Hallazgos nasales y paranasales incidentales en resonancia magnética y tomografía computarizada: un estudio prospectivo / Incidental Nasal and Paranasal Findings on MRI and CT Scans-A Prospective Study

Objective: Morphological changes in sinuses are commonly observed through routine Magnetic Resonance Imaging (MRI) and Computed Tomography (CT) scans. The present study aims to assess the prevalence of nasal and sinus pathology in the Jordanian patients undergoing head MRI or CT scans for a non-ENT cause. Materials and Methods: Prospective study was conducted at Alkarak hospital, Jordan. CT/MRI scan images of patients were reviewed over a period of 6-months. Data about ENT symptoms, history of allergic rhinitis, and abnormalities was also collected. Results: Of the 600 patients (445 MRI, 145 CT Scans), sinus pathology was observed in 170 patients (28.33%). The most common sinus abnormality was mucosal thickening (n=135, 79.41%), followed by complete opacification and cysts. A significant correlation was observed between sex, sinonasal symptoms, facial pain, and asthma in both sinus pathology and nasal pathology. Nasal obstruction (p=0.000) and allergic rhinitis (p=0.000) were significantly correlated with nasal pathology. Conclusion: A significant correlation between incidental sinonasal pathology and both facial pain and allergic rhinitis was observed. However, the incidental findings are overestimated due to lack of correlation to symptoms and underlying conditions

A Critical Review for Developing Accurate and Dynamic Predictive Models Using Machine Learning Methods in Medicine and Health Care.

Recently, Artificial Intelligence (AI) has been used widely in medicine and health care sector. In machine learning, the classification or prediction is a major field of AI. Today, the study of existing predictive models based on machine learning methods is extremely active. Doctors need accurate predictions for the outcomes of their patients' diseases. In addition, for accurate predictions, timing is another significant factor that influences treatment decisions. In this paper, existing predictive models in medicine and health care have critically reviewed. Furthermore, the most famous machine learning methods have explained, and the confusion between a statistical approach and machine learning has clarified. A review of related literature reveals that the predictions of existing predictive models differ even when the same dataset is used. Therefore, existing predictive models are essential, and current methods must be improved.

Defective cytokine production following autologous stem cell transplantation for solid tumors and hematologic malignancies regardless of bone marrow or peripheral origin and lack of evidence for a role for interleukin-10 in delayed immune reconstitution.

A substantial body of evidence accumulated in recent years indicates a protracted delay in immune reconstitution following autologous stem cell transplantation. In order to investigate the cellular basis of this phenomenon, peripheral blood mononuclear cells were studied from recipients of autologous stem cell transplantation for solid tumors and hematological malignancies. On stimulation with phytohemagglutinin and phorbol 12-myristate 13-acetate, transplant-derived peripheral blood mononuclear cells demonstrate statistically significant depressed production of interleukin 3 (IL-3), IL-4, granulocyte-macrophage-colony-stimulating factor, and gamma-interferon as compared to normal controls, during the first 6 months following engraftment, which recover to normal levels 6 months or more posttransplant. When the overall group of transplant recipients is compared to the control group, there is a statistically significant lower production of IL-2. In addition, no differences were observed regardless of the source of the engrafted stem cells, whether from bone marrow alone (autologous bone marrow transplantation), from peripheral blood stem cells alone, or from a combination of autologous bone marrow transplantation and peripheral blood stem cells. The defect persisted past 6 months postengraftment. Transplant-derived peripheral blood mononuclear cells were stimulated with combinations of either phytohemagglutinin plus the calcium ionophore A23187, thereby circumventing the requirement for accessory cell function, or with phorbol 12-myristate 13-acetate plus anti-CD28 monoclonal antibody, mimicking the CD28-B7 cell surface-ligand interaction capable of triggering and stabilizing IL-2 gene transcription. In both situations, decreased production of IL-2 as compared to controls was observed in individuals within 6 months of transplantation. Quantitative polymerase chain reaction indicates that decreased transcription of IL-2 mRNA following transplantation is not due solely to a decrease in the absolute numbers of CD4+ T-cells but is secondary to reduced numbers of transcript copies per cell. Production of IL-10 was found to be decreased regardless of whether the autologous graft was of bone marrow or peripheral blood origin. These findings are consistent with the conclusion that: (a) multiple dysregulations exist in the production of cytokines important in immune homeostasis; (b) a defect occurs at or prior to the level of transcription of IL-2 mRNA; (c) IL-10 does not play a direct role in the pathogenesis of posttransplantation immunosuppression; and (d) there is no evidence that peripheral blood stem cells may be superior to bone marrow-derived stem cells in accelerating immune reconstitution.

Transcription of genes encoding granulocyte-macrophage colony-stimulating factor, interleukin 3, and interleukin 6 receptors and lack of proliferative response to exogenous cytokines in nonhematopoietic human malignant cell lines.

Studies in recent years have suggested that human tumor cell lines are capable of responding in vitro to hematopoietic growth factors. In the present study, we investigate the transcription of the alpha and beta subunits of granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor, the alpha and beta subunits of interleukin 3 (IL-3) receptor, and the single subunit of interleukin 6 (IL-6) receptor and its associated gp130 transduction protein by PCR amplification of reverse-transcribed cellular mRNA in 34 malignant cell lines derived from a variety of histological cell types. mRNA for only a single subunit polypeptide was found in a significant minority of cell lines (23%), while in 20% both the alpha and beta subunits of either the GM-CSF receptor or the IL-3 receptor were detected among a number of different histological cell types. Transcription of the gene encoding the IL-6 receptor was found in 38% of cell lines, and all lines transcribed the gp130 transduction protein, consistent with previous observations on the ubiquity of that polypeptide. In order to test the in vitro effect of exogenously added growth factors on those malignant cell lines transcribing complete cytokine receptor, either GM-CSF, IL-3, or IL-6 was added in therapeutic concentrations (20-500 ng/ml) and cellular proliferation was measured by incorporation of [3H]thymidine. No stimulation was seen at either 3 and 6 days of culture. Production of cytokine by these cell lines was investigated at the level of transcription and by assay of peptide product. None transcribed mRNA for either GM-CSF or IL-3, while 5 of 6 (STD, DOZ, ADE, Hep-2, and Detroit) expressed IL-6 mRNA. Of these latter, 2 cell lines (ADE and Hep-2) produced IL-6 as determined by bioassay, while none produced GM-CSF or IL-3 by enzyme-linked immunosorbent assay. This suggests that in the case of GM-CSF and IL-3, failure to proliferate on addition of cytokine is not due to the prior presence of endogenous production. In contrast, at least a subset of malignant cell lines may involve a closed IL-6 autocrine loop saturating cell surface sites. These findings suggest that the ability to transcribe the genes encoding cytokine receptor is by itself insufficient to render cells cytokine responsive and that malignant cells may lack the cellular machinery for cytokine-induced proliferation. This in turn suggests that therapeutic administration of either GM-CSF, IL-3, or IL-6 may involve no additional risk of tumor regrowth in vivo.

Blunted rise in intracellular calcium in CD4+ T cells in response to mitogen following autologous bone marrow transplantation.

Following autologous bone marrow transplantation (ABMT), both impaired T cell activation and defective production of the principal T cell growth factor, interleukin-2 (IL-2), has been observed. These processes are dependent on a rise of intracellular calcium ([Ca2+]i), a step which follows binding of T cell receptor (TCR) and transduction of signal via the generation of cytoplasmic second messengers. In order to better understand the nature of defective cellular immunity in ABMT, in the present study we investigated the rise of [Ca2+]i in T cells of recipients of ABMT. By concomitant labelling lymphocytes with anti-CD4 antibody and addition of fluo-3 as fluorescent calcium indicator, we have selected for the T cell subset which is the principal source of IL-2. Short-term (less than 1 year post-transplantation) recipients of ABMT show a statistically significant blunted rise in [Ca2+]i in response to concanavalin A as compared to normal controls not accounted for solely by a decreased percentage of CD4+ cells in these patients. The [Ca2+]i response of CD4+ cells from long-term (greater than 1 year post-transplant) recipients was lower than that of the normal group although not to a statistically significant level. These findings suggest that following ABMT is a defect in the early stages of T cell activation involving either T cell receptor binding or early signal transduction ultimately resulting in depressed transcription of IL-2 mRNA. These defects are analogous to findings in both allogeneic transplantation where factors of histoincompatibility and graft-versus-host disease (GVHD) come into play, as well as in the defective T cell activation of the normal ageing process.