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Biomedical subjects

P Grillo

Publications and source records attributed to P Grillo.

10 recordsLinked to original sources
PubMed2006

Effects of exposure to air pollution on blood coagulation.

BACKGROUND: Consistent evidence has indicated that air pollution increases the risk of cardiovascular diseases. The underlying mechanisms linking air pollutants to increased cardiovascular risk are unclear. OBJECTIVES: We investigated the association between the pollution levels and changes in such global coagulation tests as the prothrombin time (PT) and the activated partial thromboplastin time (APTT) in 1218 normal subjects from the Lombardia Region, Italy. Plasma fibrinogen and naturally occurring anticoagulant proteins were also evaluated. METHODS: Hourly concentrations of particulate (PM10) and gaseous pollutants (CO, NO2, SO2, and O3) were obtained from 53 monitoring sites covering the study area. Generalized additive models were applied to compute standardized regression coefficients controlled for age, gender, body mass index, smoking, alcohol, hormone use, temperature, day of the year, and long-term trends. RESULTS: The PT became shorter with higher ambient air concentrations at the time of the study of PM10 (coefficient = -0.06; P < 0.05), CO (coefficient = -0.11; P < 0.001) and NO2 (coefficient =-0.06; P < 0.05). In the 30 days before blood sampling, the PT was also negatively associated with the average PM(10) (coefficient = -0.08; P < 0.05) and NO2 (coefficient = -0.08; P < 0.05). No association was found between the APTT and air pollutant levels. In addition, no consistent relations with air pollution were found for fibrinogen, antithrombin, protein C and protein S. CONCLUSIONS: This investigation shows that air pollution is associated with changes in the global coagulation function, suggesting a tendency towards hypercoagulability after short-term exposure to air pollution. Whether these changes contribute to trigger cardiovascular events remains to be established.

Adolescent↗
PubMed2006

Polymorphisms in Th1-type cell-mediated response genes and risk of gastric cancer.

Helicobacter pylori infection, the dominant risk factor for gastric cancers, has been shown to elicit T helper type 1 (Th1) polarized immunological responses. We conducted a population-based study of 305 gastric cancer cases and 427 age- and gender-matched controls in Warsaw, Poland, to evaluate the association with several variants in genes responsible for Th1-cell-mediated response. Genotyping was performed on genomic DNA by TaqMan(TM) assays to determine TNFA (-308 G>A, -417 G>A, -555 G>A, -1036 C>T, -1042 C>A, -1210 T>C), IL1A (-889 C>T), IFNGR2 (Ex7-128 T>C, Ex2-34 C>G and Ex2-16 A>G) and IL12A (IVS2-798 T>A, IVS2-701 C>A and Ex7+277 G>A) polymorphisms. We used unconditional logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs), adjusting for sex, age, education and smoking status. Out of six single nucleotide polymorphisms (SNPs) tested in TNFA, gastric cancer risk was significantly associated with the TNFA (-308 G>A) polymorphism, with ORs of 1.4 (95% CI: 1.0-2.0) for the G/A and 2.5 (95% CI: 1.3-4.9) for the A/A genotype carriers, when compared with the more frequent genotype (G/G) (P-trend < 0.001). Among the three tested SNPs in the IFNGR2 gene, only the Ex7-128C>T polymorphism was associated with increased risk, with ORs of 1.5 (95% CI: 1.0-2.3) for T/C and 1.7 (95% CI: 1.1-2.7) for C/C carriers when compared with T/T carriers (P-trend = 0.01). Subjects carrying both IFNGR2 Ex7-128 C/C and TNFA -308 A/A genotypes had the highest risk (OR = 5.5, 95% CI: 1.5-19.4), although the interaction was not statistically significant. IL1A (-889 C>T) and the three examined IL12A variants were unrelated to gastric cancer risk. Our findings suggest that two Th1-related polymorphisms (TNFA -308 A>G and IFNGR2 Ex7-128 C>T) may increase the risk of gastric cancer.

Adult↗
PubMed2006

[Intracerebral haemorrhage, what's new?].

Haemorrhagic stroke is frequent and associated with a high mortality and morbidity. Less than 30% of patients are still alive five years after onset and few patients regain functional independence. The worsening effect of anticoagulation has been demonstrated and the failure to rapidly normalize coagulation further increases haematoma expansion. In a recent phase II trial, recombinant activated factor VII given within 4 hours of stroke onset, reduced haematoma growth, mortality and disability. An aggressive blood pressure and intracranial pressure control early after the haemorrhage seems beneficial. A large prospective randomized study (the STICH trial) did not demonstrate any beneficial effect of surgery.

Animals↗
PubMed2001

Arrhythmogenic right ventricular cardiomyopathy: clinicopathologic correlation based on a revised definition of pathologic patterns.

Different morphologic features of arrhythmogenic right ventricular cardiomyopathy (ARVC) have been described. However, it is still unclear whether they correspond to distinct forms of the same disease. A pathologic study was performed on a series of ARVC (15 from heart transplant and 12 from autopsy) from 2 Italian referral university hospitals. Based on both myocellular features and the nature of myocardial replacement, hearts were divided into 2 groups: infiltrative, with a lacelike pattern of transmural fatty infiltration and strands of normal residual cardiomyocytes (n = 11); and cardiomyopathic, with massive myocardial replacement by fibro fatty tissue and cardiomyopathic changes (such as hypertrophy and myofibril loss) of residual cardiomyocytes (n = 16). Hearts from the infiltrative group were mostly obtained at autopsy of patients who died suddenly. Fatty substitution was limited almost exclusively to the right ventricle. Mitral valve dysplasia (prolapse or cleft) was frequently present. Hearts from the cardiomyopathic group came mainly from heart transplants for congestive heart failure. Fibro fatty replacement was more extensive, usually biventricular. Active myocarditis and features suggestive of myocardial transdifferentiation were also observed. Despite these differences in clinical outcome and morphologic features, patients from the 2 groups showed similar mean age, sex distribution, occurrence of threatening ventricular arrhythmias, and prevalence of family history of sudden death, arrhythmias, or cardiomyopathy. Infiltrative and cardiomyopathic patterns represent different clinical and pathologic subsets of ARVC. Myocellular features are an important clue in the distinction between the two entities. The differentiation between the 2 patterns is feasible on endomyocardial biopsy and could give important prognostic information.

Adipose Tissue↗
PubMed1989

Absence of cinoxacin-induced DNA fragmentation and mutations in the rat granuloma pouch.

The mutagenic and DNA-damaging activities of cinoxacin were evaluated in the rat granuloma pouch assay (GPA) in order to assess its genotoxic potential in vivo. High doses of this antimicrobial quinolone, either directly injected into the pouch or administered by gavage, did not induce mutation at the hgprt locus or DNA fragmentation in granuloma cells. Moreover, DNA damage was absent in the liver and kidney of rats given cinoxacin by the oral route.

Animals↗
PubMedDate not supplied

DNA damage in stomach, kidney, liver and lung of rats treated with atrazine.

The genotoxic activity of atrazine, a widely used triazine herbicide, was assayed by the DNA alkaline elution technique in rats given orally a single high dose or repeated daily doses. DNA breaks (and/or alkali-labile lesions) were detected in cell suspensions obtained from stomach, kidney and liver, but not in those from lung.

Animals↗
PubMedDate not supplied

Eosinophilic infiltration immediately following transplantation: recurrent hypersensitivity reaction?

Hypersensitivity myocarditis is a well-known complication of pharmaceutical therapy, often requiring heart transplantation. We report the unusual case of pre-transplant hypersensitivity myocarditis with eosinophilic myocardial infiltration in the donor heart, demonstrated by needle biopsy at the time of transplant ('time-zero' biopsy). At first the myocarditic process was temptatively attributed to a pre-transplant pathology in the donor heart, but the close similarity between the pre-transplant and the post-transplant infiltrate and the clinical data of an eosinophilic peak of the recipient during the transplant procedure brought to the diagnosis of early recurrent hypersensitivity myocarditis.

Adult↗