This paper explores how Dutch wax print has become interconnected within Central and Western African society and culture as well as throughout the diaspora. More than merely a fabric for many, Dutch wax print is an important signifier of African identity and heritage. The fabric also stands as evidence of the complex history of its traveled and cross-cultural past. During the early to mid-nineteenth century, Dutch colonizers began imitating wax resist-dyed batik fabric from Java, Indonesia, with newly developed machine technology. This was done with the intent to infiltrate the local Javanese textile market but did not succeed in doing so. Instead, the imitation batik was rejected by the Javanese market. This disapproval of the fabric in Java eventually led Dutch producers to conduct trade activity with West Africa, where a new market developed. The popularity of Dutch wax print and its association with African identity is linked to the long-standing communications between Dutch wax print distributors and West African women that sold the fabrics. These merchants would receive the fabrics and give them culturally-relevant and significant meanings related to proverbs and local sayings. Through the custom of integrating and redefining imported Dutch wax print, Africans have infused the fabric with deep cultural meaning and importance. For many in the diaspora, Dutch wax print is also a medium for expression. Contemporary artists Njideka Akunyili Crosby and Yinka Shonibare both include the fabrics into their art as a way to communicate ideas about their identity as well as the cultural heritage and multifaceted history of Africans over time. Today, throughout much of Africa and the diaspora, the fabric is a powerful medium for which to communicate ideas and concepts through cultural exchange.

Proprotein convertase subtilisin kexin 9 (PCSK9) is a circulating protein which binds with the low-density lipoprotein cholesterol receptor (LDL-R) and reduces the elimination of LDL-cholesterol from blood. Thus, PCSK9 inhibition has been used as a therapeutic strategy to treat cardiovascular disease. However, PCSK9 inhibition increases the expression of LDL-R by hepatocyte and is raising the hepatic load of cholesterol which is associated with the subsequent liver injury. Bile acids (BAs) are major cholesterol metabolites that serve as important signaling molecules for nutrient homeostasis under physiological levels and contribute to the hepatotoxicity at exceedingly high concentrations. The aim of this study is to investigate the role of PCSK9 inhibition in the development of liver toxicity through the accumulation of toxic bile acid profiles in high fat high cholesterol diet (HFHC). We quantified the liver BA profile (LC-MS) and BA-processing gene expression (RT-qPCR) from both WT and PCSK9-null mice fed a HFHC diet (0.75%) for 9 months (n=6-12 per group). In livers of WT mice, high cholesterol diet increased the total hepatic BAs, whereas such increase was further significantly amplified (p<0.05) in livers of PCSK9-null mice. High cholesterol diet down-regulated the major basolateral BA-uptake transporter Ntcp (p<0.001) and the BA-conjugation enzyme Baat (p<0.05). In livers of PCSK9-null mice, high cholesterol diet further decreased the expression of Ntcp (p<0.05) and also decreased the expression of the major canalicular BA-efflux transporter Bsep (p<0.05). The augmented BA increase in livers of PCSK9-null mice may be due to a decrease in Bsep expression, leading to BA hepatic accumulation. In summary, the present study showed that PCSK9 deficiency leads to an increased accumulation of hepatic BAs following a high cholesterol diet, and this may be explained by reduced hepatic efflux. This is important to further understand the impact of HFHC diets compounded with PCSK9 drug treatments.

The gut microbiome is a critical modifier of the host xenobiotic (foreign particle) biotransformation and is important in modulating the reduction and hydrolysis reactions of drugs and other chemicals. The Nuclear factor erythroid 2-related factor 2 (Nrf2) is a major oxidative stress sensor of the host and is highly conserved during evolution. Nrf2 is highly expressed in multiple important metabolic organs including the gastrointestinal tract. Following activation, Nrf2 detoxifies harmful free radicals and electrophiles, maintaining a reducing environment. Genetic variations of Nrf2 within the human population have been linked to cancer risks. My goal is to test the hypothesis that the Nrf2 genotype impacts gut microbiome as an additional mechanism to regulate the susceptibility to certain host diseases. Fecal microbial DNA was isolated from adult male wild type(MWT), female wild type(FWT), male Nrf2-knockout(MKO), and female Nrf2-knockout(FKO) mice (n=5 per group) using the EZNA stool kit. Amplified ribosomal DNA sequences used to identify specific bacteria (16S rDNA V4 libraries) were sequenced using the Illumina second generation sequencing platform(250bp paired-end). Data were analyzed using QIIME. Statistical significance was determined by two-way analysis of variance (ANOVA) followed by Tukey’s post hoc test(p < 0.05) using the multcomp (multiple comparisons analysis) package in R. Alpha Diversity showed that the richness of the fecal microbiome was lower in female than male mice in a Nrf2 dependent manner, and Nrf2 deficiency normalized the gender difference. In male mice, both the upregulation of the secondary bile acid-generating Clostridium and the downregulation of the carbohydrate metabolizing Rumminococcus flavefaciens were Nrf2-dependent. In female mice, the pro-inflammatory Rumminococcus gnavus was up regulated in the absence of Nrf2. In conclusion, the presence of the host Nrf2 gene is important for gender-divergent richness of the gut microbiome, as well as predicted microbial functions including inflammation, secondary bile acid synthesis, and carbohydrate metabolism.