Induced Inflammatory and Oxidative Markers in Cerebral Microvasculature by Mentally Depressive Stress.

Background: Cerebrovascular disease (CVD) is recognized as the leading cause of permanent disability worldwide. Depressive disorders are associated with increased incidence of CVD. The goal of this study was to establish a chronic restraint stress (CRS) model for mice and examine the effect of stress on cerebrovascular inflammation and oxidative stress responses. Methods: A total of forty 6-week-old male C57BL/6J mice were randomly divided into the CRS and control groups. In the CRS group (n = 20), mice were placed in a well-ventilated Plexiglas tube for 6 hours per day for 28 consecutive days. On day 29, open field tests (OFT) and sucrose preference tests (SPT) were performed to assess depressive-like behaviors for the two groups (n = 10/group). Macrophage infiltration into the brain tissue upon stress was analyzed by measuring expression of macrophage marker (CD68) with immunofluorescence in both the CRS and control groups (n = 10/group). Cerebral microvasculature was isolated from the CRS and controls (n = 10/group). mRNA and protein expressions of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), interleukin-6 (IL-6), vascular cell adhesion molecule-1 (VCAM-1), and macrophage chemoattractant protein-1 (MCP-1) in the brain vessels were measured by real-time PCR and Western blot (n = 10/group). Reactive oxygen species (ROS), hydrogen peroxide (H2O2), and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) activities were quantified by ELISA to study the oxidative profile of the brain vessels (n = 10/group). Additionally, mRNA and protein expressions of NOX subunits (gp91phox, p47phox, p67phox, and p22phox) in the cerebrovascular endothelium were analyzed by real-time PCR and Western blot (n = 10/group). Results: CRS decreased the total distances (p < 0.05) and the time spent in the center zone in OFT (p < 0.001) and sucrose preference test ratio in SPT (p < 0.01). Positive ratio of CD68+ was increased with CRS in the entire region of the brain (p < 0.001), reflecting increased macrophage infiltration. CRS increased the expression of inflammatory factors and oxidative stress in the cerebral microvasculature, including TNF-α (p < 0.001), IL-1ß (p < 0.05), IL-6 (p < 0.05), VCAM-1 (p < 0.01), MCP-1 (p < 0.01), ROS (p < 0.001), and H2O2 (p < 0.001). NADPH oxidase (NOX) was activated by CRS (p < 0.01), and mRNA and protein expressions of NOX subunits (gp91phox, p47phox, p67phox, and p22phox) in brain microvasculature were found to be increased. Conclusions: To our knowledge, this is the first study to demonstrate that CRS induces depressive stress and causes inflammatory and oxidative stress responses in the brain microvasculature.

MicroRNA-29b Suppresses Inflammation and Protects Blood-Brain Barrier Integrity in Ischemic Stroke.

Objectives: Following cerebral ischemia, microRNA- (miR-) 29b in circulating blood is downregulated. This study investigates the underlying mechanism and implications of miR-29b in leukocyte induction. Methods: miR-29b from stroke patients and rats with middle cerebral artery occlusion (MCAO) were assessed using real-time polymerase chain reaction (PCR). miR-29b agomir was used to increase miR-29b expression in leukocytes via intravenous injection. C1q and tumor necrosis factor (C1QTNF) 6, interleukin- (IL-) 1ß, zonula occludens- (ZO-) 1, occludin, and ischemic outcomes were assessed in MCAO rats. Additionally, hCMEC/D3 cells were subjected to oxygen-glucose deprivation (OGD) and cocultured with HL-60 cells. Results: miR-29b levels in neutrophils were found to be significantly lower in stroke patients compared with healthy controls, which may indicate its high diagnostic sensitivity and specificity for stroke. Moreover, miR-29b levels in leukocytes showed a negative correlation with National Institute of Health Stroke Scale (NIHSS) scores and C1QTNF6 levels. In MCAO rats, miR-29b overexpression reduced brain infarct volume and brain edema, decreasing IL-1ß levels in leukocytes and in the brain 24 hours poststroke. miR-29b attenuated IL-1ß expression via C1QTNF6 inhibition, leading to decreased blood-brain barrier (BBB) disruption and leukocyte infiltration. Moreover, miR-29b overexpression in HL-60 cells downregulated OGD-induced hCMEC/D3 cell apoptosis and increased ZO-1 and occludin levels in vitro. Conclusion: Leukocytic miR-29b attenuates inflammatory response by augmenting BBB integrity through C1QTNF6, suggesting a novel miR-29b-based therapeutic therapy for ischemic stroke.

Vestibular function is associated with immune inflammatory response.

Association between vestibular function and immune inflammatory response has garnered increasing interest. Immune responses can lead to anatomical or functional alterations of the vestibular system, and inflammatory reactions may impair hearing and balance. Vestibular disorders comprise a variety of conditions, such as vestibular neuritis, benign paroxysmal positional vertigo, Meniere's disease, vestibular migraine, posterior circulation ischemia, and bilateral vestibular disease. Moreover, some patients with autoimmune diseases develop vestibulocochlear symptom. This paper offers an overview of prevalent vestibular diseases and discusses associations between vestibular dysfunction and immune diseases.

Risk factors for not reaching minimal clinically important difference at 90 days and 1 year after elective lumbar spine surgery: a cohort study.

OBJECTIVE: Patient-perceived functional improvement is a core metric in lumbar surgery for degenerative disease. It is important to identify both modifiable and nonmodifiable risk factors that can be evaluated and possibly optimized prior to elective surgery. This case-control study was designed to study risk factors for not achieving the minimal clinically important difference (MCID) in Patient-Reported Outcomes Measurement Information System Function 4-item Short Form (PROMIS PF) score. METHODS: The authors queried the Michigan Spine Surgery Improvement Collaborative database to identify patients who underwent elective lumbar surgical procedures with PROMIS PF scores. Cases were divided into two cohorts based on whether patients achieved MCID at 90 days and 1 year after surgery. Patient characteristics and operative details were analyzed as potential risk factors. RESULTS: The authors captured 10,922 patients for 90-day follow-up and 4453 patients (40.8%) did not reach MCID. At the 1-year follow-up period, 7780 patients were identified and 2941 patients (37.8%) did not achieve MCID. The significant demographic characteristic-adjusted relative risks (RRs) for both groups (RR 90 day, RR 1 year) included the following: symptom duration > 1 year (1.34, 1.41); previous spine surgery (1.25, 1.30); African American descent (1.25, 1.20); chronic opiate use (1.23, 1.25); and less than high school education (1.20, 1.34). Independent ambulatory status (0.83, 0.88) and private insurance (0.91, 0.85) were associated with higher likelihood of reaching MCID at 90 days and 1 year, respectively. CONCLUSIONS: Several key unique demographic risk factors were identified in this cohort study that precluded optimal postoperative functional outcomes after elective lumbar spine surgery. With this information, appropriate preoperative counseling can be administered to assist in shaping patient expectations.

Hypoxic postconditioning drives protective microglial responses and ameliorates white matter injury after ischemic stroke.

BACKGROUND: Ischemic stroke (IS) is a cerebrovascular disease with high incidence and mortality. White matter repair plays an important role in the long-term recovery of neurological function after cerebral ischemia. Neuroprotective microglial responses can promote white matter repair and protect ischemic brain tissue. AIMS: The aim of this study was to investigate whether hypoxic postconditioning (HPC) can promote white matter repair after IS, and the role and mechanism of microglial polarization in white matter repair after HPC treatment. MATERIALS & METHODS: Adult male C57/BL6 mice were randomly divided into three groups: Sham group (Sham), MCAO group (MCAO), and hypoxic postconditioning group (HPC). HPC group were subjected to 45 min of transient middle cerebral artery occlusion (MCAO) immediately followed by 40 min of HPC. RESULTS: The results showed that HPC reduced the proinflammatory level of immune cells. Furthermore, HPC promoted the transformation of microglia to anti-inflammatory phenotype on the third day after the procedure. HPC promoted the proliferation of oligodendrocyte progenitors and increased the expression of myelination-related proteins on the 14th day. On the 28th day, HPC increased the expression of mature oligodendrocytes, which enhanced myelination. At the same time, the motor neurological function of mice was restored. DISCUSSION: During the acute phase of cerebral ischemia, the function of proinflammatory immune cells was enhanced, long-term white matter damage was aggravated, and motor sensory function was decreased. CONCLUSION: HPC promotes protective microglial responses and white matter repair after MCAO, which may be related to the proliferation and differentiation of oligodendrocytes.

Phenothiazines reduced autophagy in ischemic stroke through endoplasmic reticulum (ER) stress-associated PERK-eIF2α pathway.

BACKGROUND: Neuroprotective effects have been the main focus of new treatment modalities for ischemic stroke. Phenothiazines, or chlorpromazine plus promethazine (C + P), are known to prevent the generation of free radicals and uptake of Ca2+ by plasma membrane; they have a potential as a treatment for acute ischemic stroke (AIS). This study aims to investigate the role of endoplasmic reticulum (ER) stress-associated PERK-eIF2α pathway underlying the phenothiazine-induced neuroprotective effects after cerebral ischemia/reperfusion (I/R) injury. METHODS: A total of 49 male Sprague Dawley rats (280-320 g) were randomly divided into 4 groups (n = 7 per group): (1) sham, (2) I/R that received 2 h of middle cerebral artery occlusion (MCAO), followed by 6 or 24 h of reperfusion, (3) MCAO treated by C + P without temperature control and (4) MCAO treated by C + P with temperature control. Human neuroblastoma (SH-SY5Y) cells were used in 5 groups: (1) control, (2) oxygen-glucose deprivation (OGD) for 2 h followed by reoxygenation (OGD/R), (3) OGD/R with C + P; (4) OGD/R with PERK inhibitor, GSK2656157, and (5) OGD/R with C + P and GSK2656157. The molecules of ER stress, unfolded protein response (UPR) (Bip, PERK, p-PERK, p-PERK/PERK, eIF2α, p-eIF2α, p-eIF2α/eIF2α), autophagy (ATG12, LC3II/I), and apoptosis (BAX, Bcl-XL) were measured at mRNA levels by real time PCR and protein levels by Western blotting. RESULTS: In ischemic rats followed by reperfusion, expression of Bip, p-PERK/PERK, p-eIF2α/eIF2α, ATG12, and LC3II/I, as well as BAX were all significantly increased. These markers were significantly reduced by C + P at both 6 and 24 h of reperfusion. Anti-apoptotic Bcl-XL expression was increased, while pro-apoptotic BAX expression was decreased by C + P. In SH-SY5Y cell lines, both C + P and GSK2656157 significantly reduced the level of autophagy and apoptosis after I/R, respectively. The combination of GSK2656157 and C + P did not promote the same effect, suggesting that C + P did not induce any neuroprotective effect by inhibiting autophagy and apoptosis through the PERK-eIF2α pathway when this pathway was already blocked by GSK2656157. In general, the reduction in body temperature by phenothiazines was associated with better neuroprotection but it did not reach significant levels. CONCLUSION: The combined treatment of C + P plays a crucial role in stroke therapy by inhibiting ER stress-mediated autophagy, thereby leading to reduced apoptosis and increased neuroprotection. Our findings highlight the PERK-eIF2α pathway as a central mechanism through which C + P exerts its beneficial effects. The results from this study may pave the way for the development of more targeted and effective treatments for stroke patients.

Where are we heading in post-China angioplasty and stenting for symptomatic intracranial severe stenosis era?

Symptomatic intracranial atherosclerotic disease (ICAD) is a globally challengeable disease. In the past 20 years, people have made a huge effort to deal with the problem including using endovascular technology and aggressive medical therapy. However, the efficacy of these methods seemed to be limited. The recent China angioplasty and stenting for symptomatic intracranial severe stenosis (CASSISS) did not support the addition of percutaneous transluminal angioplasty and stenting to medical therapy for the treatment of patients with symptomatic severe ICAD. So where are we heading in the post-CASSISS era?

Serum Bilirubin Associated with Stroke Severity and Prognosis: Preliminary Findings on Liver Function after Acute Ischemic Stroke.

OBJECTIVE: This study investigates relationships between serum bilirubin, stroke severity, and prognosis of patients with acute ischemic stroke (AIS) to elucidate the roles of the liver in AIS. METHODS: This retrospective study collected data from 527 patients diagnosed with AIS within 24 hours after their symptom onset. Stroke severity was assessed using the National Institutes of Health Stroke Scale (NIHSS). Mild stroke was defined as NIHSS≤5. Prognosis was assessed with modified Rankin Scale (mRS) on 90 days after AIS and good prognosis was defined as mRS≤2. The patients were divided based on their total bilirubin (Tbil) and direct bilirubin (Dbil) levels to study these serum markers' association with the severity of stroke. Tbil levels were measured and compared with mRS on 90 days to analyze prognosis of mild stroke patients. RESULTS: Both Tbil abnormal (NIHSS = 6.8 ± 5.3) and Dbil abnormal groups (NIHSS = 7.3 ± 5.7) had higher NIHSS scores on admission than the normal groups (p< 0.05 or p< 0.01, respectively). Severity of stroke at discharge was similar between these groups (p = 0.025 and 0.019, respectively). Serum bilirubin levels were independently associated with stroke severity on admission and discharge after risk factors were adjusted (p< 0.001 and p< 0.05, respectively; ß (95%CI) were 0.116 (0.064-0.167) and 0.058 (0.012-0.103), respectively). The average Tbil levels of mild stroke with good prognosis was 15.1 ± 6.4umol/l versus 11.8 ± 3.1umol/l with poor prognosis; this difference was statistically significant (p = 0.003). The same difference was observed with Dtil levels but it did not reach a significant level. CONCLUSION: High Tbil and Dbil level within 48 hours of symptom onset could be an independent marker of severity of stroke on admission and discharge for all AIS patients. For patient with mild stroke, elevation of bilirubin after AIS suggests a good prognosis. These findings imply that the liver play the key roles in the mechanism of AIS.

Large vessel occlusion stroke outcomes in diabetic vs. non-diabetic patients with acute stress hyperglycemia.

Objective: This study assesses whether stress-induced hyperglycemia is a predictor of poor outcome at 3 months for patients with acute ischemic stroke (AIS) treated by endovascular treatment (EVT) and impacted by their previous blood glucose status. Methods: This retrospective study collected data from 576 patients with AIS due to large vessel occlusion (LVO) treated by EVT from March 2019 to June 2022. The sample was composed of 230 and 346 patients with and without diabetes mellitus (DM), respectively, based on their premorbid diabetic status. Prognosis was assessed with modified Rankin Scale (mRS) at 3-month after AIS. Poor prognosis was defined as mRS>2. Stress-induced hyperglycemia was assessed by fasting glucose-to-glycated hemoglobin ratio (GAR). Each group was stratified into four groups by quartiles of GAR (Q1-Q4). Binary logistic regression analysis was used to identify relationship between different GAR quartiles and clinical outcome after EVT. Results: In DM group, a poor prognosis was seen in 122 (53%) patients and GAR level was 1.27 ± 0.44. These variables were higher than non-DM group and the differences were statistically significant (p < 0.05, respectively). Patients with severe stress-induced hyperglycemia demonstrated greater incidence of 3-month poor prognosis (DM: Q1, 39.7%; Q2, 45.6%; Q3, 58.6%; Q4, 68.4%; p = 0.009. Non-DM: Q1, 31%; Q2, 32.6%; Q3, 42.5%; Q4, 64%; p < 0.001). However, the highest quartile of GAR was independently associated with poor prognosis at 3 months (OR 3.39, 95% CI 1.66-6.96, p = 0.001), compared to the lowest quartile in non-DM patients after logistic regression. This association was not observed from DM patients. Conclusion: The outcome of patients with acute LVO stroke treated with EVT appears to be influenced by premorbid diabetes status. However, the poor prognosis at 3-month in patients with DM is not independently correlated with stress-induced hyperglycemia. This could be due to the long-term damage of persistent hyperglycemia and diabetic patients' adaptive response to stress following acute ischemic damage to the brain.

Branch atheromatous disease and treatment.

Branch atheromatous disease (BAD) is a subtype of ischemic stroke caused by perforating arteries occlusion due to proximal atherosclerosis of the arteries. Early neurological deterioration and recurrent stereotyped transient ischemic attacks are typical clinical manifestations of BAD. The optimal treatment for BAD has not been determined. This article explores a possible mechanism of BAD and effective treatment measures to prevent early progression and attack of transient ischemic events. This article explains the current status of intravenous thrombolysis, tirofiban, and argatroban for BAD and subsequent prognosis.

A case of unilateral recurrent cerebral cortical encephalitis with anti-myelin oligodendrocyte glycoprotein antibodies.

Myelin oligodendrocyte glycoprotein (MOG)-antibody-associated disease (MOGAD) is an independent inflammatory demyelinating disease. A rare phenotype of MOGAD is cerebral cortical encephalitis (CCE). This case report presents unilateral recurrent cerebral cortical encephalitis (CCE) with positive anti-MOG antibodies from a 55 year old man who was admitted with headache, fever and aphasia. This case highlights the findings of hyperintense lesions in the cortex of the right temporal gyrus with slight swelling on T2 FLAIR and anti MOG antibodies in serum (1:20) and CSF (1:80) when the patient presented again to hospital after the initial improvement with IVIG and glucocorticoids. In addition, the patient was found to have atrophy of the whole brain, especially the right temporal lobe, after becoming symptom-free with glucocorticoids. In summary, anti-MOG-associated CCE can be diagnosed with headache, fever, and seizures associated with the presence of anti-MOG antibodies. Unilateral CCE is a special clinical feature of MOGAD and cerebral atrophy can be found. Steroid therapy remains to be the standard treatment.

Building First-Year Medical Students' Skills in Finding, Evaluating, and Visualizing Health Information Through a "Debunking Medical Myths" Curricular Module.

To provide an online service learning opportunity for medical students during the COVID-19 pandemic, medical faculty and librarians developed and implemented a "Debunking Medical Myths" module in which students learned to search for emerging medical literature, evaluate evidence, and use that evidence to create an infographics debunking a COVID-19-related myth for a non-medical audience. The resultant infographics are visually appealing and designed to make complex health information easy to understand. The module was well-received by students, who demonstrated a nuanced understanding of the use of infographics to convey health information, and students' work was evaluated highly by community members. Supplementary Information: The online version contains supplementary material available at 10.1007/s40670-022-01541-w.

Effects of remote ischemic conditioning on sleep complaints in Parkinson's disease-rationale, design, and protocol for a randomized controlled study.

Objective: Sleep disturbances are common non-motor symptoms of Parkinson's disease. The symptoms affect the quality of patients' life by impeding normal sleep cycles and causing excessive daytime sleepiness. Remote Ischemic Conditioning (RIC) is a therapy often used for ischemic stroke patients to minimize infarct size and maximize post-stroke neurological function. Animal experiments have shown that RIC plays a protective role for retinal ganglion cells and other critical areas of the brain of Parkinson's disease. However, whether RIC improves excessive daytime sleepiness (EDS) for patients with Parkinson's disease remains to be determined. Methods: This is a single-center, double-blind, and randomized controlled trial, which includes patients with Parkinson's disease with EDS. All recruited patients will be randomly assigned either to the RIC or the control group (i.e., sham-RIC) with 20 patients in each group. Both groups receive RIC or sham-RIC treatment once a day for 28 days within 24 h of enrollment. Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI), Parkinson Disease Sleep Scale-2 (PDSS-2), Parkinson's Disease Questionnaire39 (PDQ39) score scales, and adverse events, such as inability to tolerate the treatment leading to suspension of the study or objective signs of tissue or neurovascular injury caused by RIC and/or sham-RIC are evaluated at 7, 14, 28, and 90 days after enrollment. Results: The primary goal of this study is to assess the feasibility of the treatments in patients with Parkinson's disease by measuring serious RIC-related adverse events and any reduced incidence of adverse events during the trial and to study potential efficacy, improvement of patients' excessive daytime sleepiness, quality of life-based on ESS, PSQI, PDSS-2, and PDQ39 scores. The secondary goal is to confirm the safety of the treatments. Conclusion: This study is a prospective randomized controlled trial to determine the safety, feasibility, and potential efficacy of RIC for patients with Parkinson's disease associated with EDS.

Advancements in our understanding of circular and long non-coding RNAs in spinal cord injury.

Spinal cord injury (SCI), either from trauma or degenerative changes, can result in severe disability and impaired quality of life. Understanding the cellular processes and molecular mechanisms that underlie SCI is imperative to identifying molecular targets for potential therapy. Recent studies have shown that non-coding RNAs, including both long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), regulate various cellular processes in SCI. In this review, we will describe the changes in lncRNA and circRNA expression that occur after SCI and how these changes may be related to SCI progression. Current evidence for the roles of lncRNAs and circRNAs in neuronal cell death and glial cell activation will also be reviewed. Finally, the possibility that lncRNAs and circRNAs are novel modulators of SCI pathogenesis will be discussed.

The Multi-Sites Trial on the Effects of Therapeutic Gardening on Mental Health and Well-Being.

Although many people affected by COVID-19 suffer from some form of psychological distress, access to proper treatment or psychosocial interventions has been limited. This study aimed to examine the feasibility and preliminary effects of a therapeutic gardening program conducted during the COVID-19 pandemic. The program consisted of 30 sessions and was conducted at 10 nationwide sites in Korea from June to November 2021. Mental health and well-being were assessed using the Mental Health Screening Tool for Depressive Disorders, Mental Health Screening Tool for Anxiety Disorders, Engagement in Daily Activity Scale, brief version of World Health Organization Quality of Life, and Mindful Attention Awareness Scale. Cohen's d value was calculated for the effect size, and a multilevel analysis was used to determine the longitudinal effects of therapeutic gardening. The effect sizes for depression, anxiety, daily activities, quality of life, and mindfulness were 0.84, 0.72, 0.61, 0.64, and 0.40, respectively. Multilevel analyses showed that all five mental health variables improved significantly over time as the therapeutic gardening program progressed. Therapeutic gardening is promising and applicable as a nature-based intervention to improve the mental health of individuals experiencing psychological distress especially in the COVID-19 pandemic.

Timing is everything: Exercise therapy and remote ischemic conditioning for acute ischemic stroke patients.

Physical exercise is a promising rehabilitative strategy for acute ischemic stroke. Preclinical trials suggest that exercise restores cerebral blood circulation and re-establishes the blood-brain barrier's integrity with neurological function and motor skill improvement. Clinical trials demonstrated that exercise improves prognosis and decreases complications after ischemic events. Due to these encouraging findings, early exercise rehabilitation has been quickly adopted into stroke rehabilitation guidelines. Unfortunately, preclinical trials have failed to warn us of an adverse effect. Trials with very early exercise rehabilitation (within 24 h of ischemic attack) found an inferior prognosis at 3 months. It was not immediately clear as to why exercise was detrimental when performed very early while it was ameliorative just a few short days later. This review aimed to explore the potential mechanisms of harm seen in very early exercise administered to acute ischemic stroke patients. To begin, the mechanisms of exercise's benefit were transposed onto the current understanding of acute ischemic stroke's pathogenesis, specifically during the acute and subacute phases. Then, exercise rehabilitation's mechanisms were compared to that of remote ischemic conditioning (RIC). This comparison may reveal how RIC may be providing clinical benefit during the acute phase of ischemic stroke when exercise proved to be harmful.

Neuroplastic Effect of Exercise Through Astrocytes Activation and Cellular Crosstalk.

Physical exercise is an effective therapy for neurorehabilitation. Exercise has been shown to induce remodeling and proliferation of astrocyte. Astrocytes potentially affect the recruitment and function of neurons; they could intensify responses of neurons and bring more neurons for the process of neuroplasticity. Interactions between astrocytes, microglia and neurons modulate neuroplasticity and, subsequently, neural circuit function. These cellular interactions promote the number and function of synapses, neurogenesis, and cerebrovascular remodeling. However, the roles and crosstalk of astrocytes with neurons and microglia and any subsequent neuroplastic effects have not been studied extensively in exercise-induced settings. This article discusses the impact of physical exercise on astrocyte proliferation and highlights the interplay between astrocytes, microglia and neurons. The crosstalk between these cells may enhance neuroplasticity, leading to the neuroplastic effects of exercise.

How to remove those bloody collections: Nonsurgical treatment options for chronic subdural hematoma.

Chronic subdural hematoma (CSDH) is one of the most prevalent neurosurgical disorders. Patients with CSDH commonly present with altered mental status, focal neurological deficit, and/or headache. The first-line treatment for CSDH is surgical evacuation. Although the surgical procedures for CSDH have been considered relatively "straightforward," they are not without any risk. The elderly are especially prone to show poor surgical outcomes. To make matters worse, many elderly patients are on anticoagulants and antiplatelet agents, increasing the risk of re-bleeding before and after surgery. These complications have led clinicians to search for nonsurgical alternatives. Dexamethasone should be used with caution for selected patients given its side effects. Tranexamic acid may be utilized as an adjunct therapy to surgery, but more randomized clinical trials are needed to evaluate its definitive efficacy. Interesting results of middle meningeal artery embolization (MMAE) have been reported from case studies. However, the risks associated with MMAE, including intracerebral hemorrhage, stroke, and vasospasm, have not been properly studied yet. The clinical benefits of atorvastatin and angiotensin-converting enzyme inhibitors are uncertain for CSDH. In conclusion, surgical intervention continues to be the first-line treatment while nonsurgical treatment options may be considered an adjunct therapy especially for recurrent hematoma or to reduce the volume of a hematoma.

Silver Nanowire-IZO-Conducting Polymer Hybrids for Flexible and Transparent Conductive Electrodes for Organic Light-Emitting Diodes.

Solution-processed silver nanowire (AgNW) has been considered as a promising material for next-generation flexible transparent conductive electrodes. However, despite the advantages of AgNWs, some of their intrinsic drawbacks, such as large surface roughness and poor interconnection between wires, limit their practical application in organic light-emitting diodes (OLEDs). Herein, we report a high-performance AgNW-based hybrid electrode composed of indium-doped zinc oxide (IZO) and poly (3,4-ethylenediowythiophene):poly(styrenesulfonate) [PEDOT:PSS]. The IZO layer protects the underlying AgNWs from oxidation and corrosion and tightly fuses the wires together and to the substrate. The PEDOT:PSS effectively reduces surface roughness and increases the hybrid films' transmittance. The fabricated electrodes exhibited a low sheet resistance of 5.9 Ωsq-1 with high transmittance of 86% at 550 nm. The optical, electrical, and mechanical properties of the AgNW-based hybrid films were investigated in detail to determine the structure-property relations, and whether optical or electrical properties could be controlled with variation in each layer's thickness to satisfy different requirements for different applications. Flexible OLEDs (f-OLEDs) were successfully fabricated on the hybrid electrodes to prove their applicability; their performance was even better than those on commercial indium doped tin oxide (ITO) electrodes.