The impact of gardening on well-being, mental health, and quality of life: an umbrella review and meta-analysis.

BACKGROUND: Gardening and horticultural therapy (HT) has been widely recognised as a multicomponent approach that has affected a broad range of health and well-being outcomes. The aim of this umbrella review and meta-analysis was to compare the findings of previous reviews on the impact of multiple gardening interventions and gardening attributes on different well-being constructs. METHODS: Electronic databases including PubMed, Web of Science, Science Direct, the Cochrane Library, and Google Scholar were searched from inception to December 2022. Interventional and observational reviews were eligible for inclusion in this umbrella review. Outcome measures included mental well-being, health status and quality of life. The key exposure variables were gardening and horticultural therapy. Narrative synthesis was used to evaluate the overall impact of gardening and HT on study outcomes. For a subsample of studies with available quantitative data, a random effect meta-analysis was conducted. RESULTS: This umbrella review included 40 studies (10 interventional studies, 2 observational studies, and 28 mixed interventional and observational studies). The reviewed studies reported an overall positive impact of gardening activities on several measures of mental well-being, quality of life, and health status. Meta-analysis showed a significant and positive effect of gardening and HT activities on well-being (effect size (ES) 0.55, 95% confidence interval (CI) 0.23, 0.87, p < 0.001). CONCLUSIONS: Evidence from observational and interventional studies supports a positive role for gardening and HT activities on well-being and general health. Interventional studies with horticultural-based therapies were effective in improving well-being and quality of life both in the general population and vulnerable subgroups. The high degree of heterogeneity in the included studies cautions against any direct clinical implications of the study findings.

A simple self-report health assessment questionnaire to identify oral diseases.

BACKGROUND: One approach to addressing oral health disparities for at-risk populations has been to increase discussion of oral health by non-dental healthcare providers. This study examined the accuracy of a simple instrument to detect individuals with a history of dental disease, which would then allow referral for an oral health evaluation. MATERIALS AND METHODS: A two-question instrument was evaluated for the relationship to oral diseases, periodontal disease, and decayed, missing and filled teeth in 391 individuals seen in a dental school clinic for non-emergent dental care over a 3-month period. Clinical dental findings were used as outcome variables. The oral health parameters were dichotomised, using different levels of disease severity. The criteria were increased and decreased in an effort to test the robustness of our method. RESULTS: While the sensitivity outcomes with one question alone showed significant ability to predict oral disease (59-71%), the addition of a second self-assessment question increased the sensitivity (76-91%) for all oral health parameters studied. As the criteria for oral disease increased so did the sensitivity of this instrument. CONCLUSION: The results presented here offer evidence that a simple two-item questionnaire is an efficient and effective method of detecting populations at-risk for oral diseases.

Inhibition of focal adhesion kinase induces apoptosis in bladder cancer cells via Src and the phosphatidylinositol 3-kinase/Akt pathway.

Focal adhesion kinase (FAK) is a 125-kDa, cytosolic, non-receptor, protein tyrosine kinase localized at focal adhesions that can be activated by multiple inputs and in different manners. FAK is implicated in signaling pathways regulating cell movement, invasion, survival, gene expression and cancer stem cell self-renewal. The aim of the present study was to investigate whether FAK plays a role in the apoptosis of bladder cancer cells. The study employed in situ deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling and Annexin V labeling flow cytometry. It was found that both the knockdown of FAK and the suppression of FAK phosphorylation were able to induce apoptosis in bladder cancer cells. Caspase-3 was activated during the apoptosis induced by the suppression of FAK phosphorylation. Src was involved in FAK-regulated apoptosis in bladder cancer cells, while the suppression of Src phosphorylation was able to inhibit FAK tyrosine phosphorylation and induce apoptosis. Furthermore, phosphatidylinositol 3-kinase (PI3K)/Akt signaling was inhibited via the suppression of FAK tyrosine phosphorylation. Conversely, the expression of neither the general nor the tyrosine-phosphorylated FAK was regulated by inhibiting PI3K/Akt, which suggested that PI3K/Akt acted downstream of FAK to regulate apoptosis in bladder cancer cells. These findings indicate the presence of a mechanism of apoptosis involving FAK-mediated oncogenic signaling. FAK may function as an important regulator of extracellular signaling-mediated apoptosis in bladder cancer and be used as a novel therapeutic target in the treatment of the condition.

Oncolytic adenovirus armed with human papillomavirus E2 gene in combination with radiation demonstrates synergistic enhancements of antitumor efficacy.

High-risk human papillomavirus (hr-HPV) E6 and E7 oncogenes are associated with resistance to radiotherapy in cervical cancer. Efforts have been taken to employ HPV E2, a crucial negative transcriptional modulator of HPV E6 and E7 oncogenes, and also an apoptosis-inducing agent, for therapeutic intervention. Despite being conceptually attractive, the potency and feasibility of current hr-HPV E2-based therapies remain limited. Here, we designed a novel recombinant adenovirus, named M5, with a 27-bp deletion in E1A conserved region-2 by which to realize tumor-specific replication, and a total HPV type 16 (HPV16) E2 gene complementary DNA inserted into the E3 coding region. In this design, M5 exploited the adenovirus E3 promoters to express HPV16 E2 gene in a viral replication-dependent manner and preferentially silenced the hr-HPV E6 and E7 oncogenes in HPV-positive cervical cancer cells. In vitro and in vivo assays confirmed that M5 exhibited potent antitumoral efficacy. Moreover, the effects of combined treatment with M5 and radiation treatment resulted in synergistically enhanced potency (P<0.01). The increase in killing efficacy of M5 was also found in HPV-negative cervical cancer cells, for which the pro-apoptotic activity of HPV16 E2 was thus responsible. Our results indicated that the use of M5 that locally delivers HPV16 E2 to cancers has broad therapeutic windows and that the combination therapy with radiation for cervical cancer will be the more effective way of improving survival.