Dynamic changes and diagnostic and prognostic significance of serum PCT, hs-CRP and s-100 protein in central nervous system infection.

The aim of the study was to analyze the dynamic changes and diagnostic and prognostic significance of serum procalcitonin (PCT), high-sensitivity C-reactive protein (hs-CRP) and s-100 protein in central nervous system infection. A total of 110 patients diagnosed with central nervous system infection in Department of Neurology in the People's Hospital of Rizhao from January 2014 to January 2016 were selected and retrospectively analyzed; they were divided into the bacterium (n=70) and virus (n=40) groups. Another 45 normal subjects were selected as the control group. PCT, hs-CRP and s-100 protein values in serum and cerebrospinal fluid were measured. The serum PCT, hs-CRP and s-100 protein levels in the bacterium group were significantly higher than those in the virus and control groups (p<0.05). The serum PCT, hs-CRP and s-100 protein levels in the bacterium and virus groups after treatment were obviously decreased compared with those before treatment (p<0.05). PCT, hs-CRP and s-100 protein levels in serum and cerebrospinal fluid in the bacterium and virus groups had no statistically significant differences after treatment (p>0.05). PCT, hs-CRP and s-100 protein levels in deaths in bacterium group were significantly higher than those in survivors (p<0.05). The serum PCT, hs-CRP and s-100 protein levels, can serve as important indexes for the diagnosis of central nervous system infection and their dynamic changes can be used to monitor the changes in disease condition, severity of bacterial infection and prognosis, providing help for the clinical treatment thereof.

OVA12 promotes tumor growth by regulating p53 expression in human cancer cells.

Ovarian cancer-associated antigen 12 (OVA12) was first identified in an ovarian carcinoma complementary DNA (cDNA) expression library and has been shown to play an important role in tumor growth. Here, we found that overexpression of OVA12 accelerated tumor growth in different tumor cells, whereas OVA12 depletion was associated with the opposite effect. Moreover, knocking down OVA12 led to a significant increase in the protein levels of p53, and the overexpression of OVA12 significantly decreased endogenous p53 levels. In addition, OVA12 stimulated p53 polyubiquitination and degradation by the proteasome and promoted tumor growth at least partially through the p53 pathway. Taken together, these results indicate that OVA12 is a negative regulator of p53 and that inhibition of OVA12 expression might serve as a therapeutic target to restore tumor suppression.