Using multimodal magnetic resonance imaging (MRI), behavioral, and immunohistochemical analyses, we examined pathological changes at the acute, sub-acute, and chronic stages, induced by permanent or temporary ischemia in the common marmoset. Animals underwent either permanent (pMCAO) or 3-h transient (tMCAO) occlusion of the middle cerebral artery (MCAO) by the intraluminal thread approach. MRI scans were performed at 1 h, 8, and 45 days after MCAO. Sensorimotor deficits were assessed weekly up to 45 days after MCAO. Immunohistological studies were performed to examine neuronal loss, astrogliosis, and neurogenesis. Remote lesions were analyzed using retrograde neuronal tracers. At day 8 (D8), the lesion defined on diffusion tensor imaging (DTI)-MRI and T2-MRI was significantly larger in pMCAO as compared with that in the tMCAO group. At D45, the former still displayed abnormal signals in T2-MRI. Post-mortem analyses revealed widespread neuronal loss and associated astrogliosis to a greater extent in the pMCAO group. Neurogenesis was increased in both groups in the vicinity of the lesion. Disconnections between the caudate and the temporal cortex, and between the parietal cortex and the thalamus, were observed. Sensorimotor impairments were more severe and long-lasting in pMCAO relative to tMCAO. The profile of brain damage and functional deficits seen in the marmoset suggests that this model could be suitable to test therapies against stroke.

Although chronic arterial hypertension (CAH) increases the risk of stroke and the severity of the resultant lesion, it is rarely integrated in preclinical studies. Here, we analyzed the impact of CAH on the acute spatiotemporal evolution of the ischemic penumbra as defined by the perfusion-weighted imaging/diffusion-weighted imaging mismatch. Sequential 7T-MRI examinations were performed from 30 minutes up to 4 hours after permanent cerebral ischemia in genetically hypertensive rats (spontaneously hypertensive rats, SHR), renovascular-hypertensive rats (RH-WKY), and their normotensive controls (Wistar-Kyoto rats, WKY). The apparent diffusion coefficient (ADC)-defined lesion was larger in hypertensive rats than in normotensive animals as early as 30 minutes after the ischemia. The ischemic penumbra was smaller in both genetically and renovascular-hypertensive rats (at 30 minutes; SHR = 66 ± 25 mm 3 , RH-WKY = 55 ± 17 mm 3 versus WKY = 117 ± 14 mm 3 ; P < 0.008) and there was no significant difference between the perfusion deficit and ADC lesion (mismatch definition of penumbra) as early as 90 minutes after the occlusion. Genetic hypertension and induced renovascular hypertension resulted in larger lesion and smaller penumbra that vanished rapidly. These data support the need to integrate CAH in preclinical studies relative to the treatment of stroke, as failure to do so may lead to preclinical results nonpredictive of clinical trials, which include hypertensive patients.

BIA, based on a CF-specific equation, is a reliable method for BC assessment and allows the identification of patients at risk of nutritional degradation and bad respiratory prognosis.

In the weeks following birth, both the brain and the vascular network that supplies it undergo dramatic alteration. While studies of the postnatal evolution of the pial vasculature and blood flow through its vessels have been previously done histologically or acutely, here we describe a neonatal reinforced thin‐skull preparation for longitudinally imaging the development of the pial vasculature in mice using two‐photon laser scanning microscopy. Starting with mice as young as postnatal day 2 (P2), we are able to chronically image cortical areas >1 mm2, repeatedly for several consecutive days, allowing us to observe the remodeling of the pial arterial and venous networks. We used this method to measure blood velocity in individual vessels over multiple days, and show that blood flow through individual pial venules was correlated with subsequent diameter changes. This preparation allows the longitudinal imaging of the developing mammalian cerebral vascular network and its physiology.

Glioblastoma is the most aggressive brain tumor and is almost always fatal. These tumors are highly vascularized and angiogenesis is one of the pre-eminent mechanisms underlying their growth. Chronic arterial hypertension (CAH) is a common and worldwide pathology that markedlly alters the structure and function of the vasculature. Yet, essential hypertension is associated in the brain with potential locally impaired vasoreactivity, disturbed perfusion supply and hypoxia phenomena. Even though CAH is a global burden and has an important impact on brain function, nothing is known about the way this frequent pathology would interact with the evolution of glioma. We sought to determine if arterial hypertension influences gliobastoma growth. In the present study, rat glioma C6 tumor cells were implanted in the caudate-putamen of spontaneously hypertensive rats (SHR) or their normotensive controls, the Wistar-Kyoto (WKY) rats. The evolution of the tumor was sequentially analyzed by multiparametric magnetic resonance imaging and the inflammatory response was examined by histochemistry. We found that CAH significantly attenuates the growth of the tumor as, at 21 days, the volume of the tumor was 85.4±34.7 and 126.1±28.8 mm(3), respectively, in hypertensive and normotensive rats (P<0.02). Moreover, cerebral blood volume and cerebral blood flow were greater in the tumors of hypertensive rats (P<0.05). The lesser growth of the tumor observed in normotensive animals was not due to an enhanced rejection of the tumor cells in WKY rats, the inflammatory response being similar in both groups. For the first time, these results show that CAH impedes the growth of glioblastoma and illustrate the need to further study the impact of hypertension on the evolution of brain tumors.

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Animal models constitute an indispensable tool to investigate human pathology. Here we describe the procedure to induce permanent and transient cerebral ischemia in the mouse and the rat. The model of transient occlusion of the middle cerebral artery (MCA) is performed by the insertion of an occlusive filament until the origin of the MCA while the permanent occlusion described in the mice is performed by a distal electrocoagulation of the MCA. Those models allow evaluating the efficiency of therapeutic strategy of ischemia from tissular aspect to behavioral and cognitive impairment assessment. They were widely used in the literature to evaluate the efficiency of different drugs including the cytokines and especially erythropoietin (EPO) or its derivatives.

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