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Biomedical subjects

G Bestetti

Publications and source records attributed to G Bestetti.

At least 55 records · Page 3Linked to original sources
PubMed1986

Hypothalamic and cortical neurons of normotensive and spontaneously hypertensive rats are differently affected by streptozotocin diabetes.

Diabetic encephalopathy is a relatively frequent late complication in human and experimental diabetes mellitus. Although it is generally assumed that microangiopathy plays a major role in its pathogenesis, many aspects of the latter are still poorly understood. To detect possible correlations between vascular and cellular changes, we examined in normotensive and spontaneously hypertensive streptozotocin diabetic rats the neurons of hypothalamic and cortical regions in which the capillary basement membrane thickness had been known from a previous study. Arcuate and ventromedial nucleus neurons of normotensive diabetic rats compared to those of corresponding controls showed a reduced cytoplasmic area after 4 but not after 8 months of experiment. No difference was found between hypertensive control and diabetic rats after either 4 or 8 months of experiment. After the 8th month cortical neurons of normotensive controls were smaller in an occipital than in a frontal region and within the same region in the following layer order: deep less than superficial less than intermediate. Neurons of hypertensive controls behaved comparably yet were generally smaller than those of normotensive controls in each corresponding region. Compared to those of control, cortical neurons of normotensive diabetic rats were smaller in superficial and deep layers of both regions and in the intermediate layer of the frontal region. Hypertension appeared to antagonize diabetes. Despite an arcuate nucleus microangiopathy found in rats from both strains after 4 and 8 months of diabetes, neuronal changes were seen only in normotensive animals after 4 months. In the intermediate cortical layer, where microangiopathy was most marked after 8 months of experiment, neurons were not or only slightly reduced in size.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Comparative analysis of different Pseudomonas strains that degrade cinnamic acid.

Strains of Pseudomonas stutzeri (CINNS) and Pseudomonas putida (CINNP and CINNW) isolated from soil with cinnamic acid as the sole carbon source were found to be simultaneously adapted to grow on phenylpropionic and p-hydroxybenzoic acids. In cinnamic acid-grown cultures, phenylpropionic acid was isolated. A catabolic plasmid of approximately equal to 75 kilobase pairs encoding the metabolism of cinnamic acid was found in strains CINNP and CINNS.

Biodegradation, Environmental↗
PubMed1985

Effect of growth hormone-releasing stimuli in streptozotocin diabetic rats.

The dynamics of growth hormone (GH) secretion in response to different GH secretagogues has been studied in adult freely moving male rats one month after induction of diabetes by single i.v. injection of streptozotocin (60 mg/kg). Baseline plasma GH concentrations and pituitary GH content were not different in streptozotocin-diabetic (St-D) rats and controls. Clonidine (0.15 mg/kg i.v.), an alpha 2-adrenergic agonist, failed to evoke GH release in St-D rats. Substitution therapy with insulin (1 IU/100 g b.wt.daily) delivered through subcutaneously implanted minipumps, allowed re-institution of a normal GH responsiveness to clonidine. At odds with clonidine, FK 33-824 (0.1 mg/kg i.v.), a potent analog of the opioid peptide Met-enkephalin, induced a similar rise in plasma GH levels in control and St-D rats. Finally, administration of a synthetic replicate of a GH-releasing hormone of human pancreatic origin, hpGRF-40 (2.5 micrograms/kg i.v.) elicited a higher GH response in St-D rats than in controls. These data indicate that in St-D rats: (1) an impaired function of noradrenergic pathways controlling GH release is present; (2) contrary to previous beliefs, an alpha 2-adrenergic mechanism is not involved in the GH-releasing effect of opioid peptides; and (3) pituitary GH responsiveness to hpGRF is increased.

Animals↗
PubMed1985

Basement membrane of hypothalamus and cortex capillaries from normotensive and spontaneously hypertensive rats with streptozotocin-induced diabetes.

Basement membrane (BM) thickness of hypothalamic arcuate nucleus capillaries was measured in normotensive (WKY) and hypertensive (SHR) rats 4 and 8 months after streptozotocin or saline injection. Three groups were studied: controls (C), diabetics (D), and animals with impaired glucose tolerance (L). For comparison, BM thickness of cortical capillaries of an occipital and a frontal area was measured in three different layers starting from the pial surface. Independently from strain, hypothalamic capillary BM was thicker in older than in younger animals. At both 4 and 8 months, BM thickness was lowest in C, highest in D, and intermediate (between C and D) in L. Hypertension combined with diabetes did not further increase BM thickness. In both C and D no difference was found between the two cortical areas. The BM thickness of C increased from the superficial to the deep layer. In C hypertension induced BM thickening in the superficial frontal and the deep occipital layer. In the intermediate and the deep layer of the frontal area BM was thicker in WKY-D than in WKY-C. In every layer BM was thicker in SHR-D than in corresponding controls. Hypertension combined with diabetes enhanced BM thickening in the intermediate and the deep layer of the frontal and in the intermediate layer of the occipital area. Degenerative changes occurred in hypothalamic and cortical pericytes. These changes were more frequent in hypertensive than in normotensive animals. In conclusion, a microangiopathy characterized by BM thickening and pericytic degeneration occurs in the brain of diabetic animals. Its intensity and enhancement by a concomitant hypertension vary from hypothalamus to cortex.

Animals↗
PubMed1985

Islet cell carcinomas in dogs.

Seven cases of dog islet cell carcinomas were studied by conventional and immunohistochemical light- and electron-microscopy. Antisera to insulin, pancreatic polypeptide, somatostatin and glucagon were used. In 6 tumours several hormones were demonstrated. Glucagon never occurred. Insulin was the only hormone present in every tumour, thus it seems to be a good marker for these neoplasms. Liver metastases contained less immunoreactive cells than primary tumours and cell types found in primary carcinomas were sometimes not present in liver metastases. In two cases a degenerative neuropathy occurred.

Adenoma, Islet Cell↗
PubMed1985

Generalized parvovirus infection with inclusion-body myocarditis in two kittens.

Two 13-day-old kittens showed a disease characterized by degeneration, inflammatory response and inclusion bodies in intestine, liver and in one case the myocardium. Inclusions contained typical parvovirus particles. Either a generalized parvovirus infection by the causal agent of feline panleukopenia or an infection due to an unknown parvovirus is considered a possible cause of the disease. A possible relationship of the agent to canine parvovirus is also considered.

Animals↗
PubMed1985

One month of streptozotocin-diabetes induces different neuroendocrine and morphological alterations in the hypothalamo-pituitary axis of male and female rats.

LHRH (median eminence) and LH (pituitary and plasma) from male and female Sprague-Dawley rats were assayed 1 month after streptozotocin injection and compared with values in controls either fed ad libitum or offered a restricted diet. Plasma LH was also assayed after stimulation with exogenous LHRH or naloxone. In diabetic males, the median eminence LHRH content and the plasma LH response to exogenous LHRH were unaltered, pituitary LH was increased, and plasma LH was decreased under basal conditions and after naloxone treatment. In diabetic females, while the median eminence LHRH content and the plasma LH response to exogenous LHRH or naloxone were reduced, pituitary and plasma LH levels were not different. Measurements made in undernourished rats excluded the possibility that the alterations found in diabetic animals were nutrition dependent. In parallel experiments, hypothalami and pituitaries were examined morphologically. In diabetic animals, degenerate axons, mainly of the LHRH type, were found in the arcuate nucleus and median eminence, and LH gonadotrophs were altered and more numerous. Strong differences between control males and females were revealed by morphometry; moreover, diabetic females had higher brain weights and fewer LH gonadotroph changes than diabetic males. These studies indicate that 1) the hypothalamo-pituitary changes that occur early in our streptozotocin-treated rats are unrelated to undernourishment and are possibly caused by insulin deficiency; 2) the LHRH axonal lesions might play a primary pathogenic role in the hypothalamo-pituitary disorder; 3) some anatomical data indicate that the brain and pituitary are less severely affected by diabetes in female than in male animals; and 4) differences between control males and females may account for some of the dissimilarities between the sexes observed under diabetic conditions.

Animals↗
PubMed1984

Molecular characterization of a plasmid from Pseudomonas fluorescens involved in styrene degradation.

In this paper evidence is given that in a strain of Pseudomonas fluorescens able to grow on styrene as the sole carbon source, the degradation pathway of styrene is inducible and plasmid dependent. The plasmid, which we have called pEG is self-transmissible between Pseudomonas strains and has a size of 37 kb. A restriction map has been constructed and evidence for an inducible transcription of two separate regions of the plasmid has been obtained.

Chromosome Mapping↗
PubMed1982

Hypothalamic changes in diabetic Chinese hamsters. A semiquantitative, light and electron microscopic study.

Eight male congenitally diabetic Chinese hamsters (DCH) and eight heterozygotic controls were studied for a period of about 20 months. Final glycemia and body weight were significantly higher in DCH (p less than 0.001). After whole body perfusion brains were removed and processed for light and electron microscopy. Qualitative and quantitative light microscopic studies of semithin sections of hypothalami revealed significant changes in DCH. Accumulation of lipid droplets was found in the external layer of the median eminence (p less than 0.001). Cell bodies of beta-tanycytes (p less than 0.01) and of arcuate nucleus neurons (p less than 0.001) were hypotrophic. By electron microscopy, the lipid droplets were localized in beta-tanycyte processes. Apical surfaces of alpha- and beta-tanycytes of DCH had fewer digitations. Intracytoplasmic organelles of arcuate nucleus neurons were reduced in number and size. These findings suggest a primary pathogenetic role of the hypothalamic-hypophyseal axis in diabetes of Chinese hamsters.

Age Factors↗
PubMed1981

Morphological changes in the hypothalamic-hypophyseal-gonadal axis of male rats after twelve months of streptozotocin-induced diabetes.

The hypothalami, pituitaries and testes from streptozotocin-treated and control male Wistar rats were examined by light and electron microscopy 12 months after induction of diabetes. Light and electron microscopic immunohistochemical techniques were employed for the localization of luteinizing hormone-releasing hormone and luteinizing hormone in the hypothalami and the pituitaries. In the hypothalami of diabetic animals swollen neuronal processes containing anti-luteinizing hormone-releasing-hormone positive material were frequent. In the pituitaries of the same animals a large number of small luteinizing hormone-gonadotrophs was found. These cells contained numerous secretory granules and were deficient in endoplasmic reticulum. The average testicular weight of the diabetic rats was significantly reduced but with marked individual variations. Histologically, the testes with the highest weights appeared normal, those with the lowest weights atrophic with few degenerating Leydig cells. these hypothalamic-hypophyseal changes are probably responsible for the testicular lesions found in experimental diabetes mellitus and may have relevance to the problem of infertility in human diabetes.

Animals↗
PubMed1981

Changes in peripheral nerves of rats four months after induction of streptozotocin diabetes. A qualitative and quantitative study.

Eight streptozotocin-injected Wistar rats and eight controls were fixed by whole-body perfusion 4 months after beginning of the experiment, the nervus radialis was dissected and processed for light and electron microscopy. After light-microscopic study standard photographs of nerve cross sections were measured by means of a semiautomatic image analyzer. The following measurements were obtained: (1) surface of fibers, axons, and myelin sheaths, (2) ratio of myelin to axon surface, and (3) percent of endoneural space. Group means and standard deviations were calculated, and cumulated size class distributions were made. Representative nerve specimens from all animals were also studied by electron microscopy. The quantitative study revealed in the diabetics a severe reduction of the average myelin surface, a mild increase of axonal cross section and of endoneural space, a reduction of myelin/axon ratio and a mild reduction in cross section of the nerve. Ultrastructural lesions of minor degree were found in the cytoplasm of Schwann and mesenchymal cells, no lesion was observed in axons. These findings demonstrate the presence of neuropathy 4 months after induction of diabetes and support the pathogenetic role of the Schwann cell in our experimental model.

Animals↗
PubMed1981

Morphological and morphometric study of peripheral nerves from rats with streptozotocin-induced diabetes mellitus.

One year after beginning of the experiment seven streptozotocin-injected Wistar rats and seven controls were fixed by whole-body perfusion, the nervus radialis was dissected and processed for light and electron microscopy. After light-microscopic study standard photographs of nerve cross sections were measured by means of a semiautomatic image analyzer. The following measurements were obtained: (1) surface of fibers, axons, and myelin sheaths; (2) ratio of myelin to axon surface; and (3) percent of endoneural space. Group means and standard errors were calculated, and cumulated class distributions were made. Ultrathin sections from all animals considered morphometrically were studied qualitatively for ultrastructural changes. The quantitative study revealed in the diabetics reduction of average myelin surface, increase of endoneural space, and reduction of myelin/axon ratio. The main ultrastructural findings were lesions of Schwann and mesenchymal cells, followed by less frequent and less severe changes in axons and endothelium. These results suggest a primary Schwann cell lesion was responsible for the observed myelin reduction.

Animals↗
PubMed1980

Hypothalamic lesions in rats with long-term streptozotocin-induced diabetes mellitus. A semiquantitative light- and electron-microscopic study.

Sixteen male Wistar rats, 1 year after injection of streptozotocin or vehicle, were fixed by whole-body perfusion, the brains were removed and processed for light and electron microscopy. Study of semithin sections from the hypothalamic area revealed changes in the arcuate nucleus and median eminence. The lesions, in comparison with controls, were subjected to a blind semiquantitative evaluation. The following changes were observed by light microscopy in diabetic rats: accumulation of glycogen (P < 0.01), degeneration of neurons (P < 0.05), hypotrophy of tanycytes (P < 0.01), and axonal changes. Electron microscopy of diabetic rats revealed that glycogen was increased in neuronal bodies and processes (axons, synapses), also in tanycytes, and glia cells. In neurons were seen: dilated and fragmented endoplasmic reticulum, degranulated ergastoplasm, loss of organelles, increased number of microtubuli, myelin figures, irregularities in the form of nuclei, and appearance of chromatin. The tanycytes in diabetic animals were reduced in volume, had an increased nuclear cytoplasmic ratio, a reduced number of organelles, short basal processes, and almost complete loss of the apical processes. These changes demonstrate the existence, under experimental conditions, of an encephalopathy pathogenetically related to streptozotocin-induced diabetes.

Animals↗
PubMed1980

Encephalopathy with Rosenthal fibre formation in a sheep.

In the brain of a 4-year-old ewe extensive Rosenthal fiber (RF) formation was found in a subpial and subependymal location and in particular in the cerebellar white matter. Here, the RFs were concentrated around blood vessels, and there was diffuse myelin rarefaction. The animal had given birth to two lambs, which were still healthy at the age of 3 weeks when their mother died after a short illness with astasia and alternating states of somnolence and hyperexcitability.

Animals↗
PubMed1980

The occurrence of cytoplasmic lamellar bodies in normal and pathologic conditions.

Lamellar bodies are stacks of parallel cisternae of approximately regular spacing derived from ergastoplasm. Their occurrence was studied in various nervous and epithelial cells of different animal species in both normal and diseased subjects. This organelle appears to be, at least for some cell types, a normal cytoplasmic feature. The number of lamellar bodies increases in some pathologic conditions and when the cell metabolism is elevated.

Animals↗