Mesoporous titania-silica composite films with highly aligned cylindrical pores are prepared by the sol-gel method using a substrate with structural anisotropy. The strong alignment effect of a rubbing-treated polyimide film on a substrate provides a narrow alignment distribution in the plane of the film regardless of the fast condensation rate of titania precursors. The collapse of the mesostructure upon the surfactant removal is effectively suppressed by the reinforcement of the pore walls with silica by exposing the as-deposited film to a vapor of a silicon alkoxide. The existence of a silica layer on the titania pore wall is proved from the distributions of Ti and Si estimated by the elemental analysis in high resolution electron microscopy. The obtained mesoporous titania-silica composite film exhibits a remarkable birefringence reflecting the highly anisotropic mesoporous structure and the high refractive index of titania that forms the pore wall. The Δn value estimated from the optical retardation and the film thickness is larger than 0.06, which cannot be achieved with the conventional mesoporous silica films with uniaxially aligned mesoporous structure even though the alignment of the pores in the films is perfect. These inorganic films with mesoscopic structural anisotropy will find many applications in the field of optics as phase plates with high thermal/chemical/mechanical stabilities.

Spinal cord injury (SCI) is a debilitating condition that can cause impaired motor function or full paralysis. In the days to weeks following the initial mechanical injury to the spinal cord, inflammation and apoptosis can cause additional damage to the injured tissues. This secondary injury impairs recovery. Brain-derived neurotrophic factor is a secreted protein that has been shown to improve a variety of neurological conditions, including SCI, by promoting neuron survival and synaptic plasticity. This study treated a mouse model of contusion SCI using a single dose of brain-derived neurotrophic factor (BDNF) mRNA nanomicelles prepared with polyethylene glycol polyamino acid block copolymer directly injected into the injured tissue. BDNF levels in the injured spinal cord tissue were approximately doubled by mRNA treatment. Motor function was monitored using the Basso Mouse Scale and Noldus CatWalk Automated Gait Analysis System for 6 weeks post-injury. BDNF-treated mice showed improved motor function recovery, demonstrating the feasibility of mRNA delivery to treat SCI.

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SUMMARY Intravascular platelet aggregation induced by ADP injection into the carotid artery of rabbits caused ipsilateral cerebrovascular injuries. We have observed the details of these in vivo vascular changes under the electron microscope. Intracytoplasmic vacuole (1.0-2.0 /xm in diameter) formation and partial deendothelialization followed by platelet thrombus formation were characteristic changes in the middle cerebral artery. These vacuoles did not contain horseradish peroxidase (HRP) which was used as a marker of vascular permeability change. Compared with these phenomenon, increased vesicular (0.05-0.2 fxm in diameter) transport was prominent, and vacuole formation was rarely seen in small vessels, namely, capillaries and arterioles in the cortex. Endothelial cell damage seemed to be more prominent in large arteries, but only the smaller vessels show marked extravasation of HRP-reaction product and perivascular edema. Blood levels of TXB 2 and 6-keto PGF la were significantly increased 3 min after the ADP injection and returned to pre-injection levels at 60 min after. These results suggest that vasoactive substances resulting from platelet activation may play an important role in producing cerebrovascular injuries caused by platelet aggregation induced with ADP. Stroke Vol 16, No 2, 1985THE APPEARANCE OF VASCULAR injuries in cerebral arteries induced by intravascular aggregation of platelets in rabbits has been previously reported.'-2 At one hour after an injection or a platelet aggregating agent such as arachidonic acid of ADP into the cerebral artery, we have found an extravasation of preinjected Evans blue around platelet thrombi in the injected side of the brain. These findings were rarely observed in the noninjected side of the brain and rarely observed in thrombocytopenic rabbits. These results suggested that released substances from platelet aggregates may induce vascular injuries in the brain. However, the precise mechanism is not yet clear. injected arachidonic acid into rat carotid arteries, and they observed platelet thrombi in the vascular lumen and suppression of the EEG, with eventual death of the animals. As a model for transient ischemic attacks, Fishi et al 5 -6 injected ADP into rabbit carotid arteries to induce platelet aggregation. In this system, they also observed intravascular platelet aggregation and disturbance of cerebral blood flow, but they did not observe vascular changes associated with platelet thrombi. In this report, we describe the ultrastructural details of vascular changes induced by platelet aggregation in vivo and have analyzed the mechanisms which effect these changes. Materials and Methods Experiment 1Forty-four white male rabbits, weighing 2 . 9^. 0 kg, were used. Under general anesthesia with sodium pentobarbital (50 mg/kg, intraperitoneally), a polyethylene catheter was inserted into a lingual artery, and its tip was advanced to the carotid bifurcation. Using this method a platelet aggregating substance was injected into the cerebral arteries without disturbing...

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