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Apr 2020 DOI 10.14302/issn.2641-5526.jmid-20-3302
Data Mining is a process of exploring against large data to find patterns in decision-making. One of the techniques in decision-making is classification. Data classification is a form of data analysis used to extract models describing important data classes. There are many classification algorithms. Each classifier encompasses some algorithms in order to classify object into predefined classes. Decision Tree is one such important technique, which builds a tree structure by incrementally breaking down the datasets in smaller subsets. Decision Trees can be implemented by using popular algorithms such as ID3, C4.5 and CART etc. The present study considers ID3 and C4.5 algorithms to build a decision tree by using the “entropy” and “information gain” measures that are the basics components behind the construction of a classifier model
Feb 2026 DOI 10.14302/issn.2372-6601.jhor-25-5944
Background Oxaliplatin, a widely used chemotherapeutic agent, is associated with hematologic toxicities such as anemia, leukopenia, and thrombocytopenia. Despite their clinical relevance, the molecular mechanisms underlying lineage-specific bone marrow suppression remain poorly understood. Methods We administered oxaliplatin to mice over eight weeks and performed RNA-sequencing (RNA integrity >8) on bone marrow alongside peripheral blood analysis and cytokine profiling. Transcriptomic data were analyzed to identify differentially expressed genes (DEGs) and enriched pathways. For that, we applied a thematic Gene Ontology (thematicGO) enrichment method that groups GO terms into biologically meaningful categories, such as hematopoietic lineage disruption, cell cycle arrest, and cytokine signaling. Results Oxaliplatin induced broad transcriptional suppression of erythropoiesis and lymphopoiesis, with 3,691 DEGs identified (FDR<0.05, |FC|>1.5). Upregulation of Cdkn1a and downregulation of E2f2 suggest G1/S cell cycle arrest, correlating with repression of key erythroid maturation genes (e.g., Spta1, Slc4a1, Alas2) and hemoglobin subunits (Hba-a1/2, Hbb-bs/t). Despite a ~3000-fold increase in renal Epo expression, bone marrow Epor was reduced, indicating erythropoietin resistance. B and T cell markers were also significantly downregulated, signifying a collapse in adaptive immunity. Notably, neutrophil populations were largely spared. Cytokine analysis in plasma revealed a pro-inflammatory shift with elevated TNF-α and reduced TGF-β, potentially exacerbating hematopoietic dysfunction. Conclusions Oxaliplatin induces a lineage-dependent suppression of hematopoiesis, driven by coordinated cell cycle arrest, metabolic stress, and disrupted cytokine signaling. RNA-seq analysis enabled integration of transcriptomic findings into coherent biological themes. These findings provide mechanistic insights into oxaliplatin’s hematologic toxicity linking bone marrow failure (potentially reversible) via interconnected inflammatory and metabolic pathways and may inform therapeutic strategies to minimize or restore myelosuppression in cancer patients.
Sep 2023 DOI 10.14302/issn.2576-2818.jfb-23-4605
Background Immunological abnormalities are currently under scrutiny to potentially unravel the etiology of frustrating cases of unexplained female infertility (UFI). Objectives To explore the prevalence of immunological abnormalities in the levels of total immunoglobulins and complements in the cases of UFI. Methods Females with a history of UFI were included in this cross sectional study. They were consulted at the clinical immunology clinic at the King Abdulaziz University Hospital (KAUH). Their demographics, clinical features, total immunoglobulins and complements tests results were collected and analyzed for any relationship. Results One hundred and twenty-one cases of UFI with an average age of 34 ± 5.6 (range from 23 to 49 years old) were studied. Secondary infertility was predominant in 99 cases (81.8%). An overall prevalence of at least one abnormal level of total immunoglobulins or complements was found in 65 cases (55.1%). The predominant immunological abnormalities were elevated levels of immunoglobulins (hypergammaglobulinemia) in 51 cases (43.2%), high IgG in 26 cases (22%), high IgA in 14 cases (11.9%), and high IgM in 11 cases (9.3%). This was followed by elevated levels of complements (hypercomplementemia) in C4 in nine cases (8.5%). A significant association was found between high C4 group and some parameters of infertility, including primary infertility (p = 0.005), no pregnancy (p = 0.001), no abortion (p = 0.047), in comparison to normal C4 group. Moreover, a statistically significant association was found between high IgA group and abortion in comparison to normal IgA group (p = 0.054). Conclusion At least one abnormal level of total immunoglobulins or complements was detected in more than half of the UFI cases. The commonest abnormalities were hypergammaglobulinemia (IgG, IgM, IgA) and hypercomplementenemia (C4), which showed a potential association with some infertility parameters. These findings may encourage the screening of general immunological tests to explore promising new immunopathology in UFI.
Feb 2022 DOI 10.14302/issn.2470-5020.jnrt-22-4092
Acute disseminated encephalomyelitis (ADEM) is a monophasic, multifocal, demyelinating, autoimmune disease that affects the central nervous system (CNS). It usually occurs after a systemic infection, usually viral, including certain coronavirus infections. A 27-year-old girl presented with complaints of left interscapular pain, paresthesias and weakness in the ipsilateral upper limb. These symptoms followed paresthesias on the fingertips of her right hand the day before her admission. she was treated two weeks earlier for pneumonia with COVID-19. Her clinical pattern resulted in a moderate weakness of the left limbs associated with tactil and algic hypoesthesia in the lower left limb ascending until the C4 level in the left side. Magnetic resonance imaging (MRI) of the brain and spinal cord showed diffuse spontaneous hypersignals on fluid-attenuated inversion recovery (FLAIR) images at the cerebral level and on T2-weighted images at the spinal level. These imaging lesions coupled with the medical history of a recent COVID-19 infection led to the diagnosis of acute disseminated encephalomyelitis (ADEM) post covid-19. The clinical condition improved rapidly with intravenous (IV) corticosteroid therapy and IV immunoglobulin combined with physiotherapy. ADEM is a demyelinating autoimmune disease which is increasingly reported during this current corona virus pandemic.
Mar 2021 DOI 10.14302/issn.2692-1537.ijcv-21-3756
In contributing to the initiative to address the COVID-19 pandemic and in order to enhance the knowledge on driving forces shaping the evolution of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) (isolated from Tunisian patients), a comparison in relation to other coronaviruses infecting humans (SARS-CoV-1, MERS-CoV, HCoV/229E, HCoV/NL63, HCoV/OC43, and HCoV/HKU1) as well as animals (SARS-CoVs in tiger, bats, civet, pangolin, bovine, and MERS-CoV in dromedary/camel), was conducted. In-depth analysis was carried out involving 115 sequences of spike glycoprotein-coding gene extracted from the international databases. Phylogeny inference allowed the reconstruction of a bifurcating tree where four distinct groups were delineated and at the same time, three animal accessions (SARS-CoV-2/tiger, MERS-CoV/camel, and SARS-CoV/bovine) shifted from the animal group and integrated the human coronaviruses clades. Nonetheless, in the presence of reticulate events such as recombination, networks described better the phylogenetic relationships rather than the classic dendrogram. Thus, networks were produced and identified four clusters containing sharply demarcated subgroups (eight subdivisions). Except networked phylogenies of SARS-CoV-1, SARS-CoV-2, and HCoV/HKU1, all the others showed edges and boxes illustrating the occurrence of incompatibilities related to the sequences of spike glycoprotein-coding gene. Thereby and consolidating this result, three methods (RDP package, GARD, and RECCO) were used to detect breakpoints in aligned sequences. Except the clades SARS-CoV-1 and SARS-CoV-2, all the remaining phylogenetic subdivisions were subject to recombination. Furthermore, the screening of selection pressure in all studied sequences by various statistics-based models of the HyPhy package, showed that, similarly, the lineages belonging to the clades SARS-CoV-1 and SARS-CoV-2 were not under selection. In contrast, all members of the remaining clades underwent, to different extents, adaptive selection as well as purifying selection.
Mar 2017 DOI 10.14302/issn.2326-0793.jpgr-17-1447
Factors that contribute to the onset of atherosclerosis may be elucidated by bioinformatic techniques applied to multiple sources of genomic and proteomic data. The results of genome wide association studies, such as the CardioGramPlusC4D study, expression data, such as that available from expression quantitative trait loci (eQTL) databases, along with protein interaction and pathway data available in Ingenuity Pathway Analysis (IPA), constitute a substantial set of data amenable to bioinformatics analysis. This study used bioinformatic analyses of recent genome wide association data to identify a seed set of genes likely associated with atherosclerosis. The set was expanded to include protein interaction candidates to create a network of proteins possibly influencing the onset and progression of atherosclerosis. Local average connectivity (LAC), eigenvector centrality, and betweenness metrics were calculated for the interaction network to identify top gene and protein candidates for a better understanding of the atherosclerotic disease process. The top ranking genes included some known to be involved with cardiovascular disease (APOA1, APOA5, APOB, APOC1, APOC2, APOE, CDKN1A, CXCL12, SCARB1, SMARCA4 and TERT), and others that are less obvious and require further investigation (TP53, MYC, PPARG, YWHAQ, RB1, AR, ESR1, EGFR, UBC and YWHAZ). Collectively these data help define a more focused set of genes that likely play a pivotal role in the pathogenesis of atherosclerosis and are therefore natural targets for novel therapeutic interventions.