Impact of iodized table salt on the sensory characteristics of bread, sausage and pickle

Abstract The impact of iodized table salt on the sensory quality of wheat bread, bologna sausage and pickled cucumber was studied. Table salt (NaCl) content of the products was 1.7, 1.2 and 1.7 g/100 g, respectively. Iodine, added as potassium iodide (KI), was incorporated at levels 0, 25, 50 and 100 mg per kg table salt. Odor, flavor, appearance, and texture were evaluated using deviation from reference descriptive analysis (12 panelists, 4 replicates). Each sample was rated against the non-iodized reference sample (0 mg iodine). The retention of iodine during processing and storage was determined chemically. The iodine level 25 mg/kg, corresponding to current recommendations, did not cause sensory changes in tested products. In sausage, 50 and 100 mg/kg levels were associated with minor changes in texture and color. The maximum retention of iodine was 83% for bread, 98% for sausage, and 51% for cucumber. We did not find any sensory obstacle to using iodized table salt in industrial food production. Due to loss in manufacturing and inadequate intakes, iodine additions higher than currently recommended should be considered.Peer reviewe

The evolutionarily conserved long non‐coding RNA <i>LINC00261</i> drives neuroendocrine prostate cancer proliferation and metastasis <i>via</i> distinct nuclear and cytoplasmic mechanisms

Metastatic neuroendocrine prostate cancer (NEPC) is a highly aggressive disease, whose incidence is rising. Long noncoding RNAs (lncRNAs) represent a large family of disease- and tissue-specific transcripts, most of which are still functionally uncharacterized. Thus, we set out to identify the highly conserved lncRNAs that play a central role in NEPC pathogenesis. To this end, we performed transcriptomic analyses of donor-matched patient-derived xenograft models (PDXs) with immunohistologic features of prostate adenocarcinoma (AR+/PSA+) or NEPC (AR-/SYN+/CHGA+ ) and through differential expression analyses identified lncRNAs that were upregulated upon neuroendocrine transdifferentiation. These genes were prioritized for functional assessment based on the level of conservation in vertebrates. Here, LINC00261 emerged as the top gene with over 3229-fold upregulation in NEPC. Consistently, LINC00261 expression was significantly upregulated in NEPC specimens in multiple patient cohorts. Knockdown of LINC00261 in PC-3 cells dramatically attenuated its proliferative and metastatic abilities, which are explained by parallel downregulation of CBX2 and FOXA2 through distinct molecular mechanisms. In the cell cytoplasm, LINC00261 binds to and sequesters miR-8485 from targeting the CBX2 mRNA, while inside the nucleus, LINC00261 functions as a transcriptional scaffold to induce SMAD-driven expression of the FOXA2 gene. For the first time, these results demonstrate hyperactivation of the LINC00261-CBX2-FOXA2 axes in NEPC to drive proliferation and metastasis, and that LINC00261 may be utilized as a therapeutic target and a biomarker for this incurable disease

Identification of a long non-coding RNA that mediates response to therapy in castration-resistant prostate cancer

Prostate cancer (PCa) is the second most commonly diagnosed neoplasm and the sixth leading cause of cancer related death in males, worldwide. It is commonly treated using androgen deprivation therapy, but around 25% of PCas develop resistance to this treatment and are therefore called Castration-Resistant Prostate Cancers (CRPCs). Effective therapies for CRPC include: the second-generation anti-androgen enzalutamide; the taxane cabazitaxel; carboplatin, which is active in androgen receptor negative CRPCs. Nevertheless, response to these therapies is often short-lived making CRPC incurable. Recent evidence suggests that long non-coding RNAs (lncRNAs) can play a role in drug resistance. Using RNA sequencing and qPCR validation, we analysed the expression of lncRNAs in a panel of patient-derived PCa xenografts (PDXs) with opposing sensitivity to castration. Our data showed that HORAS5 was the most consistently up-regulated lncRNA among the CRPC vs. hormone-sensitive PDXs. Moreover, HORAS5 protected CRPC cells from androgen-deprivation induced apoptosis. We next investigated whether HORAS5 had any effect on PCa cells` response to therapies. We analysed the expression and sub-cellular localization of HORAS5 in CRPC cell lines with endogenous or lentiviral-induced expression of HORAS5. CRPC cells were treated with different concentrations of cabazitaxel, carboplatin and enzalutamide. Upon treatment, the expression of HORAS5 was tested via RT-qPCR. Our data showed a significant, dose-dependent increase in HORAS5 expression in cells exposed to cabazitaxel (p<0.01; maximum fold change: 95.07918) and carboplatin (p<0.01; maximum fold change: 71.324). We did not register any significant increase in HORAS5 expression after treatment with enzalutamide. Hence, our results revealed that the expression of HORAS5 can be modulated by two chemotherapeutics in a dose-dependent manner. We are currently evaluating whether HORAS5 silencing affects CRPC cells` response to these drugs. Our data demonstrated that HORAS5 is located mainly in the cytoplasm of PCa cells, and we have predicted that HORAS5 may bind several microRNAs. We therefore hypothesized the involvement of HORAS5 in RNA-induced silencing, where it could act like a competitive endogenous RNA. Our findings suggest that HORAS5 could have a role in CRPC cells` response to therapy. We will further investigate the molecular mechanisms by which HORAS5 drives this phenomenon

The role of epigenetics and long noncoding RNA MIAT in neuroendocrine prostate cancer

Neuroendocrine prostate cancer (NEPC) is the most lethal prostatic neoplasm. NEPC is thought to originate from the transdifferentiation of AR-positive adenocarcinoma cells. We have previously shown that an epigenetic/noncoding interactome (ENI) orchestrates cancer cells' plasticity, thereby allowing the emergence of metastatic, drug-resistant neoplasms. The primary objective of this manuscript is to discuss evidence indicating that some components of the ENI (Polycomb genes, miRNAs) play a key role in NEPC initiation and progression. Long noncoding RNAs represent vast and largely unexplored component of the ENI. Their role in NEPC has not been investigated. We show preliminary evidence indicating that a lncRNA (MIAT) is selectively upregulated in NEPCs and might interact with Polycomb genes. Our results indicate that long noncoding RNAs can be exploited as new biomarkers and therapeutic targets for NEPC