No abstract available.
C-Reactive Protein* ; Pregnancy*

No abstract available.
C-Reactive Protein* ; Tocolysis*

No abstract available.
C-Reactive Protein*

BACKGROUND: Several immunological abnormalities, such as decreased T-cell interleukin-2 production and abnormal cellular and humoral reactivity to neurons, had been associated with patients who have schizophrenia. Several researches have been conducted to study the correlation of elevated inflammatory markers with the symptomatology of schizophrenia. OBJECTIVES: The aim of this study is to determine the levels of C-reactive protein, which is a general marker for infection and inflammation, in patients with Schizophrenia in acute exacerbation and compare these to the levels of C-reactive protein in patients with Schizophrenia in remission. METHODS: A cross-sectional study was carried out on in-patients at the Veterans Memorial Medical Center Department of Psychiatry. Serum levels of C-reactive protein in adult patients were determined during an acute exacerbation of Schizophrenia. These were compared to Creactive protein levels of patients with Schizophrenia in remission. PASW Statistics 18 (SPSS) was used for data management, tabulation and analysis. RESULTS: Cases of eighty-six (86) patients, seen by the principal investigator during OPD consults were reviewed, 43 of which had Schizophrenia in Acute Exacerbation and also 43 of patients were in Remission. The mean CRP level of patients in acute exacerbation was 7.05 mg/L (SD=0.23), which was higher than the mean CRP level of patients in remission at 5.30 mg/L (SD=0.30). CONCLUSION This study demonstrated that a stronger association exists between an acute exacerbation of Schizophrenia and elevated C-Reactive protein, in the absence of another systemic inflammatory disease when compared to the association between levels of Creactive protein in patients with Schizophrenia, in remission. This finding could pave the way for initiation of studies examining whether adjunct treatment of anti-inflammatory drugs with anti-psychotics will improve disease outcome.
C-Reactive Protein ; Schizophrenia

No abstract available.
Myocardium* ; Protein Kinase C* ; Protein Kinases*

No abstract available.
Protein C Deficiency* ; Protein C* ; Purpura Fulminans* ; Purpura*

No abstract available.
Plasma ; Protein C Deficiency* ; Protein C* ; Purpura Fulminans* ; Purpura* ; Warfarin

OBJECTIVETo analyze genetic mutations and explore its molecular pathogenesis for an hereditary protein C (PC) deficiency pedigree.

METHODSThe pedigree has included 15 individuals from 4 generations. Plasma levels of PC activity (PC:A), PC antigen (PC:Ag) and other coagulant parameters were determined for members of the family. The 9 exons and intron-exon boundaries of protein C gene (PROC) of the proband were amplified with PCR and analyzed with direct sequencing. Detected mutations were confirmed with reverse sequencing. Corresponding PCR fragments from the family members were also directly sequenced.

RESULTSPlasma PC:A and PC:Ag for the proband was 26% and 18.60%, respectively, both being lower than normal references. Seven members from the pedigree also had lower PC:A, six had lower PC:Ag. A compound heterozygous missense mutation, including a T to G transition at position 6128 of exon 7, which results in Phe139Val, and a G to C transition at position 8478 in exon 9, which results in Asp255His, were identified in the proband. The paternal grandma, father and two aunts were heterozygous for g.6128 T to G, whilst the mother, the second uncle, sister and son were heterozygous for g.8478 G to C. There were lower PC:A in family members with g.8478 G to C.

CONCLUSIONThe proband had inherited two independent mutations of the PROC gene including g.6128 T to G in exon 7 and g.8478 G to C in exon 9 from her father and mother, respectively. The resulting compound heterozygous mutation has caused a serious hereditary protein C deficiency.

Humans ; Infant, Newborn ; Male ; Protein C ; metabolism ; Protein C Deficiency

No abstract available.
C-Reactive Protein ; Cardiovascular Diseases