Background and purpose:Brucine is one of the active components from Strychnos nux vomica,with signifi cant analgesic,anti-inflammatory and platelet-aggregating inhibitory properties.Due to its cytotoxic effect,the anti-tumor effect of brucine has increasingly been appreciated.In this study,we investigated the impact of brucine on A549 cells proliferation,apoptosis as well as the underlying mechanisms.Methods:MTT assay was used to examine the cell viability,flow cytometric analysis and fluorescent microscope were applied to examine cell apoptosis,ELISA method was used to examine the effect of brucine on PGE2 release from A549 cells and RT-PCR analysis was used to measure mRNA content,western blotting analysis was used to measure protein expression and luciferase activity was detected to examine the effect of brucine on COX-2 promoter activity.Results:Brucine was able to suppress the proliferation of A549 cells and induce cell apoptosis to time-dependent and dose-dependent manner.To understand the mechanisms,COX-2 was identifi ed to be an important target molecule involved in the apoptosis induced by brucine because brucine could suppress the COX-2 mRNA,protein expressions as well as PGE2 release in A549 cells in a timedependent manner.Furthermore,overexpression of COX-2 abrogated brucine-induced cell apoptosis,in contrast,when A549 cells were transfected with COX-2 siRNA,the apoptotic effect of brucine was dramatically enhanced.Further analysis revealed that brucine was able to suppress COX-2 transcriptional activation.Conclusion:Brucine was able to induce lung cancer apoptosis via downregulation of COX-2.

Objective To explore the dynamic responses of Sertoli cells to depletion of spermatogonial stem cells by busulfan.Methods After intraperitoneal injection of 15, 30 or 44 mg/kg busulfan to mice, the spermatogenesis and the expression of GDNF, PLZF, Nanog and GFRɑ1 mRNA were assessed by real-time quantitative PCR at 5 and 28 days after the busulfan treatment.Results Glial cell line-derived neutrophic factor ( GDNF ) was significantly increased and showed a dose-dependent trend at 5 days after busulfan treatment, but no significant difference was seen in the expression of promyelocytic leukemia zinc finger(PLZF) and GDNF family receptorα-1(GFRα1).The testicular histology also appeared no significant difference at 5 days after busulfan treatment.At 28 days after busulfan treatment, the relative expression lev-els of GDNF, PLZF, Nanog and GFRɑ1 mRNA were drastically increased.Morphological observation showed that spermat-ogenesis damages became even more severe as the busulfan dose increased.Conclusions Sertoli cell response to the de-pletion of spermatogonia occurs as early as the fifth day after busulfan treatment.Production of GDNF in Sertoli cells shows a compensatory increase, which may stimulate spermatogonial stem cells to accelerate their self-renewal, reflected by the enhancing expression of Nanog and PLZF, and ultimately promote the restoration of spermatogenesis.

In 2017,the Diabetes Management Center was founded in Shandong Third Provincial Hospital.On the basis of the center,a network was established which integrated the tertiary hospital,district hospitals,community health service institutions and family of patients forming the"Four in One"model of diabetes management.This article introduces the background,application,and preliminary accomplishments in individualized and standardized diabetic management of this internet plus model.The challenges and suggestions for future development of the "Four in One" model are also discussed.

Beijing has been one of the epicenters attacked most severely by the SARS-CoV (severe acute respiratory syndrome-associated coronavirus) since the first patient was diagnosed in one of the city's hospitals. We now report complete genome sequences of the BJ Group, including four isolates (Isolates BJ01, BJ02, BJ03, and BJ04) of the SARS-CoV. It is remarkable that all members of the BJ Group share a common haplotype, consisting of seven loci that differentiate the group from other isolates published to date. Among 42 substitutions uniquely identified from the BJ group, 32 are non-synonymous changes at the amino acid level. Rooted phylogenetic trees, proposed on the basis of haplotypes and other sequence variations of SARS-CoV isolates from Canada, USA, Singapore, and China, gave rise to different paradigms but positioned the BJ Group, together with the newly discovered GD01 (GD-Ins29) in the same clade, followed by the H-U Group (from Hong Kong to USA) and the H-T Group (from Hong Kong to Toronto), leaving the SP Group (Singapore) more distant. This result appears to suggest a possible transmission path from Guangdong to Beijing/Hong Kong, then to other countries and regions.
Genome, Viral ; Haplotypes ; Humans ; Mutation ; Open Reading Frames ; Phylogeny ; SARS Virus ; genetics

We report a complete genomic sequence of rare isolates (minor genotype) of the SARS-CoV from SARS patients in Guangdong, China, where the first few cases emerged. The most striking discovery from the isolate is an extra 29-nucleotide sequence located at the nucleotide positions between 27,863 and 27,864 (referred to the complete sequence of BJ01) within an overlapped region composed of BGI-PUP5 (BGI-postulated uncharacterized protein 5) and BGI-PUP6 upstream of the N (nucleocapsid) protein. The discovery of this minor genotype, GD-Ins29, suggests a significant genetic event and differentiates it from the previously reported genotype, the dominant form among all sequenced SARS-CoV isolates. A 17-nt segment of this extra sequence is identical to a segment of the same size in two human mRNA sequences that may interfere with viral replication and transcription in the cytosol of the infected cells. It provides a new avenue for the exploration of the virus-host interaction in viral evolution, host pathogenesis, and vaccine development.
Base Sequence ; China ; Cluster Analysis ; Gene Components ; Genetic Variation ; Genome, Viral ; Genotype ; Molecular Sequence Data ; Phylogeny ; Reverse Transcriptase Polymerase Chain Reaction ; SARS Virus ; genetics ; Sequence Analysis, DNA ; Severe Acute Respiratory Syndrome ; genetics