peptidase/edema

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Effect of neuropeptide Y on inflammatory paw edema in the rat: involvement of peripheral NPY Y1 and Y5 receptors and interaction with dipeptidyl-peptidase IV (CD26).

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Several lines of evidence suggest that neuropeptide Y (NPY) may exert regulatory effects in local inflammatory responses. Here, we show that intraplantarly (i.pl.) applied NPY, peptide YY (PYY), and an NPY Y5 receptor-selective agonist dose-dependently potentiate concanavalin A (Con A)-induced paw

Impact of Systemic Dipeptidyl Peptidase-4 Inhibitor Use in Diabetic Macular Edema.

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To evaluate impact of baseline systemic dipeptidyl peptidase-4 (DPP-4) inhibitor use in diabetic macular edema (DME).This was a post hoc exploratory analysis of previously completed randomized, controlled clinical trials (VISTA and VIVID) in patients with

Clinical analysis of pre-existing diabetes mellitus and dipeptidyl peptidase-4 inhibitors in patients with remitting seronegative symmetrical synovitis and pitting edema syndrome.

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Objectives: To analyze the association among remitting seronegative symmetrical synovitis with pitting edema (RS3PE) syndrome, diabetes mellitus (DM), and antidiabetic drugs. Methods: We retrospectively analyzed the clinical and serologic manifestations of patients who had RS3PE

Sulfidopeptide-leukotriene peptidases in pulmonary edema fluid from patients with the adult respiratory distress syndrome.

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The human pulmonary edema fluid concentrations of LTC4 and of LTD4 and LTE4, derived peptidolytically from LTC4, were assessed by radioimmunoassays of the mediators resolved by reverse-phase high-performance liquid chromatography. The mean pulmonary edema fluid concentration (+/- SD) of LTD4 of 19.2

Dipeptidyl peptidase IV deficiency increases susceptibility to angiotensin-converting enzyme inhibitor-induced peritracheal edema.

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BACKGROUND Serum dipeptidyl peptidase IV (DPPIV) activity is decreased in some individuals with ACE inhibitor-associated angioedema. ACE and DPPIV degrade substance P, an edema-forming peptide. The contribution of impaired degradation of substance P by DPPIV to the pathogenesis of ACE

[Clinical study of the efficacy of and tolerance to seaprose S in inflammatory venous disease. Controlled study versus serratio-peptidase].

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This study was designed to compare the efficacy and safety of seaprose S and serratio-peptidase in the treatment of venous inflammatory disease. Forty patients entered the study (11 males, 29 females), mean age 54.3 years (range 30-77), mean weight 74.8 kg (range 51-96), with superficial

Pharmacokinetic and pharmacodynamic assessments of the dipeptidyl peptidase-4 inhibitor PHX1149: double-blind, placebo-controlled, single- and multiple-dose studies in healthy subjects.

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BACKGROUND PHX1149 is a dipeptidyl peptidase-4 (DPP4) inhibitor that is currently in clinical development for the treatment of type 2 diabetes mellitus. PHX1149 is a small (molecular weight = 241.16 Da), highly water-soluble (>2 g/mL), orally active molecule with a selectivity index of 15- to

Remitting seronegative symmetrical synovitis with pitting edema syndrome in individuals with type 2 diabetes mellitus or impaired glucose tolerance.

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An association between remitting seronegative symmetrical synovitis with pitting edema (RS3PE) syndrome and insulin or dipeptidyl peptidase-4 (DPP4) inhibitor therapy were previously reported. We encountered four cases of RS3PE syndrome with type 2 diabetes mellitus or impaired glucose tolerance

Proteasome peptidase activities parallel histomorphological and functional consequences of ischemia-reperfusion injury in the lung.

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Several lines of evidence suggest that the proteasome contributes to ischemia-reperfusion injury (I-RI) of organs. Although I-RI contributes to multiple disease processes in the lung, the regulation of proteasome activities during pulmonary I-RI is unknown. Thus, the authors performed a pilot study

Peptidase neurolysin is an endogenous cerebroprotective mechanism in acute neurodegenerative disorders.

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Stroke and traumatic brain injury (TBI) are significant clinical problems characterized by high rate of mortality and long-lasting disabilities, and an unmet need for new treatments. Current experimental stroke and TBI research are evolving to focus more on understanding the brain's self-protective

The role of incretins in salt-sensitive hypertension: the potential use of dipeptidyl peptidase-IV inhibitors.

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OBJECTIVE Incretin mimetics, such as glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), as well as dipeptidyl peptidase-IV (DPP-IV) inhibitors, are used in the treatment of type 2 diabetes mellitus (T2DM). In addition to stimulating insulin secretion from

Recovery from Diabetic Macular Edema in a Diabetic Patient After Minimal Dose of a Sodium Glucose Co-Transporter 2 Inhibitor.

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BACKGROUND Diabetic macular edema (DME) causes serious visual impairments in diabetic patients. The standard treatments of DME are intra-vitreous injections of corticosteroids or anti-vascular endothelial growth factor antibodies and pan-photocoagulation. These treatments are unsatisfactory in their

Comparison of dipeptidyl peptidase-4 inhibitors and pioglitazone combination therapy versus pioglitazone monotherapy in type 2 diabetes: A system review and meta-analysis.

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BACKGROUND Dipeptidyl peptidase-4 (DPP-4) inhibitor and pioglitazone combination therapy have been widely used for patients with inadequate glycemic control on monotherapy. This meta-analysis assessed the efficacy and safety of this combination therapy in patients with type 2 diabetes mellitus

The efficacy and safety of dipeptidyl peptidase-4 inhibitors for treatment of type 2 diabetes mellitus patients with severe renal impairment: a meta-analysis.

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OBJECTIVE Dipeptidyl peptidase-4 (DPP-4) inhibitors are a new class of oral antidiabetic agents, and have been increasingly and widely used in the treatment of diabetes mellitus (DM). However, information of DPP-4 inhibitors in type 2 DM patients with severe renal impairment (RI) is limited. Our

Peptidase neurolysin functions to preserve the brain after ischemic stroke in male mice.

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Previous studies documented upregulation of peptidase neurolysin (Nln) after brain ischemia, however the significance of Nln function in the post-stroke brain remained unknown. The aim of this study was to assess the functional role of Nln in the brain after ischemic stroke. Administration of a

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