Research progress on the role of adipocyte exosomes in cancer progression.

Exosomes, minute vesicles ubiquitously released by diverse cell types, serve as critical mediators in intercellular communication. Their pathophysiological relevance, especially in malignancies, has garnered significant attention. A meticulous exploration of the exosomal impact on cancer development has unveiled avenues for innovative and clinically valuable techniques. The cargo conveyed by exosomes exerts transformative effects on both local and distant microenvironments, thereby influencing a broad spectrum of biological responses in recipient cells. These membrane-bound extracellular vesicles (EVs) play a pivotal role in delivering bioactive molecules among cells and organs. Cellular and biological processes in recipient cells, ranging from stromal cell reprogramming to immunological responses, extracellular matrix formation, and modulation of cancer cell activation, expansion, and metastasis, are subject to exosome-mediated cell-to-cell communication. Moreover, exosomes have been implicated in endowing cancer cells with resistance to treatment. Extensive research has explored the potential of exosomes as therapeutic targets and diagnostic indicators. This comprehensive review seeks to provide an in-depth understanding of the pivotal components and roles of exosomes in tumorigenesis, growth, progression, and therapeutic responses. The insights into the multifaceted involvement of exosomes in malignant cancers are essential for the scientific community, fostering the development of novel therapeutic and diagnostic strategies in the relentless pursuit of cancer.

Elastin-like polypeptide-functionalized nanobody for column-free immunoaffinity purification of aflatoxin B1.

A column-free immunoaffinity purification (CFIP) technique for sample preparation of aflatoxin B1 (AFB1) was developed using an AFB1-specific nanobody (named G8) and an elastin-like polypeptide (ELP). The reversible phase transition between liquid and solid in response to temperature changes was exhibited by the ELP which was derived from human elastin. The G8 was tagged with ELPs of various lengths (20, 40, 60, and 80 repeat units) at the C-terminus using recursive directional ligation (RDL). Coding sequences were then subcloned into pET30a at the multiple cloning sites. Bioactive recombinant proteins were produced by expressing them as inclusion bodies in Escherichia coli BL21 (DE3), then dissolved and refolded. Analysis by indirect competitive enzyme-linked immunosorbent assay (icELISA) and transition temperature (Tt) measurement confirmed that the refolded G8-ELPs preserved the ability to recognize AFB1 as well as phase transition when the temperature rose above Tt. To establish the optimal conditions for cleaning AFB1, the effects of various parameters on recovery were investigated. The recovery in ELISA tests was 95 ± 3.67% under the optimized CFIP workflow. Furthermore, the CFIP-prepared samples were applied for high-performance liquid chromatography (HPLC) detection. The recovery in the CFIP-HPLC test ranged from 54 ± 1.86% to 98 ± 3.58% for maize, rice, soy sauce, and vegetable oil samples. To the best of our knowledge, this is the first report combining the function of both nanobody and ELP to develop a cleanup technique for small molecules in a complex matrix. The CFIP for the sample pretreatment was easy to use and inexpensive. In contrast to conventional immunosensitivity materials, the reagent utilized in the CFIP was entirely biosynthesized without any chemical coupling reactions. This suggests that the nanobody-ELP may serve as a useful dual-functional reagent for the development of sample cleaning or purification methods.

Comparison of thyroid surgery techniques: a retrospective cohort study and meta-analysis of traditional electric knife vs. straight bipolar electrocoagulation forceps.

Background: In recent years, advancements in surgical techniques for thyroidectomy have led to varying outcomes and efficiencies. Understanding these differences is crucial to optimize patient care and surgical success. This study compared intra- and postoperative parameters of thyroid surgery for thyroidectomy or thyroid cancer. One approach involved the traditional electric knife, employing traditional clamp-ligation skills and an electric knife. The other approach utilized straight bipolar electrocoagulation forceps for micro-hemostasis and micro-cutting. Methods: Data were analyzed retrospectively for 228 patients who underwent thyroidectomy at the Third Affiliated Hospital of Kunming Medical University from January 2014 to November 2018. Surgery was performed either as traditional open surgery (n=150) or as a meticulous anatomical procedure involving bipolar electrocoagulation (n=78). In addition, data from published studies comparing the two surgical procedures were meta-analyzed. Results: The bipolar electrocoagulation procedure was associated with significantly shorter total operation time, lower intraoperative blood loss and lower rate of hypocalcemia. The two procedures were associated with similar rates of hoarseness. Meta-analysis of eight studies involving 2,080 patients showed that bipolar electrocoagulation was associated with significantly shorter total operation time than the traditional approach (mean difference =-21.29 min, 95% CI: -26.32 to -16.27) and with less intraoperative bleeding (mean difference =-12.87 min, 95% CI: -23.81 to -1.93). Conclusions: Straight bipolar electrocoagulation forceps can be used to perform fine dissection during thyroid surgery. Performing "micro-hemostasis" and "micro-cutting" manipulations with these straight bipolar forceps can smoothly dissect nerves and parathyroid glands and may reduce intraoperative bleeding, operation time and rates of postoperative complications, might accelerate recovery after surgery.

Discrepancies between general and central obesity in arterial stiffness: observational studies and Mendelian randomization study.

BACKGROUND: Obesity has been linked to arterial stiffness, while no consensus was reached on the association. We aimed to clarify the association of general and central obesity with arterial stiffness by combining observational studies and Mendelian randomization (MR) study. METHODS: Two cross-sectional studies were performed in UK Biobank and Fuqing Cohort, respectively. Two-sample MR study was conducted using summary data of GWASs from GIANT consortium and UK Biobank. General obesity and central obesity were measured using body mass index (BMI) and waist circumference (WC), respectively. Arterial stiffness was measured by arterial stiffness index (ASI) in UK Biobank or branchial-ankle pulse wave velocity (baPWV) in Fuqing Cohort. RESULTS: Two observational studies found a consistent positive association of BMI and WC with arterial stiffness when adjusting for age, sex, education, smoking, alcohol drinking, physical activity, and LDL cholesterol. However, when additionally adjusting for metabolic traits (i.e., systolic blood pressure, diastolic blood pressure, blood glucose, triglycerides, high-density lipoprotein cholesterol, and WC or BMI), the association with BMI changed to be inverse. As compared to the lowest quintile group, the adjusted ORs across groups of second to fifth quintile were 0.93, 0.90, 0.83, and 0.72 in UK Biobank and 0.88, 0.65, 0.63, and 0.50 in Fuqing Cohort. In contrast, the positive relationship with WC remained stable with the adjusted ORs of 1.23, 1.46, 1.60, and 1.56 in UK Biobank and 1.35, 1.44, 1.77, and 1.64 in Fuqing Cohort. MR analyses provided supportive evidence of the negative association with BMI (OR = 0.97, 95%CI = 0.94-1.00) and the positive association with WC (OR = 1.14, 95%CI = 1.08-1.20). CONCLUSIONS: Observational and genetic analyses provide concordant results that central obesity is independently related to arterial stiffness, while the role of general obesity depends on metabolic status.

Finotonlimab with chemotherapy in recurrent or metastatic head and neck cancer: a randomized phase 3 trial.

Immunotherapy combined with chemotherapy regimen has been shown to be effective in recurrent or metastatic (R/M) head and neck squamous cell carcinoma (HNSCC). However, due to the small number of patients, its efficacy remains controversial in Asian populations, particularly in mainland China. Here a randomized, double-blind phase 3 trial evaluated the efficacy and safety of finotonlimab (SCT-I10A), a programmed cell death 1 (PD-1) monoclonal antibody, combined with cisplatin plus 5-fluorouracil (C5F) for the first-line treatment of R/M HNSCC. Eligible patients (n = 370) were randomly 2:1 assigned to receive finotonlimab plus C5F (n = 247) or placebo plus C5F (n = 123). The primary endpoint was overall survival (OS). In the finotonlimab plus C5F group, OS was 14.1 months (95% confidence interval (CI) 11.1-16.4), compared with 10.5 months (95% CI 8.1-11.8) in the placebo plus C5F group. The hazard ratio was 0.73 (95% CI 0.57-0.95, P = 0.0165), meeting the predefined superiority criteria for the primary endpoint. Finotonlimab plus C5F showed significant OS superiority compared with C5F alone and acceptable safety profile with R/M HNSCC, supporting its use as a first-line treatment option for R/M HNSCC. These results validate the efficacy and safety of the combination of finotonlimab and C5F in Asian patients with R/M HNSCC. ClinicalTrials.gov identifier: NCT04146402 .

Anti-Ferroptosis: A Promising Therapeutic Method for Thyroid Cancer.

At present, many problems remain to be solved in studying the pathogenesis of thyroid cancer. Ferroptosis is a programmed cell death mode discovered in recent years, and many studies have found that ferroptosis plays a significant role in the prognosis and progression of thyroid cancer. The researchers showed that ferroptosis-related genes are essential in diagnosing thyroid cancer. Therefore, this paper summarizes some pathological and clinical characteristics of thyroid cancer and makes a series of combs on the relationship between ferroptosis and the basis and function of thyroid cancer, thus providing specific ideas for the diagnosis and treatment of thyroid cancer.

Mechanisms of cancer cell death induction by triptolide: A comprehensive overview.

The need for naturally occurring constituents is driven by the rise in the cancer prevalence and the unpleasant side effects associated with chemotherapeutics. Triptolide, the primary active component of "Tripterygium Wilfordii", has exploited for biological mechanisms and therapeutic potential against various tumors. Based on the recent pre-clinical investigations, triptolide is linked to the induction of death of cancerous cells by triggering cellular apoptosis via inhibiting heat shock protein expression (HSP70), and cyclin dependent kinase (CDKs) by up regulating expression of P21. MKP1, histone methyl transferases and RNA polymerases have all recently identified as potential targets of triptolide in cells. Autophagy, AKT signaling pathway and various pathways involving targeted proteins such as A-disintegrin & metalloprotease-10 (ADAM10), Polycystin-2 (PC-2), dCTP pyro-phosphatase 1 (DCTP1), peroxiredoxin-I (Prx-I), TAK1 binding protein (TAB1), kinase subunit (DNA-PKcs) and the xeroderma-pigmentosum B (XPB or ERCC3) have been exploited. Besides that, triptolide is responsible for enhancing the effectiveness of various chemotherapeutics. In addition, several triptolide moieties, including minnelide and LLDT8, have progressed in investigations on humans for the treatment of cancer. Targeted strategies, such as triptolide conjugation with ligands or triptolide loaded nano-carriers, are efficient techniques to confront toxicities associated with triptolide. We expect and anticipate that advances in near future, regarding combination therapies of triptolide, might be beneficial against cancerous cells.

Therapeutic, diagnostic and prognostic values of TRIM proteins in prostate cancer.

Prostate cancer is the second most prevalent cancer in men worldwide. The TRIM (tripartite motif) family of proteins is involved in the regulation of various cellular processes, including antiviral immunity, apoptosis, and cancer progression. In recent years, several TRIM proteins have been found to play important roles in prostate cancer initiation and progression. TRIM proteins have indicated oncogenic activity in prostate cancer by enhancing androgen or estrogen receptor signaling and promoting cancer cell growth. Inhibition of TRIM proteins has been raised as a potential therapeutic strategy for the treatment of prostate cancer. Overall, these studies suggest that TRIM family proteins exert tumor-promoting effects in prostate cancer, and targeting these proteins can provide a promising therapeutic strategy for prostate cancer treatment. On the other hand, some TRIM proteins can be differentially expressed in prostate cancer cells compared to normal cells, thus providing novel diagnostic/prognostic biomarkers for prostate cancer.

A Specific Mini-Intrabody Mediates Lysosome Degradation of Mutant Huntingtin.

Accumulation of misfolded proteins leads to many neurodegenerative diseases that can be treated by lowering or removing mutant proteins. Huntington's disease (HD) is characterized by the intracellular accumulation of mutant huntingtin (mHTT) that can be soluble and aggregated in the central nervous system and causes neuronal damage and death. Here, an intracellular antibody (intrabody) fragment is generated that can specifically bind mHTT and link to the lysosome for degradation. It is found that delivery of this peptide by either brain injection or intravenous administration can efficiently clear the soluble and aggregated mHTT by activating the lysosomal degradation pathway, resulting in amelioration of gliosis and dyskinesia in HD knock-in (KI-140Q) mice. These findings suggest that the small intrabody peptide linked to lysosomes can effectively lower mutant proteins and provide a new approach for treating neurodegenerative diseases that are caused by the accumulation of mutant proteins.

Emerging Roles for DNA 6mA and RNA m6A Methylation in Mammalian Genome.

Epigenetic methylation has been shown to play an important role in transcriptional regulation and disease pathogenesis. Recent advancements in detection techniques have identified DNA N6-methyldeoxyadenosine (6mA) and RNA N6-methyladenosine (m6A) as methylation modifications at the sixth position of adenine in DNA and RNA, respectively. While the distributions and functions of 6mA and m6A have been extensively studied in prokaryotes, their roles in the mammalian brain, where they are enriched, are still not fully understood. In this review, we provide a comprehensive summary of the current research progress on 6mA and m6A, as well as their associated writers, erasers, and readers at both DNA and RNA levels. Specifically, we focus on the potential roles of 6mA and m6A in the fundamental biological pathways of the mammalian genome and highlight the significant regulatory functions of 6mA in neurodegenerative diseases.

Developing a Core Outcome Set for Assessing Clinical Safety Outcomes of Prostate Cancer in Clinical Trials of Traditional Chinese Medicine: Protocol for a Mixed Methods Study.

BACKGROUND: Among the common malignant tumors in men worldwide, the incidence of prostate cancer ranks second to lung cancer. This disease will bring an economic burden to patients and their families and can reduce the quality of life of patients. Researchers have conducted numerous clinical trials on the efficacy and safety of different interventions in the treatment of prostate cancer with traditional Chinese medicine (TCM) combined with standard treatment regimens. However, the currently published clinical trials exhibit inconsistent and irregular reporting of outcome measures. OBJECTIVE: The objective of this paper is to emphasize the need for a core outcome set (COS) to facilitate future prostate cancer research, aiming to improve the quality of trials and generate high-quality evidence. METHODS: This mixed methods project has three phases, as follows: (1) a scoping review of the literature to identify outcomes that have been reported in clinical trials and systematic reviews of interventions involving TCM for the treatment of prostate cancer as well as a qualitative component using interviews to obtain the views of patients with prostate cancer, their families, and their caregivers who have a history of TCM treatment; (2) a Delphi survey among stakeholders to prioritize the core outcomes-Participants will include traditional Chinese and Western medicine clinicians in prostate cancer-related directions, nurses, and methodology experts who will participate in 2 rounds of the Delphi method expert consultation to score each outcome in the list of outcome indicators; and (3) a face-to-face consensus meeting to discuss and agree on the final COS for the application of TCM in the treatment of prostate cancer. RESULTS: The protocol has been registered in PROSPERO (CRD42022356184) before the start of the review process, and we will initiate the review on August 1, 2023; results should be expected by September 1, 2023. The Delphi survey among stakeholders is expected to start in October 2023. CONCLUSIONS: The development of a core outcome set for assessing clinical safety outcomes of prostate cancer in clinical trials of TCM will provide a significant first step to assist Chinese doctors, researchers, and policy makers. TRIAL REGISTRATION: PROSPERO CRD42022356184; https://tinyurl.com/ysakz74r. INTERNATIONAL REGISTERED REPORT IDENTIFIER (IRRID): PRR1-10.2196/46794.

Rhes depletion promotes striatal accumulation and aggregation of mutant huntingtin in a presymptomatic HD mouse model.

Introduction: Huntington's disease (HD) is caused by CAG trinucleotide repeats in the HTT gene. Selective neurodegeneration in the striatum is prominent in HD, despite widespread expression of mutant HTT (mHTT). Ras homolog enriched in the striatum (Rhes) is a GTP-binding protein enriched in the striatum, involved in dopamine-related behaviors and autophagy regulation. Growing evidence suggests Rhes plays a critical role in the selective striatal degeneration in HD, but its specific function in this context remains complex and controversial. Methods: In this study, we utilized CRISPR/Cas9 to knockdown Rhes at different disease stages through adeno-associated virus (AAV) transduction in HD knock-in (KI) mice. Immunoblotting and immunofluorescence were employed to assess the impact of Rhes depletion on mHTT levels, neuronal loss, astrogliosis and autophagy activity. Results: Rhes depletion in 22-week-old HD KI mice (representing the presymptomatic stage) led to mHTT accumulation, reduced neuronal cell staining, and increased astrogliosis. However, no such effects were observed in 36-week-old HD KI mice (representing the symptomatic stage). Additionally, Rhes deletion in 22-week-old HD KI mice resulted in increased P62 levels, reduced LC3-II levels, and unchanged phosphorylation of mTOR and beclin-1, unchanged mTOR protein level, except for a decrease in beclin-1. Discussion: Our findings suggest that knockdown Rhes promotes striatal aggregation of mutant huntingtin by reducing autophagy activity in a mTOR-independent manner. Rhes plays a protective role during the presymptomatic stage of HD KI mice.

Participation of protein metabolism in cancer progression and its potential targeting for the management of cancer.

Cancer malignancies may broadly be described as heterogeneous disorders manifested by uncontrolled cellular growth/division and proliferation. Tumor cells utilize metabolic reprogramming to accomplish the upregulated nutritional requirements for sustaining their uncontrolled growth, proliferation, and survival. Metabolic reprogramming also called altered or dysregulated metabolism undergoes modification in normal metabolic pathways for anabolic precursor's generation that serves to continue biomass formation that sustains the growth, proliferation, and survival of carcinogenic cells under a nutrition-deprived microenvironment. A wide range of dysregulated/altered metabolic pathways encompassing different metabolic regulators have been described; however, the current review is focused to explain deeply the metabolic pathways modifications inducing upregulation of proteins/amino acids metabolism. The essential modification of various metabolic cycles with their consequent outcomes meanwhile explored promising therapeutic targets playing a pivotal role in metabolic regulation and is successfully employed for effective target-specific cancer treatment. The current review is aimed to understand the metabolic reprogramming of different proteins/amino acids involved in tumor progression along with potential therapeutic perspective elucidating targeted cancer therapy via these targets.

PHF5A as a new OncoTarget and therapeutic prospects.

PHF5A (PHD-finger domain protein 5A) is a highly conserved protein comprised of 110 amino acids that belong to PHD zinc finger proteins and is ubiquitously expressed in entire eukaryotic nuclei from yeast to man. PHF5A is an essential component of the SF3B splicing complex regulating protein-protein or protein-DNA interactions; particularly involved in pre-mRNA splicing. Besides its basic spliceosome-associated attributes encompassing the regulation of alternative splicing of specific genes, PHF5A also plays a pivotal role in cell cycle regulation and morphological development of cells along with their differentiation into particular tissues/organs, DNA damage repair, maintenance of pluripotent embryonic stem cells (CSCs) embryogenesis and regulation of chromatin-mediated transcription. Presently identification of spliceosome and non-spliceosome-associated attributes of PHF5A needs great attention based on its key involvement in the pathogenesis of cancer malignancies including the prognosis of lung adenocarcinoma, endometrial adenocarcinoma, breast, and colorectal cancer. PHF5A is an essential splicing factor or cofactor actively participating as an oncogenic protein in tumorigenesis via activation of downstream signaling pathway attributed to its regulation of dysregulated splicing or abnormal alternative splicing of targeted genes. Further, the participation of PHF5A in regulating the growth of cancer stem cells might not be ignored. The current review briefly overviews the structural and functional attributes of PHF5A along with its hitherto described role in the propagation of cancer malignancies and its future concern as a potential therapeutic target for cancer management/treatment.

Loss of TDP-43 promotes somatic CAG repeat expansion in Huntington's disease knock-in mice.

TAR binding protein 43 (TDP-43) is normally present in the nucleus but mislocalized in the cytoplasm in a number of neurodegenerative diseases including Huntington's disease (HD). The nuclear loss of TDP-43 impairs gene transcription and regulation. However, it remains to be investigated whether loss of TDP-43 influences trinucleotide CAG repeat expansion in the HD gene, a genetic cause for HD. Here we report that CRISPR/Cas9 mediated-knock down of endogenous TDP-43 in the striatum of HD knock-in mice promoted CAG repeat expansion, accompanied by the increased expression of the DNA mismatch repair genes, Msh3 and Mlh1, which have been reported to increase trinucleotide repeat instability. Furthermore, suppressing Msh3 and Mlh1 by CRISPR/Cas9 targeting diminished the CAG repeat expansion. These findings suggest that nuclear TDP-43 deficiency may dysregulate the expression of DNA mismatch repair genes, leading to CAG repeat expansion and contributing to the pathogenesis of CAG repeat diseases.

RGN as a prognostic biomarker with immune infiltration and ceRNA in lung squamous cell carcinoma.

Regucalcin (RGN) is a potent inhibitory protein of calcium signaling and expresses in various tissues. However, the role of RGN in the tumor immunological microenvironment in lung squamous cell carcinoma (LUSC) remains unclear. This study identified the expression of RGN from public databases and immunohistochemistry with clinical specimen. The association between RGN and the tumor immune microenvironment (TIME) was investigated in LUSC by ESTIMATE and CIBERSORT algorithms. Similarly, the Tumor IMmune Estimation Resource (TIMER) database was used to identify the correlation between RGN and immune cells. The ceRNA network was established based on the data obtained from public databases. Finally, prediction of drug response to chemotherapy and immunotherapy was performed to evaluate clinical significance. This study found that RGN expression was significantly downregulated in tumor tissues and closely related to clinical factors and prognosis of LUSC patients. Differentially expressed genes (DEGs) grouped by the expression of RGN were mostly involved in immunobiological processes such as humoral immune response and leukocyte mediated immunity. RGN and its related miRNA (has-miR-203a-3p) and lncRNAs (ZNF876P and PSMG3-AS1) constructed the novel prognosis-related ceRNA network. Plasma cells, T cells CD4 memory resting, Macrophages M0, Macrophages M1, Mast cells resting, Mast cells activated and Neutrophils showed significantly different levels of infiltration between high and low RGN expression groups. The TIMER database showed that RGN expression was positively correlated with certain immune infiltrating cells. High RGN expression group showed a higher TIDE score, a higher dysfunction score and a lower MSI score, presenting a possible lower efficacy after accepting the immunotherapy than low RGN expression group. RGN expression was closely associated with prognosis of LUSC patients and played an important role in tumor microenvironment. This suggests that RGN could be a promising biomarker for assessing immunotherapy efficacy and prognosis.

Efficacy and safety of KL-A167 in previously treated recurrent or metastatic nasopharyngeal carcinoma: a multicenter, single-arm, phase 2 study.

Background: KL-A167 is a fully humanized monoclonal antibody targeting programmed cell death-ligand 1. This phase 2 study aimed to evaluate the efficacy and safety of KL-A167 in Chinese patients with previously treated recurrent or metastatic (R/M) nasopharyngeal carcinoma (NPC). Methods: This was a multicentre, single-arm, phase 2 study of KL-A167 in R/M NPC (KL167-2-05-CTP) (NCT03848286), conducted at 42 hospitals across the People's Republic of China. Eligible patients had histologically confirmed non-keratinising R/M NPC, and had failed at least two lines of chemotherapy. Patients received KL-A167 900mg intravenously once every 2 weeks until confirmed disease progression, intolerable toxicity, or withdrawal of informed consent. The primary endpoint was objective response rate (ORR) assessed by the independent review committee (IRC) according to RECIST v1.1. Findings: Between Feb 26th, 2019 and Jan 13th, 2021, 153 patients were treated. Totally, 132 patients entered full analysis set (FAS) and were evaluated for the efficacy. As of data cutoff date on Jul 13th, 2021, the median follow-up time was 21.7 months (95%CI 19.8-22.5). For FAS population, the IRC-assessed ORR was 26.5% (95%CI 19.2-34.9%), and disease control rate (DCR) was 56.8% (95%CI 47.9-65.4%). Median progression-free survival (PFS) was 2.8 months (95%CI 1.5-4.1) . Median duration of response was 12.4 months (95%CI 6.8-16.5), and median overall survival (OS) was 16.2 months (95%CI 13.4-21.3). When using the cutoff of 1000 copies/ml, 5000 copies/ml and 10,000 copies/ml for plasma EBV DNA titer, baseline low plasma EBV DNA was consistently related with better DCR, PFS and OS. Dynamic change of plasma EBV DNA was significantly associated with ORR and PFS. Among 153 patients, treatment related-adverse events (TRAEs) occurred in 73.2% of patients, and grade ≥3 TRAEs were in 15.0% of patients. No TRAE leading to death was reported. Conclusion: In this study, KL-A167 showed promising efficacy and an acceptable safety profile in patients with previously treated R/M NPC. Baseline plasma EBV DNA copy number might be a potentially useful prognostic biomarker for KL-A167 treatment, and post-treatment EBV DNA decrease might be correlated with better response to KL-A167. Funding: Sichuan Kelun-Biotech Biopharmaceutical Co., Ltd., China National Major Project for New Drug Innovation (2017ZX09304015).

CO2-Repurification Microemulsion Detergent for Oil-Based Slurry Cleaning.

In order to solve problems such as environmental pollution and pipeline blockage caused by oily wastewater after washing, N,N-dimethylcyclohexylamine (DMCHA) with CO2 response was selected as the oil phase, and an O/W microemulsion wellbore cleaning fluid with CO2 switching characteristics was successfully prepared with erucamide propyl betaine (EAB-40), sodium dodecyl benzene sulfonate (SDBS), n-butanol, silicone defoamer, and water. The water content of the microemulsion was 89.99%, and it had good stability at 40 and -5 °C. The emulsion was rapidly demulsified after being injected with CO2 in the CO2-repurification microemulsion detergent, and CO2 was removed with a N2 detergent. The emulsion was restored to its original state, which demonstrated the CO2/N2 switching properties of the emulsion. It is proven that the switching microemulsion has a good wetting transformation ability by cleaning the steel sheet and quartz sheet contaminated by oil-based slurry. The switching microemulsion system can clean the simulated wellbore contaminated by oil-based slurry, and the cleaning efficiency is above 99%. CO2 can be used at room temperature to separate oil and water from oily wastewater after cleaning.