MEMS粘片工艺应力抑制技术

粘片工艺过程中产生的热机械应力是微电子机械系统(MEMS)芯片的主要误差源之一。为了降低粘片工艺应力对MEMS芯片的影响,提高MEMS芯片的稳定性,开展了MEMS粘片工艺应力抑制技术的研究。分析了胶体粘片工艺过程,通过解析模型进行应力来源的分析与计算;建立了有限元仿真模型,分析了MEMS芯片粘片过程中热机械应力的主要形成机理与分布情况;进行了相关工艺实验,得出了优化后的工艺方案,采用溢胶的点胶方式和杨氏模量较低的粘片胶是可抑制热机械应力的工艺方案,降低了粘片固化过程中的温度变化对MEMS芯片诱发的残余热机械应力,从而提高了MEMS芯片的稳定性。

静态应力转移及地震触发:看不到应力下限吗?

本研究的主要目标是检验地震触发是否存在更低的阈值.解决这个问题对于理解地震机制及灾害分析来说都是十分重要的。我们通过叠加每个 M≥4.5地震前所有前面的 M≥4.5地震产生的应力变化,求出这种变化的时间函数,从而计算加在1969～1998年间加利福尼亚中部的63个 M≥4.5地震上的累积静态应力变化。我们发现,应力变化量级>10 kPa(>0.1 bar)时,地震破裂时85%的累加应力变化为正,应力变化<10 kPa(<0.1 bar)及<1 kPa 时,70%为正。将这些结果与地震时间或震源机制随机的合成地震目录作比较,说明这种触发的程度几乎不可能在随机目录中找到.因此,我们的结论是,在加利福尼亚中部至今未发现地震触发的应力下限.我们的结果表明,抑制破裂应力变化的时间分布与时间延迟随应力变化增大而加长的理论预测是一致的。

Reactivation of hepatitis B virus infection after cytotoxic chemotherapy or immunosuppressive therapy

Reactivation of hepatitis B is defined as the recurrence or an abrupt rise in hepatitis B virus(HBV) replication,often accompanied by an increase in serum transaminase levels,and both events occurring in a patient with a previous inactive hepatitis B infection.This reactivation can occur in situations in which the ratio of HBV replication and immune response is altered.It can happen during the treatment of hemato-oncological malignancies with chemotherapy and in immunosuppression of autoimmune diseases.Clinical manifestations of hepatitis B reactivation are variable and can range from asymptomatic to acute hepatitis,which are sometimes serious and result in acute liver failure with risk of death,and usually occur in the periods between cycles or at the end of chemotherapy.Immunosuppressive drugs such as corticosteroids or azathioprine can induce HBV reactivation in patients carrying hepatitis B virus surface antigen(HBsAg) or anti-HBc,but much less frequently than chemotherapy treatments.The tumor necrosis factorαinhibitors infliximab,etanercept and adalimumab may cause reactivation of hepatitis B,and the overall frequency with infliximab may be similar(50%-66%) to that caused by chemotherapy.Baseline HBV serology is recommended for all patients receiving chemotherapy and immunosuppressive drugs,and HBsAg positive patients should receive anti-HBV prophylaxis to decrease virus reactivation and death rates.

Influence of intermediate principal stress on failure mechanism of hard rock with a pre-existing circular opening

Based on particle flow theory, the influences of the magnitude and direction of the intermediate principal stress on failure mechanism of hard rock with a pre-existing circular opening were studied by carrying out true triaxial tests on siltstone specimen. It is shown that peak strength of siltstone specimen increases firstly and subsequently decreases with the increase of the intermediate principal stress. And its turning point is related to the minimum principal stress and the direction of the intermediate principal stress. Failure characteristic(brittleness or ductility) of siltstone is determined by the minimum principal stress and the difference between the intermediate and minimum principal stress. The intermediate principal stress has a significant effect on the types and distributions of microcracks. The failure modes of the specimen are determined by the magnitude and direction of the intermediate principal stress, and related to weakening effect of the opening and inhibition effect of confining pressure in essence: when weakening effect of the opening is greater than inhibition effect of confining pressure, the failure surface is parallel to the x axis(such as σ2=σ3=0 MPa); conversely, the failure surface is parallel to the z axis(such as σ2=20 MPa, σ3=0 MPa).

Hydrogen sulfide attenuates gastric mucosal injury induced by restraint water-immersion stress via activation of KATPchannel and NF-κB dependent pathway

AIMTo explore the effect of hydrogen sulfide (H2S) on restraint water-immersion stress (RWIS)-induced gastric lesions in rats and the influence of adenosine triphosphate (ATP)-sensitive potassium (KATP) channels and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway on such an effect.METHODSMale Wistar rats were randomly divided into a control group, a physiological saline (PS) group, a sodium hydrosulfide (NaHS) group, a glibenclamide (Gl) group, Gl plus NaHS group, a pyrrolidine dithiocarbamate (PDTC) group, and a PDTC plus NaHS group. Gastric mucosal injury was induced by RWIS for 3 h in rats, and gastric mucosal damage was analyzed after that. The PS, NaHS (100 μmol/kg body weight), Gl (100 μmol/kg body weight), Gl (100 μmol/kg or 150 μmol/kg body weight) plus NaHS (100 μmol/kg body weight), PDTC (100 μmol/kg body weight), and PDTC (100 μmol/kg body weight) plus NaHS (100 μmol/kg body weight) were respectively injected intravenously before RWIS.RESULTSRWIS induced serious gastric lesions in the rats in the PS pretreatment group. The pretreatment of NaHS (a H2S donor) significantly reduced the damage induced by RWIS. The gastric protective effect of the NaHS during RWIS was attenuated by PDTC, an NF-κB inhibitor, and also by glibenclamide, an ATP-sensitive potassium channel blocker, in a dose-dependent manner.CONCLUSIONThese results suggest that exogenous H2S plays a protective role against RWIS injury in rats, possibly through modulation of KATP channel opening and the NF-κB dependent pathway.

Proteasomal degradation unleashes the pro-death activity of androgen receptor

Androgen receptor （AR） is able to promote stress-induced cell death independently of its transcription activity in androgen-independent prostate cancer cells. Yet, the underlying mechanism is incompletely understood. Here, we report that stress-induced proteasomal degradation of AR contributes to its pro-death activity. Upon exposure to ul- traviolet fight and staurosporine, AR underwent proteasomal degradation. Blockade of AR degradation significantly suppressed stress-induced apoptosis in androgen-independent prostate cancer cells. Ectopic expression of the AR N-terminal （AR-N） domain, which lacks DNA- and ligand-binding abilities, led to cell death without any additional death stimuli. Truncation analysis revealed that AR-N domain contains several sub-domains that regulate the pro- death activity of AR, specifically the first 105 amino acids, which function as a minimal pro-death domain acting upstream of caspases. The pro-apoptotic activity of AR N-terminal fragments was suppressed by ectopic expression of Bcl-2 or selected caspase inhibitors. Thus, our results reveal a novel mechanism by which AR promotes stressinduced cell death in androgen-independent prostate cancer cells.

Decreased prolactin-inducible protein expression exhibits inhibitory effects on the metastatic potency of breast cancer cells

Objective:The aim of the research was to study the effects of prolactin-inducible protein(PIP) downregulation on metastatic abilities of human breast cancer MDA-MB-453 cells.Methods:PIP-siRNA was transfected into human breast cancer MDA-MB-453 cells through liposome.Reverse transcription PCR and immunocytochemistry were employed to detect the downregulated expression of PIP.Cell migration,adhesion and invasion assays were performed to assess the impacts of PIP downregulation on cell migration,adhesion and invasion respectively.Results:Knockdown of PIP obviously inhibited cell migration,the migrated cells were decreased by 83.1% compared with the negative control group.Cell adhesion was also reduced,the adhesion rates at 30 min and 60 min were decreased by 42.6% and 48.5% respectively compared with the negative control group.Moreover,PIP downregulation resulted in decreased invasion rate by 73.9%.Conclusion:Reduced PIP expression in MDA-MB-453 cells can inhibit the abilities of migration,adhesion and invasion,which suggests that PIP plays an important role in the metastatic potency of breast cancer cells.

Synthesis and application of a novel combined kinetic hydrate inhibitor

In oil and gas exploration and transportation, low dosage hydrate inhibitors （LDHIs） are more favorably utilized to inhibit the formation of hydrates than thermodynamic inhibitors （THs） as a trend. However, there are no industrial products of LDHIs available domestically, and the corresponding application experience is in urgent need. In this paper, a combined hydrate inhibitor （HY-1） was synthesized after a series of reaction condition optimization, and its performance on THF hydrate inhibition was investigated using kinetic hydrate inhibitor evaluation apparatus with 6 cells bathing in air. The results show that when the reaction temperature is 60℃, the reaction time is 6 h, and the monomer： solvent ratio is 1：2, the product has the best kinetic hydrate inhibitor performance on THF hydrate. On these bases, the scale-up production of this combined hydrate inhibitor was carried out. Although the scale-up product （HY-10） performs less effectively on the THF hydrate inhibition than HY-1, it functions better than a commercial product （Inhibex501） during in-house tests. HY-10 was successfully applied to the gas production process. Field trials in northem Shaanxi PetroChina Changqing Oilfield Company （PCOC） show that 2 wt% of HY-10 is effective on natural gas hydrate inhibition. It is found through economic analysis that the use of HY-10 has obvious economi- cal advantage over methanol and Inhibex501.