ABSTRACTare collectins, members of the C-type lectin family (4). The collectins are composed of four domains: a short aminoterminal region with interchain disulfide bonds, a long collagen-like domain, a coiled-coil neck region and a calciumdependent carbohydrate recognition domain. The basic structural unit of each collectin is a trimer based on the collagenlike triple helix, but the arrangement of multiple trimers into higher order oligomers varies (4). The close linkage of the mouse collectin genes on chromosome 14 suggests the collectins arose by ancestral gene duplication (5).It is not known whether the genetic and structural relationships among the collectins lead to related functions. There are variable degrees of evidence for each of the collectins having a role in innate immunity (for review, see ref. 6). Humans with low levels of MBP secondary to gene mutations are predisposed to infections (7,8), and mice deficient in SP-A secondary to gene targeting have delayed clearing of certain intratracheal bacterial challenges (9). Consistent with a possible role in innate immunity, SP-D binds to both microbes and phagocytic cells in vitro (6, 10), yet there is no direct evidence that SP-D has a role in host defense in vivo.Although SP-D was initially called a SP because it was expressed in the alveolar type II cell and had striking biochemical similarities to SP-A (1), a role for SP-D in surfactant homeostasis has not been established. Some surfactant phospholipid is associated with SP-D purified from alveolar lavage (11), and SP-D will interact with surfactant phospholipids in vitro under certain circumstances (12-14). SP-D also binds to both type II cell apical membranes and alveolar macrophages (6), cells that participate in alveolar surfactant metabolism (15). To develop a model to test the role of SP-D, we have produced mice lacking in SP-D secondary to the disruption of the single copy mouse SP-D gene by homologous recombination. Initial characterization of the phenotype demonstrates a progressive alveolar surfactant accumulation and a striking increase in foamy alveolar macrophages and alteration in type II cell morphology. These findings differ markedly from the results of SP-A gene targeting (16,17) and show that deletion of SP-D alters surfactant homeostasis. MATERIALS AND METHODS Generation of SP-D-Deficient Mice.A murine 129 strain genomic library (Stratagene) was screened by using a 1.2-kb full-length SP-D cDNA to obtain a 15-kb genomic fragment containing all but the extreme 3Ј end of the structural gene. A replacement-type targeting vector containing 1.2-kb and 4.3-kb homology regions was constructed by standard methods (Fig. 1a). Pgk-neo (1.8 kb) for positive selection replaced all of exon 2, including the translation start site for murine SP-D, and short segments of flanking intronic sequence (2.8 kb). Pgk-tk was inserted 5Ј to the regions of homology for negative selection. The targeting vector was linearized by using a unique NotI site and electroporated into CB1-4 embryonic stem cells as des...

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A pilot scale adsorber apparatus was designed and constructed to investigate water and ethanol adsorption/ desorption kinetics on 3A zeolite for the design purposes of a fuel ethanol dehydration pressure swing adsorption (PSA) process. Equilibrium studies have shown that 3A zeolite adsorbed a significant amount of water while very weak ethanol adsorption was observed. The breakthrough curves were utilized to study the effects of column pressure, temperature, flow rate, pellet size, and adsorbate concentration on the overall mass transfer resistance. Based on experimentally observed trends, both macropore and micropore diffusion were identified as relevant mass transfer mechanisms. A mathematical model for a bench scale adsorption bed included the linear driving force (LDF) adsorption rate model and the variation of axial velocity. A detailed heat transfer model was a necessity since the bed dynamics was affected by heat transfer in the bed wall. The model was used to analyze the experimental data and extract values of pertaining diffusion coefficients.

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In Zaire, infants with HIV infection have an 11-fold increased risk of death from diarrhea, largely persistent diarrhea, which is often preceded by recurrent episodes of acute diarrhea, malnutrition, or immunosuppression. Illness and death of the mother increase that risk, even among her uninfected infants.