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Perbandingan filogenetik protein antigen-I yang berpotensi sebagai calon diagnostik dan vaksin terhadap Parasit Cryptocaryon Irritans)

Lokanathan Y, Adura Mohd-Adnan, Sheila Nathan

Sains Malaysiana, 2016;45:1969-1979.

Protein antigen-i parasit ikan C. irritans berpotensi tinggi digunakan sebagai calon dalam pembangunan vaksin komersial terhadap C. irritans. Walau bagaimanapun, kewujudan variasi pada antigen-i serotip C. irritans yang berbeza mempengaruhi tahap perlindungan yang bakal diberikan terhadap varians C. irritans yang berbeza apabila antigen-i digunakan sebagai vaksin. Kajian ini dijalankan untuk membandingkan jujukan pelbagai antigen-i pencilan C. irritans di Malaysia berbanding antigen-i pencilan C. irritans yang pernah dilaporkan. Perbandingan filogenetik dijalankan untuk meramalkan potensi protein tersebut dalam usaha membangunkan calon serodiagnostik dan pemvaksinan terhadap pencilan C. irritans yang berlainan. Penjajaran jujukan berbilang bagi jujukan asid amino antigen-i dilakukan dengan perisian CLUSTALX dan analisis filogenetik antigen-i dilakukan menggunakan kaedah parsimoni maksimum (MP) dan kaedah Bayes. Sembilan transkrip unik (TU) C. irritans yang mempunyai padanan signifikan dengan antigen-i di pangkalan data protein NCBI didapati mempunyai peratus kesamaan antara 41% hingga 71%. Kedua-dua pohon MP dan Bayesian yang dijana menunjukkan varians antigen-i cn56 and cn57 terkelompok bersama dalam satu kumpulan manakala varians antigen-i yang lain terbahagi kepada dua kumpulan berasingan dan pengkelompokan ini disokong oleh kehadiran asid amino yang terpulihara dalam kumpulan masing-masing. Kajian lanjutan boleh dilakukan untuk mengenal pasti varians antigen-i yang sesuai sebagai calon serodiagnosis dan juga dapat memberi perlindungan silang terhadap pelbagai pencilan C. irritans di serata dunia.

Matched MeSH terms: Protein C
Discovery of plant-based phytochemical as effective antivirals that target the non-structural protein C of the Nipah virus through computational methods

Sureshan M, Prabhu D, Joshua SN, Sasikumar SV, Rajamanikandan S, Govindhapriya M, et al.

J Biomol Struct Dyn, 2024 Apr;42(7):3568-3578.
PMID: 37222609 DOI: 10.1080/07391102.2023.2214236

Nipah Virus (NiV) belongs to the Paramyxoviridae family and was first identified during an outbreak in Malaysia. Some initial symptoms include mild fever, headache and sore throat, which could escalate to respiratory illness and brain inflammation. The mortality rate of NiV infection can range from 40% to 75%, which is quite high. This is mainly due to the lack of efficient drugs and vaccines. In most instances, NiV is transmitted from animals to humans. Non-Structural Proteins (C, V and W) of the Nipah virus impede the host immune response by obstructive the JAK/STAT pathway. However, Non-Structural Proteins - C (NSP-C) plays a vital role in NiV pathogenesis, which includes IFN antagonist activity and viral RNA production. In the present study, the full-length structure of NiV-NSP-C was predicted using computational modelling, and the stability of the structure was analysed using 200 ns molecular dynamic (MD) simulation. Further, the structure-based virtual screening identified five potent phytochemicals (PubChem CID: 9896047, 5885, 117678, 14887603 and 5461026) with better binding affinity against NiV-NSP-C. DFT studies clearly showed that the phytochemicals had higher chemical reactivity, and the complex MD simulation depicted that the identified inhibitors exhibited stable binding with NiV-NSP-C. Furthermore, experimental validation of these identified phytochemicals would likely control the infection of NiV.Communicated by Ramaswamy H. Sarma.

Matched MeSH terms: Protein C/metabolism
Heparin-induced thrombocytopenia and recent advances in its therapy

Hassan Y, Awaisu A, Aziz NA, Aziz NH, Ismail O

J Clin Pharm Ther, 2007 Dec;32(6):535-44.
PMID: 18021330

To highlight therapeutic controversies, and present a critical review of the most recent evidence on the management of heparin-induced thrombocytopenia (HIT).

Matched MeSH terms: Protein C/therapeutic use
Life-saving percutaneous intervention in young patient with massive pulmonary embolism

Yaakob ZH, Undok AW, Abidin IZ, Wan Ahmad WA

Ann Saudi Med, 2012 6 19;32(4):433-6.
PMID: 22705620

Massive pulmonary embolism (PE) is not an uncommon condition, and it usually carries a high risk of mortality. It is one of the fatal conditions that commonly affect young patients. A definitive treatment for patients with massive PE is still lacking, and surgical intervention carries a substantial mortality risk. Thus, percutaneous intervention (clot fragmentation and/or aspiration) remains an option in some patients, specifically in those with a risk of bleeding, contraindicating the use of thrombolysis. There have been no randomized trials to validate percutaneous intervention in massive PE. A sufficient level of evidence is still lacking, and its use depends upon the expert committee's opinion and study of previous case reports. We present a 23-year-old man with first onset massive PE secondary to protein C deficiency, who was treated successfully with the combination of systemic thrombolysis and percutaneous interventions.

Matched MeSH terms: Protein C Deficiency/complications*
Thrombophilic mutations in pre-eclampsia and pregnancy-induced hypertension

Omar SZ, Qvist R, Khaing SL, Muniandy S, Bhalla S

J Obstet Gynaecol Res, 2008 Apr;34(2):174-8.
PMID: 18412778 DOI: 10.1111/j.1447-0756.2008.00755.x

The aim of the present study was to determine the existence or prevalence of thrombophilic markers such as Factor V Leiden, prothrombin G20210A, protein S, protein C, activated protein C and anti-thrombin in pre-eclampsia and pregnancy-induced hypertensive patients.

Matched MeSH terms: Protein C/genetics; Protein C/metabolism
Shortened activated partial thromboplastin time, a hemostatic marker for hypercoagulable state during acute coronary event

Abdullah WZ, Moufak SK, Yusof Z, Mohamad MS, Kamarul IM

Transl Res, 2010 Jun;155(6):315-9.
PMID: 20478546 DOI: 10.1016/j.trsl.2010.02.001

Various factors may contribute to a hypercoagulable state and acute vascular thrombosis. A prospective study was conducted involving 165 coronary heart disease (CHD) patients from the Cardiology Unit, Hospital Universiti Sains Malaysia. The purpose of this study was to investigate the relationship among factor VIII (FVIII), prothrombin time (PT), activated partial thromboplastin time (APTT), and activated protein C resistance (APC-R) state among CHD patients and to look for potential clinical applications from these laboratory findings. There were 110 cases diagnosed as acute coronary syndrome (ACS), whereas another 55 were stable coronary artery disease (SCAD) patients. PT, APTT, FVIII, and APC-R assays were performed on all subjects. There was a significant difference between the FVIII level and the APTT results (P value < 0.0001). A negative relationship was found between the FVIII level and the APTT from linear regression analysis (R(2) = 10%, P value < 0.0001). For each 1% increase in the FVIII level, the APTT was reduced by 0.013 s (95% confidence interval (CI) between -0.019 and -0.007). Interestingly, none of the SCAD patients had abnormally short APTT. Approximately 68.4% of cases with a positive APC-R assay were found to have a high FVIII level. In conclusion, the APTT test is a potential hemostatic marker for hypercoagulable state including in arterial thrombosis.
Study site: Cardiology unit (outpatient and inpatient), Hospital Universisti Sains Malaysia (HUSM), Kelantan, Malaysia

Matched MeSH terms: Protein C/metabolism
Hemostatic abnormalities in nephrotic syndrome

Abdullah R

Vet. Clin. North Am. Small Anim. Pract., 1988 Jan;18(1):105-13.
PMID: 3282374

Nephrotic syndrome is often associated with a hypercoagulable state and thrombotic complications. Thrombosis may be due to a number of abnormalities in blood, including AT III deficiency, increased concentrations of fibrinogen, factors V and VIII, and platelet hyperaggregability. The therapeutic approach to thrombosis in nephrotic syndrome is the use of anticoagulants as a preventive measure or an attempt at thrombolysis with streptokinase, urokinase, or stanozolol.

Matched MeSH terms: Protein C/physiology
Fulltext Ets and GATA transcription factors play a critical role in PMA-mediated repression of the ckβ promoter via the protein kinase C signaling pathway

Kuan CS, Yee YH, See Too WC, Few LL

PLoS One, 2014;9(12):e113485.
PMID: 25490397 DOI: 10.1371/journal.pone.0113485

Choline kinase is the most upstream enzyme in the CDP-choline pathway. It catalyzes the phosphorylation of choline to phosphorylcholine in the presence of ATP and Mg2+ during the biosynthesis of phosphatidylcholine, the major phospholipid in eukaryotic cell membranes. In humans, choline kinase (CK) is encoded by two separate genes, ckα and ckβ, which produce three isoforms, CKα1, CKα2, and CKβ. Previous studies have associated ckβ with muscle development; however, the molecular mechanism underlying the transcriptional regulation of ckβ has never been elucidated.

Matched MeSH terms: Proto-Oncogene Protein c-ets-1/metabolism*
Fulltext Technique of anaesthesia in pulmonary hypertension and thrombophilia in early pregnancy

Chuah KH, Mansor M, Rajen G, Wang CY, Chan YK

Med J Malaysia, 2006 Mar;61(1):114-6.
PMID: 16708749 MyJurnal

Pulmonary hypertension in pregnancy is a rare condition but is associated with a high mortality. We report the case of a 29 year old female in early pregnancy with Protein C and S deficiency with recurrent deep venous thrombosis and pulmonary embolism and subsequent secondary pulmonary hypertension. The patient was counselled and consented for termination of pregnancy with tubal sterilization. She was administered continuous spinal anaesthesia with invasive monitoring. The successful anaesthetic management of this condition is described.

Matched MeSH terms: Protein C Deficiency/physiopathology
Activated protein C resistance: a study among 60 thromboembolic patients in the Singapore population

Lim LC, Tan HH, Lee LH, Tien SL, Abdul Ghafar A

Ann Acad Med Singap, 1999 Mar;28(2):252-5.
PMID: 10497677

Resistance to activated protein C (APC-R) is the commonest inherited cause of thrombosis among Caucasians. Few studies have been carried out on its prevalence in Asians. We conducted a prospective study on 60 patients with thromboembolism to determine its prevalence in our local population. The Factor V Leiden (VaQ506) mutation associated with this condition was detected by amplification of the Factor V gene by polymerase chain reaction (PCR) and digestion of the fragment with Mnl I. Three patients were found to be heterozygous for this mutation. None of the 3 patients had other concomitant hypercoagulable states. In addition, we studied the prevalence of this condition in Malays which was found to be 0.5%. Our study suggests that the incidence of APC-R is much lower here compared to the West.

Matched MeSH terms: Activated Protein C Resistance/genetics*
Prothrombotic markers in Thalassemia major patients: A paradigm shift

Sultan S, Irfan SM, Zaidi SM

Med J Malaysia, 2018 08;73(4):185-189.
PMID: 30121679

BACKGROUND: It is being increasingly recognised that thalassemia major patients, like intermedia, have increased propensity for thromboembolism. Deficiency of natural anticoagulants is more recently defined finding contributing to the hypercoagulable state. The aim this study is to determine natural anticoagulants levels and their correlation with maternal characteristics, haematological and biochemical markers.
METHODS: This is a prospective case-control study. We registered 80 patients and 60 healthy controls from Jan 2009 to Dec 2013. Complete blood counts, prothrombin time, activated partial thromboplastin time, protein C, protein S, antithrombin, serum ferritin, liver enzymes; HbsAg and Anti- HCV were evaluated.
RESULT: There were 42 males and 38 females with mean age of 12.30±5.50 years. The mean protein C, protein S and antithrombin in patients and control were 58.25±22.5 versus 110.67±22.60, 67.90±19.58 versus 98.70±21.54 and 89.73±18.09 versus 104.0±10.98 (p<0.001) respectively. Protein C was predominantly deficient in 65% followed by protein S and antithrombin in 35% and 20% respectively. Protein C deficiency divulged positive correlation with protein S deficiency (p = 0.035) and antithrombin deficiency with hemoglobin of ≤8gm% (p<0.0025). No significant correlation of prothrombotic markers was established with maternal characteristics, hepatic dysfunction, hepatitis and serum ferritin.
CONCLUSION: Substantial decrement in prothrombotic markers, primarily protein C, may be implicated in elevated thrombosis; however follow-up data is required to establish definitive thromboembolic events.

Matched MeSH terms: Protein C/analysis
Differential effects of activated protein C on synovial fibroblasts in response to hypoxia and normoxia

Park YG, Choi J, Song I, Park SY, Seol JW, Jackson CJ

Sains Malaysiana, 2017;46:1895-1902.

Rheumatoid arthritis (RA) is a chronic disease characterized by inflammation of the joints and their lining or synovium. Previous studies showed that the synovium in RA patients is more hypoxic than normal synovium. Activated protein C (APC) has anticoagulant and anti-inflammatory effects and is highly expressed in the joints of RA patients. We examined the effect of APC on RA and normal synovial fibroblasts under hypoxic conditions. Human synovial fibroblasts were isolated from the synovial tissues of RA patients and normal controls and cells were exposed to recombinant APC under normoxic (21% oxygen) or hypoxic (1% oxygen) conditions. Cell proliferation was measured using MTT assays. Cell lysates and conditioned media were collected and assayed for matrix metalloproteinase (MMP)-2, MMP-9 and p38 using zymography and western blots. Proliferation of both normal and RA synovial fibroblasts dose-dependently increased after APC treatment in normoxic conditions. Under hypoxia, APC enhanced RA cell proliferation but had no effect on normal fibroblasts. MMP-2 production and activation were significantly augmented by APC in both cell types under normoxia and hypoxia conditions. However, activated MMP-2 was more reduced in cells under hypoxia than normoxia. APC substantially reduced the phosphorylation of p38 in normal and RA synovial fibroblasts under hypoxia. No difference in p38 phosphorylation was observed under normoxia. The receptor for APC, endothelial protein C receptor (EPCR), was elevated in normal fibroblasts under hypoxic conditions whereas in RA cells, EPCR was highly expressed under both normoxic and hypoxic conditions. We found that hypoxia enhanced the effect of APC on RA synovial fibroblasts through activation of MMP2 and inhibition of p38 phosphorylation. Our results suggested that APC may suppress joint destruction and progression of inflammation in a hypoxic RA environment.

Matched MeSH terms: Protein C
Fulltext Serotype-specific host responses in rhesus macaques after primary dengue challenge

Hickey AC, Koster JA, Thalmann CM, Hardcastle K, Tio PH, Cardosa MJ, et al.

Am J Trop Med Hyg, 2013 Dec;89(6):1043-57.
PMID: 24062475 DOI: 10.4269/ajtmh.13-0145

Dengue virus (DENV) is considered to be the most important arthropod-borne viral disease and causes more than 100 million human infections annually. To further characterize primary DENV infection in vivo, rhesus macaques were infected with DENV-1, DENV-2, DENV-3, or DENV-4 and clinical parameters, as well as specificity and longevity of serologic responses, were assessed. Overt clinical symptoms were not present after infection. However, abnormalities in blood biochemical parameters consistent with heart, kidney, and liver damage were observed, and changes in plasma fibrinogen, D-dimers, and protein C indicated systemic activation of the blood coagulation pathway. Significant homotypic and heterotypic serum immunoglobulins were present in all animals, and IgG persisted for at least 390 days. Serum neutralizing antibody responses were highly serotype specific by day 120. However, some heterotypic neutralizing activity was noted in infected animals. Identification of serotype-specific host responses may help elucidate mechanisms that mediate severe DENV disease after reinfection.

Matched MeSH terms: Protein C/analysis
Microvascular thrombosis in pediatric multiple organ failure: Is it a therapeutic target?

Nguyen T, Hall M, Han Y, Fiedor M, Hasset A, Lopez-Plaza I, et al.

Pediatr Crit Care Med, 2001 Jul;2(3):187-196.
PMID: 12793940

PURPOSE: To discuss the current rationale for the use of specific and nonspecific therapies for thrombotic microangiopathy in thrombocytopenia-associated pediatric multiple organ failure syndromes. Methods: Pertinent PubMed and MEDLINE citations and proceedings of recent critical care meeting presentations were reviewed. RESULTS: Critical care clinicians have reported using antithrombin III concentrate, protein C concentrate, activated protein C, prostacyclin and its analogues, heparin, tissue factor pathway inhibitor concentrate, plasma infusion, plasma exchange, whole blood exchange, pentoxifylline, tissue plasminogen activator, urokinase, and streptokinase with perceived therapeutic benefits in patients with thrombocytopenia-associated multiple organ failure, including those with thrombotic thrombocytopenic purpura/hemolytic uremic syndrome, disseminated intravascular coagulation syndrome, and secondary thrombotic microangiopathy syndrome without prolonged prothrombin time/activated partial thromboplastin time. CONCLUSION: Assuming that underlying disease is remediable, a consensus has developed that thrombotic microangiopathy is a therapeutic target in children with thrombocytopenia-associated multiple organ failure syndromes. Studies are warranted to delineate efficacious use of specific and nonspecific therapies to prevent and reverse thrombotic microangiopathy in these patients.

Matched MeSH terms: Protein C

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