Omeprazole treatment of chronic duodenal ulceration

Omeprazole, a substituted benzimidazole, is an acid pump inhibitor, introduced for treatment of chronic duodenal ulceration. In a study of 116 patients with endoscopically documented chronic duodenal ulcers, omeprazole affected healing in 77 (66.3%) patients after two weeks and 106 (91.4%) patients after four weeks, with symptoms relief in 102 (88%) patients within the first week of treatment. There was significantly higher healing rate in females (p < 0.05) and diffuse ulceration rather than single ulcers (p < 0.05). In meta-analysis comparing omeprazole to other antiulcer drugs reported in this country, there was a significant higher healing rate (p < 0.01) and symptom relief (p < 0.01) in favour of omeprazole. It proved to be effective and safe for the short term treatment of chronic duodenal ulceration.     

Species makeup and some characteristics of the physiology of the bacteria isolated in sugar manufacture

Nineteen pregnant women with burn areas ranging from 6 to 92% of the total body surface area were treated at the US Army Institute of Surgical Research between 1951 and 1974. A review of these cases led to the following observations and conclusions: 1) Pregnancy does not alter the maternal outcome after thermal injury. 2) Maternal survival is usually accompanied by fetal survival. 3) If the gravida's injury is lethal, the pregnancy will usually terminate spontaneously prior to her death. 4) Obstetric intervention is indicated only in the gravely ill woman whose complications (hypotension, hypoxia, or sepsis) jeopardize the life of the fetus. 5) A better understanding of the complications of major burns and the care available in modern burn units should improve the prognosis for burned pregnant patients.     

Depth distribution of ion-implanted argon in gadolinium and samarium films

The development of a model and theoretically evaluated distributions for impurities injected by ion bombardment into growing films are given. The influence of ion range distribution function, diffusion, impurity-defect interaction and film and substrate material differences upon the impurity concentration profiles is investigated. The possibility of uniform impurity distribution in the main part of the film with a sharp concentration gradient into the substrate is shown. The influence of diffusion leads to a decrease of gaseous impurity concentration in the film and penetration of impurities into the substrate; the relation of impurity diffusion coefficients and the segregation coefficient value is essential when the film and the substrate are made of different materials. Taking into account the trapping of impurities by defects we found that the distribution of the ‘free’ (mobile) impurities is inhomogeneous with a maximum near the growth boundary, this inhomogeneity is decreased with increased diffusion, while defect concentration increases. The concentration profiles of the trapped impurities (impurity-defect complexes) are very different, the complexes become distributed more homogeneously and the concentration of complexes increases as diffusion and the defect concentration increase.By use of secondary ion mass-spectrometry (SIMS) a distribution of ion-implanted argon through the film and part of the substrate depth was investigated as well as the distribution of the film and substrate materials themselves, using gadolinium and samarium films obtained by vacuum condensation on (100) molybdenum monocrystal under simultaneous 100 and 600 eV argon irradiation. The argon distribution through the film is found to be almost uniform with an exponential decrease in the substrate for gadolinium films at an energy of 100 eV. A considerable argon accumulation at the film-substrate boundary is found at an energy of 600 eV. For samarium films at an energy of 100 eV an anomalous argon and samarium penetration into the substrate as well as argon penetration into the layer deposited without irradiation of the film is obtained.     

A max-algebra approach to the robust distributed control of repetitive AGV systems

This paper presents a new approach for distributed control of automatic guided vehicle systems (AGVS) that uses max-algebra formalism to model system operation. The proposed method differs from previous works on performance analysis and control of such systems in that it constructs a feasible schedule by exploiting the repetitive character of the flow of automated guided vehicles. The AGVS is treated as a distributed system composed of autonomous and repetitive processes of AGV flows. Its periodic behaviour follows from the type of operation characterizing the job shops considered. The proposed approach employs a concept of asynchronous traffic semaphores that provide the local mechanism for vehicle flow synchronization. Setting the timing of particular semaphores results in distributed control of vehicle flows possessing self-synchronization capabilities.     

葛根的化学成分研究

系统地回顾了近30年来葛根化学成分研究概况，着重介绍了国内外对葛根中异黄酮、三萜及葛酚苷类等具显著生理活性的化学成分研究进展。     

p21(Waf1/Cip1) inhibition of cyclin E/Cdk2 activity prevents endoreduplication after mitotic spindle disruption

During a normal cell cycle, entry into S phase is dependent on completion of mitosis and subsequent activation of cyclin-dependent kinases (Cdks) in G1. These events are monitored by checkpoint pathways. Recent studies and data presented herein show that after treatment with microtubule inhibitors (MTIs), cells deficient in the Cdk inhibitor p21(Waf1/Cip1) enter S phase with a >/=4N DNA content, a process known as endoreduplication, which results in polyploidy. To determine how p21 prevents MTI-induced endoreduplication, the G1/S and G2/M checkpoint pathways were examined in two isogenic cell systems: HCT116 p21(+/+) and p21(-/-) cells and H1299 cells containing an inducible p21 expression vector (HIp21). Both HCT116 p21(-/-) cells and noninduced HIp21 cells endoreduplicated after MTI treatment. Analysis of G1-phase Cdk activities demonstrated that the induction of p21 inhibited endoreduplication through direct cyclin E/Cdk2 regulation. The kinetics of p21 inhibition of cyclin E/Cdk2 activity and binding to proliferating-cell nuclear antigen in HCT116 p21(+/+) cells paralleled the onset of endoreduplication in HCT116 p21(-/-) cells. In contrast, loss of p21 did not lead to deregulated cyclin D1-dependent kinase activities, nor did p21 directly regulate cyclin B1/Cdc2 activity. Furthermore, we show that MTI-induced endoreduplication in p53-deficient HIp21 cells was due to levels of p21 protein below a threshold required for negative regulation of cyclin E/Cdk2, since ectopic expression of p21 restored cyclin E/Cdk2 regulation and prevented endoreduplication. Based on these findings, we propose that p21 plays an integral role in the checkpoint pathways that restrain normal cells from entering S phase after aberrant mitotic exit due to defects in microtubule dynamics.