression reversed miR-21-induced apoptosis and inflammation status and showed synergic effects with miR-21 inhibitor in LPS-treated HPAEpiC. In conclusion, inhibition of miR-21 could ameliorate apoptosis and inflammation by restoring the expression of Bcl-2 in LPS-induced HPAEpiC and mice, which might provide therapeutic strategies for the treatment of ALI.

Background Leaf colour mutations are universally expressed at the seedling stage and are ideal materials for exploring the chlorophyll biosynthesis pathway, carotenoid metabolism and the flavonoid biosynthesis pathway in plants. Results In this research, we analysed the different degrees of albinism in apple ( Malus domestica ) seedlings, including white-leaf mutants (WM), piebald leaf mutants (PM), light-green leaf mutants (LM) and normal leaves (NL) using bisulfite sequencing (BS-seq) and RNA sequencing (RNA-seq). There were 61,755, 79,824, and 74,899 differentially methylated regions (DMRs) and 7566, 3660, and 3546 differentially expressed genes (DEGs) identified in the WM/NL, PM/NL and LM/NL comparisons, respectively. Conclusion The analysis of the methylome and transcriptome showed that 9 DMR-associated DEGs were involved in the carotenoid metabolism and flavonoid biosynthesis pathway. The expression of different transcription factors (TFs) may also influence the chlorophyll biosynthesis pathway, carotenoid metabolism and the flavonoid biosynthesis pathway in apple leaf mutants. This study provides a new method for understanding the differences in the formation of apple seedlings with different degrees of albinism.

CDK2-associated cullin domain 1 (CAC1) is as a novel cell cycle regulator widely expressed in colorectal cancer (CRC). However, its expression and function in drug resistant CRC cells remains elusive. Therefore, the present study aimed to assess the biochemical function and relevance of CAC1 in drug resistant CRC cells, and detect the potential mechanism. For this purpose, a total of 83 CRC cases were collected for the immunohistochemical analysis of CAC1 expression. Functional studies (stable transfection, flow cytometry, colony formation, and invasion and migration assays) were performed in SW480, LoVo and their corresponding 5-FU resistant cells. In addition, a nude mice xenograft model was established for further observation in vivo. In the present study, CAC1 protein expression was higher in CRC tissues than that in normal tissues (P<0.05). Furthermore, CAC1 protein expression was higher in SW480/5-FU cells than in SW480 cells. CAC1 knockdown arrested 5-FU resistant cells at the G1/S phase and increased the sensitivity of 5-FU resistant cells to 5-FU by inducing apoptosis. In addition, CAC1 reduced the invasive and migration ability of SW480/5-FU and LoVo/5-FU cells in vitro, and reduced their tumorigenicity and metastatic ability in vivo. Finally, CAC1 knockdown resulted in decreased P-glycoprotein and MRP-1 protein expression. Based on these results, it can be concluded that CAC1 plays an important role in the occurrence and promotion of drug resistance in CRC. Therefore, the knockdown of CAC1 may be considered as a new strategy for the development of CRC drug resistance treatments in the future.

A major goal of cancer biology is to understand the mechanisms driven by somatically acquired mutations. Two distinct methodologies—one analyzing mutation clustering within protein sequences and 3D structures, the other leveraging protein-protein interaction network topology—offer complementary strengths. We present NetFlow3D, a unified, end-to-end 3D structurally-informed protein interaction network propagation framework that maps the multiscale mechanistic effects of mutations. Built upon the Human Protein Structurome, which incorporates the 3D structures of every protein and the binding interfaces of all known protein interactions, NetFlow3D integrates atomic, residue, protein and network-level information: It clusters mutations on 3D protein structures to identify driver mutations and propagates their impacts anisotropically across the protein interaction network, guided by the involved interaction interfaces, to reveal systems-level impacts. Applied to 33 cancer types, NetFlow3D identifies 2 times more 3D clusters and incorporates 8 times more proteins in significantly interconnected network modules compared to traditional methods. Multiple computational methods have been developed to understand how mutations drive tumourigenesis, but their insights are largely non-overlapping. Here, the authors introduce NetFlow3D, a framework for integrating protein structure and interaction networks to map the mechanistic effects of somatic mutations in cancer.