Delayed-Onset Continuous Bruxism with Olivary Hypertrophy After Top of the Basilar Syndrome

Delayed-onset continuous bruxism due to brain stem infarction has not yet been reported. A 49-year old man presented with quadriplegia and ophthalmoplegia. Brain MRI showed acute infarction in the bilateral midbrain, right thalamus and the superior cerebellum. One month later, the patient developed bruxism which persisted during sleep. A palatal myoclonus was not observed. Follow up MRI taken 4 months later showed bilateral olivary hypertrophy. We suggest that the patient's bruxism may be related to the olivary hypertrophy. The bruxism generator may be located in the pontine-reticular-formation (PRF). Bilateral large midbrain lesions interrupting the cortical inhibition may have produced bilateral olivary hypertrophy, which could stimulate the PRF, producing continuous bruxism

Synthesis of polypyrrole-modified Fe3O4/SiO2/TiO2 nanocomposite microspheres and their photocatalytic activity

A polypyrrole-modified Fe _3 O _4 /SiO _2 /TiO _2 composite material was successfully synthesized on the FST surface by in situ polymerization of pyrrole. Structural, morphological and magnetic response of Fe _3 O _4 /SiO _2 /TiO _2 /PPy(FST/PPy) were characterized by transmission electron microscopy, scanning electron microscopy, X-ray diffraction pattern, Fourier transform infrared spectroscopy and energy-dispersive X-ray spectroscopy, etc. Through SEM images, the crystal sizes of the prepared FST/PPy nanoparticles were determined to be about 110 nm. The catalytic activity of FST/PPy was evaluated by the degree of decomposition of rhodamine B under ultraviolet and visible light, respectively. FST/PPy had the photocatalytic activity under the action of the light: the degradation rate of rhodamine B reached 92.8% and 63.5% after 3 h of UV and Vis light irradiation, respectively. Especially, compared with FST, the degradation rate has shown obvious improvement under the action of Vis light. Furthermore, FST/PPy photocatalyst could be easily recycled using a magnet

Serial changes of lung morphology and biochemical profiles in a rat model of bronchopulmonary dysplasia induced by intra-amniotic lipopolysaccharide and postnatal hyperoxia

Aim: To investigate serial changes of lung morphology and biochemical profiles in a rat model of bronchopulmonary dysplasia (BPD) induced by intra-amniotic lipopolysaccharide (LPS) administration and postnatal hyperoxia (85%). Methods: We evaluated histological changes of the lungs and compared the levels of interleukin-6 (IL-6), vascular endothelial growth factor (VEGF), and protein carbonyl in lung tissue on days 1, 7, and 14 after birth in a rat model of BPD. Results: The inhibition of alveolarization was sustained in the LPS plus hyperoxia group from day 7 to 14, whereas alveolarization resumed in the hyperoxia group after oxygen exposure was withdrawn at day 7. Administration of LPS alone did not adversely affect lung morphometry. IL-6 levels showed transient overexpression at day 1 in the LPS-treated groups, but decreased at days 7 and 14. VEGF protein levels were elevated in the LPS-treated groups, but not in the hyperoxia and control groups at days 1, 7, and 14. Exposure to hyperoxia affected protein carbonyl levels in the hyperoxia group at days 7 and 14. Conclusion: Lung injury induced by intra-amniotic inflammation and postnatal hyperoxia may be due to inhibition of alveolarization without recovery even after withdrawal of oxygen.Normann E, 2009, PEDIATR RES, V65, P430Choi CW, 2009, PEDIATR RES, V65, P323Cheah FC, 2008, PEDIATR RES, V63, P274Thebaud B, 2007, NEONATOLOGY, V91, P291, DOI 10.1159/000101344Ueda K, 2006, PEDIATR RES, V59, P396, DOI 10.1203/01.pdr.0000200796.86858.caRojas M, 2005, AM J PHYSIOL-LUNG C, V288, pL333, DOI 10.1152/ajplung.00334.2004Kramer BW, 2005, BIOL NEONATE, V88, P202, DOI 10.1159/000087583Kallapur SG, 2004, AM J PHYSIOL-LUNG C, V287, pL1178, DOI 10.1152/ajplung.00049.2004Pollet I, 2003, BLOOD, V102, P1740, DOI 10.1182/blood-2003-01-0288SPEER CP, 2003, SEMIN NEONATOL, V8, P29JOBE AH, 2003, SEMIN NEONATOL, V8, P9SAUGSTAD OD, 2003, SEMIN NEONATOL, V8, P39Kramer BW, 2002, AM J PHYSIOL-LUNG C, V283, pL452, DOI 10.1152/ajplung.00407.2001Van Marter LJ, 2002, J PEDIATR, V140, P171, DOI 10.1067/mpd.2002.121381Schock BC, 2001, AM J PHYSIOL-LUNG C, V281, pL1386Willet KE, 2000, PEDIATR RES, V48, P782Yoon BH, 1999, AM J OBSTET GYNECOL, V181, P773Flohe S, 1999, CYTOKINE, V11, P796Cines DB, 1998, BLOOD, V91, P3527Yoshida S, 1997, MOL CELL BIOL, V17, P4015Aono K, 1997, J CELL BIOCHEM, V65, P349Watterberg KL, 1996, PEDIATRICS, V97, P210FRANK L, 1987, PEDIATR RES, V21, P109WEIBEL ER, 1963, MORPHOMETRY HUMAN LU