Thermomechanical modelling of laser surface glazing for H13 tool steel

A two-dimensional thermomechanical finite element (FE) model of laser surface glazing (LSG) has been developed for H13 tool steel. The direct coupling technique of ANSYS 17.2 (APDL) has been utilised to solve the transient thermomechanical process. A H13 tool steel cylindrical cross-section has been modelled for laser power 200 W and 300 W at constant 0.2 mm beam width and 0.15 ms residence time. The model can predict temperature distribution, stress–strain increments in elastic and plastic region with time and space. The crack formation tendency also can be assumed by analysing the von Mises stress in the heat-concentrated zone. Isotropic and kinematic hardening models have been applied separately to predict the after-yield phenomena. At 200 W laser power, the peak surface temperature achieved is 1520 K which is below the melting point (1727 K) of H13 tool steel. For laser power 300 W, the peak surface temperature is 2523 K. Tensile residual stresses on surface have been found after cooling, which are in agreement with literature. Isotropic model shows higher residual stress that increases with laser power. Conversely, kinematic model gives lower residual stress which decreases with laser power. Therefore, both plasticity models could work in LSG for H13 tool steel

Towards systemic sclerosis and away from primary biliary cirrhosis: The case of PTPN22

Primary biliary cirrhosis (PBC) is a chronic cholestatic liver disease characterized by immune-mediated destruction of the small and medium size intrahepatic bile ducts. PBC patients often have concomitant autoimmune diseases, which are most often autoimmune thyroid disease, as well as Sicca syndrome. Occasionally, some PBC patients will also have systemic sclerosis of the limited cutaneous type (lcSSc). Conversely, up to one-fourth of SSc patients are positive for antimitochondrial antibody, the serologic hallmark of PBC. It is also common for SSc patients to have concomitant autoimmune disease, which may include PBC in rare cases. This has led to speculation of shared environmental and/or genetic factors, which lead to the development of PBC in SSc patients and vice versa. Recent genetic studies have revealed associations with several genes in both SSc and PBC. PTPN22 is one gene that has been associated with SSc, but not with PBC. It may be argued that some SSc patients with a particular genotype, which shares genes found in both conditions may develop PBC. Likewise, particular genes such as PTPN22 may infer susceptibility to SSc alone. The presence of PTPN22 may also contribute to the development of SSc in PBC patients. The lack of a large number of overlapping genes may, in part, explain the relative rarity of PBC with SSc and vice versa. This review will examine the literature surrounding the genetic associations of PBC and SSc, and the role of PTPN22 in particular. © 2011 Springer-Verlag

A Workshop on Measuring the Progression of Atrophy Secondary to Stargardt Disease in the ProgStar Studies: Findings and Lessons Learned

The Progression of Atrophy Secondary to Stargardt Disease (ProgStar) studies were designed to measure the progression of Stargardt disease through the use of fundus autofluorescence imaging, optical coherence tomography, and microperimetry. The overarching objectives of the studies were to document the natural course of Stargardt disease and identify the most appropriate clinical outcome measures for clinical trials assessing the efficacy and safety of upcoming treatments for Stargardt disease. A workshop organized by the Foundation Fighting Blindness Clinical Research Institute was held on June 11, 2018, in Baltimore, MD, USA. Invited speakers discussed spectral-domain optical coherence tomography, fundus autofluorescence, and microperimetry methods and findings in the ProgStar prospective study. The workshop concluded with a panel discussion of optimal endpoints for measuring treatment efficacy in Stargardt disease. We summarize the workshop presentations in light of the most current literature on Stargardt disease and discuss potential clinical outcome measures and endpoints for future treatment trials