Biomedical subjects

A Volk

Publications and source records attributed to A Volk.

40 records · Page 3Linked to original sources

PubMedDate not supplied

MRI description of cerebral atrophy in mouse lemur primates.

We assessed cerebral atrophy in mouse lemur primates (Microcebus murinus) by estimating CSF volume in their brains from 4.7 Tesla T2-weighted magnetic resonance images. Thirty animals aged from 1 to 10.3 years were imaged, 14 of them were followed for up to 2 years. Seven of these animals were examined for neuropathology. In 12 out of 17 animals older than 3.5 years, CSF volumes were increased. A subgroup of six animals had severe atrophy of the temporal lobe. Another subgroup of five animals displayed diffuse atrophy in addition to the temporal atrophy. One animal had a dilation of the external part of the temporal horn of the lateral ventricle in addition to the temporal atrophy. The three animals with diffuse atrophy that could be studied for neuropathology had diffuse cerebral amyloid deposits detected by immunocytochemistry. The other animals did not display amyloid deposits. Relations between the different types of atrophy as well as their causes will have to be assessed in future studies.

Age Factors↗

PubMedDate not supplied

T2-weighted MRI studies of mouse lemurs: a primate model of brain aging.

Previous histological and behavioral studies of aging mouse lemurs have demonstrated changes similar to those observed in elderly humans and in patients with Alzheimer's disease. We explored 18 animals of ages 6 months to 9 years. Axial T2-weighted images of the brain were performed on a 4.7 Tesla Bruker Biospec 47/30 system. We estimated cerebral atrophy by adding measures of high signal areas characteristic of cerebrospinal fluid (interlobular and sylvian fissures, lateral and third ventricles) of four contiguous cortical slices. We observed a significant increase of cerebral atrophy with aging and one case of an apathetic 8-year-old animal presenting a considerably higher cerebral atrophy. We also observed high correlations between decreased signal intensities and age for the pallidum, the substantia nigra, and the putamen. These results suggest that aging mouse lemurs present similar magnetic resonance images of cerebral alterations to those encountered in aging humans and that high-field T2-weighted magnetic resonance images can help in the early detection, in vivo, of animals suspected of pathological aging.

Aging↗

PubMedDate not supplied

Cerebral T2-weighted signal decrease during aging in the mouse lemur primate reflects iron accumulation.

4.7 Tesla T2-weighted magnetic resonance images showed a highly significant signal decrease in the pallidum, substantia nigra, putamen, and a less significant decrease in the thalamus and the caudate of aging mouse lemurs (Microcebus murinus). We evaluated the contribution of iron deposits to the signal decrease comparing Perls' stained histological sections of six mouse lemurs brains aged 1 to 10 years to magnetic resonance images. In young animals, none of the brain structures was stained. A large number of iron deposits were visible in the pallidum and substantia nigra of aged animals and a moderate number in the middle aged ones. In the putamen, few iron deposits were visible in aged and middle-aged animals. The thalamus and the caudate appeared unstained with Perls' technique; iron was too low to be detected. The intensification of the reaction by diaminobenzidine revealed iron deposits in the thalamus of aging animals. This study suggests that in mouse lemurs, iron deposits are responsible for T2-weighted signal decrease in the central gray nuclei.

Aging↗

PubMedDate not supplied

Ischemic preconditioning attenuates portal venous plasma concentrations of purines following warm liver ischemia in man.

BACKGROUND/AIMS: Degradation of adenine nucleotides to adenosine has been suggested to play a critical role in ischemic preconditioning (IPC). Thus, we questioned in patients undergoing partial hepatectomy whether (i) IPC will increase plasma purine catabolites and whether (ii) formation of purines in response to vascular clamping (Pringle maneuver) can be attenuated by prior IPC. METHODS: 75 patients were randomly assigned to three groups: group I underwent hepatectomy without vascular clamping; group II was subjected to the Pringle maneuver during resection, and group III was preconditioned (10 min ischemia and 10 min reperfusion) prior to the Pringle maneuver for resection. Central, portal venous and arterial plasma concentrations of adenosine, inosine, hypoxanthine and xanthine were determined by high-performance liquid chromatography. RESULTS: Duration of the Pringle maneuver did not differ between patients with or without IPC. Surgery without vascular clamping had only a minor effect on plasma purine concentrations. After IPC, plasma concentrations of purines transiently increased. After the Pringle maneuver alone, purine plasma concentrations were most increased. This strong rise in plasma purines caused by the Pringle maneuver, however, was significantly attenuated by IPC. When portal venous minus arterial concentration difference was calculated for inosine or hypoxanthine, the respective differences became positive in patients subjected to the Pringle maneuver and were completely prevented by preconditioning. CONCLUSION: These data demonstrate that (i) IPC increases formation of adenosine, and that (ii) the unwanted degradation of adenine nucleotides to purines caused by the Pringle maneuver can be attenuated by IPC. Because IPC also induces a decrease of portal venous minus arterial purine plasma concentration differences, IPC might possibly decrease disturbances in the energy metabolism in the intestine as well.

Adenosine↗