APOBEC3 is a class of cytidine deaminase, which is considered as a new member of the innate immune system, and APOBEC3G belongs to this family. The research about APOBEC3G is a new direction of innate immune defense mechanism against virus. APOBEC3G has the restrictive activity on many viral replications, which deaminates dC to dU in the viral genome and then induces extensive hypermutation. APOBEC3G can also interrupt viral replication at several phases such as reverse transcription, replication, nucleocapsid and so on by non-deamination mechanisms. However, virus can encode viral proteins to counteract the restriction activity of APOBEC3G. Elucidation of the antagonistic interaction between APOBEC3G and the virus will be contributed to development of new antiviral drugs in the future.
APOBEC-3G Deaminase ; Animals ; Cytidine Deaminase ; genetics ; metabolism ; DNA Replication ; Deamination ; HIV-1 ; physiology ; Hepacivirus ; genetics ; physiology ; Hepatitis B virus ; genetics ; physiology ; Humans ; Paramyxoviridae ; genetics ; physiology ; Retroviridae ; physiology ; Virus Replication ; vif Gene Products, Human Immunodeficiency Virus ; metabolism

Ectopia Cordis ; surgery ; Humans ; Infant, Newborn ; Male

Purple bacteria are extensively used in bacterial photosynthesis research. This review describes the structure of light-harvesting I, light-harvesting II and reaction center of photosynthetic apparatus of pur- ple bacteria and discusses the regulation mechanisms of photosynthesis (PS) gene transcription, with an emphasis laid on the transcriptional regulation of PS gene by PpsR/AppA system.

OBJECTIVETo investigate the protective effect of ginsenoside Rg1 on oxygen-glucose deprivation (OGD) in PC-12 cells, and preliminarily discuss the potential molecular mechanism of mTOR/Akt/FoxO3 signaling pathway.

METHODThe OGD PC-12 cell model was established. The cell viability was measured by MTT assay. After the pretreatment with Rg1 with the concentration of 10, 20, 40 micromol x L(-1) for 24 h, the cell viability was observed. Lactate dehydrogenase (LDH) release, superoxide dismutase (SOD) ac- tivity and malondialdehyde (MDA) level were detected by colorimetry assay. mTOR, p-Akt(ser473), p-Akt(tjr308), Akt, p-FoxO3, FoxO3 in cytoplasm and nucleus, and total FoxO3 protein expression were detected by Western blot assay.

RESULTOGD could significantly in- hibit cell proliferation in 4-24 h in a time-dependent manner. After pretreatment for 24 h, Rg1 (20, 40 micromol x L(-1)) could notably elevate the cell viability and SOD viability and reduce the LDH release and MDA content. Besides, Rg1 also inhibited OGD-induced mTOR and p-Akt(ser473) decreases. After treatment for 6 h, OGD could reduce FoxO3 phosphorylation and promote FoxO3 in cytoplasm. This data suggested that Rg1 could protect PC-12 cell injury through mTOR/p-Akt/FoxO3 signaling pathway.

CONCLUSIONGinsenoside Rg1 could attenuate OGD-induced PC-12 cell injury. Its action mechanism may be closely related to activation of mTOR/p-Akt/FoxO3 signaling pathway.

Animals ; Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Cell Survival ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Forkhead Box Protein O3 ; Forkhead Transcription Factors ; genetics ; metabolism ; Ginsenosides ; pharmacology ; Glucose ; metabolism ; Oxygen ; metabolism ; PC12 Cells ; Protective Agents ; pharmacology ; Proto-Oncogene Proteins c-akt ; genetics ; metabolism ; Rats ; Signal Transduction ; drug effects ; TOR Serine-Threonine Kinases ; genetics ; metabolism

Background:X-linked inhibitor of apoptosis (XIAP) is a vital factor in the anti-apoptosis mechanism of tumors and is highly expressed in renal cell carcinoma (RCC).However,the mechanism through which XIAP regulates DNA damage repair is unknown.This study investigated the regulatory mechanism of XIAP in etoposide-induced apoptosis in two Caki-1 cell lines with high or low XIAP expression.Methods:The two cell lines were established using RNA interference technology.The differentially expressed proteins in the two cell lines were globally analyzed through an isobaric tags for relative and absolute quantitation-based quantitative proteomics approach.Proteomic analysis revealed 255,375,362,and 5 differentially expressed proteins after 0,0.5,3,and 12 h of drug stimulation,respectively,between the two cell lines.The identified differentially expressed proteins were involved in numerous biological processes.In addition,the expression of histone proteins (H1.4,H2AX,H3.1,H3.2,and H3.3) was drastically altered,and the effects of XIAP silencing were accompanied by the marked downregulation of H2AX.Protein-protein interactions were assessed and confirmed through immunofluorescence and Western blot analyses.Results:The results suggested that XIAP may act as a vital cell signal regulator that regulates the expression of DNA repair-related proteins,such as H2AX,and influences the DNA repair process.Conclusions:Given these functions,XIAP may be the decisive factor in determining the sensitivity of RCC cell apoptosis induction in response to chemotherapeutic agents.

OBJECTIVETo study the influence of human cytomegalovirus (HCMV) infection on cell cycle and the expression of replication licensing factor Cdt1 in human embryonic lung fibroblastic (HEL) cells and to explore the pathogenesis of HCMV infection.

METHODSHEL cells were synchronized in the G0/G1 phase by the serum starvation method. The synchronized HEL cells were infected with HCMV, and those that were not subjected to HCMV infection were used as the control group. The HEL cells were harvested at 12, 24, 48, 72 and 96 hrs of HCMV infection. The cell cycle of HEL cells was detected by the flow cytometry. The expression of Cdt1 mRNA in HEL cells was determined by reverse transcription-polymerase chain reaction (RT-PCR).

RESULTSThe cells in the G1 phase in the control group was significantly more than in the HCMV-infected group 12 and 24 hrs after infection (P < 0.01). The expression of Cdt1 mRNA in the HCMV-infected group was significantly lower 12 and 24 hrs after infection but increased significantly 48 hrs after infection compared with the control group (P < 0.05). The expression of Cdt1 mRNA reached a peak at 12 hrs of infection in the control group, but at 48 hrs of infection in the HCMV-infected group, which markedly lagged behind the control group.

CONCLUSIONSHCMV infection arrests the cell cycle of HEL cells at the G1 phase. HCMV infection makes Cdt1 expression delay. HCMV infection can interfere cell cycle of HEL cells possibly through affecting the expression of Cdt1.

Cell Cycle ; Cell Cycle Proteins ; genetics ; Cells, Cultured ; Cytomegalovirus ; pathogenicity ; Embryo, Mammalian ; cytology ; Fibroblasts ; cytology ; metabolism ; Humans ; Lung ; cytology ; metabolism ; RNA, Messenger ; analysis

OBJECTIVETo determine the location on outer envelope and natural antibody response and types of genus-specific lipoprotein antigen LipL41s in patients with Leptospira interrogans.

METHODSMicroscope agglutination test (MAT) was used to examine leptospirosis patients' serum samples from Sichuan area, China. Ni-NTA affinity chromatography was performed to extract the target recombinant rLipL41/1 and rLipL41/2 products that expressed under inducement of IPTG. Western blot assay was performed to detect the immunoreactivity between the sera from the patients infected with different serogroups of L. interrogans and rLipL41s. Immune aurosol electron microscopy was selected to locate the position of LipL41s on leptospiral envelope. ELISA based on rLipL41s was established to confirm the level and types of specific antibody.

RESULTSL. interrogans serogroup icterohaemorrhagiae remained to be the most dominant leptospiral serogroup in Sichuan area. All the sera from patients infected with different serogroups of L. interrogans could efficiently recognize the LipL41s which were the protein molecular that located on the external surface of leptospiral envelope. In the 156 serum samples from MAT positive leptospirosis patients, the positive rates for rLipL41/1 or rLipL41/2 specific IgM appeared to be 84.6%-87.8% and 78.2%-83.3%, respectively, while for rLipL41/1 or rLipL41/2 specific IgG they were 69.2%-81.4% and 75.0%-80.1%, respectively.

CONCLUSIONLipL41s were the leptospiral superficial protein antigen of L. interrogans. Both the LipL41/1 and LipL41/2 could induce serum antibodies IgM and IgG with extensive antigenic-cross reaction during natural infection of L. interrogans in general populations. Hence, rLipL41/1 or rLipL41/2 could be used as the antigen candidate for developing universal genetic engineering vaccine and detection kit.

Antibodies, Bacterial ; blood ; immunology ; Antigens, Bacterial ; metabolism ; Bacterial Outer Membrane Proteins ; metabolism ; Cell Membrane ; metabolism ; Cross Reactions ; Humans ; Immunoglobulin G ; blood ; immunology ; Immunoglobulin M ; blood ; immunology ; Leptospira interrogans ; metabolism ; ultrastructure ; Leptospirosis ; immunology ; Species Specificity

OBJECTIVETo summarize the new knowledge of the anaplastic thyroid carcinoma (ATC).

METHODSThe clinical data of 58 patients (35 men, 23 women, aged 28 to 79 years) with ATC that were treated with various therapeutic modalities from 1981 to 2005 were retrospectively analyzed. Among them, 25 patients received surgery alone (SA group) and 33 received surgery plus radiation (S + R group). The dosage of postoperative radiotherapy was 40-70 Gy. Four patients received biopsy, 24 received palliative surgery, and 30 received radical surgery. Only 2 patients received complete chemotherapy.

RESULTSATC invaded trachea in 40 patients (69.0%), esophagus in 32 patients (55.2%), and carotid in 17 patients (29.3%). The cervical lymph node metastases occurred in 19 patients (32.8%). The overall 1-year survival rate was 37.8%, 3-year survival rate 31.2%, and 5-year survival rate 25.9%. The 5-year survival rate was 37.8% in S + R group but was only 9.9% in SA group (P = 0.0000). The 5-year survival rate was 41.4% in radical surgery subgroup but was only 12.4% in palliative surgery subgroup (P = 0.0023). In < or = 45-year-old subgroup (n = 4), the 5-year survival rate was 50.0%; however, in > 45-year-old subgroup, it was only 21.3%. In postoperative radiation < 60 Gy subgroup , the 5-year survival rate was 19.3%; however, in > or = 60 Gy group, it was 53.7% (P = 0.0000). Among all the 58 patients, some patients received palliative surgery because of tumor invasion in trachea (n = 16, 27.6%), esophagus (n = 8, 13.8%), carotid (n = 8, 13.8%), and other sites (n = 13, 22.4%). Twenty-four patients (61.5%) died of localrelapse, 2 (5.1%) of cervical lymphnode failure, 9 (23.1%) of metastasis, and 4 (10.3%) of other reasons.

CONCLUSIONSThe prognosis of ATC is poor. Radical surgery and postoperative radiation > or = 60 Gy can improve the survival rate. Tumor invasion in trachea, esophagus, and carotid are the main reasons of palliative surgery. Local relapse is lethal.

Adult ; Aged ; Carcinoma ; pathology ; surgery ; Carcinoma, Squamous Cell ; pathology ; surgery ; Female ; Humans ; Lymphatic Metastasis ; Male ; Middle Aged ; Neoplasm Recurrence, Local ; Retrospective Studies ; Thyroid Neoplasms ; pathology ; surgery

OBJECTIVETo investigate the cytotoxic mechanism of cadmium (Cd) on cerebral cortical neurons.

METHODSThe primary cultures of rat cerebral cortical neurons were treated with different concentrations of cadmium acetate (0, 5, 10, and 20 micromol/L), and then the cell viability, apoptosis, ultrastructure, intracellular [Ca2+], and reactive oxygen species (ROS) levels, mitochondrial membrane potential (delta psi), activities of catalase (CAT) and superoxide dismutase (SOD) were measured.

RESULTSA progressive loss in cell viability and an increased number of apoptotic cells were observed. In addition, Cd-induced apoptotic morphological changes in cerebral cortical neurons were also demonstrated by Hoechst 33258 staining. Meanwhile, ultrastructural changes were distortion of mitochondrial cristae and an unusual arrangement. Simultaneously, elevation of intracellular [Ca2+]i and ROS levels, depletion of Delta Psi were revealed in a dose-dependent manner during the exposure. Moreover, CAT and SOD activities in the living cells increased significantly.

CONCLUSIONExposure of cortical neurons to different doses of Cd led to cellular death, mediated by an apoptotic mechanism, and the apoptotic death induced by oxidative stress may be a potential reason. And the disorder of intracellular homeostasis caused by oxidative stress and mitochondrial dysfunction may be a trigger for apoptosis in cortical neurons.

Animals ; Apoptosis ; drug effects ; Cadmium ; toxicity ; Cerebral Cortex ; cytology ; drug effects ; metabolism ; In Vitro Techniques ; Neurons ; drug effects ; metabolism ; Oxidative Stress ; drug effects ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species ; metabolism

The purpose of this study was to determine whether the Ca2+ signaling pathway is involved in the ability of osteoprotegerin (OPG) to inhibit osteoclast differentiation and maturation. RAW264.7 cells were incubated with macrophage colony-stimulating factor (M-CSF) + receptor activator of nuclear factor-kappaB ligand (RANKL) to stimulate osteoclastogenesis and then treated with different concentrations of OPG, an inhibitor of osteoclast differentiation. The intracellular Ca2+ concentration [Ca2+]i and phosphorylation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) in the different treatment groups were measured by flow cytometry and Western blotting, respectively. The results confirmed that M-CSF + RANKL significantly increased [Ca2+]i and CaMKII phosphorylation in osteoclasts (p < 0.01), and that these effects were subsequently decreased by OPG treatment. Exposure to specific inhibitors of the Ca2+ signaling pathway revealed that these changes varied between the different OPG treatment groups. Findings from the present study indicated that the Ca2+ signaling pathway is involved in both the regulation of osteoclastogenesis as well as inhibition of osteoclast differentiation and activation by OPG.
Animals ; Calcium/*metabolism ; *Calcium Signaling ; *Cell Differentiation/drug effects ; Cell Line ; Cell Survival/drug effects ; Gene Expression Regulation/drug effects ; Macrophage Colony-Stimulating Factor/metabolism ; Mice ; Osteoclasts/*cytology/*drug effects/*metabolism ; Osteoprotegerin/*pharmacology ; RANK Ligand/metabolism