This experiment was carried out in young adult albino mice,which were injectedwith Ehrlich ascites tumor cells intraperitoneally to produce Ehrlich ascites tumor.The animals were divided into 2 groups.The first group received cAMP plusaminophylline for 5 to 13 days after inoculation.The second group received saline ascontrol.We found that in the administration of cAMP together with aminophylline,thegrowth of Ehrlich ascites tumor cells was inhibited to the extent of 53% at the 9thdays after inoculation.Early or later than the 9th day,the inhibitory rates were marklylower.By using cAMP immunocytochemical method,it was found that on the9th day of inoculation,there was an increase of the intensity of intracellualr cAMPspecific fluorescence in tumor cells of the cAMP treated mice in comparison withthose of the control.It also inhibited the 3',5'-cAMP-PDE activity on the 5th to 7thday after inoculation.Under the dark field microscope on the surface of the Ehrlich tumor cells therewere numerous“brush-like”microvilli,but they were not visible on the surfaceafter treated with cAMP together with aminophylline.The agglutination by theCon.A,was decreased markly on the 7th to 9th day after the inoculation.The possible relationship between the level of intracellular cAMP and of the3',5'-cAMP-PDE,and especially the inhibition of the formation of microvilli onthe treated tumor cell surface is discussed in this paper.

The experiments was conducted on the fibroblasts of human prepuce in vitro todemonstrate the distribution of cytoplasmic microfilaments with Coomassie Blue R250.It has been found that the distribution of the cytoplasmic microfilaments canbe disturbed by the specific inhibitor,Cytochalasin B.We also observed the inhi-bition by Cytochalasin B was reversible.The cytoplasmic microfilaments regainedtheir normal distribution after the Cytochalasin B was removed.This result further confirmed that the staining method of Coomassie BrilliantBlue R 250 is reliable to demonstrate microfilaments in cultured fibrablasts.

The distribution of receptor sites for concanavalin A (Con A) on the cellsurface of human gastric cancer cell line (MGC 80-3) and fibroblast cell cultures wasstudied with electron and light microscope after application of Con A-peroxidasemethod.The cytochemical reaction of the majority of non-prefixed MGC 80-3 cellsshows a striking tendency to be more uneven distribution than on fibroblasts.Clustering,patching and capping of Con A binding sites on the cancer cells anduniform distribution on the fibroblasts were observed.The effects of incubationtemperature,prefix treatment,different phase of cell cycles and cell growth condi-tions on the distribution of Con A receptor complexes were observed.The possiblereasons for the more irregular distribution of the cytochemical reaction product onthe MGC 80-3 cells than the fibroblasts are discussed.

Avian leukosis virus subgroup J (ALV-J) is an avian retrovirus that can induce myelocytomas. A high-frequency mutation in gene envelope endows ALV-J with the potential for cross-species transmission. We wished to ascertain if the ALV-J can spread across species under selection pressure in susceptible and resistant hosts. First, we inoculated (in turn) two susceptible host birds (specific pathogen-free (SPF) chickens and turkeys). Then, we inoculated three resistant hosts (pheasants, quails and ducks) to detect the viral shedding, pathologic changes, and genetic evolution of different isolates. We found that pheasants and quails were infected under the selective pressure that accumulates stepwise in different hosts, and that ducks were not infected. Infection rates for SPF chickens and turkeys were 100% (16/16), whereas those for pheasants and quails were 37.5% (6/16) and 11.1% (3/27). Infected hosts showed immune tolerance, and inflammation and tissue damage could be seen in the liver, spleen, kidneys and cardiovascular system. Non-synonymous mutation and synonymous ratio (NS/S) analyses revealed the NS/S in hypervariable region (hr) 2 of pheasants and quails was 2.5. That finding suggested that mutation of isolates in pheasants and quails was induced by selective pressure from the resistant host, and that the hr2 region is a critical domain in cross-species transmission of ALV-J. Sequencing showed that ALV-J isolates from turkeys, pheasants and quails had moved away from the original virus, and were closer to the ALV-J prototype strain HPRS-103. However, the HPRS-103 strain cannot infect pheasants and quails, so further studies are needed.
Amino Acid Sequence ; Animals ; Avian Leukosis ; transmission ; virology ; Avian Leukosis Virus ; classification ; genetics ; physiology ; Chickens ; Ducks ; virology ; Galliformes ; virology ; Host Specificity ; Molecular Sequence Data ; Poultry Diseases ; transmission ; virology ; Quail ; virology ; Sequence Alignment ; Turkeys ; virology ; Viral Envelope Proteins ; chemistry ; genetics ; metabolism

A rat monoclonal antibody of the IgG1 class, McAb B5A8, specific for the cAMP-dependent protein kinase(PKA) was produced. Western blot analysis revealed specific binding of the antibody to protein of 52-56 kd.The affinity-purified McAb BSA8 was labeled with FITC. Immunofluorescent localization of PKA was examined in human fibroblasts, gastric cancer cell line (MGc 80-3)and EAC cells. The distribution of PKA on the cytoplasmic microtubule network, Golgi region and nucleoli were observed. PKA was localized in the nuclear region in G2 phase of synchronized MGc 80-3 cells, and it was only found around the nuclei of MGc 80-3 cells which were incubated with DBcAMP. The changes in the distribution of PKA in cells are discussed.