Background Around 70% of breast cancers (BCs) are estrogen receptor-α (ERα)-positive. Adjuvant endocrine therapy is used to reduce estrogen levels and inhibit signal transduction through the ER. The anti-estrogen drugs that are most commonly used in endocrine therapy belong to the selective ER modulator (SERM) class and include tamoxifen. Although it has been used for three decades in cases of early-stage and ERα-positive BC, resistance to tamoxifen is a common problem. microRNAs (miRNAs) have a potential role in demonstrating BC resistance to tamoxifen therapy. Hence, there is a need to investigate the expression of miRNA-221 (miR-221) in luminal-subtype BC patients receiving tamoxifen therapy. Methods This case-control study investigated luminal-subtype BC patients who had undergone endocrine therapy for at least 1 year. The case group comprised patients with local or metastatic recurrence, and the control group comprised patients without local or metastatic recurrence. Results There was a significant difference in miR-221 expression ( p = 0.005) between the case and control groups. There were no significant differences between the groups that were positive and negative for the progesterone receptor (PR) ( p = 0.25), had high and low marker of proliferation Ki-67 levels ( p = 0.60), were positive and negative for lymphovascular invasion ( p = 0.14), and had stage 2 and stage 3 cancer ( p = 0.25). Conclusion miR-221 expression was higher in tamoxifen-resistant BC cases. miR-221 is a potential biomarker of tamoxifen resistance.
The formation of a scar after Mycobacterium bovis Bacillus Calmette-Guérin ( BCG) vaccination influences the effectiveness of protection against Mycobacterium tuberculosis (MTB) infection. The innate immunity plays a critical role both in the pathophysiology of tuberculosis (TB) and BCG vaccination protection mechanism. Parts of innate immunity: macrophages, dendritic cells, and neutrophils, have microbial recognition surface receptors called Toll-like receptors (TLR) 2 and 4. The objective of this study is to compare the serum levels of TLR2 and TLR4 in BCG-vaccinated pediatric patients with pulmonary and extrapulmonary TB. This cross-sectional study included children aged less than 18 years old with contracted TB disease and had received BCG vaccination. The subjects were recruited by convenience sampling from both outpatient and inpatient care at Bhakti Medicare and Jakarta Islamic Hospital, from November 2018 to December 2019. Serum TLR2 and TLR4 levels measured using ELISA of the two groups of subjects: children with pulmonary TB (PTB) and extrapulmonary TB (EPTB), were then compared. The presence of BCG scars was included in the analysis. Independent T-test, ANOVA test, and Kolmogorov-Smirnov normality tests on the SPSS program were used to statistically analyze the results. Serum TLR2 and TLR4 levels were higher in EPTB group, but the difference was not significant (TLR2 p = 0.758 and TLR4 p = 0.646, respectively). Subjects with BCG scars in both groups have significantly higher serum TLR2 and TLR4 levels than those without BCG scars in the EPTB group (EPTB p = 0.001 and p = 0.004, respectively); (PTB p < 0.001 and p < 0.001, respectively). BCG vaccination and MTB infection stimulate better innate immune response in EPTB than in PTB and serum TLR2 and TLR4 levels in those with BCG scars were higher when compared to those without BCG scars.
Background and aim: The prevalence of typhoid fever is reportedly high, especially in Asia. When a pathogen enters the human body, there are markers in the form of molecules that will be known by the innate immune system. Specific molecular markers of gram negative bacteria, which are Lipopolysaccharides (LPS) and Toll-Like receptors-4 will interact with LPS. The binding between LPS and TLR-4 will give rise to activation signals that will activate innate immune cells. Immune cells will release a number of proinflammatory cytokines, such as TNF-α, IL-1, and IL-6. While Vitamin D Receptors (VDR) are expressed in large amounts in tumor tissue and infected cells. This study aimed to prove the role of IL-6, TNF-α, and VDR in inhibiting bacterial growth in mice that have been induced by S.Typhi. Methods: This research was a real experimental pre-post test design to investigate the level of IL-6, TNF-α and VDR in suppressing the growth of bacteria in the peritoneal fluid of S. Typhi, male, mice BALB/c. Mice were divided into three groups comprised of 10 mice each. All mice in groups A and B were intraperitoneally inoculated with S. Typhi strain Thy1 in study day 0. Group A was treated with antibiotic Levofloxacine, on study day 4th. Another study group, group B, was used as a placebo and received aquades on study day 4th. While group C as a control was not inoculated with S. Typhi. Blood samples from three groups for the calculation of serum Il-6, TNF-α, and VDR were collected. This examination was taken four times; at baseline, 4th day, 10th day, and 30th day. For the calculation of bacterial colony, peritoneal fluid retrieval was collected three times, which is on 4th day, 10th day, and 30th day. Results: A repeated measure ANOVA in group A (antibiotic) and group B (placebo) group showed that mean IL-6, TNF-α, and VDR level differed statistically significant between times (p-value 0.000). There was a strong negative correlation between bacterial colony count and VDR level, which was statistically significant in both groups (group A; r = -0.875, p-value = 0.000 vs group B; r = -0.470, p-value = 0.002). IL-6 and TNF-α didn't give significant statistical correlation with bacterial colony count. Conclusion: VDR, IL-6, and TNF-α play an important role in killing bacteria. From the results of this study, IL-6 level is related to the number of bacterial colonies, the lower the IL-6 level, the less the number of bacterial colonies. Similarly, TNF-α levels have a positive correlation with the number of bacterial colonies. While VDR levels are also related to the number of bacterial colonies, the higher the VDR level, the lower the number of bacterial colonies.
is an International, peer-reviewed scientific journal that publishes original article in experimental & clinical medicine and related disciplines such as molecular biology, biochemistry, genetics, biophysics, bio-and medical technology. JMS is issued four times per year on paper and in electronic format.
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