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1 ns that can be targeted therapeutically with antiproteases.
2 teases as well as the inhibition of specific antiproteases.
3  cell death regulators and the inhibition of antiproteases.
4 les suggested decreased abundance of several antiproteases.
5        They show immunomodulatory as well as antiprotease activity and may be useful for treatment of
6                                 Insufficient antiprotease activity because of AAT deficiency in the l
7 ffect of SLPI was largely independent of its antiprotease activity because SLPI muteins, with signifi
8 rease in alpha1-AT concentration, functional antiprotease activity could not be detected.
9 onsidered to be an imbalance of protease and antiprotease activity in the lower respiratory tract lea
10                     An imbalance of protease-antiprotease activity is also detected in the airways of
11 ops is based on an imbalance of protease and antiprotease activity leading to the degradation of elas
12 hat of bikunin, which is responsible for the antiprotease activity of IalphaI.
13 es that could potentiate fibrosis, namely an antiprotease activity that inhibits the generation of pl
14 cause SLPI muteins, with significantly lower antiprotease activity, also suppressed the induction of
15  independent of its previously characterized antiprotease activity, appears to reside in disruption o
16 uitment into the lung may be linked to their antiprotease activity, directed, perhaps, at the intrace
17 latory properties of A1AT independent of its antiprotease activity.
18  bacterial infection regulating protease and antiprotease activity.
19 d anti-inflammatory functions independent of antiprotease activity.
20 of its specific physiological inhibitor, the antiprotease alpha(2)-antiplasmin.
21  neutrophil influx and degranulation, alpha1-antiprotease (alpha1-AP) concentrations, and unopposed N
22                       Prominent protease and antiprotease alterations were also noted in these mice.
23        They also link inflammation, protease/antiprotease alterations, and protease-dependent apoptos
24  inhibition of extracellular NE by BAL fluid antiproteases and its binding to leukocytes.
25 in residues, was found to exhibit antiviral, antiprotease, and antiintegrase activity.
26 terleukin 13 receptor components, proteases, antiprotease, and apoptosis regulators via Smad 2/3-inde
27                                              Antiprotease antibodies did not significantly alter IgA1
28 ing second order rate constants for protease-antiprotease associations (kass) by 3700-, 32-, and 60-f
29   Thus, chronic vaping disrupts the protease-antiprotease balance by increasing proteolysis in lung,
30 ell activation while disrupting the protease/antiprotease balance in the intestine, contributing to e
31 ve importance in maintenance of the protease-antiprotease balance in the microenvironment of inflamma
32 hysema and alterations in pulmonary protease/antiprotease balance when expressed in pulmonary tissues
33                                 The protease-antiprotease balance, controlled by serine and cysteine
34 ated by changes in the interstitial protease/antiprotease balance.
35  various growth factors/cytokines, proteases/antiproteases, cell adhesion molecules, and extracellula
36 ed alterations in chemokines, proteases, and antiproteases comparable to those seen after C10/CCL6 ne
37 eased over time, whereas neutrophil elastase antiprotease complexes (NEAPCs) and secretory leukoprote
38 he small volume of apical surface fluid, the antiprotease component of this protein was concentrated
39  an imbalance between cysteine proteases and antiproteases could be seen, which negatively affects ep
40 ly exacerbated by the loss of the endogenous antiprotease cystatin SN.
41                             We conclude that antiprotease defenses in lower respiratory tract secreti
42  nuclear factor kappaB (NF-kappaB), impaired antiprotease defenses, DNA damage, cellular senescence,
43 04 L, mean +/- SEM), five of whom had alpha1-antiprotease deficiency, performed two incremental cycli
44                                     Targeted antiprotease delivery paralleled hpIgR expression in the
45 ase inhibition or induce expression of known antiproteases, did not alter keratinocyte migration or p
46         The activities of some proteases and antiproteases found in inflammatory fluids can be modifi
47              PI-6, also known as cytoplasmic antiprotease, has been characterized as an intracellular
48                                     Protease-antiprotease imbalance and oxidative stress are consider
49 s, these assessments clarified that protease-antiprotease imbalance and oxidative stress are critical
50           Although inflammation and protease/antiprotease imbalance have been postulated to be critic
51 teinases and because the concept of protease/antiprotease imbalance is an important concept regarding
52 sema has supported the concept that protease/antiprotease imbalance mediates cigarette smoke-induced
53 rophilic inflammation, and a severe protease-antiprotease imbalance.
54 luenced by FNf and the ratio of protease and antiproteases in the cells' microenvironment.
55 inase activity, and unlike prostasins resist antiproteases, including leupeptin, aprotinin, serpins,
56  1-antitrypsin (alpha1-AT), the primary PR-3 antiprotease, inhibited the anti-PR-3 induced IL-8 relea
57           An imbalance between proteases and antiproteases is thought to play a role in the inflammat
58                                 In contrast, antiprotease levels were unchanged.
59      The possibility that H. pylori releases antiproteases may explain, in part, why this bacterium i
60 at coincides with downregulation of WFDC2-an antiprotease molecule that we find to be expressed by go
61  this system is capable of concentrating the antiprotease of the fusion protein, in the thin film of
62  PAI-1 proteins that possessed either intact antiprotease or vitronectin-binding activity to bleomyci
63  in genes involved in the digestive protease-antiprotease pathway has lent additional support to the
64                                     Specific antiprotease production in a patients with genetically d
65 ored area of A1AT biology independent of its antiprotease properties.
66    In addition to its primary function as an antiprotease, SLPI may also influence cellular functions
67 th the ability to deliver therapeutics, like antiproteases, specifically to the lumenal surface of th
68 eukocyte protease inhibitor (SLPI), a 12-kDa antiprotease, suppresses the growth of C. albicans in vi
69 al frequency of CD49e(+) monocytes contained antiproteases that partially blocked FNf-induced monocyt
70              A combination of surfactant and antiprotease therapy may improve therapeutic prospects.
71 d by changes in the balance of proteases and antiproteases, tissue damage by oxidative stress, or a c
72 s human tracheal xenografts and delivers the antiprotease to the apical surface to a much greater ext
73 oped a strategy that permits the delivery of antiproteases to the inaccessible CF airways by targetin
74 er adding alpha1-antitrypsin (alpha1-AT), an antiprotease, to surfactant improves its in vivo functio
75  value in CF, preferably in conjunction with antiprotease treatment.
76                   The proresolving effect of antiproteases was also observed in a model of monosodium
77 ession for several cytokines, proteases, and antiproteases was quantified in nasal tissue from non-CR
78    Since secreted Z alpha1AT is a functional antiprotease, we hypothesized that interrupting cataboli
79              Cell-cell adhesion proteins and antiproteases were reduced, and leukocyte recruitment (i