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Prilutsky D.,National Institute of Biotechnology in the Negev | Rogachev B.,Soroka Medical Center | Marks R.S.,National Institute of Biotechnology in the Negev | Marks R.S.,Ben - Gurion University of the Negev
Analytical Chemistry | Year: 2011

Oftentimes the etiological diagnostic differentiation between viral and bacterial infections is problematic, while clinical management decisions need to be made promptly upon admission. Thus, alternative rapid and sensitive diagnostic approaches need to be developed. Polymorphonuclear leukocytes (PMNs) or phagocytes act as major players in the defense response of the host during an episode of infection, and thereby undergo functional changes that differ according to the infections. PMNs functional activity can be characterized by quantification and localization of respiratory burst production and assessed by chemiluminescent (CL) byproduct reaction. We have assessed the functional states of PMNs of patients with acute infections in a luminol-amplified whole blood system using the component CL approach. In this study, blood was drawn from 69 patients with fever (>38 °C), and diagnosed as mainly viral or bacterial infections in origin. Data mining algorithms (C4.5, Support Vector Machines (SVM) and Naïve Bayes) were used to induce classification models to distinguish between clinical groups. The model with the best predictive accuracy was induced using C4.5 algorithm, resulting in 94.7% accuracy on the training set and 88.9% accuracy on the testing set. The method demonstrated a high predictive diagnostic value and may assist the clinician one day in the distinction between viral and bacterial infections and the choice of proper medication. © 2011 American Chemical Society.

Harlev A.,Ben - Gurion University of the Negev | Aricha-Tamir B.,Ben - Gurion University of the Negev | Shaco-Levy R.,Health Science University | Tarnovscki T.,National Institute of Biotechnology in the Negev | And 8 more authors.
Journal of Maternal-Fetal and Neonatal Medicine | Year: 2014

Objective: To examine if, as in obesity, pregnancies complicated by gestational diabetes mellitus (GDM) exhibit increased macrophage infiltration and activated MAP-kinases in omental adipose tissue. Methods: Paired omental (OM) and abdominal subcutaneous (SC) fat samples were collected from 11 GDM and 20 normal pregnancies during cesarean delivery. Tissues were stained to detect macrophages, and analyzed to assess MAP-kinases. Results: OM had higher macrophage counts than SC in GDM (6.10±2.20 versus 2.53±1.45, p=0.04), but not in normal pregnancies (p=0.346). GDM pregnancies had more macrophages than normal pregnancies in OM (6.10±2.20 versus 1.29±0.55, p=0.01), while only a trend was observed in SC fat (p=0.08). Significant correlation (R=0.619, p=0.005) was observed between OM-macrophage infiltration and insulin resistance. Using multivariate analysis, only obesity independently associated with GDM. Expression of total p38MAP-kinase was higher in OM versus SC in both normal and GDM pregnancies, without significant differences between these groups. However, expression of activated p-p38MAP-kinase, and its upstream kinase MKK4, was comparable between fat depots. Conclusion: GDM pregnancies demonstrate increased macrophage infiltration to OM fat, correlating with higher insulin resistance. As in non-pregnant-patients obesity and OM macrophage infiltration may be on the same causal pathway, leading to GDM. Yet, this occurs without activation of p38MAP-kinase signaling. © 2014 Informa UK Ltd. All rights reserved: reproduction in whole or part not permitted.

Feinstein M.,National Institute of Biotechnology in the Negev | Markus B.,National Institute of Biotechnology in the Negev | Noyman I.,Ben - Gurion University of the Negev | Shalev H.,Ben - Gurion University of the Negev | And 9 more authors.
American Journal of Human Genetics | Year: 2010

Pelizaeus-Merzbacher disease is an X-linked hypomyelinating leukodystrophy caused by PLP1 mutations. A similar autosomal-recessive phenotype, Pelizaeus-Merzbacher-like disease (PMLD), has been shown to be caused by homozygous mutations in GJC2 or HSPD1. We report a consanguineous Israeli Bedouin kindred with clinical and radiological findings compatible with PMLD in which linkage to PLP1, GJC2, and HSPD1 was excluded. Through genome-wide homozygosity mapping and mutation analysis, we demonstrated in all affected individuals a homozygous frameshift mutation that fully abrogates the main active domain of AIMP1, encoding ARS-interacting multifunctional protein 1. The mutation fully segregates with the disease-associated phenotype and was not found in 250 Bedouin controls. Our findings are in line with the previously demonstrated inability of mutant mice lacking the AIMP1/p43 ortholog to maintain axon integrity in the central and peripheral neural system. © 2010 by The American Society of Human Genetics. All rights reserved.

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