基于加权损失函数的粘连白细胞分割算法

针对粘连白细胞很难精准分割的问题,提出一种基于深度学习的粘连白细胞分割算法.首先,将急性淋巴细胞白血病患者的血液细胞显微图像的色彩空间由RGB转换至HSV,滤除红细胞并提取白细胞;其次,对提取结果中的粘连白细胞,将细胞边界设定为除前景和背景外的第三类,在深度学习分割模型训练过程中引入基于类别权重的加权交叉熵损失函数,使...     

连续铸钢用中间包衬里损伤的红外检测分析

利用一维稳态传热模型,计算中间包底面温度,建立了底面温度与中间包衬里损伤程度间的对应关系,发现中间包底面温度随着衬里损伤程度增加而增加.红外热像检测表明:中间包底面温度随着包龄的增加而增加;红外热像技术可以有效地对中间包衬里损伤进行检测;利用所建立的理论关系式,可以实现对中间包红外热像的定量分析.     

Role of the prolyl isomerase Pin1 in protecting against age-dependent neurodegeneration

The neuropathological hallmarks of Alzheimer's disease and other tauopathies include senile plaques and/or neurofibrillary tangles. Although mouse models have been created by overexpressing specific proteins including beta-amyloid precursor protein, presenilin and tau, no model has been generated by gene knockout. Phosphorylation of tau and other proteins on serine or threonine residues preceding proline seems to precede tangle formation and neurodegeneration in Alzheimer's disease. Notably, these phospho(Ser/Thr)-Pro motifs exist in two distinct conformations, whose conversion in some proteins is catalysed by the Pin1 prolyl isomerase. Pin1 activity can directly restore the conformation and function of phosphorylated tau or it can do so indirectly by promoting its dephosphorylation, which suggests that Pin1 is involved in neurodegeneration; however, genetic evidence is lacking. Here we show that Pin1 expression is inversely correlated with predicted neuronal vulnerability and actual neurofibrillary degeneration in Alzheimer's disease. Pin1 knockout in mice causes progressive age-dependent neuropathy characterized by motor and behavioural deficits, tau hyperphosphorylation, tau filament formation and neuronal degeneration. Thus, Pin1 is pivotal in protecting against age-dependent neurodegeneration, providing insight into the pathogenesis and treatment of Alzheimer's disease and other tauopathies.     

网络教育在数学教改中的初探

计算机辅助数学教学是今后数学教学改革的方向之一,本文从数学网络教学模式的设计,CAI课件的制作,网络教学的实施策略,实施步骤及其存在的问题进行探讨.     

集束射流氧枪的设计与应用

利用软件CFX10.0对电炉炼钢氧枪在集束射流和普通射流两种状态下的特征进行了数值模拟.通过结果对比,论证了集束射流氧枪的优越性,并且在安阳一炼轧厂100t竖式电炉使用并对其使用效果进行了分析.结果表明,安阳一炼轧厂电炉使用集束氧枪后,吨钢电耗平均降低了30kW·h,吨钢氧耗和生产成本等方面都有明显的优势.冶炼周期略有增加,主要在于采用的原料中铁水比例增加,导致周期增加.当热装铁水比处于50%左右时,吨钢氧耗、吨钢电耗、冶炼周期和生产成本均变化不大,所以建议铁水比保持在50%.     

转炉炼钢氧气射流技术

为了研究转炉炼钢氧气射流的应用情况,利用FLUENT软件模拟研究了集束氧气射流,并对比了集束射流和超音速射流的射流特性.在某厂35t转炉进行了集束射流的初步工业试验.试验结果表明:使用集束氧枪后的转炉炼钢脱磷效率提高,钢铁料消耗及氧气消耗均有所下降.     

正态型位置参数Bayes估计中基于P值的验前分布可信度建模

基于Bayes方法完成对战技指标的分析,首要和关键的问题是选择合理可信的验前分布.以正态分布位置参数的Bayes分析为研究对象,构建了基于P值的验前可信度计算模型.首先,对验前分布可信度研究的基本假设和必要性进行了阐述.然后,对于正态分布的位置参数,分为方差未知和已知两种情况,分别建立了基于t分布的验前P值计算模型,和基于正态分布的验前P值计算模型,并给出了不同验前可信度取值范围下验前分布的选择与判断准则.其次,对于正态分布的变形,构建了基于非中心t分布的验前P值计算模型,和基于正态分布的验前P值计算模型.通过四个示例对验前分布P值模型的构建和分析过程进行了阐述,验证了方法的有效性.     

回火硬度对新型中碳弹簧钢应变疲劳特性的影响

对两种新型中碳弹簧钢应变疲劳特性及其回火硬度影响进行了研究,并和中高碳弹簧钢60Si_2Mn进行了对比。结果表明:两个新型弹簧钢和60Si_2Mn都具有循环软化;在应变疲劳曲线(△ε/2～2N_f)上,弹性线和塑性线的交点随弹簧钢回火硬度的升高而向低循环寿命移动;在Monson-Coffin方程中的回归常数b和C与循环应变硬化指数n的关系大体符合b=-n/(1+5n),C=-1/(1+5n)。各钢的应变疲劳特性、组织特征和断口形貌之间有一定的对应关系。同样硬度下新钢较老钢有更高的过载抗力。     

放宽高炉喷吹煤粉粒度的工业实验

在安钢炼铁厂l#高炉喷吹瘦煤时进行了煤粉粒度放宽的工业试验。将小于74μm(—200目)的比例由70％放宽到30％后，磨煤能力提高了21％。采用粒度较粗的煤粉，风口前循环区变长，煤粉的置换比和喷煤比都有所提高，置换比和喷煤比提高的程度随富氧率升高而增加，使高炉生产效益有了一定的改进。     

The prolyl isomerase Pin1 regulates amyloid precursor protein processing and amyloid-beta production

Neuropathological hallmarks of Alzheimer's disease are neurofibrillary tangles composed of tau and neuritic plaques comprising amyloid-beta peptides (Abeta) derived from amyloid precursor protein (APP), but their exact relationship remains elusive. Phosphorylation of tau and APP on certain serine or threonine residues preceding proline affects tangle formation and Abeta production in vitro. Phosphorylated Ser/Thr-Pro motifs in peptides can exist in cis or trans conformations, the conversion of which is catalysed by the Pin1 prolyl isomerase. Pin1 has been proposed to regulate protein function by accelerating conformational changes, but such activity has never been visualized and the biological and pathological significance of Pin1 substrate conformations is unknown. Notably, Pin1 is downregulated and/or inhibited by oxidation in Alzheimer's disease neurons, Pin1 knockout causes tauopathy and neurodegeneration, and Pin1 promoter polymorphisms appear to associate with reduced Pin1 levels and increased risk for late-onset Alzheimer's disease. However, the role of Pin1 in APP processing and Abeta production is unknown. Here we show that Pin1 has profound effects on APP processing and Abeta production. We find that Pin1 binds to the phosphorylated Thr 668-Pro motif in APP and accelerates its isomerization by over 1,000-fold, regulating the APP intracellular domain between two conformations, as visualized by NMR. Whereas Pin1 overexpression reduces Abeta secretion from cell cultures, knockout of Pin1 increases its secretion. Pin1 knockout alone or in combination with overexpression of mutant APP in mice increases amyloidogenic APP processing and selectively elevates insoluble Abeta42 (a major toxic species) in brains in an age-dependent manner, with Abeta42 being prominently localized to multivesicular bodies of neurons, as shown in Alzheimer's disease before plaque pathology. Thus, Pin1-catalysed prolyl isomerization is a novel mechanism to regulate APP processing and Abeta production, and its deregulation may link both tangle and plaque pathologies. These findings provide new insight into the pathogenesis and treatment of Alzheimer's disease.