Background: MicroRNA-129 (miR-129) is a tumor suppressor involved in regulating oncogenic pathways, but its role in gastric adenocarcinoma and its potential connections to vascular and neurological dysfunction remain insufficiently defined. Objectives: To assess gastric juice-derived miR-129 as a diagnostic and prognostic biomarker for gastric cancer and to explore its associations with systemic inflammation, vascular impairment, and neurodegenerative changes. Methods: A prospective study was conducted in 38 patients undergoing upper gastrointestinal endoscopy (22 with histologically confirmed gastric adenocarcinoma, 16 controls). Gastric juice was aspirated prior to biopsy, and miR-129-2-3p expression was quantified by means of RT-qPCR normalized to U6 RNA. Tumor stage, serum biomarkers (CEA, CA 19-9, LDH, and CRP), carotid index (Doppler ultrasound), and neuroimaging (MRI) were recorded. Statistical analyses included ANOVA, Mann–Whitney U, ROC curve analysis, and correlation testing. Results: miR-129 expression was significantly reduced in gastric cancer compared with controls (ANOVA: F(3,34) = 3.70, p = 0.021, η² = 0.25). ΔCt values increased progressively from controls to T2–T4 tumors, indicating stage-dependent downregulation. ROC analysis demonstrated moderate diagnostic performance (AUC = 0.75, 95% CI 0.54–0.92). Lower miR-129 levels correlated inversely with serum tumor markers (CEA, CA 19-9), LDH, and CRP. Patients with elevated carotid index (>1.3) and abnormal brain imaging findings exhibited significantly lower miR-129 expression (both p < 0.05). Conclusion: Gastric juice-derived miR-129 is downregulated in gastric adenocarcinoma, with progressive decline across tumor stages. Its inverse association with systemic tumor and inflammatory markers, as well as vascular and neurological impairment, suggests that miR-129 may function as a minimally invasive, multi-system biomarker for integrated cancer and vascular–neurological risk assessment.

Background/Objectives: Periodontitis has been linked to ischemic stroke through systemic inflammation, but the evidence remains inconsistent. We examined whether C-reactive protein (CRP), the neutrophil-to-lymphocyte ratio (NLR) and periodontal status are associated with a history of ischemic stroke. Methods: This retrospective cross-sectional study included 346 adults aged 30–82 years who underwent a full-mouth periodontal examination at a military hospital in Sibiu, Romania, between May 2022 and October 2024. Associations were estimated with Firth penalized logistic regression adjusted for age and sex, and discrimination was described with receiver operating characteristic curves. Results: Twenty-four patients (6.9%) had a history of ischemic stroke and 215 (62.1%) had periodontitis. CRP and NLR were higher in patients with prior stroke (median 13.5 vs. 5.0 mg/L and 11.6 vs. 4.6) and remained associated with stroke after adjustment (NLR: odds ratio [OR] 1.62 per unit, 95% confidence interval [CI] 1.40–1.96; CRP: OR 1.43 per mg/L, 95% CI 1.28–1.64). Periodontitis was not significantly associated with stroke (adjusted OR 1.74, 95% CI 0.71–4.83), CRP or NLR. CRP and NLR were strongly correlated (ρ = 0.94), and their separate contributions could not be distinguished. Conclusions: A history of ischemic stroke was associated with higher CRP and NLR but not with periodontal status. Because of the cross-sectional design and the small number of events, these markers may reflect the consequences of stroke and should not be interpreted as predictors of stroke risk.

Background: Styloid process abnormalities, classically associated with Eagle syndrome, have increasingly been implicated in cerebrovascular events through mechanical interaction with cervical vessels. Methods: This study combined a structured narrative review of the relationship between styloid process anatomy and internal carotid artery dissection with a single-center retrospective observational cohort. Consecutive patients with acute ischemic stroke were evaluated to identify cases of extracranial internal carotid artery dissection, in whom styloid process anatomy, carotid morphology, and potential mechanical triggers were subsequently assessed. The narrative review was supported by a structured PubMed/MEDLINE search and a PRISMA-style study-selection process. No formal meta-analysis was performed, and the institutional cohort did not include an age- and sex-matched control group. Results: The literature search identified 34 eligible reports for the narrative synthesis. Among 1621 consecutive ischemic stroke admissions, 17 patients (1.04%) had extracranial internal carotid artery dissection. Elongated styloid processes (≥30 mm) were identified in 11/17 patients (64.7%), and carotid tortuosity was present in 10/17 patients (58.8%). Several patients had identifiable mechanical or traumatic precipitating factors. Conclusions: Styloid process elongation and carotid tortuosity were frequently observed in patients with extracranial internal carotid artery dissection. These findings support careful assessment of styloid–carotid anatomy in selected patients with carotid dissection. However, the small sample size, retrospective design, and absence of a control group preclude causal inference and require validation in larger controlled studies.

Background: Parenchymal fluid-attenuated inversion recovery (FLAIR) hyperintensity within an acute diffusion-weighted imaging (DWI) lesion is a marker of ischemic tissue evolution, but whether it identifies patients at higher risk of hemorrhagic transformation after mechanical thrombectomy (MT) is uncertain. Methods: We conducted a structured narrative review of cohort studies relating pretreatment lesion FLAIR signal to hemorrhage after reperfusion therapy. Four PubMed searches (1051 unique records) were supplemented by reference-list screening. Studies were classified by treatment, FLAIR construct and hemorrhage endpoint, and synthesized by direction and precision of effect without pooling. Results: Eleven cohort studies (49–412 patients each; 1726 in total) and one meta-analysis were included; four were MT or MT-predominant cohorts. The point estimate favored more hemorrhage with FLAIR positivity in nine studies. Associations were consistent for any hemorrhage, which is dominated by hemorrhagic infarction (59% vs. 39% in an MT cohort; odds ratio 20.0 in an intravenous-thrombolysis cohort imaged within 3 h). For parenchymal hematoma and symptomatic hemorrhage, three studies reported significant associations, whereas the largest MT cohort (n = 412) found no significant difference in parenchymal hematoma type 2 (10.7% vs. 6.8%, p = 0.193), and four further cohorts reported null or near-null estimates. No study isolated early-onset M1-occlusion patients with near-complete reperfusion. Conclusions: The evidence is directionally consistent but imprecise and does not show that FLAIR positivity independently predicts clinically important hemorrhage after MT. FLAIR positivity alone should not be used to withhold MT. Adequately powered studies with standardized FLAIR reading and separately reported parenchymal hematoma and symptomatic hemorrhage are needed.