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Ear filling injection of hyaluronic acid (HA) is emerging as a new application of HA filling in clinical practice. However, its risks and complications have not been sufficiently investigated. Herein, we report a case of 25-year-old female with embolization of ophthalmic artery, a severe complication caused by ear filling of HA. Injection of HA at the triangular fossa immediately induced amaurosis and dizziness, and complete loss of light sensation in the right eye 10 min after injection. These symptoms did not resolve after emergency treatment, and she was sent to our hospital for treatment. A diagnosis of central retinal arterial occlusion (CRAO) was made, for which the patient received intravascular interventional therapy as an emergency treatment. Following surgery, the patient received a multifaceted treatment approach to promote nerve health, improve blood circulation, reduce edema, and enhance oxygen delivery through hyperbaric oxygen therapy. This treatment regimen restored light perception and resolved mottled skin discoloration. This case report expands our understanding of the potential mechanisms and anatomical factors involved in embolization associated with ear filler injections. Furthermore, it highlights the importance of prompt intervention, providing valuable insights for reducing the complication rate and improving patient outcomes following such procedures.Level of Evidence IV This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

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BACKGROUND: Growing demand for facial rejuvenation drives advancements in these therapies, including laser, radiofrequency, and focused ultrasound, alongside thermal stimulation adjuncts. These methods, known for stimulating collagen regeneration, skin tightening, and lifting, have gained popularity due to their minimal side effects, low trauma, and high safety, demonstrating favorable outcomes in clinical practice. OBJECTIVE: We sought to assess the efficacy of ultrasound skin tightening for brow lift within the scope of a procedure addressing facial sagging across the entire face. Our aim was to explore a noninvasive method capable of effectively enhancing mild to moderate brow ptosis by tightening and lifting the skin in the upper facial region. METHODS: This was a rater-blinded, prospective cohort study. The upper facial region of the participants was treated with the new device, micro-focused ultrasound (MFU), in model D3.0/D2.0/M3.0. Outcomes of brow lift were measured in comparison of pretreatment and posttreatment photographs and three-dimensional (3D) vector analysis. RESULTS: A total of 42 participants (37 females) were enrolled, with 2 participants withdrawing from the trial, resulting in 40 subjects who completed 180-day-follow-up and evaluation. 35 (87.5%) were deemed to have clinically significant brow elevation by two blinded assessors (experienced clinicians) at 180-day posttreatment (p < 0.01). The mean change in brow height after 90-day was 2.16 ± 0.63 mm at the frontal position (straight-ahead gaze) (p < 0.01). The 3D vector analysis reveals varying magnitudes of vector displacement in the upward and outward directions of the skin on the frontal region above the eyebrows. CONCLUSION: Focused ultrasound appears to be a safe and effective method for upper facial skin rejuvenation. A single focused ultrasound treatment on the forehead and temple areas resulted in an average brow elevation of 2.1 mm.

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Poly-L-lactic acid (PLLA), a well-established biostimulator that induces collagenases, is widely used among clinical practice to treat skin aging. However, the precise regulatory effect of PLLA on different dermal cell subsets beyond fibroblast has not been fully elucidated. In this study, we constructed in vivo PLLA injection and in vitro PLLA-adipocyte co-culture models to analyze the regulatory effects of PLLA on the volume, differentiation, lipolysis, and thermogenic capacity of dermal adipocyte. We found that PLLA injection significantly reduced the thickness of dermal fat in mice. In co-culture assay, PLLA showed no effect on adipogenesis, but stimulated the lipolysis activity. Interestingly, PLLA also enhanced the differentiation of fat cells into beige fat cells, which possess higher thermogenic capacity. In mechanical study, we blocked adipocyte lactate uptake with a monocarboxylate transporter (MCT1/4) inhibitor and found that the regulatory effect of PLLA on dermal adipocyte relies on its metabolite lactate. In summary, our results suggest that PLLA has complex regulatory effects on the dermal cells, and its ability to improve skin aging is not fully attributed to stimulating collagen synthesis, but also partially involves adipocytes.No Level Assigned This journal requires that authors assign a level of evidence to each submission to which Evidence-Based Medicine rankings are applicable. This excludes Review Articles, Book Reviews, and manuscripts that concern Basic Science, Animal Studies, Cadaver Studies, and Experimental Studies. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

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The inflammatory response plays a vital role in cerebral aneurysm (CA) formation and progression. Tanshinone  IIA (Tan IIA) is one of the major active components of Chinese medicine Danshen (Salvia miltiorrhiza Bunge) and is widely used for the treatment of cardiovascular diseases, due to its anti­inflammatory effects. The aim of the present study was to investigate whether Tan IIA can attenuate CA formation in rat models, and determine its underlying mechanisms. CAs were induced in rats surgically and through high­salt diet treatments. The Tan IIA­treated group displayed relatively mild symptoms, as compared with the control group. Tan IIA treatment reduced macrophage infiltration and nuclear factor (NF)­κB activation in aneurysmal walls. Next, lipopolysaccharide (LPS)­stimulated RAW 264.7 murine macrophage cells were used to examine the anti­inflammatory effects of Tan IIA on macrophages. It was found that Tan IIA reversed LPS­induced differentiation of RAW 264.7 cells and suppressed NF­κB pathway activation. In conclusion, these findings demonstrated that Tan IIA can suppress CA formation by inhibiting inflammatory responses in macrophages.

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The present study examines the hypothesis that endogenous neural progenitor cells isolated from the neocortex of ischemic brain can differentiate into neurons or glial cells and contribute to neural regeneration. We performed middle cerebral artery occlusion to establish a model of cerebral ischemia/reperfusion injury in adult rats. Immunohistochemical staining of the cortex 1, 3, 7, 14 or 28 days after injury revealed that neural progenitor cells double-positive for nestin and sox-2 appeared in the injured cortex 1 and 3 days post-injury, and were also positive for glial fibrillary acidic protein. New neurons were labeled using bromodeoxyuridine and different stages of maturity were identified using doublecortin, microtubule-associated protein 2 and neuronal nuclei antigen immunohistochemistry. Immature new neurons coexpressing doublecortin and bromodeoxyuridine were observed in the cortex at 3 and 7 days post-injury, and semi-mature and mature new neurons double-positive for microtubule-associated protein 2 and bromodeoxyuridine were found at 14 days post-injury. A few mature new neurons coexpressing neuronal nuclei antigen and bromodeoxyuridine were observed in the injured cortex 28 days post-injury. Glial fibrillary acidic protein/bromodeoxyuridine double-positive astrocytes were also found in the injured cortex. Our findings suggest that neural progenitor cells are present in the damaged cortex of adult rats with cerebral ischemic brain injury, and that they differentiate into astrocytes and immature neurons, but most neurons fail to reach the mature stage.

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Several lines of direct evidence show that gliomas express high levels of vascular endothelial growth factor (VEGF). VEGF can promote the growth of gliomas through angiogenesis. It is believed that gliomas originate in the brain tumor stem cells (BTSCs). However, the direct effect of VEGF on the biological behavior of BTSCs has not been completely elucidated. In this study, we established C6 glioma stem cells (C6GSCs) from the C6 glioma cells. Furthermore, we suppressed the VEGF expression of C6GSCs using lentiviral vector-VEGF shRNA. After transfection, the VEGF expression of C6GSCs was downregulated significantly. The proliferation and invasion capacity of transfected C6GSCs was impaired and the ability of differentiation was enhanced. The data demonstrate that downregulation of VEGF expression attenuates malignant biological behavior of C6GSCs. RNA interference of VEGF expression implies an effective anti-gliomas strategy.

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Although it is believed that glioma is derived from brain tumor stem cells, the source and molecular signal pathways of these cells are still unclear. In this study, we used stable doxycycline-inducible transgenic mouse brain tumor models (c-myc(+)/SV40Tag(+)/Tet-on(+)) to explore the malignant trans-formation potential of neural stem cells by observing the differences of neural stem cells and brain tumor stem cells in the tumor models. Results showed that chromosome instability occurred in brain tumor stem cells. The numbers of cytolysosomes and autophagosomes in brain tumor stem cells and induced neural stem cells were lower and the proliferative activity was obviously stronger than that in normal neural stem cells. Normal neural stem cells could differentiate into glial fibrillary acidic protein-positive and microtubule associated protein-2-positive cells, which were also negative for nestin. However, glial fibrillary acidic protein/nestin, microtubule associated protein-2/nestin, and glial fibrillary acidic protein/microtubule associated protein-2 double-positive cells were found in induced neural stem cells and brain tumor stem cells. Results indicate that induced neural stem cells are similar to brain tumor stem cells, and are possibly the source of brain tumor stem cells.