Acceptance of low-sugar yoghurt among Latvian teenagers

Over a thousand year history, yoghurt has become one of a widely consumed product in the world. Its reputation as a healthy food has been undermined recently by concerns over the high sugar content. The majority of consumers expects and prefers yoghurts to be sweet. However, governments across Europe are calling for significant cuts in the amount of added sugar used in yoghurt production. The aim of the study was to evaluate the acceptance of low-sugar yoghurt produced by different commercial β-galactosidases by teenagers. Standardised milk with fat content 2.0% (SC Tukuma piens) was pasteurized at 95 ± 1 °C 5 min, cooled down till 43 ± 1 °C and fermented with β-galactosidase and starter YC-X11 (Chr. Hansen, Denmark) and fermented till pH 4.50 ± 0.20. Different commercial β-galactosidases: Nola™ Fit 5500, Ha-Lactase 5200 (Chr. Hansen, Denmark), GODO-YNL2 (Danisco, Denmark) and BrennZyme (Brenntag PolskaSp, Poland) were used. Fermented samples were gently mixed and cooled down till 6 ± 1 °C and 5% (w/w) of sugar was added to each sample. Sensory evaluation of the yoghurt’s samples was performed by teenagers (14–18 years, n = 50) at Aizputes Secondary School (Latvia). Lactose and monosaccharides concentration prior to sugar addition was detected by HPLC (Shimadzu LC 20 Prominence, Japan). The lactose hydrolysis into glucose and galactose by the use of β-galactosidase helps to increase sweetness through an occurrence of natural sugars in milk. During sensory evaluation, teenagers admitted the yoghurt with reduced sugar as sweet, significantly sweeter (P < 0.05) was yoghurt sample with Nola™ Fit 5500. The results demonstrated that it is possible to reduce sugar in yoghurt production and to gain consumer acceptance through the occurrence of glucose and galactose, but it is problematic to offer lactose-free or reduced lactose products to consumers without lactose intolerance

Human RSPO1/R-spondin1 Is Expressed during Early Ovary Development and Augments β-Catenin Signaling

Human testis development starts from around 42 days post conception with a transient wave of SRY expression followed by up-regulation of testis specific genes and a distinct set of morphological, paracrine and endocrine events. Although anatomical changes in the ovary are less marked, a distinct sub-set of ovary specific genes are also expressed during this time. The furin-domain containing peptide R-spondin1 (RSPO1) has recently emerged as an important regulator of ovary development through up-regulation of the WNT/β-catenin pathway to oppose testis formation. Here, we show that RSPO1 is upregulated in the ovary but not in the testis during critical early stages of gonad development in humans (between 6–9 weeks post conception), whereas the expression of the related genes WNT4 and CTNNB1 (encoding β catenin) is not significantly different between these tissues. Furthermore, reduced R-spondin1 function in the ovotestis of an individual (46,XX) with a RSPO1 mutation leads to reduced β-catenin protein and WNT4 mRNA levels, consistent with down regulation of ovarian pathways. Transfection of wild-type RSPO1 cDNA resulted in weak dose-dependent activation of a β-catenin responsive TOPFLASH reporter (1.8 fold maximum), whereas co-transfection of CTNNB1 (encoding β-catenin) with RSPO1 resulted in dose-dependent synergistic augmentation of this reporter (approximately 10 fold). Furthermore, R-spondin1 showed strong nuclear localization in several different cell lines. Taken together, these data show that R-spondin1 is upregulated during critical stages of early human ovary development and may function as a tissue-specific amplifier of β-catenin signaling to oppose testis determination

Different populations and sources of human mesenchymal stem cells (MSC): A comparison of adult and neonatal tissue-derived MSC

The mesenchymal stroma harbors an important population of cells that possess stem cell-like characteristics including self renewal and differentiation capacities and can be derived from a variety of different sources. These multipotent mesenchymal stem cells (MSC) can be found in nearly all tissues and are mostly located in perivascular niches. MSC have migratory abilities and can secrete protective factors and act as a primary matrix for tissue regeneration during inflammation, tissue injuries and certain cancers

Schimke immunoosseous dysplasia: defining skeletal features

Schimke immunoosseous dysplasia (SIOD) is an autosomal recessive multisystem disorder characterized by prominent spondyloepiphyseal dysplasia, T cell deficiency, and focal segmental glomerulosclerosis. Biallelic mutations in swi/snf-related, matrix-associated, actin-dependent regulator of chromatin, subfamily a-like 1 (SMARCAL1) are the only identified cause of SIOD, but approximately half of patients referred for molecular studies do not have detectable mutations in SMARCAL1. We hypothesized that skeletal features distinguish between those with or without SMARCAL1 mutations. Therefore, we analyzed the skeletal radiographs of 22 patients with and 11 without detectable SMARCAL1 mutations. We found that patients with SMARCAL1 mutations have a spondyloepiphyseal dysplasia (SED) essentially limited to the spine, pelvis, capital femoral epiphyses, and possibly the sella turcica, whereas the hands and other long bones are basically normal. Additionally, we found that several of the adolescent and young adult patients developed osteoporosis and coxarthrosis. Of the 11 patients without detectable SMARCAL1 mutations, seven had a SED indistinguishable from patients with SMARCAL1 mutations. We conclude therefore that SED is a feature of patients with SMARCAL1 mutations and that skeletal features do not distinguish who of those with SED have SMARCAL1 mutations