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Space-occupying cerebellar infarction can be catastrophic, leading to brainstem compression, transtentorial herniation, and obstructive hydrocephalus. Herein, we investigated the association between the venous outflow pattern based on transverse sinus (TS) shape and the outcome of space-occupying cerebellar infarction. Patients with space-occupying cerebellar infarctions were enrolled, and data on baseline demographics, clinical factors, and venous outflow patterns, including the type of TS were collected. Low-functioning ipsilateral TS was defined as aplasia, occlusion, or hypoplasia on the side ipsilateral to the space-occupying cerebellar infarction. Conversely, properly functioning ipsilateral TS was defined as: 1) bilateral symmetric TS and 2) normal ipsilateral TS with aplasia, occlusion, or hypoplasia observed on the side contralateral to the space-occupying cerebellar infarction. The primary outcome was the attainment of a modified Rankin Scale (mRS) score of 0–2 at three months. Among 42 patients, low-functioning ipsilateral TS was observed in 17 (40.5 %). Initial National Institutes of Health Stroke Scale score was significantly higher in patients with properly functioning ipsilateral TS (0.0 [0.0–1.0] vs. 2.0 [1.0–3.0], P=0.010). Moreover, the primary outcome was significantly more favorable in patients with low-functioning ipsilateral TS (1.0 [1.0–2.0] vs. 3.0 [1.0–3.0], P=0.016). Multivariable logistic regression analysis showed that patients with low-functioning ipsilateral TS (P=0.040) was associated with functional independence. Patients with low-functioning ipsilateral TS exhibit more favorable outcomes than those with properly functioning ipsilateral TS in space-occupying cerebellar infarctions. The assessment of venous outflow functionality is a potential predictor of functional outcomes in space-occupying cerebellar infarctions. •We investigated the predictors of outcomes in space-occupying cerebellar infarction.•We focused on the venous outflow pattern based on transverse sinus (TS) shape.•Ipsilateral TS aplasia, hypoplasia, occlusion were associated with favorable outcomes.•Venous outflow might be a predictor of outcomes in space-occupying cerebellar infarctions.

Chronic kidney disease (CKD) increases blood pressure variability (BPV) and affects stroke outcomes. However, the effect of BPV on early neurological deterioration (END) may be different according to the renal function. We enrolled ischemic stroke patients with a National Institutes of Health Stroke Scale of [less than or equal to]5. END was defined as worsening of [greater than or equal to]1 point in motor power or [greater than or equal to]2 points in total score. BPV was calculated with BP measured during the first 5 days and presented as standard deviation (SD) and coefficient of variation (CoV). Renal function was classified using the Kidney Disease Improving Global Outcomes (KDIGO) classification of CKD. Variables were compared between those with (KDIGO classification: moderate- to very-high-risk) and without renal impairment (KDIGO classification: low-risk) and factors associated with END were investigated. Among the 290 patients (136 [46.9%] renal impairment), END was observed in 59 (20.3%) patients. BPV parameters and the risk of END increased as renal function was impaired. Renal function and systolic BP (SBP) mean, SD, CoV, and diastolic BP (DBP) mean, SD were independently associated with END. We found no association between BPV parameters and END in normal renal function patients; however, among impaired renal function patients, SBP SD (odds ratio [OR]: 1.20, 95% confidence interval [CI]: 1.09-1.32, P<0.001) and CoV (1.30 [1.12-1.50], P<0.001) were associated with END. The association between END and BPV parameters differs according to renal function in minor ischemic stroke; BPV was associated with END in patients with renal impairment, but less in those with normal renal function.

Background Detection of atrial fibrillation (AF) in patients with embolic stroke of undetermined source (ESUS) is important for the secondary prevention of stroke. We investigated the factors associated with the detection of newly diagnosed AF in ESUS patients during follow-up. Methods Patients with acute ischemic stroke classified as ESUS were included. All patients underwent transthoracic echocardiography and Holter to detect the source of embolism. Structural, electrophysiological markers of left atrial cardiopathy (i.e., left atrial enlargement [LAE], non-sustained tachycardia [NSAT]) as well as lesion patterns of ischemic stroke were examined. Implantable loop recorder (ILR) was implanted in selective patients. Sensitivity and positive predictive value analysis was used to assess the predictive value for AF detection. Results Among 312 patients with ESUS, AF was detected in 24 (7.7%) patients during follow-up. Patients with AF had a higher prevalence of LAE, NSAT, and the imaging pattern of confluent plus additional lesions in a single vascular territory. Multivariable analysis showed that ILR implantation (hazards ratio 11.497 [95% confidence interval 3.795–34.818]), LAE (3.204 [1.096–9.370]), NSAT (4.070 [1.378–12.018]), and confluent plus additional lesions (4.977 [1.649–15.019]) were independent predictors of AF detection. The sensitivity of detecting AF in those with LAE, NSAT, or confluent plus additional lesions pattern was 91.7%. The positive predictive value of detecting AF in those with LAE, NSAT and confluent plus additional lesions pattern was 40.0%. Conclusion In conclusion, patients with LAE, NSAT, or confluent plus additional lesions may benefit from ILR monitoring detecting new AF.

The risk of ischemic stroke with intracranial stenosis is associated with various serum lipid levels. However, the effects of changes in the lipid profile on the risk of in-stent restenosis have not been verified. Therefore, we investigated the association between the occurrence of in-stent restenosis at 12-month follow-up and changes in various lipid profiles. In this retrospective cohort study, we included ischemic stroke patients who had undergone intracranial stenting for symptomatic intracranial stenosis between February 2010 and May 2020. We collected data about serum low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC), and triglyceride (TG) levels, and calculated the TC/HDL-C and LDL-C/HDL-C ratios at baseline and after 12 months. We conducted multivariable logistic regression analyses to verify the association between various lipid profile changes and in-stent restenosis at 12 months. Among the 100 patients included in the study (mean age, 60.8 ± 10.0 years; male: 80 [80.0%]), in-stent restenosis was found in 13 (13.0%) patients. The risk of in-stent restenosis of more than 50% was significantly decreased when TC/HDL-C ratio (odds ratio [OR] 0.22, [95% confidence interval (CI) 0.05-0.87]) and LDL-C/HDL-C ratio (OR 0.23, [95% CI 0.06-0.93]) decreased or when HDL-C levels (OR 0.10, [95% CI 0.02-0.63]) were increased at 12 months compared with baseline measurements. Improvement of HDL-C levels, TC/HDL-C ratio, and LDL-C/HDL-C ratio were associated with decreased risk of in-stent restenosis at 12-month follow-up. Management and careful monitoring of various lipid profiles including HDL-C levels, TC/HDL-C ratio, and LDL-C/HDL-C ratio may be important to prevent in-stent restenosis in patients with intracranial stenting.

Background Prognosis after vertebrobasilar stenting (VBS) may differ from that after carotid artery stenting (CAS). Here, we directly compared the incidence and predictors of in-stent restenosis and stented-territory infarction after VBS and compared them with those of CAS. Methods We enrolled patients who underwent VBS or CAS. Clinical variables and procedure-related factors were obtained. During the 3 years of follow-up, in-stent restenosis and infarction were investigated in each group. In-stent restenosis was defined as reduction in the lumen diameter > 50% compared with that after stenting. Factors associated with the occurrence of in-stent restenosis and stented-territory infarction in VBS and CAS were compared. Results Among 417 stent insertions (93 VBS and 324 CAS), there was no statistical difference in in-stent restenosis between VBS and CAS (12.9% vs. 6.8%, P  = 0.092). However, stented-territory infarction was more frequently observed in VBS than in CAS (22.6% vs. 10.8%; P  = 0.006), especially a month after stent insertion. HbA1c level, clopidogrel resistance, and multiple stents in VBS and young age in CAS increased the risk of in-stent restenosis. Diabetes (3.82 [1.24–11.7]) and multiple stents (22.4 [2.4–206.4]) were associated with stented-territory infarction in VBS. However, in-stent restenosis (odds ratio: 15.1, 95% confidence interval: 3.17–72.2) was associated with stented-territory infarction in CAS. Conclusions Stented-territory infarction occurred more frequently in VBS, especially after the periprocedural period. In-stent restenosis was associated with stented-territory infarction after CAS, but not in VBS. The mechanism of stented-territory infarction after VBS may be different from that after CAS.

Two different stroke mechanisms are involved in small vessel disease: branch atheromatous disease (BAD) and lipohyalinotic degeneration (LD). We compared mechanisms of stroke in lenticulostriate arteries (LSA) vs. anterior pontine arteries (APA) and verified factors associated with stroke mechanisms, including shape of middle cerebral artery (MCA) and basilar artery (BA). We retrospectively reviewed patients with acute ischemic stroke with penetrating artery territory confirmed by MRI. The mechanisms of stroke were categorized based on diffusion-weighted imaging; BAD was defined as lesion larger than 10 mm in LSA and lesions involving basal pontine in APA. Other lesions were classified as LD. The shapes of MCA and BA were classified as straight, with one angle, or with two angles (U, C or S shape, respectively) using anterior–posterior view. The study included 221 patients. LD was more common in LSA infarcts, but BAD was more common in APA infarcts (p < 0.001). Low initial National Institutes of Health Stroke Scale [Adjusted Odds ratio (aOR) = 0.78; p < 0.001], absence of hyperlipidemia [aOR = 0.31; p = 0.002], previous statin use [aOR = 4.35; p = 0.028] LSA infarcts [reference = APA territory; aOR = 11.07; p < 0.001], and S-shaped vessels (reference = straight shaped vessels; aOR = 3.51; p = 0.004) were independently associated with LD. Angulations in the mother vessels may be more associated with true small vessel disease more with LD than BAD.

BackgroundWe aimed to investigate the radiation dose to the eye lens (lens dose) during cerebral angiography and to evaluate the effectiveness of the lens dose reduction protocol for 3-dimensional rotational angiography (3D-RA) in reducing overall lens dose exposure.MethodsWe conducted a randomized, controlled clinical trial at a tertiary hospital with patients undergoing cerebral angiography. The lens dose reduction protocol in 3D-RA involved raising the table to position the patient’s eye lens away from the rotation axis. The lens dose was estimated by measuring the entrance surface air kerma using a photoluminescent glass dosimeter. The lens doses of 3D-RA, overall examination, and image quality were analyzed and compared between the two groups.ResultsA total of 20 participants (mean age, 58±9.4 years; including 12 men [60%]) were enrolled and randomly assigned to either the conventional group or the dose reduction group. The median lens dose in 3D-RA was significantly lower in the dose reduction group compared with the conventional group (1.1 mGy vs 4.5 mGy, p<0.001). The total dose was significantly lower in the dose reduction group (median of 7.5 mGy vs 10.2 mGy, p=0.003). In the conventional group, 3D-RA accounted for 46% of the total lens dose, while in the dose reduction group, its proportion decreased to 16%. No significant differences were observed in the image quality between the groups.ConclusionThe lens dose reduction protocol resulted in a significant reduction in the lens dose of the 3D-RA as well as entire cerebral angiography, while maintaining the image quality.

Three-dimensional rotational angiography (3D-RA) is increasingly used for the evaluation of intracranial aneurysms (IAs); however, radiation exposure to the lens is a concern. We investigated the effect of head off-centering by adjusting table height on the lens dose during 3D-RA and its feasibility in patient examination. The effect of head off-centering during 3D-RA on the lens radiation dose at various table heights was investigated using a RANDO head phantom (Alderson Research Labs). We prospectively enrolled 20 patients (58.0 ± 9.4 years) with IAs who were scheduled to undergo bilateral 3D-RA. In all patients' 3D-RA, the lens dose-reduction protocol involving elevation of the examination table was applied to one internal carotid artery, and the conventional protocol was applied to the other. The lens dose was measured using photoluminescent glass dosimeters (GD-352M, AGC Techno Glass Co., LTD), and radiation dose metrics were compared between the two protocols. Image quality was quantitatively analyzed using source images for image noise, signal-to-noise ratio, and contrast-to-noise ratio. Additionally, three reviewers qualitatively assessed the image quality using a five-point Likert scale. The phantom study showed that the lens dose was reduced by an average of 38% per 1 cm increase in table height. In the patient study, the dose-reduction protocol (elevating the table height by an average of 2.3 cm) led to an 83% reduction in the median dose from 4.65 mGy to 0.79 mGy ( < 0.001). There were no significant differences between dose-reduction and conventional protocols in the kerma area product (7.34 vs. 7.40 Gy·cm², = 0.892), air kerma (75.7 vs. 75.1 mGy, = 0.872), and image quality. The lens radiation dose was significantly affected by table height adjustment during 3D-RA. Intentional head off-centering by elevation of the table is a simple and effective way to reduce the lens dose in clinical practice.

HOCl is a highly reactive and biologically important reactive oxygen species. Yoon and co-workers describe how to prepare a rhodamine-based probe that is specific for HOCl and is suitable for imaging experiments in Drosophila and mouse cells. During infection, nicotinamide adenine dinucleotide phosphate-oxidase of innate immune cells generates important microbicidal reactive oxygen species (ROS) such as hypochlorous acid (HOCl) to kill the invading pathogens. However, excess amounts of HOCl induce oxidative damage of functional biomolecules such as DNA and proteins, which may cause chronic inflammatory diseases. Herein, we outline protocols for the preparation of a rhodamine-based HOCl probe, as well as applications thereof, with which to detect HOCl in living cells and organisms. The probe (R19S) can be prepared from a commercially available rhodamine, rhodamine 6G, in two steps. When R19S is treated with HOCl, the sulfur atom is replaced by an oxygen atom, resulting in opening of the lactone ring; thus, nonfluorescent R19S is converted to highly fluorescent rhodamine 19 (R19). R19S exhibits high selectivity for HOCl over other ROS and high sensitivity in a weakly acidic environment. In addition, we describe fluorescence imaging assays of HOCl in mouse neutrophils and Drosophila targeted using this probe. The approximate amount of time required to synthesize the probe is 2–3 d, after which it can be used for up to 5 h in the bioimaging of living cells.

Pseudomonas aeruginosa is an opportunistic pathogen, known to develop robust biofilms. Its biofilm development increases when antibiotics are presented at subminimal inhibitory concentrations (MICs) for reasons that remain unclear. In order to identify genes that affect biofilm development under such a sublethal antibiotic stress condition, we screened a transposon (Tn) mutant library of PAO1, a prototype P. aeruginosa strain. Among ∼5000 mutants, a fiuA gene mutant was verified to form very defective biofilms in the presence of sub-MIC carbenicillin. The fiuA gene encodes ferrichrome receptor A, involved in the iron acquisition process. Of note, biofilm formation was not decreased in the ΔpchΔpvd mutant defective in the production of pyochelin and pyoverdine, two well-characterized P. aeruginosa siderophore molecules. Moreover, ΔfiuA, a non-polar fiuA deletion mutant, produced a significantly decreased level of elastase, a major virulence determinant. Mouse airway infection experiments revealed that the mutant expressed significantly less pathogenicity. Our results suggest that the fiuA gene has pleiotropic functions that affect P. aeruginosa biofilm development and virulence. The targeting of FiuA could enable the attenuation of P. aeruginosa virulence and may be suitable for the development of a drug that specifically controls the virulence of this important pathogen. Antibiotics stimulate biofilm formation in P. aeruginosa for reasons to be further explored. A mutant of ferrichrome receptor A was defective in antibiotic-inducible biofilm formation and exhibited concomitant virulence attenuation.