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Biomedical subjects

G Moonen

Publications and source records attributed to G Moonen.

135 records · Page 8Linked to original sources

Variability of the effects of serum-free medium, dibutyryl-cyclic AMP or theophylline on the morphology of cultured new-born rat astroblasts.

The effects of serum deprivation, of dibutyryl-cyclic AMP (dBcAMP) and of theophylline on the morphology of cultured new-born rat astroblasts have been studied using Eagle's basal medium (BME) or Eagle's minimum essential medium (MEM) as culture media. Serum deprivation had no effect on cells cultured in BME, while in MEM, deprivation induced a rapid morphological transformation involving the appearance of multiple processes. This phenomenon was rapidly reversible when serum was again added. In serum-supplemented BME, dB-cAMP (1 mM) and theophylline (1 mM) had no effect. In serum-supplement MEM, theophylline (1 mM) had no effect while dB-cAMP (1 mM) induced a slower and poorly reversible morphological alteration. On the other hand cells in serum-free BME showed multiple processes after addition of dB-cAMP (1 mM) or theophylline (1 mM). This rapid alteration was completely reversed either by removal of dB-cAMP and theophylline or by addition of serum.

Animals↗

[Culture of dissociated cells from cerebral hemisphere of essentially neuronal make up].

Four methods are described to obtain pure neuronal cultures from chick embryo cerebral hemispheres. In our experimental conditions the proliferation of the glial cells in inhibited and cultures of either low or high neuronal density are obtained. The isolated neurons, however, did not survive longer than 8 to 10 days; the contact with glial cells seems to be necessary for the maintenance of the neurons in long-term cultures.

Animals↗

Effects of synthetic tripeptide on the differentiation of dissociated cerebral hemisphere nerve cells in culture.

Dissociated cells from 7-day-old chick embryo cerebral hemispheres were cultivated on collagen in Falcon Petri dishes in the presence of various concentrations of fetal calf serum and of a chemically synthesized tripeptide Gly-His-Lys. Four different culture conditions were employed in the composition of the nutrient medium in which the cells were cultivated: a low serum concentration of 1, 2 or 5% (group A), a low serum concentration with 200 ng/ml tripeptide (group B), a serum concentration of 10 to 20% (group C) and a serum concentration of 10 or 20% with 200 ng/ml tripeptide (group D). Within the first 24 h of cultivation the cells settled on the collagen substrate and outgrowth of neuronal processes started in all four culture conditions. After 48 h in culture, differences between the groups became evident. In group A most isolated nerve cells had disappeared and glial cells proliferated from the remaining clumps. In group B the neurons had differentiated in absence of glial cells, the proliferation of which was greatly suppressed. In group C and D a differentiation of neurons occurred in a similar way to group B, but in addition the glial cells had proliferated. After 7-8 days in culture the cells in group A and B suddenly degenerated. In group C and D the nerve cells maintained for up to 3 weeks. The optimum concentrations of tripeptide in which the neuroblasts grew fibers and maintained in culture during 7-8 days were in the range of 100-400 ng/ml. The role of the tripeptide in the differentiation and maintenance of nerve cells is discussed.

Animals↗

Oxidative stress-induced apoptosis of cochlear sensory cells: otoprotective strategies.

Apoptosis is an important process, both for normal development of the inner ear and for removal of oxidative-stress damaged sensory cells from the cochlea. Oxidative-stressors of auditory sensory cells include: loss of trophic factor support, ischemia-reperfusion, and ototoxins. Loss of trophic factor support and cisplatin ototoxicity, both initiate the intracellular production of reactive oxygen species and free radicals. The interaction of reactive oxygen species and free radicals with membrane phospholipids of auditory sensory cells creates aldehydic lipid peroxidation products. One of these aldehydes, 4-hydroxynonenal, functions as a mediator of apoptosis for both auditory neurons and hair cells. We present several approaches for the prevention of auditory sensory loss from reactive oxygen species-induced apoptosis: 1) preventing the formation of reactive oxygen species; (2) neutralizing the toxic products of membrane lipid peroxidation; and 3) blocking the damaged sensory cells' apoptotic pathway.

Animals↗

[Reversible posterior leukoencephalopathy syndrome].

Reversible posterior leukoencephalopathy refers to a clinicoradiological syndrome observed in patients presenting with acute or subacute symptoms of various intensity including seizures, headache, vomiting, confusion and visual abnormalities. The radiological features are reversible bilateral white matter abnormalities predominantly located in the posterior regions of the cerebral hemispheres, demonstrated by computed tomography or, better, by magnetic resonance imaging. This syndrome mostly occurs in patients with hypertensive encephalopathy or in immunosuppressed patients. The recognition of this syndrome is critical as delay in the diagnosis or treatment can result in permanent neurological deficit while early prompt control of blood pressure or withdrawal of causative drugs can reverse the syndrome.

Adult↗

[Diabetic peripheral neuropathy].

Peripheral neuropathy is a very frequent consequence of diabetes mellitus. Its clinical expression is quite variable. A specific therapy is sometimes necessary. Early diagnosis of diabetic neuropathy is a cornerstone of patient's follow-up. Differential diagnosis of diabetic neuropathy is sometimes difficult from another type of neuropathy or a focal, even systemic, disease. It is mandatory to know how a diabetic neuropathy may express. Pathophysiological mechanisms involved in diabetic neuropathy are complex and interrelated. Hyperglycaemia alone, even mild or moderate, vascular disorders and dysimmune factors may be combined to induce axonal injury. Glycaemic control is the cornerstone of effective treatment for neuropathy associated with diabetes. Specific pain control and therapies of autonomic disturbances are regularly required.

Diabetes Complications↗