Constructing Reversible Li Deposition Interfaces by Tailoring Lithiophilic Functionalities of a Heteroatom-Doped Graphene Interlayer for Highly Stable Li Metal Anodes.

Lithium (Li) metal has been regarded as the ideal anode for rechargeable batteries due to its low reduction potential and high theoretical capacity. However, the formation of fatal Li dendrites during repeated cycling shortens the battery life and causes serious safety concerns. Functionalized separators with electrically conductive and lithiophilic coating layers potentially inhibit dendrite formation and growth on Li metal anodes by providing nucleation sites for reversible Li deposition/stripping. In this work, we propose functionalized separators incorporating heteroatom-doped (N or B) graphene interlayers to modulate the Li nucleation behavior. The electronegative N-doping and electropositive B-doping were investigated to understand their regulation of the Li deposition behavior. With the heteroatom-doped graphene-coated separators, we observe significantly improved cycling stability along with enhanced charge transfer kinetics and low Li nucleation overpotential. This is attributed to the heteroatom-doped graphene interlayer expanding the surface area of the Li metal anode while providing additional space for uniform Li deposition/stripping, thus preventing undesirable side reactions. As a result, the formation of dendrites and pits on the Li metal anode surface is suppressed, demonstrating the protective effect of the Li metal anode. Interestingly, N-doped graphene-coated separators exhibit lower Li nucleation overpotentials than B-doped graphene-coated separators but rather lower average Coulombic efficiencies and reduced cycling stability. This implies that adequate adsorption on B-based sites, as opposed to the strong adsorption on N-based sites, improves the reversibility. Notably, the Li adsorption strength of the lithiophilic functional groups critically affects the reversibility, as observed by Li nucleation barrier measurements and atomistic simulations. This work suggests that interface engineering using conductive and lithiophilic materials can be a promising strategy for controlling Li deposition in advanced Li metal batteries.

Modeling of the brain-lung axis using organoids in traumatic brain injury: an updated review.

Clinical outcome after traumatic brain injury (TBI) is closely associated conditions of other organs, especially lungs as well as degree of brain injury. Even if there is no direct lung damage, severe brain injury can enhance sympathetic tones on blood vessels and vascular resistance, resulting in neurogenic pulmonary edema. Conversely, lung damage can worsen brain damage by dysregulating immunity. These findings suggest the importance of brain-lung axis interactions in TBI. However, little research has been conducted on the topic. An advanced disease model using stem cell technology may be an alternative for investigating the brain and lungs simultaneously but separately, as they can be potential candidates for improving the clinical outcomes of TBI.In this review, we describe the importance of brain-lung axis interactions in TBI by focusing on the concepts and reproducibility of brain and lung organoids in vitro. We also summarize recent research using pluripotent stem cell-derived brain organoids and their preclinical applications in various brain disease conditions and explore how they mimic the brain-lung axis. Reviewing the current status and discussing the limitations and potential perspectives in organoid research may offer a better understanding of pathophysiological interactions between the brain and lung after TBI.

Non-Mitochondrial Aconitase-2 Mediates the Transcription of Nuclear-Encoded Electron Transport Chain Genes in Fission Yeast.

Aconitase-2 (Aco2) is present in the mitochondria, cytosol, and nucleus of fission yeast. To explore its function beyond the well-known role in the mitochondrial tricarboxylic acid (TCA) cycle, we conducted genome-wide profiling using the aco2ΔNLS mutant, which lacks a nuclear localization signal (NLS). The RNA sequencing (RNA-seq) data showed a general downregulation of electron transport chain (ETC) genes in the aco2ΔNLS mutant, except for those in the complex II, leading to a growth defect in respiratory-prone media. Complementation analysis with non-catalytic Aco2 [aco2ΔNLS + aco2(3CS)], where three cysteines were substituted with serine, restored normal growth and typical ETC gene expression. This suggests that Aco2's catalytic activity is not essential for its role in ETC gene regulation. Our mRNA decay assay indicated that the decrease in ETC gene expression was due to transcriptional regulation rather than changes in mRNA stability. Additionally, we investigated the Php complex's role in ETC gene regulation and found that ETC genes, except those within complex II, were downregulated in php3Δ and php5Δ strains, similar to the aco2ΔNLS mutant. These findings highlight a novel role for nuclear aconitase in ETC gene regulation and suggest a potential connection between the Php complex and Aco2.

Pulsed Radiofrequency Neuromodulation for Post-Stroke Shoulder Pain in Patients with Hemorrhagic Stroke.

Objective: Post-stroke shoulder pain (PSSP) is a common complication that limits the range of motion (ROM) of the shoulder, the patient's rehabilitation and in turn, affects the patients' quality of life (QOL). Several treatment modalities such as sling, positioning, strapping, functional electrical stimulation (FES), and nerve block have been suggested in literatures, however none of the treatments had long-term effects for PSSP. In this study, the authors evaluated clinical efficacy of pulsed radiofrequency (PRF) neuromodulation on the suprascapular nerve for PSSP, and suggested it as a potential treatment with long-term effect. Methods: This retrospective case series was conducted at a single center, a private practice institution. From 2013 to 2021, 13 patients with PSSP underwent PRF neuromodulation of the suprascapular nerve. The primary outcome measure was the visual analog scale (VAS) score. The secondary outcome measurements included the shoulder ROM, disability assessment scale (DAS), modified Ashworth scale (mAS), modified Rankin scale (mRS), and EuroQol-5 dimension-3L questionnaire (EQ-5D-3L) scores. These parameters were evaluated before PRF modulation, immediately after PRF modulation, and every three months until the final follow-up visit. Results: Six men and seven women were enrolled, and all patients were followed-up for a minimum of 12 months. The mean VAS score was 7.07 points before PRF neuromodulation and 2.38 points immediately post-procedure. Shoulder ROM for abduction and flexion, DAS for pain, mRS, and EQ-5D-3L demonstrated marked improvement. No complications were reported. Conclusion: PRF neuromodulation of the suprascapular nerve is an effective modality in patients with PSSP, and has long-term effect of pain relief, improvement of QOL.

Tat-RAN attenuates brain ischemic injury in hippocampal HT-22 cells and ischemia animal model.

Oxidative stress plays a key role in the pathogenesis of neuronal injury, including ischemia. Ras-related nuclear protein (RAN), a member of the Ras superfamily, involves in a variety of biological roles, such as cell division, proliferation, and signal transduction. Although RAN reveals antioxidant effect, its precise neuroprotective mechanisms are still unclear. Therefore, we investigated the effects of RAN on HT-22 cell which were exposed to H2O2-induced oxidative stress and ischemia animal model by using the cell permeable Tat-RAN fusion protein. We showed that Tat-RAN transduced into HT-22 cells, and markedly inhibited cell death, DNA fragmentation, and reactive oxygen species (ROS) generation under oxidative stress. This fusion protein also controlled cellular signaling pathways, including mitogen-activated protein kinases (MAPKs), NF-κB, and apoptosis (Caspase-3, p53, Bax and Bcl-2). In the cerebral forebrain ischemia animal model, Tat-RAN significantly inhibited both neuronal cell death, and astrocyte and microglia activation. These results indicate that RAN significantly protects against hippocampal neuronal cell death, suggesting Tat-RAN will help to develop the therapies for neuronal brain diseases including ischemic injury.

Protective Effects of PEP-1-GSTA2 Protein in Hippocampal Neuronal Cell Damage Induced by Oxidative Stress.

Glutathione S-transferase alpha 2 (GSTA2), a member of the glutathione S-transferase family, plays the role of cellular detoxification against oxidative stress. Although oxidative stress is related to ischemic injury, the role of GSTA2 against ischemia has not been elucidated. Thus, we studied whether GSTA2 prevents ischemic injury by using the PEP-1-GSTA2 protein which has a cell-permeable protein transduction domain. We revealed that cell-permeable PEP-1-GSTA2 transduced into HT-22 cells and markedly protected cell death via the inhibition of reactive oxygen species (ROS) production and DNA damage induced by oxidative stress. Additionally, transduced PEP-1-GSTA2 promoted mitogen-activated protein kinase (MAPK), and nuclear factor-kappaB (NF-κB) activation. Furthermore, PEP-1-GSTA2 regulated Bcl-2, Bax, cleaved Caspase-3 and -9 expression protein levels. An in vivo ischemic animal model, PEP-1-GSTA2, markedly prevented the loss of hippocampal neurons and reduced the activation of microglia and astrocytes. These findings indicate that PEP-1-GSTA2 suppresses hippocampal cell death by regulating the MAPK and apoptotic signaling pathways. Therefore, we suggest that PEP-1-GSTA2 will help to develop the therapies for oxidative-stress-induced ischemic injury.

Outcome Analysis of External Neurolysis in Posture-Induced Compressive Peroneal Neuropathy and the Utility of Magnetic Resonance Imaging in the Treatment Process.

OBJECTIVE: We aimed to analyze the effectiveness of external neurolysis on the common peroneal nerve (CPN) in patients with posture-induced compressive peroneal neuropathy (PICPNe). Further, we aimed to examine the utility of magnetic resonance imaging (MRI) in assessing the severity of denervation status and predicting the postoperative prognosis. METHODS: We included 13 patients (eight males and five females) with foot drop who underwent CPN decompression between 2018 and 2020. We designed a grading system for assessing the postoperative functional outcome. Additionally, we performed MRI to evaluate the denervation status of the affected musculature and its effect on postoperative recovery. RESULTS: The median time to surgery was 3 months. The median preoperative ankle dorsiflexion and eversion grades were both 3, while the average functional grade was 1. Posterior crural intermuscular septum was the most common cause of nerve compression, followed by deep tendinous fascia and anterior crural intermuscular septum. There was a significant postoperative improvement in the median postoperative ankle dorsiflexion and eversion grades and average postoperative functional (4, 5, and 2.38, respectively). Preoperative ankle eversion was significantly correlated with denervation status. Additionally, the devernation status on MRI was positively correlated with the outcome favorability. However, denervation atrophy led to a less favorable outcome. CONCLUSION: Among patients with intractable PICPNe despite conservative management, surgical intervention could clinically improve motor function and functional ability. Additionally, MRI examination of the affected muscle could help diagnose CPNe and assess the postoperative prognosis.

Tat-Thioredoxin-like protein 1 attenuates ischemic brain injury by regulation of MAPKs and apoptosis signaling.

Thioredoxin-like protein 1 (TXNL1), one of the thioredoxin superfamily known as redox-regulator, plays an essential in maintaining cell survival via various antioxidant and anti-apoptotic mechanisms. It is well known that relationship between ischemia and oxidative stress, however, the role of TXNL1 protein in ischemic damage has not been fully investigated. In the present study, we aimed to determine the protective role of TXNL1 against on ischemic injury in vitro and in vivo using cell permeable Tat-TXNL1 fusion protein. Transduced Tat-TXNL1 inhibited ROS production and cell death in H2O2-exposed hippocampal neuronal (HT-22) cells and modulated MAPKs and Akt activation, and pro-apoptotic protein expression levels in the cells. In an ischemia animal model, Tat-TXNL1 markedly decreased hippocampal neuronal cell death and the activation of astrocytes and microglia. These findings indicate that cell permeable Tat-TXNL1 protects against oxidative stress in vitro and in vivo ischemic animal model. Therefore, we suggest Tat-TXNL1 can be a potential therapeutic protein for ischemic injury. [BMB Reports 2023; 56(4): 234-239].

Fabrication and Characterization of Novel Silk Fiber-Optic SERS Sensor with Uniform Assembly of Gold Nanoparticles.

Biocompatible optical fibers and waveguides are gaining attention as promising platforms for implantable biophotonic devices. Recently, the distinct properties of silk fibroin were extensively explored because of its unique advantages, including flexibility, process compatibility, long-term biosafety, and controllable biodegradability for in vitro and in vivo biomedical applications. In this study, we developed a novel silk fiber for a sensitive optical sensor based on surface-enhanced Raman spectroscopy (SERS). In contrast to conventional plasmonic nanostructures, which employ expensive and time-consuming fabrication processes, gold nanoparticles were uniformly patterned on the top surface of the fiber employing a simple and cost-effective convective self-assembly technique. The fabricated silk fiber-optic SERS probe presented a good performance in terms of detection limit, sensitivity, and linearity. In particular, the uniform pattern of gold nanoparticles contributed to a highly linear sensing feature compared to the commercial multi-mode fiber sample with an irregular and aggregated distribution of gold nanoparticles. Through further optimization, silk-based fiber-optic probes can function as useful tools for highly sensitive, cost-effective, and easily tailored biophotonic platforms, thereby offering new capabilities for future implantable SERS devices.

Heteroatom-Doped Graphenes as Actively Interacting 2D Encapsulation Media for Mg-Based Hydrogen Storage.

Nanoencapsulation using graphene derivatives enables the facile fabrication of two-dimensional (2D) nanocomposites with unique microstructures and has been generally applied to many fields of energy materials. Particularly, metal hydrides such as MgH2 encapsulated by graphene derivatives have emerged as a promising hybrid material for overcoming the disadvantageous properties of Mg-based hydrogen storage. Although the behavior of the graphene-Mg nanoencapsulation interface has been studied for many composite materials, the direct modification of graphene with nonmetal foreign elements for changing the interfacial behavior has been limitedly reported. In this regard, using B-doped graphene and N-doped graphene as nanoencapsulation media for tuning the interfacial behavior of graphene derivative-Mg nanoparticles, we present altered hydrogen storage kinetics of heteroatom-doped (B and N) graphene-Mg composites. The effect of heteroatom doping is studied in terms of bonding configurations and heteroatom doping concentrations. The enhancement in hydrogen uptake was observed for all of the heteroatom-doped graphene-Mg nanocomposites. On the other hand, a few samples exhibit significantly low activation energy at the early stage of desorption, which can be related to the facilitated nucleus formation. Density functional theory calculation indicates that B-doping and N-doping accelerate hydrogen absorption kinetics in different ways, aiding charge transfer and inducing surface deformation of Mg nanoparticles, respectively. Their effects can be augmented in the presence of structural defects on graphene, such as vacancies, pores, or graphene edges. These results demonstrate that hydrogen storage kinetics of Mg-based systems can be altered by utilizing heteroatom-doped graphene oxide derivatives as 2D nanoencapsulation media, suggesting that the addition of a nonmetal doping element can also be applied to Mg-based hydrogen storage by modifying the nanoencapsulation interface without forming Mg alloy phases.

Multiple Impact Damage in GLARE Laminates: Experiments and Simulations.

Experiments and finite element simulations for multiple impact were performed on GLARE 5-2/1 and aluminum 2024-T3. Experiments were conducted on aluminum 2024-T3 and GLARE 5-2/1 at diverse impact energies to produce BVID (barely visible impact damage) and CVID (clearly visible impact damage). The finite element model was developed for multiple impact analysis using ABAQUS software and was confirmed by comparing the finite element analysis outcomes with experimental results. The two- and three-dimensional failure criteria model was applied to predict multiple impact behavior such as load-time history, maximum deflection-impact energy history, and damage progression. In addition, a user subroutine VUMAT was created to represent a three-dimensional progressive failure and was linked with ABAQUS. FEM results showed good agreement with experimental data.

Transduced Tat-PRAS40 prevents dopaminergic neuronal cell death through ROS inhibition and interaction with 14-3-3σ protein.

Proline rich Akt substrate (PRAS40) is a component of mammalian target of rapamycin complex 1 (mTORC1) and activated mTORC1 plays important roles for cellular survival in response to oxidative stress. However, the roles of PRAS40 in dopaminergic neuronal cell death have not yet been examined. Here, we examined the roles of Tat-PRAS40 in MPP+- and MPTP-induced dopaminergic neuronal cell death. Our results showed that Tat-PRAS40 effectively transduced into SH-SY5Y cells and inhibited DNA damage, ROS generation, and apoptotic signaling in MPP+-induced SH-SY5Y cells. Further, these protective mechanisms of Tat-PRAS40 protein display through phosphorylation of Tat-PRAS40, Akt and direct interaction with 14-3-3σ protein, but not via the mTOR-dependent signaling pathway. In a Parkinson's disease animal model, Tat-PRAS40 transduced into dopaminergic neurons in mouse brain and significantly protected against dopaminergic cell death by phosphorylation of Tat-PRAS40, Akt and interaction with 14-3-3σ protein. In this study, we demonstrated for the first time that Tat-PRAS40 directly protects against dopaminergic neuronal cell death. These results indicate that Tat-PRAS40 may provide a useful therapeutic agent against oxidative stress-induced dopaminergic neuronal cell death, which causes diseases such as PD.

Reversing the Irreversible: Thermodynamic Stabilization of LiAlH4 Nanoconfined Within a Nitrogen-Doped Carbon Host.

A general problem when designing functional nanomaterials for energy storage is the lack of control over the stability and reactivity of metastable phases. Using the high-capacity hydrogen storage candidate LiAlH4 as an exemplar, we demonstrate an alternative approach to the thermodynamic stabilization of metastable metal hydrides by coordination to nitrogen binding sites within the nanopores of N-doped CMK-3 carbon (NCMK-3). The resulting LiAlH4@NCMK-3 material releases H2 at temperatures as low as 126 °C with full decomposition below 240 °C, bypassing the usual Li3AlH6 intermediate observed in bulk. Moreover, >80% of LiAlH4 can be regenerated under 100 MPa H2, a feat previously thought to be impossible. Nitrogen sites are critical to these improvements, as no reversibility is observed with undoped CMK-3. Density functional theory predicts a drastically reduced Al-H bond dissociation energy and supports the observed change in the reaction pathway. The calculations also provide a rationale for the solid-state reversibility, which derives from the combined effects of nanoconfinement, Li adatom formation, and charge redistribution between the metal hydride and the host.

Removal of malformation in cerebral proliferative angiopathy: illustrative case.

BACKGROUND: Cerebral proliferative angiopathy (CPA) is a rare vascular disorder distinct from arteriovenous malformation. Because of the disorder's rarity, there is still a controversy on the most promising treatment method for CPA. However, several meta-analysis articles suggest indirect vascularization such as encephalo-duro-arterio-synangiosis as an effective way of treating symptoms that are medically uncontrolled. OBSERVATIONS: The authors describe a case of an 11-year-old boy with this disease, who had epilepsy that was intractable despite conservative management. The patient recovered from his symptoms after the vascular malformation was surgically removed. This is the first reported case of surgical removal in CPA. LESSONS: Although further investigation on the best treatment for CPA is needed, the authors believe surgical intervention may also be an effective treatment modality when a patient presents with persisting symptoms.

A Prospective Observational Study of Return to Work after Single Level Lumbar Discectomy.

OBJECTIVE: Lumbar disc herniation (LDH) is a common disease, and lumbar discectomy (LD) is a common neurosurgical procedure. However, there is little previous data on return to work (RTW) after LD. This study investigated the period until the RTW after LD prospectively. Clinically, the pain state at the time of RTW also checked. RTW failure rate 6 months after surgery also investigated. METHODS: Patients with daily/regular jobs undergoing LD between September 2014 and December 2018 were enrolled. Pain was assessed by the Oswestri Disability Index (ODI) and the Numeric Rate Scale (NRS). Employment type was divided into self-employed, regular and contracted. Monthly telephone interviews were conducted to check RTW status and self-estimated work capability after surgery. RESULTS: Sixty-seven patients enrolled in this study. Three patients failed to RTW, and three others resigned within 6 months after surgery. The preoperative NRS and ODI were 7.2±1.2 and 22.1±7.9, respectively. The average time to RTW was 5.1±6.0 weeks. At RTW, NRS was 1.5±1.8 and ODI was 6.3±3.9. Amongst patients that successfully returned to work were 16 self-employed workers, 42 regular employees, and three contracted workers. The time to RTW of self-employed, regular, and contracted workers were 5.9±8.8, 4.2±4.3 and 13.3±2.3 weeks, respectively (p=0.011). Thirty-six of the patients that returned to work self-reported a 22.8±15.6% reduction in work capability at 6 months. CONCLUSION: RTW may vary depending on the employment status. In this study, we found that while employment type may affect the length to RTW, most patients were able to RTW and >40% of patients reported no loss of work capabilities 6 months postoperatively, hopefully alleviating some patient hesitation towards LD.

Tat-indoleamine 2,3-dioxygenase 1 elicits neuroprotective effects on ischemic injury.

It is well known that oxidative stress participates in neuronal cell death caused production of reactive oxygen species (ROS). The increased ROS is a major contributor to the development of ischemic injury. Indoleamine 2,3-dioxygenase 1 (IDO-1) is involved in the kynurenine pathway in tryptophan metabolism and plays a role as an anti-oxidant. However, whether IDO-1 would inhibit hippocampal cell death is poorly known. Therefore, we explored the effects of cell permeable Tat-IDO-1 protein against oxidative stress-induced HT-22 cells and in a cerebral ischemia/reperfusion injury model. Transduced Tat-IDO-1 reduced cell death, ROS production, and DNA fragmentation and inhibited mitogen-activated protein kinases (MAPKs) activation in H2O2 exposed HT-22 cells. In the cerebral ischemia/ reperfusion injury model, Tat-IDO-1 transduced into the brain and passing by means of the blood-brain barrier (BBB) significantly prevented hippocampal neuronal cell death. These results suggest that Tat-IDO-1 may present an alternative strategy to improve from the ischemic injury. [BMB Reports 2020; 53(11): 582-587].

Tat-Biliverdin Reductase A Exerts a Protective Role in Oxidative Stress-Induced Hippocampal Neuronal Cell Damage by Regulating the Apoptosis and MAPK Signaling.

Reactive oxygen species (ROS) is major risk factor in neuronal diseases including ischemia. Although biliverdin reductase A (BLVRA) plays a pivotal role in cell survival via its antioxidant function, its role in hippocampal neuronal (HT-22) cells and animal ischemic injury is not clearly understood yet. In this study, the effects of transducible fusion protein Tat-BLVRA on H2O2-induced HT-22 cell death and in an animal ischemia model were investigated. Transduced Tat-BLVRA markedly inhibited cell death, DNA fragmentation, and generation of ROS. Transduced Tat-BLVRA inhibited the apoptosis and mitogen activated protein kinase (MAPK) signaling pathway and it passed through the blood-brain barrier (BBB) and significantly prevented hippocampal cell death in an ischemic model. These results suggest that Tat-BLVRA provides a possibility as a therapeutic molecule for ischemia.

Retrospective Chronologic Computed Tomography Analysis of Bone Flap Fusion and Resorption After Craniotomy and Autologous Cryopreserved Cranioplasty.

BACKGROUND: In open brain surgery, fixation of the bone flap is the final procedure. The bone flaps then fuse naturally. The objective of this study was to investigate the chronological process of bone fusion after craniotomy and autologous cranioplasty. METHODS: Retrospective data were collected from patients who underwent craniotomy or cranioplasty after August 2004 and had at least 1 computed tomography (CT) scan at 3 months postsurgery. The patients were divided into a craniotomy group and a cranioplasty group. Head CT scans were analyzed to evaluate bone fusion and resorption. RESULTS: Records from 978 patients who underwent craniotomy or cranioplasty between September 2004 and November 2015 were reviewed; 369 patients were eligible for the final analysis (craniotomy, n = 276; cranioplasty, n = 93). The mean cryopreservation period for the bone flap in the cranioplasty group was 49.3 days. The mean patient age was 51.4 ± 18.1 years in the craniotomy group and 51.6 ± 17.1 years in the cranioplasty group. Head CT scans showed bone fusion rates of 76.6% in the craniotomy group and 53.3% in the cranioplasty group at 6 months postsurgery (P = 0.015) and 78.6% and 78.1%, respectively, at 1 year postsurgery (P = 0.951). There was also a significant difference in the bone flap resorption rate between the 2 groups. CONCLUSIONS: Bone flap fusion rates after craniotomy and cranioplasty were significantly different before 12 months, but not significantly different thereafter. Bone resorption occurred more frequently in the cranioplasty group over time.

A Research on the Shamanistic Medical Activities as Seen in the Recipes for Fifty-two Ailments Written in the Mawangdui Silk Manuscript.

The main thesis of this research is to discuss the shamanistic medical activities as seen in the Recipes for Fifty-two Ailments written in the Mawangdui Silk Manuscript, to corroborate them with handed-down literature and other underground written attestations in early China, and to inquire its characteristics. In the Eastern Zhou dynasty, medicine already emerged with specialized and professional properties, but did not disengage from the ideology of shamanism in Eastern Zhou society. In other words, the shamanistic treatment of diseases was one of the most important works of shamans because the specialized knowledge of medical treatment always interlaced with superstitious and mediumistic treatment methods. This article examines the details of shamanistic medical activities, for example, the 'zhuyou', the 'zhuyichuxiong', curing maggots activities, and so on, by analyzing the Recipes for Fifty-two Ailments written in the Mawangdui Silk Manuscript. The origin and development of this early Chinese medical treatment had an influence on ancient Korea, Japan, and other places. Through this research, we can learn more about the initial development stage of the early traditional medicine in ancient societies of East Asia.

Effects of silk solution against laminectomy-induced dural adhesion formation and inflammation in a rat model.

The authors investigated the effects of a silk solution against laminectomy-induced dural adhesion formation and inflammation in a rat model. They found that it significantly reduced postlaminectomy dural adhesion formation and inflammation. Dural adhesion formation, thought to be an inevitable consequence of laminectomy, is one of the most common complications following spinal surgery, and the authors' results indicate that the silk solution might be a potential novel therapeutic agent for dural adhesion formation.