Vibration reduction during milling of highly flexible workpieces using active workpiece holder system.

The milling of highly flexible workpieces, such as thin-walled structures used in turbine blades, aerospace equipment, and jet engine compressors, requires vibration compensation to improve the quality of the workpiece surface. Vibration can be reduced by selecting appropriate cutting parameters. However, this approach reduces system productivity. This paper presents an active workpiece holder that controls the vibration of general computer numerical control machine tools. The proposed holder, which comprises a flexible guide mechanism, driver, and sensor, measures vibration and actively controls it using piezoactuators. A high-rigidity flexure mechanism was designed for the holder, and finite element method simulation and modal analysis were performed. Finally, the proposed system was fabricated, and experimental verification indicated that the system reduced vibration. The surface quality obtained using the controlled system was ∼50% better than that obtained using the uncontrolled system.

The effect of sphingosine-1-phosphate on bone metabolism in humans depends on its plasma/bone marrow gradient.

BACKGROUND: Although recent studies provide clinical evidence that sphingosine-1-phosphate (S1P) may primarily affect bone resorption in humans, rather than bone formation or the osteoclast-osteoblast coupling phenomenon, those studies could not determine which bone resorption mechanism is more important, i.e., chemorepulsion of osteoclast precursors via the blood to bone marrow S1P gradient or receptor activator of NF-κB ligand (RANKL) elevation in osteoblasts via local S1P. AIM: To investigate how S1P mainly contributes to increased bone resorption in humans, we performed this case-control study at a clinical unit in Korea. METHODS: Blood and bone marrow samples were contemporaneously collected from 70 patients who underwent hip surgery due to either osteoporotic hip fracture (HF) (n = 10) or other causes such as osteoarthritis (n = 60). RESULTS: After adjusting for sex, age, BMI, smoking, alcohol, previous fracture, diabetes, and stroke, subjects with osteoporotic HF demonstrated a 3.2-fold higher plasma/bone marrow S1P ratio than those without HF, whereas plasma and bone marrow S1P levels were not significantly different between these groups. Consistently, the risk of osteoporotic HF increased 1.38-fold per increment in the plasma/bone marrow S1P ratio in a multivariate adjustment model. However, the odds ratios for prevalent HF according to the increment in the plasma and bone marrow S1P level were not statistically significant. CONCLUSION: Our current results using simultaneously collected blood and bone marrow samples suggest that the detrimental effects of S1P on bone metabolism in humans may depend on the S1P gradient between the peripheral blood and bone marrow cavity.

The roles of fractalkine/CX3CR1 system in neuronal death following pilocarpine-induced status epilepticus.

Although fractalkine is one of chemokines involved in mediation of neuronal/microglial interaction, it is not known whether fractalkine/CX3CR1-mediated pathogenesis occurs in the rat brain following epileptogenic insults. In order to elucidate the roles of the fractalkine/CX3CR1 system in microglial activation and neurodegeneration induced by status epilepticus (SE), we investigated changes in fractalkine/CX3CR1 system within the rat hippocampus following SE. In non-SE induced animals, fractalkine and CX3CR1 immunoreactivity was detected in neurons and microglia, respectively. Following SE, fractalkine immunoreactivity was transiently increased in neurons and astrocytes. CX3CR1 immunoreactivity was also transiently detected in neurons (particularly in CA1 pyramidal cells). Intracerebroventricular infusions of recombinant rat fractalkine aggravated SE-induced neuronal damage, while fractalkine IgG or CX3CR1 IgG infusion alleviated it, compared to saline-infused animals. These findings suggest that fractalkine/CX3CR1 system may play an important role in SE-induced neuronal damages via neuron-microglial interactions.

Sympathetic influence on biomechanical skin properties after spinal cord injury.

STUDY DESIGN: Case-control study. OBJECTIVES: To investigate changes of biomechanical skin properties and their relationship with paralysis following spinal cord injury (SCI). SETTING: South Korea. METHODS: A total of 48 male subjects with chronic SCI and 48 age-matched healthy controls were enrolled into this study. The C4 shoulder group and L2 thigh group were prescribed by two measured anatomical regions that represented the C4 and L2 American Spinal Injury Association sensory dermatomes. Each anatomical group was comprised of one control subgroup and three SCI subgroups determined by sympathetic paralysis at the measured region and somatic completeness. The following biomechanical skin properties were compared between the subgroups in each anatomical group by using Cutometer, a non-invasive suction device: distensibility (Uf), elasticity (Ua/Uf and Ur/Uf) and viscoelasticity (Uv/Ue and H). The impact of sympathetic and somatic sensory paralysis, somatic completeness, age, smoking, body mass index and duration of injury on the indices of skin properties were analyzed. RESULTS: In each anatomical group, sympathetic paralyzed subgroups regardless of somatic sensory completeness showed lower value of skin distensibility (Uf), and higher values of elasticity (Ua/Uf and Ur/Uf) and viscoelasticity (Uv/Ue and H), compared with other subgroups. Age and duration of injury had significant impact on biomechanical skin properties. CONCLUSION: The non-invasive suction method is useful for quantitative evaluation of skin affected by SCI. In chronic SCI patients, biomechanical skin properties are significantly altered in the skin with sympathetic paralysis rather than somatic sensory paralysis.

Differential expressions of aquaporin subtypes in astroglia in the hippocampus of chronic epileptic rats.

In order to elucidate the roles of aquaporins (AQPs) in astroglial responses, we investigated AQP expressions in the experimental epileptic hippocampus. In control animals, AQP1 protein expression was restricted to the ventricular-facing surface of the choroid plexus. AQP4 was expressed in astrocyte foot processes near blood vessels and in ependymal and pial surfaces in contact with cerebrospinal fluid. AQP9 protein has been detected in cells lining the cerebral ventricles, and in astrocytes. Six to eight weeks after status epilepticus (SE), AQP1 expression was mainly, but not all, detected in vacuolized astrocytes, which were localized in the stratum radiatum of the CA1 region. AQP4 was negligible in vacuolized CA1 astrocytes, although AQP4 immunoreactivity in non-vacuolized astrocytes was increased as compared to control level. AQP9 expression was shown to be mainly induced in non-vacuolized CA1 astrocytes. Therefore, our findings suggest that AQP subunits may play differential roles in various astroglial responses (including astroglial swelling and astroglial loss) in the chronic epileptic hippocampus.