X-ray or UV adjustment of MOS threshold voltage: Analytical and numerical modeling

A model is formulated that describes how radiation-induced charge accumulates in the gate oxide of a MOS structure and how it decays through tunneling and thermal emission. The model is used in a numerical analysis of the x-ray or UV adjustment of threshold voltage in MOS-circuit manufacture. The limits of this process technique are evaluated.     

Murine thymic lymphoma is associated with a species-specific hematopoietic progenitor cell subpopulation

Many strains of laboratory mouse are uniquely susceptible to the development of T cell lymphoma/leukemia, either spontaneously or as a result of chemical or radiation exposure. In contrast, T cell leukemias or lymphomas which are relatively uncommon in human populations, are not easily induced by radiation, and are not generally associated with chemotherapy or chemical exposure. Evidence is presented to suggest that differences in the susceptibility to the development of these malignancies is related to subtle but important variations in the regulation of hematopoietic stem cell differentiation between these two species.     

Identification of in vitro phosphorylation sites in the growth cone protein SCG10. Effect Of phosphorylation site mutants on microtubule-destabilizing activity

SCG10 is a neuron-specific, membrane-associated protein that is highly concentrated in growth cones of developing neurons. Previous studies have suggested that it is a regulator of microtubule dynamics and that it may influence microtubule polymerization in growth cones. Here, we demonstrate that in vivo, SCG10 exists in both phosphorylated and unphosphorylated forms. By two-dimensional gel electrophoresis, two phosphoisoforms were detected in neonatal rat brain. Using in vitro phosphorylated recombinant protein, four phosphorylation sites were identified in the SCG10 sequence. Ser-50 and Ser-97 were the target sites for protein kinase A, Ser-62 and Ser-73 for mitogen-activated protein kinase and Ser-73 for cyclin-dependent kinase. We also show that overexpression of SCG10 induces a disruption of the microtubule network in COS-7 cells. By expressing different phosphorylation site mutants, we have dissected the roles of the individual phosphorylation sites in regulating its microtubule-destabilizing activity. We show that nonphosphorylatable mutants have increased activity, whereas mutants in which phosphorylation is mimicked by serine-to-aspartate substitutions have decreased activity. These data suggest that the microtubule-destabilizing activity of SCG10 is regulated by phosphorylation, and that SCG10 may link signal transduction of growth or guidance cues involving serine/threonine protein kinases to alterations of microtubule dynamics in the growth cone.     

Apoptosis and delayed neuronal damage after carbon monoxide poisoning in the rat

Delayed neurological damage after CO hypoxia was studied in rats to determine whether programmed cell death (PCD), in addition to necrosis, is involved in neuronal death. In rats exposed to either air or CO (2500 ppm), microdialysis in brain cortex and hippocampus was performed to determine the extent of glutamate release and hydroxyl radical generation during the exposures. Groups of control and CO-exposed rats also were tested in a radial maze to assess the effects of the CO exposures on learning and memory. At 3, 7, and 21 days after CO exposure brains were perfusion-fixed and hematoxylin-eosin (H&E) was used to assess injury and to select regions for further examination. DNA fragmentation was sought by examining cryosections with the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) reaction. We found significant increases in glutamate release and .OH generation during and immediately after CO hypoxia. CO-exposed rats showed learning and memory deficits after exposure associated with heterogeneous cell loss in cortex, globus pallidus, and cerebellum. The frontal cortex was affected most seriously; the damage was slight at Day 3, increased at Day 7, and persistent at Day 21 after CO exposure. TUNEL staining was positive at all three time points, and TUNEL-labeled cells were distributed similarly to eosinophilic cells. The number of cells stained by TUNEL was less than by H&E and amounted to 2 to 5% of all cell nuclei in regions of injury. Ultrastructural features of both neuronal necrosis and apoptosis also were observed readily by electron microscopy. These findings indicate that both necrosis and apoptosis (PCD) contribute to CO poisoning-induced brain cell death.     

Effect of preoperative supplementation with alpha-tocopherol and ascorbic acid on myocardial injury in patients undergoing cardiac operations

Augmentation of antioxidant defenses may help protect tissues against ischemia-reperfusion injury associated with operations involving cardiopulmonary bypass. In this study we examined the effect of pretreating patients with alpha-tocopherol (vitamin E) and ascorbic acid (vitamin C) or placebo on injury to the myocardium. Seventy-six subjects undergoing elective coronary artery bypass grafting participated in a prospective, double-blind, placebo-controlled randomized trial, receiving either placebo or both 750 IU dl-alpha-tocopherol per day for 7 to 10 days and 1 gm ascorbic acid 12 hours before the operation. Plasma alpha-tocopherol concentrations, raised fourfold by supplementation, fell by 70% after the operation in the supplemented group and to negligible levels in the placebo group. There were no significant differences between the groups with respect to release of creatine kinase MB isoenzyme over 72 hours, nor in the reduction of the myocardial perfusion defect determined by thallium 201 uptake. Electrocardiography provided no evidence of a benefit from antioxidant supplementation. Thus the supplementation regimen prevented the depletion of the primary lipid soluble antioxidant in plasma, but provided no measurable reduction in myocardial injury after the operation.     

Construction of recombination-deficient strains of Streptococcus gordonii by disruption of the recA gene

Degenerate oligonucleotide primers were used in a polymerase chain reaction (PCR) to amplify a region of the recA sequence of Streptococcus gordonii Challis. The resulting PCR fragment was cloned into the suicide vector pAM6199 and introduced into strain Challis, giving rise to recombination-deficient strains in which the recA gene was specifically inactivated.     

The current aspects of seroepidemiological research in combined foci of leishmaniasis

The accuracies of ultrasonography (US) and computed tomography (CT) for determining tumor invasion of the chest wall in lung cancer were compared in a retrospective study of 120 patients. US findings were evaluated preoperatively according to the following criteria: disruption of pleura, extension through the chest wall, and fixation of tumor during breathing. CT findings were evaluated with the following criteria: obtuse angle of the mass to the pleural surface, more than 3 cm contact with the pleural surface, and visible pleural thickening associated with the mass. Chest wall invasion was judged as positive when at least two of the three findings were present with either technique. Nineteen of the 120 patients had chest wall invasion by tumor. The sensitivity of US was 100% and the specificity was 98%. The sensitivity of CT was 68% and the specificity was 66%. The accuracy of US and CT were 98% and 67%, respectively.     

混合信号芯片设计处理关键的转折阶段

通过简单地剪切和粘贴知识产权(IP)内核可以加快无工厂半导体公司的系统级芯片(SOC)设计。 过去十年中,涌现出大量的为系统制造商提供专用芯片(ASIC)的小型IC设计公司。这些被称为无工厂企业(因为他们将IC制造过程转交给商业芯片制造工厂),需要的启动资金较少,而且如果市场接受他们的产品的话,能够获得丰厚的回报。在大量设计工具的支持下,这些无工厂设计企业在历史悠久的大型芯片制造商,如IBM、Intel、Motorola和德州仪器公司所主导的市场中赢得了一席之地。     

Intrathecal fentanyl with small-dose dilute bupivacaine: better anesthesia without prolonging recovery

Recent concern regarding lidocaine neurotoxicity has prompted efforts to find alternatives to lidocaine spinal anesthesia. Small-dose dilute bupivacaine spinal anesthesia yields a comparably rapid recovery profile but may provide insufficient anesthesia. By exploiting the synergism between intrathecal opioids and local anesthetics, it may be possible to augment the spinal anesthesia without prolonging recovery. Fifty patients undergoing ambulatory surgical arthroscopy were randomized into two groups receiving spinal anesthesia with 3 ml 0.17% bupivacaine in 2.66% dextrose without (Group I) or with (Group II) the addition of 10 microg fentanyl. Median block levels reached T7 and T8, respectively (P = not significant [NS]). Mean times to two-segment regression, S2 regression, time out of bed, time to urination, and time to discharge were 53 vs 67 min (P < 0.01), 120 vs 146 min (P < 0.05), 146 vs 163 min (P = NS), 169 vs 177 min (P = NS), and 187 vs 195 min (P = NS) respectively. Motor blockade was similar between groups, but sensory blockade was significantly more intense in Group II (P < 0.01). Six of 25 blocks failed in Group I, whereas none failed in Group II. The addition of 10 microg fentanyl to spinal anesthesia with dilute small-dose bupivacaine intensifies and increases the duration of sensory blockade without increasing the intensity of motor blockade or prolonging recovery to micturition or street fitness. IMPLICATIONS: Concerns about the neurotoxicity of lidocaine have prompted efforts to find alternatives to lidocaine spinal anesthesia. We studied 50 patients undergoing ambulatory surgical arthroscopy and found that although small-dose bupivacaine alone is inadequate for this procedure, the addition of fentanyl makes it reliable.     

Electroconvulsive therapy of acute manic episodes: a review of 50 years' experience

OBJECTIVE: The most common indication for electroconvulsive therapy (ECT) is major depression. It is less recognized that ECT is effective also in the treatment of acute mania. This article aims to provide a comprehensive and critical review of the literature on the use of ECT for manic patients. METHOD: All published papers in the English language on the use of ECT in acute mania that could be found were reviewed with regard to efficacy, frequency and number of treatments, bilateral versus unilateral electrode placement, predictors of antimanic response, stability of therapeutic response, cognitive consequences, and other relevant issues. RESULTS: The evidence indicates that ECT is associated with remission or marked clinical improvement in 80% of manic patients and that it is an effective treatment for patients whose manic episodes have responded poorly to pharmacotherapy. Manic patients do not require a high frequency or prolonged course of treatments to respond to ECT. The seizure threshold appears to be lower in manic patients than in depressed patients. The issues of relapse following response to ECT, cognitive consequences of ECT, and the relative merits of unilateral versus bilateral ECT in manic patients require further study. CONCLUSIONS: ECT is an effective and safe treatment for acute mania. Remission of mania following ECT reflects a primary therapeutic effect rather than a secondary consequence of an ECT-induced organic brain syndrome.