A study on fibre addition to gluten free bread: its effects on bread quality and in vitro digestibility.

The aim of this study was to assess the impact of fibre addition on gluten-free (GF) dough properties and bread technological quality, and on protein and starch in vitro digestibility. Soluble (Inulin, In) and insoluble fibres (oat fibre, OF, and type IV resistant starch, RSIV) were used at 5 and 10% substitution levels. Dough firmness increased when insoluble fibres were added, and decreased when In was used. Incorporation of insoluble fibres resulted into bread with a low specific volume (SBV) since firmer dough were more difficult to expand during proofing and baking. Staling rate was reduced after fibre addition, with the exception being OF 10%, as its lower SBV may have favoured molecule re-association. In general, protein and starch digestibility increased when fibres were added at 5%, and then decreased after further increasing the level. Fibres may have disrupted bread crumb structure, thus increasing digestibility, although the higher addition may have led to a physical and/or chemical impediment to digestion. Inulin has well-known physiological effects, while RS presented the most important effect on in vitro starch digestibility (GI). These results showed the possibility of adding different fibres to GF bread to decrease the GI and increase protein digestibility, while obtaining an overall high quality end-product.

Differences in body condition of gilts that are maintained from mating to the end of gestation affect mammary development.

The goal of this project was to determine if different body conditions in late gestation that are due to varying body conditions at mating affect mammary development and mammary gene expression of gilts. Gilts that were fed ad libitum in the growing period were selected based on their backfat depths to form 3 groups at mating, namely, low backfat (LBF; 12-15 mm; = 14), medium backfat (MBF; 17-19 mm; = 15), and high backfat (HBF; 22-26 mm; = 16). During gestation, LBF, MBF, and HBF gilts were fed approximately 1.25, 1.43, and 1.63 times maintenance requirements to maintain their differences in body condition. Feed intake was increased by 1 kg in the last 10 d of gestation. Backfat depths of gilts were ultrasonically measured at mating and on d 30, 50, 70, 100, and 109 of gestation. Blood samples were obtained at mating and on d 109 of gestation to measure concentrations of IGF-1, glucose, insulin, estradiol, urea, free fatty acids, leptin, and adiponectin. Gilts were slaughtered on d 110 of gestation to collect mammary glands for compositional analyses. Mammary extraparenchymal tissue weight was lesser in LBF and MBF gilts than in HBF gilts (1,259.3, 1,402.7, and 1,951.5 ± 70.4 g, respectively; < 0.01). The weight of parenchymal tissue was not affected by treatment ( > 0.10), but its composition was altered. Concentrations of DNA and RNA decreased as backfat depth increased ( < 0.05), whereas percent fat and DM increased ( < 0.05). Circulating concentrations of leptin tended to be lower at mating ( < 0.10) and were lower on d 109 of gestation ( < 0.05) in LBF gilts than in HBF gilts. On d 109 of gestation, concentrations of insulin ( < 0.01) and IGF-1 ( < 0.05) were lower in LBF and MBF gilts than in HBF gilts, whereas those of urea were greater ( < 0.05). The mRNA abundance in parenchymal tissue for all genes studied was not affected by treatments ( > 0.10) with the exception of , which had a greater expression level in LBF gilts than in MFB or HBF gilts ( < 0.05). Percent of Ki-67-positive cells, used to assess mammary cell proliferation rate, was greater in HBF gilts than in LBF gilts ( < 0.05). When differences in body conditions of gilts that were present at mating were maintained throughout gestation, it had an impact on mammary development. Extraparenchymal tissue mass was affected and, more importantly, composition of parenchymal tissue was altered, indicating a beneficial effect of gilts being in the thinner treatment groups at mating.

Body condition of gilts at the end of gestation affects their mammary development.

The impact of body condition at 110 d of gestation on mammary gland development, mammary gene expression, and hormonal and metabolite status of gilts was studied. Thirty-nine gilts were equally divided into 3 groups based on their backfat thickness at the end of gestation: 1) low backfat (LBF; 12-15 mm), 2) medium backfat (MBF; 17-19 mm), or 3) high backfat (HBF; 21-26 mm). Gilts had similar BW (138.1 ± 8.2 kg) and backfat thicknesses (16.4 ± 1.0 mm) at mating and the 3 groups were achieved via ingestion of varying amounts of feed throughout gestation. Jugular blood samples were obtained from all gilts at mating and at 109 d of gestation to assess hormonal and metabolic statuses, and animals were slaughtered on d 110 to collect mammary glands for compositional analyses and for measure of gene expression. The LBF gilts had less extraparenchymal tissue ( < 0.01) and parenchymal tissue ( < 0.05) than HBF gilts. Mammary parenchyma from LBF gilts also tended to contain less DM ( < 0.10), contained more protein ( < 0.05), and had greater RNA concentrations ( < 0.01) than that from HBF gilts. None of the 15 genes studied in mammary parenchymal tissue differed in terms of expression level, and the rate of mammary cell proliferation was similar among treatments ( > 0.10). There was a tendency for circulating leptin concentrations on d 109 of gestation to be lower in LBF gilts than in MBF gilts ( < 0.10), whereas values for HBF gilts did not differ from those of the other treatments ( > 0.10). Current results demonstrate that being too thin at the end of gestation (12-15 mm backfat) has a negative impact on mammary development in gilts, whereas having backfats varying from 17 to 26 mm seems to have no detrimental effects on mammogenesis. Backfat thickness in late pregnancy must therefore be considered to achieve optimal sow lactation performance.

Dietary genistein stimulates mammary hyperplasia in gilts.

The possible role of the phytoestrogen genistein on prepubertal development of mammary glands, hormonal status and bone resorption was investigated in gilts. Forty-five gilts were fed a control diet containing soya (CTLS, n = 15), a control diet without soya (CTL0, n = 15) or the CTLS diet supplemented with 2.3 g of genistein daily (GEN, n = 15) from 90 days of age until slaughter (day 183 ± 1). Both basal diets were isonitrogenous and isocaloric. Jugular blood samples were obtained on days 89 and 176 to determine concentrations of isoflavone metabolites (on day 176 only), prolactin, estradiol, progesterone, insulin-like growth factor 1 (IGF1), and N-telopeptide of type I collagen (NTx; on day 176 only). At slaughter, mammary glands were excised, parenchymal and extraparenchymal tissues were dissected, and composition of parenchymal tissue (protein, fat, dry matter (DM), DNA) was determined. Histochemical analyses of mammary parenchyma were performed. Dietary genistein increased parenchymal protein (P < 0.05) while decreasing DM (P < 0.05) and tending to lower fat content compared with the CTLS, but not the CTL0, diet. There was more parenchymal DNA (1.26 v. 0.92 mg/g, P < 0.05) in GEN than CTLS gilts, likely reflecting an increase in the quantity of mammary epithelial cells. Circulating concentrations of genistein were increased in GEN gilts (P < 0.001) but concentrations of hormones or NTx (indicator of bone collagen resorption) were not affected by GEN (P > 0.1). Percentage of estradiol receptor alpha (ERα)-positive epithelial cells was lower (P < 0.05) in GEN than CTLS gilts, whereas 5-bromo-2'-deoxyuridine labeling index was unaltered (P > 0.1). Transcript levels for ERα, ERß, IGF1, epidermal growth factor (EGF), epidermal growth factor receptor and transforming growth factor alpha were not altered by treatments. Supplementation of the diet with genistein during the growing phase in gilts, therefore, led to hyperplasia of mammary parenchymal tissue after puberty; yet, even though circulating genistein was increased, this was not accompanied by changes in mammary expression of selected genes or circulating hormone levels.

Circulating haemopoietic and endothelial progenitor cells are decreased in COPD.

Circulating CD34+ cells are haemopoietic progenitors that may play a role in tissue repair. No data are available on circulating progenitors in chronic obstructive pulmonary disease (COPD). Circulating CD34+ cells were studied in 18 patients with moderate-to-severe COPD (age: mean+/-sd 68+/-8 yrs; forced expiratory volume in one second: 48+/-12% predicted) and 12 controls, at rest and after endurance exercise. Plasma concentrations of haematopoietic growth factors (FMS-like tyrosine kinase 3 (Flt3) ligand, kit ligand), markers of hypoxia (vascular endothelial growth factor (VEGF)) and stimulators of angiogenesis (VEGF, hepatocyte growth factor (HGF)) and markers of systemic inflammation (tumour necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-8) were measured. Compared with the controls, the COPD patients showed a three-fold reduction in CD34+ cell counts (3.3+/-2.5 versus 10.3+/-4.2 cells.microL-1), and a 50% decrease in AC133+ cells. In the COPD patients, progenitor-derived haemopoietic and endothelial cell colonies were reduced by 30-50%. However, four COPD patients showed progenitor counts in the normal range associated with lower TNF-alpha levels. In the entire sample, CD34+ cell counts correlated with exercise capacity and severity of airflow obstruction. After endurance exercise, progenitor counts were unchanged, while plasma Flt3 ligand and VEGF only increased in the COPD patients. Plasma HGF levels were higher in the COPD patients compared with the controls and correlated inversely with the number of progenitor-derived colonies. In conclusion, circulating CD34+ cells and endothelial progenitors were decreased in chronic obstructive pulmonary disease patients and could be correlated with disease severity.

Impacts of dietary protein level and feed restriction during prepuberty on mammogenesis in gilts.

The possible roles of dietary protein level and feed restriction in regulating mammary development of prepubertal gilts were investigated. Cross-bred gilts were fed a commercial diet until 90 d of age and then divided into four nutritional regimens based on two pelleted diets (as-fed basis): a high-protein diet (HP = 13.8 MJ of ME, 1.0% total lysine, 18.7% CP) and a low-protein diet (LP = 13.8 MJ of ME, 0.7% total lysine, 14.4% CP). Nutritional regimens were as follows: 1) HP ad libitum until slaughter (n = 22, T1); 2) HP ad libitum until 150 d of age followed by LP until slaughter (n = 20, T2); 3) LP ad libitum until slaughter (n = 21, T3); and 4) HP with a 20% feed restriction until slaughter (n = 19, T4). Gilts were weighed, their backfat thickness was measured, and jugular blood samples were obtained on d 90, 150, and at slaughter to determine concentrations of prolactin, IGF-I, leptin, and glucose. Gilts were slaughtered 8+/-1 d after their first or second estrus (202.7+/-14.5 d of age). Mammary glands were excised, parenchymal and extraparenchymal tissues were dissected, and composition of parenchymal tissue (protein, fat, DM, DNA, protein/DNA) was determined. The T4 gilts weighed less (P < 0.01) and had less backfat (P < 0.01) than did gilts on other treatments on d 150 and at slaughter. Treatments had no significant effects on prolactin, IGF-I, or glucose concentrations, but there was a treatment x day interaction (P < 0.01) for leptin, with concentrations being lower at slaughter in restricted-fed (T4) vs. LP (T3) gilts (P < 0.05). There was less extraparenchymal mammary tissue (P < 0.01) in T4 gilts than in gilts from the other groups and a tendency (P = 0.13) for the amount of parenchymal tissue to be lower in T4 gilts. In conclusion, a lower lysine intake during prepuberty did not hinder mammary development of gilts, but a 20% feed restriction decreased mass of parenchymal and extraparenchymal tissues. The effect of feed restriction on extraparenchymal tissue is most likely associated with the lower fat deposition.

c-erbB-2 and episialin challenge host immune response by HLA class I expression in human non-small-cell lung cancer.

The role of major histocompatibility complex expression in cancer prognosis and pathogenesis is contradictory. The aim of the current study was to compare the expression of HLA class I molecules and of oncoproteins that may be sources of peptides presented by HLA class I antigens in non-small-cell lung cancer. For this purpose, the expression of HLA class I antigen and TAP-1 molecule (a transporter in the antigen-processing 1 transport protein) were studied with epidermal growth factor, receptor; c-erbB-2; episialin; wild-type and mutant p53; bcl-2 oncoprotein expression; and angiogenic factor expression (vascular endothelial growth factor and thymidine phosphorylase). The degree of lymphocytic stromal infiltration and of platelet-endothelial cell adhesion molecule-expressing lymphocytes was also studied. A strong association of c-erbB-2 and MUC1 (episialin) expression with HLA class I expression was observed (p = 0.005 and 0.009, respectively). Intense CD31-positive lymphocytic infiltration was also more frequent in HLA class I-positive cases (p = 0.05). Although there was no association of HLA class I expression with survival, loss of the HLA class I expression in MUC1 or c-erbB-2 overexpressing cases conferred a poorer clinical outcome (p = 0.04). Both c-erbB-2 and MUC1 are well-known targets of T-cell-mediated cytotoxicity and cell-cell or cell-matrix adhesion-regulating proteins. The authors provide evidence that the sequence of cell adhesion-disrupting oncoprotein expression, HLA class I induction, and enhanced epitope presentation followed by lymphocytic response is an important pathogenetic three-step sequence of events that define, in part, the clinical outcome in non-small-cell lung cancer.

Asthma controller therapy: role of antileukotrienes, a new therapeutic class.

Asthma is a chronic disease and should be treated with both controller and reliever drugs. Asthma controller therapy is not used sufficiently widely, probably due to low compliance with inhaled drugs, lack of response in some patients to low-medium doses of inhaled steroids and possible adverse events. This review analyses a new class of antiasthmatic drugs, leukotriene receptor antagonists (antileukotrienes). At present, two antileukotrienes are available in Italy: zafirlukast and montelukast. Antileukotrienes improve symptoms and also inhibit the effects of some of the inflammatory mediators involved in the pathogenesis of asthma; therefore, antileukotrienes may be used in monotherapy. In addition, the oral administration route is an advantage for compliance. Antileukotrienes significantly improve pulmonary function, asthma symptoms and inhaled and oral steroid and short-acting beta 2-agonist use. Moreover, antileukotrienes produce a 50% mean reduction in the incidence of asthma exacerbations compared with placebo. From the economic point of view, asthma controller therapy using antileukotrienes is associated with a > 50% (compared with placebo) reduction in healthcare costs (hospitalization due to asthma exacerbation, healthcare contact and absenteeism from work or school), which globally account for 93% of asthma-related costs. Antileukotrienes are indicated in the treatment of persistent mild-to-severe asthma, seasonal allergic asthma, exercise-induced asthma and aspirin-induced asthma. Antileukotrienes are well tolerated independently of the duration of treatment and the incidence of the observed adverse events is substantially similar to that observed using placebo. Owing to good tolerability and compliance and the economic advantages, these agents may be considered a valid therapeutic option for the control and management of asthma as a chronic disease.

Platelet-derived growth factor in asthma.

Platelet-derived growth factor (PDGF) controls cellular growth, migration, and differentiation. It is secreted by various cell types, including macrophages, and participates in tissue repair and epithelial regeneration. PDGF may therefore be involved in airway remodeling in asthma. This study compared the immunoreactivity of PDGF and its receptors (R alpha and R beta) in bronchial biopsies and the levels of PDGF in bronchoalveolar lavage (BAL) fluid of asthmatics and control subjects. Bronchial biopsies were done in a subsegmental bronchus of 11 asthmatics and 11 control subjects by flexible bronchoscope. PDGF AA and BB, and PDGF receptors R alpha and R beta were studied with monoclonal antibodies and revealed by immunoperoxidase staining. The percentage of subjects presenting positive staining with PDGFs and its receptors was studied in the epithelium and submucosa. PDGF AA, AB, and BB were measured in BAL fluid of 18 asthmatics and 10 controls by specific ELISA. In biopsies, there was no significant difference between asthmatics and controls for PDGF AA, BB, PDGF-R alpha and R beta (Fisher's exact test and Bonferroni's correction). Moreover, the levels of PDGF, AA, AB, and BB were similar in asthmatics and controls. This study does not support a role for PDGF in the repair processes of asthma.