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In this work, the effect of vacuum ion-plasma treatment on the wear resistance of the medical screws surface made of VT6 titanium alloy is studied as well as on the mechanical characteristics of the screws in contact with the plate for osteosynthesis. It is shown that the TiN titanium nitride deposition on the screw head increases the surface microhardness by 3 times and also provides lowering the torque during removal of the screw out of the plate.

Background: Rete middle cerebral artery (MCA) is a rare anomaly of the intracranial circulation that mimics congenital Moyamoya disease (MMD). Similar to MMD, it is reported almost exclusively in East-Asian ethnicities. Here, we report 13 patients with rete MCA anomaly from a predominantly non-Asian background in the USA., Methods: Consecutive patients (≥18 years of age) with rete MCA seen in the neurovascular clinic at Columbia University Medical Center (2014-2024) were included. We retrieved demographics, clinical presentation, imaging findings, neurosurgical interventions, and clinical outcomes., Results: 13 patients were identified (mean age 42±21 years, 83.3% female): 7 were White (53.8%), 3 were multiracial Hispanic (23.1%), 2 were South-Asian (15.4%), and 1 was Black (7.7%). Rete MCA was unilateral in all (n=13) and collaterals typical of MMD were absent. MRI vessel wall imaging (n=6) did not show enhancement characteristic of MMD. With serial imaging (n=12), there was no progression or contralateral MCA involvement. Strokes occurred in 5 (38.5%): subarachnoid hemorrhage (n=2), intracerebral hemorrhage (n=2), and ischemic stroke (n=1) from cardioembolism (n=1). 5 (38.5%) underwent neurosurgical bypass (encephaloduroarteriosynangiosis) due to presumed initial diagnosis of MMD (n=4), or for hypoperfusion on imaging related to rete MCA (n=1). Over a 4±3-year mean follow-up, there were no acute neurovascular events., Conclusions: Rete MCA anomaly occurs in non-Asian populations, and is likely benign relative to MMD. The diagnosis should be considered with unilateral, non-progressive findings, and absent MMD-type collaterals. Neurosurgical bypass appears safe, but studies are required to assess the natural history and stroke risk in this condition., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2024. No commercial re-use. See rights and permissions. Published by BMJ Group.)

Gliomas and Glioblastomas represent a significant portion of central nervous system (CNS) tumors associated with high mortality rates and variable prognosis. In 2021, the World Health Organization (WHO) updated its Glioma classification criteria, most notably incorporating molecular markers including CDKN2A/B homozygous deletion, TERT promoter mutation, EGFR amplification, + 7/-10 chromosome copy number changes, and others into the grading and classification of adult and pediatric Gliomas. The inclusion of these markers and the corresponding introduction of new Glioma subtypes has allowed for more specific tailoring of clinical interventions and has inspired a new wave of Radiogenomic studies seeking to leverage medical imaging information to explore the diagnostic and prognostic implications of these new biomarkers. Radiomics, deep learning, and combined approaches have enabled the development of powerful computational tools for MRI analysis correlating imaging characteristics with various molecular biomarkers integrated into the updated WHO CNS-5 guidelines. Recent studies have leveraged these methods to accurately classify Gliomas in accordance with these updated molecular-based criteria based solely on non-invasive MRI, demonstrating the great promise of Radiogenomic tools. In this review, we explore the relative benefits and drawbacks of these computational frameworks and highlight the technical and clinical innovations presented by recent studies in the landscape of fast evolving molecular-based Glioma subtyping. Furthermore, the potential benefits and challenges of incorporating these tools into routine radiological workflows, aiming to enhance patient care and optimize clinical outcomes in the evolving field of CNS tumor management, have been highlighted., (© 2024. The Author(s).)

Objectives: Although lower hemoglobin levels associate with worse intracerebral hemorrhage (ICH) outcomes, causal drivers for this relationship remain unclear. We investigated the hypothesis that lower hemoglobin relates to increased hematoma expansion (HE) risk and poor outcomes using human observational data and assessed causal relationships using a translational murine model of anemia and ICH., Methods: ICH patients with baseline hemoglobin measurements and serial CT neuroimaging enrolled between 2010-2016 to a multicenter, prospective observational cohort study were studied. Patients with systemic evidence of coagulopathy were excluded. Separate regression models assessed relationships of baseline hemoglobin with HE (≥33% and/or ≥6mL growth) and poor long-term neurological outcomes (modified Rankin Scale 4-6) after adjusting for relevant covariates. Using a murine collagenase ICH model with serial neuroimaging in anemic vs. non-anemic C57/BL6 mice, intergroup differences in ICH lesion volume, ICH volume changes, and early mortality were assessed., Results: Among 1190 ICH patients analyzed, lower baseline hemoglobin levels associated with increased odds of HE (adjusted OR per -1g/dL hemoglobin decrement: 1.10 [1.02-1.19]) and poor 3-month clinical outcomes (adjusted OR per -1g/dL hemoglobin decrement: 1.11 [1.03-1.21]). Similar relationships were seen with poor 6 and 12-month outcomes. In our animal model, anemic mice had significantly greater ICH lesion expansion, final lesion volumes, and greater mortality, as compared to non-anemic mice., Conclusions: These results, in a human cohort and a mouse model, provide novel evidence suggesting that anemia has causal roles in HE and poor ICH outcomes. Additional studies are required to clarify whether correcting anemia can improve these outcomes., Competing Interests: Potential Conflicts of Interest: none

Background and Objectives: Red blood cell (RBC) concentrations are known to associate with ischemic stroke. It is unclear whether RBC concentrations associate specifically with small vessel disease lacunar infarcts. We investigated the hypothesis that RBC concentrations associate with both chronic covert and acute symptomatic brain MRI lacunar infarcts., Methods: A cross-sectional observational analysis was performed across 2 cohorts with available hematocrit (as the assessment of RBC concentration exposure) and MRI outcome data. The primary setting was a population-based cohort of stroke-free, older adult (>50 years) participants from the Northern Manhattan Study (NOMAS) enrolled between 2003 and 2009. A second replication sample consisted of patients admitted with acute stroke and enrolled into the Columbia Stroke Registry (CSR) between 2005 and 2020. Associations of hematocrit with (1) chronic, covert lacunar infarcts and (2) symptomatic (i.e., acute) lacunar strokes were separately assessed from the NOMAS and CSR cohorts, respectively, using general additive models after adjusting for relevant covariates., Results: Of 1,218 NOMAS participants analyzed, 6% had chronic, covert lacunar infarcts. The association between hematocrit and these covert lacunar infarcts was U-shaped (χ 2 = 9.21 for nonlinear associations; p = 0.03), with people with hematocrit extremes being more likely to have covert lacunar infarcts. Of the 1,489 CSR patients analyzed, 23% had acute lacunar strokes. In this sample, only the relationships of increased hematocrit concentrations and lacunar strokes were replicated (adjusted coefficient β = 0.020; SE = 0.009; p = 0.03)., Discussion: We identified relationships of hematocrit with MRI lacunar infarcts in both stroke-free and ischemic stroke cohorts, respectively. The relationship between increased hematocrit concentrations with lacunar infarcts was replicated in both cohorts. Further studies are required to clarify the mechanisms behind the relationships of hematocrit with ischemic cerebral small vessel disease.