The effect of thyrosine kinase, calmodulin and voltage-dependent Ca²⁺ channel on the proliferation of hepatoma cells induced by EGF was studied. Hepatoma cell line SMMC7721 was cultured in RPMI1640 serum-free medium. DNA synthesis rate of hepatoma cells was measured by H-TdR incorporation. 10⁻⁹ mol/L EGF could significantly stimulate the proliferation of hepatoma cells (P<0.05), and this effect might be significantly inhibited by tyrosine kinase inhibitor (P<0.001). Calmodulin inhibitor W-7 had no effect on the basic phase of cultured hepatoma cells (P>0.05), but it had very significantly inhibitory effect on the proliferation of hepatoma cells induced by EGF (P<0.001). Voltage-dependent Ca²⁺ channel inhibitor Varapamil had no inhibition on the proliferation of hepatoma cells induced by EGF (P>0.05). It had no effect on the basic phase of cultured hepatoma cells, (P>0.05). It is suggested that tyrosine kinase and Ca²⁺-calmodulin-dependent pathway may play a critical role on the proliferation of heptoma cells induced by EGF and voltage-dependent Ca²⁺ channel is independent of the effect of EGF.

The effects of carvedilol on cardiomyocyte apoptosis and expression of bcl-2, bax genes following ischemia (0.5 h) and reperfusion (48 h)in vivo and the possible biological mechanism of carvedilol inhibiting cardiomyocyte apoptosis were studied. The left anterior descending artery in Wistar rats were ligated to establish ischemia-reperfusion (I/R) models. The model animals were divided into two groups: I/R group, the model rats not subject to other treatments except ischemia-reperfusion (n=8): carvedilol-treated group (n=8), I/R model rats treated with carvedilol. Eight rats in the sham-operated group were subjected to only experimental open operation. The number of apoptotic cardiomyocyte was determined by TUNEL staining. Immunohistochemistry andin situ hybridization histochemistry (ISHH) were used to detect the expression of bcl-2 and bax genes. Image processing system was used to quantitatively dispose the positive metric substances of both immunohistochemistry and ISHH through the average optical density (OD) value. The results showed that the number of the apoptotic cells were 36.18±9 (I/R group), 0–1 (sham-operated group) and 9.5±3 (carvedilol-treated group) in each visual field respectively with the difference being very significant among the groups (P<0.001). The OD values of bcl-2 protein in sham-operated group, I/R group and carvedilol-treated group were 0.14±0.01, 0.08±0.02 and 0.15±0.03, respectively. The OD values of bcl-2 mRNA in sham-operated group, I/R group and carvedilol-treated group were 0.08±0.01, 0.06±0.01 and 0.09±0.01, respectively. There was no significant difference between carvedilol-treated group and I/R group (P>0.05). The OD values of bax protein in I/R group, sham-operated and carvedilol-treated-treated group were 0.13±0.02, 0.07±0.01, 0.06±0.01, respectively. There was very significant difference between carvedilol-treated group and I/R group (P<0.01). Bcl-2/bax ratio was 1.07±0.14 (I/R group), 1.28±0.16 (sham-operated group), 2.5±0.26 (carvedilol-treated group) respectively with the difference being very significant between carvedilol-treated group and I/R group (P<0.05). It was indicated that carvedilol could inhibit cardiomyocyte apoptosis following ischemia and reperfusion, which was related to the increased bcl-2/bax ratio due to inhibition of bax gene expression.

To investigate the distribution of variant genotypes of Fc gamma receptor III a (FcγRIII a) in healthy Chinese population of Zhengzhou city, genomic DNA was extracted from peripheral blood of healthy donators. The genotypes of FcγRIII a-158 were determined by nested polymerase chain reaction (PCR) in 137 healthy people in Zhengzhou city. The results showed that frequencies of variant genotypes FF, VV and VF were 42.3%, 48.9% and 8.8% respectively. The distribution of FcγRIII a-158 in healthy Chinese population of Zhengzhou city was polymorphic and different from that of African Americans (AA) and Caucasian Americans (CA).

This paper was designed to investigate the expression of p53, p21 of A549 cell strains under hypoxic condition and the effect of trichostatin A (TSA), the inhibitor of histone deacetylasel (HDAC1) on their expression. The authors designed 1 normoxia group (control group) and 6 hypoxia groups (experiemntal group): hypoxia 6 h group (A), TSA + hypoxia 6 h (B), hypoxia 12 h group (C), hypoxia 24 h group (D), TSA+hypoxia 24 h (E) hypoxia 48 h group (F). The expression of HDAC1 in A549 cells was examined by using Western blot and the expression of p53, p21 in A549 cells and the effect of TSA on them were determined by using immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR). The A value expressed by HDAC1 in A549 cell strains was 138±11 in the control group, 78±4, 86±5, 124±3, 120±9 in experimental groups A, C, D, F, respectively. The A value of the expression of the protein and mRNA of p53 in A549 cell strains were 0.12±0.02, 0.62±0.02 in the control group, 0.10±0.03, 0.32±0.03; 0.11±0.01, 0.33±0.02, 0.13±0.03, 0.58±0.01, 0.12±0.02, 0.56±0.02 in experimental group A, B, D, E, respectively. The A value of the expression of the protein and mRNA of p21 in A549 cell strains were 0.17±0.03, 0.62±0.03 in the control group, 0.16±0.02, 0.50±0.02; 0.14±0.02, 0.36±0.02; 0.15±0.03, 0.49±0.03; 0.13±0.02, 0.33±0.02 in experimental groups A, B, D, E, respectively. These results indicate that the expression of HDAC1 is regulated by hypoxia and the effect of TSA is closely related to the expression of P21 under hypoxia condition.