江西井冈山国家级自然保护区爬行动物多样性研究

2002～2005年对井冈山国家级自然保护区的爬行动物进行了调查,发现当地5种新记录：乌龟（Chinemys reevsii）、平胸龟（Platyternon megacephalum）、多疣壁虎（Gekko japonicus）、银环蛇（Bungarus muhicinctus）和短尾蝮（Agkistrodon brevicaudus）。井冈山自然保护区共有爬行动物41种,隶属于3目9科27属,其中蛇类占80．49％。保护区的爬行动物以东洋界种为主占总数的82．93％,其次是广布种占总数的17．07％,无古北界种。结果表明井冈山自然保护区爬行动物种类丰富,这与保护区所处的地理位置和特殊的地形和气候条件等相关。     

濒危植物长柄双花木自然种群生殖构件的时空动态

根据野外观测数据,研究了濒危植物长柄双花木(Disanthus cercidifolius var.longipes)在不同生境条件下自然种群开花物候变异以及生殖构件的时空动态.结果表明,不同群落类型中长柄双花木开花物候存在一定差异,在纯林中个体的平均花期最长,达75d,而个体间开花同步性最低,仅为0.717;竹林中的个体花期最短,只有47d,而同步指数最高,达0.968.生殖枝数量及花序数均随个体年龄增长而增加,在年龄为30～35年时达最高,此后又呈下降趋势;在海拔为810m左右处,个体生殖枝数及着生的花序数均达最大值,且冠层间差异明显.纯林中个体着生的生殖枝数及每生殖枝上着生的花序数均最高,分别为411.39和7.857;竹林中个体每生殖枝着生的花序数显著低于其它群落.年龄小的个体,各时期生殖构件败育率均高于年龄大的个体;另外,生殖构件的败育与海拔高度间无相关性,而与构件发育时间、分布的树冠层次以及所处的群落类型相关.影响生殖构件败育的主要因子是光照条件.     

二型花柱植株金荞麦繁殖特征

开花物候及繁殖分配是植物适应环境的重要因素。对金荞麦开花物候、繁殖分配及策略进行了研究。结果如下:金荞麦的花果期为每年的8—11月,9月集中开花,其集中开花模式有助于吸引昆虫传粉,提高繁殖成功率;金荞麦单花开花持续时间为1—2 d,种群花期均为85d。L型花序花期为15—26d,S型花序花期为14—27d,两者没有显著差异;L型单花序开花数为26—131朵,S型单花序开花数为36—147朵,两者没有显著差异。L型和S型花序开花动态呈现单峰曲线,在花序开花后第11天L型和S型都达到最大值,分别为7.30%和7.20%,且两种花型具有较高的开花同步性,这有助于其繁殖适应性的提高。同一个花型中,雌蕊长、雄蕊长之间存在极显著负相关,但雌雄总长不存在显著差异,表明雌蕊长、雄蕊长可能存在权衡关系;金荞麦的繁殖器官和营养器官生物量在L型和S型间不存在显著差异,但其花生物量与植株生物量表现出极显著正相关关系。金荞麦L型花生物量分配极显著大于S型,而总生物量不存在显著差异,说明金荞麦植株的营养生长与有性繁殖间存在权衡关系。     

二型花柱植物金荞麦的繁殖生态学研究

通过野外实验观察和人工控制套袋等方法,从金养麦的花部基本特征、开花动态、花粉胚珠比(P/O)、花粉活力、柱头可授性、杂交指数、套袋实验及访花昆虫等方面对其繁殖生态学进行了研究.结果显示:(1)金荞麦在同一居群中同时具有长柱型(L-型)和短柱型(S-型)两种花型,短花柱花直径(7.25±0.11 mm)显著大于长花柱花直径(6.79±0.11 mm),长花柱花的柱头和花药高分别为3.39±0.04 mm和1.80±0.02 mm,短花柱花的柱头和花药高则分别为1.89±0.04 mm和3.19±0.06 rnm,表现出互补式雌雄异位的花部特征.(2)金荞麦8～10月开花,单花序的花期为15～23 d,单花的花期为1～3 d,开花进程中,内轮雄蕊先散粉,外轮雄蕊后散粉;S-型花的花粉活力高于L型花的花粉活力,但其单花花粉量低于L-型花,显示了两种花型的自我调控机制.(3)套袋实验表明,金荞麦自花自交不亲和,但具有型内和型间亲和性,L型和S-型花的P/O值分别为810±40.48和526.5±42.24,表明其繁育系统为兼性异交,需要传粉者,但L-型花更倾向异交.(4)金荞麦的主要访花昆虫为膜翅目(Hymenoptera)、双翅目(Diptera)、鳞翅目(Lepidoptera)、半翅目(Hemiptera)和蜻蜒目(Odonata) 19个科37种昆虫,其中,两种花型拥有12种共同的访花昆虫,L-型花访花昆虫14种,S-型花访花昆虫35种,表明S-型花对昆虫具有更强的吸引力.研究表明,金荞麦是典型的二型花柱植物,虽然具有严格的自交不亲和性,但显示一定的型内亲和性.     

H2O2-induced secretion of tumor necrosis factor-α evokes apoptosis of cardiac myocytes through reactive oxygen species-dependent activation of p38 MAPK

P38 mitogen-activated protein kinases (p38 MAPK) and tumor necrosis factor-α (TNF-α) play important roles in oxidative stress-induced apoptosis in cardiac myocytes. However, the regulation and functional role of cross-talk between p38 MAPK and TNF-α pathways have not yet been fully characterized in cardiac myocytes. In this study, we found that inhibition of p38 MAPK with SB-203580 (SB) reduced H₂O₂-stimulated secretion of TNF-α, whereas pre-activation of p38 MAPK with sodium arsenite (SA) enhanced H₂O₂-stimulated secretion of TNF-α. In addition, pretreatment of cells with TNF-α increased basal and H₂O₂-stimulated p38 MAPK and apoptosis of cardiac myocytes, and p38 MAPK-associated apoptosis of cardiac myocytes induced by TNF-α was blocked by inhibition of p38 MAPK with SB. Finally, H₂O₂-induced apoptosis was attenuated by the inhibitors of p38 MAPK or reactive oxygen species (ROS), whereas it was enhanced by p38 MAPK agonist SA. These results suggest that H₂O₂-induced secretion of TNF-α increases apoptosis of cardiac myocytes through ROS-dependent activation of p38 MAPK. This may represent a novel mechanism that TNF-α partly interplays with p38 MAPK pathways during oxidative stress-modulated apoptosis in cardiac myocytes.     

Multi-Q: a fully automated tool for multiplexed protein quantitation

The iTRAQ labeling method combined with shotgun proteomic techniques represents a new dimension in multiplexed quantitation for relative protein expression measurement in different cell states. To expedite the analysis of vast amounts of spectral data, we present a fully automated software package, called Multi-Q, for multiplexed iTRAQ-based quantitation in protein profiling. Multi-Q is designed as a generic platform that can accommodate various input data formats from search engines and mass spectrometer manufacturers. To calculate peptide ratios, the software automatically processes iTRAQ's signature peaks, including peak detection, background subtraction, isotope correction, and normalization to remove systematic errors. Furthermore, Multi-Q allows users to define their own data-filtering thresholds based on semiempirical values or statistical models so that the computed results of fold changes in peptide ratios are statistically significant. This feature facilitates the use of Multi-Q with various instrument types with different dynamic ranges, which is an important aspect of iTRAQ analysis. The performance of Multi-Q is evaluated with a mixture of 10 standard proteins and human Jurkat T cells. The results are consistent with expected protein ratios and thus demonstrate the high accuracy, full automation, and high-throughput capability of Multi-Q as a large-scale quantitation proteomics tool. These features allow rapid interpretation of output from large proteomic datasets without the need for manual validation. Executable Multi-Q files are available on Windows platform at http://ms.iis.sinica.edu.tw/Multi-Q/.     

p53 Transgenic mice are highly susceptible to 4-nitroquinoline-1-oxide-induced oral cancer

In this study, we did a bioassay employing mice with a dominant-negative p53 mutation (p53(Val135/WT)) to assess whether a germ-line p53 mutation predisposed mice toward the development of squamous cell carcinomas (SCC) in the oral cavity. Treatment of the mouse oral cavity with 4-nitroquinoline-1-oxide produced a 66%, 91%, and 20% tumor incidence in the oral cavity, esophagus, and forestomach/stomach, respectively, in p53(Val135/WT) mice. In contrast, only a 25%, 58%, and 4% tumor incidence was observed in oral cavity, esophagus, and forestomach/stomach, respectively, in wild-type littermates (p53(WT/WT)). The most striking difference between p53(Val135/WT) and p53(WT/WT) mice following the carcinogen treatment was the higher prevalence and more rapid development of SSC in p53(Val135/WT) mice than in wild-type mice. To identify the precise genes or pathways involved in these differences during tumor development, we examined gene expression profiles of 4-nitroquinoline-1-oxide-treated normal tongues as well as tongue SCC in p53(Val135/WT) and p53(WT/WT) mice. Microarray and GenMAPP analysis revealed that dominant-negative p53 ((135)Valp53) affects several cellular processes involved in SCC development. Affected processes included apoptosis and cell cycle arrest pathways, which were modulated in both tumor and normal epithelium. These results showed that reduction of p53-dependent apoptosis and increases in cell proliferation might contribute to the observed increase in oral cavity and gastroesophageal malignancies in p53(Val135/WT) mice as well as to the more rapid growth and progression of tumors.     

小鼠细胞核富集着丝粒部分特性的研究

我们从分离核获得的颗粒状小鼠着丝粒富集部分的特性是用间接免疫荧光法,微管组织中心(MTOC)活性的测试,SDS-PAGE 及荧光标记原位杂交法进行研讨的。这部分中的多数颗粒是DNA 和动点蛋白质的复合物,并且显示具有MTOC 活性。从这部分提出的DNA 杂交于小鼠腹水癌细胞所有的染色体的初级缢痕处。从这部分的蛋白质中检出的动点蛋白质,其主要蛋白质的分子量是55及59 KD。以上事实说明,就如我们过去已报告过的,这一部分是核富含着丝粒的部分。     

Amino acids and their roles in tumor immunotherapy of breast cancer

Breast cancer is the most commonly diagnosed cancer among women. The primary treatment options include surgery, radiotherapy, chemotherapy, targeted therapy and hormone therapy. The effectiveness of breast cancer therapy varies depending on the stage and aggressiveness of the cancer, as well as individual factors. Advances in early detection and improved treatments have significantly increased survival rates for breast cancer patients. Nevertheless, specific subtypes of breast cancer, particularly triple-negative breast cancer, still lack effective treatment strategies. Thus, novel and effective therapeutic targets for breast cancer need to be explored. As substrates of protein synthesis, amino acids are important sources of energy and nutrition, only secondly to glucose. The rich supply of amino acids enables the tumor to maintain its proliferative competence through participation in energy generation, nucleoside synthesis and maintenance of cellular redox balance. Amino acids also play an important role in immune-suppressive microenvironment formation. Thus, the biological effects of amino acids may change unexpectedly in tumor-specific or oncogene-dependent manners. In recent years, there has been significant progress in the study of amino acid metabolism, particularly in their potential application as therapeutic targets in breast cancer. In this review, we provide an update on amino acid metabolism and discuss the therapeutic implications of amino acids in breast cancer.