Histone Deacetylase Inhibitors and Breast Cancer Metastasis: A Review and Exploration of HDAC(i)s and Other Chemotherapeutic Agents

The traditional perspective of Histone Deacetylase enzymes is focused on their inherent epigenetic modification characteristics. While it is true that the histone modification these enzymes exhibit play a role in cancer and related diseases, Histone Deacetylase has a variety of non-histone targets. The non-histone targets include microtubules and are of specific interest because of the microtubules’ role in cell line differentiation, replication, apoptosis, and cancer metastasis. Using a variety of Histone Deacetylase Inhibitors (HDACi) and other chemotherapeutic compounds, our research group explored the HDACi effect on breast cancer cell lines. Our goal was to indicate the presence of HDACi cell-line dependent cancer growth inhibition and to study the hypothesized non-histone mechanism of microtubule modification in HDACi(s). The experiment consisted of three parts: viability assay, clonogenic assay, and combination assay which analyzed HDACi(s) possible synergistic character with microtubule-stabilizing compounds. The specific breast cancer cell lines used were MDA-MB-231 clones LM-4175 and BOM-1833, and MCF7-BOM. The results of our experiments indicated that there was cell line dependent growth inhibition with the treatment of HDACi(s). Specifically, MCF7-BOM showed to be more susceptible to treatment, and this could be due to it being an estrogen receptor positive ER+ cell line. However, the growth inhibition never reached complete inhibition and was most prominent at the highest concentrations of HDACi(s). Higher concentrations of HDACi(s) also had the most prominent effect on colony growth inhibition in the clonogenic assay. The combination assay had an interesting result indicating an antagonistic trend between microtubule stabilizers and HDACi(s)

Inelastic scattering of broadband electron wave packets driven by an intense mid-infrared laser field

Intense, 100 fs laser pulses at 3.2 and 3.6 um are used to generate, by multi-photon ionization, broadband wave packets with up to 400 eV of kinetic energy and charge states up to Xe+6. The multiple ionization pathways are well described by a white electron wave packet and field-free inelastic cross sections, averaged over the intensity-dependent energy distribution for (e,ne) electron impact ionization. The analysis also suggests a contribution from a 4d core excitation in xenon

Erratum to: EuPRAXIA Conceptual Design Report – Eur. Phys. J. Special Topics 229, 3675-4284 (2020), https://doi.org/10.1140/epjst/e2020-000127-8

International audienceThe online version of the original article can be found at http://https://doi.org/10.1140/epjst/e2020-000127-8</A

The bile salt glycocholate induces global changes in gene and protein expression and activates virulence in enterotoxigenic Escherichia coli

Pathogenic bacteria use specific host factors to modulate virulence and stress responses during infection. We found previously that the host factor bile and the bile component glyco-conjugated cholate (NaGCH, sodium glycocholate) upregulate the colonization factor CS5 in enterotoxigenic Escherichia coli (ETEC). To further understand the global regulatory effects of bile and NaGCH, we performed Illumina RNA-Seq and found that crude bile and NaGCH altered the expression of 61 genes in CS5 + CS6 ETEC isolates. The most striking finding was high induction of the CS5 operon (csfA-F), its putative transcription factor csvR, and the putative ETEC virulence factor cexE. iTRAQ-coupled LC-MS/MS proteomic analyses verified induction of the plasmid-borne virulence proteins CS5 and CexE and also showed that NaGCH affected the expression of bacterial membrane proteins. Furthermore, NaGCH induced bacteria to aggregate, increased their adherence to epithelial cells, and reduced their motility. Our results indicate that CS5 + CS6 ETEC use NaGCH present in the small intestine as a signal to initiate colonization of the epithelium

Reassurance: A Mechanism by Which the Presence of Others Reduces Anxiety

The current investigation was designed to test the hypothesis that reassurance is at least one mechanism by which the presence of others reduces anxiety. In two separate experiments Ss (female undergraduates n = 38 and n = 40, respectively) waited to participate in an anxiety provoking shock experiment with two Cs. In one condition the Cs were reassuring and in the other they were not. Results of both experiments showed anxiety reduction only when the Cs were reassuring. Birth order differences could not be found; nor could the results of Experiment 2 confirm the hypothesis that reassurance causes people cognitively to re-evaluate the anxietyarousing situation