[Significances of the elevated activity of serum creatine phosphokinase and transaminase in progressive muscular dystrophy].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to E Abe.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND CONTEXT: Some biomechanical studies have demonstrated that bone mineral density of the lumbar spine (BMD) affects the stability of pedicle screws in vitro. PURPOSE: To investigate influence of BMD on loosening and related failure of pedicle screws in vivo. STUDY DESIGN/SETTING: A clinical study of 52 patients who underwent pedicle screw fixation augmenting posterior lumbar interbody fusion (PLIF). PATIENT SAMPLE: There were 13 men and 39 women, with an average age of 63 years (range, 45-76 years) at the time of operation. The mean follow-up period was 2.8 years (range, 2-6 years). OUTCOME MEASURES: Relationship between BMD, screw loosening, and its related failures were statistically analyzed. METHODS: BMD was measured by the dual energy X-ray absorptiometry (DEXA) method. Radiographic assessments were done by the first author and independently by another orthopedist who was not informed of the values of BMD. RESULTS: The mean BMD of all patients was 0.879 +/- 0.215 (mean +/- S.D.) g/cm2. The mean BMD in patients with and without screw loosening was 0.720 +/- 0.078 g/cm2 (n=11) and 0.922 +/- 0.221 g/cm2 (n=41). There was a significant difference between the mean BMD of patients with and without screw loosening (P<.01). The mean BMD of patients with "union," "nonunion" and "undetermined union" was 0.934 +/- 0.210 g/cm2 (n=40), 0.674 +/- 0.104 g/cm2 (n=4) and 0.710 +/- 0.116 g/cm2 (n=8), respectively. The mean BMD of patients with "union" was significantly greater than those with "nonunion" and "undetermined union" (P<.05). CONCLUSION: It could be concluded that BMD has a close relation with the stability of pedicle screws in vivo, and BMD value below 0.674 +/- 0.104 g/cm2 suggests a potential increased risk of "nonunion" when pedicle screw fixation is performed in conjunction with PLIF.
It is often assumed that it is not possible to alter the properties of magnetic materials once they have been prepared and put into use. For example, although magnetic materials are used in information technology to store trillions of bits (in the form of magnetization directions established by applying external magnetic fields), the properties of the magnetic medium itself remain unchanged on magnetization reversal. The ability to externally control the properties of magnetic materials would be highly desirable from fundamental and technological viewpoints, particularly in view of recent developments in magnetoelectronics and spintronics. In semiconductors, the conductivity can be varied by applying an electric field, but the electrical manipulation of magnetism has proved elusive. Here we demonstrate electric-field control of ferromagnetism in a thin-film semiconducting alloy, using an insulating-gate field-effect transistor structure. By applying electric fields, we are able to vary isothermally and reversibly the transition temperature of hole-induced ferromagnetism.
Cytokines that transduce their signals either through glycoprotein 130 (gp130) homodimers or gp 130/leukemia inhibitory factor (LIF) receptor beta heterodimers are potent inducers of osteoclast development in vitro as well as in vivo; and interleukin (IL)-6 has been recognized as an important pathogenic factor in diseases characterized by increased bone remodeling, such as the osteoporosis of sex steroid deficiency. Based on evidence that the same cytokines can also promote committed osteoblast differentiation and stimulate bone formation in vitro and in vivo and that mesenchymal cell differentiation toward the osteoblast lineage may be a prerequisite for osteoclastogenesis, we have investigated whether gp130 activation can affect the differentiation of uncommitted mesenchymal progenitors. Using as our model murine embryonic fibroblasts (EF), we found that IL-6 or IL-11 in combination with their soluble receptors (sIL-6R or sIL-11R) increased dose-dependently the number of alkaline phosphatase (AP)-positive cells in 3-6-day-long cultures. Moreover, EF cells maintained with IL-6/sIL-6R in the presence of ascorbic acid and beta-glycerophosphate expressed osteocalcin messenger RNA (mRNA) by 2 weeks and formed a matrix containing mineralized collagen fibers by 3 weeks. This prodifferentiation effect was specific for the osteoblastic lineage, as we found no evidence for increased differentiation of chondrocytes, adipocytes, or muscle cells. Unlike IL-6/sIL-6R, LIF, oncostatin M (OSM), and ciliary neurotrophic factor (CNTF) did not promote osteoblastic differentiation of EF cells. This pattern of specificity was accounted for by the finding that EF cells express gp130, but not the ligand-binding subunit of the IL-6 receptor (gp80) nor the LIF receptor beta. These observations add credence to the contention that increased production of gp130-utilizing cytokines and their receptors in pathological conditions like sex steroid deficiency is indeed responsible for not only the increased osteoclastogenesis, but also the increased osteoblastogenesis, and thereby for the increased rate of bone remodeling.