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Exploration in the Lishui West Sag of the East China Sea Basin is limited by the scarcity of offshore drilling sites, and the prediction of deep, high-quality reservoirs is challenging using only geophysical methods. This study introduces a quantitative approach to diagenetic facies division in individual wells based on logging data, providing a new method and perspective for the prediction of deep, high-quality reservoirs. We employed comprehensive data from core, logging, thin-section casting, cathodoluminescence, scanning electron microscopy, and X-ray diffraction analyses from five wells to study the petrology, physical properties, diagenetic types and strength, and diagenetic minerals of the Paleocene sandstone reservoirs in the Lishui West Sag. Apparent compaction rate, apparent cementation rate, and other quantitative characterization parameters were used to calculate the comprehensive diagenetic coefficient (Cg), and the diagenetic facies were divided into compaction, cementation, and dissolution facies. A logging calculation model for the comprehensive diagenetic coefficient (Cg) and a quantitative identification method for diagenetic facies in individual well reservoirs were established through a fitting analysis between Cg and logging curve parameters. Continuous quantitative identification of vertical diagenetic facies in the five wells in the study area showed that the high-quality reservoirs in wells L1, L2, and L3 within the L1 gas field are characterized by extensive development of dissolution facies, while wells L4 and L5 are dominated by compaction and cementation facies, with poor reservoir properties and no industrial gas flow output. The results demonstrate the reliability of the model method. The establishment of this quantitative characterization method for diagenetic facies using logging data provides guidance for the prediction of favorable reservoirs.

Abstract Background Mesenchymal stem cells (MSCs) have been considered to be the attractive vehicles for delivering therapeutic agents toward various tumor diseases. This study was to explore the distribution pattern, kinetic delivery of adenovirus, and therapeutic efficacy of the MSC loading of E1A mutant conditionally replicative adenovirus Adv-Stat3(-) which selectively replicated and expressed high levels of anti-sense Stat3 complementary DNA in breast cancer and melanoma cells. Methods We assessed the release ability of conditionally replicative adenovirus (CRAd) from MSC using crystal violet staining, TCID50 assay, and quantitative PCR. In vitro killing competence of MSCs carrying Adv-Stat3(-) toward breast cancer and melanoma was performed using co-culture system of transwell plates. We examined tumor tropism of MSC by Prussian blue staining and immunofluorescence. In vivo killing competence of MSCs carrying Adv-Stat3(-) toward breast tumor was analyzed by comparison of tumor volumes and survival periods. Results Adv-Stat3(-) amplified in MSCs and were released 4 days after infection. MSCs carrying Adv-Stat3(-) caused viral amplification, depletion of Stat3 and its downstream proteins, and led to significant apoptosis in breast cancer and melanoma cell lines. In vivo experiments confirmed the preferential localization of MSCs in the tumor periphery 24 hours after tail vein injection, and this localization was mainly detected in the tumor parenchyma after 72 hours. Intravenous injection of MSCs carrying Adv-Stat3(-) suppressed the Stat3 pathway, down-regulated Ki67 expression, and recruited CD11b-positive cells in the local tumor, inhibiting tumor growth and increasing the survival of tumor-bearing mice. Conclusions These results indicate that MSCs migrate to the tumor site in a time-dependent manner and could be an effective platform for the targeted delivery of CRAd and the amplification of tumor killing effects.

Abstract Background P21(WAF1/Cip1) binds to cyclin-dependent kinase complexes and inhibits their activities. It was originally described as an inhibitor of cancer cell proliferation. However, many recent studies have shown that p21 promotes tumor progression when accumulated in the cell cytoplasm. So far, little is known about the correlation between cytoplasmic p21 and drug resistance. This study was aimed to investigate the role of p21 in the cisplatin resistance of ovarian cancer. Methods RT-PCR, western blot and immunofluorescence were used to detect p21 expression and location in cisplatin-resistant ovarian cancer cell line C13* and its parental line OV2008. Regulation of cytoplasmic p21 was performed through transfection of p21 siRNA, Akt2 shRNA and Akt2 constitutively active vector in the two cell lines; their effects on cisplatin-induced apoptosis were evaluated by flow cytometry. Tumor tissue sections of clinical samples were analyzed by immunohistochemistry. Results p21 predominantly localizes to the cytoplasm in C13* compared to OV2008. Persistent exposure to low dose cisplatin in OV2008 leads to p21 translocation from nuclear to cytoplasm, while it had not impact on p21 localization in C13*. Knockdown of cytoplasmic p21 by p21 siRNA transfection in C13* notably increased cisplatin-induced apoptosis through activation of caspase 3. Inhibition of p21 translocation into the cytoplasm by transfection of Akt2 shRNA into C13* cells significantly increased cisplatin-induced apoptosis, while induction of p21 translocation into the cytoplasm by transfection of constitutively active Akt2 in OV2008 enhanced the resistance to cisplatin. Immunohistochemical analysis of clinical ovarian tumor tissues demonstrated that cytoplasmic p21 was negatively correlated with the response to cisplatin based treatment. Conclusions Cytoplasmic p21 is a novel biomarker of cisplatin resistance and it may represent a potential therapeutic target for ovarian tumors that are refractory to conventional treatment.

Background The CD47-SIRPα pathway acts as an important myeloid cell immune checkpoint and targeting the CD47/SIRPα axis represents a promising strategy to promote antitumor immunity. Several CD47-targeting agents show encouraging early activity in clinical trials. However, due to ubiquitous expression of CD47, the antigen sink and hematologic toxicity, such as anemia and thrombocytopenia, are main problems for developing CD47-targeting therapies. Considering the limited expression of SIRPα, targeting SIRPα is an alternative approach to block the CD47-SIRPα pathway, which may result in differential efficacy and safety profiles.Methods SIRPα-targeting antibody BR105 was generated by hybridoma fusion and following humanization. BR105 was characterized for binding to human SIRPα alleles and blockade of the interaction with CD47. The functional activity was determined in in vitro phagocytosis assays by using human macrophages. The effect of BR105 on human T cell activation was studied using an OKT3-induced T-cell proliferation assay and an allogeneic mixed lymphocyte reaction. Human SIRPα-humanized immunodeficient mice were used in cancer models for evaluating the in vivo antitumor efficacy of BR105. Safety was addressed in a repeat-dose toxicity study in cynomolgus monkeys, and toxicokinetic analysis was further evaluated.Results BR105 shows broad binding activity across various SIRPα variants, and potently blocks the interaction of SIRPα and CD47. In vitro functional assays demonstrated that BR105 synergizes with therapeutic antibodies to promote phagocytosis of tumor cells. Moreover, the combination of BR105 and therapeutic antibody significantly inhibits tumor growth in a xenograft tumor model. Although BR105 may slightly bind to SIRPγ, it does not inhibit T cell activation, unlike other non-selective SIRPα-targeting antibody and CD47-targeting agents. Toxicity studies in non-human primates show that BR105 is well tolerated with no treatment-related adverse effects noted.Conclusions The novel and differentiated SIRPα-targeting antibody, BR105, was discovered and displays promising antitumor efficacy in vitro and in vivo. BR105 has a favorable safety profile and shows no adverse effects on T cell functionality. These data support further clinical development of BR105, especially as a therapeutic agent to enhance efficacy when used in combination with tumor-targeting antibodies or antibodies that target other immune checkpoints.

ABSTRACT: Avian infectious bronchitis (IB), a highly contagious disease hazardous to the poultry industry, is caused by an etiological agent called the infectious bronchitis virus (IBV). Some IBV strains (IBVs) alone usually do not cause high mortality in field conditions if not with secondary pathogens including Escherichia coli (E. coli). Herein, we established an IBV and E. coli co-infection model to evaluate the protective efficacy of two IBV vaccine strains against a new emerging genotype GVI-1 with mild virulence in experimental conditions. Chickens were inoculated with IBV field isolate ZQX (genotype GVI-1) and challenged 4 dlater with the E. coli strain MS160427 (serotype O8). Subsequently, these chickens were euthanized at seven days postchallenge (d.p.c.) with E. coli. An autopsy revealed that lesions in the IBV plus E. coli co-infection group were more severe than those in the IBV-infected group. This pathological model was used to assess the protective effect of two commonly used vaccine strains (H120 and 4/91) against the IBV ZQX strain, and a significantly better protective efficacy was observed for 4/91 compared with H120. Thus, IBV and E. coli co-infection could be employed in assessing the protective efficacy of IBV vaccines.

The utilization of 6,6-dimethyl-3-((trimethylsilyl)oxy)cyclohex-2-en-1-one made from an unsymmetrical 4,4-dimethylcyclohexane-1,3-dione in iridium-catalyzed allylic enolization involving keto-enol isomerization is accomplished under mild conditions. The chemoselectivity, regioselectivity, and enantioselectivity are facilitated by the quaternary carbon and adjusting the reaction conditions. This method provides the substituted 2-(but-3-en-2-yl)-3-hydroxy-6,6-dimethylcyclohex-2-en-1-ones in good to high yields with high level of chemo-, regio-, and enantioselectivities. The chiral carbon-fluorine bond formation is induced by an adjacent chiral carbon center of the allylated 3-hydroxy-6,6-dimethylcyclohex-2-en-1-one, as well.

Efficiently removing clouds from remote sensing imagery presents a significant challenge, yet it is crucial for a variety of applications. This paper introduces a novel sparse function, named the tri-fiber-wise sparse function, meticulously engineered for the targeted tasks of cloud detection and removal. This function is adept at capturing cloud characteristics across three dimensions, leveraging the sparsity of mode-1, -2, and -3 fibers simultaneously to achieve precise cloud detection. By incorporating the concept of tensor multi-rank, which describes the global correlation, we have developed a tri-fiber-wise sparse-based model that excels in both detecting and eliminating clouds from images. Furthermore, to ensure that the cloud-free information accurately matches the corresponding areas in the observed data, we have enhanced our model with an extended box-constraint strategy. The experiments showcase the notable success of the proposed method in cloud removal. This highlights its potential and utility in enhancing the accuracy of remote sensing imagery. [ABSTRACT FROM AUTHOR]

β-acetoxyisovalerylalkannin (β-AIVA) is one of shikonin/alkannin derivative, which were mainly extracted from Boraginaceae family. The effects of β-AIVA on human melanoma A375 cells and U918 cells were investigated in vitro. The CCK-8 assay showed that β-AIVA inhibited proliferation of cells. Results from flow cytometry, ROS assay and JC-1 assay showed that β-AIVA increased late apoptosis rate, induced the production of ROS and promoted mitochondrial depolarization in cells. β-AIVA regulated expressions of BAX and Bcl-2 proteins, and increased the expression of cleaved caspase-9 and cleaved caspase-3. These findings suggest that β-AIVA may be a potential therapeutic drug for treating melanoma. [ABSTRACT FROM AUTHOR]