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Biomedical subjects

J E Cardoso

Publications and source records attributed to J E Cardoso.

14 recordsLinked to original sources
PubMed2004

A novel melon flexivirus transmitted by whitefly.

In recent years, a viral disease on melon plants has become a serious problem in Brazil. Symptoms were principally yellowing and mottling on older leaves. Long filamentous virus particles, resembling those of carlaviruses, were seen in symptomatic leaves. In this study, the 3' terminal region of the virus genome isolated from an infected plant, including the last two ORFs, was cloned and sequenced. The sequence comprised a polyadenilated tail and two ORFs, one exhibiting similarity to potexvirus and carlavirus coat protein gene and the second to a carlavirus protein with potential nucleic acid-binding property. The sequence analysis, the genome organization and the particle morphology indicated that the virus could be classified as a novel whitefly-transmitted flexivirus. The name Melon yellowing-associated virus (MYaV) is tentatively suggested for this virus.

Amino Acid Sequence↗
PubMed2000

Histological and histoquantitative study of the rat parotid gland after Trypanosoma cruzi infection.

The present study deals with the morphology of the rat parotid gland and its changes after Trypanosoma cruzi infection. The glands of control and infected animals were analyzed by histologic and histoquantitative methods. After 18 days of infection with T. cruzi, a significant reduction of the density of the volume of the acini and duct system, as well as a significant increase in the amount of connective tissue was noted. In addition, these animals displayed an increase in the number of cells undergoing mitosis. In the 45 day infected rats, there was return to the normal pattern. It is suggested that in the infected animals the decrease in body weight could be responsible for retarded sexual maturity, leading to the lower level of testosterone. It can be assumed that decreased levels of epidermal growth factor (EGF) and neural growth factor (NGF) caused by the lack of testosterone in infected animals also contribute to the atrophy of the parotid gland and to the proliferation of the connective tissue.

Acute Disease↗
PubMed1998

Hepatic regeneration in the isolated perfused rat liver followed by liver transplantation.

Controlling the S phase of the hepatocyte cell cycle would be of considerable help for stable retroviral foreign gene transfer. The aim of this article is to study hepatocyte regeneration during S phase in isolated, perfused rat liver followed by liver transplantation. Normal livers (G I: n = 7) were perfused with blood from normal rats for 6.1+/-0.3 hours. Regenerating livers (G II; n = 7) obtained 18 hours after partial hepatectomy were perfused for 6.0+/-0.3 hours with blood from rats partially hepatectomized 18 hours before. Regenerating livers (G III; n = 7) obtained 22 hours after partial hepatectomy were perfused for 2.4+/-0.1 hours with blood from normal rats. In the normothermal perfusion system, a bolus of 25 mg of 5-bromo-2'-deoxyuridine (BrdU) was added to the perfusate. Liver biopsies were taken at the end of each experiment. In group II, a biopsy was also taken 1 hour after BrdU introduction. At the end of each experiment, livers were orthotopically transplanted. The percentage of BrdU positive hepatocyte nuclei was 0.2% in G I; 14.8% and 38.4% after 1 hour and 6.1 hours, respectively, in G II; and 46.5% after 2.4 hours in G III. In G I, five rats died at day 1, 5, 6, 7, and 48 and two rats were still alive after 17 months. In G II, all the rats died before day five. In G III, two rats died at day one, one at day six, and four were still alive after 12 months. This study shows that, after 6 hours of normothermal perfusion, organ viability allows successful liver transplantation and that rat hepatocyte regeneration during cell cycle S phase in isolated normothermal conditions progresses in a similar way-quantity and timing-to liver regeneration found in vivo after partial hepatectomy.

Animals↗
PubMed1994

Liver function improvement following increased portal blood flow in cirrhotic rats.

BACKGROUND/AIMS: Liver microcirculation in cirrhosis is characterized by development of intrahepatic shunts and capillarization of sinusoids secondary to cell necrosis and deposition of new collagen, resulting in both decreased drug elimination and increased vascular resistance with portal hypertension. The aim of this study was to examine the effects of increased portal blood flow on hepatic microcirculation and drug elimination in 13 perfused livers from cirrhotic rats. METHODS: Intrahepatic resistance was assessed under basal conditions (21.2 +/- 0.3 mL/min) and 1 hour after doubling the flow (41.6 +/- 1.0 mL/min). A multiple indicator dilution technique was used at both flow rates to measure sinusoidal volume, albumin and sucrose extravascular volumes, and cellular water volume. Hepatic elimination of labeled taurocholate and propranolol was also measured, and the recovery of 15-microns microspheres was used to evaluate large intrahepatic shunts. RESULTS: After doubling the flow, intrahepatic resistance decreased by 31%. Sinusoidal and extravascular volume increased significantly without a change in microsphere recovery. However, there was a marked increase in taurocholate and propranolol elimination by cirrhotic livers. Moreover, during high flow, significant correlations were found between changes in albumin extravascular volume and taurocholate and propranolol elimination. CONCLUSIONS: Increased portal blood flow in cirrhotic rats induces a decrease in intrahepatic resistance without changes in intrahepatic shunting and improves drug elimination by the liver without deleterious effects on hepatocyte viability.

Animals↗
PubMed1994

Portal pumping: a new perspective for treatment of variceal hemorrhage and liver failure in end-stage cirrhosis?

In end-stage cirrhosis complicated by variceal hemorrhage, attempts to reduce portal pressure by treatments such as portosystemic shunts also decrease sinusoidal perfusion and risk impairing liver function. It has been suggested that encouraging portal flow to pass through the cirrhotic liver by mechanical action could cause a decrease in distal (splanchnic) portal pressure on one hand, and improve liver function on the other. The aim of this work was to evaluate the hemodynamic and functional effects of a 30-min pump-driven increase in portal blood flow through the liver of patients with end-stage cirrhosis before the anhepatic phase of liver transplantation. Basel portal flow (800 +/- 270 ml.min-1) was increased two fold (n = 10) or four fold (n = 9). When the flow was doubled, splanchnic portal pressure decreased 17.9 +/- 11.3% (from 31.8 +/- 5.3 to 26.0 +/- 5.8 mmHg, n = 10; p < 0.001); when flow was increased four fold, splanchnic portal pressure decreased 39.2 +/- 15.4% (from 32.8 +/- 5.0 to 19.9 +/- 6.0 mmHg, n = 9; p < 0.001). The comparison of indocyanine green clearance between basal and doubled portal flow demonstrated an increase of 32.1 +/- 26.9% (n = 5; p = 0.053). Histological analysis demonstrated sinusoidal dilatation in three out of ten livers. These results, as well as previous studies using isolated perfused cirrhotic rat or human livers, suggest that portal pumping should be explored as a treatment for certain sclerotherapy-resistant cirrhotic patients, with variceal hemorrhage and liver failure.

Adolescent↗
PubMed1994

Augmentation of portal blood flow improves function of human cirrhotic liver.

In cirrhotic livers, the intrahepatic resistance is increased and drug elimination and portal transhepatic flow are decreased. The aim of our work was to study the effect of a twofold increase in portal blood flow during 2 hr on the hemodynamic parameters, drug elimination and hepatic viability in eight isolated perfused human cirrhotic livers. Using an oxygenated recirculating system with independent arterial and portal flows, we perfused livers with Kreb's buffer bicarbonate solution, bovine serum albumin (20 gm.L-1) and human red blood cells (hematocrit 20%). The flow was maintained at a basal level of 0.713 +/- 0.19 L/min for 1 hr and then increased and maintained for 2 hr at twice the basal flow. Portal pressure-portal flow curve slopes were linear (27.04 +/- 21.06 mm Hg.L-1 x min; range = 6.43 to 60.8) and correlated with intrahepatic resistance during the basal-flow period (r = 0.87, p < 0.01). Parameters registered during the basal- and high-flow periods were compared by use of Student's t test: portal pressure increased from 23.5 +/- 7 to 37.3 +/- 16.7 mm Hg (p < 0.05); arterial pressure increased from 80.3 +/- 19 to 103.5 +/- 26 mm Hg (p < 0.005); hepatic artery flow resistance increased 31.9% (from 690.1 +/- 218 to 899.4 +/- 269 mm Hg.L-1 x min; p < 0.005); indocyanine green clearance increased by 28.2% (from 86.0 +/- 58.3 to 109.2 +/- 74.8 ml.min-1 x kg liver-1; p < 0.04). No significant differences were observed in enzyme release, biliary flow (n = 5) and oxygen consumption. Histological examinations demonstrated sinusoidal dilatations in six of eight cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Augmented portal flow in the isolated perfused cirrhotic rat liver: a haemodynamic and morphological study.

1. Isolated perfused cirrhotic rat livers were used to study the effects of an increase in portal perfusion pressure and portal flow on the microcirculation and viability of the hepatocytes. Cirrhosis was induced by CCl4, and Krebs-Ringer bicarbonate buffer solution was used as the perfusate. Portal perfusion pressures were increased incrementally between 25 and 45 cm H2O. The viability of the livers was assessed and histological studies were performed under light and electron microscopy. 2. An increase in portal perfusion pressure induced an increase in hepatic flow in all the experiments (P < 0.05). Hepatic flow was 2.52 ml min-1g-1 of liver (SD 0.67; n = 5) at basal pressure compared with 4.19 ml min-1g-1 of liver (SD 0.93; n = 5) and 5.91 ml min-1g-1 of liver (SD 0.63; n = 5) when pressures were raised to 25 and 45 cmH2O, respectively. Portal perfusion pressure and hepatic flow were correlated (r = 0.908; P < 0.001; n = 30). 3. Production of the enzyme alanine aminotransferase (EC 2.6.1.2) increased significantly from 5.69i.u. ml-1min g-1 of liver (SD 3.62; n = 5) to 23.53i.u. ml-1min g-1 of liver (SD 16.7; n = 5) when the perfusion pressure was raised from baseline to 30 cmH2O. In all the cases the porto-caval gradient of enzyme production was within the normal range. No correlation existed between the release of enzyme and portal perfusion pressures.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

In situ retrovirus-mediated gene transfer into dog liver.

Dogs were used as a large animal model to assess the feasibility and safety of a surgical method for gene transfer into hepatocytes in vivo. This method, which we previously described in rats, consists of a partial hepatectomy aimed at inducing liver regeneration, followed by the selective in situ perfusion of the remnant liver parenchyma with a retrovirus preparation. Isolation of the liver was obtained by clamping the afferent and efferent blood vessels, a procedure that prevented retroviral vector dissemination and genetic modification of nonhepatic organs. A helper-free retrovirus vector encoding beta-galactosidase targeted to the nucleus was perfused in the liver of 5 golden retriever dogs. Volumes up to 1,650 ml of fresh or concentrated vector stocks were perfused and the procedure was well tolerated. Gene transfer, observed in 3 of 5 treated dogs when documented on liver biopsy fragments obtained at day 4, involved 0.15-0.6% hepatocytes and persisted at equivalent levels at the time of sacrifice, 6 weeks later. No propagation of the vector to other tissues was detected. These observations suggest that the selective perfusion of the regenerating liver might be considered an alternative to liver transplantation for the treatment of certain severe genetic liver disorders, or for the delivery of a therapeutic protein into the serum.

Animals↗
PubMed1990

Two modes of idiotypic stimulation of T lymphocytes from patients with Chagas' disease: correlations with clinical forms of infection.

Patients with chronic Trypanosoma cruzi infections have peripheral auto-anti-idiotype (Id) T cells that proliferate on exposure to immunoaffinity-purified antibodies against T. cruzi epimastigote antigens (EPI). The responses of some patients' (group 1) peripheral blood mononuclear cells (PBMC) to anti-EPI antibodies from sera of patients with the cardiac form of Chagas' disease (Id-C) were inhibited by chloroquine, but responses of other patients' (group 2) PBMC to Id-C were not inhibited. PBMC responses of both group-1 and -2 patients to anti-EPI antibodies from asymptomatic (indeterminate) patients (Id-I) were inhibited by chloroquine, as were their responses to the antigens in EPI. Most patients (69%) in group 1 had indeterminate Chagas' disease, and 100% of the patients in group 2 had severe, cardiac or digestive Chagas' disease. Both the direct (chloroquine-insensitive) and indirect (processed) modes of stimulation by anti-EPI antibodies required adherent cells. In group 2 (direct stimulation), this requirement was met by exogenous IL-1, and neither anti-HLA-DR,DP(DQ) monoclonal antibody (mAb) nor sodium azide inhibited T-cell proliferation. Indirect Id stimulation of group-1 cells by Id-I or Id-C, and group-2 cells by Id-I or EPI, was inhibited by anti-HLA-DR,DP(DQ) mAb or sodium azide, and exogenous IL-1 alone did not support this processed, MHC-mediated T-cell stimulation, but live adherent cells did. The mode of activation of auto-anti-Id T cells from patients with Chagas' disease depends on the clinical form of infection of both the cell donor and the donor of the stimulating anti-EPI antibodies.

Adult↗
PubMed1990

Rat adrenal gland in experimental American trypanosomiasis: immunocytochemical study of tissue parasitism.

The rat adrenal gland is poorly parasitized during the experimental infection with Y strain of Trypanosoma cruzi. In both cortical and medullary regions, the parasitism peaked at day 10 and was characterized by the predominance of single amastigotes over nests containing 2 or more parasites. After day 10 of infection, the tissue parasitism dropped rapidly to become practically null at day 32 of infection. In cortical tissue, the amastigotes occurred mainly inside the endocrine cells. In the medulla, they found mainly in glial cells and non-identified stromal cells. In both cortex and medulla, inflammatory processes were found till day 20 of infection. Our data do not support the hypothesis that a corticoid rich environment would favor T. cruzi parasitism in adrenal medulla.

Adrenal Cortex↗
PubMed1988

Anti-Trypanosoma cruzi and anti-laminin antibodies in chagasic patients after specific treatment.

The antibody response to Trypanosoma cruzi epimastigote and trypomastigote stages, as well as to laminin, was studied in several groups of chagasic patients. In six patients who were cured of the parasite, the serum antibody titers as revealed by indirect immunofluorescence and hemagglutination tests against epimastigotes (conventional serology) and a complement-mediated lysis test with living trypomastigotes did not differ from those of normal individuals. In seven presumably cured patients, although the complement-mediated lysis test turned negative, conventional serology remained positive. Sera from this group of so-called "dissociated" patients presented significant lower mean antibody titers against epimastigote but not trypomastigote stages than did sera from 14 untreated patients (P less than 0.01). Most of the antibodies against trypomastigotes, including the residual levels found in cured patients, were absorbed by mouse laminin. In fact, significantly higher titers of anti-laminin antibodies were observed in sera from untreated chagasic patients (1.131 +/- 0.458) and cured patients (1.103 +/- 0.572) than in sera from eight normal individuals (0.459 +/- 0.402) (P less than 0.01). The anti-laminin titers were higher in sera of patients of blood group A or O than in those of patients of group B or AB. In Western blotting (immunoblotting) analysis against trypomastigotes, sera from chronic untreated patients recognized many polypeptide bands ranging from 26 to 160 kilodaltons, whereas no protein bands were observed with sera from cured patients. Only faint bands of parasite proteins were observed with sera of dissociated patients. In conjunction, the above data suggest that the anti-trypomastigote antibodies which persist after parasitological cure of patients with Chagas' disease are due mainly to cross-reactive epitopes from mouse laminin.

Animals↗