30,816 research outputs found
Pentraxin 3 : a multifunctional soluble pattern recognition receptor involved in inflammation and tissue remodelling
No full textnul
Disturbo di panico e condizioni mediche generali
No full textObjective. While there is accumulating literature on the association between panic disorder (PD) and high utilization of health care services, few papers have focused on the medical comorbidity associated with PD. The aim of the present study is to compare the clinical characteristics in PD patients with and without medical comorbidity. Methods. 108 out-patients with a principal diagnosis of PD (DSM-IV; SCID) were included in the present study: of them, 27 with and 81 without medical comorbidity. All patients were assessed using a semistructured clinical interview for: 1) socio-demographic data; 2) Axis I and Axis II diagnosis (SCID-I and II); 3) clinical features of PD. For statistical comparison the sample was divided into two groups according to the presence or absence of associated medical diseases. Results. We found that most common pathologies were cardiovascular followed by gastroenteric and respiratory. No differences were observed in sociodemographic features. Clinically Sheehan Clinician Rated Anxiety Scale (SCRAS) scores were significantly higher for DP patients with medical illnesses in comorbidity. Concerning symptomatolgy of attack "dyspnea, asphyxia sensation" and "sudden blush or chill" were significantly more frequent in PD patients with medical comorbidity. Discussion. Our study confirms that DP is frequently complicated by comorbidity with medical diseases, principally cardiovascular and gastroenteric pathologies. PD with medical diseases associated is a more serious form with specific symptomatological characteristics
DEFICIENCY OF THE SOLUBLE PATTERN RECOGNITION RECEPTOR PENTRAXIN-3 INCREASES SUSCEPTIBILITY TO TUMOR GROWTH AND METASTASIS
No full textThe long pentraxin PTX3 is a multifunctional soluble pattern recognition receptor involved in innate immunity, inflammation, tissue remodelling and female fertility. Moreover PTX3 binds fibroblast growth factor-2 (FGF-2) and inhibits its angiogenic activity. PTX3 is elevated in several pathological conditions reflecting in particular the involvement of the vascular bed as ischemic heart disease, atherosclerosis, small vessel vasculitis and preeclampsia. PTX3 plasma levels are elevated in cancer patients, such as in soft tissue liposarcoma and chondrosarcoma. As PTX3 is a structural component of the cumulus oophorus extracellular matrix in human and mouse, through the interaction with hyaluronic acid binding proteins TNF- α -stimulated gene-6 (TSG-6) and inter-α-trypsin inhibitor (IαI), we hypothesized that PTX3 could be a component of other extracellular matrices such as in the tumor stroma. Moreover, being produced by tumor stromal cells (endothelial cells, fibroblasts, leukocytes), PTX3 could play a role in modulating inflammation associated with tumor growth. To address the involvement of PTX3 in tumor growth, we used a model of non immunogenic and metastatic murine fibrosarcoma (MN/MCA1) and we observed an increased tumor growth and metastatic potential associated with PTX3 deficiency. Moreover in a model of immunogenic fibrosarcoma (MCA203) we observed an accelerated tumor growth in PTX3 knock out mice compared to wild type mice. Mechanisms potentially involved in the mentioned phenotypes range from regulation of angiogenesis and inflammation to organization of the extracellular matrix (ECM) through the direct interaction with ECM components and are currently under investigation. The preliminary results obtained in this study suggest that PTX3 could be a potential therapeutic target in tumor growth
First trimester PTX3 levels in women who subsequently develop preeclampsia and fetal growth restriction
No full textPentraxin 3 (PTX3) and C-reactive protein (CRP) levels were measured in the first trimester of pregnancy in women who
subsequently developed preeclampsia (PE, n 16) and fetal growth restriction (FGR, n 12) requiring iatrogenic delivery before 37 weeks, and those who had uncomplicated pregnancies delivering at term (n 60). Mean PTX3 levels were significantly higher in women who subsequently developed PE (7.31 ng/ml, SD 4.12) when compared to those with
normal pregnancy outcome (4.92 ng/ml, SD 1.94, p 0.0046). There were no significant differences between PTX3 levels in women with FGR (4.82 ng/ml, SD 2.35) compared to normal pregnancy outcome (p 0.88). The median CRP levels did not vary significantly between the three groups (p 0.26). PTX3 levels in women who subsequently develop PE are already elevated in the first trimester, but not in those that develop FGR. This supports the hypothesis of an excessive
maternal inflammatory response to pregnancy in the etiology of PE
Bias in macrophage activation pattern influences non-alcoholic steatohepatitis (NASH) in mice
No full textIn humans, there is large inter-individual variability in the evolution of NAFLD (non-alcoholic fatty liver disease) to NASH (non-alcoholic steatohepatitis). To investigate this issue, NASH was induced with an MCD (methionine–choline-deficient) diet in C57BL/6 and Balb/c mice that are characterized by different biases in Th1/Th2 and macrophage (M1/M2) responses. Following 4 weeks on the MCD diet, steatosis and lobular inflammation were prevalent in C57BL/6 (Th1, M1 oriented) than in Balb/c (Th2, M2 oriented) mice. Consistently, hepatic TNFα (tumour necrosis factor α) mRNA expression and circulating TNFα levels were higher in MCD-fed C57BL/6 than in MCD-fed Balb/c mice. The Th1/Th2 bias did not account for the increased NASH severity, as in both strains MCD feeding did not significantly modify the liver mRNA expression of the Th1 markers IFNγ (interferon γ) and T-bet or that of the Th2 markers IL-4 (interleukin 4) and GATA-3. Conversely, MCD-fed C57BL/6 mice displayed higher liver mRNAs for the macrophage M1 activation markers iNOS (inducible NO synthase), IL-12p40 and CXCL10 (CXC chemokine ligand 10) than similarly treated Balb/c mice, without effects on the M2 polarization markers IL-10 and MGL-1 (macrophage galactose-type C-type lectin-1). Circulating IL-12 was also higher in MCD-fed C57BL/6 than in MCD-fed Balb/c mice. The analysis of macrophages isolated from the livers of MCD-fed animals confirmed an enhanced expression of M1 markers in C57BL/6 mice. Among all of the MCD-treated mice, liver iNOS, IL-12p40 and CXCL10 mRNA levels positively correlated with the frequency of hepatic necro-inflammatory foci. We concluded that the macrophage M1 bias in C57BL/6 mice may account for the increased severity of NASH in this strain, suggesting macrophage responses as important contributors to NAFLD progression.</jats:p
PTX3 as a potential endothelial dysfunction biomarker for severity of preeclampsia and IUGR
No full textEndothelial dysfunction typical of preeclampsia (PE) is the result of an excessive maternal inflammatory response to pregnancy. We investigated PTX3 in maternal, fetal and placental compartments in complicated pregnancies. Maternal blood samples were collected during the third trimester in 53 PE, 43 IUGR (intrauterine growth restriction) and 50 normal pregnancies. Fetal samples were collected from the umbilical vein in 26 PE, 23 IUGR and 26 normal pregnancies at elective cesarean section. Pattern and site of expression of PTX3 were studied by immunohistochemistry (IHC) on placenta, decidual bed and maternal peritoneum. PE and IUGR pregnancies had significantly higher maternal PTX3 levels compared to normal pregnancies, with IUGR significantly lower than PE. Maternal peritoneum expressed a significantly higher signal in the endothelium of pathological compared to normal pregnancies. The maternal increase of PTX3 correlated with the severity of disease with higher PTX3 concentrations in severe PE. Increased PTX3 levels in PE and IUGR mothers, together with IHC data represent the expression of altered endothelial function on the maternal side. IUGR fetuses had higher PTX3 values than controls and the increase was related to IUGR severity, likely reflecting the hypoxic environment. These data confirm the relevance of PTX3 in support the hypothesis that PE is a disease associated with altered maternal endothelial function. The PTX3 increase in IUGR fetuses deserves further investigation
- …
