Underwater three-dimensional imaging with an amplitude-modulated laser radar at a 405 nm wavelength.

We report the results of underwater imaging with an amplitude-modulated single-mode laser beam and miniaturized piezoactuator-based scanning system. The basic elements of the device are a diode laser source at 405 nm with digital amplitude modulation and a microscanning system realized with a small-aperture aspheric lens mounted on a pair of piezoelectric translators driven by sawtooth waveforms. The system has been designed to be a low-weight and rugged imaging device suitable to operate at medium range (approximately 10 m) in clear seawater as also demonstrated by computer simulation of layout performance. In the controlled laboratory conditions a submillimeter range accuracy has been obtained at a laser amplitude modulation frequency of 36.7 MHz.

Cognitive impairment and chronic cerebral hypoperfusion: what can be learned from experimental models.

The relation between chronic cerebral hypoperfusion and cognitive functions has not been completely clarified. The resolution of cerebral hypoperfusion states, such as those induced by arteriovenous malformations or carotid stenosis/occlusion, has been reported to improve mental decline in humans. Subcortical vascular dementia is another human condition supposed to be linked with chronic cerebral hypoxia/ischemia. The extent of this cause/effect relation is, however, difficult to be assessed in humans, where different factors, such as ageing or subtle degenerative processes, can coexist and interact influencing cognitive performances. Experimental studies can help to elucidate this relation because they can use models of pure chronic/moderate cerebral hypoperfusion. An experimental model of chronic ischemia is the bilateral common carotid artery occlusion in the rat. In this paper, we present a review of experimental studies that evaluated cognitive functions in the rat with bilateral common carotid artery occlusion. We then present an experimental model of bilateral common carotid artery occlusion in the rat modified with respect to previous papers regarding both the surgical procedure and the neurocognitive evaluation that is focused on cognitive domains depending on subcortical-frontal circuits. We propose this model to investigate subcortical vascular dementia.

Persistent impairment of gait performances and working memory after bilateral common carotid artery occlusion in the adult Wistar rat.

BACKGROUND: The clinical and pathophysiological effects of a chronic reduction of cerebral blood flow in humans are not completely known. We investigated whether rats subjected to bilateral common carotid artery occlusion (bCCA-o) developed focal neurological deficits, gait dysfunction, and working memory alterations. METHODS: Eighteen male Wistar rats were subjected to bCCA-o, 13 were sham-operated. We assessed sensorimotor functions, gait on a 60 cm-long elevated bridge, and working memory (object recognition and Y maze tests) before and 30, 60, and 90 days after surgery. Histological analysis was performed in a subgroup of 10 rats. RESULTS: No rat showed sensorimotor alterations after surgery. Although gait performances of both bCCA-o and sham-operated rats declined over time, the differences reached statistical significance only for the bCCA-o group (mean+/-SE: 26.8+/-5.0; 22.4+/-4.9; 24.5+/-5.5 cm at 30, 60, and 90 days, respectively) in comparison with baseline (52.9+/-5.2 cm; P<0.05). At 60 and 90 days, bCCA-o rats in comparison with sham-operated rats showed decreased performances on object recognition (discrimination index: 0.15+/-0.03 vs. 0.29+/-0.05 at 60 days and 0.10+/-0.04 vs. 0.41+/-0.07 at 90 days; P<0.05) and on Y maze test (alternating rats: 9.9 vs. 85.7% at 60 days and 16.6 vs. 100% at 90 days; P<0.01). In none of the animals were cerebral infarcts detected. Selective neuronal necrosis was observed in the cortex and hippocampus of both bCCA-o and sham-operated rats without any obvious difference. CONCLUSIONS: bCCA-o in the Wistar rat induces persistent and progressive gait and working memory impairment without producing sensorimotor deficit or cerebral infarcts. This model may help to elucidate some physiopathological aspects of neurological impairment associated with states of cerebral chronic ischemia.