Soft Tooling-Friendly Inductive Mold Heating-A Novel Concept.

In order to economize injection molded prototypes, additive manufacturing of, e.g., curable plastics based tools, can be employed, which is known as soft tooling. However, one disadvantage of such tools is that the variothermal process, which is needed to produce polymeric parts with small features, can lead to a shorter lifespan of the tooling due to its thermally impaired material properties. Here, a novel concept is proposed, which allows to locally heat the mold cavity via induction to circumvent the thermal impairment of the tooling material. The developed fabrication process consists of additive manufacturing of the tooling, PVD coating the mold cavity with an adhesion promoting layer and a seed layer, electroplating of a ferromagnetic metal layer, and finally patterning the metal layer via laser ablation to enhance the quality and efficiency of the energy transfer as well as the longevity by geometric measures. This process chain is investigated on 2D test specimens to find suitable fabrication parameters, backed by adhesion tests as well as environmental and induction tests. The results of these investigations serve as proof of concept and form the base for the investigation of such induction layers in actual soft tooling cavities.

p.H1069Q mutation in ATP7B and biochemical parameters of copper metabolism and clinical manifestation of Wilson's disease.

We compared the effect of the p.H1069Q mutation and other non-p.H1069Q mutations in ATP7B on the phenotypic expression of Wilson's disease (WD), and assessed whether the clinical phenotype of WD in compound heterozygotes depends on the type of mutation coexisting with the p.H1069Q. One hundred forty-two patients with clinically, biochemically, and genetically diagnosed WD were studied. The mutational analysis of ATP7B was performed by direct sequencing. A total number of 26 mutations in ATP7B were identified. The p.His1069Gln was the most common mutation (allelic frequency: 72%). Seventy-three patients were homozygous for this mutation. Of compound heterozygotes, 37 had frameshift/nonsense mutation, and 20 had other missense mutation on one of their ATP7B alleles. Twelve patients had two non-p.H1069Q mutations. Patients homozygous for the p.H1069Q mutation had the less severe disturbances of copper metabolism and the latest presentation of first WD symptoms. The most severely disturbed copper metabolism and the earliest age at initial disease manifestation was noticed in non-p.H1069Q patients. In compound heterozygotes, the type of mutation coexisting with the p.H1069Q to a small extent influenced WD phenotype. The phenotype of WD varied considerably among patients with the same genotype. The p.H1069Q mutation is associated with late WD manifestation and with a mild disruption of copper metabolism. In compound heterozygotes, the phenotype of WD to a small extent depends on the type of mutation coexisting with the p.H1069Q. Besides genotype, additional modifying factors seem to determine WD manifestations.