RESUMO
BACKGROUND: The role of echocardiography in the diagnostic and prognostic assessment of pulmonary hypertension (PH) has been widely studied recently. However, these findings have not undergone normative evaluation and may provide confusing evidence for clinicians. To evaluate and summarize existing evidence, we performed an umbrella review. METHODS: Systematic reviews and meta-analyses were searched in PubMed, Embase, Web of Science, and Cochrane Library from inception to September 4, 2022. The methodological quality of the included studies was assessed using Assessment of Multiple Systematic Reviews (AMSTAR), and the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system was used to evaluate the quality of evidence. RESULTS: Thirteen meta-analyses (nine diagnostic and four prognostic studies) were included after searching four databases. The methodological quality of the included studies was rated as high (62%) or moderate (38%) by AMSTAR. The thirteen included meta-analyses involved a total of 28 outcome measures. The quality of evidence for these outcomes were high (7%), moderate (29%), low (39%), and very low (25%) using GRADE methodology. In the detection of PH, the sensitivity of systolic pulmonary arterial pressure is 0.85-0.88, and the sensitivity and specificity of right ventricular outflow tract acceleration time are 0.84. Pericardial effusion, right atrial area, and tricuspid annulus systolic displacement provide prognostic value in patients with pulmonary arterial hypertension with hazard ratios between 1.45 and 1.70. Meanwhile, right ventricular longitudinal strain has independent prognostic value in patients with PH, with a hazard ratio of 2.96-3.67. CONCLUSION: The umbrella review recommends echocardiography for PH detection and prognosis. Systolic pulmonary arterial pressure and right ventricular outflow tract acceleration time can be utilized for detection, while several factors including pericardial effusion, right atrial area, tricuspid annular systolic displacement, and right ventricular longitudinal strain have demonstrated prognostic significance. TRIAL REGISTRATION: PROSPERO (CRD42022356091), https://www.crd.york.ac.uk/prospero/ .
Assuntos
Fibrilação Atrial , Hipertensão Pulmonar , Derrame Pericárdico , Humanos , Ecocardiografia , Hipertensão Pulmonar/diagnóstico por imagem , Prognóstico , Revisões Sistemáticas como Assunto , Metanálise como AssuntoRESUMO
Caffeine is a purine alkaloid and is widely consumed in coffee, soda, tea, chocolate and energy drinks. To date, a growing number of studies have indicated that caffeine is associated with many diseases including colorectal cancer. Caffeine exerts its biological activity through binding to adenosine receptors, inhibiting phosphodiesterases, sensitizing calcium channels, antagonizing gamma-aminobutyric acid receptors and stimulating adrenal hormones. Some studies have indicated that caffeine can interact with signaling pathways such as transforming growth factor ß, phosphoinositide-3-kinase/AKT/mammalian target of rapamycin and mitogen-activated protein kinase pathways through which caffeine can play an important role in colorectal cancer pathogenesis, metastasis and prognosis. Moreover, caffeine can act as a general antioxidant that protects cells from oxidative stress and also as a regulatory factor of the cell cycle that modulates the DNA repair system. Additionally, as for intestinal homeostasis, through the interaction with receptors and cytokines, caffeine can modulate the immune system mediating its effects on T lymphocytes, B lymphocytes, natural killer cells and macrophages. Furthermore, caffeine can not only directly inhibit species in the gut microbiome, such as Escherichia coli and Candida albicans but also can indirectly exert inhibition by increasing the effects of other antimicrobial drugs. This review summarizes the association between colorectal cancer and caffeine that is being currently studied.
RESUMO
Colorectal cancer (CRC), a multifactorial disease, is usually induced and developed through complex mechanisms, including impact of diet and lifestyle, genomic abnormalities, change of signaling pathways, inflammatory response, oxidation stress, dysbiosis, and so on. As natural polyphenolic phytochemicals that exist primarily in tea, tea polyphenols (TPs) have been shown to have many clinical applications, especially as anticancer agents. Most animal studies and epidemiological studies have demonstrated that TPs can prevent and treat CRC. TPs can inhibit the growth and metastasis of CRC by exerting the anti-inflammatory, anti-oxidative or pro-oxidative, and pro-apoptotic effects, which are achieved by modulations at multiple levels. Many experiments have demonstrated that TPs can modulate several signaling pathways in cancer cells, including the mitogen-activated protein kinase pathway, phosphatidylinositol-3 kinase/Akt pathway, Wnt/ß-catenin pathway, and 67 kDa laminin receptor pathway, to inhibit proliferation and promote cell apoptosis. In addition, novel studies have also suggested that TPs can prevent the growth and metastasis of CRC by modulating the composition of gut microbiota to improve immune system and decrease inflammatory responses. Molecular pathological epidemiology, a novel multidisciplinary investigation, has made great progress on CRC, and the further molecular pathological epidemiology research should be developed in the field of TPs and CRC. This review summarizes the existing in vitro and in vivo animal and human studies and potential mechanisms to examine the effects of tea polyphenols on CRC.