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  • 1
    Electronic Resource
    Electronic Resource
    Vitamin K prophylaxis to prevent neonatal vitamin K deficient intracranial haemorrhage in Shizuoka prefecture (1996)
    Oxford, UK : Blackwell Publishing Ltd
    BJOG 103 (1996), S. 0 
    Details
    ISSN: 1471-0528
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Objective To compare three methods of vitamin K prophylaxis for neonatal vitamin K deficient intracranial haemorrhage.Design We designed three strategies for vitamin K prophylaxis: 1. therapeutic administration of vitamin K in a mass screening system using the hepaplastin test; 2. routine oral administration of vitamin K to newborn infants; and 3. administration of vitamin K to lactating mothers during the late neonatal period in addition to the routine method. We evaluated the efficacy of these methods by determining hepaplastin test values at the first month of age.Population 66,076 full term healthy newborn infants without any complications.Results Of 55,513 infants in the mass screening system, 3068 infants received vitamin K therapeutically. At the first month of age, in the group where vitamin K was administered therapeutically, 56 infants (1.83%) exhibited low hepaplastin test values (〈 40%) despite vitamin K administration. But extremely low values (〈 20%), indicating a very high risk of neonatal intracranial haemorrhage, were observed in 34 (0.06%) of 52,445 infants who did not receive vitamin K. In the routine administration system, oral administration of vitamin K twice within the first week of life showed a lower incidence (0.19%) of low level cases than a single administration (1.56%). An additional administration of vitamin K to lactating mothers throughout the late neonatal period showed an effective result.Conclusions These findings suggest that vitamin K prophylaxis might reduce the risk of developing neonatal intracranial haemorrhage, but a complete prevention of this disease could not be achieved by oral administration of vitamin K. The transmission of vitamin K through breast milk would be a suitable method of vitamin K prophylaxis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-0528.1996.tb09586.x
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  • 2
    Electronic Resource
    Electronic Resource
    A soybean Kunitz trypsin inhibitor reduces tumor necrosis factor-α production in ultraviolet-exposed primary human keratinocytes (2005)
    Oxford, UK; Malden, USA : Munksgaard International Publishers
    Experimental dermatology 14 (2005), S. 0 
    Details
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background:  Cytokines are produced as a consequence of photo-damaged DNA and oxidative stress in ultraviolet (UV)-exposed keratinocytes. A soybean Kunitz trypsin inhibitor (KTI) down-regulates the expression of proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) in tumor cells and inflammatory cells.Aim:  The effect of KTI on TNF-α production in UV-exposed primary human keratinocytes was analyzed.Results:  We show (i) UV induced up-regulation of TNF-α mRNA and protein expression in keratinocytes; (ii) cells treated with KTI before UV irradiation showed a significantly lower accumulation of TNF-α protein in a dose-dependent manner and a reduced UV-induced up-regulation of TNF-α mRNA expression; (iii) KTI inhibited the induction of TNF-α target molecules interleukin-1β (IL-1β) and IL-6 proteins; (iv) UV irradiation transiently activated c-Jun N-terminal kinase (JNK) and Akt signaling but only weakly activated extracellular signal-regulated kinase (ERK) and p38; (v) KTI specifically inhibited UV-induced activation of ERK, JNK, and p38, but not Akt; (vi) treatment of cells with SP600125, a pharmacological inhibitor of JNK, predominantly suppressed UV-induced up-regulation of TNF-α expression; and (vii) KTI did not enhance suppression of UV-induced JNK phosphorylation by SP600125.Conclusions:  KTI specifically inhibited UV-induced up-regulation of cytokine expression predominantly through suppression of JNK signaling pathway.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0625.2005.00359.x
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  • 3
    Electronic Resource
    Electronic Resource
    Suppression of lipopolysaccharide-induced cytokine production of gingival fibroblasts by a soybean, Kunitz trypsin inhibitor (2005)
    Oxford, UK : Munksgaard International Publishers
    Journal of periodontal research 40 (2005), S. 0 
    Details
    ISSN: 1600-0765
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background:  Human bikunin, a Kunitz-type trypsin inhibitor, inhibits inflammation by down-regulating the expression of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) in tumor cells and inflammatory cells.Objectives:  We analyzed the effect of a soybean-derived Kunitz trypsin inhibitor (KTI) on TNF-α production in human gingival fibroblasts stimulated by lipopolysaccharide (LPS), an inflammatory inducer.Material and methods:  Mitogen-activated protein kinase (MAPK) activation and cytokine levels were monitored using western blot and a specific enzyme-linked immunosorbent assay (ELISA).Results:  Here, we show (i) a soybean KTI abrogates LPS-induced up-regulation of TNF-α mRNA and protein expression in a dose-dependent manner in gingival fibroblasts, (ii) KTI also blocks the induction of TNF-α target molecules interleukin-1β (IL-1β) and IL-6 proteins, (iii) inhibition by KTI of TNF-α induction correlates with the suppressive capacity of extracellular signal-regulated kinase 1/2 (ERK1/2) and p38 signaling pathways, implicating repressed ERK1/2 and p38 signalings in the inhibition, and (iv) pretreatment of cells with KTI blocked LPS-induced nuclear factor κB (NFκB) activation.Conclusion:  Our results indicate that KTI inhibits LPS-induced up-regulation of cytokine expression possibly through suppression of ERK1/2 and p38 kinase-mediated NFκB activation. These findings may identify anti-inflammatory properties of KTI at the level of gingival fibroblasts and may be relevant to the use of KTI in modulating inflammation, including periodontal disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-0765.2005.00824.x
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  • 4
    Electronic Resource
    Electronic Resource
    Internalization of urinary trypsin inhibitor in human uterine fibroblasts (1998)
    Springer
    Pflügers Archiv 436 (1998), S. 16-25 
    Details
    ISSN: 1432-2013
    Keywords: Key words Internalization ; Link protein ; Urinary trypsin inhibitor ; Urinary trypsin inhibitor binding protein ; Urinary trypsin inhibitor receptor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  We have characterized the molecular species and internalization of urinary trypsin inhibitor (UTI) in human uterine fibroblasts. Link protein (LP) has previously been identified as one of the cell-associated UTI binding proteins. The truncated forms of UTI were readily detectable in the cells after incubating the cells with purified UTI. Immunoblotting analysis with a panel of domain-specific antibodies revealed that the UTI species lacked the amino-terminal domain of UTI, but contained the carboxyl-terminal domain. We have examined whether LP is involved in the UTI internalization in the cells. Internalization of 125I-labelled UTI was blocked by the intact UTI, but not by the carboxyl-terminal domain of UTI. Treatment with a polyclonal antibody to the UTI binding domain of LP partially inhibited UTI binding to the cells, but did not significantly prevent UTI internalization. In addition, preincubation of the cells with hyaluronidase reduced the UTI binding to the cells, but had no effect on the rate with which UTI was internalized. These data allow us to conclude that there are at least two different mechanisms for internalization of UTI. The major one is via unknown UTI receptors in a Ca2+, Mg2+-sensitive manner and another is via LP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050599
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  • 5
    Electronic Resource
    Electronic Resource
    Immunolocalization of hyaluronic acid and inter-alpha-trypsin inhibitor in mice (1999)
    Springer
    Cell & tissue research 296 (1999), S. 587-597 
    Details
    ISSN: 1432-0878
    Keywords: Key words Hyaluronic acid ; Immunohistochemistry ; Inter-alpha-trypsin inhibitor ; Localization ; Mouse (CD-1)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract  The direct interaction of hyaluronic acid (HA) and heavy chain (HC) of the inter-alpha-trypsin inhibitor (IαI) family plays a critical role in the organization and stabilization of the extracellular matrix. The aim of the present investigation was to elucidate the distribution of the IαI HC and HA in adult mouse tissues. An immunohistochemical method using a rabbit polyclonal antibody raised against mouse IαI heavy-chain peptide and a specific probe for HA (biotinylated HA-binding protein) was used to demonstrate an immunolocalization of IαI HC and HA. Distribution and localization of HA was of three types, namely, colocalization with IαI HC itself (cartilaginous tissue and ovary), localization around IαI HC immunostaining (lung, intestine and skeletal muscle), and localization at a small distance from IαI HC or a different distribution pattern (brain, liver, skin and kidney). These results indicate that IαI HC could function as an HA-rich matrix stabilizer on the cells of cartilage and maturing ovary, in which IαI HC shows colocalization with its predominant ligand, HA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004410051320
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  • 6
    Electronic Resource
    Electronic Resource
    Urinary trypsin inhibitor (UTI) and fragments derived from UTI by limited proteolysis efficiently inhibit tumor cell invasion (1994)
    Springer
    Clinical & experimental metastasis 12 (1994), S. 117-128 
    Details
    ISSN: 1573-7276
    Keywords: elastase ; invasion ; limited proteolysis ; plasmin ; trypsin ; urinary trypsin inhibitor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the effects of purified human urinary trypsin inhibitor (UTI) and fragments derived from UTI by proteolysis on the invasive potential of ovarian cancer cells (HOC-I) and gestational choriocarcinoma cells (SMT-ccl) using anin vitro reconstituted basement membrane invasion assay. These cells express cell-associated plasmin and functional uPA receptors that are partially occupied by ligands. SMT-ccl cells, which express threefold higher levels of cell-associated plasmin activity than HOC-I cells, showed approximately twofold increase in their invasive potential. For the invasion assay, HOC-I cells were primed with exogenous plasminogen, but SMT-ccl cells were not. Human leukocyte elastase (HLE)-digested UTI (22 kDa fragment; UTI-22) inhibited plasmin practically with the same strength as native UTI. Trypsindigested UTI (20 kDa fragment; UTI-20), however, did not inhibit plasmin significantly. Treatment of cells with UTI or UTI-22 reduced the incidence of tumor cell invasive capacity, whereas the inhibitory effect of UTI-20 was not remarkable. The inhibitory effect on tumor cell invasion was dose-dependent and non-toxic; moreover, it was not mediated by inhibition of the tumor cell chemotactic response or of cell attachment to matrigel. These results indicate that inhibition of the proteolytic enzyme plasmin specifically reduced the invasive capacity of tumor cellsin vitro.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01753978
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