A novel multimodal needs assessment to inform the longitudinal education program for an international interprofessional critical care team.

BACKGROUND: The current global pandemic has caused unprecedented strain on critical care resources, creating an urgency for global critical care education programs. Learning needs assessment is a core element of designing effective, targeted educational interventions. In theory, multimodal methods are preferred to assess both perceived and unperceived learning needs in diverse, interprofessional groups, but a robust design has rarely been reported. Little is known about the best approach to determine the learning needs of international critical care professionals. METHOD: We conducted multimodal learning needs assessment in a pilot group of critical care professionals in China using combined quantitative and qualitative methods. The assessments consisted of three phases: 1) Twenty statements describing essential entrustable professional activities (EPAs) were generated by a panel of critical care education experts using a Delphi method. 2) Eleven Chinese critical care professionals participating in a planned education program were asked to rank-order the statements according to their perceived learning priority using Q methodology. By-person factor analysis was used to study the typology of the opinions, and post-ranking focus group interviews were employed to qualitatively explore participants' reasoning of their rankings. 3) To identify additional unperceived learning needs, daily practice habits were audited using information from medical and nursing records for 3 months. RESULTS: Factor analysis of the rank-ordered statements revealed three learning need patterns with consensual and divergent opinions. All participants expressed significant interest in further education on organ support and disease management, moderate interest in quality improvement topics, and relatively low interest in communication skills. Interest in learning procedure/resuscitation skills varied. The chart audit revealed suboptimal adherence to several evidence-based practices and under-perceived practice gaps in patient-centered communication, daily assessment of antimicrobial therapy discontinuation, spontaneous breathing trial, and device discontinuation. CONCLUSIONS: We described an effective mixed-methods assessment to determine the learning needs of an international, interprofessional critical care team. The Q survey and focus group interviews prioritized and categorized perceived learning needs. The chart audit identified additional practice gaps that were not identified by the learners. Multimodal methods can be employed in cross-cultural scenarios to customize and better target medical education curricula.

ETS Proto-Oncogene 1-activated muskelin 1 antisense RNA drives the malignant progression of hepatocellular carcinoma by targeting miR-22-3p to upregulate ETS Proto-Oncogene 1.

Long noncoding RNA muskelin 1 antisense RNA (MKLN1-AS) acted as an oncogenic regulator in hepatocellular carcinoma (HCC). This study was performed to investigate the functional mechanism of MKLN1-AS. MKLN1-AS, microRNA-22-3p (miR-22-3p) and ETS Proto-Oncogene 1 (ETS1) levels were examined using reverse transcription-quantitative polymerase-chain reaction. Protein expression was detected by Western blot. The target relation was analyzed by dual-luciferase reporter assay, RNA immunoprecipitation assay and RNA pull-down assay. Cell proliferation ability was determined through cell counting kit-8 assay, colony formation assay and ethylenediurea assay. Angiogenesis was examined by tube formation assay. Cell migration and invasion were assessed via transwell assay. In vivo research was conducted by xenograft tumor model in nude mice. MKLN1-AS was upregulated in HCC tissues and cells. ETS1 promoted the ETS1 expression by binding to the 582-596 sites. Silence of MKLN1-AS suppressed cell growth, angiogenesis, migration, and invasion. MKLN1-AS interacted with miR-22-3p in HCC cells. The function of MKLN1-AS downregulation was relieved by miR-22-3p inhibition in HCC cells. ETS1 was validated as a target of miR-22-3p, and MKLN1-AS upregulated the ETS1 expression by sponging miR-22-3p. Overexpression of miR-22-3p retarded HCC progression by downregulating the level of ETS1. Tumor growth in vivo was also enhanced by MKLN1-AS through the regulation of miR-22-3p/ETS1 axis. These data demonstrated that ETS1-mediated MKLN1-AS contributed to the malignant phenotypes of HCC cells via depending on the miR-22-3p/ETS1 regulatory axis.

Observation and analysis of clinical efficacy of breast-conserving therapy integrated with neoadjuvant chemotherapy on Breast Cancer.

To investigate the efficaciousness of breast-conserving therapy in connection with neoadjuvant chemotherapy on breast cancer. 68 patients, who were confirmed going down with breast cancer and hospitalized from June 2015 and June 2017, were sampled and divided into two groups using the random digit table, i.e. the observation group (n=34) and the control group (n=34). Patients in the observation group experienced breast-conserving therapy integrated with neoadjuvant chemotherapy, but those in the control group received the radical resection of breast cancer. Patients' condition in surgery, incidence of post-surgery complications as well as patient survivals were compared and coded. In the observation group, surgical duration, intraoperative bleeding amount, length of stay in hospital and incidence rate of post-surgery complications were all lower than the patients with the similar conditions in the control group with evident distinctions in statistics (p<0.05). In the observation group, survival ratios of one-to-five-year living patients were evidently higher than those in the control group. The distinctions owned evident significance in calculations (p<0.05). In comparison of the recurrence ratio of disease and the rate of distant metastasis between the observation group (5.88% and 8.82%) and the control group (11.76% and 8.82%), differences had no statistical significance (p>0.05). Before treatment, compared with the score of life quality in the two groups, no evident distinction in statistical exists (p>0.05), however, after that, the life quality in the observation group evidently outweighs the quality in the control group, which shows the distinctions in statistics (p<0.05). Breast-conserving therapy in combination with neoadjuvant chemotherapy shows promising clinical value in ameliorating the life quality, decreasing the mortality rate and the incidence of adverse reaction, which is expected to be applied in clinical practices as a kind of safe and effective method.

MiR-125b inhibits anaplastic thyroid cancer cell migration and invasion by targeting PIK3CD.

Emerging evidences indicate that dysregulated microRNAs are implicated in the process of tumorigenesis and progression. The miRNA-125b (miR-125b) is downregulated and identified as tumor supressor in various cancers including thyroid cancer. However, the role and mechanism of miR-125b in anaplastic thyroid cancer (ATC) migration and invasion remain unknown. In the present study, the expression levels of miR-125b were downregulated and the expression levels of phosphoinositide 3-kinase catalytic subunit delta (PIK3CD) were upregulated in ATC tissues and cell lines. Moreover, miR-125b expression was negatively related to PIK3CD expression in ATC tissues. A computational search and luciferase assay identified PIK3CD as a direct target of miR-125b in ATC and PIK3CD expression was downregulated by miR-125b in ATC cells. In terms of function, miR-125b repressed migration and invasion of ATC cells, whereas PIK3CD overexpression reversed this effect. Furthermore, we showed that exogenous miR-125b decreased the PI3K, phospho-Akt, and phospho-mTOR expression in ATC cells. In conclusion, these results indicated that miR-125b suppressed ATC cell migration and invasion by targeting PIK3CD expression, and suggested novel potential therapeutic targets for the treatment of ATC.

The expressions of NEDD9 and E-cadherin correlate with metastasis and poor prognosis in triple-negative breast cancer patients.

BACKGROUND: Neural precursor cell expressed, developmentally downregulated 9 (NEDD9), a member of Crk-associated substrate family, is involved in cancer cell adhesion, migration, invasion, and epithelial-mesenchymal transition. E-cadherin is a key event in the cellular invasion during the epithelial-mesenchymal transition mechanism. The aim of this study was to evaluate the association among NEDD9 expression, E-cadherin expression, and survival in triple-negative breast cancer (TNBC) patients. METHODS: NEDD9 and E-cadherin expressions were analyzed by immunohistochemistry in 106 TNBC patients and 120 non-TNBC patients. And the association of clinicopathological factors with survival was analyzed using Kaplan-Meier analysis and Cox regression in TNBC patients. RESULTS: The results revealed that the rate of increased expression of NEDD9 and reduced expression of E-cadherin was significantly higher in TNBC group than that in non-TNBC group (P<0.001, both). Comparison of features between TNBC and non-TNBC groups showed that histological type (P=0.026) and lymph node metastasis (P=0.001) were significantly different. Correlation analysis showed that positive NEDD9 expression and negative E-cadherin expression were significantly correlated with lymph node metastasis and tumor-node-metastasis stage (P<0.05). In addition, the enhanced NEDD9 expression was significantly associated with a reduced 5-year survival for TNBC patients (overall survival [OS]: P=0.013; disease-free survival [DFS]: P=0.021). Negative E-cadherin expression showed a significantly worse 5-year OS and DFS (OS: P=0.011; DFS: P=0.012). Multivariate analysis showed that lymph node metastasis (OS: P=0.006; DFS: P=0.004), tumor-node-metastasis stage (OS: P=0.012; DFS: P=0.001), NEDD9 (OS: P=0.046; DFS: P=0.022), and E-cadherin (OS: P=0.022; DFS: P=0.025) independently predicted a poor prognosis of OS and DFS. Moreover, patients with NEDD9-positive/E-cadherin-negative expression had a significantly worse outcome than other groups (OS: P=0.004; DFS: P=0.001). CONCLUSION: Our finding demonstrated the potential value of NEDD9 and E-cadherin expression levels as prognostic molecular markers and a target for new therapies for TNBC patients.

Improved antitumor activity of epirubicin-loaded CXCR4-targeted polymeric nanoparticles in liver cancers.

A liver-targeted drug delivery system (CX-EPNP) composed of PLGA/TPGS was prepared and characterized. The surface of nanoparticle was conjugated with LFC131 peptide to increase the specific interaction of carrier with CXCR4 overexpressing liver cancers to enhance the Epirubicin (EPI) delivery to tumors. The particles were nanosized with size than 150 nm and portrayed a sustained release kinetics suggesting its suitability for cancer targeting. The in vitro cell uptake results showed that the introduction of LFC131 to the nanoparticles could increase significantly the affinity to human hepatic carcinoma cells (HepG2) with approximately a 3-fold improvement in cellular uptake than non-targeted one. A specific receptor-mediated uptake was observed by confocal laser scanning microscopy. In addition, CX-EPNP showed remarkable cytotoxicity towards HepG2 cells, and could effectively inhibit tumor growth. The more significant EPI accumulation from CX-EPNP in the cancer cells gave rise to the enhanced EPI cytotoxicity and cell apoptosis. The CX-EPNP distributed mostly in the xenograft tumor after intravenous administration to mice and adequately remained in the blood for at least 24h. It seemed that CX-EPNP upon intravenous injection avoided rapid recognition by Kupffer cells and adequately remained in the blood. These findings suggest that CX-EPNP could effectively inhibit the growth of liver tumors in situ and could potentially reduce the systemic side effects. However, extensive investigation is still needed to assess the possible applications of the CX-EPNP in humans.

Association between single nucleotide polymorphisms of upstream transcription factor 1 (USF1) and susceptibility to papillary thyroid cancer.

BACKGROUND: Thyroid cancer, predominantly by papillary thyroid cancer (PTC), is a malignant tumour of endocrine system with increasing incidence rate worldwide. Upstream transcription factor 1 (USF1) regulates a variety of biological processes by transactivation of functional genes. In this study, we investigated the association between USF1 polymorphisms and PTC risk. MATERIAL & METHODS: A total of 334 patients with PTC, 186 patients with benign nodules (BN) and 668 healthy controls were enrolled in our study. Tag-SNPs were identified in Chinese Han in Beijing (CHB) from International HapMap Project Databases. Genomic DNAs were extracted by TaqMan Blood DNA kits. SNPs of USF1 were genotyped by TaqMan SNPs genotyping assay. Odds ratios (OR) and corresponding 95% confidence interval (CI) were used to assess the association between USF1 genetic variants and PTC risk. The statistical analyses were carried out with spss 13.0 software. RESULTS: Five tag-SNPs were retrieved to capture all the genetic variants of USF1. Among the five tag-SNPs, genetic variants in rs2516838, rs3737787 and rs2516839 have significant association with PTC risk. The rs2516838 polymorphisms dominant model (CG+GG vs CC: OR = 0·71; 95% CI: 0·52-0·97; P = 0·033) and allelic model (C vs G: OR = 0·031; 95% CI: 0·56-0·97; P = 0·031) indicated it may act as a protective factor against PTC. On the contrary, the results of rs3737787 polymorphisms: dominant model (CT+TT vs CC: OR = 1·55; 95%CI: 1·09-2·02; P = 0·001) and allelic model (C vs T: OR = 1·35; 95%CI: 1·10-1·64; P = 0·003), as well as the results of rs2516839 polymorphisms: dominant model (GA+AA vs GG: OR = 1·77; 95%CI: 1·31-2·38; P < 0·001) and allelic model (G vs A: OR = 1·36; 95%CI: 1·13-1·63; P = 0·014), revealed that they may act as risk factors for PTC. CONCLUSION: In this study, we found the SNPs of rs2516838 (mutant G alleles vs wild C alleles), rs3737787 (mutant T alleles vs wild C alleles) and rs2516839 (mutant A alleles vs wild G alleles) were significantly associated with PTC risk. Further large-scale studies with different ethnicities are still needed to validate our findings and explore the underlying mechanism of USF1 in PTC development.

MicroRNA-26a inhibits proliferation by targeting high mobility group AT-hook 1 in breast cancer.

OBJECTIVES: To investigate the crucial role of miR-26a in breast cancer and to validate whether miR-26a could regulate proliferation of breast cancer cells by targeting high mobility group AT-hook 1 (HMGA1). METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) was used to quantify the expression levels of miR-26a in breast cancer and adjacent non-cancerous breast tissues. MTT, cell migration and invasion assay were carried out to characterize the miR-26a function. Finally, to validate the target gene of miR-26a, luciferase reporter assay was employed, followed by RT-PCR and Western blot confirmation. RESULTS: Compared with normal tissues, a significant down-regulation of miR-26a expression was observed in breast cancer tissues (P=0.002). miR-26a suppresses MDA-MB-231 and Mcf-7 breast cancer cell lines proliferation and motility. The luciferase activity was significantly decreased after co-transfection with psiCHECK-2/HMGA1 3'-UTR and miR-26a mimics in comparison with control cells, and qRT-PCR and Western blotting analysis found that HMGA1 expression at the mRNA and protein levels decreased in the miR-26a mimic-treatment group relative to NC. MTT assay showed that down regulation of HMGA1 by siRNA could significantly enhance the tumor-suppressive effect of miR-26a (P < 0.05). CONCLUSIONS: The results of the present study indicate that miR-26a may be associated with human breast carcinogenesis, which inhibits tumor cell proliferation by targeting HMGA1.

Genetic variations of CAV1 gene contribute to HCC risk: a case-control study.

Hepatocellular carcinoma (HCC) is the sixth common cancer and the third common cause of cancer mortality worldwide. However, the exact molecular mechanism of HCC remains uncertain. Caveolin-1 (CAV1) is the main protein in the caveolin family and plays an important role in tumorigenesis signaling. However, the contribution of CAV1 genetic variants to HCC is still unknown. The purpose of this study was to evaluate the association between the tagSNPs of the CAV1 gene and HCC risk. In this case-control study, we enrolled 1,000 HCC patients and 1,000 cancer-free controls, which were frequency-matched by age, gender, and HBV infection status. We found that CAV1 rs729949 was statistically associated with increased risk of HCC (odds ratio (OR) = 1.28; 95% confidence interval (CI), 1.11-1.48; P = 8.53 × 10(-4)), even after Bonferroni correction (P = 5.97 × 10(-3)); the expression levels of CAV1 in cancer tissues were significantly lower than those in adjacent normal tissues (P = 0.012). We also detected a significant association for CAV1 rs3807989 under the log-additive model (OR = 0.85; 95% CI, 0.74-0.98; P = 0.026). Significant associations were also detected for CAV1 rs6466583 (GG vs AA: OR = 2.53; 95% CI, 1.24-5.17; P = 0.011) and CAV1 rs3807986 (AG vs AA: OR = 3.16; 95% CI, 1.68-5.91; P = 3.36 × 10(-4)) among genotype comparisons. These findings indicated that genetic variants n CAV1 might contribute to HCC susceptibility.

Inhibition of lymphatic metastases by a survivin dominant-negative mutant.

Metastasis is the most lethal attribute of human malignancy. High-level expression of survivin is involved in both carcinogenesis and angiogenesis in cancer. Previous studies indicate that a mutation of the threonine residue at position 34 (Thr34Ala) of survivin generates a dominant-negative mutant that induces apoptosis, inhibits angiogenesis, and suppresses highly metastatic breast carcinoma in mouse models. We investigated the efficacy of gene therapy with a survivin dominant-negative mutant and possible factors related to lymph node metastasis. The metastasis rate was compared between each group in order to find a survivin-targeted therapy against lymphangiogenesis in its earliest stages. We established lymph node metastasis models and treated animals with H22 tumors with Lip-mSurvivinT34A (Lip-mS), Lip-plasmid (Lip-P), or normal saline (NS). Eight days after the last dose, five randomly chosen mice from each group were sacrificed. We detected the apoptotic index, microvessel density (MVD), lymphatic microvessel density (LMVD), and the expression of VEGF-D with immunohistochemistry. After the remaining animals were sacrificed, we compared the tumor-infiltrated lymph nodes in each group. Administration of mSurvivinT34A plasmid complexed with cationic liposome (DOTAP/chol) resulted in the efficacious inhibition of tumor growth and lymph node metastasis within the mouse H22 tumor model. These responses were associated with tumor cell apoptosis, and angiogenesis and lymphangiogenesis inhibition. Our results suggested that Lip-mSurvivinT34A induced apoptosis and inhibited tumor angiogenesis and lymphangiogenesis, thus suppressing tumor growth and lymphatic metastasis. The mSurvivinT34A survivin mutant is a promising strategy of gene therapy to inhibit lymphatic metastasis.

Therapeutic effects of survivin dominant negative mutant in a mouse model of prostate cancer.

PURPOSE: Patients with localized prostate cancer can usually achieve initial response to conventional treatment. However, most of them will inevitably progress to advanced disease stage. There is a clear need to develop innovative and effective therapeutics for prostate cancer. Mouse survivin T34A (mS-T34A) is a phosphorylation-defective Thr34 → Ala dominant negative mutant, which represents a potential promising target for cancer gene therapy. This study was designed to determine whether mS-T34A plasmid encapsuled by DOTAP-chol liposome (Lip-mS) has the anti-tumor activity against prostate cancer, if so, to further investigate the possible mechanisms. METHODS: In vitro, TRAMP-C1 cells were transfected with Lip-mS and examined for apoptosis by PI staining and flow cytometric analysis. In vivo, subcutaneous prostate cancer models were established in C57BL/6 mice, which were randomly assigned into three groups to receive i.v. administrations of Lip-mS, pVITRO2-null plasmid complexed with DOTAP-chol liposome (Lip-null) or normal saline every 2 days for eight doses. Tumor volume was measured. Tumor tissues were inspected for apoptosis by TUNEL assay. Microvessel density (MVD) was determined by CD31 immunohistochemistry. Alginate-encapsulated tumor cell test was conducted to evaluate the treatment effect on angiogenesis. RESULTS: Administration of Lip-mS resulted in significant inhibition in the growth of mouse TRAMP-C1 tumors. The anti-tumor response was associated with increased tumor cell apoptosis and decreased microvessel density. CONCLUSIONS: The present study may be of importance in the exploration of the potential application of Lip-mS in the treatment of a broad spectrum of tumors.

[Anti-prostate cancer activity of Survivin-T34A mutant in vitro and in vivo].

OBJECTIVE: To investigate the effect of Survivin-T34A mutant on murine prostate cancer and its apoptosis-inducing efficacy in vivo and in vitro. METHODS: In vitro, prostate cancer cells TRAMP-C1 were transfected with Survivin-T34A plasmid encapsulated by cationic liposome. The apoptosis of TRAMP-C1 was evaluated with flow cytometry. C57BL/6 mice model with TRAMP-C1 prostate cancer was established. Twenty four male mice with TRAMP-C1 prostate cancers were divided randomly into three groups, which were intravenously injected with normal saline, empty vector PORF-9-null encapsulated by cationic liposome and Survivin-T34A plasmid encapsulated by cationic liposome respectively twice a week for eight doses. The size of tumors was measured and the tumor sections of each group were stained with TUNEL reagent for apoptosis detection. RESULTS: An apoptotic index of 46% of TRAMP-C1 transfected with Survivin-T34A plasmid encapsulated by cationic liposome was observed. The tumor volume of Survivin-T34A group of C57BL/6 mice with TRAMP-C1 prostate cancer was far smaller than those in the control groups (P < 0.05) and the tumors treated with Survivin-T34A showed significant increase of apoptosis compared with those of control groups (P < 0.05). CONCLUSION: Survivin-T34A mutant efficiently inhibits the growth of prostate cancer, which is based on the mechanism of Survivin-T34A mutant inducing apoptosis of tumor cells.

Enhancement of cisplatin sensitivity in Lewis Lung carcinoma by liposome-mediated delivery of a survivin mutant.

BACKGROUND: A high concentration of cisplatin (CDDP) induces apoptosis in many tumor cell lines. CDDP has been administered by infusion to avoid severe toxicity. Recently, it has been reported that changes in survivin expression or function may lead to tumor sensitization to chemical and physical agents. The aim of this study was to determine whether a dominant-negative mouse survivin mutant could enhance the anti-tumor activity of CDDP. METHODS: A plasmid encoding the phosphorylation-defective dominant-negative mouse survivin threonine 34-->alanine mutant (survivin T34A) complexed to a DOTAP-chol liposome (Lip-mS) was administered with or without CDDP in Lewis Lung Carcinoma (LLC) cells and in mice bearing LLC tumors, and the effects on apoptosis, tumor growth and angiogenesis were assessed. Data were analyzed using one-way analysis of variance(ANOVA), and a value of P < 0.05 was considered to be statistically significant. RESULTS: LLC cells treated with a combination of Lip-mS and CDDP displayed increased apoptosis compared with those treated with Lip-mS or CDDP alone. In mice bearing LLC tumors and treated with intravenous injections of Lip-mS and/or CDDP, combination treatment significantly reduced the mean tumor volume compared with either treatment alone. Moreover, the antitumor effect of Lip-mS combined with CDDP was greater than their anticipated additive effects. CONCLUSION: These data suggest that the dominant-negative survivin mutant, survivin T34A, sensitized LLC cells to chemotherapy of CDDP. The synergistic antitumor activity of the combination treatment may in part result from an increase in the apoptosis of tumor cells, inhibition of tumor angiogenesis and induction of a tumor-protective immune response.

Enhanced tumor radiosensitivity by a survivin dominant-negative mutant.

Radiosensitivity of tumors is due to a complex interaction of various factors, it has been reported that survivin also acts as a constitutive and inducible radioresistance factor in a panel of tumor cells and approaches designed to inhibit survivin expression or function may lead to tumor sensitisation to chemical and physical agents. Previously, we found that the plasmid encoding the phosphorylation-defective mouse survivin threonine 34-->alanine mutant complexed to DOTAP-chol liposome (Lip-mS) can suppress murine primary breast carcinoma. However, little is known regarding the biological effect of Lip-mS combined with radiation. The present study was designed to determine whether Lip-mS could enhance the anti-tumor activity of radiation. The Lewis Lung Carcinoma (LLC) cells treated with a combination of Lip-mS and radiation displayed apparently increased apoptosis compared with those treated with Lip-mS or radiation alone. Mice bearing LLC tumors were treated with intravenous injections of Lip-mS and radiation, the combined treatment significantly reduced mean tumor volume compared with either treatment alone. Moreover, the anti-tumor effect of Lip-mS combined with radiation was greater than their additive effect when compared with the expected effect of the combined treatment. These data suggest that inhibition of survivin using a dominant-negative mutant, survivin T34A, could sensitize LLC cells to radiation efficiently and the synergistic anti-tumor activity may in part result from increasing the apoptosis of tumor cells, inhibiting tumor angiogenesis and inducing a tumor-protective immune response in the combined treatment.

A laboratory study of sediment and contaminant release during gas ebullition.

Significant quantities of gas are generated from labile organic matter in contaminated sediments. The implications for the gas generation and subsequent release of contaminants from sediments are unknown but may include enhanced direct transport such as pore water advection and diffusion. The behavior of gas in sediments and the resulting migration of a polyaromatic hydrocarbon, viz phenanthrene, were investigated in an experimental system with methane injection at the base of a sediment column. Hexane above the overlying water layer was used to trap any phenanthrene migrating out of the sediment layer. The rate of suspension of solid particulate matter from the sediment bed into the overlying water layer was also monitored. The experiments indicated that significant amounts of both solid particulate matter and contaminant can be released from a sediment bed by gas movement with the amount of release related to the volume of gas released. The effective mass transfer coefficient of gas bubble-facilitated contaminant release was estimated under field conditions, being around three orders of magnitude smaller than that of bioturbation. A thin sand-capping layer (2 cm) was found to dramatically reduce the amount of contaminant or particles released with the gas because it could prevent or at least reduce sediment suspension. Based on the experimental observations, gas bubble-facilitated contaminant transport pathways for both uncapped and capped systems were proposed. Sediment cores were sliced to obtain phenanthrene concentration. X-ray computed tomography (CT) was used to investigate the void space distribution in the sediment penetrated by gas bubbles. The results showed that gas bubble migration could redistribute the sediment void spaces and may facilitate pore water circulation in the sediment.