CDKL5-mediated developmental tuning of neuronal excitability and concomitant regulation of transcriptome.

Cyclin-dependent kinase-like 5 (CDKL5) is a serine-threonine kinase enriched in the forebrain to regulate neuronal development and function. Patients with CDKL5 deficiency disorder (CDD), a severe neurodevelopmental condition caused by mutations of CDKL5 gene, present early-onset epilepsy as the most prominent feature. However, spontaneous seizures have not been reported in mouse models of CDD, raising vital questions on the human-mouse differences and the roles of CDKL5 in early postnatal brains. Here, we firstly measured electroencephalographic (EEG) activities via a wireless telemetry system coupled with video-recording in neonatal mice. We found that mice lacking CDKL5 exhibited spontaneous epileptic EEG discharges, accompanied with increased burst activities and ictal behaviors, specifically at postnatal day 12 (P12). Intriguingly, those epileptic spikes disappeared after P14. We next performed an unbiased transcriptome profiling in the dorsal hippocampus and motor cortex of Cdkl5 null mice at different developmental timepoints, uncovering a set of age-dependent and brain region-specific alterations of gene expression in parallel with the transient display of epileptic activities. Finally, we validated multiple differentially expressed genes, such as glycine receptor alpha 2 and cholecystokinin, at the transcript or protein levels, supporting the relevance of these genes to CDKL5-regulated excitability. Our findings reveal early-onset neuronal hyperexcitability in mouse model of CDD, providing new insights into CDD etiology and potential molecular targets to ameliorate intractable neonatal epilepsy.

Perinatal blockade of neuronal glutamine transport sex-differentially alters glutamatergic synaptic transmission and organization of neurons in the ventrolateral ventral media hypothalamus of adult rats.

Compared to male pups, perinatal female rats rely heavily on neuronal glutamine (Gln) transport for sustaining glutamatergic synaptic release in neurons of the ventrolateral ventral media nucleus of the hypothalamus (vlVMH). VMH mainly regulates female sexual behavior and increases glutamate release of perinatal hypothalamic neurons, permanently enhances dendrite spine numbers and is associated with brain and behavioral defeminization. We hypothesized that perinatal interruption of neuronal Gln transport may alter the glutamatergic synaptic transmission during adulthood. Perinatal rats of both sexes received an intracerebroventricular injection of a neuronal Gln uptake blocker, alpha-(methylamino) isobutyric acid (MeAIB, 5 mM), and were raised until adulthood. Whole-cell voltage-clamp recordings of miniature excitatory postsynaptic currents (mEPSCs) and evoked EPSCs (eEPSCs) of vlVMH neurons in adult rats with the perinatal pretreatment were conducted and neuron morphology was subjected to post hoc examination. Perinatal MeAIB treatment sex-differentially increased mEPSC frequency in males, but decreased mEPSC amplitude and synaptic Glu release in females. The pretreatment sex-differentially decreased eEPSC amplitude in males but increased AMPA/NMDA current ratio in females, and changed the morphology of vlVMH neurons of adult rats to that of the opposite sex. Most alterations in the glutamatergic synaptic transmission resembled the changes occurring during MeAIB acute exposure in perinatal rats of both sexes. We conclude that perinatal blockade of neuronal Gln transport mediates changes via different presynaptic and postsynaptic mechanisms to induce sex-differential alterations of the glutamatergic synaptic transmission and organization of vlVMH neurons in adult rats. These changes may be permanent and associated with brain and behavior feminization and/or defeminization in rats.

Barley endosomal MONENSIN SENSITIVITY1 is a target of the powdery mildew effector CSEP0162 and plays a role in plant immunity.

Encasements formed around haustoria and biotrophic hyphae as well as hypersensitive reaction (HR) cell death are essential plant immune responses to filamentous pathogens. In this study we examine the components that may contribute to the absence of these responses in susceptible barley attacked by the powdery mildew fungus. We find that the effector CSEP0162 from this pathogen targets plant MONENSIN SENSITIVITY1 (MON1), which is important for the fusion of multivesicular bodies to their target membranes. Overexpression of CSEP0162 and silencing of barley MON1 both inhibit encasement formation. We find that the Arabidopsis ecotype No-0 has resistance to powdery mildew, and that this is partially dependent on MON1. Surprisingly, we find the MON1-dependent resistance in No-0 not only includes an encasement response, but also an effective HR. Similarly, silencing of MON1 in barley also blocks Mla3-mediated HR-based powdery mildew resistance. Our results indicate that MON1 is a vital plant immunity component, and we speculate that the barley powdery mildew fungus introduces the effector CSEP0162 to target MON1 and hence reduce encasement formation and HR.

A Highly Accurate Method for Deformation Reconstruction of Smart Deformable Structures Based on Flexible Strain Sensors.

Smart deformable structures that integrate designing, sensing, and controlling technology have been widely applied in the fields of aerospace, robotics, and biomedical engineering due to their multi-functional requirements. The deformation reconstruction method essential for security monitoring and shape controlling, especially for the large deflection deformation, remains a challenge on accuracy and efficiency. This paper takes a wind tunnel's fixed-flexible nozzle (FFN) plate as the research object to develop a highly accurate deformation reconstruction method based on sensing information from flexible strain sensors. The mechanical behaviors of the FFN plate with large deflection deformation, which is modeled as a cantilever beam, are studied to analyze the relationship of the strain and moment. Furthermore, the large deflection factor and shell bending theory are creatively utilized to derive and modify the strain-moment based reconstruction method (SMRM), where the contour of the FFN plate is solved by particular elliptic integrals. As a result, structural simulation based on ABAQUS further demonstrates that the reconstruction error of SMRM is 21.13% less than that of the classic Ko-based reconstruction method (KORM). An FFN prototype accompanied by customized flexible sensors is developed to evaluate the accuracy and efficiency of the SMRM, resulting in a maximum relative error of 3.97% that is acceptable for practical applications in smart deformable structures, not limited to the FFN plate.

Dopaminergic loss of cyclin-dependent kinase-like 5 recapitulates methylphenidate-remediable hyperlocomotion in mouse model of CDKL5 deficiency disorder.

Cyclin-dependent kinase-like 5 (CDKL5), a serine-threonine kinase encoded by an X-linked gene, is highly expressed in the mammalian forebrain. Mutations in this gene cause CDKL5 deficiency disorder, a neurodevelopmental encephalopathy characterized by early-onset seizures, motor dysfunction, and intellectual disability. We previously found that mice lacking CDKL5 exhibit hyperlocomotion and increased impulsivity, resembling the core symptoms in attention-deficit hyperactivity disorder (ADHD). Here, we report the potential neural mechanisms and treatment for hyperlocomotion induced by CDKL5 deficiency. Our results showed that loss of CDKL5 decreases the proportion of phosphorylated dopamine transporter (DAT) in the rostral striatum, leading to increased levels of extracellular dopamine and hyperlocomotion. Administration of methylphenidate (MPH), a DAT inhibitor clinically effective to improve symptoms in ADHD, significantly alleviated the hyperlocomotion phenotype in Cdkl5 null mice. In addition, the improved behavioral effects of MPH were accompanied by a region-specific restoration of phosphorylated dopamine- and cAMP-regulated phosphoprotein Mr 32 kDa, a key signaling protein for striatal motor output. Finally, mice carrying a Cdkl5 deletion selectively in DAT-expressing dopaminergic neurons, but not dopamine receptive neurons, recapitulated the hyperlocomotion phenotype found in Cdkl5 null mice. Our findings suggest that CDKL5 is essential to control locomotor behavior by regulating region-specific dopamine content and phosphorylation of dopamine signaling proteins in the striatum. The direct, as well as indirect, target proteins regulated by CDKL5 may play a key role in movement control and the therapeutic development for hyperactivity disorders.

Transgenic plant generated by RNAi-mediated knocking down of soybean Vma12 and soybean mosaic virus resistance evaluation.

Soybean mosaic virus (SMV) is one of the most destructive viral diseases in soybean and causes severe reduction of soybean yield and destroys the seed quality. However, the production of SMV resistant plants by transgenic is the most effective and economical means. Based on our previous yeast two-hybrid assay, the GmVma12 was selected as a strong candidate gene for further function characterization. Here we transformed soybean plants with a construct containing inverted repeat of-GmVma12 sequence to analyze the role of GmVma12 during SMV invasion. Totals of 33 T0 and 160 T1 plants were confirmed as positive transgenic plants through herbicide application, PCR detection and LibertyLink® strip screening. Based on the segregation ratio and Southern Blot data, T1 lines No. 3 and No. 7 were selected to generate T2 plants. After SMV-SC15 inoculation, 41 T1 and 38 T2 plants were identified as highly resistant, and their quantification disease levels were much lower than non-transformed plants. The transcript level of GmVma12 in T2 plants decreased to 70% of non-transformed plants. The expression level of SMV-CP transcript in T2 transgenic plants was lower than that in non-transformed plants and SMV CP protein in T2 plants could not be detected by Enzyme-linked Immunosorbent assay, which indicated that SMV production would be inhibited in transgenic plants. Moreover, coat mottles of T2 seeds were obliterated significantly. In conclusion, inverted repeat of the hairpin structure of GmVma12 interfered with the transcription of GmVma12, which can induce resistance to SMV in soybean. This research lays the foundation for the mechanism of SMV pathogenesis, and provides new ideas for SMV prevention and control.

Comprehensive Analysis of Soybean Mosaic Virus P3 Protein Interactors and Hypersensitive Response-Like Lesion-Inducing Protein Function.

Soybean mosaic virus (SMV) is one of the most prevalent and important pathogens of soybean, which produces 11 proteins, and the third protein, P3, was suggested to be involved in virus movement and replication, as well as host infection. During the virus infection, host proteins are essential in the virus cycle. However, there is no comprehensive report on the network of host proteins that interact with P3. Fifty-one interactors were identified by using the P3 protein as the bait against the SMV SC15 strain-challenged soybean cDNA library. These proteins were classified into five groups, including transport and protein transport-related proteins, defense and disease-related proteins, photosynthesis proteins, cellular metabolic proteins, and unknown proteins. Among these proteins, the protein defined as hypersensitive response-like lesion-inducing (HRLI) appeared multiple times and showed strong affinity with P3, which indicated its important role in SMV infection. Thus, it was chosen for further investigation. Phylogenetic classification showed that paralog proteins GmHRLI-1 and GmHRLI-2 clustered together and shared 90% homologous identity. Bimolecular fluorescence complementation (BiFC) assay was carried out to confirm the interaction, and fluorescence was detected at the cell periplasmic as well as at the nucleus. Subcellular localization showed that GmHRLI was localized to the cell periplasmic, while the co-localization of GmHRLI and P3 signals was also observed in the nucleus, suggesting that GmHRLI could interact with P3 and promoted the translation of P3 to the nucleus. Moreover, the gene expression of GmHRLI was abundant in the roots, leaves, and flowers, and could be induced by SMV infection, suggesting its involvement in SMV infection. Our results together lay the foundation to explore the mechanisms of P3 in the HR process and the HRLI protein function in SMV response.

Psychomotor Dysfunction in Rett Syndrome: Insights into the Neurochemical and Circuit Roots.

Rett syndrome (RTT) is a monogenic neurodevelopmental disorder caused by mutations in the methyl-CpG binding protein 2 (MECP2) gene. Patients with RTT develop symptoms after 6-18 months of age, exhibiting characteristic movement deficits, such as ambulatory difficulties and loss of hand skills, in addition to breathing abnormalities and intellectual disability. Given the striking psychomotor dysfunction, numerous studies have investigated the underlying neurochemical and circuit mechanisms from different aspects. Here, I review the evidence linking MeCP2 deficiency to alterations in neurotransmission and neural circuits that govern the psychomotor function and discuss a recently identified pathological origin underlying the psychomotor deficits in RTT.

Evolution mechanism of surface roughness during ion beam sputtering of fused silica.

Ultrasmooth surfaces with sub-nanometer roughness and low damage are a great challenge for optical fabrication. Ion beam sputtering (IBS) has obvious advantages on the improvement of surface quality and the removal of surface defects. However, surface defects with different properties and structures display different evolution laws during the IBS process, which affects the roughness change and needs classification studies. In this paper, classification experiments are carried out to study the surface topography evolution of plastic scratches, brittle scratches, and micro-particles during the IBS process. The plastic scratches and micro-particles can be removed, while the brittle scratches can be passivated, so that surface defects can be reduced and surface quality improved. The corresponding evolution mechanisms are discussed in depth, and we show that micro-topography characteristics and material properties are important factors affecting the evolution of surface topography. Through the summary of evolution laws of different surface states, the Gaussian distribution law of surface roughness is established. The evolution regularity and mechanism of surface roughness during the IBS process are expounded upon from the perspective of microscopic morphology, which lays a foundation for ultra-smooth surface manufacturing with low damage.

Loss of CDKL5 disrupts respiratory function in mice.

Cyclin-dependent kinase-like 5 (CDKL5) is an X-linked gene encoding a serine-threonine kinase that is highly expressed in the central nervous system. Mutations in CDKL5 cause neurological and psychiatric symptoms, including early-onset seizures, motor dysfunction, autistic features and sleep breathing abnormalities in patients. It remains to be addressed whether loss of CDKL5 causes respiratory dysfunction in mice. Here, we examined the respiratory pattern of male Cdkl5-/y mice at 1-3 months of age during resting breathing and respiratory challenge (i.e., hypoxia and hypercapnia) via whole body plethysmography. The results demonstrated that the resting respiratory frequency and tidal volume of Cdkl5-/y mice was unaltered compared to that of WT mice at 1 month of age. However, these mutant mice exhibit transient reduction in tidal volume during respiratory challenge even the reduction was restored at 2 months of age. Notably, the sigh-breathing pattern was changed in Cdkl5-/y mice, showing a transient reduction in sigh volume at 1-2 month of age and long-term attenuation of peak expiratory airflow from 1 to 3 month of age. Therefore, loss of CDKL5 causes breathing deficiency, supporting a CDKL5-mediated regulation of respiratory function in mice.

Mice lacking cyclin-dependent kinase-like 5 manifest autistic and ADHD-like behaviors.

Neurodevelopmental disorders frequently share common clinical features and appear high rate of comorbidity, such as those present in patients with attention-deficit hyperactivity disorder (ADHD) and autism spectrum disorders (ASD). While characterizing behavioral phenotypes in the mouse model of cyclin-dependent kinase-like 5 (CDKL5) disorder, a neurodevelopmental disorder caused by mutations in the X-linked gene encoding CDKL5, we found that these mice manifested behavioral phenotypes mimicking multiple key features of ASD, such as impaired social interaction and communication, as well as increased stereotypic digging behaviors. These mice also displayed hyper-locomotion, increased aggressiveness and impulsivity, plus deficits in motor and associative learning, resembling primary symptoms of ADHD. Through brain region-specific biochemical analysis, we uncovered that loss of CDKL5 disrupts dopamine synthesis and the expression of social communication-related key genes, such as forkhead-box P2 and mu-opioid receptor, in the corticostriatal circuit. Together, our findings support that CDKL5 plays a role in the comorbid features of autism and ADHD, and mice lacking CDKL5 may serve as an animal model to study the molecular and circuit mechanisms underlying autism-ADHD comorbidity.

Autophagy and its link to type II diabetes mellitus.

Autophagy, a double-edged sword for cell survival, is the research object on 2016 Nobel Prize in Physiology or Medicine. Autophagy is a molecular mechanism for maintaining cellular physiology and promoting survival. Defects in autophagy lead to the etiology of many diseases, including diabetes mellitus (DM), cancer, neurodegeneration, infection disease and aging. DM is a metabolic and chronic disorder and has a higher prevalence in the world as well as in Taiwan. The character of diabetes mellitus is hyperglycemia resulting from defects in insulin secretion, insulin action, or both. Type 2 diabetes mellitus (T2DM) is characterized by insulin resistance and failure of producing insulin on pancreatic beta cells. In T2DM, autophagy is not only providing nutrients to maintain cellular energy during fasting, but also removes damaged organelles, lipids and miss-folded proteins. In addition, autophagy plays an important role in pancreatic beta cell dysfunction and insulin resistance. In this review, we summarize the roles of autophagy in T2DM.

Neurotensin-Conjugated Reduced Graphene Oxide with Multi-Stage Near-Infrared-Triggered Synergic Targeted Neuron Gene Transfection In Vitro and In Vivo for Neurodegenerative Disease Therapy.

Delivery efficiency with gene transfection is a pivotal point in achieving maximized therapeutic efficacy and has been an important challenge with central nervous system (CNS) diseases. In this study, neurotensin (NT, a neuro-specific peptide)-conjugated polyethylenimine (PEI)-modified reduced graphene oxide (rGO) nanoparticles with precisely controlled two-stage near-infrared (NIR)-laser photothermal treatment to enhance the ability to target neurons and achieve high gene transfection in neurons. First-stage NIR laser irradiation on the cells with nanoparticles attached on the surface can increase the permeability of the cell membrane, resulting in an apparent increase in cellular uptake compared to untreated cells. In addition, second-stage NIR laser irradiation on the cells with nanoparticles inside can further induce endo/lysosomal cavitation, which not only helps nanoparticles escape from endo/lysosomes but also prevents plasmid DNA (pDNA) from being digested by DNase I. At least double pDNA amount can be released from rGO-PEI-NT/pDNA under NIR laser trigger release compared to natural release. Moreover, in vitro differentiated PC-12 cell and in vivo mice (C57BL/6) brain transfection experiments have demonstrated the highest transfection efficiency occurring when NT modification is combined with external multi-stage stimuli-responsive NIR laser treatment. The combination of neuro-specific targeting peptide and external NIR-laser-triggered aid provides a nanoplatform for gene therapy in CNS diseases.

Current concepts regarding developmental mechanisms in diabetic retinopathy in Taiwan.

Diabetic retinopathy (DR) is one of the most feared complications of diabetes and is a leading cause of acquired blindness in working adults. The prevalence of undiagnosed diabetes in Taiwan is about 4%, and the annual incidence of T2D (Type 2 Diabetes) in Taiwan is 1.8% following the 1985 WHO criteria. Multiple mechanisms have been shown in T2DR with some signaling pathways, including the polyol pathway, PKC pathway, AGEs pathway, and MAPK pathway. However, the cause of vision loss in diabetic retinopathy is complex and remains incompletely understood. Herein, we try to fully understand the new concepts regarding hyperglycemia-induced biochemical pathways contributing to DR pathophysiology. Our work may be able to provide new strategies for the prevention and treatment of diabetic vascular complications.

Detailed subsurface damage measurement and efficient damage-free fabrication of fused silica optics assisted by ion beam sputtering.

Formation of subsurface damage has an inseparable relationship with microscopic material behaviors. In this work, our research results indicate that the formation process of subsurface damage often accompanies with the local densification effect of fused silica material, which seriously influences microscopic material properties. Interestingly, we find ion beam sputtering (IBS) is very sensitive to the local densification, and this microscopic phenomenon makes IBS as a promising technique for the detection of nanoscale subsurface damages. Additionally, to control the densification effect and subsurface damage during the fabrication of high-performance optical components, a combined polishing technology integrating chemical-mechanical polishing (CMP) and ion beam figuring (IBF) is proposed. With this combined technology, fused silica without subsurface damage is obtained through the final experimental investigation, which demonstrates the feasibility of our proposed method.

Structure optimization and fabricating capability analysis of an ion-beam machine for a subnanometer optical surface.

Ultraprecise and ultrasmooth surfaces become critical requirements for some high-performance optical systems. Ion-beam figuring (IBF) is a good and highly deterministic method for the final precision optical figuring. However, the uniform convergences of all spatial frequency surface errors are strongly dependent on the dynamic performance and ion-beam stability of the IBF machine. In this paper, only the dynamic performance is discussed, which is limited by the acceleration and velocity of the motion system. So we discuss these problems and their influences on figuring optical surfaces in detail. The structure optimization principle is based on the fabricating capability of ultraprecise surface errors in all spatial frequency ranges. With this requirement, the structure optimization of a quick-response platform is performed to improve its dynamic performance. Manufacturing experiments on a fused silica spherical concave surface (Φ135.7 mm, radius of curvature 340.5 mm) are accomplished, and the IBF machine can effectively correct the figure errors and improve the surface quality simultaneously. The IBF process realizes the uniform convergence of surface errors in all spatial frequency ranges, which is reduced down to 0.368 nm RMS, 0.204 nm RMS, and 0.087 nm RMS, respectively. The final results indicate that the performance of the new designed IBF machine meets the requirements well for the fabrication of a subnanometer optical surface.

PTPRD silencing by DNA hypermethylation decreases insulin receptor signaling and leads to type 2 diabetes.

Genome-wide association study (GWAS) data showed that the protein tyrosine phosphatase receptor type delta (PTPRD) is associated with increased susceptibility to type 2 diabetes (T2D) in Han Chinese. A replication study indicated that PTPRD is involved in the insulin signaling pathway; however, the underlying mechanism remains unclear. We evaluated PTPRD expression in patients with T2D and controls. PTPRD expression levels were lower in patients and were correlated with the duration of the disease. Overexpression of the human insulin receptor PPARγ2 in HepG2 cells induced overexpression of PTPRD and the insulin receptor. PTPRD knockdown, using a shRNA, resulted in down-regulation of the insulin receptor. These results indicate that PTPRD activates PPARγ2 in the insulin signaling pathway. Similar results for PTPRD expression were found using a T2D mouse model. Silencing of PTPRD was caused by DNA methylation in T2D mice and patients, and correlated with DNMT1 expression. Furthermore, we showed that a DNMT1 SNP (rs78789647) was correlated with susceptibility to T2D. This study shows for the first time that DNMT1 caused PTPRD DNA hypermethylation and induced insulin signaling silencing in T2D patients. Our findings contribute to a better understanding of the crucial roles of these regulatory elements in human T2D.

Characterization of Soybean mosaic virus resistance derived from inverted repeat-SMV-HC-Pro genes in multiple soybean cultivars.

KEY MESSAGE: Soybean mosaic virus resistance was significantly improved in multiple soybean cultivars through genetic transformation induced by inverted repeat-SMV- HC - Pro genes based on RNAi and post-transcriptional gene silencing. Here, we demonstrate Soybean mosaic virus (SMV) resistance in transgenic soybean plants. Transformation of five soybean genotypes with a construct containing inverted repeat-SMV-HC-Pro genes-induced high-level SMV resistance. Through leaf-painting assays, polymerase chain reaction (PCR) verification and LibertyLink(®) strip detection, 105 T0 and 1059 T1 plants were confirmed as transgene-positive. Southern blotting confirmed insertion of the T-DNA into the genomic DNA and revealed a low-copy integration pattern. Most T0 plants were fertile and transmitted the exogenous genes to their progenies (ratios of 3:1 or 15:1). In the T1 generation, virus resistance was evaluated visually after inoculation with SMV (strain SC3) and 441 plants were highly resistant (HR). SMV disease rating was classified on a scale with 0 = symptomless and 4 = mosaic symptoms with severe leaf curl. In the positive T1 plants, the disease rating on average was 1.42 (range 0.45-2.14) versus 3.2 (range 2-4) for the nontransformed plants. With the T2 generation, 75 transgene-positive plants were inoculated with SC3, and 57 HR plants were identified. Virus-induced seed coat mottling was eliminated in the resistant lines. Analysis of SMV levels in the plants was performed using quantitative real-time PCR and double-antibody sandwich enzyme-linked immunosorbent assays; the results revealed no virus or a gradual reduction over time in the viral content, thereby supporting the visual examination results. This is the first report demonstrating pathogen-derived resistance to SMV induced by inverted repeat-SMV-HC-Pro genes in multiple soybean cultivars. Our findings contribute positively to the study of transgenic SMV-resistance using RNA interference.

MeCP2 in the rostral striatum maintains local dopamine content critical for psychomotor control.

Methyl-CpG binding protein 2 (MeCP2) is a chromatin regulator highly expressed in mature neurons. Mutations of MECP2 gene cause >90% cases of Rett syndrome, a neurodevelopmental disorder featured by striking psychomotor dysfunction. In Mecp2-null mice, the motor deficits are associated with reduction of dopamine content in the striatum, the input nucleus of basal ganglia mostly composed of GABAergic neurons. Here we investigated the causal role of MeCP2 in modulation of striatal dopamine content and psychomotor function. We found that mice with selective removal of MeCP2 in forebrain GABAergic neurons, predominantly in the striatum, phenocopied Mecp2-null mice in dopamine deregulation and motor dysfunction. Selective expression of MeCP2 in the striatum preserved dopamine content and psychomotor function in both males and females. Notably, the dopamine deregulation was primarily confined to the rostral striatum, and focal deletion or reactivation of MeCP2 expression in the rostral striatum through adeno-associated virus effectively disrupted or restored dopamine content and locomotor activity, respectively. Together, these findings demonstrate that striatal MeCP2 maintains local dopamine content in a non-cell autonomous manner in the rostral striatum and that is critical for psychomotor control.

Translation-reduced ion beam figuring.

A translation-reduced ion beam figuring (TRIBF) technique for five-axis ion beam figuring (IBF) plants is proposed to process large size components which cannot be processed in the traditional way. This novel technique enhances the capability of five-axis IBF plants by taking advantage of their rotation axes. The IBF kinematic model is described and the TRIBF processing technique is established by solving the motion parameters. Verification experiments are conducted on a 150 mm diameter planar mirror. This mirror was processed by TRIBF technique with only a 100 mm translation stage. The surface error was reduced from initial 10.7 nm rms to 1.3 nm rms within 97 minute processing time. The result indicates that the TRIBF processing technique is feasible and effective.