Tool life and hole surface integrity studies for hole-making of Ti6Al4V Alloy

With a significant growth in the use of titanium alloys in the aviation manufacturing industry, the key challenge of making high-quality holes in the aircraft assembly process needs to be addressed. In this work, case studies deploying traditional drilling and helical milling technologies are carried out to investigate the tool life and hole surface integrity for hole-making of titanium alloy. Results show that the helical milling process leads to much longer tool life, generally lower hole surface roughness, and higher hole subsurface microhardness. In addition, no plastically deformed layer or white layer has been observed in holes produced by helical milling. In contrast, a slightly softened region was always present on the drilled surface. The residual stress distributions within the hole surface, including compressive and tensile residual stress, have also been investigated in detail.

Enabling ultra high precision on hard steels using surface defect machining

This paper is an extension to an idea coined during the 13th EUSPEN Conference (P6.23) named "surface defect machining" (SDM). The objective of this work was to demonstrate how a conventional CNC turret lathe can be used to obtain ultra high precision machined surface finish on hard steels without recourse to a sophisticated ultra precision machine tool. An AISI 4340 hard steel (69 HRC) workpiece was machined using a CBN cutting tool with and without SDM. Post-machining measurements by a Form Talysurf and a Scanning Electron Microscope (FEI Quanta 3D) revealed that SDM culminates to several key advantages (i) provides better quality of the machined surface integrity and offers (ii) lowering feed rate to 5μm/rev to obtain a machined surface roughness of 30 nm (optical quality).

Advances in the surface defect machining (SDM) of hard steels

This paper reports the realisation of precision surface finish (Ra 30 nm) on AISI 4340 steel using a conventional turret lathe by adapting and incorporating a surface defect machining (SDM) method [Wear, 302, 2013 (1124-1135)]. Conventional ways of machining materials are limited by the use of a critical feed rate, experimentally determined as 0.02 mm/rev, beyond which no appreciable improvement in the machined quality of the surface is obtained. However, in this research, the novel application of an SDM method was used to overcome this minimum feed rate limitation ultimately reducing it to 0.005 mm/rev and attaining an average machined surface roughness of 30 nm. From an application point of view, such a smooth finish is well within the values recommended in the ASTM standards for total knee joint prosthesis. Further analysis was done using SEM imaging, white light interferometry and numerical simulations to verify that adapting SDM method provides improved surface integrity by reducing the extent of side flow, microchips and weldments during the hard turning process.

Insulin and insulin-like growth factor signaling increases proliferation and hyperplasia of the ovarian surface epithelium and decreases follicular integrity through upregulation of the PI3-kinase pathway

BACKGROUND: The ovarian surface epithelium responds to cytokines and hormonal cues to initiate proliferation and migration following ovulation. Although insulin and IGF are potent proliferative factors for the ovarian surface epithelium and IGF is required for follicle development, increased insulin and IGF activity are correlated with at least two gynecologic conditions: polycystic ovary syndrome and epithelial ovarian cancer. Although insulin and IGF are often components of in vitro culture media, little is known about the effects that these growth factors may have on the ovarian surface epithelium morphology or how signaling in the ovarian surface may affect follicular health and development.

METHODS: Ovaries from CD1 mice were cultured in alginate hydrogels in the presence or absence of 5 μg/ml insulin or IGF-I, as well as small molecule inhibitors of IR/IGF1R, PI 3-kinase signaling, or MAPK signaling. Tissues were analyzed by immunohistochemistry for expression of cytokeratin 8 to mark the ovarian surface epithelium, Müllerian inhibiting substance to mark secondary follicles, and BrdU incorporation to assess proliferation. Changes in gene expression in the ovarian surface epithelium in response to insulin or IGF-I were analyzed by transcription array. Extracellular matrix organization was evaluated by expression and localization of collagen IV.

RESULTS: Culture of ovarian organoids with insulin or IGF-I resulted in formation of hyperplastic OSE approximately 4-6 cell layers thick with a high rate of proliferation, as well as decreased MIS expression in secondary follicles. Inhibition of the MAPK pathway restored MIS expression reduced by insulin but only partially restored normal OSE growth and morphology. Inhibition of the PI 3-kinase pathway restored MIS expression reduced by IGF-I and restored OSE growth to a single cell layer. Insulin and IGF-I altered organization of collagen IV, which was restored by inhibition of PI 3-kinase signaling.

CONCLUSIONS: While insulin and IGF are often required for propagation of primary cells, these cytokines may act as potent mitogens to disrupt cell growth, resulting in formation of hyperplastic OSE and decreased follicular integrity as measured by MIS expression and collagen deposition. This may be due partly to altered collagen IV deposition and organization in the ovary in response to insulin and IGF signaling mediated by PI 3-kinase.

Wild-type measles virus infection of primary epithelial cells occurs via the basolateral surface without syncytium formation or release of infectious virus

The lymphotropic and myelotropic nature of wild-type measles virus (wt-MV) is well recognized, with dendritic cells and lymphocytes expressing the MV receptor CD150 mediating systemic spread of the virus. Infection of respiratory epithelial cells has long been considered crucial for entry of MV into the body. However, the lack of detectable CD150 on these cells raises the issue of their importance in the pathogenesis of measles. This study utilized a combination of in vitro, ex vivo and in vivo model systems to characterize the susceptibility of epithelial cells to wt-MV of proven pathogenicity. Low numbers of MV-infected epithelial cells in close proximity to underlying infected lymphocytes or myeloid cells suggested infection via the basolateral side of the epithelium in the macaque model. In primary cultures of human bronchial epithelial cells, foci of MV-infected cells were only observed following infection via the basolateral cell surface. The extent of infection in primary cells was enhanced both in vitro and in ex vivo cornea rim tissue by disrupting the integrity of the cells prior to the application of virus. This demonstrated that, whilst epithelial cells may not be the primary target cells for wt-MV, areas of epithelium in which tight junctions are disrupted can become infected using high m.o.i. The low numbers of MV-infected epithelial cells observed in vivo in conjunction with the absence of infectious virus release from infected primary cell cultures suggest that epithelial cells have a peripheral role in MV transmission.