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Biomedical subjects

E Sanna

Publications and source records attributed to E Sanna.

86 records · Page 5Linked to original sources
PubMed1987

Isolation from rat brain tissue of an inhibiting activity for dihydropyridine binding sites and voltage-dependent CA2+ uptake.

Nitrendipine binding-inhibitory activity was extracted and partially purified from rat brain. This preparation also decreased veratridine-stimulated Ca2+ uptake in cultured cerebellar granule cells. It failed to inhibit 3H-nitrendipine binding by sequestering Ca2+ that is required for the high affinity binding of nitrendipine. An allosteric modulation of nitrendipine recognition sites by this preparation is suggested.

Animals↗
PubMed1986

Striato-nigral denervation increases type II benzodiazepine receptors in the substantia nigra of the rat.

The degeneration of the striato-nigral projection induced by the injection of kainic acid into the striatum produced a 30% increase in the density of type II benzodiazepine binding sites (measured as the proportion of [3H]flunitrazepam which remained after the addition of 2 X 10(-7) M CL 218872). The lesion did not change the number of type I benzodiazepine binding sites (measured using [3H]ethyl-beta-carboline-3-carboxylate). The increase of type II benzodiazepine binding sites persisted and was markedly enhanced in the substantia nigra, previously lesioned with kainic acid. In fact, the injection of kainic acid into the nigra caused, 3 weeks after the treatment, a 80% decrease in the total number of type I benzodiazepine binding sites, and no change in the number of type II benzodiazepine binding sites. The density of type II sites increased by 70% following a subsequent injection of kainic acid into the striatum, homolateral to the lesioned substantia nigra. The results suggest that type I benzodiazepine binding sites in the nigra are located on kainic acid-sensitive elements (probably intrinsic neurones), while type II benzodiazepine binding sites, the number of which increased after degeneration of the striato-nigral pathway, are localized on kainic acid-resistant structures (probably axons or terminals) that receive an input from striatal afferents and from interneurones in the nigra.

Animals↗
PubMed1986

Evidence for a selective localization of voltage-sensitive Ca2+ channels in nerve cell bodies of corpus striatum.

Specific binding sites for [3H]nitrendipine, an organic Ca2+ channel antagonist, were abolished in crude synaptosomal membranes of kainic acid-lesioned caudate nuclei. In contrast, specific lesions of dopaminergic or serotonergic axon terminals in caudate nuclei failed to alter the density or the affinity of [3H]nitrendipine binding sites. In addition, the basal and veratridine-stimulated 45Ca2+ accumulations were greatly impaired in slices prepared from kainic acid-lesioned caudate nuclei. The veratridine-elicited accumulation of 45Ca2+ in control slices was attenuated by addition of tetrodotoxin in the incubation medium. The present data provide evidence that most of the [3H]nitrendipine binding sites and the voltage-dependent Ca2+ channels are located in intrinsic neurons or interneurons in caudate nucleus. In contrast, destruction of dopaminergic or serotonergic nerve terminals emanating from other brain areas and innervating the caudate nucleus failed to change the apparent Bmax value for [3H]nitrendipine binding.

5,7-Dihydroxytryptamine↗
PubMed1986

Enhancement of gamma-aminobutyric acid binding by quazepam, a benzodiazepine derivative with preferential affinity for type I benzodiazepine receptors.

We evaluated the effect of the two N-trifluoroethyl benzodiazepines, quazepam and its 2-oxo metabolite SCH 15725, which possess preferential affinity for type I benzodiazepine recognition sites, on the binding of [3H] gamma-aminobutyric acid ([3H]GABA) to rat brain membrane preparations. The study also included compounds such as diazepam and N-desalkyl-2-oxoquazepam (SCH 17514), which have equal affinity for the type I and type II receptor subtypes. Binding of [3H]GABA was studied in frozen-thawed and repeatedly washed cortical membranes incubated in 20 mM KH2PO4 plus 50 mM KCl, pH 7.4, at 4 degrees C in the absence and presence of quazepam or its metabolites. Addition of 10(-6) M quazepam increased by 30% specific [3H]GABA binding; as revealed by Scatchard plot analysis, the effect was due to an increase in the total number of GABA receptors. The effect of quazepam was concentration dependent, and it was shared by its active metabolite SCH 15725. The potency of quazepam and SCH 15725 in enhancing [3H]GABA binding was similar to that of diazepam, whereas CL 218872 and SCH 17514 were less active. Moreover, the [3H]GABA binding-enhancing effect of quazepam was mediated by an occupancy of benzodiazepine receptors, because it was specifically antagonized by 5 X 10(-6) M Ro15-1788.

Animals↗
PubMed1985

Increase in nigral type II benzodiazepine recognition sites following striatonigral denervation.

In the rat substantia nigra Type II benzodiazepine recognition sites (measured as the portion of [3H]flunitrazepam binding which remain after the addition of 2 X 10(-7) M Cl 218872) represent 50% of the total benzodiazepine recognition sites. The density of Type II sites was increased by 35% following the degeneration of the striatonigral afferents induced by the intrastriatal injection of kainic acid. On the other hand the same lesion failed to change the density of the remaining nigral Type I sites. The results indicate that denervation induces supersensitivity to nigral Type II benzodiazepine recognition sites.

Animals↗
PubMed1985

Evidence for down-regulation of 3H-nitrendipine recognition sites in mouse brain after long-term treatment with nifedipine or verapamil.

Mice were fed powdered food which contained nifedipine, verapamil or diltiazem for 28 days. Long lasting treatment with nifedipine (0.28 mg/g b.w./day) or verapamil (0.27 mg/g b.w./day), but not with diltiazem (0.38 mg/g b.w./day) reduced the number of 3H-nitrendipine recognition sites in membranes prepared from cerebral cortex, caudate nucleus, and hippocampus. In addition, the veratridine-elicited stimulation of 45Ca-uptake in slices of the same brain areas was decreased in mice which were fed nifedipine or verapamil for 28 days.

Animals↗
PubMed1982

High prevalence of Werner's syndrome in Sardinia. Description of six patients and estimate of the gene frequency.

Several patients with Werner's syndrome in a large family group in Sardinia were ascertained three years ago and reported briefly by Rabbiosi and Borroni (1979). Since then two sisters from a second family and a single case from a third family were ascertained. The three families originated from the Northern part Sardinia and no connection between them was found. We provide a detailed clinical description of six of these patients and attempt to estimate the prevalence and the gene frequency of Werner's syndrome in Sardinia. The prevalence was calculated as 1:94,914 for the two districts of Sassari and Nuoro and as 1:202,766 for the whole island. This is the highest prevalence thus far ascertained. Using Dahlberg's formula we obtained an estimate of the gene frequency q = 0.003288 and thus a frequency of Werner's syndrome of 1:92,515. A more rigorous estimate gave a gene frequency q = 0.001483 and thus a frequency of Werner's syndrome of 1:454,505, but because of the small sample size this estimate should be taken with caution.

Adult↗
PubMedDate not supplied

Association of jaagsiekte sheep retrovirus with pulmonary carcinoma in Sardinian moufflon (Ovis musimon).

Bronchiolo-alveolar carcinoma has been described in man and in several animal species, including cattle, dogs, opossums, goats and sheep. In sheep, a bronchiolo-alveolar carcinoma, known as ovine pulmonary carcinoma (OPC), is caused by jaagsiekte sheep retrovirus (JSRV), an exogenous type D retrovirus. In the mid-1980s, a severe outbreak of a disease resembling OPC was described in captive Sardinian moufflon (Ovis musimon). In the present study, the use of polymerase chain reaction (PCR) amplification of nucleic acids extracted from archival material established that JSRV was associated with OPC in affected moufflon. JSRV was detected in the lungs and mediastinal lymph nodes. Immunohistochemical and in-situ PCR demonstrated that in the lungs, JSRV proviral DNA was localized in transformed and untransformed type II pneumocytes and in the alveolar macrophages. In the mediastinal lymph nodes, JSRV DNA was mainly located in the cortical follicles and paracortex. These data suggest that JSRV is the cause of OPC in Sardinian moufflon, as it is in Sardinian sheep.

Animals↗
PubMedDate not supplied

Changes in body and head dimensions in urban Sardinian children (3-5 years) from 1986 to 2001.

PRIMARY OBJECTIVES: The study describes and discusses the changes in body and head dimensions of urban pre-school children from Sardinia in a 15-year period. METHODOLOGY: The mean values of 11 anthropometric variables measured in 2001 in 414 children (209 males, 205 females) from 3 to 5 years old were compared with those measured in 1986 in 262 coeval children (131 males, 131 females). The t-test was used to evaluate whether the differences between the two samples, divided by sex, were statistically significant. RESULTS: For each age class and sex, the differences between the means were significant for the following anthropometric variables: weight, stature, estimated lower limb length, biacromial breadth, bicristal breadth, body mass index, relative sitting height index, head length, and cephalic index. In contrast, the differences between the means were not significant for sitting height and head breadth. CONCLUSIONS: The pre-school children of Cagliari measured in 2001 were on average taller and especially heavier than their same-sex peers measured in 1986; the increase in height was clearly due to the increased length of the lower limbs. The transverse dimensions of the trunk also increased, while its length remained largely the same. Head length also increased, while the relative sitting height and cephalic indexes decreased.

Anthropometry↗
PubMedDate not supplied

Age at menarche in Sardinia (Italy).

The median age at menarche in 1080 Sardinian girls (ages 11.00-16.49 years) was calculated with the status quo method and probit analysis as 12.78 +/- 0.06 years.

Adolescent↗