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F Resta

Publications and source records attributed to F Resta.

32 records · Page 2Linked to original sources
PubMed1998

[The use of HIV-1 protease inhibitors. Their effects on AIDS-correlated outpatient and hospitalization activities. A catchment area study].

OBJECTIVE: To evaluate the effects of the use of protease inhibitors (IP) on the out-patient department's activities and hospitalizations of HIV-1 infected subjects. METHODS: From the December 1996 IP was available in our hospital, so the years 1996 and 1997 were studied. RESULTS: In the year 1997, 336 patients were visited with an increase of the 41% compared with the year 1996. In the 1997 the 45.2% of hospitalizations were related to AIDS, while in the year 1996 the 65.4% of them were related to AIDS. CONCLUSIONS: The use of IP had increased the activities of the out-patient department and certainly had a role in reducing the hospitalizations related to AIDS.

AIDS-Related Opportunistic Infections↗
PubMed1994

A new Italian case of lipoprotein lipase deficiency: a Leu365- > Val change resulting in loss of enzyme activity.

We describe a second Italian family with primary Lipoprotein Lipase deficiency. A new mutation in exon 8 causes a Leu365- > Val change resulting in severe mass reduction and loss of enzyme activity. We suggest that this change interferes with the correct folding and stability of the protein and impairs the assembly of the active homodimer. The procedures applied are useful to screen a large sample of population for genetic variants and allow the clear identification of asymptomatic heterozygous subjects at risk from atherosclerosis disease.

Adult↗
PubMed1992

A G----C change at the donor splice site of intron 1 causes lipoprotein lipase deficiency in a southern-Italian family.

We describe a new case of lipoprotein lipase deficiency in a proband from a Southern-Italian family. Enzyme activity and mass were absent. Amplification and sequencing of individual exons, intron boundaries and the regulatory region revealed only one homozygous G----C transversion at the first nucleotide of intron 1. The single strand conformation polymorphism analysis proved to be a helpful tool for the identification of the single base mutation. Northern hybridization failed to reveal the presence of mature lipoprotein lipase mRNA. The mutation, which destroys the conserved dinucleotide at the junction site of intron 1, causes defective mRNA splicing and it is responsible for the deficiency.

Adult↗
PubMed1992

Apo C-II deficiency type Bari.

We formerly studied an Italian family with apo C-II deficiency. Two probands were homozygous for the defect (unmeasurable circulating apolipoprotein C-II and absence of C-II bands on immunoelectrophoresis). We documented the synthesis of the protein at the intestinal level in the probands with immunohistological techniques. With the purpose of investigating the molecular basis of the defect, Southern analysis, polymerase chain reaction (PCR) amplification and sequence analysis were carried out on one of the two cases. We identified a point mutation C to G transversion in the third exon of the gene causing a premature stop codon. Our hypothesis is that the truncated protein of 36 aa., instead of 79 aa., lacks its functional domain. This causes inefficiency in the activation of lipoprotein lipase (LPL) and the instability of the circulating molecule, which could have an higher catabolic rate compared to a normal protein. The faster disappearance from the circulating compartment make it unmeasurable. The mutation destroys a Rsa I site, present in the normal gene sequence. We suggest the use of this site for a rapid Restriction Fragment Length Polymorphism (RFLP) on PCR amplification products to screen this defect in the Italian population.

Apolipoprotein C-II↗
PubMed1991

[The treatment of gastrointestinal infections with ciprofloxacin].

The authors have evaluated the efficacy and tolerability of ciprofloxacin, a new broad-spectrum fluor-quinolone, in the therapy of gastrointestinal infections. The authors have studied 24 patients suffering from above-mentioned infections clinically diagnosed (11 microbiologically diagnosed too). All the patients took ciprofloxacin tablets 500 mg b.i.d. for 10 days (average). All the patients were restored to health and the tolerability was excellent.

Adolescent↗
PubMed1988

Apolipoprotein C-II deficiency: detection of immunoreactive apolipoprotein C-II in the intestinal mucosa of two patients.

Recent data suggest that mutant immunoreactive forms of apolipoprotein C-II (apoC-II) can be detected in the plasma of patients with the apoC-II deficiency syndrome. We studied the possible presence of apoC-II mutants in the plasma of two patients with apoC-II deficiency by immunological means. The patients were hypertriglyceridemic, and apoC-II was undetectable in plasma as determined by radial immunodiffusion, electroimmunoassay, and immunonephelometry. Furthermore, apoC-II was undetectable either by electrophoresis or by immunoblotting in the plasma of the probands, while apoC-II was present in the plasma of their parents, although at less than half-normal concentration. Immunochemical localization of apoC-II, however, showed that the apoprotein could be detected within the enterocytes obtained from the intestinal mucosa of the patients. From these data we conclude that the patients synthesize apoC-II, at least in the intestine.

Apolipoprotein C-II↗
PubMed1988

Cell-mediated immune response in patients with type IIa, type IIb and type IV primary hyperlipoproteinaemia.

Plasma lipoproteins inhibit immune function. Polymorphonuclear cell (PMN) and monocyte activities, and pokeweed mitogen (PWM)-driven B cell differentiation in patients with type IIa, type IIb and type IV primary hyperlipoproteinaemia were evaluated. Evidence is provided for a selective impairment of these functional capacities in type IIa and type IIb hyperlipoproteinaemic patients, while immune responsiveness is unaffected in type IV primary hyperlipoproteinaemia. The data suggest a specific immune dysfunction in patients with type IIa and type IIb primary hyperlipoproteinaemia.

Adult↗
PubMed1984

Effect of procetofen on serum lipids and apoproteins.

The effect of procetofen (fenofibrate) on lipids and apoproteins was studied in ten patients affected with familial type II-A and II-B hyperlipoproteinemia. Following stabilization with an isocaloric diet for 2 months, the patients were given 300 mg/day of procetofen for 3 months, then placebo for 1 month. Plasma cholesterol and triglycerides were decreased by 15% and 46%, respectively. Plasma apo B was lowered by 17%. The predominant decrease in lipids and apoproteins occurred in VLDL, whereas in HDL cholesterol increased significantly but not its major apoprotein, apo A-I. A mechanism of action involving increased catabolism of VLDL and reduced synthesis of LDL and VLDL is proposed.

Adult↗
PubMedDate not supplied

Prurigo nodularis (Hyde's prurigo) disclosing celiac disease.

A case of prurigo nodularis (Hyde's prurigo) preceding by 15 years the diagnosis of celiac disease is presented. In particular, the association between the clinical course of prurigo nodularis and the compliance with gluten-free diet is reported and discussed.

Aged↗
PubMedDate not supplied

Oxidative burst and lysosomal enzyme release by polymorphonuclear cells in type IIa, type IIb and type IV primary hyperlipoproteinaemia.

Several findings pint out the occurrence of a strict relationship between lipoproteins and immunoresponsiveness. In this regard, in vitro lipoproteins pretreatment of mononuclear cell suspensions leads to an inhibition of Natural Killer (NK) cytotoxicity or T- and B-mediated immune functions. These results have an in vivo counterpart, since an impairment of either T-driven B cell polyclonal differentiation or phagocyte chemotaxis, phagocytosis and killing has been shown in patients with type IIa and type IIb primary hyperlipoproteinaemia. On the contrary, these activities fall within normal range in type IV hyperlipoproteinaemic subjects. To further address the potential role of polymorphonuclear cells (PMN) in atherosclerotic process, in the present report PMN-mediated superoxide anion (O2-) generation, hydrogen peroxide (H2O2) production, beta-glucuronidase and myeloperoxidase release have been assessed in similar groups of patients. Results provide a clearcut evidence for a significant enhancement of oxidative metabolism by either suspended or adherent to plastic PMN in type IIa primary hyperlipoproteinaemia only. These data were further confirmed by the observation that the same cell suspensions exhibit a significant increase of H2O2 generation and/or beta-glucuronidase and myeloperoxidase release. By contrast, PMN metabolic pathway in type IIb and type IV patients mimics that observed in healthy individuals. In the light of the well known increase of serum low-density lipoproteins (LDL) in type IIa primary hyperlipoproteinaemia, these findings suggest that also PMN may play an important role in the development of atherosclerosis. The augmented oxidative responsiveness may, in fact, give rise to LDL oxidation, which is in turn responsible for foam cell generation through an exaggerated uptake of oxidized LDL by macrophages.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗