Tantalum-based diffusion barriers in Si/Cu VLSI metallizations

We have studied sputter-deposited Ta, Ta36Si14, and Ta36Si14N50 thin films as diffusion barriers between Cu overlayers and Si substrates. Electrical measurements on Si n + p shallow junction diodes demonstrate that a 180-nm-thick Ta film is not an effective diffusion barrier. For the standard test of 30-min annealing in vacuum applied in the present study, the Ta barrier fails after annealing at 500 °C. An amorphous Ta74Si26 thin film improves the performance by raising the failure temperature of a /Ta74Si26(100 nm)/Cu(500 nm) metallization to 650 °C. Unparalled results are obtained with an amorphous ternary Ta36Si14N50 thin film in the Si/Ta36Si14N50 (120 nm)/Cu(500 nm) and in the Si/TiSi2(30 nm)/Ta36SiN50 (80 nm)/Cu(500 nm) metallization that break down only after annealing at 900 °C. The failure is induced by a premature crystallization of the Ta36Si14N50 alloy (whose crystallization temperature exceeds 1000 °C) when in contact with copper

Thermal oxidation of reactively sputtered amorphous W_(80)N_(20) films

The oxidation behavior of reactively sputtered amorphous tungsten nitride of composition W_(80)N_(20) was investigated in dry and wet oxidizing ambient in the temperature range of 450 °C–575 °C. A single WO_3 oxide phase is observed. The growth of the oxide follows a parabolic time dependence which is attributed to a process controlled by the diffusivity of the oxidant in the oxide. The oxidation process is thermally activated with an activation energy of 2.5 ± 0.05 eV for dry ambient and 2.35 ± 0.05 eV for wet ambient. The pre‐exponential factor of the reaction constant for dry ambient is 1.1×10^(21) Å^2/min; that for wet ambient is only about 10 times less and is equal to 1.3×10^(20) Å^2/min

Thermal oxidation of amorphous ternary Ta36Si14N50 thin films

The oxidation kinetics of reactively sputtered amorphous Ta36Si14N50 thin films are studied in dry and wet ambient in the temperature range of 650-850-degrees-C by backscattering spectrometry, Dektak profilometer, and x-ray diffraction analyses. The dry oxidation is well described by a parabolic time dependence which corresponds to a process controlled by the diffusion of the oxidant in the oxide. The growth of the oxide in wet ambient is initially very rapid and then proceeds linearly which means that the process is reaction limited. Both oxidation rates are thermally activated. The activation energies are 2.0 eV for dry and 1.4 eV for wet ambient. The pre-exponential factors are 0.17 x 10^(16) angstrom 2/min and 7.4 x 10^(8) angstrom/min, respectively. Both the dry and wet oxidation of the amorphous ternary Ta36Si14N50 film result in the formation of an x-ray amorphous Ta14Si5.5O80 layer

Electrocautery causes more ischemic peritoneal tissue damage than ultrasonic dissection

Contains fulltext : 96869.pdf (publisher's version ) (Open Access)BACKGROUND: Minimizing peritoneal tissue injury during abdominal surgery has the benefit of reducing postoperative inflammatory response, pain, and adhesion formation. Ultrasonic dissection seems to reduce tissue damage. This study aimed to compare electrocautery and ultrasonic dissection in terms of peritoneal tissue ischemia measured by microdialysis. METHODS: In this study, 18 Wistar rats underwent a median laparotomy and had a peritoneal microdialysis catheter implanted in the left lateral sidewall. The animals were randomly assigned to receive two standard peritoneal incisions parallel to the catheter by either ultrasonic dissection or electrocautery. After the operation, samples of microdialysis dialysate were taken every 2 h until 72 h postoperatively for measurements of pyruvate, lactate, glucose, and glycerol, and ratios were calculated. RESULTS: The mean lactate-pyruvate ratio (LPR), lactate-glucose ratio (LGR), and glycerol concentration were significantly higher in the electrocautery group than in the ultrasonic dissection group until respectively 34, 48, and 48 h after surgery. The mean areas under the curve (AUC) of LPR, LGR, and glycerol concentration also were higher in the electrocautery group than in the ultrasonic dissection group (4,387 vs. 1,639, P=0.011; 59 vs. 21, P=0.008; 7,438 vs. 4,169, P=0.008, respectively). CONCLUSION: Electrosurgery causes more ischemic peritoneal tissue damage than ultrasonic dissection.01 juni 201

Predictors of brain injury after experimental hypothermic circulatory arrest:an experimental study using a chronic porcine model

Abstract There is a lack of reliable methods of evaluation of brain ischemic injury in patients undergoing cardiac surgery. The present study was, therefore, planned to evaluate whether serum S100β protein (I), brain cortical microdialysis (II), intracranial pressure (III) and electroencephalography (EEG) (IV) are predictive of postoperative death and brain ischemic injury in an experimental surviving porcine model of hypothermic circulatory arrest (HCA). One hundred and twenty eight (128) female, juvenile (8 to 10 weeks of age) pigs of native stock, weighing 21.0 to 38.2 kg, underwent cardio-pulmonary bypass prior to, and following, a 75-minute period of HCA at a brain temperature of 18°C. During the operation, hemodynamic, electrocardiograph and temperature monitoring was performed continuously. Furthermore, metabolic parameters were monitored at baseline, end of cooling, at intervals of two, four and eight hours after HCA and before extubation. Electroencephalographic recording was performed in all animals, serum S100β protein measurement in 18 animals, cortical microdialysis in 109 animals, and intracranial pressure monitoring in 58 animals. After the operation, assessment of behavior was made on a daily basis until death or elective sacrifice on the seventh postoperative day. All four studies showed that these parameters were predictive of postoperative outcome. Animals with severe histopathological injury had higher serum S100β protein levels at every time interval after HCA. Analysis of cortical brain microdialysis showed that the lactate/glucose ratio was significantly lower and the brain glucose concentration significantly higher among survivors during the early postoperative hours. Intracranial pressure increased significantly after 75 minutes of HCA, and this was associated with a significantly increased risk of postoperative death and brain infarction. A slower recovery of EEG burst percentage after HCA was significantly associated with the development of severe cerebral cortex, brain stem and cerebellum ischemic injury. In conclusion, serum S100β protein proved to be a reliable marker of brain ischemic injury as assessed on histopathological examination. Cerebral microdialysis is a useful method of cerebral monitoring during experimental HCA. Low brain glucose concentrations and high brain lactate/ glucose ratios after HCA are strong predictors of postoperative death. Increased intracranial pressure severely affected the postoperative outcome and may be a potential target for treatment. EEG burst percentage as a sum effect of anesthetic agent and ischemic brain damage is a useful tool for early prediction of severe brain damage after HCA. Among these monitoring methods, brain cortical microdialysis seems to be the most powerful one in predicting brain injury after experimental hypothermic circulatory arrest