Developing of thin chromium-free multifunctional treatments on hot dip galvanized steel: strategy, implementation and experience

Since the use of hexavalent chromium in automotive and electronic equipment is largely prohibited, manydifferent hexavalent chromium free conversion layers have been developed. In this work, different Crfreephosphate and polycarboxylate based conversion coatings were characterized (with electron microscopyand other surface analytical methods) for the usage of a multifunctional property layer for hot dipgalvanised steel strips. The different corrosion resistance of such conversion coatings on ZM [1](ZnAlMg) and Z (Zn) will be another topic of this paper [2]. The corrosion protection properties ofthese phosphate based conversion coatings on Z and ZM were characterized in a standardized salt spray test.Finally the conversion layers and the barrier protection effect on Cr-free treated zinc and zinc magnesium wasinvestigated by cyclovoltammetry

Microstructure of Ag2BI4 (B = Ag, Cd) superionics studied by SEM, impedance spectroscopy and fractal dimension analysis

Two silver ion conducting solid electrolytes, Ag2HgI4 and Ag2CdI4, representing a wide class of AgI-based halogenide superionics have been the subjects of study by means of electrical impedance spectroscopy, SEM, porosity measurements and fractal dimension analysis. Even though both materials have been obtained by the same method under strictly identical conditions they were found to exhibit certain differences at the microstructural level. Thus, by the direct measurements of porosity and density it was found that the grain boundaries are better developed in silver mercuric iodide. On the assumption that pore geometry in the materials under study displays fractal character it was shown that the fractal dimension of the pore contours is larger in the case of Ag2HgI4. These results are in agreement with electrical studies which indicated that the grain boundary capacitance in Ag2CdI4 is two orders of magnitude smaller than that of the silver mercuric iodide

A role for endothelial nitric oxide synthase in intestinal stem cell proliferation and mesenchymal colorectal cancer

Abstract Background Nitric oxide (NO) has been highlighted as an important agent in cancer-related events. Although the inducible nitric oxide synthase (iNOS) isoform has received most attention, recent studies in the literature indicate that the endothelial isoenzyme (eNOS) can also modulate different tumor processes including resistance, angiogenesis, invasion, and metastasis. However, the role of eNOS in cancer stem cell (CSC) biology and mesenchymal tumors is unknown. Results Here, we show that eNOS was significantly upregulated in VilCre ERT2 Apc fl/+ and VilCre ERT2 Apc fl/fl mouse intestinal tissue, with intense immunostaining in hyperproliferative crypts. Similarly, the more invasive VilCre ERT2 Apc fl/+ Pten fl/+ mouse model showed an overexpression of eNOS in intestinal tumors whereas this isoform was not expressed in normal tissue. However, none of the three models showed iNOS expression. Notably, when 40 human colorectal tumors were classified into different clinically relevant molecular subtypes, high eNOS expression was found in the poor relapse-free and overall survival mesenchymal subtype, whereas iNOS was absent. Furthermore, Apc fl/fl organoids overexpressed eNOS compared with wild-type organoids and NO depletion with the scavenger carboxy-PTIO (c-PTIO) decreased the proliferation and the expression of stem-cell markers, such as Lgr5, Troy, Vav3, and Slc14a1, in these intestinal organoids. Moreover, specific NO depletion also decreased the expression of CSC-related proteins in human colorectal cancer cells such as β-catenin and Bmi1, impairing the CSC phenotype. To rule out the contribution of iNOS in this effect, we established an iNOS-knockdown colorectal cancer cell line. NO-depleted cells showed a decreased capacity to form tumors and c-PTIO treatment in vivo showed an antitumoral effect in a xenograft mouse model. Conclusion Our data support that eNOS upregulation occurs after Apc loss, emerging as an unexpected potential new target in poor-prognosis mesenchymal colorectal tumors, where NO scavenging could represent an interesting therapeutic alternative to targeting the CSC subpopulation

Texture effects in TiB2 coatings electrodeposited from a NaCl-KCl-K2TiF6-NaF-NaBF4 melt at 700 °c

TiB2 layers have been electrodeposited on steel and molybdenum substrates from a molten salt electrolyte at 700 °C by either direct current (DC) or pulsed plating techniques. The crystallographic textures of the coatings obtained are described and discussed

4-PBA Treatment Improves Bone Phenotypes in the Aga2 Mouse Model of Osteogenesis Imperfecta.

Osteogenesis imperfecta (OI) is a genetically heterogenous disorder most often due to heterozygosity for mutations in the type I procollagen genes, COL1A1 or COL1A2. The disorder is characterized by bone fragility leading to increased fracture incidence and long-bone deformities. Although multiple mechanisms underlie OI, endoplasmic reticulum (ER) stress as a cellular response to defective collagen trafficking is emerging as a contributor to OI pathogenesis. Herein, we used 4-phenylbutiric acid (4-PBA), an established chemical chaperone, to determine if treatment of Aga2+/- mice, a model for moderately severe OI due to a Col1a1 structural mutation, could attenuate the phenotype. In vitro, Aga2+/- osteoblasts show increased protein kinase RNA-like endoplasmic reticulum kinase (PERK) activation protein levels, which improved upon treatment with 4-PBA. The in vivo data demonstrate that a postweaning 5-week 4-PBA treatment increased total body length and weight, decreased fracture incidence, increased femoral bone volume fraction (BV/TV), and increased cortical thickness. These findings were associated with in vivo evidence of decreased bone-derived protein levels of the ER stress markers binding immunoglobulin protein (BiP), CCAAT/-enhancer-binding protein homologous protein (CHOP), and activating transcription factor 4 (ATF4) as well as increased levels of the autophagosome marker light chain 3A/B (LC3A/B). Genetic ablation of CHOP in Aga2+/- mice resulted in increased severity of the Aga2+/- phenotype, suggesting that the reduction in CHOP observed in vitro after treatment is a consequence rather than a cause of reduced ER stress. These findings suggest the potential use of chemical chaperones as an adjunct treatment for forms of OI associated with ER stress. © 2022 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR)

HIC1 attenuates Wnt signaling by recruitment of TCF-4 and β-catenin to the nuclear bodies

The hypermethylated in cancer 1 (HIC1) gene is epigenetically inactivated in cancer, and in addition, the haploinsufficiency of HIC1 is linked to the development of human Miller–Dieker syndrome. HIC1 encodes a zinc-finger transcription factor that acts as a transcriptional repressor. Additionally, the HIC1 protein oligomerizes via the N-terminal BTB/POZ domain and forms discrete nuclear structures known as HIC1 bodies. Here, we provide evidence that HIC1 antagonizes the TCF/β-catenin-mediated transcription in Wnt-stimulated cells. This appears to be due to the ability of HIC1 to associate with TCF-4 and to recruit TCF-4 and β-catenin to the HIC1 bodies. As a result of the recruitment, both proteins are prevented from association with the TCF-binding elements of the Wnt-responsive genes. These data indicate that the intracellular amounts of HIC1 protein can modulate the level of the transcriptional stimulation of the genes regulated by canonical Wnt/β-catenin signaling