Representation of Hispanics, especially Hispanic women, is notoriously low in data science programs in higher education and in the tech industry. The engagement of undergraduate students in research, often and early in their path towards degree completion, has been championed as one of the principal reforms necessary to increase the number of capable professionals in STEM. The benefits attributed to undergraduate research experiences have been reported to disproportionately benefit individuals from groups that have been historically underrepresented in STEM. The IDI-BD2K (Increasing Diversity in Interdisciplinary Big Data to Knowledge) Program funded by the NIH at the XXXXXXwas designed to bridge the increasing digital and data divide at the university. The college's population is 98% Hispanic, it is one of the top 20 producers of Hispanic PhDs in Science and Engineering and yet there is no formal data science program. There also exists a gender imbalance in computing at the College of Natural Sciences at the XXXX. Over 60% of the undergraduate students in Biology are women. However, the percentage of women in Computer Science hovers around 15%. The IDI-BD2K was created to address these concerns and increase the participation of Hispanics in interdisciplinary computational and quantitative research in XXXX. The Interdisciplinary and Quantitative Biology Research Experience for Undergraduates (IQ-Bio-REU) summer program forked off from the IDI-BD2K and was created to engage ten (10) underrepresented undergraduate students from the US and its territories in authentic research experiences in emerging fields of biology which integrate quantitative and computational approaches to projects ranging from molecular biosciences to bioinformatics to ecology to bridge the digital and data divide for Hispanics and women in computing. This paper documents the additions to curriculum as a result of the IDI-BD2K, the first summer of the IQ-Bio-REU and highlights the importance of mutually beneficial collaborations with top research institutions to make it possible.

Abstract-InfiniBand is widely accepted as a high performance networking technology for datacenters and HPC clusters. It uses the Remote Direct Memory Access (RDMA) where communication tasks that are typically assigned to CPUs are offloaded to the Channel Adapters (CAs), resulting in a significant increase of the throughput and reduction of the latency and CPU load. In this paper, we make an introduction to InfiniBand and IP over InfiniBand (IPoIB), where the latter is a protocol proposed by the IETF to run traditional socket-oriented applications on top of InfiniBand networks. We also evaluate the performance of InfiniBand using different transport protocols with several benchmarking tools in a testbed. For RDMA communications, we consider three transport services: (1) Reliable Connection, (2) Unreliable Connection, and (3) Unreliable Datagram. For UDP and TCP, we use IPoIB. Our results show significant differences between RDMA and IPoIB communications, encouraging the coding of new applications with InfiniBand verbs. Also, it is noticeable that IPoIB in datagram mode and in connected mode have similar performance for small UDP and TCP payload. However, the differences get important as the payload size increases.

Prostate Cancer (PCa) is the second leading diagnosed cancer and the fifth cause of cancer mortality in men worldwide. The combination of chemotherapy with phytochemicals have been widely studied in different types of cancer including PCa. Andrographolide, a labdane diterpenoid that is the main bioactive component of the medicinal plant Andrographis paniculata, have shown a wide range of biological activities including anticarcinogenic properties. Previous studies from our laboratory has shown that Andrographolide induces a DNA damage response involving cell grown suppression, cell cycle arrest and apoptosis in PCa in vitro. In this study we aim to evaluate the role of Andrographolide in carbohydrate metabolism and mitochondrial function in PCa. Tumors from a mouse xenograft model in which the anterior prostate lobes of SCID mice were injected with 22RV1 cells and treated with Andrographolide during 4 weeks, were used for microarray analysis. The global gene expression profile was identified and analyzed using the Affymetrix GeneChip® Human Gene 2.0 array. Ingenuity Pathway Analysis (IPA) revealed alterations in carbohydrate metabolism and predicted the upregulation of mitochondrial associated genes DAP3 and HIFa. The microarray results were confirmed by real-time quantitative PCR (RT-qPCR) for some representative genes. Mitochondrial function was assessed using the Seahorse Mito Stress assay in androgen-dependent (22RV1) and androgen-independent (PC3) cell lines treated with Andrographolide (25µM). RT-qPCR showed that ZNF676, ZNF766, TXNL4 were up-regulated in PC3 PCa cells treated with Andrographolide, and ZNF676, TXNL4B, SASS6 and FBXL4 in 22Rv1 PCa cells treated with Andrographolide. The Seahorse Mito Stress assay showed a reduction of ATP Production, Basal Respiration and Spare Respiratory Capacity in 22RV1 PCa cells when treated with Andrographolide 25mM at 24hrs and 48hrs. ATP production was reduced in PC3 PCa cells treated with 25mM Andrographolide for 24hrs and 48hrs. Our data confirmed that Andrographolide alters the regulation of genes associated with carbohydrate metabolism, and the mitochondrial function. Our ongoing studies are evaluating the effect of Andrographolide on mtDNA damage and mtDNA expression in PCa cells. This data suggests a novel mechanism in which Andrographolide up-regulates nuclear carbohydrate metabolism's genes and suppress the mitochondrial activity in PCa. Citation Format: Jesus M. Sosa Rivera, Andres Lopez Rivas, Yarelis Roque Reyes, Desiree Arroyo Villegas, Maria Sanchez Velazquez, Humberto Ortiz Zuazaga, Carlos Torres Ramos, Magaly Martinez Ferrer. Andrographolide induces metabolic changes and suppresses mitochondrial activity in prostate cancer [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 4784.

Prostate cancer (PCa) is the second most common diagnosed cancer and the fifth cause of cancer mortality in men worldwide. In the United States, PCa is the most common diagnosed cancer and the third cause of cancer mortality in men. PCa is often treated using radiation, chemotherapy or radical prostatectomy. However, the combination of natural products with the standard of care treatment is an emerging area of cancer therapeutics. Previous studies from our laboratory showed that Andrographolide inhibits prostate cancer progression through a DNA damage response mechanism. In this study, we investigated the role of Andrographolide in metabolic function. Tumor development was performed by using an orthotopic xenograft model in which the prostates of SCID mice were injected with the prostate cancer cell line 22RV1. These mice were treated three times per week with Andrographolide 10 or 25 mg/kg for 4 weeks. Tumor tissue was collected to evaluate the effect of Andrographolide in tumor gene expression. Microarray analysis identified carbohydrate metabolism, connective tissue development and function, and cell cycle as a major molecular and cellular function altered in tumors treated with Andrographolide. Specifically, we found that the expression profiles of SASS6, FBXL4, MYDGF, TKK, MRSP33 and ZNF766 were significantly altered, suggesting that Andrographolide may be altering tumor metabolism. To confirm this observation, bioenergetics profile was determined using an Extracellular Flux Analyzer (Seahorse XF Mito Stress assay). The results of these experiments indicate that Andrographolide treatment decreases the Maximum and Spare Respiratory Capacity of PCa cells. These data suggest that Andrographolide disrupts the bioenergetics profile of PCa cells.Support or Funding InformationWork funded by Institutional funds from the University of Puerto Rico Comprehensive Cancer Center and the School of Pharmacy. HOZ was supported in part by NIH‐NCI grant U54CA096297. MARC grant 5T34GM007821‐38.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.