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BackgroundDepression is the leading burden of mental disease, especially in low-and-middle-income countries like Vietnam. The Stepped Care Model is a promising approach to managing depression in the community with low resources. This is the first study that implemented the adapted Stepped Care Model for depression management in the Vietnamese context and evaluated the initial effectiveness of this community-based intervention in the Thai Nguyen community.Materials and methodsA quasi-experimental study with a 3-month follow-up was conducted in 10 selected communes in Thai Nguyen province. The most important modifications in the Stepped Care Model for depression management were the screening focused on the high-risk individuals living in the community; the combination of 8-session group psychotherapy with animation activities at commune health stations (CHS); and using psychotherapy as first-line treatment. From August 2020 to January 2021, quantitative data were collected using the Patient Health Questionnaire-9, the Generalized Anxiety Disorder-7, and the Quality of Life Enjoyment and Satisfaction Questionnaire-Short Form. The descriptive analyses were performed to describe the demographic characteristics and the change in the questionnaires' mean score at the baseline and 3-month follow-up.ResultsA total of 1,891 people were approached in the community, of which 359 voluntary people met the study criteria and attended group psychotherapy. During group psychotherapy, the average PHQ-9 scores gradually decreased, and after the 8th session, this figure dropped by 2.65 times compared to the beginning. After 3 months, the percentage of the group with mild-moderate depression shrank from 95.5 to 9.3%, and there were no more severe cases. Moreover, life satisfaction increased by 32% and the anxiety level significantly dropped according to Q-LES-Q-SF and GAD-7 accordingly.ConclusionThe preliminary results after 3-month follow-up showed that the Stepped Care Model with group psychotherapy at the CHS was promising to manage the depression in the community. This task shifting approach with limited resources should be further disseminated and studied for long-term effectiveness in low-and-middle-income countries like Vietnam.
AimHealthcare workers have directly provided care for COVID-19 patients, and have faced many additional sources leading to poor mental health. The study aimed to investigate the mental health problems and related factors among healthcare staff in Vietnam.MethodsA descriptive cross-sectional mixed methods study, combining quantitative and qualitative research methods, was performed among 400 healthcare workers working at the National Hospital for Tropical Diseases and Ninh Binh General Hospital from the first day of treatment for COVID-19 patients to May 01, 2020.ResultsThe results showed that 8.0% of participants had stress, 17.5% of participants had anxiety, and 14.8% of participants had depression. Approximately 50% of participants reported that they had at least one of these symptoms. The findings illustrated that stress, anxiety, and depression were associated with the position in a hospital, health status during the COVID-19 pandemic, family members/relatives infected with COVID-19, physical and mental support from friends, family, and community, department, years of working, and the average work hours per day of healthcare workers exposed to COVID-19.ConclusionDuring the COVID-19 pandemic, healthcare workers who worked in the hospital providing treatment and care for COVID-19 patients dealt with mental health problems such as stress, anxiety, and depression. It is necessary to promote mental health among healthcare workers, to contribute to the fight against the COVID-19 outbreak in Vietnam.
Human papillomavirus (HPV), high-risk type 18, is directly associated with approximately 98% incidence of invasive cervical cancer. Epithelial cells infected with HPV-18 become transformed and exhibit overexpression of telomerase activity and chromosomal instability. As a result of this transformation, E6 and E7 oncoproteins are perpetually expressed: E6 degrades the tumor suppressor p53; E7 inhibits the tumor suppressor pRB, leading to uncontrollable growth and the extension of telomere length. While a few studies explored the chromosomal instability induced by HPV E6 and E7 oncoproteins, the full scope of the problem has not been clearly characterized. In this research we investigated HPV-18 acquired genomic instability by E6 and E7 oncoproteins. HPV-positive cervical cancer cells, HeLa, were studied through spectral karyotyping (SKY), Giemsa banding (G-banding), telomere length, and telomerase activity using PCR ELISA assay and the TRAPeze XL Kit, which uses fluorescence energy transfer. With the use of SKY, G-banding, and chromosomal instability analysis, HeLa cells exhibited many aneuploidies. In our results, there were consistent translocations on chromosomes 4 and 11, with deletions on chromosomes 11 and 20. There were also other translocations on chromosomes 9 and 20, with deletions on chromosome 10. Additionally, copies of chromosome 5 and unidentifiable marker chromosomes were noted. Moreover, telomerase data suggest that upregulated expression of telomerase activity correlates with the increase in chromosomal instability. The aforementioned aneuploidy is demonstrative of the induced chromosomal instability from HPV-18 infection. In addition to the tumor-suppressor disruption acquired by E6 and E7 oncoproteins, HeLa cells showed gene deletion on chromosome 11. The ATM gene, which is specifically located between distal regions 11q22.3 and 11q23 of chromosome 11, is known to help identify breaks in DNA and plays a crucial role in DNA repair. Damage to the ATM gene may further play an important role in increasing cancer progression. Citation Format: Mai Do, Nichelle Cox, Naomi Long, Liliana Zarate, Chinelo Ezechukwu, Jenna Cormier, Hyun Chung, Meidrah Tyler, Judith Okoro, Diondra Harris, Victoria Vidal, Jerica Watson, Ellie Canty, Shyam Arya, Benjamin Liu, Roland Pattillo, Billy Ballard, Jay Vadgama, Eva McGhee. Molecular characterization of HPV type 18 cervical cancer: Upregulation of telomerase expression and induced chromosomal instability by E6 and E7 oncoproteins [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 3388.
Human Papillomavirus (HPV), a non-enveloped epitheliotropic double stranded DNA virus, is an etiological agent of oral cancer. Oral cancer is related to the persistent infection by high-risk HPV type 16, E6/E7 oncoproteins. The E6/E7 oncoproteins significantly contribute to the carcinogenic genetic instability effect of high-risk HPV through the degradation of two gatekeeper proteins, p53 and pRB, respectively. The ATM gene, also known as a gatekeeper protein plays a central role in the complex processes that repair DNA strand breaks. The ATM gene is located at 11q22.3 and belongs to a protein family known as the PI3K. Many studies have tried to clarify the epigenetic instability role of ATM in cancer function and susceptibility. However, there are no studies addressing the relationship between HPV infection-oral cancer, ATM/PI3K expression, and genomic instability. The aim of this study is to analyze the influence of HPV16 E6/E7 oncoproteins in oral cancer and the epigenetic profile. In our experimental procedures, we proposed a novel approach to study HPV-induced epigenetic changes with reconstructed human oral epithelium in SCID mouse. We used HPV-16, which is the most common HPV type found in oral cancer. Two plasmids were used to produce HPV-16 E6/E7. The first plasmid p16sheLL expresses the two viral capsid proteins, L1 and L2. The second plasmid pBR322HPV16 contains the full length HPV-16 genome. This approach closely mimics the architecture of normal human oral epithelium. In our study, we first focused on analyzing selected cellular gene loci where DNA methylation profiles are known to be altered, either by HPV infection or in oral cancer. We examined the following gene promoters DcR1/DcR2 (apoptosis regulation), p16 (cell cycle control), DAPK (cancer metastasis), and MGMT (DNA repair). We also analyzed progressive morphological and cytopathic changes in the HPV-infected oral epithelia. These data indicate that HPV E6/E7 oncoproteins can promote increased upregulation of apoptosis, disrupt cell cycle regulation, and decrease DNA double strand break repair. Epigenetics and chromosomal instability events were noted, specifically, the deletion of the distal region of chromosome 11q22-23 in the E6/E7 transfected keratinocytes. These results indicate that HPV-16, E6/E7 oncoproteins induced epigenetic changes in mouse keratinocytes, which may further promote oral carcinogenesis. Citation Format: Eva McGhee, Mengtao Li, Yi-Ling Lin, Liliana Zarate, Naomi Long, Mai Do, Chinelo Ezechukwu, Nichelle Cox, Hyun Chung, Jenna Cormier, Meidrah Tyler, Victoria Vidal, Billy Ballard, Roland Pattillo, Jay Vadgama. Upregulation of epigenetic changes acquired by HPV16 E6/E7 oncoproteins in mouse keratinocytes: Targeting ATM/PI3K [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 3326.
Purpose: Provision of mental health psychosocial support can reduce psychological distress experienced by cancer patients, which can in turn improve their treatment adherence and outcomes. In this study, we present the results from the pilot trial of Stronger Together, a culturally adapted peer-to-peer support program, conducted in Vietnam. Methods: We recruited eligible women from four hospitals in Vietnam (K3 National Cancer Hospital, Hue Central Hospital Oncology Center, Can Tho Oncology Hospital, and Hung Vong Women’s Hospital Oncology Unit). Participants were newly diagnosed with breast or gynecologic cancers, and self-selected into either the control (usual care) or intervention arm (mentees who were matched up with trained peer mentors). Validated questionnaires were administered at baseline (0), 2-, 4-, and 6-months. We conducted a difference-in-difference (DID) analysis for the primary outcomes (assessed by the Depression, Anxiety, and Stress Scale [DASS-21]), comparing the difference in scores from baseline to 6 months and between intervention arms (mentees vs. usual care). Results: The analytic sample included n=186 participants (mentees: 91; usual care: 95), with the majority having breast cancer (85.5%), followed by cervical cancer (7.5%) and ovarian cancer (7.0%). There were no statistically significant differences between study arms in demographic and cancer characteristics (cancer type and stage). DID analyses showed that compared to usual care participants, mentees (those who received peer support) showed greater reductions in depression, anxiety, and stress scores between baseline and 6 months. Adjusting for age, education, marital status, and cancer stage, statistically significant reductions in stress scores (β=-1.47; 95%CI: [-2.9,-0.02]; p=0.047) were observed. Among breast cancer patients only, adjusted models showed significant reductions in depression scores (β=-1.80; 95%CI: [-3.0,-0.48]; p=0.007) and stress scores (β=-1.9; 95%CI: [-3.3,-0.37; p=0.015). Conclusion: The Stronger Together pilot study study shows that utilizing peer cancer survivors is a promising strategy to address the psychosocial needs of newly diagnosed cancer patients in low-resource settings. Future research should test this intervention model in larger samples or other similar populations and settings. Citation Format: PhuongThao Le, Carolyn Taylor, Rachel Monahan, Mai Do, Linh Nguyen, Minh Tri Phan, Cong Wang, Huong Tran, Ophira Ginsburg. Implementation of a Hospital-Based Peer Support Intervention Model for Cancer Patients: Results From a Pilot Study in Vietnam [abstract]. In: Proceedings of the 11th Annual Symposium on Global Cancer Research; Closing the Research-to-Implementation Gap; 2023 Apr 4-6. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2023;32(6_Suppl):Abstract nr 52.
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