1.Effect of potential categories of cumulative ecological risk on academic engagement among vocational college students
Chinese Journal of School Health 2025;46(2):229-233
Objective:
To explore the effects of potential categories of cumulative ecological risk on academic engagement, so as to provide theoretical basis for promoting academic engagement among vocational college students.
Methods:
In May 2024, a convenience sampling method was used to select 1 666 students from three grades of six vocational colleges in Xuzhou City, Jiangsu Province. A survey was conducted on the cumulative ecological risk and academic engagement, and latent profile analysis was used to explore the potential categories of cumulative ecological risk and test its effect on academic engagement.
Results:
There were four latent classes of cumulative ecological risk among vocational college students, namely, complete family-low risk group, complete family-medium risk group, incomplete family-medium risk group, complete family-moderate to high risk group, accounting for 11.8%, 44.8%, 21.0% and 22.4%. There were significant differences in academic engagement among different potential categories of cumulative ecological risk of students ( F =138.03, P <0.01), with the highest level of academic engagement in the complete family-low risk group (102.95±15.74), followed by the complete family-medium risk group (87.67±14.26), incomplete family-medium risk group (84.53±19.25) and complete family-moderate to high risk group (73.24±20.13). The potential categories of cumulative ecological risk significantly predicted academic engagement ( P <0.01). When the complete family-low risk group was used as a reference, the regression coefficients for the complete family-medium risk, incomplete family-medium risk, and complete family-moderate to high risk were -0.40, -0.40 and -0.65, respectively.
Conclusion
The potential categories of cumulative ecological risks among vocational college students significantly predict their academic engagement, and vocational colleges need to pay attention to the cumulative ecological risks and different potential categories of students when promoting their academic engagement.
2.Alectinib (CH5424802) antagonizes ABCB1- and ABCG2-mediated multidrug resistance in vitro, in vivo and ex vivo.
Ke YANG ; Yifan CHEN ; Kenneth Kin Wah TO ; Fang WANG ; Delan LI ; Likun CHEN ; Liwu FU
Experimental & Molecular Medicine 2017;49(3):e303-
Alectinib, an inhibitor of anaplastic lymphoma kinase (ALK), was approved by the Food and Drug Administration (FDA) for the treatment of patients with ALK-positive non-small cell lung cancer (NSCLC). Here we investigated the reversal effect of alectinib on multidrug resistance (MDR) induced by ATP-binding cassette (ABC) transporters, which is the primary cause of chemotherapy failure. We provide the first evidence that alectinib increases the sensitivity of ABCB1- and ABCG2-overexpressing cells to chemotherapeutic agents in vitro and in vivo. Mechanistically, alectinib increased the intracellular accumulation of ABCB1/ABCG2 substrates such as doxorubicin (DOX) and Rhodamine 123 (Rho 123) by inhibiting the efflux function of the transporters in ABCB1- or ABCG2-overexpressing cells but not in their parental sensitive cells. Furthermore, alectinib stimulated ATPase activity and competed with substrates of ABCB1 or ABCG2 and competed with [125I] iodoarylazidoprazosin (IAAP) photolabeling bound to ABCB1 or ABCG2 but neither altered the expression and localization of ABCB1 or ABCG2 nor the phosphorylation levels of AKT and ERK. Alectinib also enhanced the cytotoxicity of DOX and the intracellular accumulation of Rho 123 in ABCB1-overexpressing primary leukemia cells. These findings suggest that alectinib combined with traditional chemotherapy may be beneficial to patients with ABCB1- or ABCG2-mediated MDR.
Adenosine Triphosphatases
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Carcinoma, Non-Small-Cell Lung
;
Doxorubicin
;
Drug Resistance, Multiple*
;
Drug Therapy
;
Humans
;
In Vitro Techniques*
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Leukemia
;
Lymphoma
;
Parents
;
Phosphorylation
;
Phosphotransferases
;
Rhodamine 123
;
United States Food and Drug Administration