Background: Stroke is accompanied by a distinguished inflammatory reaction that is initiated by the infiltration of immunocytes, expression of cytokines, and other inflammatory mediators. As natural killer cells (NK cells) are a type of cytotoxic lymphocyte critical to the innate immune system, we investigated the mechanism of NK cells-induced brain injuries after cerebral ischemia and the chemotactic effect of IP-10 simultaneously. Methods: NK cells infiltration, interferon-gamma (IFN-γ) and IP-10 expression were detected by immunohistochemistry, immunofluorescence, PCR and flow cytometry in human and C57/BL6 wild type mouse ischemic brain tissues. The ischemia area was detected via 2,3,5-triphenyltetrazolium chloride staining. CXCR3 mean fluorescence intensity of isolated NK cells was measured by flow cytometry. The neuronal injury made by NK cells was examined via apoptosis experiment. The chemotactic of IP-10 was detected by migration and permeability assays. Results: In human ischemic brain tissue, infiltrations of NK cells were observed and reached a peak at 2 to 5 days. In a permanent middle cerebral artery occlusion (pMCAO) model, infiltration of NK cells into the ischemic infarct region reached their highest levels 12 hours after ischemia. IFN-γ-positive NK cells and levels of the chemokine IP-10 were also detected within the ischemic region, from 6 hours up to 4 days after pMCAO was performed, and IFN-γ levels decreased after NK cells depletion in vivo. Co-culture experiments of neural cells with NK cells also showed that neural necrosis was induced via IFN-γ. In parallel experiments with IP-10, the presence of CXCR3 indicates that NK cells were affected by IP-10 via CXCR3, and the effect was dose-dependent. After IP-10 depletion in vivo, NK cells decreased. In migration assays and permeability experiments, disintegration of the blood-brain barrier (BBB) was observed following the addition of NK cells. Moreover, in the presence of IP-10 this injury was aggravated. Conclusions: All findings support the hypothesis that NK cells participate in cerebral ischemia and promote neural cells necrosis via IFN-γ. Moreover, IP-10 intensifies injury to the BBB by NK cells via CXCR3.

2 Technical Efficacy: Stage 3 J. Magn. Reson. Imaging 2018;47:1350-1358.

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IntroductionThe aim of this study was to explore whether patients with chronic obstructive pulmonary disease (COPD) develop vasogenic cerebral edema, and whether this edema contributes to the COPD‐related disability.MethodsEighteen stable patients with COPD and 17 matched healthy volunteers were enrolled. Apparent diffusion coefficient (ADC) values were calculated by voxel‐based analysis using DTI‐Studio software based on diffusion tensor imaging. COPD‐related disability was calculated using activities of daily living (ADL) scale.ResultsIn patients with COPD, ADC increased in the white matter fiber tracts including the bilateral anterior cingulum and posterior corpus callosum and in the white matter fibers connecting the bilateral insular cortices, sub‐lobar cortices, and pars triangularis cortices and the left rectus and olfactory gyrus. However, after further controlling for cigarette smoking, the difference in ADC values in the posterior corpus callosum between groups disappeared. Patients with COPD had significantly higher scores in ADL than that in controls. Moreover, ADL scores were positively correlated with the increased regional ADC values.ConclusionVasogenic cerebral edema occurs in patients with COPD. Cigarette smoking may be a risk factor for COPD‐related vasogenic edema. Vasogenic cerebral edema may be related to the COPD‐related ADL impairment.

Extensive evidence supports the claim that serum neurofilament light chain (sNfL) can be used as a biomarker for monitoring disease severity in patients with spinocerebellar ataxia type 3 (SCA3). However, little is known about the associations between sNfL levels and neurochemical alterations in SCA3 patients. Serum samples were collected from ATXN3 mutation carriers (n = 20) and normal controls (n = 14). sNfL levels, measured by a single-molecule array, were compared between SCA3 patients and controls. We explored the relationship between sNfL levels and metabolic changes via magnetic resonance spectroscopy (MRS) scans. sNfL levels in SCA3 patients were higher than those in healthy controls, and these levels were correlated with disease severity. Associations emerged between the elevation of sNfL levels and lower brain metabolite changes, reflected as N-acetyl aspartate/creatine (NAA/Cr). These associations remained significant after multiple comparison corrections. Our results confirmed that serum sNfL levels are increased in SCA3 and are correlated with cerebellar hemisphere metabolic changes. Brain metabolic changes and sNfL levels show promise as potential complementary biomarkers for clinical trials for patients with SCA3.

Emotional and cardiac responses to audio erotica and their gender differences are relatively unclear in the study of the human sexual response. The current study was designed to investigate gender differences regarding positive and negative emotional responses to erotica, as well as its association with cardiac response. A total of 40 healthy participants (20 women) were exposed to erotic, neutral, and happy audio segments during which emotions and heart rate changes were evaluated. Our data showed distinct emotional responses to erotica between genders, in which women reported a higher level of shame than men and rated erotic audios as less pleasant than happy audios. Meanwhile, men reported erotic and happy audios as equally pleasant. These results were independent of cardiac changes, as both sexes demonstrated comparable heart rate deceleration when exposed to erotica relative to neutral and happy stimuli. Our results highlight the role of sociocultural modulation in the emotional response to erotica.