Case report and literature review: fatal cerebral fat embolism following facial autologous fat graft

BackgroundSevere cerebral artery embolism is a rare complication of facial autologous fat injection. However, its incidence has markedly increased with the recent rise in facial cosmetic procedures.Case presentationWe report a 31-year-old Chinese woman who presented with unconsciousness 6 h after having undergone a facial autologous fat injection. A neurological examination revealed stupor, bilaterally diminished pupillary light reflexes, right-sided central facial palsy, and no reaction to pain stimulation of right limbs. Diffusion-weighted imaging displayed patchy hyperintense lesions in the left frontal, parietal, and temporal lobes. Magnetic resonance angiography demonstrated fat embolism in the left internal carotid artery, anterior cerebral artery, and middle cerebral artery. We immediately performed mechanical thrombectomy under sufficient preoperative preparations but failed to achieve complete recanalization. Pathological examination of the embolus confirmed the presence of adipocytes. Although we actively administered symptomatic and supportive treatments, the patient eventually died due to the progression of cerebral herniation and systemic infection.ConclusionDue to the ineffectiveness of current treatment and the inferior prognosis, fat embolism, a severe complication of autologous fat graft, should draw the attention of both plastic surgeons and neurologists so that actions may be taken for both its prevention and treatment

Development of Research and Innovation Capacity Index of HEIs on Disaster Resilience Related Studies

Research capacity development is one of the most critical challenges facing HEIs in the Asian countries. Growing the number and quality of researchers is a strategic issue. For academia, developing research capacity can help enhance academic fulfilment as well as provide career advancement. The notion that excellent people are a resource to be treasured has led to increased attention being paid to how to attract, support and retain them, thereby building research capacity. This paper is part of an Erasmus plus co-funded project called ASCENT, which focuses on building the research and innovation capacity (R&I) of Higher Education Institutions (HEI) on disaster resilience related studies. This paper particularly aims at reviewing the current context and gaps in the literature with regards to the indices used to assess the research capacity of the higher education institutions. Qualitative systematic review approach was adopted at the initial stage, followed by three-round Focus Group Discussion with high -level academics from 14 countries in Asia and Europe. Twenty-one Key Performance Indicators (KPIs) of HEIs Research and Innovation Capacity were identified, which were grouped into three themes: Structure, System, and Policy; Skills and Training; and Staff

Melatonin-mediated cytoprotection against hyperglycemic injury in Müller cells.

Oxidative stress is a contributing factor to the development and progression of diabetic retinopathy, a leading cause of blindness in people at working age worldwide. Recent studies showed that Müller cells play key roles in diabetic retinopathy and produce vascular endothelial growth factor (VEGF) that regulates retinal vascular leakage and proliferation. Melatonin is a potent antioxidant capable of protecting variety of retinal cells from oxidative damage. In addition to the pineal gland, the retina produces melatonin. In the current study, we investigated whether melatonin protects against hyperglycemia-induced oxidative injury to Müller cells and explored the potential underlying mechanisms. Our results show that both melatonin membrane receptors, MT1 and MT2, are expressed in cultured primary Müller cells and are upregulated by elevated glucose levels. Both basal and high glucose-induced VEGF production was attenuated by melatonin treatment in a dose-dependent manner. Furthermore, we found that melatonin is a potent activator of Akt in Müller cells. Our findings suggest that in addition to functioning as a direct free radical scavenger, melatonin can elicit cellular signaling pathways that are protective against retinal injury during diabetic retinopathy

Melatonin-mediated inhibition of VEGF production from Müller cells.

<p>(A) Cells were treated with either 30 mM glucose (HG) or glucose and 100 µM melatonin (HG+Mel) for indicated time. The amount of VEGF secreted in the conditioned media was measured by ELISA. (B) Dose-dependent inhibition of VEGF production by melatonin. VEGF production was measured at 48 hr after high glucose stimulation in the presence of different concentrations of melatonin. Data presented are the average of 2 separate experiments. *P<0.05 one-way ANOVA and Tukey’s post-hoc test.</p

Primer sequences for RT-PCR analyses.

<p>Primer sequences for RT-PCR analyses.</p

High glucose-induced upregulation of melatonin receptors in Müller cells.

<p>(A) Immunostaining of MT1 and MT2 in cultured primary rat Müller cells. Nuclei were counterstained with SYTO green, Scale bar = 20 µm. (B) High glucose-induced mRNA expression of both melatonin receptors. Cells were treated with 30 mM glucose for 24 and 48 hr. MT1/MT2 expression was measured by Real-time RT-PCR and normalized to β-actin mRNA. CTL: untreated control; Mann: 24.5 mM mannitol as osmolarity control. (C) Western blot of MT1/MT2 proteins in Müller cells treated with high glucose. (D) Quantification data from the Western blots after normalizing to β-actin. Data presented are the average from 3 to 5 separate experiments (mean ± SD). *P<0.05, **P<0.01, as determined by either one-way ANOVA (B) or Student’s t-test (D).</p

Effects of melatonin on Nrf2 expression and localization in Müller cells.

<p>(A) The mRNA level of Nrf2 was measured by real-time RT-PCR after 24 and 48 hr exposure to high glucose with or without melatonin. (B) Immunostaining of Nrf2 localization after high glucose and melatonin treatment. The nuclei were counterstained with DAPI. Scale bar = 5 µm. (C) Western blot analyses of Nrf2 protein after 24 and 48 hr treatment. (D) Effects of luzindole on Nrf2. Data presented are representative of three independent experiments. (*P<0.05).</p

Protection against high glucose-induced oxidative stress by melatonin.

<p>(A) Measurement of cellular glutathione contents in Müller cells exposed to high glucose. Cells were treated with 30 mM glucose (HG) alone or in together with 0.1 mM melatonin (Mel), 50 µM luzindole (Luz) or 50 µM LY294002 (Ly2). Glutathione was measured by the DTNB method. (B) Upregulation of GCLc and GCLm measured by real-time RT-PCR and normalized to β-actin mRNA. (C) Western blot analyses of HO-1 expression after co-treatment with high glucose and indicated concentrations of melatonin (Mel). (D) Effects of luzindole on melatonin-induced upregulation of HO-1. Data presented are average from 3 to 5 experiments (*P<0.05; **P<0.01).</p