Ultrasonographic evaluation of changes in the muscle architecture of the gastrocnemius with botulinum toxin treatment for lower extremity spasticity in children with cerebral palsy.

BACKGROUND: Botulinum toxin A treatment involves injecting botulinum toxin A to relax muscle spasticity. Using ultrasonography, this study examined changes in the muscle architecture before and after treatment to evaluate the influence of botulinum toxin A injection on muscles. METHODS: The participants included 18 children (mean age, 6.2 years) with cerebral palsy who were treated with botulinum toxin A for lower extremity spasticity and 27 healthy children (mean age, 6.4 years) as a control group. In all cases, botulinum toxin A was injected into the gastrocnemius muscle. The muscle length, muscle width, and pennation angle (which indicates the degree of muscle fiber tone), were measured using B-mode ultrasonography before and 12 weeks after injection. RESULTS: The muscle length and muscle width were shorter in the cerebral palsy group than in the control group. The pennation angle in the cerebral palsy group significantly decreased after injection from 28.2 ± 3.6° to 25.8 ± 2.5° in the resting position of the ankle and from 18.6 ± 2.8° to 15.9 ± 1.7° in the maximum dorsiflexion position of the ankle. In the control group, the pennation angle was 25.9 ± 3.2° in the resting position of the ankle and 15.1 ± 2.5° in the maximum dorsiflexion position of the ankle. The rate of increase of fascicle length during passive movement from the resting position of the ankle to the maximum dorsiflexion position was 143.9% in the cerebral palsy group, which was significantly less than the value of 157.7% in the control group. After botulinum toxin A treatment, the rate of increase of fascicle length in the cerebral palsy group increased to 155.1%. CONCLUSIONS: The decrease in the pennation angle after botulinum toxin A treatment is considered to be the result of a reduction of spasticity and subsequent structural changes in flaccid muscle fibers.

Single-crystalline boron-doped diamond superconducting quantum interference devices with regrowth-induced step edge structure.

Superconducting quantum interference devices (SQUIDs) are currently used as magnetic flux detectors with ultra-high sensitivity for various applications such as medical diagnostics and magnetic material microstructure analysis. Single-crystalline superconducting boron-doped diamond is an excellent candidate for fabricating high-performance SQUIDs because of its robustness and high transition temperature, critical current density, and critical field. Here, we propose a fabrication process for a single-crystalline boron-doped diamond Josephson junction with regrowth-induced step edge structure and demonstrate the first operation of a single-crystalline boron-doped diamond SQUID above 2 K. We demonstrate that the step angle is a significant parameter for forming the Josephson junction and that the step angle can be controlled by adjusting the microwave plasma-enhanced chemical vapour deposition conditions of the regrowth layer. The fabricated junction exhibits superconductor-weak superconductor-superconductor-type behaviour without hysteresis and a high critical current density of 5800 A/cm2.

High relative biologic effectiveness of carbon ion radiation on induction of rat mammary carcinoma and its lack of H-ras and Tp53 mutations.

PURPOSE: The high relative biologic effectiveness (RBE) of high-linear energy transfer (LET) heavy-ion radiation has enabled powerful radiotherapy. The potential risk of later onset of secondary cancers, however, has not been adequately studied. We undertook the present study to clarify the RBE of therapeutic carbon ion radiation and molecular changes that occur in the rat mammary cancer model. METHODS AND MATERIALS: We observed 7-8-week-old rats (ACI, F344, Wistar, and Sprague-Dawley) until 1 year of age after irradiation (0.05-2 Gy) with either 290 MeV/u carbon ions with a spread out Bragg peak (LET 40-90 keV/mum) generated from the Heavy-Ion Medical Accelerator in Chiba or (137)Cs gamma-rays. RESULTS: Carbon ions significantly induced mammary carcinomas in Sprague-Dawley rats but less so in other strains. The dose-effect relationship for carcinoma incidence in the Sprague-Dawley rats was concave downward, providing an RBE of 2 at a typical therapeutic dose per fraction. In contrast, approximately 10 should be considered for radiation protection at low doses. Immunohistochemically, 14 of 18 carcinomas were positive for estrogen receptor alpha. All carcinomas examined were free of common H-ras and Tp53 mutations. Importantly, lung metastasis (7%) was characteristic of carbon ion-irradiated rats. CONCLUSIONS: We found clear genetic variability in the susceptibility to carbon ion-induced mammary carcinomas. The high RBE for carbon ion radiation further supports the importance of precise dose localization in radiotherapy. Common point mutations in H-ras and Tp53 were not involved in carbon ion induction of rat mammary carcinomas.

Colitis associated with Clostridium difficile in specific-pathogen-free C3H-scid mice.

Soft feces and a decreased delivery rate were observed in a specific-pathogen-free (SPF) C3H-scid mouse breeding colony. Grossly, the ceca were shrunken and edematous in the affected mice. Histopathologically, severe edema in the cecal submucosa as well as infiltration of inflammatory cells in the lamina propria and submucosa of the ceca and colon were observed. No pathogenic microorganisms were detected by the routine microbiological tests. By anaerobic bacterial-examination, Clostridium (C.) difficile with toxin A was isolated from the cecal contents of the affected mice. The mice were diagnosed with C. difficile-associated colitis. This case appears to be the first report of natural infection with C. difficile in SPF mice with clinical signs.

Radiation-induced germline mutations detected by a direct comparison of parents and first-generation offspring DNA sequences containing SNPs.

Germline mutation induction has been detected in mice but not in humans. To estimate the genetic risk of germline mutation induction in humans, new techniques for extrapolating from animal data to humans or directly detecting radiation-induced mutations in man are expected to be developed. We have developed a new method to detect germline mutations by directly comparing the DNA sequences of parents and first-generation offspring. C3H male mice were irradiated with gamma-rays of 3, 2 and 1 Gy and 3 weeks later were mated with C57BL female mice of the same age. The nucleotide sequences of 160 UniSTS markers containing 300-900 bp and SNPs of the DNA of parent and offspring mice were determined by direct sequencing. At each dose of radiation, a total of 5 Mb DNA sequences were examined for radiation-induced mutations. We found 7 deletions in 3 Gy-irradiated mice, 1 deletion in 2 Gy-irradiated mice, 1 deletion in 1 Gy-irradiated mice and no mutations in control mice. The maximum mutation frequency was 2.0 x 10(-4)/locus/Gy at 3 Gy, and these results suggested that a non-linear increase of mutations with dose.

Neuropathology of delayed encephalopathy in cats induced by heavy-ion irradiation.

AIM: The pathogenesis of delayed encephalopathy induced by heavy-ion irradiation was investigated experimentally in cats. The left cerebral hemispheres were irradiated with 15-40 Gy of heavy ions (carbon), and histologically and morphometrically examined 12 months later. RESULTS: In the irradiated cerebral white matter the following occurred as the dose increased: astrocytic swelling, then the dilatation of small blood vessels with a fibrous thickening of the wall, and then loosening of the white matter with cavity formation and diffuse albumin deposition. Pathological features of these cavities suggested that they are induced by long-standing edema. Although the dilated vessels were arteries, veins, and capillaries, arteriovenous shunt and damage of the smooth muscle cells of the arterial media were absent. Changes of the cerebral cortex were scarce. Morphometrically, the irradiated cerebral white matter was swollen, and the capillary density tended to be reduced in the deep cortex and subcortical white matter, but this effect was not dose dependent. CONCLUSION: Heavy-ion irradiation induces delayed encephalopathy in cats, preferentially involving the white matter. The cardinal pathogenesis was long-standing edema of the white matter due to vascular hyperpermeability, and the vascular dilatation seemed to be caused by a reduction in the vascular bed and/or hemoconcentration due to hyperpermeability.