包钢BG-Ⅲ型无钟炉顶布料器

BG型无钟炉顶布料器是包钢（集团）公司炼铁厂开发的专利产品。包钢（集团）公司自1985年开始使用BG型无钟炉顶布料器，先后用于3号高炉、1号高炉。2004年2号高炉扩容和5号高炉的新建也采用了该BG型布料器，2005年9月将4号高炉的PW型布料器也改为BG型布料器。20年的使用实践证明：BG型无钟炉顶布料器的各项技术指标满足高炉使用要求。     

钢多BG-Ⅲ型无钟炉顶布料器

BG型无钟炉顶布料器是包钢（集团）公司炼铁厂开发的专利产品。包钢（集团）公司自1985年开始使用BG型无钟炉顶布料器，先后用于3号高炉、1号高炉。2004年2号高炉扩容和5号高炉的新建也采用了该BG型布料器，2005年9月将4号高炉的PW型布料器也改为BG型布料器。20年的使用实践证明：BG型无钟炉顶布料器的各项技术指标满足高炉使用要求。[第一段]     

包钢BG-Ⅱ型无钟炉顶布料器

BG型无钟炉顶布料器是包钢（集团）公司炼铁厂开发的专利产品。包钢（集团）公司自7985年开始使用BG型无钟炉顶布料器，先后用于3号高炉、1号高炉。2004年2号高炉扩容和5号高炉的新建也采用了该BG型布料器，     

包钢7#高炉炉顶布料器的改进

文章通过对包钢型布料器的工作原理以及在包钢7#高炉炉顶布料器的应用情况做了简要说明,分析了布料器寿命短的原因,并对布料器改进前后的性能特点进行了比较,介绍了新型布料器(秦冶布料器)在7#高炉的更换过程,更换后的布料器达到了高炉按角度布料的要求,对高炉的稳定顺产起到了积极作用。     

包钢布料器在大型高炉的应用与改进

文章介绍了包钢拥有自主知识产权的布料器逐步发展过程,以及近年来在大高炉的应用情况,并针对在包钢特殊炉况情况下布料器在大高炉出现的故障,针对性的对布料器中心喉管、托架等做了改进措施,提高了包钢布料器在大高炉应用的能力。     

BGⅢ型高炉布料器运动分析

文章通过对包钢BGⅢ型布料器结构进行分析,求出溜槽在整个旋转和倾动过程中对布料器各部件产生的最大值负荷。构建了合理的力学模型,核算了电机及油缸的负载能力,证明了原设计选型的合理性。同时为布料器其它部件的结构改进和受力计算提供基础数据支撑,为布料器的结构优化提供理论支持。     

BT型布料器的改进及在中小高炉上的应用

由于BT型布料器具有独特的优点,已成功应用于大型高炉上,现在有必要在中小型高炉上推广应用.在介绍BT型布料器结构、原理的基础上,针对中、小型高炉的具体情况,提出了对BT型布料器的改进思想,并说明了改造后BT-Ⅲ型布料器的结构、原理和主要优点.实践证明,改造后的BT-Ⅲ型布料器更适合中、小型高炉的工艺特点,可以在中小型高炉上推广使用.     

高炉无料钟炉顶布料器的冷却分析

首钢一号高炉无料钟炉顶布料器是水冷、氮气密封的结构,对影响布料器冷却的各主要参数进行了分析,得出各个参数对布料器齿轮箱内温度的影响程度,在此基础上提出了一种旋转圆筒结构的改进方案,此方案可大幅度降低布料器内的温度,并可大量节省冷却水用量。     

包钢BG-Ⅱ型无料钟炉顶布料器的现状与展望

简要介绍了包钢BG-Ⅱ型无料钟炉顶布料器原理、特点及现在使用状况,并提出了对该布料器作进一步改进的设想。     

无钟炉顶布料器在包钢的使用与发展

介绍了由包头钢铁设计研究院自行设计、改进的无钟炉顶布料器在包钢的使用与发展过程。较详细地阐述了ＢＧ－Ⅱ型布料器的结构、工作原理和使用效果。     

Prefabricated Vertical Drains Flow Resistance under Vacuum Conditions

The results of experimental research are presented and discussed with focus on the internal well resistance of prefabricated vertical drains (PVD) under vacuum-induced water flow. Measured results included fluid flow rates for two different cross-sectional hydraulic profiles (Types I and II PVDs). Experimental results indicated linear relationships, independent of the PVD widths, between extracted fluid velocity and the applied hydraulic gradient. Data showed a laminar flow regime to predominate for test velocities corresponding to hydraulic gradients <0.5. The larger nominal hydraulic radius of the Type II PVD is credited with providing a flow rate equal to approximately 3.2 times that of the Type I PVD at approximately the same operating total head. There was no apparent dependency of the transmissivity θ on the width or lengths (3, 4, and 5 m) of the PVDs tested. In the case of the 100-mm-wide Type I PVD, θ = 618 mm2∕s was estimated from the measured data versus θ = 1,996 mm2∕s for Type II PVD with the same dimensions.     

高炉矮式液压泥炮

本文针对高炉炉前设备液压泥炮的发展进行概述 ,叙述了目前国内外较为先进的典型矮式液压泥炮 ,PW型、MHG型、IHI型、BG型和DDS型。     

Pharmacokinetics of O6-benzylguanine and its active metabolite 8-oxo-O6-benzylguanine in plasma and cerebrospinal fluid after intrathecal administration of O6-benzylguanine in the nonhuman primate

O6-Benzylguanine (O6BG) irreversibly inactivates the single-turnover DNA repair protein alkylguanine-alkyltransferase. Thus, O6BG increases tumor-cell sensitivity to alkylating agents such as carmustine, lomustine, procarbazine, and temozolomide. We investigated the pharmacokinetic behavior of O6BG and O6-benzyl-8-oxoguanine (8-oxo-O6BG) in cerebrospinal fluid (CSF) and plasma after intraventricular administration of O6BG in a nonhuman primate model. In our study, three animals received a single 1-mg dose of O6BG into the lateral ventricle. CSF from the 4th ventricle and plasma samples were collected after administration, and O6BG and 8-oxo-O6BG concentrations were measured by high-performance liquid chromatography. Four additional animals received 1 mg of O6BG via the intralumbar route weekly for 6 weeks to assess the feasibility and toxicity of this route of administration. The peak O6BG CSF concentration was 412+/-86 microM, the t1/2 was 0.52+/-0.02 h, the clearance was 0.22+/-0.01 ml/min, and the area under the concentration-time curve was 319+/-15 microM x h in 4th ventricular CSF. The peak CSF concentration of 8-oxo-O6BG in CSF was 1.9+/-0.4 microM, the t1/2 was 0.76+/-0.03 h, and the area under the concentration-time curve was 5.0+/-1.1 microM x h. Both O6BG and 8-oxo-O6BG were detected in the plasma 0.5-3 h after intraventricular O6BG administration. The plasma peak concentration of O6BG was 0.4 microM at 30 min, and the concentration was <0.1 microM by 3 h. The plasma concentration of 8-oxo-O6BG was 0.2 microM at 30 min and 0.6 microM at 3 h. The animals tolerated the single intraventricular dose and 6 weekly intralumbar doses of O6BG without toxicity. We concluded that intrathecal administration of O6BG is well tolerated in the nonhuman primate and seems to have a substantial pharmacokinetic advantage over systemic administration for meningeal tumors.     

Differential regulation of genes encoding 1-aminocyclopropane-1-carboxylate (ACC) synthase in etiolated pea seedlings: effects of indole-3-acetic acid, wounding, and ethylene

OBJECTIVE: To compare the efficacy of the short-acting insulin analog lispro (LP) with that of regular insulin in IDDM patients treated with an external pump. RESEARCH DESIGN AND METHODS: Thirty-nine IDDM patients (age, 39.4 +/- 1.5 years; sex ratio, 22M/17W; BMI, 24.4 +/- 0.4 kg/m2; diabetes duration, 22.5 +/- 1.6 years) who were treated by external pump for 5.1 +/- 0.5 years were involved in an open-label, randomized, crossover multicenter study comparing two periods of 3 months of continuous subcutaneous insulin infusion with LP or with Actrapid HM, U-100 (ACT). Boluses were given 0-5 min (LP) or 20-30 min (ACT) before meals. Blood glucose (BG) was monitored before and after the three meals every day. RESULTS: The decrease in HbA1c was more pronounced with LP than with ACT (-0.62 +/- 0.13 vs. -0.09 +/- 0.15%, P = 0.01). BG levels were lower with LP (7.93 +/- 0.15 vs. 8.61 +/- 0.18 mmol/l, P < 0.0001), particularly postprandial BG levels (8.26 +/- 0.19 vs. 9.90 +/- 0.20 mmol/l, P < 0.0001). Standard deviations of all the BG values (3.44 +/- 0.10 vs. 3.80 +/- 0.10 mmol/l, P = 0.0001) and of postprandial BG values (3.58 +/- 0.10 vs. 3.84 +/- 0.10 mmol/l. P < 0.02) were lower with LP. The rate of hypoglycemic events defined by BG < 3.0 mmol/l did not significantly differ between LP and ACT (7.03 +/- 0.94 vs. 7.94 +/- 0.88 per month, respectively), but the rate of occurrences of very low BG, defined as BG < 2.0 mmol/l, were significantly reduced with LP (0.05 +/- 0.05 vs. 0.47 +/- 0.19 per month, P < 0.05). At the end of the study, all but two (95%) of the patients chose LP for the extension phase. CONCLUSIONS: When used in external pumps, LP provides better glycemic control and stability than regular insulin and does not increase the frequency of hypoglycemic episodes.     

Treatment of human brain tumor xenografts with O6-benzyl-2'-deoxyguanosine and BCNU

O6-Methylguanine-DNA methyltransferase (MGMT), a constitutively expressed DNA repair protein, removes alkyl groups from the O6-position of guanine in DNA. Tumor cells with high MGMT activity are resistant to nitrosoureas and other agents that form toxic O6-alkyl adducts. O6-Benzylguanine (BG) inactivates the MGMT protein and thereby enhances the sensitivity of tumor cells to alkylating drugs. However, the therapeutic potential of BG is limited by its poor solubility and its nonspecific inactivation of MGMT in normal tissues as well as in tumor tissues. Consequently, BG analogues are being developed to identify agents that have more favorable pharmacological characteristics. We evaluated O6-benzyl-2'-deoxyguanosine (dBG), the 2'-deoxyribonucleoside analogue of BG, for its ability to inhibit MGMT and to potentiate 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) in a MGMT-positive human brain tumor xenograft, Daoy. When given i.p. 1 h before BCNU (25 mg/m2) to animals bearing s.c. tumors, dBG (134 mg/m2) produced a growth delay of 24.7 days, compared to 21.6 days after treatment with an equimolar dose of BG (90 mg/m2) plus BCNU and -0.6 days after treatment with BCNU alone. The combination of dBG + BCNU also increased the survival of animals bearing intracranial tumors by 65%. By increasing the dose of dBG to 300 mg/m2 (the maximum dose that could be delivered i.p. in a standard treatment volume), the growth delay of s.c. tumors increased from -0.1 days with BCNU alone to 39.3 days. dBG suppressed both tumor and liver MGMT activity to less than 1.5% of baseline, and dBG + BCNU induced extensive perivascular apoptosis. Because dBG is a 10-fold less potent MGMT inhibitor than BG in HT-29 cell extracts, these results illustrate the capacity of BG analogues to potentiate BCNU toxicity, despite less in vitro activity than the parent compound, and emphasize the importance of in vivo evaluation of BG analogues.     

Does suppression of postprandial blood glucose excursions by the alpha-glucosidase inhibitor miglitol improve insulin sensitivity in diet-treated type II diabetic patients?

OBJECTIVE: Insulin sensitivity is impaired in patients with type II diabetes and is exacerbated by high mean blood glucose (BG). Potentially, large postprandial swings in BG could result in further decrements of insulin sensitivity. Because alpha-glucosidase inhibitors cause a marked reduction in the amplitude of BG changes, the aim of this study was to determine if such a BG-smoothing effect improves insulin sensitivity in well-controlled type II diabetic subjects treated with diet alone. RESEARCH DESIGN AND METHODS: Patients received either miglitol (BAY m 1099) (50 mg three times daily) or placebo for 8 weeks in a randomized double-blind parallel study. The miglitol (9 men, 2 women) and placebo (7 men, 3 women) groups were well matched (mean +/- SD) for age, weight, and blood glucose control (fasting BG, 6.4 +/- 1.0 vs. 6.9 +/- 1.6 mmol/l; HbA1, 7.7 +/- 1.0 vs. 7.9 +/- 0.4%; fructosamine, 0.99 +/- 0.08 vs. 1.07 +/- 0.17 mmol/l). The glucose metabolic clearance rate was calculated during the last 30 min of a 150 min glucose/insulin sensitivity test (glucose, 6 mg . kg-1 . min-1; insulin, 0.5 U . kg-1 . min-1). RESULTS: There was no significant improvement in metabolic clearance rate (0.21 +/- 0.27 vs. 0.16 +/- 0.35 l . kg-1 . min-1) for the miglitol- and placebo-treated groups, respectively. There were no statistically significant differences between miglitol and placebo for changes from baseline in BG (0.1 +/- 0.1 vs. -0.1 +/- 0.2 mmol/l), HbA1 (0.1 +/- 0.1 vs. 0.3 +/- 0.1%), and fructosamine (-0.06 +/- 0.02 vs. -0.03 +/- 0.02 mmol/l). CONCLUSIONS: Alpha-glucosidase-induced improvement in postprandial hyperglycemia does not result in increased insulin sensitivity.     

Retroviral transfer of a bacterial alkyltransferase gene (ada) into human bone marrow cells protects against O6-benzylguanine plus 1, 3-bis(2-chloroethyl)-1-nitrosourea cytotoxicity

The antitumor activity of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) is limited by the O6-alkylguanine-DNA alkyltransferase (ATase) in tumor cells and by delayed myelosuppression. Inactivation of neoplastic ATase by O6-benzylguanine (BG) improves the therapeutic index for BCNU. We have demonstrated previously that BG + BCNU-induced myelosuppression in mice is reduced by expression of the BG-resistant ATase ada in murine bone marrow. We have now generated an amphotropic retrovirus containing the ada gene and tested the effectiveness of ada expression in preventing BG + BCNU cytotoxicity in human hematopoietic progenitor cells. A retroviral producer clone with a biological titer of 6.5 x 10(4) colony-forming units/ml and 4.4 pmol ATase/mg protein was used for transduction of bone marrow. Cocultivation of these ada producer cells with progenitor cells from six normal individuals resulted in 1.9-3. 9-fold protection against BG + BCNU-induced cytotoxicity in committed progenitor cell assays. Furthermore, this cytoprotective effect was associated with a high transduction efficiency (40%) and a 2-fold increase of ATase activity in the surviving committed progenitor cell colonies. These data provide a basis for testing the clinical effectiveness of retroviral ada gene transfer into hematopoietic cells to increase the therapeutic index of BG + BCNU.     

Hydraulic Models of the Flow Distribution in a Four Branch Open Channel Junction with Supercritical Flow

Intense rainfall on urban areas can generate severe flooding in the city, and if the conditions are right, the flow in the streets can be supercritical. The redistribution of the flow in street intersections determines the flow rates and water levels in the street network. We have investigated the flow that occurs when two supercritical flows collide in a 90° junction formed by streets of identical cross section. Several flow configurations within the intersection are possible, depending on the position of the hydraulic jumps that form in and upstream of the intersection. Previous work has identified three flow types, with Type II flows being further classified into three subregimes. Hydraulic models have been developed, based on the principles of the conservation of flow and momentum flux in the intersection, which predict the angles at which the jumps will form. These models can be used to determine the flow type that will occur. Moreover, additional models have been developed for computing the outflow discharge distribution. For Type I flows, it has not been possible to develop such a hydraulic model for the discharge distribution, but some data are provided for one configuration to indicate the influence of different parameters. For Type II and Type III flows, such models are developed, and their predictions agree with data obtained from the channel intersection facility at the Laboratory of Fluid Mechanics and Acoustics in Lyon.     

Enhanced susceptibility of low-density lipoprotein to in vitro oxidation in type 1 and type 2 diabetic patients

Macrovascular disease represents a major cause of morbidity and mortality in patients with diabetes mellitus. Low-density lipoprotein (LDL) is involved in the pathogenesis of atherosclerotic lesions, through modifying processes such as oxidation. We examined the in vitro susceptibility to oxidation and the oxidizability of LDL isolated from the plasma of Type 1 and Type 2 diabetic patients. Two groups of diabetic patients (20 Type 1, 20 Type 2) were compared with sex- and age-matched non-diabetic control groups. In vitro oxidation of the purified LDL preparations was assessed by determination of the kinetics for the formation of conjugated dienes (lag phase duration, maximal rate and maximal dienes concentration) and by measurement of thiobarbituric acid-reacting substances (TBARS) in the presence of copper ions. LDL from both Type 1 and Type 2 diabetic patients exhibited a shorter lag phase duration for conjugated dienes formation (94 +/- 14 vs. 108 +/- 20 and 97 +/- 26 vs. 112 +/- 18 min for Type 1 and Type 2 diabetic groups vs. respective control groups, P < 0.05). We also observed an increase in maximal rate of conjugated dienes formation (2.21 +/- 0.55 vs. 1.52 +/- 0.31 and 2.02 +/- 0.55 vs. 1.52 +/- 0.31 nmol/mg LDL/min, P < 0.01) and of maximal production of TBARS (77.9 +/- 11.8 vs. 65.5 +/- 10.4 and 76.7 +/- 9.9 vs. 65.3 +/- 9.4 nmol/mg LDL protein, P < 0.05) in diabetic groups. Our results demonstrate both a higher susceptibility to oxidation and a higher oxidizability of LDL from diabetic patients, as much for Type 1 as Type 2 diabetic subjects with or without pre-existent vascular complications. This enhanced propensity of LDL oxidation in patients with diabetes mellitus could at least partly be attributable to quantitative and qualitative alterations in the chemical composition of LDL and to the glycoxidation process occurring on these lipoproteins.     

Isolation of human O6-alkylguanine-DNA alkyltransferase mutants highly resistant to inactivation by O6-benzylguanine

The activity of O6-alkylguanine-DNA alkyltransferase (AGT) protects cells from killing by methylating or chloroethylating agents. AGT is strongly inhibited by O6-benzylguanine (ED50, 0.2 microM), and this drug is presently undergoing clinical trials to enhance chemotherapy by alkylating agents. Point mutations such as P140A (ED50, 5 microM) render AGT resistant to O6-benzylguanine (BG). Selection for such mutants may prove to be a problem in the use of BG, and a better knowledge of the factors underlying resistance to BG will enable the rational design of improved inhibitors able to inactivate these mutants. BG-resistant AGT mutants may also be valuable for expression in bone marrow stem cells to reduce myelosuppression brought about by alkylating agents, to increase the therapeutic index of therapies including BG, and for use as a selectable marker to allow other genes to be expressed in such stem cells. We have therefore set up a general screen to obtain such mutants by using the ability of AGT to protect Escherichia coli GWR109 lacking endogenous AGT from killing by N-methyl-N'-nitro-N-nitrosoguanidine. When the cells were rendered permeable to BG by mutating the lipopolysaccharide membrane component forming strain TRG8, the protection by AGT expression was abolished by treating the cells with BG. The known P140A mutant was used to test the system and was highly selected for by treatment with 50 microM BG and 40 microg/ml N-methyl-N'-nitro-N-nitrosoguanidine. The sequence coding for PVP at positions 138-140 in AGT was replaced with a random nucleotide sequence, and this library was used to transform TRG8. All of the 59 colonies analyzed having AGT activity that survived the selection from the pool of 36,000 transformants were resistant to BG. Many (69%) of these mutants contained lysine at position 140, and all of these showed the highest level of resistance with <10% loss of activity when crude cell extracts were incubated with 1.2 mM BG. This result was confirmed with three mutants (P138K/V139L/P140K, P138M/V139L/P140K, and P140K), which were purified to homogeneity. The next most common residues found at position 140 were arginine (7%) and asparagine (7%). Studies carried out with purified preparations of mutants P140R and P140N revealed that these mutations also provided resistance to BG but to a lesser extent than P140K (ED50s of 190 and 7 microM, respectively). These results indicate that: (a) this screening method can be used to evaluate BG resistance of single or multiple changes throughout the AGT sequence; and (b) replacement of proline-140 with lysine is the most effective point mutation at this site causing BG resistance and is more than 200 times more effective than replacement with alanine.