Reciprocal Changes Following Cervical Realignment Surgery

Over the last few decades, the importance of the sagittal plane and its contour has gained significant recognition. Through full-body stereoradiography, the understanding of compensatory mechanisms, and the concept of global balance and reciprocal change has expanded. There have been a few reports describing how cervical realignment surgery affects global spinal alignment (GSA) and global balance. Despite the research efforts, the concept of reciprocal change and global balance is still perplexing. Understanding the compensatory status and main drivers of deformity in a patient is vital because the compensatory mechanisms may resolve reciprocally following cervical realignment surgery. A meticulous preoperative evaluation of the whole-body alignment, including the pelvis and lower extremities, is paramount to appreciate optimal GSA in the correction of spinal malalignment. This study aims to summarize relevant literature on the reciprocal changes in the whole body caused by cervical realignment surgery and review recent perspectives regarding cervical compensatory mechanisms

Clinical Impact and Correlations of Odontoid Parameters Following Multilevel Posterior Cervical Fusion Surgery

Objective C2 slope (C2S), a cervical parameter mathematically approximated as T1 slope minus cervical lordosis (T1S–CL), predicts functional improvement in cervical deformity patients. Nonetheless, C2S is a positional parameter based only on the horizontal axis. The current study aims to introduce novel odontoid parameters and establish their relationships with patient-reported health-related quality of life (HRQoL). Methods Lateral plain radiographs of 32 adults who underwent multilevel posterior cervical fusion were analyzed. The odontoid parameters included odontoid incidence (OI), C2S, odontoid tilt (OT), and gravity line-C2 distance (GL-C2), while the cervical parameters were the Cobb angle at C0–1, C1–2, C0–2, C2–7, C2–7 sagittal vertical axis (cSVA), T1 slope, and T1S–CL. The range of motion (ROM) of the occipito-atlantoaxial complex was measured in flexion and extension plain radiographs. Scores on the Neck Disability Index (NDI) and visual analogue scale (VAS) for axial neck (VASn) and arm pain were measured. Results Compared to asymptomatic subjects, patients had larger C2S, cSVA, and T1S–CL, and smaller OT. Preoperatively, OI was significantly correlated with the ROM of C1–2 (r = 0.37, p < 0.05) and C0–2 (r = 0.46, p < 0.01). OT and C2S had significant correlations with the C0–1, C1–2, and C0–2 angles, GL-C2, and T1S–CL. Postoperative NDI scores were significantly correlated with OI (r = -0.40, p < 0.05) and OT (ρ = -0.37, p < 0.05). VASn was significantly correlated with GL-C2 (r = -0.35, p < 0.05). Conclusion The odontoid parameters were significantly correlated with established cervical parameters and HRQoL measures. OI is a constant parameter representing the individual's compensatory reservoir at the upper cervical spine

Inhibitory effect of a tyrosine-fructose Maillard reaction product, 2,4-bis(p-hydroxyphenyl)-2-butenal on amyloid-β generation and inflammatory reactions via inhibition of NF-κB and STAT3 activation in cultured astrocytes and microglial BV-2 cells

<p>Abstract</p> <p>Background</p> <p>Amyloidogenesis is linked to neuroinflammation. The tyrosine-fructose Maillard reaction product, 2,4-bis(<it>p</it>-hydroxyphenyl)-2-butenal, possesses anti-inflammatory properties in cultured macrophages, and in an arthritis animal model. Because astrocytes and microglia are responsible for amyloidogenesis and inflammatory reactions in the brain, we investigated the anti-inflammatory and anti-amyloidogenic effects of 2,4-bis(<it>p</it>-hydroxyphenyl)-2-butenal in lipopolysaccharide (LPS)-stimulated astrocytes and microglial BV-2 cells.</p> <p>Methods</p> <p>Cultured astrocytes and microglial BV-2 cells were treated with LPS (1 μg/ml) for 24 h, in the presence (1, 2, 5 μM) or absence of 2,4-bis(<it>p</it>-hydroxyphenyl)-2-butenal, and harvested. We performed molecular biological analyses to determine the levels of inflammatory and amyloid-related proteins and molecules, cytokines, Aβ, and secretases activity. Nuclear factor-kappa B (NF-κB) DNA binding activity was determined using gel mobility shift assays.</p> <p>Results</p> <p>We found that 2,4-bis(<it>p</it>-hydroxyphenyl)-2-butenal (1, 2, 5 μM) suppresses the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) as well as the production of nitric oxide (NO), reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) in LPS (1 μg/ml)-stimulated astrocytes and microglial BV-2 cells. Further, 2,4-bis(<it>p</it>-hydroxyphenyl)-2-butenal inhibited the transcriptional and DNA binding activity of NF-κB--a transcription factor that regulates genes involved in neuroinflammation and amyloidogenesis via inhibition of IκB degradation as well as nuclear translocation of p50 and p65. Consistent with the inhibitory effect on inflammatory reactions, 2,4-bis(<it>p</it>-hydroxyphenyl)-2-butenal inhibited LPS-elevated Aβ₄₂levels through attenuation of β- and γ-secretase activities. Moreover, studies using signal transducer and activator of transcription 3 (STAT3) siRNA and a pharmacological inhibitor showed that 2,4-bis(<it>p</it>-hydroxyphenyl)-2-butenal inhibits LPS-induced activation of STAT3.</p> <p>Conclusions</p> <p>These results indicate that 2,4-bis(<it>p</it>-hydroxyphenyl)-2-butenal inhibits neuroinflammatory reactions and amyloidogenesis through inhibition of NF-κB and STAT3 activation, and suggest that 2,4-bis(<it>p</it>-hydroxyphenyl)-2-butenal may be useful for the treatment of neuroinflammatory diseases like Alzheimer's disease.</p

Increased Corticomuscular Coherence in Idiopathic REM Sleep Behavior Disorder

The authors hypothesized that if locomotor drive increases along with rapid eye movement (REM) sleep without atonia in idiopathic REM sleep behavior disorder (RBD), then RBD patients would have greater corticomuscular coherence (CMC) values during REM sleep than at other sleep stages and than in healthy control subjects during REM sleep. To explore this hypothesis, we analyzed beta frequency range CMC between sensorimotor cortex electroencephalography (EEG) and chin/limb muscle EMG in idiopathic RBD patients. Eleven drug naive idiopathic RBD patients and 11 age-matched healthy control subjects were included in the present study. All participants completed subjective sleep questionnaires and underwent polysomnography for one night. The CMC value between EEGs recorded at central electrodes and EMGs acquired at leg and chin muscles were computed and compared by repeated measures analysis of variance (ANOVA). Sleep stages and muscle (i.e., chin vs. leg) served as within-subject factors, and group served as the between-subject factor. Repeated measures ANOVA revealed no significant main effect of group (F1,20 = 0.571, p = 0.458) or muscle (F1,20 = 1.283, p = 0.271). However, sleep stage was found to have a significant main effect (F2.067,41.332 = 20.912, p < 0.001). The interaction between group and sleep stage was significant (F2.067,41.332 = 3.438, p = 0.040). RBD patients had a significantly higher CMC value than controls during REM sleep (0.047 ± 0.00 vs. 0.052 ± 0.00, respectively, p = 0.007). This study reveals increased CMC during REM sleep in patients with RBD, which indicates increased cortical locomotor drive. Furthermore, this study supports the hypothesis that sufficient locomotor drive plays a role in the pathophysiology of RBD in addition to REM sleep without atonia

Effects of Korean Red Ginseng on Cognitive and Motor Function: A Double-blind, Randomized, Placebo-controlled Trial

Ginseng has a long history of use for health enhancement, and there is some evidence from animal studies that it has a beneficial effect on cognitive performance. The purpose of this study was to investigate the effect of Korean red ginseng on cognitive performance in humans. A total of 15 healthy young males with no psychiatric or cognitive problems were selected based on an interview with a board-certified psychiatrist. The subjects were randomly assigned to receive a daily dose of 4,500 mg red ginseng or placebo for a 2-week trial. There were 8 subjects in the red ginseng group and 7 subjects in the placebo group. All of the subjects were analyzed with the Vienna test system and a P300 event-related potential (ERP) test. There were no significant differences in the Vienna test system scores between the red ginseng group and the placebo group. In the event-related potential test, the C3 latency of the red ginseng group tended to decrease during the study period (p=0.005). After 2 wk, significant decreases were observed in the P300 latencies at Cz (p=0.008), C3 (p=0.005), C4 (p=0.002), and C mean (p=0.003) in the red ginseng group. Our results suggest that the decreased latency in ERP is associated with improved cognitive function. Further studies with a higher dosage of ginseng, a larger sample size, and a longer follow-up period are necessary to confirm the clinical efficacy of Korean red ginseng.OAIID:oai:osos.snu.ac.kr:snu2012-01/102/2014017262/7SEQ:7PERF_CD:SNU2012-01EVAL_ITEM_CD:102USER_ID:2014017262ADJUST_YN:YEMP_ID:A079623DEPT_CD:801CITE_RATE:0DEPT_NM:의학과SCOPUS_YN:NCONFIRM:

The Orphan Nuclear Receptor ERRγ Regulates Hepatic CB1 Receptor-Mediated Fibroblast Growth Factor 21 Gene Expression

BACKGROUND: Fibroblast growth factor 21 (FGF21), a stress inducible hepatokine, is synthesized in the liver and plays important roles in glucose and lipid metabolism. However, the mechanism of hepatic cannabinoid type 1 (CB1) receptor-mediated induction of FGF21 gene expression is largely unknown. RESULTS: Activation of the hepatic CB1 receptor by arachidonyl-2'-chloroethylamide (ACEA), a CB1 receptor selective agonist, significantly increased FGF21 gene expression. Overexpression of estrogen-related receptor (ERR) γ increased FGF21 gene expression and secretion both in hepatocytes and mice, whereas knockdown of ERRγ decreased ACEA-mediated FGF21 gene expression and secretion. Moreover, ERRγ, but not ERRα and ERRβ, induced FGF21 gene promoter activity. In addition, deletion and mutation analysis of the FGF21 promoter identified a putative ERRγ-binding motif (AGGTGC, a near-consensus response element). A chromatin immunoprecipitation assay revealed direct binding of ERRγ to the FGF21 gene promoter. Finally, GSK5182, an ERRγ inverse agonist, significantly inhibited hepatic CB1 receptor-mediated FGF21 gene expression and secretion. CONCLUSION: Based on our data, we conclude that ERRγ plays a key role in hepatic CB1 receptor-mediated induction of FGF21 gene expression and secretion

Ultraviolet nanoimprinted polymer nanostructure for organic light emitting diode application

Light extraction efficiency of a conventional organic light emitting diode (OLED) remains limited to approximately 20% as most of the emission is trapped in the waveguide and glass modes. An etchless simple method was developed to fabricate two-dimensional nanostructures on glass substrate directly by using ultraviolet (UV) curable polymer resin and UV nanoimprint lithography in order to improve output coupling efficiency of OLEDs. The enhancement of the light extraction was predicted by the three-dimensional finite difference time domain method. OLEDs integrated on nanoimprinted substrates enhanced electroluminance intensity by up to 50% compared to the conventional device

Clinicopathological findings of pediatric NTRK fusion mesenchymal tumors

Background While ETV6- NTRK3 fusion is common in infantile fibrosarcoma, NTRK1/3 fusion in pediatric tumors is scarce and, consequently, not well known. Herein, we evaluated for the presence of NTRK1/3 fusion in pediatric mesenchymal tumors, clinicopathologically and immunophenotypically. Methods We reviewed nine NTRK fusion-positive pediatric sarcomas confirmed by fluorescence in situ hybridization and/or next-generation sequencing from Seoul National University Hospital between 2002 and 2020. Results One case of TPR-NTRK1 fusion-positive intracranial, extra-axial, high-grade undifferentiated sarcoma (12-year-old boy), one case of LMNA-NTRK1 fusion-positive low-grade infantile fibrosarcoma of the forehead (3-year-old boy), one case of ETV6-NTRK3 fusion-positive inflammatory myofibroblastic tumor (IMT) (3-months-old girl), and six cases of ETV6-NTRK3 fusion-positive infantile fibrosarcoma (median age: 2.6 months, range: 1.6–5.6 months, M: F = 5:1) were reviewed. The Trk immunopositivity patterns were distinct, depending on what fusion genes were present. We observed nuclear positivity in TPR-NTRK1 fusion-positive sarcoma, nuclear membrane positivity in LMNA-NTRK1 fusion-positive sarcoma, and both cytoplasmic and nuclear positivity in ETV6-NTRK3 fusion-positive IMT and infantile fibrosarcomas. Also, the TPR-NTRK1 fusion-positive sarcoma showed robust positivity for CD34/nestin, and also showed high mitotic rate. The LMNA-NTRK1 fusion-positive sarcoma revealed CD34/S100 protein/nestin/CD10 coexpression, and a low mitotic rate. The IMT with ETV6-NTRK3 fusion expressed SMA. Six infantile fibrosarcomas with ETV6-NTRK3 fusion showed variable coexpression of nestin (6/6)/CD10 (4/5)/ S100 protein (3/6). Conclusions All cases of NTRK1 and NTRK3 fusion-positive pediatric tumors robustly expressed the Trk protein. A Trk immunopositive pattern and CD34/S100/nestin/CD10/SMA immunohistochemical expression may suggest the presence of NTRK fusion partner genes. LMNA-NTRK1 fusion sarcoma might be a low-grade subtype of infantile fibrosarcoma. Interestingly, more than half of the infantile fibrosarcoma cases were positive for S100 protein and CD10. The follow-up period of TPR-NTRK1 and LMNA-NTRK1 fusion-positive tumors are not enough to predict prognosis. However, ETV6-NTRK3 fusion-positive infantile fibrosarcomas showed an excellent prognosis with no evidence of disease for an average of 11.7 years, after gross total resection of the tumor.This work was supported by the Institute for Information & Communications Technology Promotion (IITP) grant funded by the Korean government (MSIP) (No.2019–0567, Development of Intelligent SW systems for uncovering genetic variation and developing personalized medicine for cancer patients with unknown molecular genetic mechanisms)