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Biomedical subjects

S Salardi

Publications and source records attributed to S Salardi.

At least 55 records · Page 3Linked to original sources
PubMed1990

Variability of growth hormone response to pharmacological and sleep tests performed twice in short children.

Forty-nine children with short stature (age range, 4.1-15.9 yr) were examined. Twenty-four (group 1) were submitted twice to an arginine and a sleep test (12-h overnight GH profile). Twenty-five patients (group 2) were submitted twice to an arginine and L-dopa test. Coefficients of variation were calculated between both the results of pharmacological (peak and area under the curve) and sleep tests [mean GH concentration (MGHC), peak, area under the curve, number of peaks above 5 micrograms/L, and peak area]. In group 1 the coefficient of variation of sleep test parameters was significantly lower than that of pharmacological tests (P less than 0.01 to less than 0.001). In the sleep test the area under the curve and MGHC were the most constant parameters. Group 2 showed no difference between the coefficients of variation of the two pharmacological tests. Considering groups 1 and 2 together, the coefficients of variation of the sleep test, in particular the MGHC and area under the curve, were lower than those of the two pharmacological tests. Eight of 24 subjects in group 1 showed a low GH level in 1 series of tests, and a normal level in the other series. Five of 18 subjects in group 2 showed an abnormally low GH response to the arginine and L-dopa tests and a normal response to the 2 repeated tests. Therefore, to prevent an erroneous interpretation of the GH test results, it is very important to perform a sleep test and repeat it whenever GH secretion seems to be deficient or at the lower limits of normalcy.

Adolescent↗
PubMed1989

A possible primary role for the kidney in essential hypertension.

The role of the kidney in "essential" or "genetic" types of hypertension has been evaluated both in a rat model such as the Milan hypertensive strain (MHS) or in humans. In both species, abnormalities of renal function have been demonstrated before the development of hypertension. Moreover hypertension could be "transplanted" with the kidney when kidney cross-transplantation was carried out between MHS and the Milan normotensive strain (MNS). Also in humans, the familiality for hypertension of the donor affected the requirement of antihypertensive therapy of the recipient. Further studies furnished results that were consistent with the hypothesis that a primary increase in Na transport across the tubular cell could be responsible for the pressor effect of the kidney in MHS or in humans. Because many similarities were found between the function of the tubular cell and the red blood cell in MHS, red blood cells were used to gain information about the molecular genetic mechanisms underlying these cellular changes. The results so far obtained showed that red blood cell abnormalities in MHS were genetically determined within the stem cells and genetically associated with the development of hypertension in F2 hybrids obtained by crossing the F1 (MHS X MNS). Moreover, the abnormal Na transport across the cell membrane may be due to an abnormal function of the membrane skeleton proteins. Studies are in progress to evaluate a possible cause-effect relationship between: membrane skeleton protein-ion transport across the cell membrane and the development of hypertension.

Animals↗
PubMed1989

Erythrocyte adducin differential properties in the normotensive and hypertensive rats of the Milan strain. Characterization of spleen adducin m-RNA.

Previous studies have shown that erythrocytes from the Milan hypertensive strain of rats (MHS) differ from erythrocytes from the control normotensive strain (MNS). These differences are determined within the stem cells, are genetically associated with the development of hypertension, and are similar to those found between the tubular cells of the two strains. Moreover they seem to be dependent upon the presence of the membrane skeleton proteins. In this paper we describe our studies aimed at identifying some precise protein difference between the membrane skeletons of the two strains, which may cause the cellular differences described above. Milan hypertensive strain and MNS rats were immunized with ghost or membrane skeleton extracts prepared from the other or their own strains. Only MHS rats immunized with MNS ghost or membrane skeleton extracts produced an antibody against a 105 KD protein in about 95% of the animals. This protein has been identified with the recently described cytoskeletal protein adducin on the following bases: the protein binds calmodulin (CaM) and protein kinase C (PKc) in a Ca2+ dependent way. It also binds phosphatidylserine, is the substrate of exogenous PKc, and finally it is purified by high salt extraction of Triton-X100 insoluble erythrocyte cytoskeletons followed by affinity chromatography on CaM-sepharose. Using this antibody the isolation from a mouse spleen library, the characterization and sequencing of a partial cDNA clone coding for this protein has been carried out. In conclusion adducin may be considered a very useful tool to test the hypothesis that the cellular differences between MHS and MNS may be caused by a difference in a membrane skeleton protein.

Amino Acid Sequence↗
PubMed1989

Clinical and laboratory features of homocystinuria.

Classic homocystinuria is an autosomal recessive metabolic disease due to a cystathionine-beta-synthase deficiency with consequent blocking of homocysteine and serine condensation for producing cystathionine. The characteristic biochemical abnormalities in the blood and urine are: abnormal accumulation of methionine, abnormal presence of homocystine and low values of cystathionine, cysteine or cystine (disulfide of the cysteine). The most frequent clinical signs are: subluxation of the lenses, mental retardation of different degrees, long bones excessively lengthened, scoliosis, susceptibility to arterial and venous thromboembolism. The latter is frequent after surgery, and may be life-threatening. This disease must be differentiated from Marfan's syndrome via laboratory tests.

Diagnosis, Differential↗
PubMed1988

Bronchial reactivity in diabetic patients. Relationship to duration of diabetes and degree of glycemic control.

Bronchial reactivity was studied via carbachol testing in 46 patients affected by type 1 diabetes mellitus and in 30 control subjects and via exercise testing in 55 diabetic patients and 60 control subjects. In all subjects, reactivity to skin allergen tests, the existence of atopic illnesses, and family history for these diseases were evaluated. Diabetic patients were less affected by asthma than control subjects, although their family history of atopy is greater. Bronchial reactivity, as expressed by the results of carbachol testing, was lower in diabetic patients than in control subjects. Furthermore, the duration of disease in diabetic patients was positively correlated with the results of carbachol testing. Reduced bronchial reactivity might be an indication of initial damage to the autonomic nervous system, which would thus appear to be both a complication and a protective factor.

Adolescent↗
PubMed1988

Pelvic ultrasonography in girls with precocious puberty, congenital adrenal hyperplasia, obesity, or hirsutism.

Real-time ultrasonography of the pelvic organs was performed on 151 girls with various complete and incomplete forms of precocious puberty, 20 girls with congenital adrenal hyperplasia, 20 with hirsutism, 18 with obesity, and 133 age-matched normal girls. Uterine and ovarian volumes were calculated and the ovarian morphologic picture was classified as homogeneous, nonhomogeneous (less than three small cystic areas), microcystic (four or more small cystic areas less than 9 mm in diameter), follicular (at least one cystic area greater than 9 mm), and macrocystic (large cystic area greater than 20 mm). Ultrasound imaging allowed an easy distinction between true precocious puberty and premature thelarche or idiopathic premature adrenarche. It was also helpful in the diagnosis of transient sexual precocity, although in these cases the differential diagnosis of precocious puberty can be difficult. In postmenarcheal patients with congenital adrenal hyperplasia, ultrasound study showed a low uterine volume and, frequently, a macrocyst in the ovary. In hirsute girls and in a few obese patients, ovaries had an increased volume and a microcystic structure, similar to those in polycystic ovary syndrome. Pelvic ultrasonography can be useful not only in diagnosing disorders in sexual development but also for greater understanding of the pathogenesis of these and other disorders.

Adrenal Hyperplasia, Congenital↗
PubMed1988

Characterization of erythrocyte adducin from the Milan hypertensive strain of rats.

Previous studies showed that erythrocytes from the Milan hypertensive strain of rats (MHS) are smaller and have a faster Na-K cotransport when compared with their normotensive controls (MNS). These characteristics are determined within the stem cell, are genetically associated with hypertension and are similar to other renal tubular cell abnormalities more directly involved in the development of hypertension in MHS. The difference in volume is maintained in ghost membranes, while the difference in transport is abolished in inside-out vesicles. Ghosts and cytoskeletons contain a 105-kilodalton protein already characterized by immunoblotting. This protein has been identified with erythrocyte adducin by several criteria, including binding to calmodulin and protein kinase C, phosphorylation and full immunological cross-reactivity with human adducin. Since only MHS rats immunized with MNS erythrocyte cytoskeletons produce anti-adducin antibodies, we suggest an immunogenic structural difference in adducin from the two strains, and an involvement of this difference in the alteration of Na-K cotransport observed.

Animals↗
PubMed1988

Renal abnormalities at the prehypertensive stage of essential hypertension.

An approach to evaluating the genetic components of essential hypertension using an animal model, the Milan hypertensive strain (MHS) of rats, and studies in human families with positive and negative histories for high blood pressure are described and discussed. Differences at renal and cellular levels between MHS and its normotensive control strain, MNS, show many similarities to those between offspring from hyper- and normotensive families in humans. These include, with respect to the former group of each species, lower erythrocyte volume and Na content, higher Na-K cotransport across red blood cell (RBC) membranes higher Na excretion after load, and greater pressor effect in transplanted kidneys. A novel protein found in rat RBC cytoskeleton appears to have a function in Na-K cotransport and it may, eventually, be possible to demonstrate in man.

Animals↗
PubMed1988

[Sodium transport and renal hemodynamics in arterial hypertension of genetic origin: primary or secondary changes?].

Essential hypertension develops from the interaction of genetic and environmental factors. In the Milan hypertensive strain (MHS) rat before the development of hypertension, there is a genetically inherited increase of tubular reabsorption which is the cause of the following increase of blood pressure. Also in young normotensive humans, predisposed to develop essential hypertension later in life, there is an abnormal pattern of renal function that may be explained by increase of tubular reabsorption. The studies of the erythrocyte membrane transport support these data and suggest that at least a subset of essential hypertensive humans may develop a form of hypertension that has pathogenetic mechanisms similar to the ones of MHS rats.

Animals↗
PubMed1987

Growth and growth factors in diabetes mellitus.

Growth of 79 children with diabetes was analysed at diagnosis and again after one to 10.7 years of treatment with insulin. Both sexes were tall at onset, whereas at the last observation boys alone showed significant growth retardation. Height standard deviation score (SDS), however, showed no significant fall either in 32 subjects reassessed after five years of disease or in 18 subjects examined at full stature. Skeletal maturity was not significantly impaired after treatment. Pubertal growth spurt was reduced, especially in girls and in subjects with onset of disease at or around puberty. We found no significant correlation between height and height velocity SDS and glycosylated haemoglobin values or secretion of growth hormone during the arginine test. Somatomedin C values were correlated with height velocity SDS in prepubertal boys. The results of this study suggest that there are interferences in the growth of children with diabetes but that they do not seem to have a significant influence on adult height.

Adolescent↗
PubMed1987

The Milan hypertensive rat as a model for studying cation transport abnormality in genetic hypertension.

Environmental factors, genetic polymorphisms, and different experimental designs have been the main impediments to evaluating a genetic association between cell membrane cation transport abnormalities and human essential or genetic hypertension. We review the results obtained in the Milan hypertensive strain of rats (MHS) and in its appropriate control normotensive strain (MNS) to illustrate our approach to defining the role of cation transport abnormality in a type of genetic hypertension. Before the development of a difference in blood pressure between the two strains, the comparison of kidney and erythrocyte functions showed that MHS had an increased glomerular filtration rate and urinary output, and lower plasma renin and urine osmolality. Kidney cross-transplantation between the strains showed that hypertension is transplanted with the kidney. Proximal tubular cell volume and sodium content were lower in MHS while sodium transport across the brush border membrane vesicles of MHS was faster. Erythrocytes in MHS were smaller and had lower sodium concentration, and Na+-K+ cotransport and passive permeability were faster. The differences in volume, sodium content, and Na+-K+ cotransport between erythrocytes of the two strains persisted after transplantation of bone marrow to irradiated F1 (MHS X MNS) hybrids. Moreover, in normal segregating F2 hybrid populations there was a positive correlation between blood pressure and Na+-K+ cotransport. These results suggest a genetic and functional link in MHS between cell membrane cation transport abnormalities and hypertension. Thus erythrocyte cell membrane may be used for approaching the problem of defining the genetically determined molecular mechanism underlying the development of a type of essential hypertension.

Animals↗
PubMed1986

Blood coagulation changes in homocystinuria: effects of pyridoxine and other specific therapy.

The aim of this study was to investigate the blood coagulation changes in three patients with homocystinuria, in baseline condition and during therapy. At baseline, antithrombin III activity and factor VII levels were reduced in all three patients; antithrombin III protein and protein C antigen were also slightly lowered in one patient, and factor X in another. beta-Thromboglobulin, a measure of platelet activation, was increased in one case. During pyridoxine treatment, antithrombin III activity was rapidly restored to normal; factor VII increased and beta-thromboglobulin decreased. These data suggest that, in addition to platelet activation, abnormalities of blood clotting, and particularly reduction of antithrombin III, may play a role in the thrombotic tendency associated with homocystinuria. The nature of these clotting alterations is still uncertain, but their improvement during active metabolic treatment suggests that the defect in amino acid transsulfuration of homocystinuria may directly affect synthesis or activity of some liver-dependent clotting factors.

Adolescent↗
PubMed1986

Genetic and experimental hypertension in the animal model-similarities and dissimilarities to the development of human hypertension.

In this article, we present the results we have obtained from experimental and genetic models of human essential hypertension, in order to investigate those findings relevant to understanding the time course and the mechanisms underlying the human disease. With experiments on the renal artery constriction in the conscious dog, we have shown that a kidney lesion can produce a form of hypertension not different, in the established phase, from the essential one and that the onset of this form follows a phasic pattern during which the initial stages are crucial for understanding the mechanisms leading to hypertension. We also consider a rat model (MHS) that spontaneously develops a form of hypertension very similar to the human disease. In this model, we have demonstrated by a kidney cross-transplantation experiment and functional studies that the kidney is responsible for the rise in blood pressure and that the organ dysfunction is probably due to a primary abnormality in ion handling of the cell membrane. This cellular alteration, detected both in MHS erythrocytes and in their kidney proximal tubular cells, should be the cause for the higher rate of kidney Na+ reabsorption observed in the MHS. Comparing this animal model with, at least, a subgroup of humans prone to develop hypertension or already hypertensive, it is possible to detect a series of similarities in the kidney function, hormonal pattern, and cellular function of the two species that allows us to argue that the MHS is a suitable model from which to draw conclusions relevant to the pathogenesis of essential hypertension in some humans.

Animals↗