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Long-Term Probability of Auto-immune Conditions other than Systemic Lupus Erythematosus throughout Cutaneous Lupus Erythematosus-Alone Sufferers: A new 10-Year Across the country Cohort Research.
As shown by in-vivo study, xenograft tumors treated by docetaxel with quercetin had poorest growth. Then, to investigate the underlying mechanisms, the differences among parental cells, docetaxel-resistant subclones and quercetin treated resistant subclones were evaluated. It was found that docetaxel-resistant subclones had stronger activation of androgen receptor and PI3K/Akt pathway, more remarkable mesenchymal and stem-like cell phenotypes, and more P-gp expression than that of parental cells. Interestingly, quercetin could reverse these transformations. Our data revealed that quercetin had docetaxel-resistance reversal effect both in vitro and in vivo and provided in-depth support for clinical use of quercetin in docetaxel-resistant prostate cancer. © The author(s).Traumatic brain injury (TBI) induces an acute inflammatory response in the central nervous system that involves both resident and peripheral immune cells. The ensuing chronic neuroinflammation causes cell death and tissue damage and may contribute to neurodegeneration. The molecular mechanisms involved in the maintenance of this chronic inflammation state remain underexplored. C-terminal binding protein (CtBP) 1 and 2 are transcriptional coregulators that repress diverse cellular processes. Unexpectedly, we find that the CtBPs can transactivate a common set of proinflammatory genes both in lipopolysaccharide-activated microglia, astrocytes and macrophages, and in a mouse model of the mild form of TBI. We also find that the expression of these genes is markedly enhanced by a single mild injury in both brain and peripheral blood leukocytes in a severity- and time-dependent manner. Moreover, we were able to demonstrate that specific inhibitors of the CtBPs effectively suppress the expression of the CtBP target genes and thus improve neurological outcome in mice receiving single and repeated mild TBIs. This discovery suggests new avenues for therapeutic modulation of the inflammatory response to brain injury. © The author(s).Repair of damaged DNA induced by radiation plays an important role in the development of radioresistance, which greatly restricts patients' benefit from radiotherapy. However, the relation between radioresistance development and DNA double-strand break repair pathways (mainly non-homologous end joining and homologous recombination) and how these pathways contribute to radioresistance are unclear. Here, we established a radioresistant breast cancer cell line by repeated ionizing radiation and studied the alteration in DNA repair capacity. Compared with parental sham-treated cells, radioresistant breast cancer cells present elevated radioresistance, enhanced malignancy, increased expression of Ataxia-telangiectasia mutated (ATM), and increased DNA damage repair efficiency, as reflected by accelerated γ-H2AX kinetic. These defects can be reversed by ATM inhibition or ATM knockdown, indicating a potential link between ATM, DNA repair pathway and radiosensitivity. We propose that cancer cells develop elevated radioresistance through enhanced DNA damage repair efficiency mediated by increased ATM expression. Our work might provide a new evidence supporting the potential of ATM as a potential target of cancer therapy. © The author(s).Purpose To compare the difference in gene expression between human limbal niche cells (LNC) and bone marrow derived mesenchymal stem cells (BMMSC). Methods LNC were isolated by collagenase and expanded in modified embryonic stem cell medium (MESCM) on a Matrigel coated plastic plate. Cell diameters were measured with Image J software. Relative gene expression levels between LNC and BMMSC were compared using Affymetrix Human Primer View Gene Expression Array. A subset of differentially expressed genes was verified by RT-qPCR. The protein level of LAMA1 and COL4A1 was confirmed by Western blot and immunostaining. Results The average diameter of LNC was 10.2±2.4 μm, which was significantly smaller than that of BMMSC (14 ±3.4 μm) (p less then 0.0001). Expression of 20,432 genes was examined by Gene Expression Array, among which expression of 349 genes in LNC was 10-fold or higher than that of BMMSC and expression of 8 genes in LNC was 100-fold or higher than that of BMMSC, while expression of 3 genes in BMMSC was 100-fold higher than that of LNC. click here GO analysis and pathway analysis showed that the differentially expressed genes were mainly enriched in the extracellular matrix receptor interaction pathway and Wnt signaling pathway. In addition, RT-qPCR results demonstrated that the expression of CD73, CD90, CD105, PDGFRβ, Vimentin, SCF, KIT (CD117), COL14A1, LAMA2, THBS2, FZD1, BMP2 and CXCL12 genes in LNC were at least 2 folds higher than BMMSC. The protein level of LAMA1 was higher but the protein level of COL4A1 was lower in LNC than that in BMMSC. Conclusion LNC exhibit differential gene expression from BMMSC in the extracellular matrix (ECM) receptor interaction pathway and Wnt signaling pathway, suggesting that LNC have their unique signaling pathways to support limbal stem cell niches. © The author(s).Background A proportion of women with pregnancies complicated by gestational hypertension/preeclampsia (GH-PE) will have persistent postpartum chronic hypertension (CHTN). Common risk factors for postpartum CHTN include older age, pre-existing CHTN, smoking, pre-pregnancy obesity (elevated BMI), and co-morbidities such as thyroid disorders. However, most of explored risk factors are pre-pregnancy factors, and were mainly based on studies with small sample size. Methods To investigate provoking pre-pregnancy and intra-pregnancy factors for postpartum CHTN in women with preceding GH-PE, the cohort study enrolled 22,798 index pregnancies to analyze individual characteristics, co-morbidities and postpartum outcomes after excluding women with pre-existing CHTN. Results Among 2,132 GH-PE pregnancies, 428 (20.1%) were complicated with postpartum CHTN. After adjustment, logistic regression analysis revealed excessive pregnant weight gain (≥10 kgw at 28 weeks' gestation) (OR 14.50, 95% CI 11.02-19.08) and gestational diabetes mellitus (GDM) (OR 6.25, 95% CI 4.98-7.85) were major risk factors for developing CHTN, other than age (OR 1.80, 95% CI 1.68-1.93), pre-pregnancy BMI (OR 3.15, 95% CI 2.75-3.60), severity of GH-PE (OR 2.46, 95% CI 1.97-3.07), smoking (OR 1.79, 95% CI 1.35-2.38), and overt DM (OR 2.30, 95% CI 1.73-3.06). Conclusion Excessive pregnant weight gain and GDM are major intra-pregnancy risk factors for postpartum CHTN in women with preceding GH-PE. Future studies should investigate interventions such as a healthy diet, appropriate physical exercise and avoidance of excessive pregnant weight gain as a means to reduce the frequency of CHTN following pregnancy. © The author(s).
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