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In recent decades, 3D printing (also known as additive manufacturing) techniques have moved beyond their traditional applications in the fields of industrial manufacturing and prototyping to increasingly find roles in scientific research contexts, such as synthetic chemistry. We present a general approach for the production of bespoke chemical reactors, termed reactionware, using two different approaches to extrusion-based 3D printing. This protocol describes the printing of an inert polypropylene (PP) architecture with the concurrent printing of soft material catalyst composites, using two different 3D printer setups. The steps of the PROCEDURE describe the design and preparation of a 3D digital model of the desired reactionware device and the preparation of this model for use with fused deposition modeling (FDM) type 3D printers. The protocol then further describes the preparation of composite catalyst-silicone materials for incorporation into the 3D-printed device and the steps required to fabricate a reactionware device. This combined approach allows versatility in the design and use of reactionware based on the specific needs of the experimental user. To illustrate this, we present a detailed procedure for the production of one such reactionware device that will result in the production of a sealed reactor capable of effecting a multistep organic synthesis. Depending on the design time of the 3D model, and including time for curing and drying of materials, this procedure can be completed in ∼3 d.

Interferon-alpha therapy has become a main stay of treatment for hepatitis-B patients. The sustained remission rates are around 30%, and the factors determining response are poorly defined. Our study aimed to search for the genetic differences between responder and non-responder patients. We have found 13 short tandem repeat markers (STR) that display different allele and/or genotype frequency between the two patient groups. Eleven out of 13 STR markers were selected to perform principal component analysis and hierarchical clustering. The study subjects could be further divided into six groups based on their genetic similarity, which correlated with the drug response rate. In conclusion, this pilot study has developed a new approach to identify genetic markers that allows us to predict the drug response in hepatitis B patients. Our study utilizing STR markers may provide an alternative approach to the utilized SNP markers in pharmacogenetic study.

The genome-wide linkage disequilibrium screen for loci associated with genetic difference between allergic and nonallergic asthma was conducted with 763 autosomal STR markers and included 190 asthmatic children. Evidence for association with differences between the two forms of asthma was observed for 36 STR markers. Marker-to-marker synergetic effect and by simulation resampling tests revealed D5S2011, D6S305, and D9S286 were important loci in allergic asthma while D6S1574, D8S1769, and D19S226 were important in nonallergic asthma. Our results show strong genetic evidence that these markers play an important role in defining allergic and nonallergic asthma and provides important candidates of susceptible genes in these two categories of asthma. This study further shows that asthma is, indeed, a heterogeneous group of underlying diseases and, although with similar clinical phenotypes, may have different clinical severities, outcomes, and need more tailor-made management.

Chromosome 5, especially the 5q31-33 region, may contain one or more loci to control total serum IgE as well as asthma and bronchial hyperresponsiveness. To investigate the regions related with IgE level in chromosome 5, we performed a case-control association study on 105 high-IgE-level and 85 normal-IgE-level asthmatic children using 43 microsatellite markers that span the whole chromosome 5 with 5 cM intervals. One of microsatellite marker, D5S2011, had significantly different allele frequency between the two asthmatic groups. E allele (143 bp) of the D5S2011 marker was more frequent in high-IgE asthmatics. CD14 is the candidate gene of atopy and asthma and is distant from D5S2011 by about 1 Mb. We analyzed the SNP genotypes in the CD14 gene region alone and in combination with microsatellite marker D5S2011. The CD14/-2984 polymorphism but not the CD14/-159 is associated with IgE level in Taiwanese asthmatic children. The CD14/-159 allele was observed only to be associated with IgE level when -159T was part of a haplotype containing a D5S2011 E allele. The combination analysis using SNP and STRP markers provided a novel method for increasing detection power in candidate gene association studies.

To evaluate basic informativeness of commercially available microsatellite markers in theTaiwanese population, 190 unrelated Taiwanese children were genotyped using ABI PRISM Linkage Mapping Set-HD5. The average heterozygosity in Taiwanese was slightly lower than that in Caucasians among these 811 microsatellite markers. There were 50 marker loci with heterozygosities lower than 50%. Moreover, allelic distributions at many of the loci were significantly different in two ethnic groups. The results reported here represent a valuable database for disease genes mapping in the Taiwanese population. This database can be easily accessed at the Web site of Vita Genomics, Inc. (http://www.vitagenomics.com/str.html).