Intermittent pyramidal claudication as presenting and sole symptom in multiple sclerosis.
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Biomedical subjects
Publications and source records attributed to M Ferrari.
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Thirty-five patients with superficial transitional carcinoma of the bladder were treated intravesically with escalating doses of recombinant alpha-2-interferon administered weekly for 8 weeks. Of the 19 patients with high-grade intraepithelial neoplasia (17 carcinoma in situ [CIS], two severe dysplasia, all cytology positive), six (32%) had complete resolution of all histologic and cytologic evidence of disease (complete response). An additional three patients (16%) had complete resolution of CIS, but the interval appearance of a low-grade transitional cell neoplasm. Five (26%) had a partial response (complete resolution of all evidence of CIS on multiple bladder biopsies but persistently positive cytologic preparations). Sixteen patients with recurrent papillary tumors and extensive prior therapy were also treated. Four (25%) had a complete response. Twenty-three of the 35 patients had prior intravesical therapy. Seven of the 23 (30%) patients with prior intravesical chemotherapy or immunotherapy had a complete or partial response to interferon, while eight of the 12 patients (67%) without prior intravesical treatment responded. These responses were achieved with minimal local and systemic toxicity. Of the ten complete responders, five remain in continuous unmaintained remission for 18+ to 37+ months. Intracavitary alpha-2-interferon is an effective new treatment for some patients with bladder cancer.
Many in vivo studies showed the accumulation of PFC particles in reticuloendothelial cells of target organs such as spleen, lungs and liver. Surprisingly, an uptake of PFCs particles by liver parenchymal cells as well was described by some authors. In order to clarify whether Kupffer cells and/or liver environmental factors could be involved in particle uptake we exposed cultured rat hepatocytes to Fluosol 43. PFC particles were noted, after a 3-hour incubation, in lysosomes. This result suggests that more attention must be paid to liver toxicity of PFC blood substitutes. Isolated mouse myocytes were exposed as well to Fluosol 43 for 3 hours. Preliminary results confirm the absence of the particle uptake previously noted also in our in vivo studies on rat and guinea pig heart-lung preparation. The possible subsequent absence of cytotoxicity at myocardial level could underline the reliability of using optimized PFCs as components of cardioplegic solutions in open heart surgery.
Pregnant cows were given the first injection of an inactivated bovine rotavirus vaccine approximately 4 weeks before calving and a second injection just before calving. This led to the enhancement of rotavirus antibody titers in their colostrum as well as in the milk for at least 5 days after parturition. Thus, when newborn calves were fed with the mammary secretions obtained from the vaccinated cows daily for 5 consecutive days they were fully refractory to experimental infection with 81/36F bovine rotavirus. By contrast, the calves which were given the mammary secretions from unvaccinated cows, had clinical signs consistent with rotavirus infection and viral shedding. Based on these results it is suggested that vaccination of cows according to the scheme followed in this experiment, i.e., two injections within the last month of pregnancy, might be a valid approach which depending on confirmation under field conditions, could help reduce the incidence of rotavirus-induced diarrhea in newborn calves.
The locus D7S23 includes a CpG-enriched methylation-free island that maps midway between the markers J3.11 and met and is genetically very close to the mutation causing cystic fibrosis (CF). We have studied the linkage disequilibrium between four polymorphic markers from this locus (KM.19, CS.7, XV-2c, and PT-3) and the CF mutation (CF) in 127 Italian families. Strong linkage disequilibrium is found between KM.19, CS.7, and CF, and weaker but significant disequilibrium is found between XV-2c, PT-3, and CF. The disequilibrium between markers and CF for the Italian population provides additional information on the origin and homogeneity of the CF defect. This panel of probes is sufficiently informative to permit accurate prenatal diagnosis of CF in most families with an affected person, and the disequilibrium also allows indirect carrier detection/exclusion in some cases.
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The acute effects of the peritoneovenous shunt (LeVeen) on hemodynamics and pulmonary gas exchange in 6 consecutive patients with intractable ascites and cirrhosis were evaluated. After opening the peritoneovenous shunt, there was a marked increase in cardiac index, (from 3.78 +/- 0.4 to 5.86 +/- 0.4 1/min. m2, p less than 0.01), and mean pulmonary artery pressure (from 17.3 +/- 1.9 to 23.3 +/- 1.5 mmHg, p less than 0.05), while a significant decrease in systemic vascular resistances (from 1086 +/- 116 to 694 +/- 52 dynes.sec.cm-5, p less than 0.05) was observed. In all patients there was a drop in arterial oxygen tension (PaO2) (from 76 +/- 3 to 67 +/- 3 torr, p less than 0.01) and an increase in venous admixture (Qsp/Qt) from 13.1 +/- 2 to 18.9 +/- 2%, p less than 0.01). The comparable increase in cardiac output and in venous admixture produced by opening the peritoneovenous shunt, might be related to the massive transfusion of ascitic fluid into the intravascular compartment. It is therefore concluded that this impairment of tas exchange further support discarding an appropriate amount of ascitic fluid at the time of shunt insertion.
Portal vein thrombosis is an infrequent complication after hepatic transplantation, but is quite dramatic when it occurs. It is usually managed by retransplantation with a significant mortality rate. We present a patient in whom portal vein thrombosis after hepatic transplantation was ultimately managed by a splenorenal shunt. The portal vein thrombosis was manifested by bleeding esophageal varices and, yet, normal hepatic function obviated the need for a new graft (one was not readily available). To the best of our knowledge, this is the first presentation of a patient with a transplant of the liver with acute portal vein occlusion and maintained hepatic function who has been successfully managed by a portosystemic shunt.
A thrombotic microangiopathy syndrome, clinically and pathologically similar to thrombotic thrombocytopenic purpura (TTP) has been reported in recipients of tissue transplants, including renal and bone marrow allografts. The diagnosis is made only after other causes of microangiopathic hemolytic anemia have been excluded. In this case report we present the outcome of the combination of plasma exchange, dipyridamole and aspirin in the management of a TTP-like syndrome that complicated the post-operative course of liver transplantation.
Refractory ascites is an infrequent complication of cirrhosis. Paracentesis and ultrafiltration of the ascitic fluid with intravenous or intraperitoneal reinfusion of the concentrated ascites has been used as therapy for this condition since 1971. The technique is cumbersome and has high morbidity and mortality rates, even if effective. In this paper we describe a new technique that couples secondary filtration for the removal of macromolecules, with ultrafiltration of ascitic fluid. In its very first application 6 patients underwent 8 treatments. No adverse effect was observed and clinical efficacy was good. Up to 60 g of albumin can be saved in a single session lasting less than 2 hours.
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First-trimester prenatal diagnoses of hemophilia A were heretofore obtained by using either intragenic factor VIII markers or linked extragenic polymorphic markers. Postulating that the combined use of all the available intragenic and extragenic markers can render such diagnoses more frequently feasible and more reliable, we carried out ten first-trimester prenatal diagnoses in male fetuses at risk for hemophilia A by DNA analysis of chorionic villus employing in combination the intragenic Bcl I polymorphism and the St 14 (DXS 52) or DX 13 (DXS 15) extragenic probes. A diagnosis of hemophilia was obtained in three fetuses, with a diagnosis of normal fetus obtained in the remaining seven. Seven diagnoses are confirmed by factor VIII assays carried out at the time of abortion, in the mid-trimester or at birth. A factor VIII probe recognizing Bcl I polymorphism was useful in 4 of 6 diagnoses; St 14, in 5 of 6; and DX 13 in 3 of 5. In two cases, St 14 was the only useful probe for diagnosis. Even though no recombination between extragenic probes and factor VIII gene was detected in this study, when only extragenic markers were informative we advised diagnostic confirmation on fetal plasma obtained by fetoscopy. Hence, first-trimester prenatal diagnosis of hemophilia A is feasible for the great majority of fetuses at risk through combined use of all the available intragenic and extragenic probes, providing key family members are available.
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