The study aimed to establish the association of miR-153-3p expression with treatment response to IM in CML patients. Sixty CML patients were included and divided into two groups consistent with their response to treatment whether sensitive or resistant to IM. Ten healthy normal participants were enrolled as control group. RNA was extracted from serum to work out miR-153-3p expression utilizing real-time quantitative reverse transcription polymerase chain reaction. The primers were supplied by Macrogen Inc. Twenty seven patients were sensitive to imatinib and 33 were resistant to imatinib. The ratio of male to female was 1.14:1. The bulk (58%) of patients were within the age range of 41-60 years. Weight and gender did not significantly differ between the two patient groups. The mean patients’ CT of miR-153-3p was significantly above the control group and the sensitive group. The mean DCT value in resistant group was significantly above that of the sensitive group while insignificantly above that of the control group. The mean DDCT in resistant group was significantly higher than that of the sensitive group. The miR-153-3p expression showed significantly lower fold change than the sensitive group. Conclusion: There is miR-153-3p expression downregulation in resistant CML patients indicating unresponsiveness to treatment with imatinib.
In this research the Empirical Bayes method is used to Estimate the affiliation parameter in the clinical trials and then we compare this with the Moment Estimates for this parameter using Monte Carlo stimulation , we assumed that the distribution of the observation is binomial distribution while the distribution with the unknown random parameters is beta distribution ,finally we conclude that the Empirical bayes method for the random affiliation parameter is efficient using Mean Squares Error (MSE) and for different Sample size .
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Background: Study looking into cardiovascular disorders (CVD) medicines or analgesics cost-saving activities during dispensing process is lacking.
Aim: To determine differences in factors and costs associated with refused CVD medicines or analgesics during dispensing process
Method: This study was approved by Medical Research and Ethics Committee (MREC) (Registration number: NMRR-20-177-53153(IIR)). Participants receiving CVD medicines or analgesics during dispensing process were recruited via convenience sampling technique between February and March 2020 at the Specialist Pharmacy Department of Jerantut Hospital, Malaysia. Refusal to medications and its reasons were asked based on the questionnaire developed by the resea
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Background: Breast cancer is the most frequently diagnosed malignancy and the second leading cause of mortality among women in Iraq forming 23% of cancer related deaths. The low survival from the disease is a direct consequence to the advanced stages at diagnoses. Aim: To document the composite stage of breast cancer among Iraqi patients at the time of diagnosis; correlating the observed findings with other clinical and pathological parameters at presentation. Patients and Methods: A retrospective study enrolling the clinical and pathological characteristics of 603 Iraqi female patients diagnosed with breast cancer. The composite stage of breast cancer was determined according to UICC TNM Classification System of Breast Cancer and the Ameri
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ntroduction. Finding a safe innate immune response stimulator is one of the greatest challenges facing immunologists and vaccine manufacturers. Gap statement. The role of sterile bacterial secretions (SBSs) of Pseudomonas aeruginosa in stimulating the innate immune response was not investigated previously. Aim. The comparative effect of SBSs and bacterial cells of P. aeruginosa isolates isolated from freshwater (PAE) and infected wounds (PAC) on the respiratory tract innate immune response. Methodology. Four test mice groups were instilled intranasally (i.n.) with 106 c.f.u of PAC, 106 c.f.u of PAE, SBS of PAC, and SBS of PAE. Two control groups were given i.n. either LB broth or PBS. Time-course changes in IL-1 beta mRNA, TNF-alpha mRNA, I
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