scholarly journals Protease inhibitors, inflammatory markers, and their association with outcome in dogs with naturally occurring acute pancreatitis

2020 ◽  
Vol 34 (5) ◽  
pp. 1801-1812
Author(s):  
Sharon Kuzi ◽  
Michal Mazaki‐Tovi ◽  
Jan S. Suchodolski ◽  
Dar Rimer ◽  
Jonathan A. Lidbury ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Protease Inhibitors ◽  
Inflammatory Markers ◽  
Naturally Occurring

Effects of QingYi decoction on inflammatory markers in patients with acute pancreatitis: A meta-analysis

Phytomedicine ◽  
2021 ◽  
pp. 153738
Author(s):  
Guanyu Wang ◽  
Dong Shang ◽  
Guixin Zhang ◽  
Shenglin Zhang ◽  
Nan Jiang ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Inflammatory Markers ◽  
Meta Analysis

scholarly journals Naturally occurring mutations to HCV protease inhibitors in treatment-naïve patients

2012 ◽  
Vol 9 (1) ◽  
pp. 245 ◽  
Author(s):  
Stefania Paolucci ◽  
Loretta Fiorina ◽  
Antonio Piralla ◽  
Roberto Gulminetti ◽  
Stefano Novati ◽  
...  
Keyword(s):  
Protease Inhibitors ◽  
Naturally Occurring ◽  
Treatment Naïve ◽  
Hcv Protease

scholarly journals Effects of vacuum-assisted closure and Drotrecogin alpha on inflammatory markers in severe acute pancreatitis

2013 ◽  
Vol 04 (08) ◽  
pp. 43-53
Author(s):  
Oscar Arias-Carvajal ◽  
José Manuel Hermosillo-Sandoval ◽  
Carlos Alberto Gutiérrez-Martínez ◽  
Fermín Paul Pacheco-Moisés ◽  
Genaro Gabriel Ortiz ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Inflammatory Markers ◽  
Vacuum Assisted Closure ◽  
Drotrecogin Alpha

Prevalence of Naturally Occurring Resistance Associated Substitutions in NS3/4A Protease Inhibitors in Iranian HCV/HIV Infected Patients

2021 ◽  
Vol 19 ◽  
Author(s):  
Kazem Baesi ◽  
Ali Akbar Velayati ◽  
Masoumeh Farrokh Ashtiani ◽  
Kamal Fakhredini ◽  
Mohammad Banifazl ◽  
...  
Keyword(s):  
Protease Inhibitors ◽  
Standard Treatment ◽  
Large Population ◽  
Host Immune Responses ◽  
Naturally Occurring ◽  
Immunodeficiency Virus ◽  
Direct Acting ◽  
Therapy Success ◽  
Cure Rates

Background: Hepatitis C virus (HCV) acts in host as a complicated mixture of related variants with the potency to genetically escape host immune responses. Direct acting antivirals (DAAs) have been approved for HCV treatment with shorter duration, better cure rates and lower side effects. However, naturally occurring resistance associated substitutions(RASs) make some obstacles to this antiviral therapy success. Objective: In this study, we aimed at determination of the naturally occurring NS3/4A RASs in HCV/human immunodeficiency virus (HIV)infected patients. Methods: A total of 120 DAA-naïve HCV-HIV co-infected patients were included. HCV NS3/4Agenome region was amplified with PCR and mutation analysis was performed by Sanger sequencing technique. The amino acid sequence diversity of the region wasanalyzed using geno2pheno HCV. Results: Phylogenetic analysis showed that 73 cases were infected by 3a and 47 subjects by subtype1a. The overall RASs among studied subjects wereobserved in 6 (5%) individuals from 120 studied cases who were infected with HCV 1a. V36M/L,Q80L,S122G/L,R155T/G,A156S,D168Y/N and S174A/N/T mutations were detected in this study. Conclusion: Although the prevalence of RASs was totally low in this study, the presence of several cases of double and triple mutants among this population suggests prior evaluation of protease inhibitors related mutations before initiation of standard treatment and also investigation on a large population could be of high value.

scholarly journals Inhibition of platelet aggregation by protease inhibitors. Possible involvement of proteases in platelet aggregation

Blood ◽  
1978 ◽  
Vol 52 (1) ◽  
pp. 1-12 ◽  
Author(s):  
N Aoki ◽  
K Naito ◽  
N Yoshida
Keyword(s):  
Platelet Aggregation ◽  
Protease Inhibitors ◽  
Serine Proteases ◽  
Human Platelet ◽  
Serotonin Release ◽  
Second Phase ◽  
Inhibition Of Platelet Aggregation ◽  
Naturally Occurring ◽  
Human Platelet Aggregation ◽  
Platelet Receptor

Abstract The possible participation of proteases in human platelet aggregation was explored using various protease inhibitors and substrates. Protease inhibitors used included naturally occurring inhibitors of serine proteases and synthetic inhibitors that modify the active site of protease. Substrates used were synthetic substrates for the trypsin type as well as for the chymotrypsin type of protease. All these inhibitors and substrates inhibited platelet aggregation and serotonin release induced by ADP, collagen, epinephrine, or thrombin. In ADP- and epinephrine-induced platelet aggregation the second phase of aggregation was most efficiently inhibited. The inhibitors suppressed the formation of malondialdehyde during platelet aggregation. Release by aggregating agents of arachidonate and its metabolites from indomethacin-treated platelets as well as nontreated platelets was also inhibited. The inhibitors apperar to interact with stimulated platelets but not with unstimulated platelets. These observations suggest that the interaction of an aggregating agent with its platelet receptor activates a unique precursor serine protease that in turn activates platelet phospholipase to liberate arachidonic acid (the precursor of the potent platelet aggregating agent thromboxane A2) from platelet phospholipids.

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