Thermal—Mechanical Fatigue Behavior and Life Analysis of Cast Ni—base Superalloy K417

In-phase(IP) and out-of-phase(OP)thermal-mechanical fatigue(TMF) behavior of cast Ni-base superalloy K417 was studied.All experiments were carried out under total strain control with temperature cycling between 400-850℃.Both in-phase and out-of-phase TMF specimens exhibited cyclic hardening followed by cyclic softening at the minimum temperature.Besides,they cyclically hardened in the early stage of life followed by cyclic softening at the minimum temperature.Besides,they cyclically hardened in the early stage of life followed by cyclic softening at the maximum temperature.OP TMF life was longer than of IP TMF.Various damage mechanisms operating in different controlled strain ranges and phasing were discussed.A few life prediction methods for isothermal fatigue were used to handle TMF fatigue and their applicability to superalloy K417 was evaluated.The SEM analysis of the fracture surface showed that transgranular fracture was the principal cracking mode for both IP and OP TMF.Oxidation was the main damage mechanism in causing shorter fatigue life for IP TMF compared with OP TMF.     

The pathogenesis of undiagnosed peritonitis in middle-aged and elderly patients with acute coronary insufficiency

Three-stage treatment using a day hospital instead of a sanatorium with regards to the pattern of a tuberculosis process can achieve the results of closure of decay and abacillation cavities, which are not inferior to those with the conventional treatment, by reducing the basic regimen through the length of a hospital stage. The efficiency of two-stage treatment (day hospital--outpatient clinic) of lung tissue decay and culture-positive patients depends on the duration of the basic regimen, patient compliance, and the presence of a concomitant abnormality.     

Comparability of self-report of familial alcoholism among male and female college students

There is a general impression in the literature that women are more accurate reporters of familial psychiatric history. In this regard, this study presents data from a large cohort of young men (n = 427) and women (n = 607) who in answering a questionnaire self-reported alcohol abuse symptoms for various biological relatives. No significant gender differences emerged for any of the family history comparisons including reports for father, mother, either parent, any first- or second-degree relatives, or men or women relatives. The findings are discussed in the context of the existing literature.     

利用扫描电镜研究三维电极主电极表面腐蚀状况

借助扫描电镜（SEM）对不同实验条件下的三维电极主电极表面腐蚀状况进行研究。结果表明，三维电极主极阳极的内侧腐蚀程度远大于其外侧，水样性质、电极材料性质对电极的腐蚀程度有很大的影响，不锈钢做三维电极主电极优于铝、铁电极。为三维电极主电极的选材提供了一定的理论依据。     

Effect of feedback from peripheral movements on neuron activity in the aplysia abdominal ganglion

We have made reasonably comprehensive measurements of action potential activity in the Aplysia californica abdominal ganglion to determine the amount of feedback the central nervous system (CNS) receives from a movement which it initiates. Voltage-sensitive dye measurements of action potential activity of cells in the ganglion were made during the gill-withdrawal reflex elicited by siphon stimulation. We compared recordings in two situations which differed dramatically in the amount the gill moved. In the control sea water, the gill withdrawal was normal; in low-Ca2+, high-Mg2+ sea water, the gill movement was blocked. Both the timing and the number of spikes of the individual neurons were similar in the two situations. Histograms of the summed spike activity versus time and histograms of the number of active neurons versus time in the two conditions were also similar. Finally, two numerical measures of trial-to-trial differences, a paired t-test and a measure we named fractional similarity, did not indicate larger differences between two trials in the different sea waters than two trials in the same sea water. Feedback from sensory neurons activated by the gill movement itself does not make a large contribution to the spike activity in the abdominal ganglion. Apparently the Aplysia CNS issues the command for the withdrawal and does not make adjustments for the magnitude of the actual withdrawal. It may not even receive the information necessary for such adjustments to be made. A second motivation for these experiments was to test whether removing the feedback might simplify the neuronal activity that occurs during the gill-withdrawal reflex. This did not occur.     

Plasma and erythrocyte alpha-tocopherol and plasma retinol concentrations in term infants fed formula enriched with long-chain polyunsaturated fatty acids

OBJECTIVE: To assess the effect of long-chain polyunsaturated fatty acids (LCPUFA)- and vitamin E-supplemented formula feeding on erythrocyte and plasma alpha-tocopherol (VE), and plasma retinol (VA) concentrations in neonates and to compare these values with those found in infants feeding on infant formula without LCPUFA or breast milk SETTING: University Hospital of Granada, Spain. SUBJECTS: 49 full-term infants. DESIGN AND INTERVENTION: Subjects who chose not to breast feed were fed either (i) unsupplemented infant formula (F) or (ii) infant formula supplemented with LCPUFA and vitamin E (FL). Alpha-tocopherol and retinol were measured at 7 days, 1 month and 3 months. RESULTS: Plasma and erythrocyte VE concentrations and plasma VE/total lipids ratio increased significantly in all groups at 1 month of life (P < 0.05), but did not change significantly between 1 month and 3 months in any group (P > 0.05). Erythrocyte VE and VA retinol concentrations were higher in infants fed an infant formula than in breast milk-fed infants at 1 month of life (P < 0.05). Finally, there were no significant differences in plasma or erythrocyte VE levels, plasma VA or plasma VE/total lipid ratio between any groups at 3 months of life (P > 0.05). CONCLUSION: Infants fed on LCPUFA- and vitamin E-supplemented infant formula for 3 months have similar vitamin E and A status to infants fed on breast milk or infant formula without LCPUFA supplementation.     

Radiolabeled nucleoside analogs in cancer diagnosis and therapy

Radiolabeled nucleosides, specifically 5-iodo-2'-deoxyuridine (IUdR) radioiodinated with the Auger-electronemitting 123I or 125I, have been shown to produce extensive DNA damage in mammalian cell systems in vitro. Such nucleosides are cycle-dependent agents that are taken up by mitotically dividing cells in the S phase of the cell cycle. The degree of damage that occurs is related to the fact that these nucleosides bind covalently to DNA bringing the decaying Augerelectron-emitting radionuclide in close proximity to the genome. The use of these radiohalogenated nucleosides in vivo is associated with several problems. The first relates to their extremely short biologic half-life in blood (T1/2 of minutes in humans). The second involves achieving therapeutic ratios in tumor cells in the face of efficient hepatic dehalogenation. The third concerns the uptake of these radiopharmaceuticals by actively proliferating normal cell renewal systems, thus potentially causing toxic side effects. The fourth, one shared with other cycle-dependent drugs, relates to the matter of labeling the whole tumor cell population. To facilitate targeting to tumors, investigators have been examining the direct introduction of these agents into the targeted area or into an arterial blood supply that immediately precedes the target. For example, radiopharmaceutical administration could be intracavitary (bladder, spinal fluid, peritoneum), intralesional (brain tumor, breast mass) or intra-arterial (liver, pancreas). In all these situations, the following conditions must be met: (a) once within the vicinity of the tumor the agent can freely diffuse through the tissues and is selectively taken up by cancerous cells; (b) once the agent has left the target area it is converted quickly into a nontoxic form and/or excreted from the body; and finally, (c) the biologic behavior of the agent is not altered by repeated injections. We report herein our experience and that of others with [123I/125I/131I]IUdR in cultured cells, animal tumor-model systems, and patients. In vitro, DNA incorporation of 123I- and 125I-labeled IUdR leads to an exponential decrease in cell survival (no shoulder on the survival curve). However, the total number of decays needed to produce a given lethal effect with [123I]IUdR is approximately twice that required with [125I]IUdR. In vivo, the scintigraphic and antineoplastic capabilities of radioiodinated IUdR have been demonstrated in an intraperitoneal murine ovarian tumor model following intraperitoneal injection; in an intracerebral rat gliosarcoma model after intracranial administration; in an intrathecal rat gliosarcoma model after intrathecal infusion; and in a rat transitional cell bladder cancer model following intravesicular infusion. [123I]IUdR, [125I]IUdR, and/or [131I]IUdR have been administered to patients with brain, breast, colorectal, or gastrointestinal cancers (intratumorally); ovarian cancer (intraperitoneally); bladder cancer (intravesically); liver metastases from colorectal cancer (through the hepatic artery, permanent intra-arterial catheter). These studies have confirmed the observations made in animal models. The data indicate that 5-iodo-2'-deoxyuridine radiolabeled with an Auger electron emitter (123I or 125I) may be a useful agent for the scintigraphic diagnosis and/or therapy of neoplastic diseases that are accessible to direct radiopharmaceutical administration. This radiopharmaceutical should serve as a prototype for, and facilitate the development of, other radiolabeled nucleoside analogs. Further investigations are certainly warranted.     

Reduced skin tumor development in cyclin D1-deficient mice highlights the oncogenic ras pathway in vivo

Cyclin D1 is part of a cell cycle control node consistently deregulated in most human cancers. However, studies with cyclin D1-null mice indicate that it is dispensable for normal mouse development as well as cell growth in culture. Here, we provide evidence that ras-mediated tumorigenesis depends on signaling pathways that act preferentially through cyclin D1. Cyclin D1 expression and the activity of its associated kinase are up-regulated in keratinocytes in response to oncogenic ras. Furthermore, cyclin D1 deficiency results in up to an 80% decrease in the development of squamous tumors generated through either grafting of retroviral ras-transduced keratinocytes, phorbol ester treatment of ras transgenic mice, or two-stage carcinogenesis.