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

HORAS5 promotes cabazitaxel resistance in castration resistant prostate cancer via a BCL2A1-dependent survival mechanism

Background: Long non-coding RNAs (lncRNAs) have been recently identified as key players in several cancer-associated pathways such as metastasis and drug resistance. Emerging evidence indicates that the HORAS5 lncRNA (i.e. linc00161) modulates drug response in different malignancies. In a recently published study, we have shown that HORAS5 promotes the survival of androgen receptor-positive (AR+) castration resistant prostate cancer (CRPC) cells. Preliminary data obtained in our lab show that HORAS5 is involved in response to cabazitaxel, in both AR+ and AR- CRPC cells.Methods: HORAS5 expression was modulated in AR+ and AR- CRPC cells with lentiviral-mediated overexpression and siRNA-based silencing. We measured cell count (Trypan Blue exclusion test) and apoptosis (caspase 3/7) of CRPC cells exposed to clinically achievable concentrations of cabazitaxel. RNA sequencing, RT-qPCR and western blot were used to identify genes regulated by HORAS5 in cabazitaxel-treated cells. We also transfected the cells with antisense oligonucleotides (ASOs), a technology that is currently being tested in clinical trials.Results: Our results show that HORAS5 overexpression increases cabazitaxel IC50 (p = 0.01), while HORAS5 silencing has an opposite effect (p = 0.003). HORAS5 also inhibits caspase activity upon cabazitaxel treatment (p 50 (p = 0.03) in response to cabazitaxel.Conclusions: Our findings show that HORAS5 mediates cabazitaxel resistance in both AR+ and AR- CRPC cells via regulation of the anti-apoptotic BCL2A1. Experiments with ASOs demonstrate the translational potential of HORAS5 inhibition. We are currently assessing HORAS5 expression in biological fluids from patients exposed (or not) to cabazitaxel.Legal entity responsible for the study: Francesco Crea.Funding: The Open University.Disclosure: All authors have declared no conflicts of interest

The sarcopenia and physical frailty in older people: multi-component treatment strategies (SPRINTT) project: description and feasibility of a nutrition intervention in community-dwelling older Europeans

Background: The “Sarcopenia and Physical Frailty in Older People: Multicomponent Treatment Strategies” (SPRINTT) project sponsored a multi-center randomized controlled trial (RCT) with the objective to determine the effect of physical activity and nutrition intervention for prevention of mobility disability in community-dwelling frail older Europeans. We describe here the design and feasibility of the SPRINTT nutrition intervention, including techniques used by nutrition interventionists to identify those at risk of malnutrition and to carry out the nutrition intervention. Methods: SPRINTT RCT recruited older adults (≥ 70 years) from 11 European countries. Eligible participants (n = 1517) had functional limitations measured with Short Physical Performance Battery (SPPB score 3–9) and low muscle mass as determined by DXA scans, but were able to walk 400 m without assistance within 15 min. Participants were followed up for up to 3 years. The nutrition intervention was carried out mainly by individual nutrition counseling. Nutrition goals included achieving a daily protein intake of 1.0–1.2 g/kg body weight, energy intake of 25–30 kcal/kg of body weight/day, and serum vitamin D concentration ≥ 75 mmol/L. Survey on the method strategies and feasibility of the nutrition intervention was sent to all nutrition interventionists of the 16 SPRINTT study sites. Results: Nutrition interventionists from all study sites responded to the survey. All responders found that the SPRINTT nutrition intervention was feasible for the target population, and it was well received by the majority. The identification of participants at nutritional risk was accomplished by combining information from interviews, questionnaires, clinical and laboratory data. Although the nutrition intervention was mainly carried out using individual nutritional counselling, other assisting methods were used as appropriate. Conclusion: The SPRINTT nutrition intervention was feasible and able to adapt flexibly to varying needs of this heterogeneous population. The procedures adopted to identify older adults at risk of malnutrition and to design the appropriate intervention may serve as a model to deliver nutrition intervention for community-dwelling older people with mobility limitations