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Biomedical subjects

G Bianchi

Publications and source records attributed to G Bianchi.

At least 145 records · Page 8Linked to original sources
PubMed1998

Donor and recipient family histories of hypertension influence renal impairment and blood pressure during acute rejections.

A previous historical prospective observational study, double blinded for knowledge of kidney donors' family history of hypertension, included 85 transplanted patients with stable renal function, not treated with cyclosporine, who were followed-up for an average of 8 yr and carefully characterized for the presence or absence of hypertension in the donor and recipient families. The recipients without a family history of hypertension, but grafted with a kidney coming from a "hypertensive" family, developed hypertension much more frequently than recipients grafted with a kidney coming from a "normotensive" family, or recipients with familial hypertension in whom the origin of the kidney did not influence the prevalence of hypertension after transplantation. In this second study of the same patients, it was found that these recipients with a "normotensive" family and a "hypertensive" kidney showed a greater increase of diastolic BP (P = 0.005) and a greater degree of acute renal damage (P = 0.004) during acute rejections than all of the other recipients. This extension study shows that a grafted kidney can transmit not only chronic hypertension, but also susceptibility to a greater rise in BP and more severe kidney impairment after an acute insult.

Acute Disease↗
PubMed1998

Strontium absorption and excretion in normocalciuric subjects: relation to calcium metabolism.

The relationships of Sr intestinal absorption and renal excretion with biohumoral factors regulating Ca metabolism were studied in 47 normocalciuric subjects with Ca kidney stones. Sr concentrations were measured in serum and urine after an oral load of stable Sr (30.2 mumol/kg body wt). Enteral absorption of the ion (9.77 +/- 0.438 mmol.L-1.min, 240 min after Sr administration), expressed as the area under the plasma concentration-time curve (AUC), and renal clearance (CRE) in these subjects during the test (2.80 +/- 0.336 mL/min) were not different from values for 27 controls. CRE was not correlated with AUCs. Plasma concentrations of parathyroid hormone (PTH) negatively correlated with AUCs (P < 0.01) and correlated with CRE after one outlier was excluded (P < 0.05). Plasma concentrations of 1,25-dihydroxyvitamin D correlated positively with AUCs (P < 0.01) when normalized to the plasma concentration of PTH. Multiple stepwise regression showed that PTH and phosphatemia were significantly related to AUC values at 240 min (P < 0.01). These findings suggest that Sr absorption and excretion reflect the regulation of Ca metabolism, but some differences in renal handling of the two ions may exist.

Administration, Oral↗
PubMed1998

PST2238: a new antihypertensive compound that antagonizes the long-term pressor effect of ouabain.

The inhibition of the long-term pressor effect of ouabain may be useful for the therapy of essential hypertension. Here, for the first time, a selective inhibitor of the ouabain pressor effect is described. In vitro, 17beta-(3-furyl)-5beta-androstane-3beta, 14beta, 17alpha-triol (PST 2238) displaced ouabain from its binding sites on purified sodium, potassium ATPase enzyme (Na-K ATPase) (IC50 1.7 x 10(-6) M) without interacting with other receptors involved in blood pressure regulation or hormonal control. In cultured renal cells, incubation with ouabain (10(-10) to 10(-8) M) for 5 days stimulated the Na-K pump at Vmax, whereas PST 2238 showed the same effect at micromolar concentration. The ouabain-dependent increase in the Na-K pump rate was abolished by PST 2238 at concentrations from 10(-14) to 10(-9) M. In rats made hypertensive by chronic infusion of 50 microg/kg/day of ouabain, PST 2238 given p.o at very low doses (0.1-1 microg/kg/day for 4 weeks) abolished the increase in blood pressure and renal Na-K ATPase activity caused by ouabain. PST 2238 did not affect either blood pressure or renal Na-K ATPase activity in normotensive rats. In conclusion, PST 2238 is a very potent compound that normalizes both blood pressure and alterations in the Na-K pump caused by ouabain. Thus it represents the prototype of a new class of antihypertensive drugs that could be effective in forms of hypertension sustained by the concomitant increase of endogenous ouabain levels and alterations in the Na-K pump.

Androstanols↗
PubMed1998

Renal staghorn calculosis: our experience with the percutaneous treatment with or without extracorporeal shock wave lithotripsy.

OBJECTIVES: In this paper we report our results in the treatment of renal staghorn stones by percutaneous lithotripsy (PCNL) with or without extracorporeal shock wave lithotripsy (ESWL). METHODS/RESULTS: Over a period of 5 years, 244 patients with renal calculosis were treated by PCNL in our Department. Seventy-four of these were cases of renal staghorn calculosis: 44 presented a partial staghorn stone and in 30 cases the stone formation completely occupied the pyelocalieal cavity. We performed first a PCNL via a rigid nephroscope. Stones were crushed using an ultrasonic lithotrite; an electrohydraulic probe was used when the calculus was resistant to ultrasound. The patients were submitted to one or more percutaneous treatments followed by extracorporeal lithotripsy to complete the operation, when required. The patients were divided into two groups according to the type of stone: the first group comprised 59 patients with a partial or complete simple staghorn stone and the second comprised 15 patients with a complete complex staghorn stone. Complete resolution was achieved in 55 of the 59 cases (93.2%) in the first group and in 9 of the 15 cases (60%) in the second. We had no complications. CONCLUSIONS: Our experience confirms that PCNL is the elective treatment for partial and complete staghorn stones and ESWL in these types of stones must be utilized only as ancillary treatment for residual fragments.

Humans↗
PubMed1998

[Leydig cell tumor of the testicle. Clinical case].

The case of a young man affected by Leydig cell tumor of the right testis, without gynecomastia and feminization signs is reported. The plasmatic level of testosterone, estrogenic hormones, APF and Beta-HCG were normal. The diagnostic and therapeutical aspects are discussed and the role of the radical orchifuniculectomy in T1N0M0 stage is pointed out.

Adult↗
PubMed1997

Role of metalloproteases in the release of the IL-1 type II decoy receptor.

The IL-1 type II receptor (decoy RII) is a nonsignaling molecule the only established function of which is to capture IL-1 and prevent it from interacting with signaling receptor. The decoy RII is released in a regulated way from the cell surface. Here, we reported that hydroxamic acid inhibitors of matrix metalloproteases inhibit different pathways of decoy RII release, including the following: (a) the slow (18 h) gene expression-dependent release from monocytes and polymorphonuclear cells exposed to dexamethasone; (b) rapid release (minutes) from myelomonocytic cells exposed to tumor necrosis factor, chemoattractants, or phorbol myristate acetate; (c) phorbol myristate acetate-induced release from decoy RII-transfected fibroblasts and B cells. Inhibition of release was associated with increased surface expression of decoy RII. Inhibitors of other protease classes did not substantially affect release. However, serine protease inhibitors increased the molecular mass of the decoy RII released from polymorphonuclear cells from 45 to 60 kDa. Thus, irrespective of the pathway responsible for release and of the cellular context, matrix metalloproteases, rather than differential splicing, play a key role in production of soluble decoy RII.

Alternative Splicing↗
PubMed1997

Polymorphism of gamma-adducin gene in genetic hypertension and mapping of the gene to rat chromosome 1q55.

Adducin (ADD) is a heterodimeric protein involved in cellular signal transduction. A mutation in the alpha subunit affects ion transport and blood pressure in primary hypertension of Milan rats (MHS) and humans. In rats this effect is modulated by another mutation in the beta subunit. The recently described gamma subunit is a new member of the ADD family that should take the place of beta subunit in cells and tissues expressing alpha but not beta-Add. A missense mutation (Q572K) has been found in the gamma subunit of the Milan rats. Nineteen normotensive and five hypertensive inbred rat strains were genotyped for the polymorphisms in alpha, beta and gamma-Add genes. A disequilibrium was evident in the distribution of MHS-like Add genotype, being more frequent between the hypertensive than the normotensive strains (Chi-Square = 13.03, p = 0.0003). In kidney, brain, spleen, liver and heart a cDNA differing from gamma subunit by an in-frame insertion of 96 nucleotides, was found by PCR amplification and confirmed by RNase protection analysis. The rat gamma-Add gene was localized to chromosome 1q55 by fluorescence in situ hybridization.

Amino Acid Sequence↗
PubMed1997

Characterization of voltage-dependent calcium influx in human erythrocytes by fura-2.

Thus far, the methods used to determine erythrocyte Ca2+ influx have not allowed the assessment of the kinetics of ion uptake. To overcome this drawback, we studied a new method, using the fluorescent Ca2+-chelator fura-2, which directly quantifies intracellular Ca2+ changes in human erythrocytes. This method has the advantage over previous techniques that it monitors continuously cellular Ca2+ levels. The Ca2+ influx is modulated by cellular membrane potential in the presence of a transmembrane Ca2+ concentration gradient and exhibits a first slow increase of the intracellular Ca2+ concentration, followed, after the reachment of a threshold value of 125 +/- 13 nM Ca2+, by a faster increase until a plateau is reached. The influx rate is inhibited by dihydropyridines in the micromolar range. These findings support the hypothesis that erythrocyte Ca2+ influx is mediated by a carrier similar to the slow Ca2+ channels and is dependent on membrane depolarization.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1997

Polymorphisms of alpha-adducin and salt sensitivity in patients with essential hypertension.

BACKGROUND: Abnormalities in renal sodium transport may be involved in hypertension. Adducin, an alpha/beta heterodimeric protein found in the renal tubule is thought to regulate ion transport through changes in the actin cytoskeleton. We investigated whether an alpha-adducin polymorphism (Gly 460 Trp) is involved in essential hypertension in two separate populations. METHODS: Linkage analysis of three DNA markers at different distances from the alpha-adducin locus (20-2500 kb) was done in 137 hypertensive sibling-pairs. 477 hypertensive and 322 normotensive individuals were genotyped for the alpha-adducin polymorphism. The blood-pressure response to acute and chronic changes in sodium balance was studied in hypertensive individuals with and without the 460 Trp alpha-adducin allele. FINDINGS: Significant linkage was found for all three markers in the sibling-pair study. The extra shared alleles (9.1%, 6.5%, and 4.7%) and the significance level for linkage (p = 0.0006, p = 0.0119, and p = 0.0211) both decreased with increasing distance from the alpha-adducin locus. There was a significant association between the 460 Trp mutation and hypertension (p = 0.0003). In the salt-sensitivity test, to assess the acute blood-pressure response to changes in body sodium in 86 hypertensive patients, the decrease in mean arterial pressure was greater in 65 patients who were heterozygous for the mutant allele (Gly/Trp) than in 21 wild-type homozygotes (Gly/Gly) (mean decrease 15.9 [SE 2.0] vs 7.4 [1.3] mm Hg; p = 0.001). Similarly, 21 heterozygous hypertensive patients showed a greater fall in mean arterial pressure in response to 2 months' treatment with hydrochlorothiazide than did 37 wild-type homozygous hypertensive patients (mean decrease 14.7 [2.2] vs 6.8 [1.4] mm Hg; p = 0.002). INTERPRETATION: Our findings of significant linkage of the alpha-adducin locus to essential hypertension and greater sensitivity to changes in sodium balance among patients with the mutant allele suggest that alpha-adducin is associated with a salt-sensitive form of essential hypertension. We suggest the alpha-adducin polymorphism may identify hypertensive patients who will benefit from diuretic treatment or manoeuvres to reduce total body sodium.

Aged↗
PubMed1997

Isozyme-dependent sensitivity of adenylyl cyclases to P-site-mediated inhibition by adenine nucleosides and nucleoside 3'-polyphosphates.

Recombinant adenylyl cyclase isozyme Types I, II, VI, VII, and three splice variants of Type VIII were compared for their sensitivity to P-site-mediated inhibition by several adenine nucleoside derivatives and by the family of recently synthesized adenine nucleoside 3'-polyphosphates (Désaubry, L., Shoshani, I., and Johnson, R. A. (1996) J. Biol. Chem. 271, 14028-14034). Inhibitory potencies were dependent on isozyme type, the mode of activation of the respective isozymes, and on P-site ligand. For the nucleoside derivatives potency typically followed the order 2',5'-dideoxyadenosine (2',5'-ddAdo) > beta-adenosine > 9-(cyclopentyl)-adenine (9-CP-Ade) >/= 9-(tetrahydrofuryl)-adenine (9-THF-Ade; SQ 22,536), with the exception of Type II adenylyl cyclase, which was essentially insensitive to inhibition by 9-CP-Ade. For the adenine nucleoside 3'-polyphosphates inhibitory potency followed the order Ado < 2'-dAdo < 2',5'-ddAdo and 3'-mono- < 3'-di- < 3'-triphosphate. Differences in potency of these ligands were noted between isozymes. The most potent ligand was 2',5'-dd-3'-ATP with IC50 values of 40-300 nM. The data demonstrate isozyme selectivity for some ligands, suggesting the possibility of isozyme-selective inhibitors to take advantage of differences in P-site domains among adenylyl cyclase isozymes. Differential expression of adenylyl cyclase isozymes may dictate the physiological sensitivity and hence importance of this regulatory mechanism in different cells or tissues.

Adenosine↗
PubMed1997

IL-2-regulated expression of the monocyte chemotactic protein-1 receptor (CCR2) in human NK cells: characterization of a predominant 3.4-kilobase transcript containing CCR2B and CCR2A sequences.

NK cells migrate in response to C-C chemokines, including monocyte chemotactic protein-1 (MCP-1) and MCP-3. Increased migration was observed in IL-2-activated NK cells. It was therefore of interest to define the expression in resting and activated NK cells of the MCP-1 receptor (CCR2) for which two cDNAs (A and B) have been described. Specific oligonucleotides and reverse-transcriptase PCR revealed the presence in activated NK cells and mononuclear phagocytes of the fragments expected on the basis of the reported cDNAs. In addition, amplification with a common A/B- and an A-specific oligonucleotide yielded an unexpected, abundant, 1649-bp fragment. Sequence analysis as well as Northern blotting and RNase protection with different probes revealed that the CCR2 gene is expressed in activated NK cells and mononuclear phagocytes as a predominant long transcript (3.4 kb) consisting of CCR2B, followed by a novel sequence (X), corresponding to an intron in the genome, and by a CCR2A-specific portion. The predominant long transcript is polyadenylated and present in the cytoplasm. The augmented migratory capacity of IL-2 activated vs resting NK cells was associated with increased CCR2 transcript levels.

Base Sequence↗
PubMed1997

Serum autoantibodies in chronic hepatitis C: comparison with autoimmune hepatitis and impact on the disease profile.

Antibodies to nuclei (ANA), smooth muscle (SMA), and liver/kidney microsomes type 1 (anti-LKM1) may occur in chronic hepatitis C. Distinct subspecificities, including ANA with the homogeneous pattern (ANA-H) and SMA with antiactin specificity (SMA-AA), are found in autoimmune hepatitis (AIH). This study was performed to characterize the hepatitis C virus (HCV)-associated autoantibodies and to evaluate their influence on the profile of the disease. Two hundred ninety consecutive patients with chronic hepatitis C and 35 control cases with AIH were screened for autoantibodies by indirect immunofluorescence (IFL) at 1:40 serum dilution. The ANA pattern was defined by IFL on HEp-2 cells and the SMA-AA identified by the presence of at least two of the following elements: 1) SMA(T) or SMA(G) pattern by IFL on kidney sections; 2) XR1 precipitating system by counterimmunoelectrophoresis; or 3) typical pattern by IFL on liver sections from phalloidin-intoxicated rats. ANA, SMA, and anti-LKM1 occurred in 9%, 20%, and 6% of chronic hepatitis C cases, respectively. The overall prevalence of autoantibodies was 30% (87 of 290). Compared with AIH, HCV-associated ANA and SMA exhibited ANA-H and SMA-AA at a lower prevalence (38% vs. 71%, P = .04 and 8% vs. 87%, P < .000001, respectively) and had a lower median titer (1:80 vs. 1:320, P < .001 and 1:40 vs. 1:320, P < .000001, respectively). The concomitant positivity for ANA-H and SMA-AA was detected in none of the HCV cases, but in 46% of AIH sera (P < .000001). Two parameters were independently associated with the autoantibodies in chronic hepatitis C: high alanine transaminase (ALT) serum levels (F = 14.04) and female gender (F = 5.03). At the univariate analysis, patients with autoantibodies had a more severe portal-periportal necroinflammation (median Scheuer's score: 2.05 vs. 1.64, P = .003). The presence of autoantibodies did not influence the response to interferon (IFN). In chronic hepatitis C, serum autoantibodies are common, but their subspecificities are distinct from those occurring in AIH. Whereas the absence of ANA-H and/or SMA-AA does not exclude AIH, the characterization of ANA and SMA may help to discriminate between the two conditions. As compared with the seronegative counterpart, autoantibody-positive chronic hepatitis C is more common in females and exhibits a more severe biochemical and histological activity. The response to IFN therapy, however, is similar.

Analysis of Variance↗
PubMed1997

IL-15 is chemotactic for natural killer cells and stimulates their adhesion to vascular endothelium.

Interleukin-15 (IL-15) is a recently described cytokine with IL-2-like stimulating activities on T lymphocytes and natural killer (NK) cells. IL-15 mediates its function through the beta- and gamma-chains of the IL-2 receptor. In this work, we have investigated the effect of IL-15 on the directional migration of NK cells in chemotaxis assays and on the ability of NK cells to bind to vascular endothelium. IL-15 (10-20 ng/mL) had chemotactic effects on freshly isolated resting NK cells as well as on long-termed IL-2-cultured NK cells. A checkerboard experiment demonstrated that migration in response to IL-15 was observed only in the presence of a positive gradient (chemotaxis). Overnight treatment of freshly isolated NK cells with IL-15 (10-20 ng/mL) augmented their binding to cultured endothelial cells (EC) in vitro, especially to resting EC. IL-15-activated NK cells bound to resting and tumor necrosis factor-activated EC by use of LFA-1/ICAM-1 and VLA-4/VCAM-1 adhesion pathways, essentially as untreated NK cells do. The fact that IL-15 increased NK cell binding to ICAM-1-transfected NIH-3T3 fibroblasts, together with the finding that IL-15 did not increase binding to extracellular matrix proteins, where the major molecules involved are VLA proteins, indicated that IL-15 primarily stimulates LFA-1-dependent adhesion. By increasing NK cell adhesion to vascular endothelium and migratory response, IL-15 is an important determinant of NK cell recruitment in tissues.

3T3 Cells↗
PubMed1997

Antibodies of the anti-Yo and anti-Ri type in the absence of paraneoplastic neurological syndromes: a long-term survey of ovarian cancer patients.

In recent years several authors have described a close correlation between circulating antineuronal antibodies of different types and the occurrence of paraneoplastic neurological syndromes. Because this has not been widely accepted, we screened 300 serum samples from 181 ovarian cancer patients for the presence of circulating antineuronal antibodies by immunofluorescence. The findings were confirmed by immunoblotting. In 11 patients circulating antineuronal antibodies were detected. In 4 patients they were classified as anti-Yo and in 7 as anti-Ri, titres ranging from 1:400 to 1: 204,800. All the patients underwent thorough neurological and neurophysiological investigations, with special regard to paraneoplastic syndrome. None of them had symptoms pointing to a paraneoplastic neurological syndrome, although patients were followed up to 2 years after the first examination. Thus the frequency of circulating antineuronal antibodies in ovarian cancer patients is higher than the frequency of paraneoplastic syndromes, and antibody positivity does not necessarily lead to the appearance of a neurological paraneoplastic syndrome.

Autoantibodies↗