Methylation of the suppressor of Cytokine Signaling 1 Gene (SOCS1) in Philadelphia-negative myeloproliferative neoplasms.

OBJECTIVE: Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway activation is initiated by mutations in the JAK2 gene. This activation is in turn, a vital pathogenetic mechanism in myeloproliferative neoplasms (MPNs). However, several factors affect the pathogenesis of MPNs other than the JAK2 gene mutations, such as the downregulation of cytokine signaling (SOCS) proteins, which are potent inhibitors of the JAK/STAT pathway. Therefore, we hypothesized that the regulation of SOCS protein system might be a possible pathogenetic mechanism of MPNs through activating the JAK/STAT pathway. PATIENTS AND METHODS: Our study aimed to investigate the status of the Suppressors of cytokine signaling 1 (SOCS1) in 125 MPNs specimens at the level of mutated points. The acquired mutations, aberrant expression, and/or CpG island hypermethylation of SOCS1 were analyzed among Philadelphia-negative myeloproliferative neoplasm patients. RESULTS: SOCS1 was identified in 20.0% of all patients with Philadelphia-negative myeloproliferative neoplasm. At the diagnosis, the prevalence of methylation was 41.0% for Polycythaemia Vera (PV), 27.7% for Essential Thrombocythaemia (ET), and 6.6% for Primary Myelofibrosis (PMF). The methylation was not detected in 20 healthy adult people. A significant association was found between disease groups (p=.077). The presence of methylated SOCS1 was found to be significantly correlated with age (p=.005), total RBCs count (p=.019), hemoglobin (Hb) concentration (p=.002), and Hematopoietic cell transplant (HCT) (p=.007) in PV patients. However, the presence of methylated SOCS1 was found to be significantly associated with age (p=.012), total RBCs count (p=.022), Hb concentration (p=.024), HCT (p=.033), and platelets count (p=.037) in ET patients. Moreover, the presence of methylated SOCS1 was significantly associated with Hb concentration (p=.046) and HCT (p=.040) in PMF patients. CONCLUSIONS: We concluded that the activation of the JAK/STAT signaling pathway in alternative or with JAK2 mutations leads to SOCS1 hypermethylation, which could represent a potential therapeutic target.

An efficient intelligent analysis system for confocal corneal endothelium images.

A confocal microscope provides a sequence of images of the corneal layers and structures at different depths from which medical clinicians can extract clinical information on the state of health of the patient's cornea. A hybrid model based on snake and particle swarm optimisation (S-PSO) is proposed in this paper to analyse the confocal endothelium images. The proposed system is able to pre-process images (including quality enhancement and noise reduction), detect cells, measure cell densities and identify abnormalities in the analysed data sets. Three normal corneal data sets acquired using a confocal microscope, and three abnormal confocal endothelium images associated with diseases have been investigated in the proposed system. Promising results are presented and the performance of this system is compared with manual and two morphological based approaches. The average differences between the manual and the automatic cell densities calculated using S-PSO and two other morphological based approaches is 5%, 7% and 13% respectively. The developed system will be deployable as a clinical tool to underpin the expertise of ophthalmologists in analysing confocal corneal images.

Average row thresholding method for mammogram segmentation.

Two novel threshold techniques are proposed for image segmentation which is a very critical task in any image processing. The two methods are based in scanning each image row by row and to find the proper threshold value. A modification of this method is developed to find the threshold value by average. The two methods are implemented on a mammogram and accordingly, a comparison between the two methods is carried out.