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Penetrating brain injury caused by a nail is an extremely rare neurosurgical emergency that poses a challenge for neurosurgeons. Nail entering the brain from the orbit and lodging within the cranial cavity is even more unusual. A 53-year-old male was found unconscious at a construction site, and brain CT revealed not only the presence of a nail beneath the inner table of the parietal bone, but also traumatic intracerebral hematoma. Consequently, accurate localization of the nail and hematoma was mandatory for surgical plan. During surgical planning, computational model reconstruction and trajectory calculation were completed using preoperative CT in 3D Slicer. Under the guidance of a head-mounted mixed-reality holographic computer, the neurosurgeon was able to visualize and interact with the hologram of the surgical plan, and intraoperative findings demonstrated that our low-cost portable wearable mixed-reality holographic navigation assisted precise localization of the nail and intracerebral hematoma, assuring less injury to the already compromised brain. After the surgery, the patient could obey commands, and postoperative imaging ruled out the possibility of brain abscess during follow-up. To the best of our knowledge, this is the first report on using a low-cost wearable mixed-reality holographic navigation to guide the management of penetrating intracranial injury caused by a nail.We assessed extracranial contamination of the near-infrared spectroscopy (NIRS) signal during administration of phenylephrine. The study was performed with NIRO 200NX which employs both the Modified Beer-Lambert (MBL) method to measure total hemoglobin (tHb, expressed in µM), and Spatially Resolved Spectroscopy (SRS) to measure total hemoglobin content (nTHI, expressed in arbitrary units (a.u.)). SRS tends to not be affected by extracranial blood flow. As vasoconstriction with phenylephrine mainly occurs in the extracranial area, we hypothesized that if NIRS measurements are indeed prone to extracranial contamination, tHb will be more affected by the administration of phenylephrine than nTHI. After ethical committee approval, 20 consenting cardiac surgery patients were included. Phenylephrine was administered whenever clinically indicated and its effect on nTHI and tHb was evaluated. To adjust for the difference in raw scale units, Z-scores were calculated. Data were analyzed with Wilcoxon Signed Ranks Test and the Hodges-Lehmann method. A total of 191 data sets were obtained in 20 patients (10 male, 65 ± 15 years, 77 ± 16 kg, 166 ± 11 cm). The median difference before and after administration of phenylephrine was - 0.006 a.u. [95%CI - 0.010 to - 0.002] (p  less then  0.001) and - 0.415 µM [95%CI - 0.665 to - 0.205] (p  less then  0.001) for nTHI and tHb, respectively. The median difference between the Z-scores of nTHI and tHb was - 0.02 [95%CI - 0.04 to - 0.003] (p = 0.03), with a higher variability in the Z-scores of tHb. Phenylephrine induced significant larger changes in MBL values compared to SRS values, indicating that the MBL method might be more prone to extracranial contamination. Trial and clinical registry Trial registration number B670201939459, ethical committee number 2019/0265, date of approval March 19, 2019.Rapamycin (RAPA) is found to have neuro-protective properties in various neuroinflammatory pathologies, including brain aging. With magnetic resonance imaging (MRI) techniques, we investigated the effect of RAPA in a lipopolysaccharide (LPS)-induced inflammaging model in rat brains. Rats were exposed to saline (control), or LPS alone or LPS combined with RAPA treatment (via food over 6 weeks). Arterial spin labeling (ASL) perfusion imaging was used to measure relative cerebral blood flow (rCBF). MR spectroscopy (MRS) was used to measure brain metabolite levels. Contrast-enhanced MRI (CE-MRI) was used to assess blood-brain barrier (BBB) permeability. Immunohistochemistry (IHC) was used to confirm neuroinflammation. RAPA restored NF-κB and HIF-1α to normal levels. RAPA was able to significantly restore rCBF in the cerebral cortex post-LPS exposure (p less then 0.05), but not in the hippocampus. In the hippocampus, RAPA was able to restore total creatine (Cr) acutely, and N-acetyl aspartate (NAA) at 6 weeks, post-LPS. Myo-inositol (Myo-Ins) levels were found to decrease with RAPA treatment acutely post-LPS. RAPA was also able to significantly restore the BBB acutely post-LPS in both the cortex and hippocampus (p less then 0.05 for both). Caspofungin mw RAPA was found to increase the percent change in BOLD signal in the cortex at 3 weeks, and in the hippocampus at 6 weeks post-LPS, compared to LPS alone. RAPA treatment also restored the neuronal and macro-vascular marker, EphB2, back to normal levels. These results indicate that RAPA may play an important therapeutic role in inhibiting neuroinflammation by normalizing brain vascularity, BBB, and some brain metabolites, and has a high translational capability.How the heat shock axis, repair pathways, and proteostasis impact the rate of aging is not fully understood. Recent reports indicate that normal aging leads to a 50% change in several regulatory elements of the heat shock axis. Most notably is the age-dependent enhancement of inhibitory signals associated with accumulated heat shock proteins and hyper-acetylation associated with marked attenuation of heat shock factor 1 (HSF1)-DNA binding activity. Because exceptional longevity is associated with increased resistance to stress, this study evaluated regulatory check points of the heat shock axis in liver extracts from 12 months and 24 months long-lived Ames dwarf mice and compared these findings with aging wild-type mice. This analysis showed that 12M dwarf and wild-type mice have comparable stress responses, whereas old dwarf mice, unlike old wild-type mice, preserve and enhance activating elements of the heat shock axis. Old dwarf mice thwart negative regulation of the heat shock axis typically observed in usual aging such as noted in HSF1 phosphorylation at Ser307 residue, acetylation within its DNA binding domain, and reduction in proteins that attenuate HSF1-DNA binding. Unlike usual aging, dwarf HSF1 protein and mRNA levels increase with age and further enhance by stress. Together these observations suggest that exceptional longevity is associated with compensatory and enhanced HSF1 regulation as an adaptation to age-dependent forces that otherwise downregulate the heat shock axis.