Encapsulation of a zinc phthalocyanine derivative in self-assembled peptide nanofibers

Cataloged from PDF version of article.In this article, we demonstrate encapsulation of octakis(hexylthio) zinc phthalocyanine molecules by non-covalent supramolecular organization within self-assembled peptide nanofibers. Peptide nanofibers containing octakis(hexylthio) zinc phthalocyanine molecules were obtained via a straight-forward one-step self-assembly process under aqueous conditions. Nanofiber formation results in the encapsulation and organization of the phthalocyanine molecules, promoting ultrafast intermolecular energy transfer. The morphological, mechanical, spectroscopic and non-linear optical properties of phthalocyanine containing peptide nanofibers were characterized by TEM, SEM, oscillatory rheology, UV-Vis, fluorescence, ultrafast pump-probe and circular dichroism spectroscopy techniques. The ultrafast pump-probe experiments of octakis(hexylthio) zinc phthalocyanine molecules indicated pH controlled non-linear optical characteristics of the encapsulated molecules within self-assembled peptide nanofibers. This method can provide a versatile approach for bottom-up fabrication of supramolecular organic electronic devices. © 2012 The Royal Society of Chemistry

The questions asked to the psychiatrists while preparing a forensic report on offences of bodily harm defined in the Turkish Penal Code

WOS: 000490862500015[No abstract available

Serotonin 5-HT7 receptor is a biomarker poor prognostic factor and induces proliferation of triple-negative breast cancer cells through FOXM1

Background Triple-negative breast cancer (TNBC) is an aggressive type of breast cancer and associated with poor prognosis and shorter survival due to significant genetic heterogeneity, drug resistance and lack of effective targeted therapeutics. Therefore, novel molecular targets and therapeutic strategies are needed to improve patient survival. Serotonin (5-hydroxytryptamine, 5-HT) has been shown to induce growth stimulatory effects in breast cancer. However, the molecular mechanisms by which 5-HT exerts its oncogenic effects in TNBC still are not well understood

Investigation of Reasons for Age Assessment Demands among Cases who Appear to Be in Children Age Bracket According to Their Birth Records: 6.5 Years of Experience [Nufus Kaydina Gore Cocuk Yas Grubunda Gorunen Olgularin Yas Tayini Raporu Istem Nedenlerinin Irdelenmesi: 6,5 Yillik Deneyim]

Age assessment remains an important subject of forensic medicine due to true age disputes caused by unorganized birth records and registrations. In this study, it is aimed to draw attention to the importance of age assessment, reasons for age assessment demands and demographics of cases who appear to be in children age bracket according to their birth records. Study consisted of cases who were evaluated at Ege University, Medicine Faculty, Department of Forensic Medicine between 01.01.2008 and 30.06.2014 for age assessment and who were under 18 at the time of application. Reports were examined retrospectively to establish gender, age according to birth record, occupation, number of siblings, birthplace, birth order, claimed age, assessed age, owner of the demand and reason for age assessment of the cases. Data were analysed using SPSS (version 18.0). Of the 214 cases involved in the study, 155 (72.4%) were female and 59 (27.6%) were male. Age according to birth record ranged between 3 and 17, mean age was 14.0±3.1 Civil Courts of First Instance ranked first (61.7%) among the owners of the demand for age assessment. Most frequent reason for age assessment demands was found to be early sexual activity and pregnancy (n=49, 22.9%) 63.6% of the cases claimed to be older than their ages according to their birth registrations. Various legal and social circumstances call for age assessment, particularly age assessment for sex crimes are prominent among children age bracket. As the hospital birth rates increase and birth registrations remain well-organized, applications for the age assessment of living individuals are expected to decline. [Med-Science 2015; 4(4.000): 2797-812

Flavopiridol Suppresses Cell Proliferation and Migration and Induces Apoptotic Cell Death by Inhibiting Oncogenic FOXM1 Signaling in IDH Wild-Type and IDH-Mutant GBM Cells

Glioblastoma multiforme (GBM) remains one of the most challenging solid cancers to treat due to its highly aggressive and drug-resistant nature. Flavopiridol is synthetic flavone that was recently approved by the FDA for the treatment of acute myeloid leukemia. Flavopiridol exhibits antiproliferative activity in several solid cancer cells and currently evaluated in clinical trials in several solid and hematological cancers. In this study, we investigated the molecular mechanisms underlying antiproliferative effects of flavopiridol in GBM cell lines with wild-type and mutant encoding isocitrate dehydrogenase 1 (IDH1). We found that flavopiridol inhibits proliferation, colony formation, and migration and induces apoptosis in IDH1 wild-type and IDH-mutant cells through inhibition of FOXM1 oncogenic signaling. Furthermore, flavopiridol treatment also inhibits of NF-KB, mediators unfolded protein response (UPR), including, GRP78, PERK and IRE1α, and DNA repair enzyme PARP, which have been shown to be potential therapeutic targets by downregulating FOXM1 in GBM cells. Our findings suggest for the first time that flavopiridol suppresses proliferation, survival, and migration and induces apoptosis in IDH1 wild-type and IDH1-mutant GBM cells by targeting FOXM1 oncogenic signaling which also regulates NF-KB, PARP, and UPR response in GBM cells. Flavopiridol may be a potential novel therapeutic strategy in the treatment of patients IDH1 wild-type and IDH1-mutant GBM

LC3 and Beclin-1 as Markers of Autophagic Activity in Breast Cancer

Autophagy is a catabolic pathway meaning "self-eating" that facilitates nutrient recycling from damaged and aged organelles and other impaired cellular components through lysosomal degradation. Regulation of this process has been associated with the development of cancer. It can play different roles at different tumors and developmental stages of tumors. In breast cancer, similarly, autophagy functions as a mechanism promoting survival or leading to death. Whereas, it is very important to define the role of autophagy as an effective treatment strategy in breast cancer cells. Therefore, in this review, the role of inhibited autophagy is discussed with specific RNAs targeting Beclin-1 and LC3 genes in breast cancer

MicroRNA profiling identifies Forkhead box transcription factor M1 (FOXM1) regulated miR-186 and miR-200b alterations in triple negative breast cancer

Breast cancer (BC) is the most commonly diagnosed malignancy. MicroRNAs (miRNAs) play important roles in the tumorigenesis, metastasis and progression of BC. Forkhead Box M1 (FOXM1) oncogenic transcription factor is involved in events considered as hallmarks of cancer. However, the specific mechanism by which FOXM1 exerts its oncogenic effects remains unclear and little is known about its effects on the regulation of miRNA expression. We have found that FOXM1 is upregulated in breast cancer cells and that its expression is associated with shortened overall survival and poor prognosis in patients with BC. Using microarray technology, we assessed the expression profiles of 752 miRNAs in highly aggressive and metastatic triple negative breast cancer (TNBC) cells in response to FOXM1 knockdown and identified 13 differentialy expressed miRNAs (3 miRNAs upregulated and 10 miRNAs down-regulated). We validated the results of the miRNA expression profile in two different TNBC cells by performing qRT-PCR and identified that miR-186-5p and miR-200b-5p were consistently down- or upregulated, respectively, after knockdown of FOXM1. We further performed KEGG pathway analysis and GO enrichment analysis for miR-186-5p and miR-200b-5p, and identified that these miRNAs are associated with cancer development and progression involving toll-like receptor signaling, cell cycle, AMPK, p53 and NF-kappa B signaling pathways. Taken together, our results suggest that increased FOXM1 expression is associated with poor patient survival and leads to induction of oncomiR miR-186-5p expression and tumor-suppressor inhibition miR200b-5p, suggesting that the FOXM1/miRNA signaling pathway may contribute to poor patient prognosis and may be a potential therapeutic target in TNBC