RESUMO
Background: Hypertension is a major risk factor for the global burden of disease, and nutrition is associated with an increased risk of mortality from multiple diseases. Few studies have explored the association of nutritional risk with all-cause mortality and cardiovascular mortality in hypertension, and our study aims to fill this knowledge gap. Method: We included data from the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2016 on a total of 10,037 elderly patients with hypertension. The nutritional status was evaluated using the Geriatric Nutrition Risk Index (GNRI). Kaplan-Meier survival analysis was performed to analyze the survival rates of different nutritional risk groups. COX proportional risk regression models were used to analyze the predictive effect of GNRI on all-cause mortality and cardiovascular mortality in hypertensive patients. Restricted cubic splines (RCS) were used to explore the nonlinear relationship between GNRI and mortality. Result: The mean age of the hypertensive patients was 70.7 years. A total of 4255 (42.3%) all-cause mortality and 1207 (17.2%) cardiovascular mortality occurred during a median follow-up period of 106 months. Kaplan-Meier showed a more significant reduction in survival for the moderate to severe malnutrition risk of GNRI. The adjusted COX proportional hazards model showed that the hazard ratios for all-cause mortality and cardiovascular mortality in the moderate to severe malnutrition risk group for GNRI were 2.112 (95% CI, 1.377,3.240) and 2.604 (95% CI, 1.603,4.229), respectively. The RCS showed that increased GNRI was associated with a reduced risk of all-cause mortality and cardiovascular mortality risk reduction. Conclusion: Malnutrition exposure assessed by GNRI effectively predicts the risk of all-cause mortality and cardiovascular mortality in the elderly with hypertension.
RESUMO
After spinal cord injury (SCI) in mammals, neuronal regeneration is limited; in contrast, such regeneration occurs quickly in zebrafish. Member A of the acidic nuclear phosphoprotein 32 (ANP32a) family is involved in neuronal development, but its function is controversial, and its involvement in zebrafish SCI remains unknown. To determine the role of zebrafish ANP32a in the neuronal regeneration of SCI embryos, we microinjected ANP32a mRNA into embryos from zebrafish transgenic line Tg(mnx1:GFP) prior to SCI. Compared to control SCI embryos, the results showed that the regeneration of spinal cord and resumption of swimming capability were promoted by the overexpression of ANP32a mRNA but reduced by its knockdown. We next combined fluorescence-activated cell sorting with immunochemical staining of anti-GFAP and immunofluorescence staining against anti-PH3 on Tg(gfap:GFP) SCI embryos. The results showed that ANP32a promoted the proliferation and cell number of radial glial cells at the injury epicenter at 24 h post-injury (hpi). Moreover, when we applied BrdU labeling to SCI embryos derived from crossing the Tg(gfap:GFP) and Tg(mnx1:TagRFP) lines, we found that both radial glial cells and motor neurons had proliferated, along with their increased cell numbers in Anp32a-overexpression SCI-embryos. On this basis, we conclude that ANP32a plays a positive role in the regeneration of zebrafish SCI embryos.