Effects of Goal-Framed Messages on Mental Health Education Among Medical University Students: Moderating Role of Personal Involvement.

Mental health problem among university students is an emerging public health issue, and mental health education has always been the focus of attention for universities. However, limited attention has been paid to the effect of students' acceptance of health messages. Previous studies have found that message framing plays a key role in the process of responding to health-promoting messages. In this backdrop, the study aimed to examine the effects of goal-framed messages on mental health education among medical university students and investigate the moderating role of personal involvement. A cross-sectional study was conducted on medical university students. An online self-administered questionnaire was used to collect data. Wilcoxon rank-sum test and ordinal logistic regression were used for data analysis. Results showed significant differences in message acceptance between the gain- and loss-framed groups ( < 0.001). Participants with high personal involvement had higher message acceptance than those with low personal involvement in gain- and loss-framed message models ( < 0.05). Specifically, participants who related to roommates with high intimacy had higher message acceptance than those who related to roommates generally ( < 0.05). Participants who were concerned about their health condition had higher message acceptance than those who were neutral about their health condition ( < 0.001). Evidence of advantages of gain- over loss-framed messages on mental health among medical university students was found. The hypothesis that personal involvement with a health issue affects the acceptance of message framing was supported. Public health advocates can use framed message as a strategy to improve the efficacy of intervention in mental health education

Goal-Framing and Temporal-Framing: Effects on the Acceptance of Childhood Simple Obesity Prevention Messages among Preschool Children’s Caregivers in China

A range of intervention models are available for childhood obesity prevention; however, few studies have examined the effectiveness of intervention messages. This study developed childhood simple obesity prevention messages on the basis of goal-framing and temporal-framing effects to improve message acceptance among the caregivers of preschool children and explored associated factors. A cross-sectional study was conducted among 592 caregivers of preschool children in urban kindergartens in China during March to April 2019. The framing messages were developed based on prospect theory and construal level theory. The majority (48.4%) of caregivers found the gain-framed, present-oriented message most salient for acceptance. We found that gender, education background, theme, and the use of negative words have impacts on goal-framing effects; and previous participation in a health related intervention, career category, and the theme have impacts on temporal-framing effects (p &lt; 0.001). Goal-framing effects and temporal-framing effects can influence each other (p &lt; 0.001). The findings suggest that the gain-framed, present-oriented message could be considered a strategy to improve the acceptance of information by caregivers. When framing a message, subtle differences like using negative words might affect the exertion of framing effects

Comparing the prognostic impact of 131I or/and Artificial Liver Support System on liver function failure combined with hyperthyroidism

Objective: Hyperthyroidism, a prevalent endocrine disorder, can lead to complications such as liver failure due to the liver's essential role in thyroid hormone metabolism. The study aimed to elucidate the respective contributions of 131I or/and ALSS in managing hyperthyroidism alongside liver failure. Methods: A retrospective analysis was carried out on 74 patients diagnosed with severe liver dysfunction in the context of Graves' disease. Patients were categorized into three groups: Group A (n=34) received 131I treatment, group B (n=17) underwent 131I and ALSS treatment, and Group C (n=24) received ALSS treatment alone. Results: Throughout the treatment period, the liver function indexes in all groups exhibited a decline trend. The thyroid function of group A and B treated with 131I was significantly improved compared with that before treatment. There was no significant change in thyroid function in group C. After the correction of hyperthyroidism, significant improvements were observed in the liver function of individuals in group A and B, particularly with more noticeable amelioration compared to group C. After two months of treatment, the efficacy rates for the three groups were 79.41%, 82.35%, and 60.87% respectively. Mortality rates of the three groups were 5.88%,17.65% and 36%(p < 0.01). Group B, receiving both 131I and ALSS treatments, exhibited a lower mortality rate than group C. Conclusion: In cases of severe liver dysfunction accompanied by hyperthyroidism, prompt administration of 131I is recommended to alleviate the adverse effects of hyperthyroidism on liver function and facilitate a conducive environment for the recovery of liver functionality

RUNX1/CBFβ Dosage Is Critical for MLL Leukemias Development

Abstract Transcription factors RUNX1/CBFβ play critical roles in hematopoiesis. Both of them are frequently involved in chromosomal translocations, point mutations, or deletions in acute leukemia. The mixed lineage leukemia (MLL) gene is also frequently involved in chromosomal translocations or partial tandem duplication in acute leukemia. We have previously shown that MLL, RUNX1, and CBFβ interact and form a regulatory complex to regulate downstream target genes. However, the functional consequence of MLL fusions on RUNX1/CBFβ activity remains unknown. To determine the impact of MLL fusion protein on RUNX1/CBFβ, we introduced either MLL, MLL-BP (longer N-terminal Flag-tagged MLL construct which contains CXXC domain; 1-1406), or MLL-fusions together with RUNX1, CBFβ, or both RUNX1 and CBFβ into 293T cells. MLL-BP and MLL fusions significantly decreased RUNX1 levels compared with controls (empty vector and MLL). CBFβ protein was mildly decreased by MLL-BP and MLL-fusions when expressed alone. However, when CBFβ was co-expressed with RUNX1, it was significantly decreased compared with controls. The expression levels of RUNX1 and CBFβ proteins in LSK cells from Mll-Af9 knock-in mice were significantly lower than those from wild-type (WT) mice. To confirm these findings in human acute myeloid leukemia (AML), we measured the expression of RUNX1 and CBFβ at both mRNA and protein levels in various leukemia cell lines. The expression levels of RUNX1 and CBFβ proteins were significantly decreased in AML cells with MLL fusion and MLL partial tandem duplication (MLL-PTD) compared with those in AML cells without MLL aberrations. MLL fusions still have CXXC domain. In MLL-PTD, the CXXC domain is duplicated. Our data showed that RUNX1 protein is not only down-regulated by MLL fusion proteins, but also by MLL-BP. Thus, to determine which region is involved in the down-regulation of RUNX1, we introduced a series of MLL deletion mutants into 293T cells and measured RUNX1 protein expression. MLL deletion mutants without CXXC domain had no effect on RUNX1 stability. The construct which contains point mutations in CXXC domain also lacked the ability to reduce RUNX1 expression. Furthermore, overexpression of only CXXC domain and flanking regions could down-regulate RUNX1 protein expression. These results suggest that MLL fusion proteins and the N-terminal MLL portion of MLL fusions down-regulate RUNX1 and CBFβ protein expression via the MLL CXXC domain and flanking regions. To understand the impact of RUNX1/CBFβ down-regulation on hematopoietic stem and progenitor cells (HSPCs), we generated RUNX1+/–/CBFβ+/– mice as a hypomorph model. The percentage of bone marrow (BM) LSK cells from RUNX1+/–/CBFβ+/– mice was significantly increased compared with that from WT mice. Using BM cells from these mice, we performed in vitro CFU assay and in vivo bone marrow transplantation (BMT) assay. BM cells from RUNX1+/–/CBFβ+/– mice provided more colonies in CFU assay compared with those from WT mice. To determine whether restoration of RUNX1 could repress the MLL mediated leukemogenesis, we retrovirally overexpressed WT RUNX1 in BM cells from Mll-Af9 knock-in mice. Using transduced BM cells, we performed in vitro CFU assay and in vivo BMT assay. RUNX1 overexpressed Mll-Af9 (Mll-Af9/RUNX1) cells underwent terminal differentiation after 2 times replating, while control vector transduced Mll-Af9 (Mll-Af9/Control) cells could still be replated more than 4 times. All the recipient mice transplanted with Mll-Af9/Control cells developed AML. In contrast, all the recipient mice transplanted with Mll-Af9/RUNX1 never develop AML. Furthermore, when we treated MLL leukemia cell lines with DOT1L inhibitor (EPZ-5676), RUNX1 protein levels in these MLL leukemia cell lines were significantly increased 48 hours after the treatment in comparing with controls treated with DMSO. However, there was no significant mRNA expression level change of RUNX1within 48 hours. Future studies are needed to fully understand the mechanism of whether this increasing RUNX1 protein level by DOT1L inhibitor is through blocking CXXC domain and flanking regions mediated degradation. In conclusion, MLL aberrations down-regulate RUNX1/CBFβ via their CXXC domain and flanking regions. Down-regulation of RUNX1/CBFβ plays critical role for MLL mediated leukemia development. Targeting RUNX1/CBFβ levels allows us to test novel therapies for MLL leukemias. Disclosures Mulloy: Celgene: Research Funding; Seattle Genetics: Research Funding; Amgen: Research Funding; NovImmune: Research Funding

Kv3.3 Channels Bind Hax-1 and Arp2/3 to Assemble a Stable Local Actin Network that Regulates Channel Gating

Mutations in the Kv3.3 potassium channel (KCNC3) cause cerebellar neurodegeneration and impair auditory processing. The cytoplasmic C terminus of Kv3.3 contains a proline-rich domain conserved in proteins that activate actin nucleation through Arp2/3. We found that Kv3.3 recruits Arp2/3 to the plasma membrane, resulting in formation of a relatively stable cortical actin filament network resistant to cytochalasin D that inhibits fast barbed end actin assembly. These Kv3.3-associated actin structures are required to prevent very rapid N-type channel inactivation during short depolarizations of the plasma membrane. The effects of Kv3.3 on the actin cytoskeleton are mediated by the binding of the cytoplasmic C terminus of Kv3.3 to Hax-1, an anti-apoptotic protein that regulates actin nucleation through Arp2/3. A human Kv3.3 mutation within a conserved proline-rich domain produces channels that bind Hax-1 but are impaired in recruiting Arp2/3 to the plasma membrane, resulting in growth cones with deficient actin veils in stem cell-derived neurons