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Despite the improvements in the diagnosis and management during the past six decades, acute aortic dissection (AAD) remains a life-threatening condition associated with significant morbidity and mortality rates. Due to the relatively rare occurrence of AAD, several clinical registries have been established to gain insights into this lethal disease in a large number of patients, such as the International Registry of Acute Aortic Dissection (IRAD), the German Registry for Acute Aortic Dissection Type A (GERAADA), and the Society of Thoracic Surgeons (STS) Adult Cardiac Surgery Database Aortic Section. This review aims to interpret and compare the latest results of the IRAD, STS and GERAADA database. It focuses on several controversial and key issues in the diagnosis and management of acute aortic dissection in hope of providing some insights and references for cardiovascular professionals engaged in the care of this deadly disease.过去60年内，尽管急性主动脉夹层的诊断治疗技术有了巨大进步，其死亡率和并发症发生率仍居高不下。由于发病率相对较低，为了通过收集大样本患者资料提高对该病的认识，国际同行建立了数个临床注册数据库，包括急性主动脉夹层国际注册数据库（IRAD）、德国急性A型主动脉夹层注册数据库（GERAADA）和美国胸外科医师协会（STS）成人心脏外科数据库主动脉分库。本文根据IRAD、GERAADA和STS主动脉数据库的最新结果，针对部分热点问题进行探讨和对比，为国内心血管专业同道提高急性主动脉夹层的诊断治疗水平提供借鉴参考。.

To explore the role of γδT cells against bladder cancer and to detect the expression of stress proteins MICA/B recognized by γδT cells in bladder cancer.γδT cells from peripheral blood drawn from 6 bladder cancer patients with pamidronate stimulating were expanded. Flow cytometry was used to detect the purity and expansion folds of γδT cells, and the expression of CD107a on γδT cells after PMA/ionomycin stimulated. The cytotoxicity assay was carried out to test the cytotoxicity of γδT cells against human bladder cancer cell lines. The expression of MICA/B on bladder cancer cell lines and in bladder cancer tissues were detected through flow cytometry and immunohistochemistry respectively.γδT cells from peripheral blood drawn from 6 bladder cancer patients were successfully expanded. The purity was 75%-94% and the expansion folds were 109-371 times. After being stimulated by PMA/ionomycin, the proportion of CD107a+ γδT cells increased significantly, reaching 40%-82%. γδT cells from the 6 bladder cancer patients showed obvious cytotoxic effects on 3 human bladder cancer cell lines which was enhanced as the effector: the target ratio increased. MICA/B were detected both in 3 bladder cancer cell lines and in 26 bladder cancer tissues. The staining score of MICA/B in invasive bladder cancer was slightly higher than that in non-invasive bladder cancer, and in advanced bladder cancer was higher than that in low grade bladder cancer, but the statistical analysis showed that the staining score of MICA/B was no significant correlation between the tissue and the tumor stages and grades.γδT cells from the peripheral blood of the bladder cancer patients could be successfully expanded in vitro, and showed significant anti-bladder cancer effect. MICA/B were detected both in bladder cancer cell lines and in bladder cancer tissues. The statistical analysis showed that there was no significant correlation between the staining scores of MICA/B in the tissue and the tumor stages and grades.

To identify the drop-off location of victims in drowning cases, and confirm whether it is a fatal drowning or the victim is thrown into the water after death by detecting part of 5.8S sequence and second internal transcribed spacer （ITS2） （5.8S+ITS2） of diatom rDNA in water and organs.Two cases identified by diatom examination, which received by Nanjing Municipal Public Security Bureau Forensic Center, were taken as the research objects. The difference of the population structure of algae in water and human tissue was analysed by length polymorphism of 5.8S+ITS2 marker.In case 1, similar species of diatom were detected from victim's lung and liver tissues and the water sample. Two kinds of DNA fragments with length of 330 bp and 376 bp were detected from victim's lung tissue and the water sample using 5.8S+ITS2 marker, which could confirm the victim was drowning before death. In case 2, there was no diatom found in victim's lung and liver tissues. Only one kind of DNA fragment with length of 331 bp and low relative fluorescence unit （RFU） was obtained from victim's lung tissue using 5.8S+ITS2 marker, thus the victim was thrown into the water after death.The experimental results of the two cases in present study are consistent with the actual facts and the result of the diatom microscopic examination. The difference of population structure of specific microorganism in water and human tissue can be detected by 5.8S+ITS2 marker, which can help to identify the drop-off location of victims in drowning cases, and confirm whether it is a fatal drowning or the victim is thrown into the water after death.藻类rDNA特异性片段长度多态性在溺死鉴定中的应用.通过检验水体和人体器官中硅藻核糖体DNA（rDNA） 5.8S部分序列、第二内转录间隔区（second internal transcribed spacer，ITS2）序列（5.8S+ITS2）的长度多态性差异，判断溺水死亡案件中受害人的落水地点以及受害人系生前落水还是死后被抛尸入水。.以南京市公安局法医中心受理的2例硅藻检验鉴定案例为对象，利用5.8S+ITS2分子标记的长度多态性，分析藻类生物在水体、人体组织中种群结构的差异。.案例1中，在受害人肺、肝组织和水体样本中均检出种类相近的硅藻，利用5.8S+ITS2分子标记在死者肺组织和水体样本中均检出330 bp和376 bp两种DNA片段，确定受害人系生前溺水。案例2中，在死者肺、肝组织中均未检出硅藻，利用5.8S+ITS2分子标记在死者肺组织中仅获得1条DNA片段，长度为331 bp，相对荧光单位值非常低，确定受害人系死后抛尸入水。.本方法检验两案例的实验结果符合实际案情和硅藻镜检的结论，利用5.8S+ITS2分子标记研究水体和人体组织中特定微生物的种群结构差异，从而判断溺水死亡的落水地点以及受害人系生前落水还是死后被抛尸入水等问题具有可行性。.法医病理学；法医遗传学；硅藻类；DNA，核糖体；第二内转录间隔区；扩增片段长度多态性分析；溺死.

To investigate the genetic polymorphism ofY-STRs loci of 580 unrelated Han males in Nanjing were amplified using AGCU Y-PLUS PCR （24） kit. The genetic parameters of 24 Y-STR loci such as gene frequency were calculated by software, and compared with the data of Hubei, Liao- ning, Guangdong, Beijing and Chengdu Han population.Total 580 haplotypes were detected among 24 Y-STR loci in 580 unrelated Han males in Nanjing. The genetic diversity （GD） of each locus was from 0.294 6 to 0.939 8, and the haplotypes diversity （HD） was 0.983 7. There was a significant difference between the GD of 6 areas.The 24 Y-STR loci such as

A series of La0.7Ca0.3MnO3 films are fabricated by pulsed laser deposition under controlling the oxygen partial pressure or adding an oxygen post-annealing process. The film after oxygen post-annealing shows an orientation change and has more non-lattice oxygen near the surface than those of the films without annealing. Moreover, only the structure of Ag/La0.7Ca0.3MnO3/Pt with the oxygen annealed film behaves a big current-voltage hysteresis and stable resistance switching properties by applying voltage pulse. Experimental results indicate that the increase of non-lattice oxygen content induced by oxygen annealing in the vicinity of the Ag/La0.7Ca0.3MnO3 interface contributes to the occurrence of resistance switching. And with the accurate controlling of the oxygen annealing parameters, the improvement of resistance switching property of the La0.7Ca0.3MnO3 film can be expected.

A noncrystalline SrTiO3 (STO) thin film was grown on Pt/Ti/SiO2/Si substrates by pulsed laser deposition. The Pt thin film was deposited on STO film as top electrode, forming a symmetric structure (Pt/STO/Pt) to exclude the influence of the electrical difference in STO-electrode interfaces. It was found that a stable bipolar resistive switching was obtained in this structure. In a current sweep, an obvious S type negative differential conductance (NDC) phenomenon was found in both polarities. And in a voltage sweep, no NDC was observed due to the current control mechanism of S type NDC effect. The possible mechanism of this effect is discussed preliminarily.

Polycrystalline NiO thin films were fabricated on Pt (111)/Ti/SiO2/Si substrates by thermal oxidation of the evaporated Ni films. Pt/NiO/Pt structures were prepared, and they showed reversible resistance switching behaviors. When the compliance set current was varied from 5 mA to 40 mA, the on-state currents increased, while the on-state resistances decreased. It is probably attributed to higher current compliance resulted in the formation of stronger and less resistive filaments, which in turn need more energy and power for their rupture. The resistive switching in NiO thin films is closely related to the formation and rupture of conducting filaments.

Bipolar resistance switching was investigated on La0.7Ca0.3MnO3 (LCMO) thin film with Al-Ag alloy top electrode (TE) including different Ag contents. The switching capability of Al-Ag/LCMO/Pt was greatly improved in Al-33%Ag TE structure compared to in Al-50%Ag TE structure. Switching times of faster than 100 ns and rewrite cycles of more than 400 were obtained while maintaining a ratio of resistance change larger than 1000%. The mechanism of resistance switching was explained by a model with interfacial nanostructured domains composed of Ag and insulator AlOx matrix, as previously proposed for Al-50%Ag/LCMO/Pt structure.

Wurtzite structure ZnMgO thin films with the energy gap (E g ) of 4.2 eV were deposited by oxygen-plasma enhanced pulsed laser deposition (PEPLD) on quartz glass. Oxygen-plasma increases the Zn content in ZnMgO thin film, which induced the evolution from cubic to hexagonal structure. The effects of target-substrate (T-S) distance on the band gap and crystal quality of ZnMgO thin film deposited by PEPLD were studied by transmittance spectra and Raman. The band gap of ZnMgO increased from 3.84 eV to 4.03 eV and the crystal quality decrease gradually when the T-S distance decreased from 9 cm to 5 cm.

Previously we have shown that dexamethasone (DEX) enhances the antitumor activity and ligand binding of the active form of vitamin D, 1alpha,25-dihydroxyvitamin D(3) (1,25-D(3)), in the murine squamous cell carcinoma model SCC VII/SF. DEX also reduces the hypercalcemia toxicity of 1,25-D(3) treatment. However, the mechanism of the enhanced antitumor activity has not been defined. Here, we demonstrate that both cell cycle arrest and apoptosis were enhanced by DEX, effects that were inhibited by RU486. We also demonstrate that vitamin D receptor (VDR) protein levels were increased by the combination of 1,25-D(3) and DEX above the level observed with 1,25-D(3) treatment alone, whereas protein levels of the heterodimeric partner of VDR, retinoid X receptor, were lower for the combination than for 1,25-D(3) alone. Glucocorticoid receptor protein levels and ligand binding were increased by 1,25-D(3) but not by the combination. Treatment with the combination of 1,25-D(3) and DEX did not result in greater activation of a vitamin D response element-reporter than 1,25-D(3) alone or of a glucocorticoid response element-reporter than DEX alone. Nevertheless, the levels of phospho-Erk1/2 and phospho-Akt, signaling molecules that are modulated in 1,25-D(3)-treated squamous cell carcinoma cells, were reduced by the combination of 1,25-D(3) and DEX more than by either agent alone. These trends were also observed in vivo. Our results suggest the involvement of the Erk and Akt signaling pathways in the antiproliferative effects of the combination of 1,25-D(3) and DEX and that phospho-Erk1/2 and phospho-Akt may be useful markers of response to this combination.

We demonstrated that calcitriol has antiproliferative activity in squamous cell carcinoma and prostatic adenocarcinoma and enhances the antitumor activity of platinum-based agents. In this study, we examined whether calcitriol also increases paclitaxel cytotoxicity. The effect of treatment on growth of the murine squamous cell carcinoma (SCCVII/SF) and human prostatic adenocarcinoma (PC-3) was determined by clonogenic assay, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and monitoring tumor growth. Treatment of SCC or PC-3 cells in vitro with calcitriol prior to paclitaxel significantly reduced clonogenic survival compared with either agent alone. Median-dose effect analysis revealed that calcitriol and paclitaxel interact synergistically. Treatment of SCC or PC-3 tumor-bearing mice with calcitriol prior to paclitaxel resulted in substantially greater growth inhibition than was achieved with either agent alone, supporting the combined use of calcitriol and paclitaxel in the treatment of solid tumors. To explore the molecular basis for the enhanced antitumor activity of this combination, the effect of treatment on p21(Waf-1) (p21), Bcl-2, and poly(ADP-ribose) polymerase expression was evaluated in PC-3. A 72-h pretreatment with calcitriol reduced p21 expression and increased paclitaxel cytotoxicity (measured after 24 h) without evidence of apoptosis [poly(ADP-ribose) polymerase cleavage]. After 48 h, paclitaxel induced apoptosis, the extent of which was increased similarly by pretreatment or concurrent treatment with calcitriol. We therefore propose a model for calcitriol enhancement of paclitaxel cytotoxicity in which the "early" (24 h) effects are schedule dependent and not attributed to enhancement of paclitaxel-induced apoptosis. In contrast, the "delayed" (48-h) enhancement of paclitaxel activity by calcitriol is schedule independent and associated with acceleration of apoptosis.

In a murine squamous cell carcinoma (SCC) model, we have demonstrated that both 1,25-dihydroxycholecalciferol (1,25-D3) and the analogue 1,25-dihydroxy-16-ene-23-yne-cholecalciferol (Ro23-7553) have significant in vitro and in vivo antitumor activity. We have examined here the cell cycle effect of 1,25-D3 and Ro23-7553 on SCCVII/SF tumor cells by quantitating nuclear DNA using a detergent-trypsin method via flow cytometry analysis. Both 1,25-D3 and Ro23-7553 resulted in a significant increase of cells in G0-G1, with an accompanying decrease of cells in S phase. The ability to arrest cells in G0-G1 has been exploited by combining Ro23-7553 with the cytotoxic agent cisplatin (cis-diamminodichloroplatinum; cDDP). Using the in vitro clonogenic assay, pretreatment with Ro23-7553 for 24-48 h significantly enhanced cDDP-mediated tumor cell kill as compared to concurrent treatment with Ro23-7553 and cDDP or cDDP alone. To examine the effect of Ro23-7553 and cDDP in vivo, C3H/HeJ mice with 9-14-day SCC tumors were treated either for 3 days with varying i.p. doses of Ro23-7553 or for 7 days continuously through the use of Alzet pumps, and on the last day of Ro23-7553 treatment, cDDP (1-6 mg/kg) was administered. Using the in vivo excision tumor cell clonogenic assay, in which tumors were removed from animals 24 h after cDDP treatment and plated in a clonogenic assay, pretreatment with Ro23-7553 markedly enhanced cDDP-mediated clonogenic tumor cell kill, even at low doses of cDDP as compared to cDDP treatment alone. Similarly, a significant decrease in fractional tumor volume and increase in tumor regrowth delay was observed when animals were pretreated before cDDP with Ro23-7553 as compared to either agent alone. These results demonstrate a significant enhanced antitumor effect with Ro23-7553 pretreatment before cDDP both in vitro and in vivo and suggest that Ro23-7553 may potentiate cDDP cytotoxicity through effects on cell cycle progression.

We have previously demonstrated that the cytokine interleukin 1 alpha (IL-1 alpha) significantly potentiates the antitumor activity of a variety of chemotherapeutic agents, including cisplatin (cDDP). In studies described here, we examined the potential of combining IL-1 alpha and the platinum analogue carboplatin (CBDCA) and compared the schedule-dependent and pharmacokinetic effects for IL-1 alpha combinations with cDDP and CBDCA. RIF-1 tumor-bearing mice (C3H/HeJ) received i.p. injections of varying doses of CBDCA, alone or concurrently with IL-1 alpha (48 or 480 micrograms/kg). Clonogenic cell kill and tumor regrowth delay were significantly increased when CBDCA was combined with IL-1 alpha, at both doses, compared to either CBDCA or IL-1 alpha alone (P0.001 and P0.01, respectively). Although pretreatment with IL-1 receptor antagonist blocked the acute tumor hemorrhagic response induced by IL-1 alpha alone, IL-1 receptor antagonist only partially blocked IL-1 alpha enhancement of CBDCA or cDDP-mediated tumor cell kill. The IL-1 alpha enhancement of CBDCA-mediated tumor cell kill was highly schedule dependent, with maximum antitumor activity observed when IL-1 alpha was administered 4-12 h before CBDCA. In contrast, administration of IL-1 alpha from 24 h before or as late as 6 h after cDDP resulted in the same antitumor activity as simultaneous administration of cDDP and IL-1 alpha. Tumor and normal tissue platinum content were significantly increased by IL-1 alpha in animals treated with CBDCA (P0.01) but not in those treated with cDDP. The observed differences between cDDP and CBDCA may be explained by their known differential rates of clearance and protein binding affinities and are compatible with an induced alteration in CBDCA pharmacokinetics.

Various DNA components which were extracted with gentle cell fractionation from the HeLa cells after 4 h vaccinia virus infection were detected by dot hybridization technique. The virus DNA mainly exist in intermediate filament-lamina-nuclear matrix complex. With DGD embedment free technique and electron microscopic autoradiography, the newly synthesized virus DNA is found to be associated with intermediate filaments. The results of southwestern hybridization demonstrate that vaccinia virus DNA has specific affinity to intermediate filaments and some nuclear matrix proteins.

In vivo administration of tumor necrosis factor-alpha (TNF) suppresses both normal and Friend virus (FVA)-infected erythroid progenitor cells (CFU-E). To examine the mechanism of erythroid suppression by TNF, we examined TNF's direct effect on normal and virus-infected cells in vitro. Productively infected fibroblast cell lines, fresh acute virus-infected spleen cells, and virus-infected CFU-E were sensitive, whereas uninfected CFU-E were resistant to TNF cytotoxicity in vitro. When FVA-infected erythroblasts were depleted from the spleen cell population in vitro with antivirus antibodies, TNF suppression of the remaining (uninfected) cells was abrogated. In contrast, both normal and virus-infected macrophage progenitor cells and immature erythroid progenitor cells were equally sensitive to TNF cytotoxicity in vitro. Normal erythroblasts had significantly fewer TNF receptors than FVA-infected erythroblasts, which also were morphologically less mature. These results suggest that TNF can differentially suppress late-stage virus-infected erythroid progenitors in vitro.

An n-type Zn1−x−yBexMgyO thin film was deposited on a p-type Si substrate by pulsed laser deposition to obtain a solar-blind photodetector. The spectral response characteristic with a cutoff wavelength of 280 nm was demonstrated to realize the photodetection of the solar-blind wave zone. The responsivity of the device was improved by inserting an Al-doped ZnO (AZO) contact layer, which was expected to enhance the carrier collection efficiency significantly. Correspondingly, the peak responsivity was improved from 0.003 to 0.11 A W−1 at zero bias, and a high external quantum efficiency of 53% at 270 nm was achieved. The fast rise time reached 20 ns. This work demonstrated the possibility of a wurtzite ZnO based oxide system to realize high performance zero-biased solar-blind photodetectors.

Epitaxial growth of a ZnO(110)/STO(001)/TiN(001)/Si(001) heterostructure has first been demonstrated on a Si(001) substrate by pulsed laser deposition. The growth process was monitored in situ by reflection high-energy electron diffraction, and the epitaxial orientation relationship was further confirmed by ex situ x-ray diffraction analysis. Results show that the high (110) oriented ZnO films are in domain-growth mode, and composed of two kinds of domains with their c-axes perpendicular to each other along STO� 110� . The excitation-density-dependent photoluminescence spectra analyses at 83K indicate that the ZnO films have good optical quality with low defect density, and no significant deep-level emission is detected. The strong near-band-edge luminescence consists of several acceptor-related emissions such as the acceptor‐bound exciton emission (3.352eV), the free electron‐acceptor emission (3.318eV) and the donor‐acceptor-pair emission (3.248eV). The presence of these acceptor-related emissions in undoped ZnO films should be attributed to structural acceptor defects, which are mainly caused by the domain-growth mode in this case. (Some figures in this article are in colour only in the electronic version)

An epitaxial ZnO heterojunction light-emitting diode with an n-ZnO/MgO/TiN/n+-Si structure is produced by pulsed-laser deposition. By introducing a thin MgO/TiN buffer and a low temperature (LT) ZnO buffer, layer-by-layer growth of high quality ZnO epi-layer on Si(1 1 1) has been realized, which was confirmed by in situ reflection high-energy electron diffraction (RHEED), transmission electron microscopy, high-resolution x-ray diffraction, resonant Raman spectra and photoluminescence spectroscopy. Combining in situ RHEED with Phi-scan XRD analysis, the in-plane epitaxial growth of ZnO[1 1 0]||MgO[1 0 ]||Si[1 0 ] has been demonstrated. The strong room temperature electroluminescence (EL) with a broad emission band ranging from 1.46 to 3.5 eV and centred at 2.31 eV could be observed from the diode under relative low injection current. Furthermore, the EL output light intensity is enhanced obviously by improving the ZnO crystal quality via inserting a ZnO LT buffer layer.

Electric-pulse-induced resistance (EPIR) switching behaviour was observed in bulk La0.7Ca0.3MnO3 polycrystalline. Temperature dependences of resistance and magnetic moment at different resistance states were studied. The metal–insulator phase transition temperature changed with the resistance states, which suggested that the EPIR phenomenon is related to the modulating bulk properties of perovskite manganites. The Curie temperature derived from the magnetic moment measurement did not change with the resistance states, which implied that there was no ferromagnetic–metal and antiferromagnetic–insulator transition occurring in perovskite manganite global materials. These results provided a new evidence for a filamentary mechanism in the EPIR effect.