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Background: Situs inversus (SI) is a rare congenital anomaly in which systemic organs and vessels are positioned in a mirror image of their normal positions. An interesting issue regarding individuals with such a condition is whether they also have reversed brain asymmetries. Most of studies on this issue indicate that, similarly to many people with normal visceral alignment, patients with SI have a left hemispheric dominance for language functions. Case presentation: We report a rare occurrence of anomalous cerebral dominance for language in a patient with complete situs inversus. The right-handed patient developed aphasia after carotid stenting, and brain magnetic resonance imaging showed cerebral infarction in the right parietal lobe. Conclusion: Anomalous cerebral dominance for language and visceral situs inversus in our patient both may result from a single, genetically coded atypicality of developmental gradient. [ABSTRACT FROM AUTHOR]

Ischemic stroke is a major cerebrovascular disease resulting from a transient or permanent local reduction of cerebral blood flow. Angiogenesis plays an important role in cerebral microvascular repair after ischemic stroke. This study aimed at investigating the effect of NF-E2-related factor 2 (Nrf2) on the angiogenesis of mouse cerebral microvascular endothelial bEnd.3 cells in a hypoxic environment. We found that Nrf2 expression was temporarily increased in hypoxia-induced bEnd.3 cells. Knockdown of Nrf2 inhibited the proliferation, migration, as well as tube formation in hypoxia-induced bEnd.3 cells. Meanwhile, vascular endothelial growth factor and PI3K/Akt signaling pathways were identified to be regulated by Nrf2 in hypoxia-induced bEnd.3 cells. It was found that silencing of Nrf2 downregulated the expression levels of NAD(P)H:quinine oxidoreductase-1, vascular endothelial growth factor, p-Akt, and heme oxygenase-1 in hypoxia-induced bEnd.3 cells. Data suggested that hypoxia induced the transient increase of Nrf2, which plays a key role in the angiogenesis of cerebral microangiogenesis, and that Nrf2 regulates the proliferation, migration, as well as tube formation likely through PI3K/Akt signaling pathway in hypoxia-induced bEnd.3 cells. Our study provides proof of concept for the modulation of Nrf2, so as to tilt the balance toward angiogenesis, representing a therapeutic strategy for hypoxia or ischemia disorders such as stroke. Key words: angiogenesis, endothelial cells, hypoxia, NF-E2-related factor 2, vascular endothelial growth factor. Resume: L'accident vasculaire cerebral (AVC) ischemique est une condition pathologique cerebrovascular majeure qui resulte d'une reduction locale transitoire ou permanente du flux sanguin dans le cerveau. L'angiogenese joue un role important dans la reparation microvasculaire cerebrale a la suite de l'AVC ischemique. Cette etude visait a examiner l'effet de facteur Nrf2 ([much less than] NF-E2-related factor 2 [much greater than]) sur l'angiogenese des cellules endotheliales microvasculaires cerebrales de souris bEnd.3 dans un environnement hypoxique. Les auteurs ont trouve que l'expression de Nrf2 etait temporairement accrue chez les cellules bEnd.3 soumises a l'hypoxie. Le knockdown de Nrf2 inhibait la proliferation et la migration cellulaires, de meme que la formation de tube endothelial par les cellules bEnd.3 soumises a l'hypoxie. Parallelement, les voies de signalisation du facteur de croissance vasculaire endothelial et de la PI3K/Akt ont ete identifiees comme cibles regulees par Nrf2 chez les cellules bEnd.3 en hypoxie. Il appert que le silen[zeta]age de Nrf2 regulait a la baisse les niveaux d'expression de la NAD(P)H : quinine oxydoreductase-1, du facteur de croissance vasculaire endothelial, de p-Akt et de l'heme-oxygenase-1 dans les cellules bEnd.3 en hypoxie. Les donnees suggeraient que l'hypoxie induisait une elevation transitoire de Nrf2 qui joue un role cle dans la micro-angiogenese cerebrale, et que Nrf2 regulait la proliferation, la migration et la formation de tube endothelial vraisemblablement par l'intermediaire de la voie de signalisation PI3K/Akt chez les cellules bEnd.3 en hypoxie. L'etude des auteurs fournit une preuve de concept de la modulation de Nrf2 qui fait pencher la balance en faveur de l'angiogenese, constituant une strategie therapeutique dans l'hypoxie ou les conditions ischemiques comme l'AVC. [Traduit par la Redaction] Mots-cles: angiogenese, cellules endotheliales, hypoxie, Nrf2, facteur de croissance vasculaire endothelial., Introduction Stroke is one of the leading causes of death and serious long-term disability worldwide (Towfighi and Saver 2011). Ischemic stroke, resulting from focal cerebral ischemia due to occlusion of [...]

Purpose: Small dense low-density lipoprotein cholesterol (S-LDL-C) has been suggested as a particularly atherogenic factor for ischemic stroke (IS) in observational studies, but the causality regarding the etiological subtype remains unclear. This study aims to explore the causal effects of small dense low-density lipoprotein cholesterol (S-LDL-C), medium (M-LDL-C) and large (L-LDL-C) subfractions on the lifetime risk of ischemic stroke (IS) and main subtypes using two-sample Mendelian randomization (TSMR) design., Methods: We identified genetic instruments for S-LDL-C, M-LDL-C and L-LDL-C from a genome-wide association study of 115 082 UK Biobank participants. Summary-level data for genetic association of any ischemic stroke (AIS), large artery stroke (LAS), small vessel stroke (SVS) and cardioembolic stroke (CES) were obtained from MEGASTROKE consortium. Accounting for the pleiotropic effects of triglycerides (TG) and high-density lipoprotein cholesterol (HDL-C), we conducted multivariable TSMR analysis., Results: In univariable TSMR, we found a causal association between genetically predicted S-LDL-C and LAS (IVW-FE: odds ratio (OR) = 1.481, 95% confidence interval (CI): 1.117-1.963, P = 0.006, q = 0.076) but not AIS, SVS or CES. No causal effects were observed for M-LDL-C or L-LDL-C in terms of AIS and IS subtype. In multivariable analysis, the causal association between S-LDL-C and LAS remained significant (IVE-MRE: OR = 1.329, 95% CI: 1.106-1.597, P = 0.002)., Conclusions: Findings supported a causal association between S-LDL-C and LAS. Further studies are warranted to elucidate the underlying mechanism and clinical benefit of targeting S-LDL-C., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer Y-XC declared a shared affiliation with the author PL to the handling editor at the time of the review., (Copyright © 2024 Yu, Shen, Zhang, Cui, Zha, Li, Li, Wang and Nan.)

Bilateral medial medullary infarction is a rare stroke subtype, and its diagnosis has become possible by brain magnetic resonance imaging. In this report, we describe a case in which acute bilateral medial medullary infarction accompanied by cerebral watershed infarction was clearly identified by diffusion-weighted imaging, and we discuss the mechanisms of bilateral medial medullary infarction accompanied by cerebral watershed infarction., (Copyright Journal of Radiology Case Reports.)