Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.59 (MIP)
 4,906 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purposes of this study were (1) to evaluate the shear bond strength of stainless steel orthodontic brackets bonded to dry and wet (with water and saliva) etched enamel with the use of the moisture-insensitive primer (MIP; Transbond; 3M Unitek, Monrovia, Calif) and (2) to evaluate the effectiveness of MIP with chemically activated (Concise; 3M Dental Products, St Paul, Minn) and light-activated (Transbond XT; 3M Unitek) resin. One hundred forty-four freshly extracted bovine teeth were divided into 12 groups (n = 12 teeth), and brackets were bonded with either of the 2 resins in combination with the conventional primer or MIP in dry or wet enamel surface conditions. The test specimens were mounted in a screw-driven mechanical testing machine (model 4204; Instron Corp, Canton, Mass) and subjected to a crosshead speed of 0.5 mm/min. The data were analyzed by 2-way analysis of variance. MIP with Concise produced slightly higher bond strengths compared with the conventional primers under wet conditions (MIP vs conventional: saliva, P <.001; water, P =.004). However, MIP in combination with Transbond XT produced comparable bond strengths on both the dry and wet etched enamel (dry, 10.14 MPa; water, 9.69 MPa; saliva, 8.90 MPa). The results of this study suggest that MIP be used only with light-activated composite resins.
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PMID:Shear bond strength of stainless steel orthodontic brackets with a moisture-insensitive primer. 1124 19

In crucifers, the ability of the stigma to differentially modulate hydration of pollen grains, depending on whether the pollen is recognized to be compatible or incompatible, represents a crucial stage in pollination. Our recent analysis of the mod mutation of Brassica, which results in a breakdown of the self-incompatibility response, led to the isolation of a gene linked to the MOD locus which is expressed at low levels in mod mutants. The gene is predicted to encode a plasma membrane-localized aquaporin-like protein and has been designated MIP-MOD. We utilized reporter gene analysis to demonstrate that the MIP-MOD promoter is active in Brassica papillar cells as well as in some vegetative tissues. The encoded protein is also likely to be plasma membrane-localized based on the observation that all plasma membrane-intrinsic aquaporin-like proteins in Brassica leaves are enriched in plasma membrane fractions. The MIP-MOD protein results in a low but measurable enhancement in osmotic water permeability of Xenopus oocytes and hence represents a functional aquaporin. The results are consistent with the notion that MIP-MOD is involved in the regulation of water transport across the stigma epidermal cell membrane.
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PMID:The brassica MIP-MOD gene encodes a functional water channel that is expressed in the stigma epidermis. 1124 6

Recent clinical trials have shown that the survival of patients with acute respiratory distress syndrome (ARDS) is improved by ventilation with reduced volumes. These studies suggested that overinflation of the lungs causes overactivation of the immune system. The present study investigated the hypothesis that ventilation with increased tidal volumes results in early responses similar to those caused by stimulation with one of the major risk factors for ARDS: bacterial lipopolysaccharide (LPS). We therefore compared the effects of ventilation (-10 cm H2O or -25 cm H2O end-inspiratory pressure) and LPS (50 microg/ml) on nuclear factor (NF)-kappaB activation, chemokine release, and cytokine release in isolated perfused lungs obtained from BALB/C mice. We found that both LPS and ventilation with -25 cm H2O (overventilation; OV) caused translocation of NF-kappaB, which was abolished by pretreatment with the steroid dexamethasone. Furthermore, both treatments resulted in similar increases in perfusate levels of alpha-chemokines (macrophage inflammatory protein; [MIP]-2; KC), beta-chemokines (macrophage chemotactic protein-1; MIP-1alpha), and cytokines (tumor necrosis factor-alpha, interleukin-6), which were largely prevented by dexamethasone pretreatment. In LPS-resistant C3H/HeJ mice, only OV, and not LPS, caused translocation of NF-kappaB and release of MIP-2. We conclude that OV evokes early inflammatory responses similar to those evoked by LPS (i.e., NF-kappaB translocation and release of proinflammatory mediators). The NF-kappaB translocation elicited by OV appears to be independent of Toll-like receptor 4 and not due to LPS contamination introduced by the ventilator. Our data further suggest that steroids might be considered as a subsidiary treatment during artificial mechanical ventilation.
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PMID:Ventilation-induced chemokine and cytokine release is associated with activation of nuclear factor-kappaB and is blocked by steroids. 1125 8

MIP family proteins can be divided into two groups according to their primary sequences. The CHIP group is predominant in the plant and animal kingdoms and functions primarily as water channels. The GLP group is a minor group with limited prevalence and functions primarily as glycerol transporters. Both prototypes are present in bacteria and may have evolved separately.
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PMID:The Dichotomy of MIP Family Suggests Two Separate Origins of Water Channels. 1139 Jul 77

With the aim of identifying cells and tissues with high expression of aquaporins (water channels) or homologous genes in Norway spruce (Picea abies), we report the expression patterns of such transcripts in seedlings, in roots of various ages, and in needles. In situ hybridization experiments with a conserved area of a tonoplast intrinsic protein (TIP) gene from P. abies gave high expression signals in differentiating vascular tissues and in the columella cells of the seedling root cap. High-staining signals were also seen in guard cells and in the bundle sheath cells of needles. Moreover, a slightly increased staining signal was seen in cells forming lateral roots as well as in adventitious roots formed from hypocotyl cuttings. By using PCR-based procedures we also identified a full-length aquaporin-like cDNA (mipr) from roots of two-week old seedlings. Sequence homology analysis of the gene suggests that it belongs to the TIP subgroup within the large MIP (major intrinsic protein) family. A phylogenetic analysis of the plant MIP family, including both plasmamembrane (PIP) and tonoplast intrinsic protein (TIP) from Picea, suggests that MIP subgroups evolved already 330 million years ago, as this is the dating of conifer and angiosperm divergence.
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PMID:Expression pattern of transcripts encoding water channel-like proteins in Norway spruce (Picea abies). 1148 76

The restrictive defect was quantified (Forced vital capacity, FVC) and their postural dependence and the respiratory muscle weakness (Maximal inspiratory and expiratory pressures, MIP and MEP) in 29 patients (12 to 46 years) with spinal injury from cervical (C) 4 to thoracic (T) 7 (30 days to 48 months post injury period). The FVC in C (seated) was 2200 +/- 560 ml (47.2%), and in T was 2940 +/- 750 ml (66.6%), p < 0.008. The postural dependence of the FVC was higher in C with an increase of 25% and only of 10% in the T (p < 0.03). This postural dependence was a function of the FVC according to the regression equation: FVC % (supine) = 24.73+ 0.7341* FVC % seated (r 0.8771, p < 0.001). The MIP in C was 61.59 (53.82%) +/- 17.26 cm H2O and in T was 87.25 (77.85%) +/- 24.27 cmH2O (p < 0.05). The MEP in C was 48.53 (24.97%) +/- 18.09 cm H2O, and in T was 58.75 (30.74%) +/- 27.67 cmH2O (p NS). No correlation was found between FVC and maximal statics respiratory pressures. In conclusion, the C showed more significant restrictive defect and a great postural dependence of the FVC. In both, the expiratory muscle weakness was more severe than the inspiratory group. Inspiratory muscle weakness was higher in C.
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PMID:[Functional respiratory evaluation in patients with high traumatic spinal injury]. 1172 18

The purpose of this study was to investigate the reactivity with water of a moisture-insensitive orthodontic primer (Transbond MIP), in conjunction with a no-mix orthodontic adhesive (Unite), and a moisture-insensitive adhesive (Smartbond), and to assess their bond strength to wet and saliva-contaminated enamel relative to the conventional application of the no-mix adhesive. The reactivity of the moisture-insensitive products with water was investigated by micro-multiple internal reflectance Fourier transform infrared spectroscopy (micro-MIR FTIR). Sixty premolars were divided into two groups of 30 teeth each and, on the buccal enamel surfaces, a standardized volume (0.1 ml) of water or fresh whole saliva was applied. Standard edgewise stainless steel brackets were then bonded to enamel surfaces as follows: (a) Unite, (b) Unite with the Transbond MIP, and (c) Smartbond. The brackets were debonded under shear force at a speed of 2 mm/min and the debonded enamel surfaces were subjected to fractographic analysis. The statistical analysis of the bond strength values was performed by two-way ANOVA with condition (water, saliva) and adhesive type serving as discriminating variables (n = 10, alpha = 0.05). The results of the fractographic analysis were evaluated by chi 2 test (alpha = 0.05). FTIR analysis showed that only Smartbond set in the presence of water. Application of water in Transbond MIP increased the extent of carboxyl ionization without inducing any setting reaction. Transbond MIP did not improve bond strength values when combined with the no-mix adhesive. Most adhesive-enamel condition combinations showed a trend to present lower bond strength in the presence of saliva; however, this was not confirmed statistically. Fractography of enamel and bracket base surfaces showed that Unite + Transbond MIP resulted in the most adhesive fractures (leaving no resin on enamel surface), whereas Smartbond presented the highest frequency of cohesive fractures (adhesive left on bracket and enamel surfaces).
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PMID:Moisture-insensitive adhesives: reactivity with water and bond strength to wet and saliva-contaminated enamel. 1188 77

The yeast Saccharomyces cerevisiae (baker's yeast or budding yeast) is an excellent eukaryotic model system for cellular biology with a well-explored, completely sequenced genome. Yeast cells possess robust systems for osmotic adaptation. Central to the response to high osmolarity is the HOG pathway, one of the best-explored MAP kinase pathways. This pathway controls via different transcription factors the expression of more than 150 genes. In addition, osmotic responses are also controlled by protein kinase A via a general stress response pathway and by presently unknown signaling systems. The HOG pathway partially controls expression of genes encoding enzymes in glycerol production. Glycerol is the main yeast osmolyte, and its production is essential for growth in a high osmolarity medium. Upon hypo-osmotic shock, yeast cells transiently stimulate another MAP kinase pathway, the so-called PKC pathway, which appears to orchestrate the assembly of the cell surface and the cell wall. In addition, yeast cells show signs of a regulated volume decrease by rapidly exporting glycerol through Fps1p. This unusual MIP channel is gated by osmotic changes and thereby plays a key role in controlling the intracellular osmolyte content. Yeast cells also possess two aquaporins, Aqy1p and Aqy2p. The production of both proteins is strictly regulated, suggesting that these water channels play very specific roles in yeast physiology. Aqy1p appears to be developmentally regulated. Given the strong yeast research community and the excellent tools of genetics and functional genomics available, we expect yeast to be the best-explored cellular organism for several years ahead, and osmotic responses are a focus of interest for numerous yeast researchers.
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PMID:Osmotic adaptation in yeast--control of the yeast osmolyte system. 1195 27

Chemokines are involved in the pathogenesis of alcoholic hepatitis and are considered to contribute to the migration of leukocytes into the liver during chronic ethanol intoxication. This work tests the hypothesis that chronic ethanol consumption selectively enhances chemokine release by Kupffer cells and hepatic sinusoidal endothelial cells and migration of inflammatory cells into the liver. Furthermore, enhanced hepatic chemokine secretion may induce an autocrine effect on the ability of Kupffer cells and endothelial cells to chemotax and ingest microbial particles. Male Wistar rats were fed with ethanol in agar block and water for 32 weeks, and were allowed free access to solid food. Results show that after 32 weeks of feeding, leukocyte infiltration and steatosis were observed in the livers of ethanol-fed rats. The majority of the infiltrated cells were CD8+ cells. Serum ALT, endotoxin, MIP-1alpha, MCP-1 and RANTES, (but not CINC and MIP-2) were also increased in the ethanol-fed rats than in the pair-fed group. Isolated Kupffer cells from ethanol-fed rats were primed for enhanced MIP-1alpha, MCP-1, and RANTES production in vitro, while the endothelial cells were primed for enhanced MIP-1alpha release only. Chronic alcohol intoxication was also associated with increased basal H2O2 formation, enhanced nuclear translocation and binding of NF-kappaB, AP-1 and MNP-1 in Kupffer Cells. Chronic ethanol feeding significantly enhanced MNP-1 binding, but not those of NF-kappaB and AP-1 in endothelial cells. Concomitantly, chemokine-induced chemotaxis, E.coli phagocytosis and f-met-leu-phe-induced superoxide anion production by Kupffer cells were downregulated in the ethanol-fed group. Taken together these data demonstrate that prolonged alcohol consumption may compromise the host to hepatitis as a result of increased chemokine production and at the same time may suppress the innate immune function of hepatic non-parenchymal cells.
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PMID:Chronic alcohol intoxication primes Kupffer cells and endothelial cells for enhanced CC-chemokine production and concomitantly suppresses phagocytosis and chemotaxis. 1204 6

Aquaporins are ubiquitous membrane channel proteins that facilitate and regulate the permeation of water across biological membranes. Aquaporins are members of the MIP family and some of them seem to be also able to transport other molecules such as urea or glycerol. In the plant kingdom, a single plant expresses a considerably large number of MIP homologues. These homologues can be subdivided into four groups (PIP, TIP, NIP, SIP) with highly conserved amino acid sequences and intron positions in each group. Since their discovery, advancing knowledge of their structure led to an understanding of the basic features of the water transport mechanism. An optimal water balance is essential to the homeostasis of most organisms, and aquaporins may be one of the mechanisms involved under changing environmental and developmental conditions. In fact, this may be one reason for the abundance and diversity of aquaporins, in particular in plants. In addition, exposure to different types of stress alters water relations and thus, aquaporins may be involved in stress responses as well. The transcriptional and/or post-translational regulation of aquaporins would determine changes in membrane water permeability. Both phosphorylation and translocation to/from vesicles have been reported as post-translational mechanisms. However, translocation in plants has not yet been shown. Although significant advances have been achieved, complete understanding of aquaporin function and regulation remains elusive.
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PMID:Plant aquaporins. 1206 Feb 33


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