Microstructure, wear, and corrosion characterization of high TiC content Inconel 625 matrix composites

Titanium carbide/Inconel 625 (nickel alloy) metal matrix composites (MMCs) are developed for the combination of the super mechanical and corrosion properties of nickel alloy matrix and the high hardness of reinforcing titanium carbide particles (TiCp). The microstructure, hardness, wear, and corrosion behavior of MMCs with different volume contents of TiCp (25, 50 and 70 vol.%) were investigated. The effect of increasing TiCp on the intermetallics and precipitates formed was examined using SEM/EDS and XRD analyses. The tribological behavior of the MMCs was investigated using wear testing with a pin-on-disk machine. The corrosion behavior was examined using potentiodynamic polarization experiments in 3% (w/v) NaCl solution. The results showed that the addition of TiCp into the Inconel 625 alloy resulted in formation of several intermetallics such as MoNi4, Cr2Ni3 and MoCr, in addition to molybdenum and chromium carbides in the matrix alloy. A great improvement in the hardness was resulted with addition of 25 vol.% TiCp and consequently the wear resistance was also improved. Further increase of TiCp from 50 to 70 vol.% did not result in more improvement of both hardness and wear resistance. The corrosion resistance of TiCp (25 vol.%) composite was comparable to that of monolithic Inconel 625 matrix alloy, while clear reduction in the corrosion resistance was found in the 50 and 70 vol.% composites. Keywords: Inconel 625, TiCp MMC, Microstructure, Hardness, Wear, Corrosio

Effect of the Si Content on the Dry and Wet Sliding Wear Behavior of the Developed Ti-15Mo-(0-2) Si Alloys for Biomedical Applications

The durability of a metallic biomaterial to withstand weight loss is a key factor in determining its service life and performance. Therefore, it is essential to create biomaterials with high wear resistance to ensure the biomaterial has a long service life. Thus, this study aims to explore the dry and wet sliding wear characteristics of the developed Ti-15Mo-xSi as-cast alloys (where x equals 0, 0.5, 1, 1.5, and 2 wt.%) in order to assess the impact of the Si addition on the microstructure, mechanical properties, and wear resistance and to consider them for biomedical applications. The wear experiments were conducted using a pin-on-desk wear testing machine at a load of 20 N and a sliding distance of 1000 m with and without applying simulated body fluid (SBF). Different techniques were utilized in the evaluation of the developed Ti-15Mo-xSi alloys. The results showed that significant grain refining was attained with the Si addition. The hardness, compressive strength, and wear resistance of the Ti-15Mo-xSi as-cast alloys increased with the increase in Si content. The Ti-15Mo-2Si as-cast alloy exhibited the highest dry and wet wear resistance of all the Ti-15Mo-xSi alloys. The worn surfaces were investigated, the roughness and main features were reported, and the wear mechanisms were also discussed

Targeting Hyaluronidase for Cancer Therapy: Antitumor Activity of Sulfated Hyaluronic Acid in Prostate Cancer Cells

The tumor cell-derived hyaluronidase HYAL-1 degrades hyaluronic acid (HA) into pro-angiogenic fragments that support tumor progression. Although HYAL-1 is a critical determinant of tumor progression and a marker for cancer diagnosis and metastasis prediction, it has not been evaluated as a target for cancer therapy. Similarly, sulfated hyaluronic acid (sHA) has not been evaluated for biological activity, although it is a HAase inhibitor. In this study we show that sHA is a potent inhibitor of prostate cancer. sHA blocked the proliferation, motility and invasion of LNCaP, LNCaP-AI, DU145 and LAPC-4 prostate cancer cells, also inducing caspase 8-dependent apoptosis associated with downregulation of Bcl-2 and phospho-Bad. sHA inhibited Akt signaling including androgen receptor (AR) phosphorylation, AR-activity, NFkb activation and VEGF expression. These effects were traced to a blockade in complex formation between PI3K and HA receptors and to a transcriptional downregulation of HA receptors, CD44 and RHAMM, along with PI3K inhibition. Angiogenic HA fragments or overexpression of myristoylated-Akt or HA receptors blunted these effects of sHA, implicating a feedback loop between HA receptors and PI3K/Akt signaling in the mechanism of action. In an animal model, sHA strongly inhibited LNCaP-AI prostate tumor growth without causing weight loss or apparent serum-organ toxicity. Inhibition of tumor growth was accompanied by a significant decrease in tumor angiogenesis and an increase in apoptosis index. Taken together, our findings offer mechanistic insights into the tumor-associated HA-HAase system and a preclinical proof-of-concept of the safety and efficacy of sHA to control prostate cancer growth and progression

<i>Khalas</i> date flavonoids inhibited cell viability, induced apoptosis and expression of the pro-autophagy LC3-B gene in human hepatocellular carcinoma cells (HepG2)

Autophagy is a protective mechanism important in human diseases as cancer. We evaluated the impact of khalas date extract (KDE) (20-60 mg/mL) on cell viability, morphological changes, DNA fragmentation and gene expression of LC3B-II associated with autophagosome on HepG2 cell line. The GC/MS identification of KDE showed its high content of flavonoids including quercetin, myricetin, kaempferol and catechol. KDE reduced cell viability of HepG2 with IC50 (31.52 mg/mL). Cells treated with KDE showed two band of DNA fragments at (30 and 40 mg) indicating that KDE induced DNA damage and apoptosis in HepG2. The analysis RT-PCR data showed a 0.2-fold increase in the expression of LC3-B in the cells treated with KDE versus control. We concluded that, KDE flavonoids such as quercetin, myricetin kaempferol exhibited anticancer properties manifested by inhibition of HepG2 cell viability and induction of apoptosis and upregulation of the pro-autophagy LC3-B gene. </p

Occupational exposure to polycyclic aromatic hydrocarbons influenced neither the frequency nor the spectrum of FGFR3 mutations in bladder urothelial carcinoma.

International audienceOccupational exposure to polycyclic aromatic hydrocarbons (PAH) is associated with an increased risk of urothelial carcinoma (UC). FGFR3 is found mutated in about 70% of Ta tumors, which represent the major group at diagnosis. The influence of PAH on FGFR3 mutations and whether it is related to the emergence or shaping of these mutations is not yet known. We investigated the influence of occupational PAH on the frequency and spectrum of FGFR3 mutations. We included on 170 primary urothelial tumors from five hospitals from France. Patients (median age, 64 yr) were interviewed to gather data on occupational exposure to PAH, revealing 104 non- and possibly PAH exposed patients, 66 probably and definitely exposed patients. Tumors were classified as follows: 75 pTa, 52 pT1, and 43 > or =pT2. Tumor grades were as follows: 6 low malignant potential neoplasms (LMPN) and 41 low-grade and 123 high-grade carcinomas. The SnaPshot method was used to screen for the following FGFR3 mutations: R248C, S249C, G372C, Y375C, A393E, K652E, K652Q, K652M, and K652T. Occupational PAH exposure was not associated with a particular stage or grade of tumors. Thirty-nine percent of the tumors harbored FGFR3 mutations. After adjustment for smoking, occupational exposure to PAH did not influence the frequency [OR, 1.10; 95% CI, 0.78-1.52], or spectrum of FGFR3 mutations. Occupational exposure to PAH influenced neither the frequency nor the spectrum of FGFR3 mutations and there was no direct relationship between these mutations and this occupational hazard