Morphology and Thermal Properties of MCPA6/ABS by in situ Polymerization of ε‐Caprolactam

Summary: In this work, blends of monomer casting polyamide 6 (MCPA6) and acrylonitrile‐butadiene‐styrene (ABS) were successfully prepared by in situ polymerization via the application of ε‐caprolactam as a reactive solvent. The morphology and thermal properties of MCPA6/ABS were investigated by means of wide angle X‐ray diffraction (WAXD), differential scanning calorimetry (DSC) and scanning electron microscopy (SEM), respectively. The domain sizes of the ABS phase in MCPA6/ABS blends were much finer than those in corresponding polyamide 6 (PA6)/ABS blends prepared by simple melt blending. With an increased amount of ABS in MCPA6, the melt enthalpy (ΔH_f), the rate of crystallization (T_c) and the degree of crystallinity (X_c(DSC)) of MCPA6 in MCPA6/ABS blends were all decreased. The degree of supercooling (ΔT_d) showed a contrary trend. However, the melting temperatures of these blends were almost unchanged. All the results could be attributed to in situ polymerization and the hydrolysis reaction of ABS that occurred during the polymerization process. Furthermore, WAXD results showed that only α‐form crystals existed in the MCPA6/ABS blends, despite the ABS content and heat treatment.

SEM micrograph of the fractured surface of an MCPA6/ABS blend with an ABS content of 20 wt.‐% (×10 000).     

丁二烯第一萃取精馏塔操作参数的优化

利用A SPEN PLU S流程模拟软件对丁二烯第一萃取精馏塔进行模拟计算,在此基础上进行操作变量对塔顶和塔釜关键组分的灵敏度分析,并对第一萃取精馏塔进行溶剂比优化,最后利用神经网络进行建模,预测不同C 4进料情况下的最佳溶剂比,并用于指导生产。实际生产情况表明该方法是有效的。     

Aggravation of necrotic death of glucose-deprived cells by the MEK1 inhibitors U0126 and PD184161 through depletion of ATP

The extracellular-regulated kinases (ERK) modulate cell proliferation and survival in response to several different stimuli and are therefore important drug targets. ERKs are activated by the dual phosphorylation kinase MEK1 and MEK1 inhibitors PD98059, U0126 and CI-1040 are now widely used to inhibit ERKs in cell and animal studies. In an analysis of ERK functions in astrocytes we found that PD98059 (100microM) failed to inhibit ERK phosphorylation but U0126 (50microM) inhibited ERK phosphorylation to approximately 80%. Surprisingly, U0126 also caused profound depletion of ATP in glucose-deprived cells, leading to death by necrosis. Since glucose-deprived cells depend mainly on mitochondrial ATP-synthase for ATP production, we tested whether U0126 or PD184161, a derivative of CI-1040, might inhibit ATP synthase activity, using 143B(Rho0) cells (which lack a functional F0 subunit) to further parse this effect. We found that the F1F0ATPase activity extracted from U0126- or PD184161-treated parental 143B cells or astrocytes was indeed inhibited by >or=80% suggesting a covalent change in the enzyme. However, F1F0ATPase activity extracted from similarly treated 143B(Rho0) cells was spared. Because F1F0ATPase activity in isolated mitochondria was not inhibited directly, we propose that U0126 and PD184161 inhibit ATP-synthase via an indirect action on F0. The MEK1 inhibitors also induced necrosis of other glucose-deprived cell types including primary neurons at the same concentrations required for inhibition of ERK phosphorylation. Thus, the MEK1/ERK signalling pathway may modulate ATP synthase function, and its inhibition may cause cells unable to perform glycolysis to die by necrosis.     

Evaluation of frequencies of HPRT mutant lymphocytes in butadiene polymer workers in a Southeast Texas facility

We examined the frequency of mutant lymphocytes (VFs) in workers (n = 30) occupationally exposed to the petrochemical, 1,3‐butadiene (BD), using the autoradiographic HPRT mutant lymphocyte assay. Current exposures were determined with organic vapor monitors that had a 12‐hr method detection limit (MDL) of 2.5 parts per billion (ppb). HPRT VFs were analyzed with respect to current exposure estimates, age in years, and occupational longevity (OL; defined as years working in the BD industry at this facility). Current exposures were low (mean 93.5 ppb, median 2.5 ppb) with only one individual's estimate (1683.5 ppb) exceeding the Occupational Safety and Health Administration's permissible exposure limit of 1,000 ppb. The majority (>50%) of current exposures were below the MDL. HPRT VFs were not significantly associated with current exposures (n = 29), and they were not significantly associated with age (n = 29). HPRT VFs were, however, significantly associated with OL (n = 29, R² = 0.107, P < 0.046). This result suggests that chronic and/or past, high‐level exposures might leave a mutagenic signature that is revealed by the HPRT assay, possibly through the retention of mutant, long‐term memory T‐cells. While it is encouraging that current occupational exposures to BD in this facility do not appear to be increasing the frequency of mutant T‐lymphocytes, evidence from workers with a lengthy history in the industry (≥30 years in this case) indicates that these individuals likely require additional biomonitoring for possible mutagenic effects resulting from chronic, past exposures. Environ. Mol. Mutagen., 2009. © 2008 Wiley‐Liss, Inc.     

丁苯橡胶的阳离子环化

应用一氯二乙基铝和苄基氯催化剂体系进行了丁苯橡胶的阳离子环化反应。研究了反应温度、苄基氯／一氯二乙基铝比例、溶剂、原胶浓度对环化的影响。发现通过控制苄基氯／一氯二乙基铝比，可在高温（１２０℃）、高原胶浓度（２～４％ｗ／ｖ）下进行丁苯橡胶的环化，制得特性粘度较原胶有大幅度降低，可溶性无凝胶的环化丁苯胶。通过对红外光谱、＾１Ｈ－ＮＭＲ谱初步解析，证实了环化反应的发生。     

氢化丁腈橡胶/受阻酚阻尼复合材料的制备与结构

将受阻酚AO-80加入氢化丁腈橡胶(HNBR)中,成功制备了氢化丁腈橡胶/受阻酚阻尼复合材料。利用差示扫描量热分析（DSC）、X射线衍射分析（XRD）、动态力学分析（DMA）、扫描电子显微镜（SEM）等测试手段对该复合材料进行了表征。测试结果表明：随着AO-80含量的增加,复合材料的阻尼因子逐渐增大,峰值对应温度逐渐移动至室温附近;在氢化丁腈橡胶（HNBR）内部,AO-80以无定形微球颗粒和无定形聚集体两种形式存在,以这两种形式存在的AO-80均可以利用氢键作用提高HNBR的阻尼性能。     

Rapid Determination of the Chemical Composition of Ethylene/Butadiene Copolymers Using FTIR Spectroscopy and Chemometrics

Fourier transform infrared spectroscopy by attenuated total reflection (ATR‐FTIR), combined with the partial least square (PLS) method provides a fast characterization of ethylene/butadiene copolymers' intricate composition. The PLS regression method is constructed to quantify ethylene, 1,2‐butadiene (vinyl), trans‐1,4‐butadiene, and 1,2‐cyclohexane units in the copolymer. These rings are formed by intramolecular cyclization during polymerization. The performance of PLS models is evaluated by comparing the result obtained by ¹³C NMR and the model for three unknown samples. It is shown that the proposed method allows to accurately estimate the chemical composition of ethylene/butadiene copolymers in a much shorter time than NMR.     

B90催化剂上丁烯氧化脱氢的反应动力学─一一种简便的建立化学动力学方程的方法

采用简便的建立化学反应动力学方程的方法，研究了Ｂ９０催化剂上丁烯氧化脱氢制丁二烯反应的动力学，即先在一较低温度下，用微分法拟合得到化学反应动力学方程中的浓度项，然后改变反应温度，求算不同温度下的反应速率常数。采用这个简便方法，只需较少的实验，即可求得该反应体系中的丁烯转化速率方程式。     

Disposition of Butadiene Epoxides in Sprague-Dawley Rats Following Exposures to 8000 ppm 1,3-Butadiene: Comparisons with Tissue Epoxide Concentrations Following Low-Level Exposures

1,3-Butadiene (BD), a compound used extensively in the rubberindustry, is weakly carcinogenic in Sprague-Dawley rats afterchronic exposures to concentrations of 1000 and 8000 ppm. Conversely,in B6C3F1 mice, tumors occur after chronic exposures to concentrationsas low as 6.25 ppm. Previously, we have shown that tissue concentrationsof the mutagenic BD metabolites, butadiene monoepoxide (BDO)and butadiene diepoxide (BDO₂), are present in greater concentrationsin mice than in rats following acute exposures to low levels(100 ppm or less). This disparity was particularly significantfor the diepoxide. We hypothesized that if these epoxides areinvolved in the carcinogenic response of BD, then they willalso be present in rat tissues at relatively high concentrationsfollowing exposures to 8000 ppm BD. In the present study, concentrationsof the BD epoxides, BDO and BDO₂, were determined in blood offemale Sprague-Dawley rats following a single 6-h exposure and10 repeated exposures to a target concentration of 8000 ppmBD. Concentrations of these epoxides were also determined ina number of other tissues, including the primary rat targetorgan—mammary gland—following 10 repeated exposures.Blood concentrations of BDO were 4030 pmol/g ± 191 followinga 6-h exposure and were 18% lower following the 10-day exposure.Blood concentrations of BDO₂, following the 8000 ppm exposures,were very similar to those previously observed after exposuresto 62.5 ppm BD (11 ± 1 and 17 ± 1 pmol/g followingexposures of 6h and 6h/day for 10 days, respectively.) Concentrationsof BDO ranged from 740 ± 110 (femur) to 8990 ±1150 (fat) pmol/g tissue. Concentrations of BDO₂ were similaramong eight tissues analyzed, ranging from 5 ± 1 (femur)to 17 ± 3 (heart) pmol/g tissue. Tissue concentrationsof butadiene mono-epoxide were increased by 17- to 50-fold intissues from rats exposed by inhalation to 8000 ppm BD as comparedto tissues from rats exposed to 62.5 ppm BD. Based on earlierstudies at our institute the internal dose of BD increases approximately14-fold in the 8000 ppm-exposed rats compared to rats exposedto 62.5 ppm BD. Concentrations of butadiene diepoxide in rattissues following an exposure to 8000 ppm BD were similar tothose observed in rat tissues following exposures to 62.5 ppmBD. This study shows that pathways responsible for the accumulationof BDO₂ in rats are saturated following low-level BD exposures.This suggests that the primary determinant of BD tumorigenicityin rats is not butadiene diepoxide. The high levels of BDO observedin rat mammary tissue suggest that this metabolite may be amore important determinant of BD carcinogenesis in the rat.     

Evaluation of respiratory effects of thermal decomposition products following single and repeated exposures of guinea pigs

Groups of guinea pigs were exposed to the thermal decomposition products (TDP) released from acrylonitrile butadiene styrene (ABS), polypropylene-polyethylene copolymer (CP), polypropylene homopolymer (HP), or plasticized polyvinyl chloride (PVC). In single 50-min exposures to the TDP, guinea pigs exhibited sensory irritation, coughing, and airways constriction. Significant decreases in respiratory frequency (f) occurred during TDP exposure which were magnified during CO₂ challenge conducted immediately post-exposure. For each resin, it was possible to demonstrate a linear relationship between the logarithm of heated mass and the percent decrease in f during CO₂ challenge. From these relationships, the mass of each resin producing a 50% decrease in f during CO₂ challenge (RD₅₀ masses of 2744, 25.2, 16.0, and 6.7 g were obtained for ABS, CP, HP, and PVC, respectively. Thus, the relative potency of their TDP was PVC > CP ≈ HP ≫ ABS. Using the RDC₅₀ mass of each resin, guinea pigs were exposed to TDP for 50 min/day on 5 consecutive days. These repeated exposures also resulted in sensory irritation, coughing, and airways constriction. However, deaths occurred during exposures, and there was evidence of cumulative respiratory effects, and slower recoveries among survivors. Data obtained in guinea pigs were compared to a previous study with mice exposed to the TDP of the same four resins (Schaper et al. 1994). On the basis of heated mass, mice were 20 500 times more sensitive to the acute respiratory effects of TDP than guinea pigs. Thus, the exposure limits of 0.63, 0.11, 0.08, and 0.35 mg/mg³ proposed by Schaper et al. (1994) on the basis of particulates released from ABS, CP, HP and PVC should prevent not only irritation, but also possible couphing, and airways constriction in workers. Received: 14 June 1994/Accepted: 18 October 1994