ABSTRACT
Objective To investigate the change and clinical significance of growth differentiation factor 15 (GDF15) and gastric cancer antigen 724 (CA724) in serum of patients with gastric cancer .Methods Serum levels of GDF15 in serum of 30 patients with gastric cancer were detected by ELISA .The levels of serum gas-tric CA724 were measured by electrochemiluminescence ,and 32 cases of benign gastric lesions and 30 healthy controls were compared .Results The levels of serum GDF15 and CA724 in patients with gastric cancer were (1 .58 ± 0 .53)ng/mL and (40 .80 ± 5 .20) IU/mL ,respectively .The levels of serum GDF15 and CA724 in pa-tients with benign gastric lesions were (0 .26 ± 0 .11) ng/mL ,(12 .90 ± 2 .30) IU/mL (P<0 .01) .The levels of GDF15 and CA724 in normal control group were (0 .17 ± 0 .08)ng/mL and (3 .80 ± 0 .90)IU/mL respectively . The levels of serum GDF15 and CA724 in gastric cancer group were significantly higher than those in benign gastric lesions and normal control group (P<0 .01) .The level of serum GDF15 was closely related to tumor size ,TNM stage and lymph node metastasis (P<0 .05) .The sensitivity of gastric cancer was 83 .3％ ,the spe-cificity was 83 .9％ and the AUC was 0 .837 .The sensitivity of CA724 was 90 .0％ ,the specificity was 76 .5％and the AUC was 0 .886 .The combined detection of AUC was 0 .920 ,which was significantly higher than that of single detection .Conclusion GDF15 is associated with the development and progression of gastric cancer .Combined detection of GDF15 and CA724 in serum is helpful for early diagnosis of gastric cancer and progno-sis .
ABSTRACT
OBJECTIVE: To analyze the ACC inhibitor drugs and their layout of global patents, thus to provide experience for the domestic pharmaceutical enterprises in the R&D and patent protection. METHODS: Using qualitative and quantitative analysis, the global patents of ACC inhibitor drugs were searched, indexed, statisticed and analyzed to draw the conclusion. RESULTS: Patent family is key for the important market and the chemical compound patent plays a major role. CONCLUSION: The global patents of ACC inhibitor drugs are still on the early stage, and the domestic pharmaceutical enterprises could construct the crystal and composition patents in the surrounding patent layouts at the right time according the R&D strategies.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the possible relationship between variation of coxsackievirus B3 (CoxB3) VP1 sequence from cerebrospinal fluid of children with severe and mild central nervous system (CNS) infection and damage to CNS in children from Shandong province.</p><p><b>METHODS</b>The enteroviruses were detected using VP1 typing and sequencing primer for enteroviruses from 73 enterovirus-infected cases confirmed by detection of cerebrospinal fluid by enteroviruses common primer. VP1 sequences (450 nucleotides) were determined and analyzed for 21 CoxB3 enteroviruses strains isolated in Qingdao and Binzhou, and were compared with that of BLAST search procedures from GeneBank in NCBI. The variation of VP1 gene and amino acids sequence of CoxB3 enteroviruses was analyzed for severe and mild CNS infection.</p><p><b>RESULTS</b>The nucleotide homogeneity of these CoxB3 appeared to be 97% - 99%, however, the homogeneity among different genotypes were 83% - 76%. Replacement of glutamine by histidine at amino acid locus 856 of VP1 CoxB3 was found in 4 cases with severe encephalitis. There were different variation in VP1 nucleotide sequence of CoxB3 in 3 cases with mild encephalitis and 14 cases with meningitis, but amino acids sequences had no regular variation. The modified Glasgow's coma score was below 7 in all the 4 cases with severe encephalitis. Of these 4 cases, 3 had consciousness disturbance for less than 3 days. Lethargy, restlessness and psychiatric symptoms were major manifestations, of whom 3 also had dysphagia, 1 had encephalatrophy obviously, Glasgow's coma score was 3, deep coma lasted for 9 days, and had concomitant fatal epileptic attacks. Of these 4 cases, 2 completely recovered, 1 had high muscle tone, 1 remained under anti-epileptic drug treatment at follow-up 6 months later.</p><p><b>CONCLUSION</b>There were a small epidemic of CoxB3 CNS infection in children in 2005 in this area. The amino acid variation of CoxB3 VP1 possibly caused increased viral virulence and caused damage to CNS.</p>