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Biomedical subjects

G Rossi

Publications and source records attributed to G Rossi.

At least 217 records · Page 12Linked to original sources
PubMed1998

A Pixel-Array Detector for Time-Resolved X-ray Diffraction.

An integrating pixel-array detector for recording time-resolved X-ray diffraction measurements on microsecond timescales has been designed and tested as a 4 x 4 pixel prototype. Operational characteristics and radiation tolerance are discussed. A 100 x 92 array with 151.2 micro m square pixels is currently under construction.

Journal Article↗
PubMed1998

Differential expression of a truncated form of the urokinase-type plasminogen-activator receptor in normal and tumor thyroid cells.

We studied the urokinase-type plasminogen activator (uPA) receptor (uPA-R) in normal and neoplastic human thyroid cells. It has recently been shown that cleaved forms of uPA-R display an extremely strong chemotactic activity. Normal human thyroid TAD-2 cells express the intact form of the uPA-R and a truncated form lacking the uPA-binding domain on their surface, in a similar manner to tumor thyroid cell lines. However, in tumor thyroid cell lines, the amount of the truncated form is variable: high in papillary carcinoma cells, very low in follicular carcinoma cells, and not detectable in anaplastic carcinoma cells. Similar studies on primary cell cultures confirm the presence of the truncated form of uPA-R in normal and in papillary carcinoma cells and its partial or total loss in follicular carcinoma cells. The presence of truncated uPA-R correlates to uPA secretion, except in papillary carcinoma cells, which express the truncated form of uPA-R but do not release uPA. uPA-R is also able to act as an adhesion receptor by binding vitronectin (VTN) and interacting with integrins. We observe that removal of uPA-R from the surface of normal thyroid and anaplastic carcinoma cells by phosphatidylinositol-specific phospholipase C or treatment with anti-uPA-R antibodies decreases the adhesion of both cell types to VTN and, less efficiently, to fibronectin or collagen. On the other hand, uPA treatment strongly increases the adhesion of anaplastic carcinoma cells specifically to VTN.

Cell Adhesion↗
PubMed1998

Relation between therapy for hyperthyroidism and the course of Graves' ophthalmopathy.

BACKGROUND: The chief clinical characteristics of Graves' disease are hyperthyroidism and ophthalmopathy. The relation between the two and the effect of treatment for hyperthyroidism on ophthalmopathy are unclear. METHODS: We studied 443 patients with Graves' hyperthyroidism and slight or no ophthalmopathy who were randomly assigned to receive radioiodine, radioiodine followed by a 3-month course of prednisone, or methimazole for 18 months. The patients were evaluated for changes in the function and appearance of the thyroid and progression of ophthalmopathy at intervals of 1 to 2 months for 12 months. Hypothyroidism and persistent nyperthyroiaism were promptly corrected. RESULTS: Among the 150 patients treated with radioiodine, ophthalmopathy developed or worsened in 23 (15 percent) two to six months after treatment. The change was transient in 15 patients, but it persisted in 8 (5 percent), who subsequently required treatment for their eye disease. None of the 55 other patients in this group who had ophthalmopathy at base line had improvement in their eye disease. Among the 145 patients treated with radioiodine and prednisone, 50 (67 percent) of the 75 with ophthalmopathy at base line had improvement, and no patient had progression. The effects of radioiodine on thyroid function were similar in these two groups. Among the 148 patients treated with methimazole, 3 (2 percent) who had ophthalmopathy at base line improved, 4 (3 percent) had worsening of eye disease, and the remaining 141 had no change. CONCLUSIONS: Radioiodine therapy for Graves' hyperthyroidism is followed by the appearance or worsening of ophthalmopathy more often than is therapy with methimazole. Worsening of ophthalmopathy after radioiodine therapy is often transient and can be prevented by the administration of prednisone.

Adolescent↗
PubMed1998

Fasciola hepatica-induced immune suppression of spleen mononuclear cell proliferation: role of nitric oxide.

The aim of the present study was to evaluate the proliferative response of spleen mononuclear cells (Spm) to mitogens in rats infected with Fasciola hepatica and its correlation with Spm and peritoneal cell (PC) nitric oxide (NO) production on Days 1, 3, 7, 14, 30, and 60 postinfection. In addition, histological changes in the liver were also studied. The proliferative response to Con A of F. hepatica-infected Spm was significantly decreased on Day 7 postinfection (P < 0.01). However, a pronounced increase of the proliferative response was detected from Day 3 until Day 60 when Spm were stimulated with LPS. In order to determine whether NO levels were modified during F. hepatica infections, we quantified nitrite in Spm and PC supernatants in cultures. Our results indicate a profound decrease of nitrite production by LPS-stimulated PC on the first and second weeks postinfection, and an increase in the levels of this mediator on LPS-stimulated Spm at the same postinfection time. The F. hepatica excretory-secretory antigen (ESA) was in part involved in the decrease of nitrite production by LPS-stimulated PC. A mechanism to avoid an immune response during the first stages of liver penetration could explain the transient suppression observed in Spm proliferative responses. On the other hand, the decrease in NO production by rat-infected PC could also be one of the strategies of the parasite to avoid the potential killing effect of NO during peritoneal migration.

Animals↗
PubMed1998

Post-hepatitis primary disease does not influence 6-year survival after liver transplantation beyond 1 year.

Orthotopic liver transplantation (OLT) is used as a definitive treatment for end-stage liver disease and prolonged posttransplant survival has already been reported. The incidence of late mortality and graft morbidity is, however, not well defined and the role of primary viral disease in the long-term follow-up results is not clear. Data of posttransplant follow-up in 213 patients, 156 adults and 57 children, who survived at least 1 year were reviewed in order to define causes of graft dysfunction, graft loss and death. In 98 patients, 103 persistent graft dysfunctions were found. Thirty-four grafts were later lost [28 deaths and 6 successful retransplantations (re-OLT)]. The results were reviewed grouping patients according to their age and viral hepatitis status at the time of the transplantation. HBV-positive patients (51) showed 4 re-OLT (1 HBV), 3 liver-related deaths (2 HBV), 24 graft dysfunctions (8 HBV, 5 HCV), and 85.2% 6-year survival (based on 100% survival at 1 year). HCV-positive adults (28) showed 1 re-OLT, 3 HCV-related deaths, 24 graft dysfunctions (19 HCV), and 68.8% 6-year survival. HBV-HCV-positive patients (14) showed no graft loss and death, 10 graft dysfunctions (7 HCV, 1 HBV, 2 HBV-HCV), and 81.8% 6-year survival. HBV-HCV-negative adults (63) showed 3 non-hepatitis-related re-OLT, 5 liver-related deaths (2 HCV), 24 graft dysfunctions (6 HCV, 2 HBV), and 83.1% 6-year survival. HBV-HCV-negative children (49) showed no re-OLT, 1 HCV-related death, 14 graft dysfunctions (3 HCV), and 92.6% 6-year survival. HCV-positive children (8) showed 1 HCV-related re-OLT, 2 HCV-related deaths, 4 graft dysfunctions (3 HCV), and 81.3% 6-year survival. The main cause of graft dysfunction was hepatitis (45 HCV and 13 HBV), followed by technical complications (21), rejection (16), recurrent alcoholism (3), HIV infection (1), and unknown causes (4). In this long-term post-transplant follow-up series, viral hepatitis led to graft dysfunction in 58/103 (56.3%) cases, late graft failure was viral hepatitis-related in 11/ 20 (55%) cases, and, as a total, HCV infection was present in 45/58 (77.5%) cases of viral hepatitis-related graft damage. Looking at the timing of hepatitis-related graft failure, in 70% of cases death occurred after the 5th post-transplant year. In our experience, the occurrence of hepatitis, particularly HCV induced, was common and led to abnormal graft function, but the 6-year post-transplant survival (based on 100% survival at 1 year) in patients surviving for at least 1 year did not differ on the basis of the pretransplant viral hepatitis status. This finding may be consistent with the slow progression of the viral damage and longer follow-up results remain to be established. Nevertheless, data from the present study suggest that in long-term liver transplant survivors, the risk of deteriorating liver damage and eventual failure after 5 years remains only in those patients experiencing a viral hepatitis infection.

Adolescent↗
PubMed1998

Rescue FK506 early conversion for refractory rejection after pediatric liver transplantation: experience in 20 children.

Tacrolimus (FK506) is an effective and relatively safe novel immunosuppressant able to revert refractory rejection after pediatric liver transplantation (LTx). Between April 1993 and October 1996, 20 pediatric patients were converted to tacrolimus for biopsy-proven, steroid-resistant liver rejection. The mean follow-up was 18 months. The median time from LTx to switch was 20 days. Tacrolimus was administered per os at a mean dosage of 0.23 mg/kg per day to maintain median blood levels of 10.8 ng/ml at 1 week and 9.2 ng/ml at 1 year from the switch. Of the 20 patients, 15 are alive and they all recovered from rejection without the need of OKT3 after conversion. The major causes of death were: one multiorgan failure, two infections (cytomegalovirus Aspergillus), one bowel perforation, and one posttransplant lymphoproliferative disease. One patient experienced late side effects and was reconverted to cyclosporine when she was already rescued from hepatic allograft rejection. The results confirm that an earlier conversion to tacrolimus should be recommended after pediatric liver transplantation in order to revert hepatic allograft rejection with the best safety profile.

Child, Preschool↗
PubMed1998

Lung resection in pediatric patients.

An evaluation of all pediatric patients with primary or secondary pulmonary disease operated upon from January 1993 to July 1996 by the same senior surgeon was carried out. The inclusion criterion was a lung resection in patients aged less than 14 years. Children were divided into two categories according to the neoplastic or non-neoplastic nature of their disease. In the first group a lobectomy was performed for primary lesions and wedge resection for secondary ones. In the second group lobar emphysema and cystic dysplasia were the major indications for lobectomy, while diagnostic wedge resections were performed for interstitial/infiltrative lesions. Several groups of techniques were identified according to the type of approach and the suture method. Video-assisted thoracoscopic surgery and a muscle-sparing approach were compared to classic posterolateral thoracotomy. The mechanical stapler-suturing method was compared to the manual suturing. Our results demonstrate the importance of mechanical suturing, particularly in decreasing anesthesia time and reducing the risk of dehiscence. The minimally invasive approach associated with mini-thoracotomy was particularly useful for patients with reduced oxygen saturation due to ventilatory and gas-exchange problems. The roles of staplers in lung parenchymal resection and minimally invasive procedures for improving the postoperative thoracic compliance of pediatric patients are stressed.

Adolescent↗
PubMed1998

Expression of GM-CSF receptor and "in vitro" effects of GM-CSF on human fibroblasts.

In the present study the effects of Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) on fibroblast growth and activity have been studied. In this regard the AA have evaluated in primary cultures of human gengival normal fibroblasts (PG1 cells): a)-the expression of GM-CSF receptor (GM-CSFR) (alfa unit) on the cell surface; b)-the in vitro effects of different doses of GM-CSF on the GM-CSFR expression and on the proliferation and activity of fibroblasts. PG1 cells have been stimulated in vitro with different concentrations of GM-CSF (10, 50, 80, 100 and 150 ng/ml) using promonocytic cell line U937 as positive control for GM-CSFR expression. GM-CSFR was investigated by flow cytometry, with mouse monoclonal antibody (mAb) against the alfa chain of the human GM-CSFR and fluorescein-conjugated goat antimouse immunoglobulin G (IgG). At high GM-CSF concentration (80 ng/ml) the AA observed: 1)-A marked increase of GM-CSFR expression evaluated as fluorescence intensity (about three fold in respect to the controls); 2)-Maximal increase of PG1 cells proliferation. Moreover immunofluorescence on fibroblasts obtained from culture plates showed increased actin stress fibers and fibronectin production with low stimulation by GM-CSF, while higher concentration of this cytokine determined increased proliferation of cells, but a decreased formation of actine fibers and vinculin plaques. These results demonstrate: 1)-The presence of GM-CSFR on the surface of fibroblasts; 2)-The proliferation and the synthesis activity of these cells (in vitro) are modulated by different concentration of GM-CSF. We hypothesize that GM-CSF until 80 ng/ml can upregulate the expression of the receptor. Therefore, on the basis of previous findings of high serum levels of GM-CSF in course of scleroderma, a disease characterized by fibroblast hyperactivity, a possible role of this cytokine in the pathogenic process of this disease can be hypothesized.

Animals↗