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    <timestamp>20250115060626000</timestamp>
    <depositor>
      <depositor_name>Editor</depositor_name>
      <email_address>editor.jddt@gmail.com</email_address>
    </depositor>
    <registrant>Universal Journal of Pharmaceutical Research</registrant>
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      <journal_metadata>
        <full_title>Universal Journal of Pharmaceutical Research</full_title>
        <abbrev_title>Univ J Pharm Res</abbrev_title>
        <issn media_type="electronic">2456-8058</issn>
        <issn media_type="print">2831-5235</issn>
      </journal_metadata>
      <journal_issue>
        <publication_date media_type="online">
          <month>01</month>
          <day>15</day>
          <year>2025</year>
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          <title>A RETROSPECTIVE INVESTIGATION OF BLOOD COAGULATIVE PARAMETERS PT, KPTT, PROTEIN C, AND ANTITHROMBON III IN 95 PATIENTS WITH LIVER DISEASE</title>
        </titles>
        <contributors>
          <person_name contributor_role="author" sequence="first">
            <surname>George Zhu</surname>
          </person_name>
          <person_name contributor_role="author" sequence="additional">
            <surname>Broekmans AW</surname>
          </person_name>
          <person_name contributor_role="author" sequence="additional">
            <surname>Bertina RM</surname>
          </person_name>
        </contributors>
        <jats:abstract xmlns:jats="http://www.ncbi.nlm.nih.gov/JATS1">
          <jats:p>Background: The liver is a crucial synthesis of blood coagulation factors and anticoagulative serine proteases such as protein C(PC) and antithrombin III (ATIII), which exerts a key role in the regulation of hemostatic balance. Activated protein C(APC) and protein S complex inactivate the activated factor Va and VIIIa, thus limiting Xa and thrombin formation. The excess protein S can drive cancer cellular proliferation and cell survival through oncogenic receptor Axl. In presence of heparin binding, antithrombin III (ATIII) and thrombin form an inactive complex in a 1:1 molar ratio. ATIII also inactivate factor IXa, Xa, XIa and XIIa at slow rate. In the setting of liver diseases, this reduced dysregulation can be attributed to decreased synthesis by the liver and increased consumption of coagulative factors and protein C and ATIII.
Methods: In current study, using routine detection for the blood coagulative parameters in 75 patients with liver diseases.
Results: The results showed that there exist one or three coagulative parameters PT, KPTT, and TT abnormal longer. Moreover, the abnormal intensity of coagulative parameters was associated to the severity of liver diseases. In our detection of 20 liver cirrhosis, the results showed significantly decreased plasma protein C antigen (PC:Ag 0.5501 vs 1.0578 µ/ml) and antithrombin III level (ATIII: Ag 21.8 vs 39.8 mg/dl, ATIII:C 40.25 vs 105.04%), respectively.
Conclusions: The measurement of multidispillary analyses of coagulative and anticoagulative system protein C and ATIII level are helpful to monitoring the liver diseases and might play a predictable marker.
                  
Peer Review History: 
Received 13 September 2024;   Reviewed 20 November; Accepted 26 December; Available online 15 January 2025
Academic Editor: Dr. Marwa A. A. Fayed, University of Sadat City, Egypt, maafayed@gmail.com
Average Peer review marks at initial stage: 6.0/10
Average Peer review marks at publication stage: 7.0/10</jats:p>
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          <day>15</day>
          <year>2025</year>
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