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Circular AMOLED panel is largely applied in smart watches. However, it has been challenged that under the difference of smaller size and irregular cutting, the mechanical strength of circular AMOLED panel is no longer suitable for the common definition in the past, compared with the ordinary rectangular shape. 4-point bending test is a common method to define the cutting strength of a panel, therefore, 4-point bending test is used to review the strength variation of circular AMOLED panel in this paper. Besides, due to the characteristics of OLED panel, a special fracture mode will also be discussed in this paper. [ABSTRACT FROM AUTHOR]

Currently, analysis of sustained ventricular tachycardia postmyocardial infarction in man is limited by the time required for single point activation mapping and the difficulty in obtaining information during hemodynamically unstable arrhythmias. To overcome these limitations, we developed a multielectrode 'basket' catheter for endocardial recording and pacing. This report describes the first clinical use of such a catheter to guide successful radiofrequency ablation of incessant sustained ventricular tachycardia postmyocardial infarction. This system may significantly shorten the time required for VT analysis and improve the results of radiofrequency catheter ablation for VT postmyocardial infarction. [ABSTRACT FROM AUTHOR]

Background: Computer-assisted surgical simulation (CASS) allows more precise orthognathic surgery. However, few studies have evaluated associations between CASS-designed bilateral sagittal split osteotomy (SSO) and bone contact surface in class II mandibular asymmetry. This study aims to evaluate the effects of using computer-assisted simulation and design modification of SSO to improve bony contact in skeletal class II asymmetry., Methods: This retrospective analysis reviewed 28 patients with class II asymmetry who underwent orthognathic surgery, including 15 with modified SSO (group CS) and 13 with conventional SSO (group C). Modified SSO was designed under CASS. Operative characteristics, postoperative outcomes, and complications were collected and compared between the two groups., Results: Bony contact was found at the distal end of the proximal segment in all group CS patients, while bone gap was noted in all group C patients ( P < 0.05). Moreover, bone graft was used in four group C patients but was not used in all cases in group CS patients ( P < 0.05). A trend toward lower operative time or perioperative bleeding was noted in group CS, but without statistical significance. After 1-year follow-up, inferior alveolar nerve disturbances were noted in two group CS patients and one group C patient. Palpable bone gap with uneven jaw line was noted in two group C patients 1 year after surgery and one patient received fat graft treatment., Conclusion: The simulation-based SSO modification provides appropriate contact surface and eliminates the bone gap between proximal and distal segments in class II asymmetry., Clinical Question/level of Evidence: Therapeutic, III., (Copyright © 2023 by the American Society of Plastic Surgeons.)

Organophosphate pesticides (OPs), which are among the most widely used synthetic chemicals for the control of a wide variety of pests, are however associated with various adverse reactions in animals and humans. Chlorpyrifos, an OP, has been shown to cause various health complications due to ingestion, inhalation, or skin absorption. The mechanisms underlying the adverse effect of chlorpyrifos on neurotoxicity have not been elucidated. Therefore, we aimed to determine the mechanism of chlorpyrifos-induced cytotoxicity and to examine whether the antioxidant vitamin E (VE) ameliorated these cytotoxic effects using DBTRG-05MG, a human glioblastoma cell line. The DBTRG-05MG cells were treated with chlorpyrifos, VE, or chlorpyrifos plus VE and compared with the untreated control cells. Chlorpyrifos induced a significant decrease in cell viability and caused morphological changes in treated cultures. Furthermore, chlorpyrifos led to the increased production of reactive oxygen species (ROS) accompanied by a decrease in the level of reduced glutathione. Additionally, chlorpyrifos induced apoptosis by upregulating the protein levels of Bax and cleaved caspase-9/caspase-3 and by downregulating the protein levels of Bcl-2. Moreover, chlorpyrifos modulated the antioxidant response by increasing the protein levels of Nrf2, HO-1, and NQO1. However, VE reversed the cytotoxicity and oxidative stress induced by chlorpyrifos treatment in DBTRG-05MG cells. Overall, these findings suggest that chlorpyrifos causes cytotoxicity through oxidative stress, a process that may play an important role in the development of chlorpyrifos-associated glioblastoma., (© 2023 Wiley Periodicals LLC.)

Glioblastoma (GBM) is the most common primary brain malignancy in adults. Despite multimodal treatment that involves maximal safe resection, concurrent chemoradiotherapy, and tumour treatment for supratentorial lesions, the prognosis remains poor. The current median overall survival is only <2 years, and the 5-year survival is only 7.2%. Thioredoxin domain-containing protein 11 (TXNDC11), also known as EF-hand binding protein 1, was reported as an endoplasmic reticulum stress-induced protein. The present study aimed to elucidate the prognostic role of TXNDC11 in GBM. We evaluated the clinical parameters and TXNDC11 scores in gliomas from hospitals. Additionally, proliferation, invasion, migration assays, apoptosis, and temozolomide (TMZ)-sensitivity assays of GBM cells were conducted to evaluate the effects of short interfering RNA (siRNA) on these processes. In addition, these cells were subjected to Western blotting to detect the expression levels of N-cadherin, E-cadherin, and Cyclin D1. High levels of TXNDC11 protein expression were significantly associated with World Health Organization (WHO) high-grade tumour classification and poor prognosis. Multivariate analysis revealed that in addition to the WHO grade, TXNDC11 protein expression was also an independent prognostic factor of glioma. In addition, TXNDC11 silencing inhibited proliferation, migration, and invasion and led to apoptosis of GBM cells. However, over-expression of TXNDC11 enhanced proliferation, migration, and invasion. Further, TXNDC11 knockdown downregulated N-cadherin and cyclin D1 expression and upregulated E-cadherin expression in GBM cells. Knock-in TXNDC11 return these. Finally, in vivo, orthotopic xenotransplantation of TXNDC11-silenced GBM cells into nude rats promoted slower tumour growth and prolonged survival time. TXNDC11 is a potential oncogene in GBMs and may be an emerging therapeutic target.

Mycotoxins are secondary metabolites produced by various kinds of fungi that can induce disease in humans. The fungal species Penicillium expansum produces patulin (C 7 H 6 O 4 ), a polyketide lactone mycotoxin found in fruits. Patulin is classified as noncarcinogen; however, recently, it has been associated with harmful effects on the central nervous system. Patulin's toxic action has been established in various brain models; however, its effect on human glioblastoma remains elusive. This study explores whether patulin induces cytotoxicity through oxidative stress in DBTRG-05MG human glioblastoma cells. This study also evaluates whether the antioxidant N-acetylcysteine (NAC) protects against patulin-induced cytotoxicity. In DBTRG-05MG cells, patulin concentration (10-60 μM) dependently induced cytotoxicity. Concerning oxidative stress, patulin (10 and 20 μM) increased the production of intracellular reactive oxygen species (ROS) but depleted reduced glutathione (GSH) contents and regulated the expressions of antioxidant-related proteins (Nrf2 and HO-1). Furthermore, patulin induced cytotoxicity via modulation of apoptosis-related protein expressions (Bax, cleaved caspase-9, and cleaved caspase-3). These cytotoxic responses were partially reversed via pretreatment with NAC (10 μM). In summary, these data help us understand the toxicology of patulin in human glioblastoma and evaluate whether NAC could clinically reduce patulin-affected brain damage., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Terahertz (THz) radiation has attracted wide attention in recent years due to its non-destructive properties and ability to sense molecular structures. In applications combining terahertz radiation with metamaterial technology, the interaction between the terahertz radiation and the metamaterials causes resonance reactions; different analytes have different resonance performances in the frequency domain. In addition, a microfluidic system is able to provide low volume reagents for detection, reduce noise from the environment, and concentrate the sample on the detection area. Through simulation, a cruciform metamaterial pattern was designed; the proportion, periodicity, and width of the metamaterial were adjusted to improve the sensing capability of the chip. In the experiments, the sensing capabilities of Type A, B, and C chips were compared. The Type C chip had the most significant resonant effect; its maximum shift could be increased to 89 GHz. In the probiotic experiment, the cruciform chip could have a 0.72 GHz shift at a concentration of 0.025 mg/50 μL, confirming that terahertz radiation combined with a metamaterial microfluidic chip can perform low-concentration detection.

Objective: Ependymomas are rare central nervous system tumors. The current treatment strategy is gross total tumor removal. Whether adjuvant therapy will be beneficial is controversial. We retrospectively analyzed 3 cases of World Health Organization (WHO) grade III posterior fossa anaplastic ependymomas treated with different treatment modalities. We aimed to identify possible treatment options for infratentorial WHO grade III anaplastic ependymoma in adults., Methods: We performed a retrospective analysis of 3 patients diagnosed with infratentorial anaplastic ependymomas in our institution from 2016 to 2020. The demographic data were documented. This case series of 3 patients does not meet the Department of Health and Human Services definition of research and does not need Institutional Review Board approval. All patients' informed consents have been obtained., Results: One patient underwent subtotal tumor resection combined with adjuvant radiotherapy and Gamma Knife radiosurgery while the other 2 patients underwent gross total tumor removal combined with Gamma Knife radiosurgery or adjuvant radiotherapy. Tumors recurred in the first patient 20 months later, while the other 2 patents did not develop recurrence. The modified Rankin scale scores of these patients were 1, 0, and 0. All patients are followed up with regular magnetic resonance imaging at our facility., Conclusions: The strategy for treating WHO grade III anaplastic ependymomas is controversial, but gross total tumor resection remains the key element. Adjuvant stereotactic radiosurgery after tumor removal might be considered if radiotherapy is not an option. The role of chemotherapy is unclear, and the use of chemotherapy should be tailored to individual patients., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Background: Susceptibility-weighted imaging (SWI) is sensitive to the accumulation of paramagnetic substances, such as hemorrhage and increased venous vasculature, both being frequently found in high-grade tumors. The purpose of this retrospective study is to differentiate high-grade and low-grade astrocytoma by objectively measuring quantitative intra-tumoral susceptibility signals (qITSS) on SWI., Methods: Precontrast SWI and 3D contrast-enhanced T1WI of 65 patients with astrocytoma were collected at 1.5 Tesla. All tumors were histologically confirmed and classified into two groups: high grade (WHO grade III and IV, n=50) and low grade (WHO grade II, n=15). After manual delineation of the tumor on T1WI, normalized contrast (NC) was calculated voxel by voxel within the tumor by using the concept of contrast to noise ratio. Thresholding on NC was applied to detect qITSS, and the volumetric percentage of qITSS can be obtained for each tumor. Two-sample t -test was applied to examine significant difference of qITSS percentage between high-grade and low-grade astrocytoma for different NC thresholds, ranging from 4 to 20. Receiver operating characteristic analysis was performed to evaluate the performance of differentiation., Results: P value was less than 0.01 for a large range of NC thresholds [4-20], reflecting significant difference of qITSS percentage between high-grade and low-grade astrocytoma. The area under the receiver operating characteristic curve was larger than 0.9 at NC thresholds from 8 to 16 and peaks at 0.949 with a NC threshold of 14. It was shown that astrocytoma grading by qITSS percentage is successful for a wide range of NC threshold, demonstrating robustness on threshold selection., Conclusions: Without relying on the selection of slice position and at the same time providing objective identification of hypointense signal in SWI, the qITSS percentage can be used to distinguish high-grade and low-grade astrocytoma reliably., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://dx.doi.org/10.21037/qims-21-58). Dr. HWC serves as an unpaid editorial board member of Quantitative Imaging in Medicine and Surgery, and Drs. TCC, YLC, WPS, HWC reported that they received grant supports from Ministry of Science and Technology (Taiwan) research grants (MOST 104-2221-E-110-039 and MOST 105-2221-E-110-054); Dr. DHL reported that he received grant support from Kaohsiung Veterans General Hospital (VGHKS107-160) in Taiwan. The other authors have no conflicts of interest to declare., (2022 Quantitative Imaging in Medicine and Surgery. All rights reserved.)

Rotenone, a plant-derived pesticide belonging to genera Derris and Lonchorcarpus, is an inhibitor of NADH dehydrogenase complex. Studies have shown that rotenone was applied as a neurotoxic agent in various neuronal models. Hydroxytyrosol [2-(3,4-dihydroxyphenyl)-ethanol] is a natural phenolic compound found in the olive (Olea europaea L.). Studies of hydroxytyrosol have dramatically increased because this compound may contribute to the prevention of neurodegenerative diseases. Although hydroxytyrosol has received increasing attention due to its multiple pharmacological activities, it is not explored whether hydroxytyrosol inhibited rotenone-induced cytotoxicity in the neuronal cell model. The aim of this study was to explore whether hydroxytyrosol prevented rotenone-induced Ca 2+ signaling, cytotoxicity and oxidative stress in HCN-2 neuronal cell line. In HCN-2 cells, rotenone (5-30 μM) concentration-dependently induced cytosolic Ca 2+ concentrations ([Ca 2+ ] i ) rises and cytotoxicity. Treatment with hydroxytyrosol (30 μM) reversed rotenone (20 μM)-induced cytotoxic responses. In Ca 2+ -containing medium, rotenone-induced Ca 2+ entry was inhibited by 2-APB (a store-operated Ca 2+ channel modulator) or hydroxytyrosol. In Ca 2+ -free medium, treatment with thapsigargin (an endoplasmic reticulum Ca 2+ pump inhibitor) or hydroxytyrosol significantly inhibited rotenone-induced [Ca 2+ ] i rises. Furthermore, treatment with hydroxytyrosol reversed ROS levels, cytotoxic responses, and antioxidant enzyme activities (SOD, GPX and CAT) in rotenone-treated cells. Together, in HCN-2 cells, rotenone induced Ca 2+ influx via store-operated Ca 2+ entry and Ca 2+ release from the endoplasmic reticulum and caused oxidative stress. Moreover, hydroxytyrosol ameliorated Ca 2+ or ROS-associated cytotoxicity. It suggests that hydroxytyrosol might have a protective effect on rotenone-induced neurotoxicity in human neuronal cells., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Cinobufagin, a bufadienolide of toad venom of Bufo bufo gargarizans, is used as a cardiotonic, central nervous system (CNS) respiratory agent, as well as an analgesic and anesthetic. However, several research showed that bufadienolide has a few side effects on the CNS, such as breathlessness or coma. Although cinobufagin was shown to display pharmacological effects in various models, the toxic effect of cinobufagin is elusive in brain cell models. The aim of this study was to explore whether cinobufagin affected viability, Ca 2+ homeostasis, and reactive oxygen species (ROS) production in Gibco® Human Astrocyte (GHA) and HCN-2 neuronal cell line. In GHA cells but not in HCN-2 cells, cinobufagin (20-60 μM) induced [Ca 2+ ] i rises. In terms of cell viability, chelation of cytosolic Ca 2+ with 1,2-bis(2-aminophenoxy)ethane-N,N,N'N'-tetraacetic acid reduced cinobufagin-induced cytotoxicity in GHA cells. In GHA cells, cinobufagin-induced Ca 2+ entry was inhibited by 2-aminoethoxydiphenyl borate or SKF96365. In a Ca 2+ -free medium, treatment with thapsigargin or U73122 abolished cinobufagin-evoked [Ca 2+ ] i rises. Furthermore, treatment with N-acetylcysteine reversed ROS production and cytotoxicity in cinobufagin-treated GHA cells. Together, in GHA cells but not in HCN-2 cells cinobufagin caused cytotoxicity that was linked to preceding [Ca 2+ ] i rises by Ca 2+ influx via store-operated Ca 2+ entry and phospholipase C-dependent Ca 2+ release from the endoplasmic reticulum. Moreover, cinobufagin induced ROS-associated cytotoxicity., (© 2021 Wiley Periodicals LLC.)

Fusarium mycotoxins are one of the largest families of mycotoxins. Among these mycotoxins, deoxynivalenol is the most widespread pollutant of grains. However, the mechanism underlying the effect of deoxynivalenol on cytotoxicity in human brain endothelial cells was still unclear. This study examined whether deoxynivalenol induced oxidative stress-associated cytotoxicity in primary human brain endothelial cells (HBEC-5i), and explored whether Vitamin E (VE), a selective antioxidant, had protective effects on deoxynivalenol-treated cells. Deoxynivalenol (10-50 μM) concentration-dependently induced cytotoxicity in HBEC-5i cells. Deoxynivalenol (IC50 = 20 μM) activated mitochondrial apoptotic pathway by modulating antioxidant protein expressions (Nrf2, HO-1 and NQO1). More significantly, pre-treatment with VE (20 μM) attenuated the deoxynivalenol-induced cytotoxicity in this cell model. Together, VE significantly alleviated the apoptotic effects of deoxynivalenol in HBEC-5i cells suggesting that it protected the cells against deoxynivalenol-induced oxidative damage. Our findings provided new insight that VE had the potential to ameliorate neurotoxicity of deoxynivalenol., (© 2021 Wiley Periodicals LLC.)

Hypaconitine, a neuromuscular blocker, is a diterpene alkaloid found in the root of Aconitum carmichaelii. Although hypaconitine was shown to affect various physiological responses in neurological models, the effect of hypaconitine on cell viability and the mechanism of its action of Ca 2+ handling is elusive in cortical neurons. This study examined whether hypaconitine altered viability and Ca 2+ signalling in HCN-2 neuronal cell lines. Cell viability was measured by the cell proliferation reagent (WST-1). Cytosolic Ca 2+ concentrations [Ca 2+ ] i was measured by the Ca 2+ -sensitive fluorescent dye fura-2. In HCN-2 cells, hypaconitine (10-50 μmol/L) induced cytotoxicity and [Ca 2+ ] i rises in a concentration-dependent manner. Removal of extracellular Ca 2+ partially reduced the hypaconitine's effect on [Ca 2+ ] i rises. Furthermore, chelation of cytosolic Ca 2+ with BAPTA-AM reduced hypaconitine's cytotoxicity. In Ca 2+ -containing medium, hypaconitine-induced Ca 2+ entry was inhibited by modulators (2-APB and SKF96365) of store-operated Ca 2+ channels and a protein kinase C (PKC) inhibitor (GF109203X). Hypaconitine induced Mn 2+ influx indirectly suggesting that hypaconitine evoked Ca 2+ entry. In Ca 2+ -free medium, treatment with the endoplasmic reticulum Ca 2+ pump inhibitor thapsigargin abolished hypaconitine-induced [Ca 2+ ] i rises. Conversely, treatment with hypaconitine inhibited thapsigargin-induced [Ca 2+ ] i rises. However, inhibition of phospholipase C (PLC) with U73122 did not inhibit hypaconitine-induced [Ca 2+ ] i rises. Together, hypaconitine caused cytotoxicity that was linked to preceding [Ca 2+ ] i rises by Ca 2+ influx via store-operated Ca 2+ entry involved PKC regulation and evoking PLC-independent Ca 2+ release from the endoplasmic reticulum. Because BAPTA-AM loading only partially reversed hypaconitine-induced cell death, it suggests that hypaconitine induced a second Ca 2+ -independent cytotoxicity in HCN-2 cells., (© 2021 John Wiley & Sons Australia, Ltd.)

Mesaconitine, one of Aconitum carmichaelii Debx bioactive compounds, was shown to evoke Ca 2+ homeostasis and its related physiological effects in endothelial cell types. However, the effect of mesaconitine on Ca 2+ signaling and cell viability in human brain microvascular endothelial cells is unclear. This study focused on exploring whether mesaconitine changed cytosolic Ca 2+ concentrations ([Ca 2+ ] i ), affected cell viability, and established the relationship between Ca 2+ signaling and viability in HBEC-5i human brain microvascular endothelial cells. In HBEC-5i cells, cell viability was measured by the cell proliferation reagent (WST-1). [Ca 2+ ] i was measured by the Ca 2+ -sensitive fluorescent dye fura-2. Mesaconitine (10-100 μM) concentration dependently induced [Ca 2+ ] i rises. Ca 2+ removal reduced the signal by approximately 25%. Mesaconitine (40-100 μM) caused cytotoxicity in HBEC-5i cells. This cytotoxic response was significantly reversed by chelation of cytosolic Ca 2+ with BAPTA/AM. In Ca 2+ -containing medium, mesaconitine-induced Ca 2+ entry was inhibited by 25% by modulators of store-operated Ca 2+ channels and protein kinase C (PKC). Furthermore, mesaconitine also induced Mn 2+ influx suggesting of Ca 2+ entry. In Ca 2+ -free medium, treatment with the endoplasmic reticulum Ca 2+ pump inhibitor thapsigargin abolished mesaconitine-evoked [Ca 2+ ] i rises. Conversely, treatment with mesaconitine abolished thapsigargin-evoked [Ca 2+ ] i rises. Inhibition of phospholipase C (PLC) with U73122 abolished mesaconitine-induced [Ca 2+ ] i rises. In sum, mesaconitine caused cytotoxicity that was triggered by preceding [Ca 2+ ] i rises. Furthermore, mesaconitine induced [Ca 2+ ] i rises by evoking Ca 2+ entry via PKC-sensitive store-operated Ca 2+ channels and PLC-dependent Ca 2+ release from the endoplasmic reticulum. It suggests that Ca 2+ signaling have a potential cytotoxic effect on mesaconitine-treated human brain microvascular endothelial cells.

Background: Intracranial solitary fibrous tumor/hemangiopericytoma (HPC) is a rare and aggressive tumor. We conducted this retrospective study to investigate the outcome of patients after treatment, the efficacy of postoperative adjuvant radiotherapy, and the factors not conducive to total resection., Methods: We conducted a retrospective review of the medical records of patients harboring fresh intracranial solitary fibrous tumor/HPC treated from January 2009 to December 2019 in our hospital. We reviewed their clinical presentations, radiologic appearances, tumor size and location, extent of resection, estimate intraoperative blood loss, treatment modalities and results, and duration of follow-up., Results: There were seven consecutive patients (three males and four females). The ages of the patients at the time of diagnosis ranged from 35 to 77 years (mean: 52.86 years). Five patients (71.43%) got tumor bigger than 5 cm in dimension and only 1 patient (14.29%) underwent gross total tumor resection in the first operation without complication. Five patients (71.43%) underwent postoperative adjuvant radiotherapy. Follow-up period ranged from 4.24 to 123.55 months and the median follow-up period was 91.36 months. Three patients had favorable outcome with Glasgow Outcome Scale (GOS) equal to 4; four patients had unfavorable outcome with GOS equal to 2 or 3. No mortality was happened., Conclusion: Gross total tumor resection in the initial surgery is very important to achieve a better outcome. Massive intraoperative bleeding and venous sinus or major vessels adjoining are factors not conducive to total resection. Radiotherapy can be administered as adjuvant therapy for cases showing an aggressive phenotype or not treated with gross total resection., Competing Interests: There are no conflicts of interest., (Copyright: © 2020 Surgical Neurology International.)

Haloperidol, a typical antipsychotic medication, has been shown to possess various biological effects in different brain models. However, the impact of haloperidol on Ca 2+ signaling in astrocytes is elusive. This study explored the effect of haloperidol on cytosolic free Ca 2+ levels ([Ca 2+ ] i ) and viability, and established these two connections in Gibco® Human Astrocytes (GHAs) and DI TNC1 rat astrocytes. Haloperidol (5-20 μM) caused [Ca 2+ ] i rises in a concentration-dependent manner in GHAs but not in DI TNC1 cells. Furthermore, removal of extracellular Ca 2+ reduced haloperidol's effect by approximately 30% in GHAs. Haloperidol (20-40 μM) evoked concentration-dependent cytotoxicity in GHAs and DI TNC1 cells. However, chelating cytosolic Ca 2+ with the Ca 2+ chelator BAPTA/AM significantly reversed haloperidol's cytotoxicity only in GHAs. In GHAs, haloperidol-induced Ca 2+ entry was inhibited by store-operated Ca 2+ modulators (2-APB and SKF96365) and the protein kinase C (PKC) inhibitor GF109203X. This Ca 2+ entry induced by haloperidol was confirmed by Mn 2+ entry-induced quench of fura-2 fluorescence. In Ca 2+ -free medium, treatment with the endoplasmic reticulum Ca 2+ pump inhibitor 2,5-di-tert-butylhydroquinone (BHQ) abolished haloperidol-induced [Ca 2+ ] i rises. Conversely, treatment with haloperidol inhibited 45% of BHQ-evoked [Ca 2+ ] i rises. Moreover, haloperidol-induced Ca 2+ release from the endoplasmic reticulum was abolished by inhibition of phospholipase C (PLC) by U73122. Together, in GHAs but not in DI TNC1 cells, haloperidol caused Ca 2+ -associated cell death, induced Ca 2+ entry via PKC-sensitive store-operated Ca 2+ channels, and evoked PLC-dependent Ca 2+ release from the endoplasmic reticulum. The protective effect of Ca 2+ chelating on haloperidol-induced cytotoxicity in human astrocytes was also demonstrated.

The purpose of this study was to investigate muscle activity and intermuscular coherence of the rectus femoris (RF) and biceps femoris (BF) during forward (FW) and backward (BW) pedaling. Sixteen healthy volunteers performed FW and BW pedaling in 30, 45, and 60 revolutions per minute (RPM), while electromyographic (EMG) signals of the RF and BF were recorded bilaterally to determine integral EMG and intermuscular coherence. BW pedaling showed a statistically significant larger EMG activity on the left BF (P = 0.023) in 30 RPM; on the left BF (P = 0.01), right BF (P = 0.05), and right RF (P = 0.006) in 45 RPM, and on the left BF (P = 0.014) and right RF (P = 0.011) in 60 RPM than FW pedaling. In 45 RPM, higher coherence was demonstrated on the left leg (P = 0.011) during the left flexor and right extensor phases and on the right leg (P = 0.043) during the right flexor and left extensor phases in BW compared with FW pedaling. In 60 RPM, higher coherence was observed on both legs (left, P = 0.037; right, P < 0.001) during the left flexor and right extensor phases in BW compared with FW pedaling. Our results suggest that BW pedaling increased the muscle activity of both biarticular muscles and intermuscular coherence., Competing Interests: None

Background: Mandibular prognathism is a common dentofacial deformity in Asia. Treatment of such condition may vary from orthodontic camouflage to surgical orthodontics with orthognathic surgery depending on the severity of the condition. Because of the prominent position of the mandible, fractures involving different locations of the mandible commonly occur in maxillofacial trauma. Anatomical reduction of maxillofacial fractures and restoration of the pretraumatic occlusion are the primary goals of acute management of facial fractures. In patients with dentofacial deformity, simultaneous surgical correction of their malocclusion and improvement of their facial aesthetics while providing open treatment to the maxillofacial fractures are rarely reported in the literature., Patients and Methods: We reported 3 cases with combined open reduction and internal fixation and surgery-first orthognathic surgery principles to correct class III malocclusion with mandibular prognathism during acute management of maxillofacial fractures. Computer-assisted surgical simulation was used in surgical planning and fabrication of surgical splint., Results: Two patients underwent mandibular osteotomies in addition to open reduction and internal fixation of maxillofacial fractures. One patient had both maxillary and mandibular osteotomies during facial fracture repair. Class I occlusion with satisfactory facial profile was achieved in all 3 cases., Conclusions: Careful patient selection with presurgical planning using computer-assisted surgical simulation is essential in achieving successful outcomes in correcting dentofacial deformities while managing maxillofacial fractures. This combined technique is a viable option in the surgical management of facial fractures in patients with dentofacial deformities.

Purpose: The purpose of this retrospective study was to investigate the differentiation of abscess and necrotic tumors, using susceptibility-weighted imaging (SWI) and apparent diffusion coefficients (ADC) either separated or combined., Methods: Imaging was performed on 26 patients with pyogenic brain abscesses, 31 patients with rim-enhancing glioblastomas, and 21 patients with rim-enhancing metastases. The degree of intralesional susceptibility signal (ILSS) was independently assessed by three observers. Average ADC in the lesion core was calculated. After receiver operating characteristic (ROC) analysis, the area under the ROC curve was compared using three different analytical models (ILSS, ADC, and ILSS-ADC combined) to differentiate abscess from the two rim-enhancing necrotic tumors., Results: The ILSS-ADC combined model had greater area under the ROC curves than ILSS or ADC used alone. In this study, the ILSS-ADC combined model showed 100% diagnostic accuracy differentiating abscesses from glioblastoma. The ADC model and the ILSS-ADC combined model performed equally well in distinguishing abscesses from metastases., Conclusion: It is concluded that SWI and ADC are complementary, and the combination of SWI and ADC may improve results compared with the use of only one model. Validation by an independent cohort is the next necessary step to broaden its applicability in routine clinical settings., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Malathion, one of commonly used organophosphate insecticides, has a wide range of toxic actions in different models. However, the effect of this compound on Ca 2+ homeostasis and its related cytotoxicity in glial cells is elusive. This study examined whether malathion evoked intracellular Ca 2+ concentration ([Ca 2+ ] i ) rises and established the relationship between Ca 2+ signaling and cytotoxicity in normal human astrocytes, rat astrocytes and human glioblastoma cells. The data show that malathion induced concentration-dependent [Ca 2+ ] i rises in Gibco ® Human Astrocytes (GHA cells), but not in DI TNC1 normal rat astrocytes and DBTRG-05MG human glioblastoma cells. In GHA cells, this Ca 2+ signal response was reduced by removing extracellular Ca 2+ . In Ca 2+ -free medium, pretreatment with the endoplasmic reticulum Ca 2+ pump inhibitor thapsigargin abolished malathion-induced [Ca 2+ ] i rises. Conversely, incubation with malathion abolished thapsigargin-induced [Ca 2+ ] i rises. Inhibition of phospholipase C (PLC) with U73122 also blocked malathion-induced [Ca 2+ ] i rises. In Ca 2+ -containing medium, malathion-induced [Ca 2+ ] i rises was inhibited by store-operated Ca 2+ channel blockers (2-APB, econazole or SKF96365) and the protein kinase C (PKC) inhibitor GF109203X. Malathion (5-25 μM) concentration-dependently caused cytotoxicity in GHA, DI TNC1 and DBTRG-05MG cells. This cytotoxic effect was partially prevented by prechelating cytosolic Ca 2+ with BAPTA-AM (a selective Ca 2+ chelator) only in GHA cells. Together, in GHA but not in DI TNC1 and DBTRG-05MG cells, malathion induced [Ca 2+ ] i rises by inducing PLC-dependent Ca 2+ release from the endoplasmic reticulum and Ca 2+ entry via PKC-sensitive store-operated Ca 2+ channels. Furthermore, malathion induced Ca 2+ -associated cytotoxicity, suggesting that Ca 2+ chelating may have a protective effect on malathion-induced cytotoxicity in normal human astrocytes., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Exposure to insecticides has been found to have deleterious effects on human health. Lambda-cyhalothrin (LCT), a mixture of isomers of cyhalothrin, is a pyrethroid insecticide routinely used in pest control programs. LCT was reported to cause neurotoxic effects in various models. However, the mechanism of underlying effect of LCT on cytotoxicity in normal human brain cells is still elusive. This study examined whether LCT affected Ca 2+ homeostasis and Ca 2+ -related physiology in Gibco® Human Astrocytes (GHA cells), and explored whether BAPTA-AM (1,2-bis(2-aminophenoxy)ethane-N,N,N'N'-tetraacetic acid), a selective Ca 2+ chelator, has protective effects on LCT-treated GHA cells. The data show that LCT (10-15 μM) concentration-dependently induced cytotoxicity in both GHA cells and DI TNC1 normal rat astrocytes but only induced intracellular Ca 2+ concentration ([Ca 2+ ] i ) rises in GHA cells. In terms of Ca 2+ signaling in GHA cells, LCT-induced [Ca 2+ ] i rises were reduced by removing extracellular Ca 2+ and were inhibited by store-operated Ca 2+ channel modulators (2-APB, econazole or SKF96365). In Ca 2+ -free medium, pretreatment with the endoplasmic reticulum Ca 2+ pump inhibitor thapsigargin abolished LCT-induced [Ca 2+ ] i rises. Conversely, incubation with LCT abolished thapsigargin-induced [Ca 2+ ] i rises. Regarding cytotoxicity, LCT evoked apoptosis by regulating apoptotic protein expressions (Bax, BCl-2, cleaved caspase-9/-3). This apoptotic response was significantly inhibited by prechelating cytosolic Ca 2+ with BAPTA-AM. Together, in GHA cells, LCT induced [Ca 2+ ] i rises by inducing Ca 2+ entry via store-operated Ca 2+ channels and Ca 2+ release from the endoplasmic reticulum. Moreover, BAPTA-AM has a protective effect on inhibiting LCT-activated mitochondrial apoptotic pathway. This study provided new insights into the molecular protective mechanism of LCT-induced cytotoxicity in normal human astrocytes., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Propofol (2,6-diisopropylphenol), one of the extensively and commonly used anesthetic agents, has been shown to affect the biological behavior of various models. Previous researches have shown that propofol-induced cytotoxicity might cause anticancer effect in different cells. However, the mechanisms underlying the effect of propofol on cytotoxicity is still elusive in human glioblastoma cells. The aims of this study were to evaluate effects of propofol on cytotoxicity, cell cycle distribution and ROS production, and establish the relationship between oxidative stress and cytotoxicity in GBM 8401 human glioblastoma cells and DI TNC1 rat astrocytes. Propofol (20-30 μM) concentration-dependently induced cytotoxicity, cell cycle arrest, and increased ROS production in GBM 8401 cells but not in DI TNC1 cells. In GBM 8401 cells, propofol induced G2/M phase cell arrest, which affected the CDK1, cyclin B1, p53, and p21 protein expression levels. Furthermore, propofol induced oxygen stresses by increasing O2- and H 2 O 2 levels but treatment with the antioxidant N-acetylcysteine (NAC) partially reversed propofol-regulated antioxidative enzyme levels (superoxide dismutase, catalase, and glutathione peroxidase). Most significantly, propofol induced apoptotic effects by decreasing Bcl-2 but increasing Bax, cleaved caspase-9/caspase-3 levels, which were partially reversed by NAC. Moreover, the pancaspase inhibitor Z-VAD-FMK also partially prevented propofol-induced apoptosis. Together, in GBM 8401 cells but not in DI TNC1 cells, propofol activated ROS-associated apoptosis that involved cell cycle arrest and caspase activation. These findings indicate that propofol not only can be an anesthetic agent which reduces pain but also has the potential to be used for the treatment of human glioblastoma., (© 2017 Wiley Periodicals, Inc.)

Tetramethylpyrazine (TMP) is a compound purified from herb. Its effect on Ca 2+ concentrations ([Ca 2+ ] i ) in renal cells is unclear. This study examined whether TMP altered Ca 2+ signaling in Madin-Darby canine kidney (MDCK) cells. TMP at 100-800 μM induced [Ca 2+ ] i rises, which were reduced by Ca 2+ removal. TMP induced Mn 2+ influx implicating Ca 2+ entry. TMP-induced Ca 2+ entry was inhibited by 30% by modulators of protein kinase C (PKC) and store-operated Ca 2+ channels. Treatment with the endoplasmic reticulum Ca 2+ pump inhibitor 2,5-di-tert-butylhydroquinone (BHQ) inhibited 93% of TMP-evoked [Ca 2+ ] i rises. Treatment with TMP abolished BHQ-evoked [Ca 2+ ] i rises. Inhibition of phospholipase C (PLC) abolished TMP-induced responses. TMP at 200-1000 μM decreased viability, which was not reversed by pretreatment with the Ca 2+  chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester. Together, in MDCK cells, TMP induced [Ca 2+ ] i rises by evoking PLC-dependent Ca 2+ release from endoplasmic reticulum and Ca 2+ entry via PKC-sensitive store-operated Ca 2+ entry. TMP also caused Ca 2+ -independent cell death., (© 2017 Wiley Periodicals, Inc.)

Researches have been conducted to explore the biological effect of gastrodin, a natural compound extracted from the rhizome of Gastrodia elata Blume, in different models. However, the effects of gastrodin on cytotoxicity, cell cycle distribution and oxidative stress in glia cells have not been explored. The aim of this study was to investigate the cytotoxic effect of gastrodin and its mechanisms in DBTRG-05MG human glioblastoma cells and CTX TNA2 rat astrocytes. In DBTRG-05MG cells but not in CTX TNA2 cells, gastrodin (20-30 μM) induced cytotoxicity, G2/M phase cell cycle arrest and apoptosis. Regarding oxidative stress, gastrodin (20-30 μM) elevated intracellular ROS levels but reduced GSH levels. Treatment with the antioxidant NAC (10 μM) partially reversed gastrodin-altered antioxidant enzymes levels. Furthermore, gastrodin induced mitochondria-associated apoptosis. The apoptotic effects evoked by gastrodin were partially inhibited by the antioxidant NAC and the pancaspase inhibitor Z-VAD-FMK. Together, in DBTRG-05MG cells, but not in CTX TNA2 cells, gastrodin activated ROS-associated mitochondrial apoptotic pathways that involved cell cycle arrest. These data provide insight into the molecular mechanisms governing the ability of gastrodin to induce cytotoxicity in human glioblastoma cells and further suggest that gastrodin is a new potential agent for the treatment of human gliblasoma., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Methoxsalen is a natural compound found in many seed plants. The effect of methoxsalen on Ca²⁺- related physiology in human osteosarcoma is unclear. This study investigated the effect of methoxsalen on cytosolic free Ca²⁺ concentrations ([Ca²⁺]i) in MG63 human osteosarcoma cells. Methoxsalen induced [Ca²⁺]i rises concentration-dependently. Methoxsalen-induced Ca²⁺ entry was confirmed by Mn²⁺-induced quench of fura-2 fluorescence. This Ca²⁺ entry was suppressed by nifedipine, econazole, and SKF96365. In Ca²⁺-free medium, incubation with the endoplasmic reticulum Ca²⁺ pump inhibitor 2,5-di-tert-butylhydroquinone (BHQ) inhibited methoxsalen-evoked [Ca²⁺]i rises by 96%. In contrast, incubation with methoxsalen abolished BHQ-evoked [Ca²⁺]i rises. Inhibition of phospholipase C (PLC) with U73122 abolished methoxsalen-induced [Ca²⁺]i rises. Methoxsalen was cytotoxic at 300-700 μM in a concentration-dependent fashion. Chelating cytosolic Ca²⁺ with 1,2-bis(2-aminophenoxy)ethane-N,N,N’,N’-tetraacetic acid/acetoxymethyl ester (BAPTA/AM) did not prevent methoxsalen-induced cytotoxicity. Collectively, our data suggest that in MG63 cells, methoxsalen induced [Ca²⁺]i rises by evoking PLC-dependent Ca²⁺ release from the endoplasmic reticulum, and Ca²⁺ entry via store-operated Ca²⁺ entry. Methoxsalen also induced Ca²⁺- disassociated cell death., Competing Interests: The authors declared no conflicts of interest.

The subcutaneous implantable cardioverter defibrillator (S-ICD) registry included very few patients with a body mass index (BMI) greater than 40. We present a case of a 40-year-old male with a BMI of 44 and ejection fraction of 25% who underwent S-ICD implantation for primary prevention of sudden cardiac death in the setting of a nonischemic cardiomyopathy. Defibrillation threshold (DFT) testing failed at high output. A posterior to anterior radiograph demonstrated migration of the components despite positioning under fluoroscopy. After repositioning, repeat DFT testing showed an inconsistent efficacy. We discuss the probabilistic nature of DFT testing, clinical factors affecting the S-ICD implant in the obese population and offer a novel insight from this specific experience., (© 2016 S. Karger AG, Basel.)

Cytochalasin B, a cell-permeable mycotoxin isolated from the fungus Phoma spp., shows a wide range of biological effects, among which its potent antitumor activity has raised great interests in different models. However, the cytotoxic activity of cytochalasin B and its underlying mechanisms have not been elucidated in breast cells. This study examined the effect of cytochalasin B on MCF 10A human breast epithelial cells and ZR-75-1 human breast cancer cells. Cytochalasin B (10-20μM) concentration-dependently induced cytotoxicity, cell cycle arrest, and [Ca 2+ ] i rises in ZR-75-1 cells but not in MCF 10A cells. In ZR-75-1 cells, cytochalasin B triggered G2/M phase arrest through the modulation of CDK1, cyclin B1, p53, p27 and p21 expressions. The Ca 2+ signal response induced by cytochalasin B was reduced by removing extracellular Ca 2+ and was inhibited by the store-operated Ca 2+ channel blocker 2-APB and SKF96365. In Ca 2+ -free medium, cytochalasin B induced Ca 2+ release through thapsigargin-sensitive endoplasmic reticulum stores. Moreover, cytochalasin B increased H 2 O 2 levels but reduced GSH levels. The apoptotic effects evoked by cytochalasin B were partially inhibited by prechelating cytosolic Ca 2+ with BAPTA-AM and the antioxidant NAC. Together, in ZR-75-1 cells but not in MCF 10A cells, cytochalasin B activated Ca 2+ -associated mitochondrial apoptotic pathways that involved G2/M phase arrest and ROS signaling. Furthermore, cytochalasin B induced [Ca 2+ ] i rises by releasing Ca 2+ from the endoplasmic reticulum and causing Ca 2+ influx through 2-APB or SKF96365-sensitive store-operated Ca 2+ entry. Our findings provide new insights into the possible application of cytochalasin B in human breast cancer therapy., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Gallic acid, a polyhydroxylphenolic compound, is widely distributed in various plants, fruits and foods. It has been shown that gallic acid passes into blood brain barrier and reaches the brain tissue of middle cerebral artery occlusion rats. However, the effect of gallic acid on Ca(2+) signaling in glia cells is unknown. This study explored whether gallic acid affected Ca(2+) homeostasis and induced Ca(2+)-associated cytotoxicity in DBTRG-05MG human glioblastoma cells and CTX TNA2 rat astrocytes. Gallic acid (20-40 μM) concentration-dependently induced cytotoxicity and intracellular Ca(2+) level ([Ca(2+)]i) increases in DBTRG-05MG cells but not in CTX TNA2 cells. In DBTRG-05MG cells, the Ca(2+) response was decreased by half by removal of extracellular Ca(2+). In Ca(2+)-containing medium, gallic acid-induced Ca(2+) entry was inhibited by store-operated Ca(2+) channel inhibitors (2-APB, econazole and SKF96365). In Ca(2+)-free medium, pretreatment with the endoplasmic reticulum Ca(2+) pump inhibitor thapsigargin abolished gallic acid-induced [Ca(2+)]i increases. Conversely, incubation with gallic acid also abolished thapsigargin-induced [Ca(2+)]i increases. Inhibition of phospholipase C with U73122 abolished gallic acid-induced [Ca(2+)]i increases. Gallic acid significantly caused cytotoxicity in DBTRG-05MG cells, which was partially prevented by prechelating cytosolic Ca(2+) with BAPTA-AM. Moreover, gallic acid activated mitochondrial apoptotic pathways that involved ROS production. Together, in DBTRG-05MG cells but not in CTX TNA2 cells, gallic acid induced [Ca(2+)]i increases by causing Ca(2+) entry via 2-APB, econazole and SKF96365-sensitive store-operated Ca(2+) entry, and phospholipase C-dependent release from the endoplasmic reticulum. This Ca(2+) signal subsequently evoked mitochondrial pathways of apoptosis that involved ROS production., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Objectives: To investigate the feasibility of using susceptibility-weighted imaging (SWI) to discriminate abscesses and necrotic tumours., Methods: Twenty-one patients with pyogenic abscesses, 21 patients with rim-enhancing glioblastomas and 23 patients with rim-enhancing metastases underwent SWI. Intralesional susceptibility signal (ILSS) was analyzed employing both qualitative (QL) and semi-quantitative (SQ) methods. Logistic regression models and receiver operating characteristic analysis were used to demonstrate the discriminating power., Results: In QL analysis, ILSSs were seen in 12 of 21 abscesses, in 20 of 21 glioblastomas, and in 16 of 23 metastases. In SQ analysis, a low degree of ILSS (85.8 %) was in the majority of abscesses and a high degree of ILSS (76.2 %) was in the majority of glioblastomas. SQ model was significantly better than QL model in distinguishing abscesses from glioblastomas (P < .001). A derived ILSS cutoff grade of 1 or less was quantified as having a sensitivity of 85.7 %, specificity of 90.5 %, accuracy of 88.1 %, PPV of 90.0 %, and NPV of 86.4 % in distinguishing abscesses from glioblastomas., Conclusions: A high-grade ILSS may help distinguish glioblastomas from abscesses and necrotic metastatic brain tumours. The lack of ILSS or low-grade ILSS can be a more specific sign in the imaging diagnosis of abscesses., Key Points: • ILSS of SWI can contribute to differential diagnosis of rim-enhanced mass. • Low-grade ILSS can be a more specific sign in abscesses. • High-grade ILSS may help distinguish necrotic glioblastomas from abscesses. • ILSS spreads across the four ILSS categories in metastases.

Eugenol, a natural phenolic constituent of clove oil, has a wide range of applications in medicine as a local antiseptic and anesthetic. However, the effect of eugenol on human glioblastoma is unclear. This study examined whether eugenol elevated intracellular free Ca(2+) levels ([Ca(2+)]i) and induced apoptosis in DBTRG-05MG human glioblastoma cells. Eugenol evoked [Ca(2+)]i rises which were reduced by removing extracellular Ca(2+). Eugenol-induced [Ca(2+)]i rises were not altered by store-operated Ca(2+) channel blockers but were inhibited by the PKC inhibitor GF109203X and the transient receptor potential channel melastatin 8 (TRPM8) antagonist capsazepine. In Ca(2+)-free medium, pretreatment with the endoplasmic reticulum Ca(2+) pump inhibitor thapsigargin (TG) or 2,5-di-tert-butylhydroquinone (BHQ) abolished eugenol-induced [Ca(2+)]i rises. The phospholipase C (PLC) inhibitor U73122 significantly inhibited eugenol-induced [Ca(2+)]i rises. Eugenol killed cells which were not reversed by prechelating cytosolic Ca(2+) with 1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester (BAPTA-AM). Eugenol induced apoptosis through increasing reactive oxygen species (ROS) production, decreasing mitochondrial membrane potential, releasing cytochrome c and activating caspase-9/caspase-3. Together, in DBTRG-05MG cells, eugenol evoked [Ca(2+)]i rises by inducing PLC-dependent release of Ca(2+) from the endoplasmic reticulum and caused Ca(2+) influx possibly through TRPM8 or PKC-sensitive channels. Furthermore, eugenol induced the mitochondrial apoptotic pathway., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

Introduction: Primary central nervous lymphoma(PCNSL) is a rare form of non-Hodgkin lymphoma confined to the central nervous system. Most of the lesions are supratentorial and periventricular, often involving deep structures such as corpus callosum and basal ganglion. Isolated intraventricular lymphoma is rare and only a few case reports. We report, to the best of our knowledge, the seventh case of isolated PCNSL in the fourth ventricle in an immunocompetent patient., Presentation of Case: A 61-year-old male presenting with 3 months of headache and dizziness followed with unsteady gait for days. The MR imaging of brain revealed a homogeneously enhancing lesion occupying almost the whole 4th ventricle.The tumor was removed subtotally via suboccipital craniotomy. Histopathology revealed the lesion be a diffuse large B-cell lymphoma., Discussion: PCNSL is an important consideration in the differential diagnosis of intracranial mass lesion. The unusual location in surgically accessible fourth ventricle in posterior fossa, the isolation of the tumor may present a compelling indication for surgical resection., Conclusion: We suggest that primary lymphoma should be considered with homogenous lesions of the 4th ventricle. Also aggressive surgical resection in this surgically accessible location, instead of biopsy only, is rational., (Copyright © 2015 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Intraspinal tumors are rare central nervous system neoplasms. The reported clinical features of intraspinal tumors have varied in previous studies. We present here the cases of 184 patients with intraspinal tumors treated surgically in our hospital and a review of the literature., Methods: We conducted a retrospective review of 184 patients with intraspinal tumors who underwent surgical treatment in our institution between 2002 and 2013. Their age, sex, initial presentation, tumor location, level of affected vertebral column, histological diagnosis, and primary origin of the metastatic tumor were reviewed and analyzed., Results: Of these 184 patients, 97 (52.7%) were men and 87 (47.3%) were women. The mean age was 56.3 years (range 7-83 years). A total of 102 (55.4%) had primary tumors, while 82 (44.6%) patients had developed metastatic tumors. The histological diagnosis of the primary tumors included 55 (53.9%) schwannomas, 16 (15.7%) meningiomas, six (5.9%) ependymomas, five (4.9%) neurofibromas, three (2.9%) hemangiomas, two (2.0%) hemagioblastomas, and 15 (14.7%) other tumor types. The most common primary sites of the metastatic tumors were the lung and breast., Conclusion: Primary tumors were more numerous than metastastic tumors in our series of patients. For the primary tumors, our study showed a higher proportion of nerve sheath cell tumors (schwannomas and neurofibromas) and fewer meningiomas and neuroepithelial tumors compared with reports from non-Asian countries. In addition, the lung was the most common origin of the metastatic tumors and more than half of these tumors were located at the thoracic spine. Back pain and radicular pain were the most common presentations in patients with intraspinal tumors., (Copyright © 2014. Published by Elsevier Taiwan.)

Flexible integrated circuits with complex functionalities are the missing link for the active development of wearable electronic devices. Here, we report a scalable approach to fabricate self-aligned graphene microwave transistors for the implementation of flexible low-noise amplifiers and frequency mixers, two fundamental building blocks of a wireless communication receiver. A devised AlOx T-gate structure is used to achieve an appreciable increase of device transconductance and a commensurate reduction of the associated parasitic resistance, thus yielding a remarkable extrinsic cutoff frequency of 32 GHz and a maximum oscillation frequency of 20 GHz; in both cases the operation frequency is an order of magnitude higher than previously reported. The two frequencies work at 22 and 13 GHz even when subjected to a strain of 2.5%. The gigahertz microwave integrated circuits demonstrated here pave the way for applications which require high flexibility and radio frequency operations.

The surgery-first approach in orthognathic surgery has recently created a broader interest in completely eliminating time-consuming preoperative orthodontic treatment. Available evidence on the surgery-first approach should be appraised to support its use in orthognathic surgery. A MEDLINE search using the keywords "surgery first" and "orthognathic surgery" was conducted to select studies using the surgery-first approach. We also manually searched the reference list of the selected keywords to include articles not selected by the MEDLINE search. The search identified 18 articles related to the surgery-first approach. There was no randomized controlled clinical trial. Four papers were excluded as the content was only personal opinion or basic scientific research. Three studies were retrospective cohort studies in nature. The other 11 studies were case reports. For skeletal Class III surgical correction, the final long-term outcomes for maxillofacial and dental relationship were not significantly different between the surgery-first approach and the orthodontics-first approach in transverse (e.g., intercanine or intermolar width) dimension, vertical (e.g., anterior open bite, lower anterior facial height) dimension, and sagittal (e.g., anterior-posterior position of pogonion and lower incisors) dimension. Total treatment duration was substantially shorter in cases of surgery-first approach use. In conclusion, most published studies related to the surgery-first approach were mainly on orthognathic correction of skeletal Class III malocclusion. Both the surgery-first approach and orthodontics-first approach had similar long-term outcomes in dentofacial relationship. However, the surgery-first approach had shorter treatment time.