A review of development methods and EOR technologies for carbonate reservoirs

Carbonate reservoirs worldwide are complex in structure,diverse in form,and highly heterogeneous.Based on these characteristics,the reservoir stimulation technologies and fluid flow characteristics of carbonate reservoirs are briefly described in this study.The development methods and EOR technologies of carbonate reservoirs are systematically summarized,the relevant mechanisms are analyzed,and the application status of oil fields is catalogued.The challenges in the development of carbonate reservoirs are discussed,and future research directions are explored.In the current development processes of carbonate reservoirs,water flooding and gas flooding remain the primary means but are often prone to channeling problems.Chemical flooding is an effective method of tertiary oil recovery,but the harsh formation conditions require high-performance chemical agents.The application of emerging technologies can enhance the oil recovery efficiency and environmental friendliness to a certain extent,which is welcome in hard-to-recover areas such as heavy oil reservoirs,but the economic cost is often high.In future research on EOR technologies,flow field control and flow channel plugging will be the potential directions of traditional development methods,and the application of nanoparticles will revolutionize the chemical EOR methods.On the basis of diversified reservoir stimulation,combined with a variety of modern data processing schemes,multichannel EOR technologies are being developed to realize the systematic,intelligent,and cost-effective development of carbonate reservoirs.

Evaluation of therapeutic effectiveness of 131I-antiEGFR-BSA-PCL in a mouse model of colorectal cancer

AIM: To investigate the biological effects of internal irradiation, and the therapeutic effectiveness was assessed of ^(131)I-labeled anti-epidermal growth factor receptor(EGFR) liposomes, derived from cetuximab, when used as a tumor-targeting carrier in a colorectal cancer mouse model.METHODS: We described the liposomes and characterized their EGFR-targeted binding and cellular uptake in EGFR-overexpressing LS180 colorectal cancer cells. After intra-tumor injections of 74 MBq(740 MBq/m L) ^(131)I-anti EGFR-BSA-PCL, we investigated the biological effects of internal irradiation and the therapeutic efficacy of ^(131)I-anti EGFR-BSA-PCL on colorectal cancer in a male BALB/c mouse model. Tumor size, body weight, histopathology, and SPECT imaging were monitored for 33 d post-therapy.RESULTS: The rapid radioiodine uptake of ^(131)I-antiEGFR-BSA-PCL and ^(131)I-BSA-PCL reached maximum levels at 4 h after incubation, and the ^(131)I uptake of ^(131)I-anti EGFR-BSA-PCL was higher than that of ^(131)I-BSAPCL in vitro. The ^(131)I tissue distribution assay revealed that ^(131)I-anti EGFR-BSA-PCL was markedly taken up by the tumor. Furthermore, a tissue distribution assay revealed that ^(131)I-anti EGFR-BSA-PCL was markedly taken up by the tumor and reached its maximal uptake value of 21.0 ± 1.01 %ID/g(%ID/g is the percentage injected dose per gram of tissue) at 72 h following therapy; the drug concentration in the tumor was higher than that in the liver, heart, colon, or spleen. Tumor size measurements showed that tumor development was significantly inhibited by treatments with ^(131)I-anti EGFR-BSA-PCL and ^(131)I-BSA-PCL. The volume of tumor increased, and treatment rate with ^(131)I-anti EGFR-BSA-PCL was 124% ± 7%, lower than that with ^(131)I-BSA-PCL(127% ± 9%), ^(131)I(143% ± 7%), and normal saline(146% ± 10%). The percentage losses in original body weights were 39% ± 3%, 41% ± 4%, 49% ± 5%, and 55% ± 13%, respectively. The best survival and cure rates were obtained in the group treated with ^(131)I-anti EGFR-BSA-PCL. The animals injected with ^(131)I-anti EGFR-BSA-PCL and ^(131)I-BSA-PCL showed more uniform focused liposome distribution within the tumor area.CONCLUSION: This study demonstrated the potential beneficial application of ^(131)I-anti EGFR-BSA-PCL for treating colorectal cancer. ^(131)I-anti EGFR-BSA-PCL suppressed the development of xenografted colorectal cancer in nude mice, thereby providing a novel candidate for receptor-mediated targeted radiotherapy.