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Dionysios J Papachristou

Publications and source records attributed to Dionysios J Papachristou.

10 recordsLinked to original sources
PubMed2006

Chronic alcohol consumption is a major risk factor for pancreatic necrosis in acute pancreatitis.

BACKGROUND: Much of the late morbidity and mortality of acute pancreatitis (AP) is attributed to complications of pancreatic necrosis (PNEC). Early diagnosis of PNEC in high-risk patients is critical to management. Hemoconcentration is one risk factor for PNEC, but additional risk factors are likely implicated. AIMS: (1) To evaluate a series of preselected clinical factors in a prospectively collected cohort with AP to identify risk factors for PNEC and (2) to verify the relative risk of any newly identified factor(s) by retrospective analysis of a large patient cohort. METHODS: Phase I: 102 AP patients were prospectively ascertained, of which 77 (mean age 49 yr; 35 women, 42 men) underwent contrast-enhanced computerized tomography (CECT) and were studied. Eleven subjects developed PNEC (14%). Binary logistic regression was performed to identify any clinical factors associated with PNEC. Phase II: 1,474 anonymized patients admitted to the hospital with a diagnosis of AP were electronically reviewed to identify 359 subjects (mean age 54 yr; 157 women, 202 men) with AP and CECT. Seventy-six of these patients (21%) exhibited CECT evidence of PNEC. The associations found in the Phase I group were compared with Phase II by logistic regression analysis. RESULTS: In Phase I, only chronic alcohol consumption was identified as a significant new risk factor for the development of PNEC (6/19 vs 5/58, p= 0.02, OR 4.8, CI 1.27-18.2). In Phase II, it was verified that excessive alcohol consumption was a significant risk factor for PNEC (18/52 vs 58/307, p= 0.012, OR 2.27, CI 1.19-4.30). CONCLUSION: Chronic alcohol consumption seems to constitute a strong risk factor for PNEC.

Alcohol Drinking↗
PubMed2006

Comparison of allelic losses in chondroblastoma and primary chondrosarcoma of bone and correlation with fluorescence in situ hybridization analysis.

Chondroblastoma (CBL) is a benign neoplasm of bone for which the genomic characteristics remain unclear. We compared the status of allelic losses of CBL with that seen in a set of chondrosarcomas (CS) to determine whether differences in their natural history and behavior are also reflected genetically. Eleven cases of CBL and 10 cases of CS of different grades were included. Tumors were subjected to microdissection and polymerase chain reaction using 17 markers located near genes on chromosomes 5, 9, 11, 13, 17, and 19. The selected chromosomes are known to be involved in several mesenchymal neoplasms. Fluorescence in situ hybridization was also performed on tumors displaying allelic losses, with dual-color probes for 9p, 17p, and 13q. Fractional allelic losses per gene ranged from 18.2% to 63.7% in CBLs and from 28.6% to 66.7% in CSs. Loss of heterozygosity (LOH) of 5q, 9p, 11p, 13q, and 19q occurred in both CBLs and CSs. Loss of heterozygosity of 17p (p53 locus) occurred in 7 of 11 CBLs and in only 1 case of recurrent CS. The pattern of allelic loss was similar in low-grade CSs and CBLs. Loci with LOH in both tumor types suggest possible involvement of the genes p53, RB1, CDKN2/p16, ERC, and XRCC in tumorigenesis. Overall correlation between LOH and fluorescence in situ hybridization results was 90% with 17p13, 80% with 9p, and 60% with 13q. The role of p53 in CBL is uncertain; however, given the benign behavior of this tumor, it is probably unrelated to tumor progression.

Adolescent↗
PubMed2006

FSH directly regulates bone mass.

Postmenopausal osteoporosis, a global public health problem, has for decades been attributed solely to declining estrogen levels. Although FSH levels rise sharply in parallel, a direct effect of FSH on the skeleton has never been explored. We show that FSH is required for hypogonadal bone loss. Neither FSHbeta nor FSH receptor (FSHR) null mice have bone loss despite severe hypogonadism. Bone mass is increased and osteoclastic resorption is decreased in haploinsufficient FSHbeta+/- mice with normal ovarian function, suggesting that the skeletal action of FSH is estrogen independent. Osteoclasts and their precursors possess G(i2alpha)-coupled FSHRs that activate MEK/Erk, NF-kappaB, and Akt to result in enhanced osteoclast formation and function. We suggest that high circulating FSH causes hypogonadal bone loss.

Animals↗
PubMed2006

Obesity increases the severity of acute pancreatitis: performance of APACHE-O score and correlation with the inflammatory response.

BACKGROUND: Obese patients appear to be at risk for complications of acute pancreatitis (AP). APACHE-O score has been suggested to improve APACHE-II accuracy in predicting severe outcome in AP. AIMS: To determine if APACHE-O adds any predictive value to APACHE-II score and to test the hypothesis that obese patients are at increased risk of severe AP (SAP) because of a more intense inflammatory response to pancreatic injury. METHODS: 102 AP patients were prospectively studied. Using a body mass index (BMI) >30, 28% of the subjects were obese. Nineteen patients developed organ dysfunction and were classified as SAP. Receiver-operating curves for prediction of SAP were calculated using admission APACHE-II and APACHE-O scores. Binary logistic regression was performed to assess if obesity is a risk for SAP and to determine the clinical factors associated with severe disease. Serum levels of IL-6, MCP-1 and CRP as well as Ranson's scores were compared between obese and non-obese patients. RESULTS: Admission APACHE-O (area under the curve AUC 0.895) and APACHE-II (AUC 0.893) showed similar accuracy in predicting severe outcome. BMI was identified as a significant risk for SAP (OR 2.8, p = 0.048) and mortality (OR 11.2, p = 0.022). CRP levels were significantly higher in obese AP patients (p = 0.0001) as well as Ranson's score (p = 0.021). IL-6 and MCP-1 levels were higher in obese patients but did not reach statistical significance. CONCLUSIONS: Obesity is an independent risk for SAP. Admission APACHE-O score is not more accurate than APACHE-II. Our study results suggest that obesity increases the severity of AP by amplifying the immune response to injury.

APACHE↗
PubMed2005

JNK/ERK-AP-1/Runx2 induction "paves the way" to cartilage load-ignited chondroblastic differentiation.

Chondro-osteogenesis and subsequently skeletal morphology are greatly influenced by mechanical loads. The exact mechanism(s) by which mechanical stimuli are transduced in chondrocytes remains obscure and appears to be equally complex with similar signal transducing systems. Here we investigated whether and to what extent the MAPK (JNK/ERK)-AP-1/Runx2 signaling pathways are engaged in this phenomenon, and assessed their involvement in the functional biology of articular cartilage. For this purpose, 14-day-old female Wistar rats were divided into 2 groups: the first group was fed hard diet (simulating physiologic temporomandibular joint (TMJ) loading), while the second group was fed soft diet (reduced TMJ loading). On day 21 (experiment initiation day - weaning day), biopsies from condyles of both groups were obtained after 6, 12 and 48 h of functional TMJ loading. Immunohistochemical methodology was employed to evaluate the expression levels of pc-Jun, c-Fos, JNK2, p-JNK, p-ERK and Runx2 due to alteration in functional load. Our data demsonstrate that the protein levels of all the aforementioned molecules were markedly increased in animals fed with the hard diet, throughout the experimental procedure. These results indicate that functional cartilage loading induces the AP-1 and Runx2 transcription factors through the JNK and ERK MAPK cascades. In as much as the above signaling mediators/effectors are considered to be crucial in the differentiation/maturation process of cartilage tissue, we pose that functional mechanical loading of condylar cartilage serves to "fine tune" chondroblastic differentiation/maturation.

Animals↗
PubMed2004

Immunohistochemical expression of vascular endothelial growth factor (VEGF) and C-KIT in cutaneous melanocytic lesions.

Vascular endothelial growth factor (VEGF) and C-KIT are involved in tumor progression in several human neoplasms. The aim of the present study has been to investigate their immunohistochemical expression in melanocytic lesions. We examined 11 compound nevi, 12 dysplastic nevi, and 18 melanomas. Immunostaining for VEGF was observed only in melanomas; c-kit expression was detected in melanomas (higher in radial than in vertical growth phase) and in nevi (predominantly in the junctional component). Our data indicate that assessment of VEGF expression might aid in the differential diagnosis between dysplastic nevi and melanomas. Moreover, VEGF might be a candidate for targeted therapy. The loss of c-kit expression might contribute to melanoma progression.

Biomarkers, Tumor↗
PubMedDate not supplied

Expression of vascular endothelial growth factor (VEGF) and association with microvessel density in benign prostatic hyperplasia and prostate cancer.

BACKGROUND: Tumor angiogenesis is an absolute requirement for tumor growth and a prognostic factor for various malignant neoplasms. Recent reports in the literature have addressed the importance of the VEGF system in benign prostatic hyperplasia (BPH) and adenocarcinoma, however the results are controversial. The aim of the present study was to determine and compare the levels of VEGF expression and vascularity in BPH and prostate carcinoma. MATERIALS AND METHODS: We examined 60 prostate adenocarcinomas and 64 benign prostatic hyperplasias. Angiogenesis was estimated by determining microvessel counts (MVC), with the use of anti-CD31 and anti-CD34 antibodies. Expression of VEGF was also evaluated immunohistochemically. RESULTS AND CONCLUSION: Our data showed that angiogenesis was more prominent in carcinomas than in BPH. Furthermore, increased MVC was significantly associated with high-grade carcinomas. Angiogenesis was correlated with VEGF expression and it was, at least in part, mediated by the latter. Thus, prostate adenocarcinoma may represent a suitable neoplasm for antiangiogenic treatment in combination with conventional therapies.

Adenocarcinoma↗
PubMedDate not supplied

Expression of vascular endothelial growth factor and its receptor, KDR/Flk-1, in soft tissue sarcomas.

The aim of the present study was to evaluate the association of vascular endothelial growth factor (VEGF) and its receptor, KDR/Flk-1, with tumor grade, microvessel density (MVD) and clinical outcome in patients with soft tissue sarcomas (STSs). Tissue specimens of 28 patients with STSs were analyzed immunohistochemically using specific monoclonal antibodies. Tissue samples were obtained prior to any treatment. Half of the STSs exhibited strong expression of VEGF that was associated statistically significantly with high tumor grade. Strong expression of KDR/Flk-1 was detected in only 2 sarcomas. No association was demonstrated between VEGF and KDR/Flk-1 expression. MVD was significantly associated with tumor grade and was higher in sarcomas with strong VEGF expression. Limited data on clinical outcome precluded solid analyses for an association with disease progression. This study provides further evidence on the role of VEGF and MVD in tumor aggressiveness in STSs.

Adolescent↗