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Biomedical subjects

A Capuano

Publications and source records attributed to A Capuano.

At least 37 records · Page 2Linked to original sources
PubMed1990

Cardiovascular impairment, dialysis strategy and tolerance in elderly and young patients on maintenance haemodialysis.

Cardiovascular impairment is considered a major cause of reduced tolerance to haemodialysis in elderly patients and is thought to require a soft dialysis strategy in these patients. To verify these observations we compared dialysis strategy and tolerance of patients over 65 years old to those of patients under 45 years, since atherosclerotic/involutional changes of vasculature should be quite different in these groups. Seventy-seven elderly and 57 young patients (age 72 +/- 5 and 35 +/- 6 years respectively, mean and SD) were selected from a population of 292 patients undergoing regular dialysis treatment exclusively on the basis of the age criterion. Cardiovascular impairment was found to be greater (as expected) in older than in younger patients, as documented by a larger proportion of diabetic patients (19% vs 3%), a greater incidence of cardiovascular manifestations both before the beginning of dialysis (27% vs 10% of patients affected) and after the beginning of dialysis (35% vs 16%), a greater incidence of ECG abnormalities (78% vs 56%), a longer exposure to hypertension (9.2 vs 3.5 years), and a greater utilisation of digitalis (36% vs 5%) and nitrates (19% vs 2%). Dialysis strategy in elderly patients differed from that in young patients only for a moderately lower blood flow rate (243 vs 279, 244 vs 279, ml/min, males and females respectively). Dialysis sessions were shorter in older than in younger males (11.8 vs 12.4 h/week). The incidence of intradialytic hypotension did not differ significantly between the two groups (44% vs 32%), although the elderly showed a greater pre-to-post-dialysis systolic arterial pressure reduction (21 vs 15 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[The role of Streptococcus mutans in human caries].

Definite proof has been found that S. mutans, and probably S. sobrinus and lactobacilli, are responsible for caries in man. The aciduria of S. mutans encourages the selection inside the plaque and is directly responsible for its cariogenicity. Other aciduric species, as S. sobrinus, cause caries on the smooth surface of the tooth, where the principal causes of the rampant caries reside. If during the eruption of the tooth the fissures become colonized in depth by S. mutans, the development of caries becomes a highly probable event. Instead, if the colonization of the tooth by S. mutans takes place after the fissure depth have been occupied by other microbic species not cariogenic, it is probable that the caries will not manifest or will appear in a less severe form. In conclusion, the knowledge already acquired on the ecology of S. mutans and the mechanism of cariogenesis clearly indicate that all factors that interfere with the colonization of the tooth by S. mutans can greatly reduce the incidence of caries in man.

Bacterial Adhesion↗
PubMed1989

[Cefatrizine in dentistry. Clinical study].

The Authors evaluated the cefatrizine clinical effects on 50 patients with infectious diseases. The statistical analysis of results show a high efficacy and safety with no relevant side effects.

Adolescent↗
PubMed1989

[MK6: a computerized diagnostic system for mandibular movement].

The authors describe the use of a new computerized diagnostic system MK6 by Myotronics Inc., Seattle, for the cranio-mandibular disorders. The conclusion of an anamnestic questionnaire, of an extraoral and intraoral standardized analysis and the computerized tridimensional tracings allow a precise and accurate diagnosis of the occlusal and neuromuscular pathology.

Diagnosis, Computer-Assisted↗
PubMed1987

Immunoradiometric quantitation of tissue plasminogen activator-related antigen in human plasma: crypticity phenomenon and relationship to plasma fibrinolysis.

A two-site immunoradiometric assay for tissue plasminogen activator (tPA) antigen has been developed using immunoaffinity purified antibody. Various treatments enhanced the detection of tPA antigen in the plasma samples. Maximum detection was obtained by acidification of plasma to pH 4.8 to 6.5 or addition of 0.5 mol/L of L-lysine or L-arginine. Acidification or addition of lysine to plasma is also required for maximum immunoadsorption of plasma tPA antigen on anti-tPA-Ig-sepharose. These results indicate that plasma tPA antigen is partially cryptic to antibody in untreated plasma. The plasma tPA antigen isolated by immunoadsorption of either untreated plasma or acidified plasma on anti-tPA-Ig-sepharose consists mainly of a 100-kd plasminogen activator species as determined by fibrin-agar zymography. The 100-kd activity is possibly a tPA:inhibitor complex. A standardized sample preparation method was conveniently adopted by mixing 3 vol of plasma and 1 vol of 2 mol/L of L-lysine for the assay. Reconstitution and recovery studies showed that the method is specific and permits full detection of both free tPA and tPA:inhibitor complex. The validity of the assay is further supported by the finding that the spontaneous plasma fibrinolysis previously demonstrated to be dependent on plasma tPA antigen is correlated with tPA antigen content. Using the standardized assay, we found that tPA antigen concentrations in 16 blood bank plasmas are equivalent to 3.7 to 20 ng of 60 kd tPA/mL. In all the plasma tested, more than half of the antigen is undetected unless the plasma is treated as described above.

Acids↗
PubMed1987

Initiation and regulation of fibrinolysis in human plasma at the plasminogen activator level.

The initiation and regulation of fibrinolysis has been studied by reconstitution of fibrinolytic activity in human plasma in vitro. Depletion of tissue plasminogen activator (tPA) antigen by immunoadsorption of human plasma with anti-tPA Ig Sepharose 4B leads to total loss of spontaneous fibrinolytic activity determined by lysis of a thrombin-induced clot. Addition of physiological concentrations of purified tPA to tPA-depleted plasma restores fibrinolytic activity as a function of the length of time between tPA addition and clotting. Addition of free tPA to tPA-depleted plasma followed by immediate clotting results in a high rate of fibrinolysis. In contrast, when free tPA is allowed to incubate in plasma for 10 to 60 minutes prior to clot formation, the fibrinolytic activity of tPA is gradually lost. The loss of tPA-induced fibrinolytic activity in unclotted plasma is accompanied by decreased partitioning of tPA antigen into fibrin after clotting and is kinetically correlated with the formation of a 100 kilodalton (kDa) tPA complex as demonstrated by SDS-gel electrophoresis and fibrin-agar zymography. These results suggest that free tPA is susceptible to complexation by the plasma inhibitor in the absence of a clot. Fibrin formation renders tPA relatively inaccessible to inhibition. The tPA antigen isolated from stored plasma consists mainly of 100 kDa activity in SDS-gel electrophoresis and zymography, indicating that the tPA complex is resistant to dissociation by SDS. Upon rezymography of the sliced gel, only a 60 kDa tPA activity is found, suggesting that the activity at 100 kDa is at least partly due to free tPA dissociated from the complex during the first zymography. Conversion of tPA complex to enzymatically active free tPA also occurs with brief SDS exposure followed by incubation in the presence of excess Triton X-100 or by hydroxylamine treatment. These results reconcile the apparent discrepancy of the 100 kDA inhibitor-tPA complex manifesting plasminogen activation activity during zymography. The plasma tPA-inhibitor complex is precipitated strongly by antisera against plasminogen activator inhibitors (PAIs) of human Hep G2 hepatoma and HT-1080 fibrosarcoma cells and weakly by antiserum against bovine aortic endothelial cell PAI but not by antiserum against a placental PAI (PAI-2) suggesting that the plasma inhibitor is immunologically related to Hep G2, HT-1080 and possibly endothedial cell PAIs. Based on the above findings, a simple model for the initiation and regulation of plasma fibrinolysis at the PA level has been formulated.

Antigens↗
PubMed1986

Carrier-linked primaquine in the chemotherapy of malaria.

The antimalarial effect of intravenously administered primaquine (PQ) can be improved and its toxicity diminished by linking it to a macromolecular carrier protein. A thiol-containing primaquine derivative 8-[[4-(2-amino-3-mercaptopropionamido)-1-methylbutyl]amino]-6- methoxyquinoline was synthesized. This compound could readily be linked via a disulfide bond to a carrier protein containing (pyridyldithio)propionate groups. The derivative was coupled to serum albumin as well as to serum albumin that contained covalently linked lactose residues. The protein-drug conjugates were tested for their antimalarial activity in mice inoculated with Plasmodium berghei. The causal prophylactic activity of the conjugate with the lactosaminated serum albumin was 2 times higher than that of the free drug; the mean causal prophylactic doses (CPD50) were 6 and 13 mg of primaquine base/kg, respectively. Moreover, its acute lethal toxicity had decreased at least 6.5-fold (mean lethal dose (LD50) greater than 85 mg of primaquine base/kg). The therapeutic index of this conjugate was at least 12 times higher than that of the free drug. This allowed the administration of a dose that cured 100% of the animals (17.5 mg of primaquine base/kg), in a single injection. With unmodified serum albumin the conjugate showed an increased therapeutic efficacy (the CPD50 was approximately 10 mg of primaquine base/kg) and a strongly reduced lethal toxicity.

Animals↗
PubMed1985

Spontaneous fibrinolysis in whole human plasma. Identification of tissue activator-related protein as the major plasminogen activator causing spontaneous activity in vitro.

Spontaneous fibrinolysis of plasma clots was studied by following the lysis of the clots formed in 125I-fibrinogen-supplemented citrated plasma. Lysis of the clots invariably follows sigmoidal kinetics with S50 (the time required for 50% clot lysis) ranging from 3.5 to 4.7 days in 8 samples of pooled blood bank plasma and in the majority of apparently healthy donor plasmas. The spontaneous lysis of factor XII-deficient and prekallikrein-deficient plasmas was found to be similar to that of normal plasma. Addition of ellagic acid or antibodies against kallikrein or urokinase to normal pooled plasma did not alter significantly its rate of spontaneous lysis. On the other hand the addition of antibody against tissue activator (t-PA) inhibited over 80% of the spontaneous fibrinolysis in a 7-day incubation period at 37 degrees C, and the clot visually persisted for more than a month. Therefore, the factor XII-dependent components and prourokinase/urokinase system do not contribute significantly in whole plasma fibrinolysis in vitro, while the t-PA-related protein appears to be the major plasminogen activator responsible for initiating spontaneous fibrinolysis in whole plasma. Exogenous addition of increasing amounts of purified HeLa cell t-PA to normal pooled plasma in the ng/ml range cause progressively faster clot lysis. By extrapolation, normal pooled plasma is found to contain endogenous tissue activator in an amount functionally equivalent to 2 ng/ml of purified 60-kDa t-PA. The molecular nature of the t-PA-related proteins in plasma was studied by zymographic and immunological methods. The major t-PA-related protein in plasma was found to have a molecular mass of 100 kDa as determined by zymography. By incubating purified HeLa 60-kDa t-PA with a t-PA-depleted plasma, the 100-kDa component can be generated in plasma, suggesting that the latter is formed as a result of the binding of 60-kDa t-PA to a binding protein in plasma.

Antibodies↗
PubMed1984

Scleroembolization for treatment of hypertension caused by intrarenal arterial fibrodysplasia.

This paper reports a 13-year-old girl with severe hypertension due to fibrodysplasia of intrarenal arterial branches in the upper pole of the left kidney. Scleroembolization of the abnormal vascular region was carried out by injecting, via a transcutaneous catheter, an 80% solution of sodium iothalamate in ethanol, followed by a suspension of Gore-Tex particles in the same solution, which resulted in complete and persistent normalization of blood pressure.

Adolescent↗