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Cation-Controlled Enantioselective along with Diastereoselective Activity of Indolines: An Autoinductive Phase-Transfer Initiated 5-endo-trig Process.
026). The main causes of bleeding were incomplete vascular ligation (30.23%), severe postoperative cervical activity (16.28%) and long-term use of anticoagulant drugs (11.63%). Overall survival at 5 years in the obese group was poor (P=0.015). Forty patients (93.02%) underwent surgical exploration and hemostasis and two patients (4.65%) underwent tracheotomy. All PH complications disappeared completely after active postoperative treatment, and all patients were discharged from hospital. Conclusion Obesity is closely associated with PH in TC patients. Therefore, in obese patients, active prevention preoperatively, complete hemostasis intraoperatively, early detection and timely treatment postoperatively are the key factors to reduce PH risk. © 2020 Li et al.Purpose The aim of this study was to analyse the expression profiles of DNMT1, DNMT3A, DNMT3B (components of DNA methylation machinery), TET2 and APOBEC3B (components of DNA demethylation machinery) in pediatric MDS patients and investigate their associations with MDS subtypes, cytogenetics, evolution to acute myeloid leukemia (AML) and p15INK4B methylation level. Patients and Methods The expressions of DNMT1, DNMT3A, DNMT3B, TET2, and APOBEC3B were evaluated in 39 pediatric MDS patients by real-time quantitative PCR (qPCR). The quantification of p15INK4B methylation levels (MtL) was performed in 20 pediatric MDS patients by pyrosequencing. Mann-Whitney test was used to evaluate possible differences between the expression levels of selected in patients and donors, according to MDS subtypes, karyotypes, evolution to AML and p15INK4B MtL. The correlations between the expression levels of the different genes were assessed by Spearman rank correlation coefficient. Results We found that DNMTs expression levels wered with DNMTs or APOBEC3B. p15INK4B MtL was higher in pediatric MDS patients compared with donors (p less then 0.03) and its hypermethylation was associated with increased DNMT1 expression (p less then 0.009). Conclusion Our results suggest that the overexpression of DNMTs and an imbalance between the expressions of the DNA methylation/demethylation machinery components play an important role in MDS development and evolution to AML. These results have clinical implications indicating the importance of DNMTs inhibitors for preventing or delaying the progression to leukemia in pediatric MDS patients. © 2020 Lamim Lovatel et al.Introduction It is known that CASC11 can promote colorectal cancer. However, the function of CASC11 in ovarian carcinoma (OC) remains elusive. Methods In this study, we measured the expression levels of CASC11 and miR-182 in both OC and healthy control samples by performing qPCR. The interaction between CASC11 and miR-182 was analyzed by the overexpression experiment and qPCR. Cell apoptosis was analyzed by cell apoptosis assay, and the prognostic value of CASC11 for OC was analyzed by survival curve analysis. Caspofungin concentration Results We found that CASC11 and microRNA-182 (miRNA-182) were upregulated in OC. Plasma CASC11 was upregulated in OC patients and predicted early-stage OC. Caspofungin concentration Follow-up study revealed that high plasma levels of CASC11 were closely correlated with poor survival conditions of OC patients. CASC11 and miRNA-182 were positively correlated in OC. Overexpression of CASC11 mediated the upregulation of miRNA-182 in cells of OC cell lines, while miRNA-182 overexpression did not significantly affect CASC11 expression. Overexpression of CASC11 and miRNA-182 promoted cancer cell proliferation and inhibited cancer cell apoptosis. Conclusion Therefore, CASC11 overexpression predicts poor prognosis and CASC11 regulates cell proliferation and apoptosis as well as microRNA-182 expression in ovarian carcinoma. © 2020 Cui et al.Background Breast cancer remains the most lethal malignancy in women worldwide. Aberrant O-glycosylation is closely related to many human diseases, including breast carcinoma; however, its precise role in cancer development is insufficiently understood. Cosmc is an endoplasmic reticulum-localized chaperone that regulates the O-glycosylation of proteins. Cosmc dysfunction results in inactive T-synthase and expression of truncated O-glycans such as Tn antigen. Here we investigated the impact of Cosmc disruption-mediated aberrant O-glycosylation on breast cancer cell development through in vitro and in vivo experiments. Materials and Methods We deleted the Cosmc gene in two breast cancer cell lines (MCF7, T47D) using the CRISPR/Cas-9 system and then measured the expression levels of Tn antigen. The proliferation of Tn-positive cells was examined by RTCA, colony formation and in vivo experiments. The effects of Cosmc deficiency on glycoprotein CD44 and MAPK pathway were also determined. Results Both in vitro and in vivo studies showed that Cosmc deficiency markedly suppressed breast cancer cell growth compared with the corresponding controls. Mechanistically, Cosmc disruption impaired the protein expression of CD44 and the associated MAPK signaling pathway; the latter plays a crucial role in cell proliferation. Reconstitution of CD44 substantially reversed the observed alterations, confirming that CD44 requires normal O-glycosylation for its proper expression and activation of the related signaling pathway. Caspofungin concentration Conclusion This study showed that Cosmc deficiency-mediated aberrant O-glycosylation suppressed breast cancer cell growth, which was likely mediated by the impairment of CD44 expression. © 2020 Du et al.Purpose Evidence suggested that procyanidin compound (PC) could inhibit the progression of cervical cancer (CC); however, the mechanism still remains unclear. We aimed to study the potential mechanism of PC acting on CC cells. Patients and Methods After a 24 hr incubation of lipopolysaccharide (LPS) (1 μg/mL), human CC SiHa and HeLa cells were cultured with various concentrations (20, 40, and 80 μg/mL) of PC for 24 hrs, then the cell viability was detected using Cell Counting Kit-8 (CCK-8). The migration and invasion abilities were assessed by scratch and Transwell assays. Apoptosis and cell cycle were detected using flow cytometry. Real-time quantitative PCR (RT-qPCR) and Western blot were used for expression analysis of the inflammatory cytokines. The pathway components were measured to evaluate the involvement of toll-like receptor 4/nuclear factor kappa-light-chain-enhancer of activated B cells (TLR4/NF-κB) pathway. Results PC inhibited the LPS-primed cell viability in a dose-dependent manner. link2 After PC treatment, cell migration and invasion were inhibited, cell number at the G2/M phase was increased. The CC cell apoptosis was triggered through upregulating levels of cleaved caspase-3 and Bax and downregulating the level of B-cell lymphoma 2 protein. A significant reduction was shown in the levels of interleukin (IL)-6, IL-1β and tumor necrosis factor (TNF)-α. Furthermore, a remarkable reduction in the ratio of TLR4 and the p-P65/t-P65 and in the progression of P65 translocation into the nucleus was observed. Conclusion Our results revealed that the inhibitory effect of PC on CC cell proliferation relies on the induction of apoptosis and inhibition of inflammatory cytokines. © 2020 Yang et al.Opioid analgesics remain a treatment option for refractory acute and chronic pain, despite their potential risk for abuse and adverse events (AEs). link2 Opioids are associated with several common AEs, but the most bothersome is opioid-induced constipation (OIC). OIC is often overlooked but has the potential to affect patient quality of life, increase associated symptom burden, and impede long-term opioid compliance. The peripherally acting µ-receptor antagonists (PAMORAs) are a class of drugs that include methylnaltrexone, naloxegol, and naldemedine. Collectively, each is approved for the treatment of OIC. PAMORAs work peripherally in the gastrointestinal tract, without impacting the central analgesic effects of opioids. However, each has unique pharmacokinetic properties that may be impacted by coadministered drugs or food. This review focuses on important metabolic and pharmacokinetic principals that are pertinent to drug interactions involving µ-opioid receptor antagonists prescribed for OIC. It highlights subtle differences among the PAMORAs that may have clinical significance. link3 For example, unlike naloxegol or naldemedine, methylnaltrexone is not a substrate for CYP3A4 or p-glycoprotein; therefore, its plasma concentration is not altered when coadministered with concomitant medications that are CYP3A4 or p-glycoprotein inducers or inhibitors. With a better understanding of pharmacokinetic nuances of each PAMORA, clinicians will be better equipped to identify potential safety and efficacy considerations that may arise when PAMORAs are coadministered with other medications. © 2020 Gudin and Fudin.Introduction The aim of this study is to assess the influence of gene CYP2C19, CYP3A4, CYP3A5 and ABCB1 polymorphisms on clopidogrel antiplatelet activity, rivaroxaban concentration equilibrium, and clinical outcomes among patients with acute coronary syndrome and non-valvular atrial fibrillation. Methods In the multicenter prospective registry study of the efficacy and safety of a combined antithrombotic therapy 103 patients with non-valvular atrial fibrillation both undergoing or not a percutaneous coronary intervention were enrolled. The trial assessed the primary outcomes (major bleeding, in-hospital death, cardiovascular death, stroketransient ischaemic attack, death/renal insufficiency) and secondary outcomes (platelet reactivity units (PRU), rivaroxaban concentration). link2 Results For none of the clinical outcomes when combined with other covariates, the carriership of polymorphisms CYP3A5*3 rs776746, CYP2C19*2 rs4244285;*17 rs12248560, ABCB1 3435 C>T, ABCB1 rs4148738 was significant. None of the markers under study (CYP3A5*3 rs776746, CYP2C19*2 rs4244285, *17 rs12248560, ABCB1 3435 C>T, ABCB1 rs4148738) has proven to affect rivaroxaban equilibrium concentration in blood plasma among patients with atrial fibrillation and acute coronary syndrome. Conclusion In situations of double or triple antithrombotic rivaroxaban and clopidogrel therapy among patients with atrial fibrillation and acute coronary syndrome, the genetic factors associated with bleeding complications risk (CYP2C19*17) may prove to be clinically relevant. © 2020 Sychev et al.The last 15 years have been the most fruitful in the history of research on the metabolic disorder alkaptonuria (AKU). link3 AKU is caused by a deficiency of homogentisate dioxygenase (HGD), the enzyme involved in metabolism of tyrosine, and is characterized by the presence of dark ochronotic pigment in the connective tissue that is formed, due to high levels of circulating homogentisic acid. link3 Almost 120 years ago, Sir Archibald Garrod used AKU to illustrate the concept of Mendelian inheritance in man. In January 2019, the phase III clinical study SONIA 2 was completed, which tested the effectiveness and safety of nitisinone in the treatment of AKU. Results were positive, and they will serve as the basis for the application for registration of nitisinone for treatment of AKU at the European Medicines Agency. Therefore, AKU might become a rare disease for which a cure will be found by 2020. We understand the natural history of the disease and the process of ochronosis much more, but at the same time there are still unanswered questions.
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