环磷酰胺、二溴氯丙烷和卡铂对小鼠和大鼠生殖细胞的细胞遗传学效应

采用精母细胞染色体分析方法检测了环磷酰胺、二溴氯丙烷和卡铂对小鼠和大鼠生殖细胞的细胞遗传学效应。环磷酰胺可使小鼠和大鼠精母细胞染色体断裂和断片率明显上升。在小鼠精母细胞的早粗线期和前细线期及大鼠精母细胞粗线期的早、中期给药时,环磷酰胺还可以使染色体易位率显著升高。

家蚕减数分裂的雌雄差异

家蚕减数分裂,国内外已有许多研究,然自发生学立场者居多。著者自遗传学角度,系统研究了减数分裂的雌雄差异,兹将结果报告于下: 材料及方法供试材料是781×(782×734),参照今井(1980),蒋同庆、郝瑜(1987)方法进行染色体制片,经尿素处理后Giemsa染色。

有丝分裂和减数分裂

分裂是生活细胞的重要特征。每个细胞都是通过分裂而来,又通过分裂而维持其生存;细胞一旦停止分裂就趋向分化,甚至衰老和死亡。有增殖能力的细胞每次分裂后都要进行生长和DNA复制,然后再进行分裂,细胞的这种生长和分裂的周期称细胞周期。它是指一次细胞分裂结束后,细胞开始生长,到下一次分裂结束所经历的过程。所以整个细胞周期包括细胞的生长、DNA复制和细胞分裂。1953年Howard和Pelc根据细胞形态和生物化学的变化把它分为G1、S、G2和M等四个时期（图1）

The impact of ^(60)Co γ-ray on cycles to Hep-2 human laryngeal cancer cell in the condition of hypoxia

Objective： The aim of the study was to investigate the impact of 60Co y-ray on apoptosis, cell cycles and the expression of protein hypoxia-inducible factor-1α （HIF-1α） to Hep-2 cell line in the conditions of normoxia and hypoxia. Methods： Hep-2 cell were divided into 2 groups： group A （normoxia） and group B （hypoxia）. All of the ceils were exposed to y-ray with dosage being 0, 1, 3, 5, 10, 20, and 40 Gy. Flow cytometry was used to measure the protein level of HIF-1α and to detect apoptosis and cell cycles. The protein level of HIF-1α was also determined by immunohistochemistry and Western blotting. Results： The protein level of HIF-1α in group B was significantly higher than that in group A. In group A, low doses （1-5 Gy） of y-ray had caused G0/G1 cell cycle arrest and high doses （10-40 Gy） had caused G2/M cell cycle arrest. In group B, without exposure of y-ray （0 Gy） had caused G0/G1 cell cycle arrest, all of the different dosage of y-ray could cause G2/M cell cycle arrest. The curve of apoptosis rate in group A was a parabola, the apoptotic rate was related to the dosage of y-ray in a dosage dependent manner. The peak was at the point of 5 Gy. The apoptosis rate in group A was significantly higher than that in group B. Conclusion： Different doses of y-ray could cause different cell cycles arrest then make different impact on apoptosis to Hep-2 ceil. The lower apoptosis rate in condition of hypoxia maybe has a relationship with G2/M cell cycle arrest. Up-regulated HIF-1α protein may be one of the reasons for G2/M cell cycle arrest.

Preparation and analysis of spermatocyte meiotic pachytene bivalents of pigs for gene mapping

Well-spread meiotic pachytene bivalents were obtained by using the prolonged hypotonic treatment com-bined with high chloroform Carnory’s fixative solution from cells of the testes of domestic pigs. Comparison in the division index and length of pachytene bivalents with metaphase chromosomes showed that those of the former are 5 times higher and 3.42(1.87-5.98) times longer than those of the latter. Comparative studies on chromomere maps of bivalents and mitotic chromosomal G-bands were conducted by using the chromo-some 12 as a example. Sex vesicle and various shapes of synaptic sex chromosomes have been observed.Two-color PRimed IN Situ (PRINS) labeling has been conducted successfully on pachytene bivalents of pigs.

全局性DNA去甲基化参与男性减数分裂重组调控

精子发生是一个复杂的发育过程,基因突变或表观遗传变异对精子发生功能的破坏可导致男性不育[1~3].在精子发生过程中,减数分裂是生殖细胞获得遗传多样性的关键,其中涉及一系列重要事件,包括前细线期精母细胞中DNA的复制、细线期中DNA双链断裂(DSBs)的形成、合子期及粗线期中发生的减数分裂重组,以及联会复合体在双线期的解离[2,4,5].随着单细胞测序技术在生殖发育领域的应用,先前的研究已初步绘制了人类精子发生过程的基因转录图谱[6~8].

HRCT Scans of Peripheral Non-Small Cell Lung Cancers and their Relationship with Cyclin D1 Expression:a Longitudinal Study

OBJECTIVE To investigate cyclin D1 expression in peripheral lung cancers and its relationship with CT signs and prognosis. METHODS Cyclin D1 expression in peripheral lung cancers and its relationship with the CT imaging and prognosis were analyzed retrospectively by means of SP immunohistochemistry and spiral CT scanning in 92 patients with peripheral lung cancer verified by pathology. RESULTS Cyclin D1 expression was related to deep lobulation,spiculate protuberance,short thin spinules sign and mediastina lymph node metastasis.Cyclin D1 expression was not related to tumor size,cavity,pleural indentation,histological type,differentiation,tumor TNM stage,age or sex.Cyclin D1 was a negative prognostic factor whose over-expression indicated a poor prognosis. CONCLUSION Cyclin D1 expression may play an important role in the occurrence,progress and CT scan results of lung cancers.Cyclin D1 was a negative factor whose over-expression implied a poor prognosis.Detection of the cyclin D1 and observation of the CT scan can be considered as indexes of clinical diagnosis and prognostic evaluation.

Effect of three suture lines on the proliferation and cell cycle of lung adenocarcinoma cell A549 in vitro

Objective： The interaction of cell and medical biomaterial is one of the significant factors to affect clinical application of medical biomaterial. This research is to investigate three of suture lines how to affect the proliferation and cell cycle of lung adenocarcinoma cell A549 in vitro. Methods： Three of suture lines were respectively cultivated with lung adenocarcinoma cell A549, after of 72 hours, we detected absorptions of each group by MTT method in order to reflect the proliferation of lung adenocarcinoma cell A549, and also examined percentage of G1 period cells and S period cells of each group by flow cytometry. Results： Different of suture lines had different effects on the proliferation and cell cycle of lung adenocarcinoma cell A549 （P 〈 0.05）. The effect of absorbent suture line was the strongest on the proliferation and cell cycle of lung arlenecarcinoma cell A549, the effect of chorda serica chirurgicalis was medium, and the effect of slide wire was poor. Different length of each suture line had different effects on the proliferation and cell cycle of lung adenocarcinoma cell A549 （P 〈 0.05）, Conclusion： Three of suture line materials have different effects on the proliferation and cell cycle of lung adenocarcinoma cell A549, with dose-effect relationship.

Green tea polyphenols induce cell death in breast cancer MCF-7 cells through induction of cell cycle arrest and mitochondrial-mediated apoptosis

In order to study the molecular mechanisms of green tea polyphenols（GTPs） in treatment or prevention of breast cancer, the cytotoxic effects of GTPs on five human cell lines（MCF-7, A549, Hela, PC3, and HepG2 cells） were determined and the antitumor mechanisms of GTPs in MCF-7 cells were analyzed. The results showed that GTPs exhibited a broad spectrum of inhibition against the detected cancer cell lines, particularly the MCF-7 cells. Studies on the mechanisms revealed that the main modes of cell death induced by GTPs were cell cycle arrest and mitochondrialmediated apoptosis. Flow cytometric analysis showed that GTPs mediated cell cycle arrest at both G1/M and G2/M transitions. GTP dose dependently led to apoptosis of MCF-7 cells via the mitochondrial pathways, as evidenced by induction of chromatin condensation, reduction of mitochondrial membrane potential（ΔΨ_m）, improvement in the generation of reactive oxygen species（ROS）, induction of DNA fragmentation, and activations of caspase-3 and caspase-9 in the present paper.

Enhancive effect of N,N'-dinitrosopiperazine on inducing precancerous lesion on nasal and/or nasopharyngeal epithelia of TgN(p53mt-LMP1)/HT mice

Objective： To investigate the enhancive effect ofN, N′-dinitrosopiperazine （DNP） on induced carcinogenesis in nasal and/or nasopharyngeal epithelia among TgN（p53mt-LMP1）/HT transgenic mice to examine the underlying mechanism for the development of nasopharyngeal carcinoma （NPC）. Methods： TgN（p53mt-LMP1）/HT transgenic mice and the same strain of C57BL/6J wild-type mice both at the age of 5 months were randomly divided into 2 groups in parallel, respectively, i.e., TgN（p53mt-LMP1）/HT cancerous lesion-inducing group （T1）, TgN（p53mt-LMP1）/HT control group （TC）, C57BL/6J cancerous lesion-inducing group （CI）, and C57BL/6J control group （CC）. TI and CI mice were treated only with DNP for 16 weeks, twice each week, while TC and CC mice were given the same volume of saline as controls.At the end of treatment, animals were sacrificed to collect epithelial tissue samples from nasal cavity and nasopharynx for pathohistological evaluation by hacmatoxylin and eosin （HE） staining and for determination on the expression ofTRAF2, c-Jun, and p 16 by immunohistochemistry. Results： Atypical hyperplasia was more significant in the samples of TI than in those of TC, CI, and CC, with the rates of lesions being 90%, 10%, 0, and 0 （P〈0.01） respectively, though DNP was used alone in a much shortened inducing period at less dosage and without the use of carcinogenic promoter 12-0-tetradecanoylphorbol-13-acetate as usual. The expressions of tumor necrosis factor （TNF） receptor-associated factor 2 （TRAF2） and c-Jun in these samples were significantly up-regulated in TI （P〈0.0 I）, while tbe expression of p16 was significantly lower in TI than in the other groups （P〈0.01）. Conclusion： TgN（p53mt-LMPI）/HT mice hold inherited constitutional defect in immune surveillance function, which can be aggravated by environmental carcinogens, such as DNP used even though in a much less strength. The enhanced carcinogenesis-inducing effect of DNP on TgN（p53mt-LMP1）/HT mice should be closely associated with abnormal signaling of activator protein-1 （AP-1） pathway, especially up-regulated expressions of TRAF2 and c-Jun, and down-regulated expression of p l6.

PGC-1α regulates the cell cycle through ATP and ROS in CH1 cells

Peroxisome proliferator-activated receptor-γ coactivator 1α（PGC-1α） is a transcriptional co-activator involved in mitochondrial biogenesis, respiratory capacity, and oxidative phosphorylation（OXPHOS）. PGC-1α plays an important role in cellular metabolism and is associated with tumorigenesis, suggesting an involvement in cell cycle progression. However, the underlying mechanisms mediating its involvement in these processes remain unclear. To elucidate the signaling pathways involved in PGC-1α function, we established a cell line, CH1 PGC-1α, which stably overexpresses PGC-1α. Using this cell line, we found that over-expression of PGC-1α stimulated extra adenosine triphosphate（ATP） and reduced reactive oxygen species（ROS） production. These effects were accompanied by up-regulation of the cell cycle checkpoint regulators Cyclin D1 and Cyclin B1. We hypothesized that ATP and ROS function as cellular signals to regulate cyclins and control cell cycle progression. Indeed, we found that reduction of ATP levels down-regulated Cyclin D1 but not Cyclin B1, whereas elevation of ROS levels down-regulated Cyclin B1 but not Cyclin D1. Furthermore, both low ATP levels and elevated ROS levels inhibited cell growth, but PGC-1α was maintained at a constant level. Together, these results demonstrate that PGC-1α regulates cell cycle progression through modulation of Cyclin D1 and Cyclin B1 by ATP and ROS. These findings suggest that PGC-1α potentially coordinates energy metabolism together with the cell cycle.