刘、柳与元、白交游始年考

刘禹锡、柳宗元与元稹、白居易交游的始年,学术界要么漠视,要么避而不谈,实在绕不过去则存疑,则云早年交游无考,如为这些诗人作年谱、编年笺注的朱金城、卞孝萱、陶敏、施子愉等,大致不外乎这几种情况。但事实上,对这段历史中的人事关系作一个精细的梳理后,便能发现,刘、柳与元、白的交游始年当在贞元十九年(803年)。考定刘、柳与元、白交游始年在贞元十九年的意义在于,通过这点我们能够更加清晰准确地理解和把握贞元、永贞、元和之际当时复杂的人事关系,尤其是对元、白早年的政治态度和倾向,能够得出新的定位和思考。

犀角地黄汤+参苓白术散+大补元煎鼻饲联合西药临床治愈呼吸机相关腹胀1例报告

报告1例犀角地黄汤＋参苓白术散＋大补元煎鼻饲联合西药临床治愈长期使用呼吸机导致相关性腹胀,出院后腹胀症状消失,大便1-2日一行。男,68岁。肢体活动不利,意识欠清1天。腹部膨隆、皮肤绷急,大便2-3日一行,脉沉细;白细胞15.06×10^9/L,中性粒细胞百分比88%,血红蛋白84g/L;C反应蛋白58.5mg/L,降钙素原0.43ng/m L,D二聚体2ug/m L;生化、凝血、肿瘤系列、心肌酶等未见明显异常;CT：双下肺炎症;颅脑左侧丘脑可见新发梗塞灶,放射冠可见陈旧性梗塞灶。西医诊断：1.脑梗塞,2.肺炎;中医诊断：1.中风（肝肾亏虚）,2.喘嗽。抗感染、营养支持等治疗,犀角地黄汤加减,水牛角、生地各30g,赤芍、丹皮、丹参、玄参各15g,麦冬20g,茯苓30g,白术15g,1剂/d,水煎200m L,早晚鼻饲,5d为1疗程。二诊以参苓白术散合大补元煎加减以健脾补肾,党参30g,茯苓20g,白术、山药各15g,薏苡仁30g,砂仁、桔梗各12g,生地、熟地各30g,杜仲、枸杞各15g,鹿角胶烊化10g,丹参15g,地龙12g,桃仁、红花各9g,甘草炙6g,1剂/d,水煎200m L,早晚鼻饲。此后每7d在此方基础上加减,服药2月,腹胀明显减轻,大便1-2日一行,服药4月,腹胀症状消失,大便1-2日一行,临床治愈。

张祜与元白诗派的离合

综合考虑张祜与元稹、自居易的交往,和他个人的诗歌创作,可以看出,他与元白诗派有离有合。就交往而言,离多于合。就诗歌创作而言,尽管可自成一家,但在浮艳与讽谏之篇并存、古题乐府和新乐府颇具元白新乐府精神、诗作中不乏浅近流丽的律绝(晚年尤多)这三点上,与元白诗派的合多于离。

Using ^(99m)Tc-MIBI to Evaluate the Effects of Chemosensitizer on P-glycoprotein in Multidrug-resistant Carcinoma Cells

To establish a method to evaluate the effects of chemosensitizer onP-glycoprotein using ^(99m)Tc-MIBI, and observe the changes of ^(99m)Tc-MIBI uptake kinetics andP-glycoprotein levels after using verapamil in MDR human breast cells MCF-7/Adr. Methods: MDR breastcarcinoma cells, MCF-7/Adr, were incubated and different protocols were performed. Protocol Ⅰ: achemosensitizer, verapamil (10 μmol/L), was added into cell culture medium, while in control group,the same volume of DMEM was given. Cells were harvested after 2 h incubation with ^(99m)Tc-MIBI.Protocol Ⅱ: Verapamil (10 μmol/L) was added into cell culture medium and incubated for 20 min, 40min, 60 min, 80 min, 8 h, 24 h, 48 h and 72 h respectively. Cells were harvested after 2 hincubation with ^(99m)Tc-MIBI. The radioactivity of the cells was measured and P-glycoproteinexpression levels were determined with immunohistochemical stain. Results: Protocol Ⅰ: After 2hincubation with verapamil the cellular uptake of ^(99m)Tc-MIBI was remarkably higher than controlgroup (t=2.33, P 【 0.05), but there was no difference in P-glycoprotein expression levels betweentwo groups (P 】 0.05). Protocol Ⅱ: In verapamil group, ^(99m)Tc-MIBI uptake was increased withincubation time prolonging (F=58.2, P 【 0.05). When verapamil incubation time surpassed 8 h the^(99m)Tc-MIBI uptake negatively correlated to the P-glycoprotein expression levels (r=-0.73, P 【0.01). However, when incubation time was less than 80 min, there was no correlation between^(99m)Tc-MIBI accumulation and P-glycoprotein levels (r=0.16, P 】 0.05). Conclusion: ^(99m)Tc-MIBImay be used to evaluate the qualitative as well as quantitative change of P-glycoprotein expressionlevels induced by the chemosensitizer, verapamil.

Construction of retroviral vector carrying HSV tk gene under control of human AFP enhancer core sequence and human pgk promotor *

AIM Tenstruct retroviral vector bringing HSV tk gene under control by human AFP enhancer core sequence and human pgk promotor.

A Low Power SRAM/SOI Memory Cell Design

A modified four transistor （4T） self-body-bias structured SRAM/SOI memory cell is proposed. The structure is designed and its parameters are obtained by performance simulation and analysis with TSUPREM4 and MEDICI.The structure saves area and its process is simplified by using the body resistor with buried p^＋ channel beneath the nMOS gate instead of the pMOS of 6T CMOS SRAM. Furthermore, this structure can operate safely with a 0.5V supply voltage, which may be prevalent in the near future. Finally, compared to conventional 6T CMOS SRAM,this structure＇s transient responses are normal and its power dissipation is 10 times smaller.

Myenteric neurons and intestinal mucosa of diabetic rats after ascorbic acid supplementation

AIM: To investigate the effect of ascorbic acid (AA) dietary supplementation on myenteric neurons and epithelial cell proliferation of the jejunum of adult rats with chronic diabetes mellitus. METHODS: Thirty rats at 90 d of age were divided into three groups: Non-diabetic, diabetic and diabetic treated with AA (DA) (1 g/L). After 120 d of treatment with AA the animals were killed. The myenteric neurons were stained for myosin-V and analyzed quantitatively in an area of 11.2 mm2/animal. We further measured the cellular area of 500 neurons per group. We also determined the metaphasic index (MI) of the jejunum mucosa layer of about 2500 cells in the intestinal crypts, as well as the dimensions of 30 villi and 30 crypts/animal. The data area was analyzed using the Olympus BX40 microscope. RESULTS: There was an increase of 14% in the neuronal density (792.6 ± 46.52 vs 680.6 ± 30.27) and 4.4% in the cellular area (303.4 ± 5.19 vs 291.1 ± 6.0) respectively of the diabetic group treated with AA when compared to control diabetic animals. There were no signifi cant differences in MI parameters, villi height or crypt depths among the groups.CONCLUSION: Supplementation with AA in the diabetic animal promoted moderate neuroprotection. There was no observation of alteration of the cellular proliferation of the jejunum mucosa layer of rats with chronic diabetes mellitus with or without supplementation with AA.

Changes of CREB in rat hippocampus, prefrontal cortex and nucleus accumbens during three phases of morphine induced conditioned place preference in rats

Objective: To investigate the changes in CREB (cAMP response element binding protein) in hippocampus, PFC (prefrontal cortex) and NAc (nucleus accumbens) during three phases of morphine induced CPP (conditioned place preference) in rats, and to elucidate the role of CREB during the progress of conditioned place preference. Methods: Morphine induced CPP acquisition, extinction and drug primed reinstatement model was established, and CREB expression in each brain area was measured by Western Blot methods. Results: Eight alternating injections of morphine (10 mg/kg) induced CPP, and 8 d saline extinction training that extinguished CPP. CPP was reinstated following a priming injection of morphine (2.5 mg/kg). During the phases of CPP acquisition and reinstatement, the level of CREB expression was significantly changed in different brain areas. Conclusion: It was proved that CPP model can be used as an effective tool to investigate the mechanisms underlying drug-induced reinstatement of drug seeking after extinction, and that morphine induced CPP and drug primed reinstatement may involve acti-vation of the transcription factor CREB in several brain areas, suggesting that the CREB and its target gene regulation pathway may mediate the basic mechanism underlying opioid dependence and its drug seeking behavior.

Maintaining cholesterol homeostasis: Sterol regulatory element-binding proteins

The molecular mechanism of how hepatocytes maintain cholesterol homeostasis has become much more transparent with the discovery of sterol regulatory element binding proteins (SREBPs) in recent years. These membrane proteins aremembers of the basic helix-loop-helix-leucine zipper (bHLHZip) family of transcription factors. They activate the expression of at least 30 genes involved in the synthesis of cholesterol and lipids. SREBPs are synthesized as precursor proteins in the endoplasmic reticulum (ER), where they form a complex with another protein, SREBP cleavage activating protein (SCAP). The SCAP molecule contains a sterol sensory domain. In the presence of high cellular sterol concentrations SCAP confines SREBP to the ER. With low cellular concentrations, SCAP escorts SREBP to activation in the Golgi. There, SREBP undergoes two proteolytic cleavage steps to release the mature, biologically active transcription factor, nuclear SREBP (nSREBP). nSREBP translocates to the nucleus and binds to sterol response elements (SRE) in the promoter/enhancer regions of target genes. Additional transcription factors are required to activate transcription of these genes. Three different SREBPs are known, SREBPs-1a, -1c and -2. SREBP-1a and -1c are isoforms produced from a single gene by alternate splicing. SREBP-2 is encoded by a different gene and does not display any isoforms. It appears that SREBPs alone, in the sequence described above, can exert complete control over cholesterol synthesis, whereas many additional factors (hormones, cytokines, etc.) are required for complete control of lipid metabolism. Medicinal manipulation of the SREBP/SCAP system is expected to prove highly beneficial in the management of cholesterol-related disease.

Hydrolysis Activities of the Particle of Agarose-Ce^(4+) Complex for Compounds Containing Phosphodiester or Peptide Bonds

Hydrolysis activities of PACC (particle of agarose-Ce4+ complex, newly made through double emulsification) forcompounds containing phosphodiester or peptide bonds were studied. The results showed that PACC could hydrolyzeorganophosphorous pesticides not only in water but also in vegetable juice or tea extract. Hydrolysis rates of methamidophos,omethoate and chlorpyrifos in water are 32.39%, 27.12% and 46.62% respectively, those of chlorpyrifos and methami-dophos in mung sprout juice 38.28% and 35.45% respectively, and that of chlorpyrifos in tea extract 59.76%. Hydrolysisrates of BSA (bovine serum albumin) in water and protein in tea extract by PACC increase by 54.30% and 86.46% respec-tively as compared with the control.

Simultaneous Cell Disruption and Aqueous Two-Phase Extraction for Isolation of Intracellular Recombinant Proteins

A new technique was developed for the integrated processing of cell disruption and aqueous two-phase extraction in a high-speed bead mill to separate intracellular proteins from microbial cells. The process was named as simultaneous cell disruption and aqueous two-phase extraction (SDATE). Advantages, such as high cell disruption efficiency, biochemical activities preservation of proteins, cell debris elimination, and prelimiary purification of the target protein were being claimed. When this technique was employed for isolating recombinant Tumor Necrosis Factor (TNF) from E. coli, overall protein concentration and TNF activity were found to have been increased. More than 95% of TNF was partitioned into the top phase and all cell debris were in the bottom phase. The partition coefficient was greater than 3 and the TNF purification factor was greater than 6. It is shown that less separation steps were being utilized in the new technique, meaning a reduction in separation time and less process extractors required.

Inhibition of the MAPK/ERK cascade: a potential transcription-depen-dent mechanism for the amnesic effect of anesthetic propofol

Intravenous anesthetics are known to cause amnesia, but the underlying molecular mechanisms remain elusive. To identify a possible molecular mechanism, we recently turned our attention to a key intracellular signaling pathway organized by a family of mitogen-activated protein kinases （MAPKs）. As a prominent synapse-to-nucleus superhighway, MAPKs couple surface glutamate receptors to nuclear transcriptional events essential for the development and/or maintenance of different forms of synaptic plasticity （long-term potentiation and long-term depression） and memory formation. To define the role of MAPK-dependent transcription in the amnesic property of anesthetics, we conducted a series of studies to examine the effect of a prototype intravenous anesthetic propofol on the MAPK response to N-methyl-D-aspartate receptor （NMDAR） stimulation in hippocampal neurons. Our results suggest that propofol possesses the ability to inhibit NMDAR-mediated activation of a classic subclass of MAPKs, extracellular signal-regulated protein kinase 1/2 （ERK1/2）. Concurrent inhibition of transcriptional activity also occurs as a result of inhibited responses of ERK1/2 to NMDA. These findings provide first evidence for an inhibitory modulation of the NMDAR-MAPK pathway by an intravenous anesthetic and introduce a new avenue to elucidate a transcription-dependent mechanism processing the amnesic effect of anesthetics.

Occurrence of cGMP/nitric oxide-sensitive store-operated calcium entry in fibroblasts and its effect on matrix metalloproteinase secretion

AIM： To examine the existence of Nitric oxide/ cGMP sensitive store-operated Ca^2＋ entry in mouse fibroblast NIH/3T3 cells and its influence on matrix metalloproteinase （MMP） production and adhesion ability of fibroblasts. METHODS： NIH/3T3 cells were cultured. Confocal laser scanning microscopy was used to examine the existence of thapsigargin-induced store-operated Ca^2＋ entry in fibroblasts. Gelatin zymography and semiquantitative reverse transcriptase-polymerase chain reaction （RTPCR） were employed to detect the involvement of [Ca^2＋]i and NO/cGMP in MMP secretion. The involvement of NO/ cGMP-sensitive Ca^2＋ entry in adhesion was determined using matrigel-coated culture plates. RESULTS： 8-bromo-cGMP inhibited the thapsigargin-induced Ca^2＋ entry in 3T3 cells. The cGMP-induced inhibition was abolished by an inhibitor of protein kinase G, KT5823 （1μmol/L）. A similar effect on the Ca^2＋ entry was observed in 3T3 cells in response to a NO donor, （±）-S-nitroso-N-acetylpenicillamine （SNAP）. The inhibitory effect of SNAP on the thapsigargin-induced Ca^2＋ entry was also observed, indicating NO/cGMP-regulated Ca^2＋ entry in 3T3 cells. Results of gelatin zymography assay showed that addition of extracellular Ca^2＋ concentration induced MMP release and activation in a dose-dependent manner. RT-PCR also showed that cGMP and SNAP reduced the production of MMP mRNA in 3T3 cells. Experiments investigating adhesion potentials demonstrated that cGMP and SNAP could upgrade 3T3 cell attachment rate to the matrigel-coated culture plates.CONCLUSION： NO/cGMP sensitive store-operated Ca^2＋ entry occurs in fibroblasts, and attenuates their adhesion potentials through its influence on MMP secretion.

Apaf-l-deficient fog mouse cell apoptosis involves hypopolarization of the mitochondrial inner membrane, ATP depletion and citrate accumulation

To explore how the intrinsic apoptosis pathway is controlled in the spontaneous fog （forebrain overgrowth） mutant mice with an Apafl splicing deficiency, we examined spleen and bone marrow cells from Apafl＋/＋ （＋/＋） and Apafl^fog/fog （fog/fog） mice for initiator caspase-9 activation by cellular stresses. When the mitochondrial inner membrane potential （△ψm） was disrupted by staurosporine, ＋/＋ cells but not fog/fog cells activated caspase-9 to cause apoptosis, indicating the lack of apoptosome （apoptosis protease activating factor 1 （Apaf-l）/cytochrome c/（d）ATP/procaspase-9） function in fog/fog cells. However, when a marginal （-20%） decrease in △ψm was caused by hydrogen peroxide （0.1 mM）, peroxynitrite donor 3-morpholinosydnonimine （0.1 mM） and UV-C irradiation （20 J/m^2）, both ＋/＋ and fog/fog cells triggered procaspase-9 auto-processing and its downstream cascade activation. Supporting our previous results, procaspase-9 pre-existing in the mitochondria induced its auto-processing before the cytosolic caspase activation regardless of the genotypes. Cellular ATP concentration significantly decreased under the hypoactive △ψm condition. Furthermore, we detected accumulation of citrate, a kosmotrope known to facilitate procaspase-9 dimerization, probably due to a feedback control of the Krebs cycle by the electron transfer system. Thus, mitochondrial in situ caspase-9 activation may be caused by the major metabolic reactions in response to physiological stresses, which may represent a mode of Apaf-l-independent apoptosis hypothesized from recent genetic studies.

The distribution of cofilin and DNase I in vivo

Actin is the principal component of the cytoskeleton, a structure that can be disassembled and reassembled in a matter of seconds in vivo. The state of assembly of actin in vivo is primarily regulated by one or more actin binding proteins (ABPs). Typically, the actions of ABPs have been studied one by one, however, we propose that multiple ABPs, acting cooperatively, may be involved in the control of actin filament length. Cofilin and DNase I are two ABPs that have previously been demonstrated to form a ternary complex with actin in vitro. This is the first report to demonstrate their co-localisation in vivo, and differences in their distributions. Our observations strongly suggest a physiological role for higher order complexes of actin in regulation of cytoskeletal assembly during processes such as cell division.

Influencing Factors of Seed Long-distance Dispersal on a Fragmented Forest Landscape on Changbai Mountains,China

Seed long-distance dispersal(LDD) events are typically rare, but are important in the population processes that determine large-scale forest changes and the persistence of species in fragmented landscapes. However, previous studies focused on species dispersed via animal-mediated LDD, and ignored those dispersed by wind. The aim of this study was to assess the effects of canopy openness, edge, seed source, and patch tree density on the LDD of seeds by wind in forest. We collected birch seeds, a typical wind-dispersed species, throughout a larch plantation. We then assessed the relationship between birch LDD and each factor that may influence LDD of seeds by wind including distance to edge, canopy openness size, distance to mature forest, and the tree density of the larch plantation. We used univariate linear regression analysis to assess the influence of those factors on birch LDD, and partial correlations to calculate the contribution of each factor to LDD. The results showed that both canopy openness and edge had significant influences on birch LDD. Specifically, a negative relationship was observed between distance to edge and birch LDD, whereas there was a positive correlation between canopy openness size and LDD. In contrast, the distance to the mature forest was not correlated with birch LDD. Our results suggest that patch tree density could potently affect the probability of LDD by wind vectors, which provides novel and revealing insights regarding the effect of fragmentation on wind dynamics. The data also provide compelling evidence for the previously undocumented effect of habitat fragmentation on wind-dispersed organisms. As such, these observations will facilitate reasonable conservation planning, which requires a detailed understanding of the mechanisms by which patch properties hamper the delivery of seeds of wind-dispersed plants to fragmented areas.

Inhibitory effect of schisandrin B on free fatty acid-induced steatosis in L-02 cells

AIM:To investigate the effects of schisandrin B (Sch B) on free fatty acid (FFA)-induced steatosis in L-02 cells.METHODS:Cellular steatosis was induced by incubating L-02 cells with a FFA mixture (oleate and palmitate at the ratio of 2:1) for 24 h.Cytotoxicity and apoptosis were evaluated by 3-(4,5-dmethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay and Annexin V/propidium iodide staining,respectively.Cellular total lipid was determined using a photocolorimetric method after Nile red staining,and triglyceride content was measured using an enzymatic kit.To study the effects of Sch B on steatosis,L-02 cells were treated with Sch B (1-100 μmol/L) in the absence or presence of 1 mmol/L FFA for 24 h,and cellular total lipid and triglyceride levels were measured.To explore the mechanisms of action of Sch B in the steatotic L-02 cells,mRNA levels of several regulators of hepatic lipid metabolism including adipose differentiation related protein (ADRP),sterol regulatory element binding protein 1 (SREBP-1),peroxisome proliferator-activated receptor (PPAR)-α and PPAR-γ were measured by quantitative real-time polymerase chain reaction (PCR),and protein levels of ADRP and SREBP-1 were measured by immunoblotting.RESULTS:Treatment with 1 mmol/L FFA for 24 h induced intracellular lipid accumulation in L-02 cells comparable to that in human steatotic livers without causing apparent apoptosis and cytotoxicity.Sch B mitigated cellular total lipid and triglyceride accumulations in the steatotic L-02 cells in a dose-dependent manner.Quantitative real-time PCR and Western blot analyses revealed that treatment of L-02 cells with 100 μmol/L Sch B reverted the FFA-stimulated up-regulation of ADRP and SREBP-1.CONCLUSION:Sch B inhibits FFA-induced steatosis in L-02 cells by,at least in part,reversing the up-regulation of ADRP and SREBP-1.

Specific HLA-DQB1 alleles associated with risk for development of hepatocellular carcinoma:A meta-analysis

AIM:To evaluate the association of human leukocyte antigen(HLA)-DQB1 alleles with hepatocellular carcinoma(HCC) through meta-analysis of published data.METHODS:Case-control studies on HLA-DQB1 allele association with HCC published up to January 2010 were included in the analyses.The odds ratios(ORs) of HLADQB1 allele distributions in HCC patients were analyzed and compared with healthy controls.The meta-analysis software REVMAN 5.0 was applied for investigating heterogeneity among individual studies and for summarizing all the studies.A meta-analysis was performed using fixed-effect or random-effect methods,depending on the absence or presence of significant heterogeneity.Seven case-control studies containing 398 cases and 594 controls were included in the final analysis.RESULTS:Among the five family alleles,two(DQB1*02 and DQB1*03) were found to be significantly associated with the risk of HCC.The combined OR for the association of DQB1*02 and DQB1*03 allele with the risk for HCC was 1.78(95% CI:1.05-3.03,P = 0.03) and 0.65(95% CI:0.48-0.89,P = 0.007),respectively.Among the 13 specific alleles,two(DQB1*0502 and DQB1*0602) were significantly associated with risk of HCC.The combined OR for the association of DQB1*0502 and DQB1*0602 allele with the risk for HCC was 1.82(95% CI:1.14-2.92,P = 0.01) and 0.58(95% CI:0.36-0.95,P = 0.03),respectively.No significant association was established for other HLA-DQB1 family alleles and specific alleles.CONCLUSION:Our results support the hypothesis that specific HLA-DQB1 allele families and alleles might influence the susceptibility or resistance to HCC,although it needs further investigations.

Construction of the Subtracted cDNA Library of Striatal Neurons Treated with Long-term Morphine

Objective To construct a morphine tolerance model in primarily cultured striatal neurons, and screen the differentially expressed genes in this model using suppression subtractive hybridization （SSH）. Methods Sbtracted cDNA libraries were constructed using SSH from normal primarily cultured striatal neurons and long-term morphine treated striatal neurons （10^-5 mol/L for 72 hours）. To check reliability of the cell culture model, RT-PCR was performed to detect the cAMP-responsive element-binding protein （CREB） mRNA expression. The subtracted clones were prescreened by PCR. The clones containing inserted fragments from forward libraries were sequenced and submitted to GenBank for homology analysis. And the expression levels of genes of interest were confirmed by RT-PCR. Results CREB mRNA expression showed a significant increase in morphine treated striatal neurons （62.85± 1.98） compared with normal striatal neurons （28.43 ± 1.46, P〈0.01）. Thirty-six clones containing inserted fragments were randomly chosen for sequence analysis. And the 36 clones showed homology with 19 known genes and 2 novel genes. The expression of 2 novel genes, mitochondrial carrier homolog 1 （Mtchl ; 96.81±2.04 vs. 44.20±1.31, P〈0.01） and thyrnoma viral proto-oncogene 1 （Akt1 ; 122.10±2.17 vs 50.11±2.01, P〈0.01）, showed a significant increase in morphine-treated striatal neurons compared with normal striatal neurons. Conclusions A reliable differential cDNA library of striatal neurons treated with long-term morphine is constructed. Mtchl and Aktl might be the candidate genes for the development of morphine tolerance.

Recent advances on study of hadrosaurid dinosaurs in Heilongjiang(Amur) River area between China and Russia

Four main dinosaur-bearing sites have been investigated in latest Cretaceous deposits from the Amur/Heilongjiang Region ： Jiayin and Wulaga in China （ Yuliangze Formation）, Blagoveschensk and Kundur in Russia （Udurchukan Formation）. More than 90% of the bones discovered in these localities belong to hollow-crested lambeosaurine hadrosaurids： Charonosaurus fiayinensis at Jiayin, Amurosaurus riabinini at Blagoveschensk, Olorotitan arharensis at Kundur, and Sahaliyania elunchunorum at Wulaga. Flat-headed hadrosaurine hadrosaurids are much less numerous, but appear well diversified as well： Kerberosaurus manakini at Blagoveschensk, Wulagasaurus dongi at Wulaga, and a new genus at Kundur. Theropods are represented by shed teeth and isolated bones; isolated scutes and teeth discovered at Kundur are tentatively attributed to nodosaurids. Palynological studies suggest that these sites are probably synchronous with the Lancian＇ vertebrate localities of western North America, which represent the youngest dinosaur faunas in this area. However, the latest Cretaceous dinosaur assemblages are completely different in the Amur/Heilongjiang region （lambeosaurines abundant, ceratopsids absent） and in western North America （ceratopsids abundant, lainbeosaurines extremely rare or absent）. This probably reflects some kind of geographical barrier between both areas by Maastrichtian time rather than strong differences in palaeoecological conditions.