Background: In many countries, nurses are ill-prepared to provide care to patients with terminal illnesses. Limited education and training affect their ability to deliver proper palliative care. Only a few studies have explored appropriate and effective training methods of palliative care in China. Therefore, we aimed to provide evidence for a palliative care training system by appraising the effects of a mixed-method intervention on participants’ knowledge of palliative care and attitudes towards dying patients and death. Methods: An e-learning intervention approach was adopted for 97 nurses from oncology departments across five hospitals, using a mobile terminal combined with a virtual forum and face-to-face interactions. We conducted a pre- and post-training evaluation through the Palliative Care Quiz of Nursing (PCQN), Frommelt Attitude Toward Care of the Dying Scale Form B (FATCOD-B), and Death Attitude Profile-Revised (DAP-R). Results: After a three-week intervention, there was a significant increase in the PCQN and FATCOD-B scores as compared to the baseline. For PCQN, the total score increased from 10.3 ± 1.9 to 11.1 ± 2.2 (p = .011) and the score for management of pain and other symptoms increased from 7.7 ± 1.7 to 8.4 ± 1.7 (p = .003). FATCOD-B scores increased noticeably from 100.6 ± 7.9 to 102.9 ± 8.9 (p = .019). The DAP-R scores showed no obvious difference between pre- and post-intervention results. Conclusions: The mixed-method intervention was effective in improving participants’ knowledge and attitudes about palliative care. The implementation of training for nurses at appropriate intervals during both education and professional life is required, especially regarding the improvement in participants’ attitudes towards death. Therefore, palliative care training in China should receive more attention.

Mitophagy alleviates neuronal damage after cerebral ischemia by selectively removing dysfunctional mitochondria. Phosphatase and tensin homolog (PTEN) induced putative kinase 1 (PINK1)/Parkin-mediated mitophagy is the most well-known type of mitophagy. However, little is known about the role of PINK1/Parkin-mediated mitophagy in ischemic tolerance induced by hypoxic postconditioning (HPC) with 8% O₂ against transient global cerebral ischemia (tGCI). Hence, we aimed to test the hypothesis that HPC-mediated PINK1/Parkin-induced mitochondrial ubiquitination and promotes mitophagy, thus exerting neuroprotection in the hippocampal CA1 subregion against tGCI. We found that mitochondrial clearance was disturbed at the late phase of reperfusion after tGCI, which was reversed by HPC, as evidenced by the reduction of the translocase of outer mitochondrial membrane 20 homologs (TOMM20), translocase of inner mitochondrial membrane 23 (TIMM23) and heat shock protein 60 (HSP60) in CA1 after HPC. In addition, HPC further increased the ratio of LC3II/I in mitochondrial fraction and promoted the formation of mitophagosomes in CA1 neurons after tGCI. The administration of lysosome inhibitor chloroquine (CQ) intraperitoneally or mitophagy inhibitor (Mdivi-1) intracerebroventricularly abrogated HPC-induced mitochondrial turnover and neuroprotection in CA1 after tGCI. We also found that HPC activated PINK1/Parkin pathway after tGCI, as shown by the augment of mitochondrial PINK1 and Parkin and the promotion of mitochondrial ubiquitination in CA1. In addition, PINK1 or Parkin knockdown with small-interfering RNA (siRNA) suppressed the activation of PINK1/Parkin pathway and hampered mitochondrial clearance and attenuated neuroprotection induced by HPC, whereas PINK1 overexpression promoted PINK1/Parkin-mediated mitophagy and ameliorated neuronal damage in CA1 after tGCI. Taken together, the new finding in this study is that HPC-induced neuroprotection against tGCI through promoting mitophagy mediated by PINK1/Parkin-dependent pathway.

Hypoxia administered after transient global cerebral ischemia (tGCI) has been shown to induce neuroprotection in adult rats, but the underlying mechan

Autophagy disruption leads to neuronal damage in hypoxic–ischemic brain injury. Rab7, a member of the Rab GTPase superfamily, has a unique role in the regulation of autophagy. Hypoxic preconditioning (HPC) provides neuroprotection against transient global cerebral ischemia (tGCI). However, the underlying mechanisms remain poorly understood. Thus, the current study explored the potential molecular mechanism of the neuroprotective effect of HPC by investigating how Rab7 mediates autophagosome (AP) maturation after tGCI in adult rats. We found that HPC attenuated AP accumulation in the hippocampal CA1 region after tGCI via restoration of autophagic flux. We also confirmed that this HPC-induced neuroprotection was not caused by the increase in lysosomes or the improvement of lysosomal function after tGCI. Electron microscopic analysis then revealed an increase in autolysosomes in CA1 neurons of HPC rats. Moreover, the inhibition of autophagosome-lysosome fusion by chloroquine significantly aggravated neuronal death in CA1, indicating that AP maturation contributes to HPC-induced neuroprotection against neuronal injury after tGCI. Furthermore, the activation of Rab7 was found to be involved in the neuroprotective effect of AP maturation after HPC. At last, the knockdown of ultraviolet radiation resistance-associated gene (UVRAG) in vivo disrupted the interaction between Vps16 and Rab7, attenuated the activation of Rab7, interrupted autophagic flux, and ultimately abrogated the HPC-induced neuroprotection against tGCI. Our results indicated that AP maturation was enhanced by the activation of Rab7 via UVRAG-Vps16 interaction, which further demonstrated the potential neuroprotective role of Rab7 in HPC against tGCI-induced neuronal injury in adult rats.

Metabolic syndrome (MetS) is an important risk factor for cerebral ischemic stroke, yet previous studies on the relationship between MetS or its components and acute cerebral infarction have been inconsistent. This study aims to evaluate the effects of MetS and its components on the short-term prognosis of patients with acute ischemic stroke. Subjects with ischemic stroke of <7-day duration (530 cases) were enrolled. MetS was defined based on the modified criteria of the International Diabetes Federation and the American Heart Association/National Heart, Lung, and Blood Institute. Demographic data, vascular risk factors, National Institutes of Health Stroke Scale score, the results of physical, laboratory and imaging examinations and clinical outcomes at 30 and 90 days were recorded. Using univariate analysis, we compared different baseline characteristics between patients with MetS and those without MetS. Further, we assessed MetS and its 5 components on the contribution to short-term prognosis of ischemic stroke with multiple logistic regression models after adjusting for age and sex. The prevalence of MetS among the patients with acute ischemic stroke in the study is 58.3 %, with more in females (70.3 %) than in males (49.7 %, p < 0.001). As expected, among the MetS components, elevated waist circumference, elevated triglyceride, high fasting blood glucose and low high density lipoprotein cholesterol (HDL-C) were significantly more prevalent in patients with MetS than those without MetS (all p < 0.001). There was no correlation between MetS itself and the short-term prognosis of acute ischemic stroke. Only hyperglycemia in the serum was shown to have impact on poor functional outcomes in 30 and 90 days after the onset of stroke. The occurrence of MetS among patients with acute ischemic stroke in our study is 58.3 %. MetS itself may not be predictive for the short-term prognosis of patients, while hyperglycemia is a significant predictor for poor functional outcomes in our study.