The objective of this study was to optimize and develop low-fat soft dough biscuits using carbohydrate-based fat replacers (combinations of polydextrose and guar gum). Central composite rotatable design was utilized to optimize the levels of sugar, composite fat (fat, polydextrose, and guar gum), ammonium bicarbonate, and water. The parameters measured were spread ratio, hardness, stress-strain ratio, and sensory properties. Composite fat and sugar were found to be important determinants of biscuit hardness. The principal effect of fat substitutes on biscuits' attributes was crisper texture but with higher brittleness. The level of water had a significant effect on spread ratio (p < 0.1), hardness (p < 0.1), and stress-strain ratio (p < 0.05). It was also observed that by varying the level of ammonium bicarbonate in the formulation from 0.5 to 2.5 g/100 g flour, the dimensions and texture of the biscuits were affected. The optimum ingredient levels on 100 g flour basis were found to be sugar 24 g, fat 10.5 g, polydextrose 24.2 g, guar gum 0.3 g, ammonium bicarbonate 2 g, and water 24 mL. It was found from the storage study that low-fat biscuit with 70% fat replacement was more oxidative stable than the control sample.

Experiments were conducted to develop low-fat soft dough biscuits using carbohydrate-based fat replacers (maltodextrin and guar gum). A central composite rotatable design was used to optimise the level of sugar 24–36%, composite fat (fat 10.5–24.5%, maltodextrin 10.4–24%, and guar gum 0.1–0.5%), ammonium bicarbonate 0.5–2.5%, and water 20–24% for production of low-fat biscuits. Diameter and stress-strain ratio decreased significantly with increase in the amount of sugar. There was a significant decrease in spread ratio at high amount of water. Hardness was significantly affected by the interactions of ammonium bicarbonate with sugar and fat . The optimum level of ingredients obtained for low-fat biscuits was sugar 31.7 g, fat 13.55 g, maltodextrin 21.15 g, guar gum 0.3 g, ammonium bicarbonate 2.21 g, and water 21 mL based on 100 g flour. The fat level in the optimised low-fat biscuit formulation was found to be 8.48% as compared to 22.65% in control; therefore, the reduction in fat was 62.5%.

Objective: Sprouty, a common antagonist of fibroblast growth factor (FGF) and epidermal growth factor signaling, is a key player regulating tracheal branching and eye development in Drosophila. Four Sprouty homologs have been identified in vertebrates and all share a cysteine-rich region. However, the physiological function(s) of the individual Sprouty homologs is unknown. mRNA of Sprouty homologs is expressed during mouse lung development. In the present study, we investigated the immunolocalization of Sprouty proteins in rat lung at different stages of development. Methods: Rabbit antibodies were raised against peptides derived from rat Sprouty-1 and Sprouty-2 and were used in Western blot analysis to determine Sprouty distribution in subcellular fractions (pellets and supernatant centrifuged at 5,000 and 20,000 g) and bronchoalveolar lavage fluid (BAL) from adult rat lungs or used in immunohistochemistry. Results: Western blot analysis revealed a 30-kDa Sprouty-1 band and a 34-kDa Sprouty-2 band in the supernatant and pellet fractions centrifuged at 20,000 g. BAL contained a band of approximately 16 kDa with Sprouty-1 antibody derived from proteolytic fragmentation of Sprouty-1. In embryonic day (E) 14 and E16 lungs, Sprouty-1 and Sprouty-2 were expressed both in epithelial and peripheral mesenchymal cells. In adult rat lung, bronchiolar and alveolar type II epithelial cells showed staining for both Sprouty-1 and Sprouty-2. Sprouty-1 expression was also seen in alveolar type I epithelial cells. Conclusion: In light of the proximity of the distribution of Sprouty to that of FGF-10 (peripheral mesenchyme) and its receptor FGFR2IIIb (distal tubular epithelium) in lung development, and the finding that FGF-9, which is expressed in mesothelial cells, upregulates FGF-10, it appears that Sprouty expression in epithelial and mesenchymal cells during branching morphogenesis is closely related to signaling by FGF-9 and FGF-10.

Possibility of using full fat soy flour (FFSF) for replacer for whole milk powder (WMP), stevia-mannitol blend as replacer for sugar and soybean oil (SBO) as replacer for cocoa butter in chocolate manufacture without impairing the sensory quality characteristics of chocolate was explored. Data on the sensory evaluation of WMP, sugar and cocoa butter substituted chocolates revealed that 40% (w/w) of WMP, sugar and cocoa butter can be successfully substituted by FFSF, stevia-mannitol blend and SBO, respectively in the preparation of high protein and low sugar chocolate without impairing the sensory attributes. Lecithin was found to be optimum at 0.32% (w/w) level of chocolate mix. Protein content of optimized formulation increased by 21.8% over control. Storage study of the product indicated an increase in hardness, free fatty acid content, peroxide value, total plate count, yeast and mold count, whereas a decrease in moisture content, pH value and sensory scores. The optimized chocolate was found acceptable (score ≥7.0) after 90 days of storage at 16 ± 1°C and ~65% RH.

In this article, our main objective is to present the use of Microsoft Software Excel 2007/2003 for teaching college and university level curriculum in science and engineering. In particular, we discuss two interesting and fascinating examples of interactive applications of Microsoft Excel targeted for undergraduate students in: 1) computational physics and physics education; and 2) computer and medical sciences. We demonstrate the tremendous amount of computational power of the most recent Microsoft Excel 2007 Software, which is employed here to perform simulations of a projectile (may be a missile) launched from an airplane so as to hit a target on the ground using the simplest assumption of no air resistance during the projectile motion in air and that of rolling of nine dice with six surfaces. For projectile motion, kinematic equations based on Newton's laws of uniform motion have been employed to simulate projectile trajectory. We are going to prove through a plot of vertical distance as a function time that the projectile motion undergoes a parabolic path. However, modification in the simulation equations of the projectile motion, which includes the effect of air resistance, change in gravitational force with altitude, curvature in the surface of Earth, Coriolis force due to Earth's spin motion about its axis of rotation, and wind speed, will be discussed in very near future. We will also plot a graph of normalized total score versus the maximum score for rolling of nine dice like in casino games.

Sproutys and Sprouty-related proteins, Spred-1 and -2, are known inhibitors of fibroblast growth factor (FGF) signaling, which plays key role in lung branching morphogenesis and the development of other tissues. The present study demonstrates that Spreds are expressed in a variety of rat embryonic tissues (brain, intestine, heart, skin) including the lung. In the embryonic lung, Spreds and Sproutys are expressed during the early stages of branching morphogenesis, but their expression profiles are both distinct and overlapping. Spreds are predominantly expressed in mesenchymal cells in contrast to Sproutys, which are abundantly expressed in epithelial cells. Spred expression is especially strong in the regions of new bud formation both in the peripheral mesenchyme as well as in the epithelium. The peripheral region also expresses FGF-10 in the mesenchymal cells and FGF-9 in the mesothelial cells. The expression profiles suggest that Spreds, Sproutys and FGF-9/FGF-10 are part of epithelial-mesenchymal interactions, which are essential for the development and maintenance of normal lung branching pattern.

A bstract : Clara cells are nonciliated, nonmucous, secretory cells of the pulmonary airways. These cells are known to secrete a variety of proteins, including Clara cell 10‐kDa protein/uteroglobin. This protein consists of a homodimer of 70–77 amino acid polypeptides arranged in antiparallel fashion. In vitro testing suggests that the protein suppresses inflammation. The physiologic role of the protein remains to be determined.

Congenital cystic adenomatoid malformation of the lung (CCAM) is a rare congenital lesion whose pathogenesis is not well defined. It is generally accepted that the various types of CCAMs originate at different levels of the tracheobronchial tree. To further define the pathogenesis of CCAM, we evaluated the cellular composition of different CCAM types by immunohistochemistry. Twenty-two CCAMs (17 CCAM type 1, two type 2, one type 3, and two type 4) were collected. The cellular composition was determined using immunohistochemical stains for type I cell-associated antigen (T1 cell-Ag), surfactant proteins and surfactant protein precursors (SP-A, SP-B, proSP-B, and proSP-C), neuroendocrine cells (GRP), Clara cells (UP-1), and the adhesion molecule CD44v6, a glycoprotein thought to be involved in cell-matrix and cell-cell interactions. Eleven fetal lungs also were analyzed to compare cytodifferentiation of the epithelial-lined cysts of the different types of CCAM with the stages of normal lung development. Our results indicate that CCAM is caused by an arrest in lung development, and, on the basis of cytodifferentiation, two major subtypes can be distinguished. One subtype consisting of CCAM types 1, 2, and 3 that shows a bronchiolar type of epithelium and a second subtype, consisting of CCAM type 4, that has an acinar-alveolar type of epithelium. Our findings also suggest that these two subtypes may arise at different stages of the branching of the bronchopulmonary tree, the first at the pseudoglandular stage and the second at the saccular stage.

Human protein 1/Clara cell Mr 10,000 protein consists of two identical subunits of seventy amino acid residues each. In the present study, eight clones of monoclonal antibodies against native protein 1 were prepared and their respective epitopes were immunochemically and immunohistochemically characterized using native protein 1, truncated recombinant protein 1 and synthesized peptides. Among the clones, three designated as TY-5, TY-7 and TY-8 recognized amino acid residues 7-16, residues 19-28, and residues 39-46, respectively, all of which comprise the hydrophobic cavity of protein 1, possibly associated with chemical binding function. With the exception of TY-4, the remaining clones recognized residues 61-68 which are exposed to solvent. The epitope of TY-4 remains undetermined. Proper selection and combination of clones and recombinant protein 1 may be useful for fundamental and clinical studies of protein 1.

In this study, we examined the effects of dexamethasone (DEX) on airway branching and subsequent lung maturation. DEX treatment of fetal rat lung explants was initiated during the early pseudoglandular stage of development. Day 14 fetal lung explants were cultured with and without DEX for 4 d. Explants treated with 10 nM or higher concentrations of DEX showed features of both distorted and accelerated maturation. DEX-treated lungs had growth retardation, distorted branching, dilated proximal tubules, and suppressed proliferation of epithelial cells of the distal tubules. Several biochemical and morphologic features of accelerated maturation were also observed: 1 ) the epithelial cells lining the distal tubules (prospective respiratory airways) were generally cuboidal or flattened; 2 ) the cuboidal cells often contained lamellar bodies and abundant glycogen; 3 ) rudimentary septa and large airspace were present; 4 ) mesenchymal tissue was attenuated and compressed between adjacent epithelial tubules; 5 ) the distribution of SP-C mRNA in distal tubules was more mature, with individual and clusters of cells expressing SP-C transcripts; and 6 ) the transcript levels of several genes related to epithelial growth [keratinocyte growth factor (KGF), KGF receptor, and hepatocyte growth factor receptor] and differentiation [surfactant proteins, SP-A, SP-B and SP-C and the Clara cell secretory protein, CC10] were precociously increased. These results show that DEX treatment of the lung during the early pseudoglandular stage accelerates the acquisition of several features of advanced maturation that normally accompany late stages of fetal development. We postulate that KGF mediates at least some effects of DEX on lung maturation and gene expression.

We have reported that dexamethasone (DEX) treatment of early embryonic rat lungs in culture induced features of both distorted and accelerated maturation. In this report, we investigated the effects of retinoids on normal and DEX-induced lung development in vitro. Lung maturation was assessed by examining the morphology and the expression of genes related to epithelial differentiation (surfactant proteins, SP-A, SP-B and SP-C and Clara cell protein, CC10) and growth [keratinocyte growth factor (KGF) and hepatocyte growth factor (HGF)]. We cultured d 14 and 15 fetal rat lungs in the presence of DEX (1-1000 nM) and/or all-trans-retinoic acid (RA)(10-7-10-5 M) for 4 d. RA at 10-6 and 10-5 M inhibited branching and dilated the distal tubules, and at 10-5 M caused dilatation of the proximal tubules destined to form the trachea and the main bronchi. The adverse effects of DEX, such as distorted branching, tubular dilatation, and suppression of both lung growth and epithelial cell proliferation, were all prevented by RA. In addition, RA inhibited several features of DEX-induced accelerated maturation, such as: 1) the increased levels of SP-A, SP-B, and CC10 mRNAs; 2) the attenuation of mesenchymal tissue; and 3) the mature distribution of cells expressing SP-C mRNA. In contrast, RA potentiated the increase of KGF and decrease of HGF transcripts induced by DEX. In conclusion, the study shows antagonism by RA of DEX-induced effects on lung morphology and gene expression. We postulate that normal lung development requires a balanced action of endogenous retinoids and glucocorticoids.

The Clara cell phospholipid-binding protein, previously referred to as CC10, is a homodimeric protein of M(r) 15,800. It is secreted into the bronchioalveolar lining layer in mammalian lung. A combination of X-ray crystallography and chemical analysis was used to determine that phosphatidylcholine and phophatidylinosital are bound to the protein as isolated from human lung lavage. We now report the crystal structure of the protein-phospholipid complex at 1.9 Angstrom resolution. The phospholipid is bound inside the protein's Targe hydrophobic cavity. A model is proposed for the manner in which a channel may open to provide access to the cavity, allowing the binding or potential release of phospholipid.

Through the use of radioactively labeled methyl isocyanate (MIC), the deposition, penetration, and clearance of this highly reactive compound in the airway at the tissue and cellular levels have been directly examined. Guinea pigs were exposed to 14C-MIC vapors at concentrations ranging from 0.38 to 15.2 ppm for periods of 1-6 hr. Solubilization of tissues from these animals showed the airway tissues to have the highest level of radioactivity. In the nasal region, 14C deposition, as monitored by histoautoradiography, was limited to the epithelial layer, was related to dose, and was dependent on the specific epithelial cell type. The squamous epithelium was minimally labeled on the surface and the label did not penetrate the cell layer. However, radioactivity was detected throughout the entire nasal respiratory epithelial layer. The lack of nasal deposition in tracheotomized animals demonstrated that the 14C accumulation at this site was due to the scrubbing action of the nasal region with no contribution from blood recirculation. Cellular localization in the tracheobronchial region showed epithelial and subepithelial deposition in a dose-dependent manner with accumulation of the label at the subepithelial region. Radioactivity penetrated to the level of the terminal bronchiole but was not detected in the alveolar region. The persistence of airway radioactivity over the 48-hr postexposure period monitored suggests the covalent modification of airway macromolecules. Despite its broad specificity and high reactivity, MIC undergoes selective reactions in the airways which are dependent on respiratory region and cell type.

A protein similar to the rat Clara cell 10-kDa protein (CC10) was isolated from mouse lung homogenate by conventional chromatography. cDNA for the mouse CC10 protein was identified in the mouse lung cDNA library by using radiolabeled rat CC10 cDNA as the probe. The isolated cDNA was sequenced and the deduced primary amino acid sequence was compared to the known sequences of rabbit and hare uteroglobins and human and rat CC10 proteins. The cDNA sequence was confirmed by N-terminal amino acid sequencing of the purified protein. The purified mouse CC10 was tested for its ability to bind progesterone, and the binding was found to be 27% lower than rat CC10 and 48% lower than rabbit uteroglobin. The relative binding of mouse, rat, and human CC10 may reflect subtle structural perturbations. The only notable difference between mouse and rat CC10 is in the beta bend between helices 1 and 2, at residue 16. This difference also exists between rat and human CC10. The mouse CC10 sequence compares favorably with human CC10, which does not bind progesterone; however, the mouse CC10 does not contain M60, which has been proposed to block the binding of progesterone with human CC10. The wide variation in progesterone binding among this family of proteins casts doubt on the importance of such binding as a physiologic function.

Pulmonary surfactant is a lipid-protein complex involved in maintaining alveolar stability. SP-A is the major surfactant-associated protein of 26 to 38 kD. A human SP-A gene (SP-A I) and two distinct SP-A cDNAs, MPSAP 1A and MPSAP 6A, have been reported previously. We have isolated and characterized a second human SP-A gene (SP-A II), which appears to code for the mRNA corresponding to the previously described MPSAP-1A cDNA. Both genes consist of five exons, a consensus recognition sequence for initiation, TATAAA, and a polyadenylation signal sequence. Significant divergence in the two genes is observed throughout. The divergence is highest in the upstream region, intron I, exon III, and noncoding portion of exon V. The coding regions of all other exons and the introns show much lower divergence. Transcripts from both genes were found in adult human lung, using gene-specific oligonucleotide probes in Northern blot analysis.