Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.1.3.1 (
alkaline phosphatase
)
47,916
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Complement component C3
was investigated in sera of a group of schistosomal patients free from obvious nephritis. C3 was studied in relation to S. mansoni egg count, presence of HBsAg, and liver functions. C3 level was low in schistosomal patients than normal individuals. Levels were low in both HBsAg --ve and HBsAG +ve schistosomal patients. No significant difference was found between HBsAg --ve and HBsAg +ve in one hand, and between patients with egg counts more than 400 and those with egg counts less than 400 eggs/1 gr as regards level of C3 on the other hand. Presence of ascites did not affect C3 concentration. Positive correlation was found with Serum albumin, but not with prothrombin concentration serum
alkaline phosphatase
or serum transaminases.
...
PMID:Factors affecting C3 in intestinal schistosomiasis. 830 53
A prominent role for complement has been identified in the linkage of innate and adaptive immunity. The liver is the main source of complement and hepatocytes are the primary sites for synthesis of complement components in vivo. We have discovered that hepatitis C virus (HCV) impairs C4 and C3 synthesis. Liver damage may diminish capacity of complement synthesis in patients. However, we observed that the changes in measured complement components in chronically HCV infected patients do not correlate with liver fibrosis or rheumatoid factor present in the blood, serum albumin, or
alkaline phosphatase
levels.
Complement component C3
is of critical importance in B cell activation and T cell-dependent antibody responses. C3 activity is required for optimal expansion of CD8
+
T cells during a systemic viral infection. Deficiencies in complement may predispose patients to infections via ineffective opsonization, and defects in lytic activity via membrane attack complex. Interestingly, C9 is significantly reduced at the mRNA level in chronically HCV infected liver biopsy specimens, while many hepatocyte derived complement components (C6, C8, Factor B, MASP1, and MBL) and unrelated genes remain mostly unaffected. This implies an HCV specific effect, not a global effect from liver disease.
...
PMID:Complement Regulation and Immune Evasion by Hepatitis C Virus. 3059 37