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Maria Serban

Abstract

Turing patterns are a class of minimal mathematical models that have been used to discover and conceptualize certain abstract features of early biological development. This paper examines a range of these minimal models in order to articulate and elaborate a philosophical analysis of their epistemic uses. It is argued that minimal mathematical models aid in structuring the epistemic practices of biology by providing precise descriptions of the quantitative relations between various features of the complex systems, generating novel predictions that can be compared with experimental data, promoting theory exploration, and acting as constitutive parts of empirically adequate explanations of naturally occurring phenomena, such as biological pattern formation. Focusing on the roles that minimal model explanations play in science motivates the adoption of a broader diachronic view of scientific explanation.

Open access

Raluca Dumache, Sorina Popescu, Radu Minciu, Serban Negru and Maria Puiu

Summary

Background: Prostate cancer (PCa) represents the second most prevalent malignancy among males, which is characterized by a high mortality rate. The aim of our study was to evaluate the methylation status of glutathione S-transferase P1 (GSTP1) in urine specimens from males with PCa and benign prostatic hyperplasia (BPH) and its usefulness in distinguishing between males with PCa and BPH by noninvasive methods.

Methods: Voided urine specimens were collected from 65 patients with PCa and 45 patients with BPH. Genomic DNA was isolated and subjected to bisulfite modification. Methylation status of the GSTP1 gene was determined by conventional methylation-specific polymerase chain reaction (MSP) analysis.

Results: Promoter hypermethylation of the GSTP1 gene in voided urine samples was found in 63 of 65 (97%) males with PCa and in 5 of 45 (11%) males with BPH. The sensitivity and specificity of GSTP1 in discriminating between PCa and BPH males were 98% and 89%, respectively.

Conclusions: Gene analysis of GSTP1 using conventional MSP in urine specimens can be used as a noninvasive biomarker to distinguish between men with malignant and benign prostatic diseases.

Open access

Mircea Dumitru Croitoru, Hermina Iulia Petkes, Ibolya Fülöp, Remus Cotârlan, Oana Elena Şerban, Titica Maria Dogaru, Şerban Andrei Gâz Florea, Béla Tőkés and Cornelia Majdik

Abstract

Free radicals are involved in the development of reperfusion injuries. Using a spin trap, the intensity of such lesions can be reduced. Nitrones (effective in vivo spin traps) were tried in this work as in vivo nitric oxide donors. Nitrite and nitrate concentration values (rabbit blood) were used as biomarkers of nitric oxide production. Most nitrones did not increase plasma concentrations of nitrite and nitrate; on the contrary, reduced plasma concentrations of these indicators were noted. However, glyoxal isopropyldinitrone, in a dose of 50 mg kg-1, was highly effective in increasing nitric oxide production. At the same time, nitrones do not react with hepatic homogenates, proving that the release of nitric oxide takes place in the tissues and is not related to hepatic metabolism. Before using nitrones in vivo, they were tested in vitro for the ability to release nitric oxide following a reaction with the hydroxyl radical.

Open access

Andreea Varga, Răzvan Constantin Șerban, Daniela Lucia Muntean, Cristina Maria Tătar, Lenard Farczadi and Ioan Tilea

Abstract

A rapid, sensitive, high-throughput liquid chromatography coupled with tandem mass spectrometry method for the quantification of rivaroxaban from human plasma has been developed and validated. For the analytical separation a Zorbax SB-C18 column with isocratic flow of mobile phase composed of 0.2% formic acid in water and acetonitril (65:35, V/V) with a flow rate of 1 mL/min at a temperature of 45ºC was used. Detection of rivaroxaban was performed using positive electrospray ionization and MS/MS mode (sum of m/z 231.1; 289.2 and 318.2 from m/z 436.3). Plasma samples were prepared using single-step protein precipitation with methanol. Method validation was performed with regards to selectivity, linearity (r >0.9927), within-run and between-run precision (CV< 13.1 %) and accuracy (bias< 9.4 %) over a concentration range of 24.00 - 960.00 ng/mL plasma. Recovery was between 96.5 - 108.5% and the lower limit of quantification of rivaroxaban was 24.00 ng/mL. The developed method is simple, rapid, and selective, requires small plasma sample volumes, and was successfully applied for therapeutic drug monitoring of rivaroxaban in treated patients.

Open access

Ioana Macovei, Daniela Lemeni, Roxana Șerban, Andreea Niculcea, Gabriel A. Popescu, Maria Nica, Anca Petrini and Grigore Mihăescu

Abstract

This study investigated the antibiotic susceptibility patterns and genetic resistance markers of 35 C. difficile strains isolated from patients with C. difficile infection. Vancomycin, metronidazole, tigecycline, teicoplanin, rifampicin, moxifloxacin, cefotaxime, tetracycline, erythromycin, clindamycin, chloramphenicol, linezolid and imipenem MICs were determined for toxigenic strains belonging to PCR ribotypes (PR) 012 (2), 014 (4), 017 (3), 018 (2), 027 (17), 046 (2), 087 (3) and 115 (2). Results showed vancomycin, metronidazole, tigecycline and teicoplanin to be active against all isolates. High resistance rates were noticed against cefotaxime (n = 35), clindamycin (n = 33), imipenem (n = 31), moxifloxacin (n = 25), erythromycin (n = 25) and rifampicin (n = 22). Linezolid-resistance was found in three isolates (PR 017/2, PR 012/1), showing complex resistance (7-9 antibiotics). PR 012, 017, 018, 027 and 046 isolates (n = 26) were resistant to 5-9 antibiotics. Twelve resistance profiles (2-9 antibiotics) were detected. Rifampicin-moxifloxacin-cefotaxime-erythromycin-clindamycin-imipenem-resistance was predominant, being expressed by 18 strains (PR 027/17, PR 018/1). PCR results suggested tetracycline-resistance to be induced by the gene tetM. Three tetM-positive isolates (PRs 012, 046), were also tndX-positive, suggesting the presence of a Tn5397-like element. Only two MLSB-resistant strains (PR 012) had the ermB gene and chloramphenicol-resistance determinant catD was not detected, leaving room for further investigating resistance mechanisms. Multidrug resistance could be attributed to most analysed strains, underlining, once more, the impact of wide-spectrum antimicrobial over prescription, still a tendency in our country, on transmission of antimicrobial resistance and emergence of epidemic C. difficile strains generating outbreaks.

Open access

Cristian Jinca, Carmen Angela Maria Petrescu, Estera Boeriu, Andrada Oprisoni, Loredana Balint-Gib, Mihaela Baica, Cristina Popa, Nicoleta Andreescu, Margit Serban, Emilia Ursu and Smaranda Arghirescu

Abstract

Introduction. The unsatisfactory results of the survival in patients with acute lymphoblastic leukemia (ALL) until 2000 in our center have led us to improve the approach of diagnosis and therapy. Since 2003 in all patients the following have been performed: flow cytometry, conventional genetic diagnosis, FISH (fluorescent in situ hybridization), and molecular biology. Objectives. Our aims were to identify solutions to increase patients’ survival. Patients and method. It is a single-center, retrospective study of 136 patients with ALL treated at 3rd Pediatric Clinic of Timisoara, over a period of 10 years (2003-2012), where survival was assessed. Results. Morphologically, 86% of the patients were L1 type, 13% L2 type and 1% L3 type. Flow citometry revealed that 68% were ALL with B precursors, and 19% with T immunophenotype. Acute leukemia with mixed phenotype (biphenotypic) was identified in 2.3% of patients and 10.7% of the forms were acute leukemia with myeloid markers. In 27.7% of patients, mutations were detected by the RT-PCR method, the most commonly identified was TEL-AML1 (ETV6- RUNX1) accounting for 12.7% of the cases. Relapse-free survival at 5 years for the entire group was 59%, and for the group treated between 2008 and 2012 it was 72%. Conclusion. Our analysis confirms the decisive value of laboratory investigations for the prognosis and improvement of supportive therapy.

Open access

Ana Maria Daraban, Adrian Pavel Trifa, Radu Anghel Popp, Diana Botezatu, Marinela Șerban, Valentina Uscatescu, Rodica Talmaci, Daniel Coriu, Carmen Ginghina and Ruxandra Oana Jurcut

Abstract

Objective: The present case-control study aimed at evaluating the contribution of thrombophilic polymorphisms to acute venous (VTE) as well as arterial thrombotic events (ATE) in a population of young women with few traditional thrombotic factors (CVRF).

Methods: We consecutively enrolled patients under 45 years of age, with less than 3 CVRF, evaluated for VTE or ATE, women and men as a comparator. The control group consisted of healthy young women. A thrombophilia panel and genetic testing for Factor V Leiden (FVL), G20210A Prothrombin and MTHFR polimorphisms were done.

Results: A total of 323 persons were enrolled: 71 women and 121 men with thromboembolic events, and 131 healthy female as controls. Hyperhomocysteinemia was more frequent in ATE (30.4%) than VTE female patients (6.25%), p<0.01. Genetic testing was available in 45 women and 84 men with acute thrombotic events and in all controls. Homozygous FVL was associated with VTE in young women (10.3% vs 0% controls, p<0.01). Prothrombin G20210A polymorphism had the lowest prevalence – 5.4% and only heterozygosity was found. MTHFR C677T heterozygosity showed no significant difference between women patients and controls (62.2 % vs 43.5% respectively, p=0.1). The homozygous status, less frequent (6.6%), was not associated with ATE or VTE. Homozygous MTHFR A1298C was associated with VTE in women (17.2% patients vs 4.5% controls, OR 4.34, p 0.02, CI 1.22-15.3).

Conclusion: In young women with few CVRF, mild hyperhomocysteinemia, homozygosity for FVL and for MTHFR A1298C polymorphisms increase the risk for VTE but not ATE. MTHFR polymorphisms are found with increased frequency in both healthy persons and patients therefore, their significance as an important thrombotic risk modifier remains unclear.

Open access

Mihai Gabriel Cucu, Ioana Streața, Anca Lelia Riza, Alina Liliana Cimpoeru, Simona Șerban-Șoșoi, Adela Ciocoiu, Răzvan Mihail Pleșea, Elena Leocadia Popescu, Ștefania Dorobanțu, Andreea Anghel, Aida Maria Stroe, Andreea Nicoleta Ștefan, Ramona Cioboată, Ileana Băzăvan, Marius Sorin Ciontea, Iulia Căpitănescu, Mihai Olteanu, Mimi Nițu, Florin Burada, Tiberiu Tătaru, Mihai Netea, Reinout van Crevel, Marian Olaru, Francisc Mixich and Mihai Ioana

Abstract

Autophagy, a homeostatic process involved in nutrient regeneration and immune responses, may be involved in intracellular killing of M. tuberculosis. Several studies linked variation in autophagy genes with susceptibility to pulmonary tuberculosis, but others did not confirm these findings.

We genotyped single nucleotide polymorphisms (SNPs) in the ATG5 (rs2245214, c.574-12777G>C) and NOD2 (rs2066844, c.2104C>T) genes for 256 pulmonary tuberculosis patients and 330 unrelated healthy controls in Romania. Both SNPs have been reported as relevant for the autophagy process and potentially for susceptibility to active pulmonary tuberculosis.

In our study, the polymorphisms in ATG5 and NOD2 were not associated with tuberculosis. This suggests that the two genetic variants we focused on are not related to the risk for developing active TB in a Romanian population.