PubMed Health⌕ Search

Biomedical subjects

A Rizzo

Publications and source records attributed to A Rizzo.

At least 19 recordsLinked to original sources
PubMed1995

Multiple actions of the coumarine derivative cloricromene and its protective effects on ischemic brain injury.

The effects of different doses (0.25, 0.5, 1 and 2 mg/kg i.p.) of cloricromene, a coumarine derivative, have been investigated on brain malondialdehyde levels, brain edema, myeloperoxidase activity, survival, locomotor hyperactivity and hippocampal neuronal loss following transient cerebral ischemia induced by temporary bilateral carotid occlusion in the Mongolian gerbil. Cloricromene reduced brain lipid peroxidation, measured through the evaluation of malondialdehyde (-82.9% with the highest dose), and the formation of post-ischemic brain edema, evaluated by water content. The increase in myeloperoxidase activity observed in the hippocampus of postischemic animals was also reduced: 0.7 +/- 0.3 U x 10(-3) vs. 3.3 +/- 0.3 U x 10(-3)/g tissue. The same treatment increased survival and reduced hyperactivity linked to neurodegeneration induced by cerebral ischemia and reperfusion. Histological observations of the pyramidal layer of CA1 showed a reduction of neuronal loss in animals that received the drug before occlusion but not in those that were treated after the occlusion. These results show that cloricromene, a drug with multiple actions, improves brain injury induced by transient cerebral ischemia.

Animals↗
PubMed1995

Growth factor and procollagen type I gene expression in human liver disease.

BACKGROUND/AIMS: Growth factors have been implicated in the pathogenesis of liver fibrosis, a major determinant of the clinical course of chronic liver disease. The aim of this study was to study the relationship of growth factor expression to inflammation and fibrosis in a variety of human liver diseases. METHODS: We studied by in situ hybridization the expression of transforming growth factor (TGF) beta 1, platelet-derived growth factor (PDGF) A and PDGF-B, and procollagen type I (pro-I) messenger RNAs (mRNAs) in liver diseases of various etiologies. RESULTS: Pro-I mRNA was expressed by mesenchymal cells at sites of inflammation and scarring, where TGF-beta 1 immunoreactivity was often found, and by perisinusoidal cells. TGF-beta 1 and PDGF-A mRNAs were expressed mainly by mononuclear cells and proliferating ductular cells. TGF-beta 1 mRNA was also expressed by perisinusoidal cells. PDGF-A gene expression was more common than that of PDGF-B. Pro-I and TGF-beta 1 expression correlated with both ductular proliferation and tissue inflammation, whereas PDGF-A and PDGF-B only correlated with ductular proliferation. CONCLUSIONS: Our data suggest that TGF-beta 1 and PDGF are involved in human liver inflammation and fibrosis. The expression of growth factor mRNAs in proliferating ductular cells may indicate a role for these cells in liver fibrogenesis and may help explain the pathophysiology of conditions such as biliary atresia progressing to fibrosis despite the absence of marked inflammation.

Gene Expression↗
PubMed1995

KP1/CD68 expression in malignant neoplasms including lymphomas, sarcomas, and carcinomas.

Expression of KP1/CD68 macrophage-associated antigen in a series of 840 selected malignant neoplasms, including immunomorphologically characterized cases of non-Hodgkin's lymphoma (NHL) (434), Hodgkin's disease (HD) (115), soft tissue sarcoma (147), carcinoma (49), and other tumors (95), was examined. KP1 expression was detected in a significant number of NHLs (107 of 434; 24.7%), most of them (65 of 107; 60.7%) of the diffuse small cell subtype. Only 14 of the 155 large cell lymphomas, compared to 10 of the 51 Ki-1/CD30+ anaplastic large cell (ALC) lymphomas examined, were KP1 positive. Conversely, none of the T-lineage NHL--other than Ki-1/CD30+ ALC lymphomas--or the HD cases tested was labeled by KP1 antibody. Among the other neoplasms tested, KP1 was reactive with a variable proportion of cases of malignant fibrous histiocytoma (19 of 24; 79.2%), malignant schwannoma (8 of 22; 36.4%), liposarcoma (3 of 9; 33.3%), leiomyosarcoma (8 of 37; 21.6%), cutaneous or metastatic melanoma (51 of 73; 69.9%), and renal cell carcinoma (3 of 5; 60%). These results indicate that KP1 shows a relatively wide spectrum of immunoreactivity with malignant neoplasms of presumed non-histiocyte origin, thus arguing against its expected specificity and high value in diagnostic pathology. Although the significance of KP1 expression by some subsets of NHLs remains to be elucidated, its close association with B-cell NHLs, mostly of the diffuse small cell type, should stimulate further pathologic and clinical investigations.

Antibodies, Monoclonal↗
PubMed1995

Platelet-activating factor increases vascular resistance in rat hindquarters by thromboxane A2.

The effects of platelet-activating factor (PAF) on vascular resistance and capillary permeability were studied in the isolated rat hindquarter. Six groups were studied (n = 30): control; PAF alone (1.4 microM); and PAF (1.4 microM) pretreated with ibuprofen (30 mg/kg), thromboxane A2 (TxA2)-receptor antagonist (BM-13505, 2 mg/kg), PAF-receptor antagonist (WEB-2086, 5 mg/kg), or dexamethasone (5 mg/kg). The vascular resistance was calculated, and the reflection coefficient (sigma) was determined as an index of capillary permeability. Exogenous PAF caused a threefold increase in vascular resistance peaking at 5 min and a 2.5-fold increase in capillary permeability. The increased vascular resistance caused by PAF alone was significantly attenuated by ibuprofen, BM-13505, and dexamethasone. The PAF-induced permeability was neither attenuated by ibuprofen nor BM-13505. However, both the increased vascular resistance and permeability were blocked and attenuated by WEB-2086 and dexamethasone, respectively. We conclude that TxA2 mediates the PAF-induced increased vascular resistance; however, the increased vascular permeability is independent of the formation of TxA2 in the isolated hindquarter.

Animals↗
PubMed1995

Adenosine A2 receptors reverse ischemia-reperfusion lung injury independent of beta-receptors.

To evaluate the adenosine systems ability to reverse the endothelial damage produced by ischemia and reperfusion (I/R), we studied several different selective adenosine-receptor agonists and antagonists, a protein kinase A inhibitor, and a beta-adrenoreceptor antagonist in isolated buffer-perfused rat lungs. I/R (45 min/105 min) produced a sixfold increase in endothelial permeability as measured by the capillary filtration coefficient. Both a selective A2-receptor agonist (CGS-21680, 300 nM) and a beta-receptor agonist (isoproterenol, 10 microM) reversed the increased microvascular permeability. A nonselective adenosine-receptor antagonist (SPT, 20 microM) and a selective A1-receptor antagonist (DPCPX, 10 nM) had no effect on increased microvascular permeability. Also, isoproterenol and CGS-21680 reversed the damage being introduced after a selective A1-receptor agonist (CCPA, 100 nM). The nonspecific adenosine A1- and A2-receptor agonist NECA (12 nM) appeared to desensitize the A2 receptors and a protein kinase A inhibitor, adenosine-3',5'-cyclic monophosphothioate (Rp-cAMPS, 100 microM), blocked the reversal of endothelial damage by isoproterenol or A2-receptor agonist. Propranolol (100 microM) blocked the effect of isoproterenol but not the effect of CGS-21680. From this study we conclude that A2-receptor activation reverses endothelial damage associated with I/R by a mechanism independent of beta-receptors or Gi protein. However, a protein kinase A-3',5',-cyclic adenosine monophosphate pathway is activated by both the adenosine systems and beta-receptor activation.

Adenosine↗
PubMed1993

Co-expression of Epstein-Barr virus latent membrane protein and vimentin in "aggressive" histological subtypes of Hodgkin's disease.

The presence of Epstein-Barr virus (EBV) genome in Hodgkin's and Reed-Sternberg (HRS) cells, as detected using in situ hybridization (ISH) with biotinylated BamHI "V" probes, along with the expression of EBV-encoded latent membrane protein (LMP) and vimentin was examined in paraffin-embedded sections of 39 immunomorphologically characterized cases of Hodgkin's disease (HD). ISH demonstrated EBV in HRS cells in 15 of 39 cases, whereas LMP expression was detected in 11 of 39 cases, only in the presence of EBV genome detection. With the exception of 1 case, in which HRS cells expressed B-cell-associated antigens, the LMP-positive cases included specimens in which HRS cells were of non-B, non-T phenotype. LMP expression showed a stronger association with lymphocyte depletion (LD) (3/3) and mixed cellularity (MC) (6/11) than with lymphocyte predominance (0/5) or nodular sclerosis (2/20) subtypes. Vimentin expression on HRS cells was found in all the LMP-expressing cases and only in a fraction (13/28) of LMP-negative cases. This study supports the view that HD represents a heterogeneous group of diseases also in terms of EBV association, LMP expression being strongly related to the "aggressive" LD and MC histological subtypes. In light of the supposed interactions between vimentin and LMP, their co-expression on HRS cells, as detected in this study, provides further evidence for a significant role of EBV in the development of a proportion of HD cases.

Antigens, CD↗
PubMed1993

Immunocytochemical demonstration of calmodulin and its activated forms in normal and carcinomatous human mammary tissue.

Using an indirect immunoperoxidase technique with a polyclonal antibody (CaMp) for calmodulin (CaM) and monoclonal antibodies against CaM activated form of cyclic nucleotide phosphodiesterase (ACAP-1) and calcium activated CaM (ACC-1), we have investigated the distribution pattern of this calcium-binding protein on frozen and paraffin sections of ductal non-infiltrating (20 cases) and infiltrating carcinomas (39 cases), lobular in situ (3 cases) and infiltrating carcinomas (8 cases); 10 metastatic axillary lymph nodes were also studied, while normal breast tissue surrounding neoplasias was tested as a control. All cases of non-infiltrating as well as infiltrating ductal and lobular carcinomas were reactive with the above-mentioned antisera, although a marked variation both in the proportion of cells stained within a tumour and in the intensity of staining of the cells was noted; the immunoreactivity showed a diffuse cytoplasmic pattern but sometimes nuclear with CaMp and ACC-1, while ACAP-1 exhibited mostly a cytoplasmic perinuclear granular expression; the same immunohistochemical pattern for CaM and CaM activated forms was observed also in metastatic elements present in axillary lymph nodes. Normal breast acini were patchily reactive for ACAP-1, whereas CaMp and ACC-1 stainings were more diffuse.

Adult↗
PubMed1992

Na+/K+/Cl- cotransport in resealed ghosts from erythrocytes of the Milan hypertensive rats.

The erythrocytes (RBC) of the Milan hypertensive rats (MHS) have a smaller volume and faster Na+/K+/Cl- cotransport than RBC from normotensive controls (MNS). The difference in Na+/K+/Cl- cotransport is no longer present in inside-out Vesicles (IOV) of RBC membrane. To differentiate between cytoplasmic or membrane skeleton abnormalities as possible causes of these differences. Resealed ghosts (RG) were used to measure ion transport systems. The following results have been obtained: (1) RG from MHS have a smaller volume than MNS (mean +/- S.E. 20.7 +/- 0.45 vs. 22.09 +/- 0.42 fl, P < 0.05). (2) RG showed a bumetanide-sensitive Na efflux that retains the characteristics of the Na+/K+/Cl- cotransport of the original RBC: it is K(+)- and Cl(-)-sensitive and dependent on the intracellular Na+ concentration. (3) The Na+/K+/Cl- cotransport was faster in RG from MHS than in those from MNS (mean +/- S.E. 0.095 +/- 0.01 vs. 0.066 +/- 0.01 rate constant h-1, P < 0.01). These results, together with those of IOV, support the hypothesis that an abnormality in the membrane skeletal proteins may play a role in the different Na+/K+/Cl- cotransport modulation between MHS and MNS erythrocytes.

Animals↗
PubMed1992

Immunohistochemical study on the pattern of 50 kd cytokeratin in psoriasis.

Three biopsies of normal skin and 15 biopsies collected from patients with psoriasis vulgaris were analyzed for the expression of the 50 kd cytokeratin using direct immunofluorescence and ABC technique before and after local treatment with anthralin 0.1% in a petrolatum base, with 0.05% betamethasone dipropionate cream, and finally, after PUVA treatment. Antiserum against the 50 kd anti-cytokeratin reacted with tissue sections of normal skin, staining cells in the basal layer, while the psoriatic skin sections before the various treatments showed a staining concerning the whole thickness of the epidermis. After the various therapies, the 50 kd cytokeratin immunoreactivity was observed only in the basal layer of those psoriatic skin sections that showed complete clinical clearing, while it was observed in the whole thickness of psoriatic patches that did not clear. These data suggest that the normalization of the 50 kd cytokeratin expression pattern can be considered as a marker of clinical remission of psoriasis.

Administration, Topical↗
PubMed1992

Passive immunization with antibodies against tumor necrosis factor (TNF-alpha) protects from the lethality of splanchnic artery occlusion shock.

Splanchnic artery occlusion shock was induced in anesthetized rats by clamping splanchnic arteries for 45 min. Survival rate, serum and macrophage tumor necrosis factor (TNF-alpha), peritoneal macrophage phagocytosis, and killing activities were evaluated. Shocked rats died within 2 hr, whilst all sham-shocked rats survived more than 6 hr. Serum and macrophage TNF-alpha was undetectable in sham-shocked rats while shocked rats exhibited increased serum (110 +/- 5 U/ml 90 min after release of occlusion) and macrophage levels (122 +/- 4.5 U/ml 90 min after release of occlusion) of TNF-alpha. Furthermore, splanchnic artery occlusion shock produced cardiovascular changes, reduced macrophage phagocytosis (23 +/- 4.6%) and killing (6 +/- 1.1%) activities, and induced a massive necrosis of the ileum. A passive immunization with a hyperimmune serum containing antibodies against murine TNF-alpha significantly protected rats from the lethal effects of splanchnic artery occlusion shock, lowered serum TNF-alpha (6 +/- 2.1 U/ml), and completely reverted the impairment in peritoneal macrophage phagocytosis (48 +/- 4.8%) and killing (13 +/- 1.5%) activities. In addition passive immunization had beneficial effects on the cardiovascular changes occurring during splanchnic artery occlusion shock and prevented necrosis of the ileum induced by this model of shock. By contrast, pretreatment with polymyxin B, an "antiendotoxin" antibiotic, did not modify the lethal effects and the TNF-alpha production induced by splanchnic artery occlusion shock. Furthermore, endotoxin was undetectable in the blood of splanchnic artery occlusion shocked rats. These findings are consistent with the involvement of TNF-alpha in splanchnic artery occlusion shock and suggest that the cytokine represents an important mediator of non-septic shock.

Animals↗
PubMed1992

Iron-binding proteins in human colorectal adenomas and carcinomas: an immunocytochemical investigation.

By immunocytochemistry, the presence of major iron-binding proteins (lactoferrin, transferrin and ferritin) was investigated in tubular adenomas (12 cases), villous adenomas (7 cases), carcinomas of the large bowel and rectum (39 cases) and lymph nodes involved in carcinomas (8 cases); 5 samples of colonic inflammatory pseudopolyps were also studied. Dysplastic areas of tubular and villous adenomas as well as adenocarcinomas and colloid carcinomas showed a variable cytoplasmic immunoreactivity for all antisera, although no staining was noted in some cases; tubular adenomas without dysplasia and colonic inflammatory pseudopolyps were always unstained. Metastatic elements present in lymph nodes maintained the immunohistochemical staining for iron-binding proteins. An autoctone production of lactoferrin, transferrin and ferritin by tumour cells may be hypothesized in relation to the increased requirement of iron for the turnover of rapidly dividing cells.

Adenoma↗
PubMed1991

Accuracy and response time of a portable pulse oximeter. The Pulsox-7 with a finger probe.

We studied the performance of a portable pulse oximeter in 123 consecutive adult patients by spot-checking with a finger probe and by spectrophotometry of oxygen saturation on a simultaneous arterial blood sample. 88 patients were overtly hypoxemic (HbO2 less than 90%) and 26 showed severe hypoxemia (HbO2 36-70%). The differences between the two methods showed a skewed distribution with a positive tail due to the over-estimation of lower saturation values by the pulse oximeter. Overall, the 95% confidence interval for the median difference ranged from -0.6 to +0.5%. The limits of agreement (distribution-free 95% confidence interval for the sample) were -5.8 to +11.6%. Pulse oximetry can be recommended as a first assessment of the respiratory balance only if a cut-off value of HbO2 equal to 90% in nonsmoking, air-breathing subjects is acceptable. The finger probe implies a response delay of approximately 30 s, making the instrument rather insensitive to short hypoxemic transients. With a predictive value around 90%, the pulse oximeter may be a useful portable screening tool.

Adolescent↗
PubMed1991

A 220 kDa coelomocyte aggregating factor involved in Holothuria polii cellular clotting.

Agglutinating molecules are released by Holothuria polii coelomocytes. In our in vitro system we observe that release depends on the number of coelomocytes but it seems not to be time- and temperature-dependent. The factor responsible for agglutination was isolated from an Edds isotonic solution coelomocyte suspension medium and purified by ammonium sulfate precipitation, gel filtration and ion exchange chromatography; it had a molecular mass of about 220 kDa on an sodium dodecyl sulfate polyacrylamide gel. The purified factor agglutinates sea cucumber coelomocytes suggesting that it could be involved in the first phase of clotting events.

Agglutination↗
PubMed1990

[Handicapped and oral pathology. Clinico-statistical survey].

Dental and periodontal conditions of 80 handicapped adults were examined. The epidemiological survey was made by following the WHO suggestions and showed that there are patients in great need of primary and secondary prevention. The results of the research point out a DMFT of 18.78 and extractions were practically the only dental therapy received by these specific patients. Periodontal diseases were surveyed by the use of the CPITN index, and exhibited high values of dental calculus in younger. Furthermore, as the patients increased in age, periodontal pockets appeared and edentulous patients increased.

Adult↗