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Biomedical subjects

F Scolari

Publications and source records attributed to F Scolari.

67 records · Page 4Linked to original sources
PubMed1982

[Effect of pretreatment with atenolol and propranolol on sympatho-adrenal and cardiovascular responses to acute insulin-induced hypoglycaemia in the hypertensive patient].

Plasma catecholamines and cardiovascular responses to acute insulin i.v. injection (0.12 U.I. per Kg of body weight) have been studied in eight patients with mild essential hypertension. The hypoglycaemia test was carried out before and after a week of atenolol treatment. In six patients the test was also repeated after propranolol treatment. Following insulin injection, blood sugar fell abruptly with a nadir at 30 m, diastolic blood pressure decreased, and systolic blood pressure and heart rate rose significantly. Atenolol treatment abolished almost completely these hemodynamic changes. By contrast, propranolol caused an increase in both systolic and diastolic blood pressures, leaving the heart rate unmodified. During hypoglycaemia, plasma adrenaline rose sharply in coincidence with the glycaemic nadir and declined thereafter during the glycaemic recovery. Plasma noradrenaline rose less markedly than adrenaline, but the increments were significant after 30 and 60 m. Neither atenolol, nor propranolol affected significantly these changes in plasma catecholamine concentration. These data indicate that beta-blockers do not alter the hypoglycaemia-induced adrenomedullary release of catecholamines. We conclude therefore that beta-blockers modify the pattern of the hemodynamic response to acute hypoglycaemia by interfering with the peripheral effects of circulating catecholamines in a way which depends on the degree of beta-1 selectivity of the drug used.

Adult↗
PubMed1982

[Thalidomide in the treatment of chronic lupus erythematosus].

The effect of thalidomide was investigated in 12 patients with chronic lupus erythematosus resistant to classical treatment (antimalarial drugs, topical steroids). 10 patients were improved and 2 were not sensitive to the treatment. The doses were 100 mg/day for a minimum period of 2 months. With the exception of 1 case, the treatment was well tolerated. The indications of thalidomide in dermatology and the mechanism of action of the drug are briefly discussed.

Adult↗
PubMedDate not supplied

Familial IgA nephropathy.

To date, more than 90 families with multiple members with IgA nephropathy have been reported. The case for genetic predisposition as a cause of familial clustering of IgA nephropathy is supported by several factors, including variable time points in the onset of the disease in relatives with IgA nephropathy; the presence of abnormalities of IgA production in both affected and unaffected family members; the clustering of the birthplaces of ancestors of large pedigrees containing multiple affected members with IgA nephropathy, which suggests the existence of a "founder effect". Immunogenetic studies does not conclusively indicate that HLA is involved in the pathogenesis of IgA nephropathy. The specific mode of inheritance of familial IgA nephropathy is difficult to establish with certainty. IgA nephropathy may be a single gene trait with incomplete penetrance. Alternatively, a multifactorial genetic disease could account for the increased prevalence of the disorder among relatives of affected individuals. Clinicians must become aware that IgA nephropathy may aggregate within families in a substantial number of cases. The availability of multiplex families offers an ideal opportunity to design a molecular genetics approach to map the gene(s) or pathway(s) responsible for the development of IgA nephropathy.

Genetic Predisposition to Disease↗
PubMedDate not supplied

Molecular analysis of uromodulin and SAH genes, positional candidates for autosomal dominant medullary cystic kidney disease linked to 16p12.

BACKGROUND: The location of a second genetic locus for autosomal dominant medullary cystic kidney disease (ADMCKD) at chromosome 16p12 led us to further investigate the molecular analysis of the critical region where two genes coding for uromodulin and SA proteins with renal specific functions, UMOD and SAH, are localized. METHODS: We characterized the intron-exon boundary sequences by screening phage and BAC DNA genomic clones for the development of new molecular tools functional to the mutation analysis of UMOD and SAH genes. RESULTS: No consistent mutations for ADMCKD2 were found in the UMOD and SAH genes. We identified a silent polymorphism in the UMOD gene at codon C174 which co-segregates with the disease in the ADMCKD2 family. CONCLUSIONS: This study excludes the involvement of uromodulin and SAH genes in ADMCKD2, and provides new tools for their molecular analysis in other diseases.

Chromosome Mapping↗
PubMedDate not supplied

Atherosclerotic renovascular disease: medical therapy versus medical therapy plus renal artery stenting in preventing renal failure progression: the rationale and study design of a prospective, multicenter and randomized trial (NITER).

BACKGROUND: Many studies suggest a major prevalence of atherosclerotic renovascular disease (ARVD), caused by mono or bilateral renal artery stenosis (RAS). Unfortunately, there is no definite therapy to cure this disease to date; therefore, ARVD is burdened by important clinical complications with high social and economic costs. The last few years have seen important advancements in both medical therapy and in interventional radiology (for example, percutaneous transluminal renal artery stenting (PTRS)). All of them could affect, in some way, the natural history of ARVD, but to date the optimal strategy has not been established. METHODS: The protocol of a prospective, multicenter, randomized trial "Nephropathy Ischemic Therapy (NITER)" is presented. It enrolls patients with stable renal failure (glomerular filtration rate (GFR) >or=30 ml/min) and hypertension, and hemodynamically significant atherosclerotic ostial RAS (>or=70%) diagnosed by duplex Doppler (DD) ultrasonography and confirmed by magnetic resonance angiography (MRA). This study aims to evaluate whether medical therapy plus interventional PTRS is superior to medical therapy alone according to the following combined primary endpoint: death or dialysis initiation or reduction by >20% in estimated GFR after 0.5, 1, and 2 yrs of follow-up and an extended follow-up until the 4th year. Medical therapy means drugs to control hypertension, improve dyslipidemia and optimize platelet anti-aggregant therapy. The sample size is estimated in 50 patients per group to achieve a statistical significance of 0.05 in case of a reduction by 50% in the combined endpoints.

Aged↗
PubMedDate not supplied

[The role of magnetic resonance angiography in the assessment of arterial stenosis in the transplanted kidney].

Artery stenosis in the transplanted kidney is the most frequent vascular complication; hypertension onset or worsening may be associated and, at an end stage, also renal insufficiency. The diagnosis must be early and accurate and provide guidelines for medical, interventional or surgical therapy. To assess the diagnostic reliability or MRA, 27 patients were examined. On the basis of clinical, biochemical, pharmacological (Captopril test) and instrumental (color-Doppler US) examinations, the artery of the transplanted kidney was considered normal in 6 patients and stenotic in 21. In the control group, MRA results were in agreement with color-Doppler findings. On the contrary, in 8 of 21 abnormal conditions, the two techniques were in disagreement. Digital angiography, considered as the gold standard, was performed in any questionable case, confirming a slight overestimation of the stenoses by MRA (3 cases) and 2 false positives by color-Doppler US. The authors believe color-Doppler US to be a reliable technique for screening stenosed arteries in the transplanted kidney. MRA is proposed as a complementary investigation useful to define stenosis type and to provide guidelines for treatment.

Adult↗
PubMedDate not supplied

Familial membranous nephropathy.

Numerous HLA studies suggest that genetic factors play an important role in the development of membranous nephropathy (MN). We studied seven patients with idiopathic MN, from three unrelated families of Italian ancestry. Complement phenotype analysis and restriction fragment length polymorphism (RFLP) typing of HLA class II and of the switch region genes were done in family members. In the first family, the father, one son, and one daughter had MN; another daughter had clinical glomerulonephritis. The three members with MN shared one HLA haplotype carrying DR beta 11; in the two siblings with the disease, the second HLA haplotype carried the DR beta 3.2 allele. In families 2 and 3, two brothers had MN: in family 2, they differed in at least one haplotype; in family 3, they differed in both haplotypes. Only family 3 was informative with regard to the RFLP of the switch region genes: the two siblings were identical for both Ig heavy chain haplotypes. No clinical, laboratory or morphologic features consistent with a secondary form of the disease were found. Familial clustering of MN suggests a genetically transmitted mechanism.

Adult↗