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.     

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.     

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.     

Androgen-dependent protein interactions within an intron 1 regulatory region of the 20-kDa protein gene

The 20-kDa protein gene is androgen regulated in rat ventral prostate. Intron 1 contains a 130-base pair complex response element (D2) that binds androgen (AR) and glucocorticoid receptor (GR) but transactivates only with AR in transient cotransfection assays in CV1 cells using the reporter vector D2-tkCAT. To better understand the function of this androgen-responsive unit, nuclear protein interactions with D2 were analyzed by DNase I footprinting in ventral prostate nuclei of intact or castrated rats and in vitro with ventral prostate nuclear protein extracts from intact, castrated, and testosterone-treated castrated rats. Multiple androgen-dependent protected regions and hypersensitive sites were identified in the D2 region with both methods. Mobility shift assays with 32P-labeled oligonucleotides spanning D2 revealed specific interactions with ventral prostate nuclear proteins. Four of the D2-protein complexes decreased in intensity within 24 h of castration. UV cross-linking of the androgen-dependent DNA binding proteins identified protein complexes of approximately 140 and 55 kDa. The results demonstrate androgen-dependent nuclear protein-DNA interactions within the complex androgen response element D2.     

Long-term effect of lisinopril and atenolol on kidney function in hypertensive NIDDM subjects with diabetic nephropathy

The aim of our study was to evaluate whether inhibition of ACE (lisinopril 10-20 mg/day) can reduce the rate of decline in kidney function more than reducing blood pressure with conventional antihypertensive treatment (atenolol 50-100 mg/day), usually in combination with a diuretic. We performed a prospective, randomized, parallel study for 42 months, double blind for the first 12 months and single blind thereafter. Forty-three (21 lisinopril and 22 atenolol) hypertensive NIDDM patients with diabetic nephropathy were enrolled. Data from 36 patients (17 lisinopril and 19 atenolol, 60 +/- 7 years of age, 27 men) who completed at least 12 months of the study period are presented. At baseline, the two groups were comparable: glomerular filtration rate (51Cr-EDTA plasma clearance) was 75 +/- 6 and 74 +/- 8 ml x min(-1) x 1.73 m(-2), mean 24-h ambulatory blood pressure (A&D TM2420) was 110 +/- 3 and 114 +/- 2 mmHg, and 24-h urinary albumin excretion rate was 961 (range 331-5,727) and 1,578 (476-5,806) mg/24 h in the lisinopril and atenolol groups, respectively. The mean follow-up time was similar, 37 and 35 months in the lisinopril and atenolol groups, respectively. Mean ambulatory blood pressure was equally reduced in the two groups, 12 +/- 2 and 10 +/- 2 mmHg in the lisinopril and atenolol groups, respectively. Glomerular filtration rate declined in a biphasic manner with a faster initial (0 to 6 months) change of 1.25 +/- 0.49 and 0.81 +/- 0.29 ml x min(-1) x month(-1) followed by a slower sustained decline (6 to 42 months) of 0.59 +/- 0.10 and 0.54 +/- 0.13 ml x min(-1) x month(-1) in the lisinopril and atenolol groups, respectively. No significant differences were observed in either initial or sustained decline in glomerular filtration rate between the two groups. Urinary albumin excretion was reduced (% reduction of baseline) more in the lisinopril than in the atenolol group, at 55 (95% CI 29-72) and 15% (-13 to 34), respectively (P = 0.01). In conclusion, the relentless decline in kidney function characteristically found in hypertensive NIDDM patients with diabetic nephropathy can be reduced equally effectively by two antihypertensive treatments, the beta-blocker atenolol and the ACE inhibitor lisinopril.     

Insulin-like growth factors-I and -II stimulate chemotaxis of osteoblasts isolated from fetal rat calvaria

Repair and regeneration of damaged bone is believed to be regulated in part by growth factors stored in the bone matrix. These growth factors are synthesized and secreted by osteoblasts and are incorporated into the developing bone. This pool of stored growth factors is then released into the immediate area following resorption of the matrix. One of the initial steps in bone repair is the recruitment of osteoblasts to the repair site. Growth factors, such as TGF-beta and PDGF, which are present in bone matrix, have been shown to be chemotactic for osteoblasts. In this study, primary cultures of osteoblasts isolated from fetal rat calvaria were examined for chemotaxis in response to IGF-I and IGF-II. IGF-I stimulated a dose-dependent increase in osteoblast chemotaxis, while IGF-II stimulated chemotaxis maximally at the lowest concentration studied (0.1 ng/ml), and had no effect at the highest concentration studied (100 ng/ml). IGF-I and -II had no effect on osteoblast proliferation at any of the concentrations examined. These results indicate that IGFs may be playing an important role in the early stages of bone repair by stimulating osteoblast chemotaxis to the repair site.     

Prostate enlargement in mice due to fetal exposure to low doses of estradiol or diethylstilbestrol and opposite effects at high doses

On the basis of results of studies using high doses of estrogens, exposure to estrogen during fetal life is known to inhibit prostate development. However, it is recognized in endocrinology that low concentrations of a hormone can stimulate a tissue, while high concentrations can have the opposite effect. We report here that a 50% increase in free-serum estradiol in male mouse fetuses (released by a maternal Silastic estradiol implant) induced a 40% increase in the number of developing prostatic glands during fetal life; subsequently, in adulthood, the number of prostatic androgen receptors per cell was permanently increased by 2-fold, and the prostate was enlarged by 30% (due to hyperplasia) relative to untreated males. However, as the free serum estradiol concentration in male fetuses was increased from 2- to 8-fold, adult prostate weight decreased relative to males exposed to the 50% increase in estradiol. As a model for fetal exposure to man-made estrogens, pregnant mice were fed diethylstilbestrol (DES) from gestation days 11 to 17. Relative to controls, DES doses of 0.02, 0.2, and 2.0 ng per g of body weight per day increased adult prostate weight, whereas a 200-ng-per-g dose decreased adult prostate weight in male offspring. Our findings suggest that a small increase in estrogen may modulate the action of androgen in regulating prostate differentiation, resulting in a permanent increase in prostatic androgen receptors and prostate size. For both estradiol and DES, prostate weight first increased then decreased with dose, resulting in an inverted-U dose-response relationship.     

Determining flow rate in discharge pipes by measuring velocity at one point of the outlet section of a convergent duct

Results are presented from a study of a method for determining flow rate in discharge pipes by measuring velocity at one point of the outlet section of a convergent duct that smoothly connects two pipes of different diameters. A metrological analysis, of the measurement method is presented. Translated from Izmeritel'naya Teknika, No. 4, pp. 40–45, April, 1996     

Low-flow measurements with roller/blade tachometric chamber transducers

Three roller/blade tachometric chamber transducers, with capacities of 2, 10, and 20 cm³/rev, have been designed for measuring low flow rates. Translated from Izmeritel'naya Tekhnika, No. 5, pp. 37–41, May, 1996.