RESUMO
Context: Severe cases of stroke can lead to cognitive impairment or even dementia. The most critical factor related to cognitive impairment after strokes is patients' lack of understanding about or attention to their conditions. Strengthening standardized management post-stroke has become a common goal for clinical workers and patients. Objective: The study intended to explore, during post-discharge follow-up, the effectiveness of standardized management of patients with post-stroke cognitive impairment, which could provide guidance for patients and doctors to improve patients' follow-up plans. Design: The research team conducted a randomized controlled trial. Setting: The study took place at Huangshi Central Hospital, an Affiliated Hospital of Hubei Polytechnic University, Edong Healthcare Group, in Huangshi, Hubei, China. Participants: Participants were 112 patients with post-stroke cognitive impairment at the hospital between February 2021 and March 2023. Intervention: The research team randomly divided the participants into two groups, using a random-number-table method: (1) a control group with 56 participants who received routine management and (2) an intervention group with 56 participants who received standardized management. Outcome Measures: At baseline and 6 months postintervention, the research team measured participants': (1) cognitive function using the Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA), (2) quality of life (QoL) using the World Health Organization Quality of Life-Bref (WHOQOL-BREF) questionnaire, and (3) self-efficacy using the General Self-Efficacy Scale (GSES). At one and 6 months postintervention, the team analyzed participants' medication adherence using the Morisky Medication Adherence Scale (MMAS-8). Results: At baseline, no significant difference (P > .05) existed between the groups in the scores: (1) for cognitive function on the MMSE or MoCA, (2) for the physiological, psychological, social, and environmental domains and the total score on the WHOQOL-BREF, or (3) for self-efficacy on the GSES scores. At 6 months postintervention, the intervention group's scores were significantly higher than those of the control group: (1) on the MMSE and MoCA (both P < .001), (2) on the four domains and total score on the WHOQOL-BREF (all P < .001), and (3) on the GSES (P < .001). At one month and six months postintervention, the intervention group's score for medication adherence on the MMAS-8 was significantly higher than those of the control group (both P < .001). Conclusions: Standardized management for patients with post-stroke cognitive impairment provided beneficial outcomes in improving their cognitive function, QoL, self-efficacy, and medication adherence, and the research team highly recommends it for wide application in clinical practice.
RESUMO
BACKGROUND: Fish oil is one of the most popular supplements in the UK and other developed countries. However, the relationship between fish oil use and chronic obstructive pulmonary disease (COPD) is unclear. OBJECTIVE: To prospectively examine the association of habitual fish oil supplementation with incident COPD risk and to evaluate potential effect modification by genetic predisposition. METHODS: This study included 484,414 participants (mean and standard deviation [SD] age: 56.5 [8.1] years) from the UK Biobank who completed a touchscreen questionnaire on habitual fish oil supplement use between 2006 and 2010 and were followed up through 2018. Cox regression models were used to estimate the hazard ratios (HRs) and 95% confidence intervals (95% CIs) with adjustment for sociodemographic and lifestyle behaviours, health conditions, and other potential confounding factors. A weighted genetic risk score (GRS) for COPD was derived from 112 validated single nucleotide polymorphisms. RESULTS: During a median follow-up of 9.0 years, 8860 incident COPD events were recorded. A total of 31.4% (152,230) of the study participants reported habitual fish oil supplementation at baseline. Habitual fish oil supplementation was significantly associated with a lower risk of incident COPD (adjusted HR: 0.88; 95% CI: 0.84-0.93). The association with COPD did not differ by GRS strata (P for interaction = 0.880). The results from subgroup and sensitivity analyses supported the robustness of our findings. CONCLUSIONS: Our findings suggest that habitual fish oil supplementation is associated with a lower risk of incident COPD, irrespective of genetic predisposition.
Assuntos
Óleos de Peixe , Doença Pulmonar Obstrutiva Crônica , Humanos , Estudos Prospectivos , Predisposição Genética para Doença , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Doença Pulmonar Obstrutiva Crônica/genética , Doença Pulmonar Obstrutiva Crônica/complicações , Fatores de Risco , Suplementos NutricionaisRESUMO
ETHNOPHARMACOLOGICAL RELEVANCE: Pennogenyl saponins, the characterized components of Rhizoma Paridis, have been reported to have anticancer activity through induction of apoptosis or anti-metastasis in cultured cells or animal models. The aim of the study was to evaluate the anticancer properties of four pennogenyl saponins (PS1-PS4) on a panel of human cancer and normal cell lines, and explore the potential mechanisms underlying the selective anticancer effects of the steroidal saponins in cancer cells. MATERIALS AND METHODS: Differences in the anticancer activity of pennogenyl saponins were examined by MTT assay in human cancer cell lines (HepG2 hepatocellular carcinoma cells, UACC-257 melanoma cells, MCF-7 breast and PC-3 prostate cancer cells) and normal human cell lines (L-02 liver cells and HEK293 kidney cells). Flow cytometry analysis, JC-1 staining and western blot analysis were applied to detect the effects of anticancer pennogenyl saponins on apoptosis, cell cycle, and expression and/or activation of main effectors involved in the potential signaling pathways. RESULTS: Among the tested four saponins, only PS1 and PS2 selectively inhibited cell growth in HepG2, MCF-7 and PC-3 cells. Moreover, PS1 and PS2 could significantly induce apoptosis and cell cycle G2/M arrest in HepG2 cells, which were at least associated with activation of mitochondrial caspase-dependent and -independent apoptotic cascades, inhibition of cyclin-dependent kinase 1 and PI3K/Akt signaling pathway, and modulation of mitogen-activated protein kinases. CONCLUSIONS: PS1 and PS2 had potent and selective anticancer activity to breast, liver and prostate cancer cells. Furthermore, the anticancer effects of PS1 and PS2 were associated with induction of apoptosis and blockage of cell cycle progression through multiple targets in HepG2 cells. These findings suggest that PS1 and PS2 can be considered as potential agents for the treatment of some cancers such as hepatoma.