Project Early Rise: Traveltimes and amplitudes

1968 ◽  
Author(s):  
David H. Warren ◽  
J.H. Healy ◽  
J.C. Hoffman ◽  
Reinis Kempe ◽  
Srinivasreddy Rauula ◽  
...  
Keyword(s):  
1974 ◽  
Vol 77 (1_Suppl) ◽  
pp. S7 ◽  
Author(s):  
P. H. Althoff ◽  
J. Happ ◽  
V. Grabs ◽  
B. Schneider ◽  
J. Beyer ◽  
...  
Keyword(s):  

1969 ◽  
Vol 74 (17) ◽  
pp. 4409-4441 ◽  
Author(s):  
H. M. Iyer ◽  
L. C. Pakiser ◽  
D. J. Stuart ◽  
D. H. Warren
Keyword(s):  

1988 ◽  
Vol 22 (3) ◽  
pp. 202-204 ◽  
Author(s):  
Merlin V. Nelson ◽  
Vickie Tutag-Lehr ◽  
R. Lee Evans

Nine normal, healthy male subjects had significantly elevated thyroid-stimulating hormone (TSH) concentrations while receiving oral lithium carbonate for two weeks. The mean minimum lithium serum concentration was 0.765 mEq/L. The TSH concentrations after 15 days on lithium were significantly correlated to the TSH concentration at baseline. No correlation was found between mean minimum lithium steady-state concentration and TSH concentration after 15 days on lithium. Further research is necessary to determine if a high baseline TSH concentration or an early rise in TSH will predict those patients who will eventually develop hypothyroidism after long-term lithium therapy.


1993 ◽  
Vol 264 (3) ◽  
pp. L323-L328 ◽  
Author(s):  
C. G. Salvaterra ◽  
W. F. Goldman

The effects of hypoxia on the cytosolic Ca2+ concentration, [Ca2+]i, were characterized in cultured pulmonary arterial smooth muscle (PASM) cells. Reducing O2 tension (PO2) from 150 to < 25 Torr induced a reversible 100-200% increase in [Ca2+]i that was characterized by two components: an early rise in [Ca2+]i that was dependent on the rate, as well as the magnitude, of decline in PO2 and a later, steady-state increase that was independent of the rate at which PO2 changed. Caffeine lowered [Ca2+]i during normoxia and blocked the early component of the response to hypoxia, whereas the steady-state hypoxic response was only partially inhibited. Like hypoxia, thapsigargin (TG) elevated [Ca2+]i, and there was no additional hypoxia-induced elevation in [Ca2+]i at any time after exposure to TG. At steady state, the hypoxic responses were completely reversed by removal of extracellular Ca2+, whereas, on average, verapamil and nifedipine attenuated the hypoxia-induced increases in [Ca2+]i by only 44 and 35%, respectively. These results suggest that hypoxia-induced elevation of [Ca2+]i in PASM cells consists of an early release of Ca2+ from the sarcoplasmic reticulum and a later influx of extracellular Ca2+, in part, through nifedipine- and verapamil-insensitive Ca2+ channels. The results are consistent with the idea that hypoxia and thapsigargin may share common mechanisms for tonically increasing [Ca2+]i.


2021 ◽  
Vol 9 (10) ◽  
pp. 1379-1385
Author(s):  
Rani Kumaravelu ◽  
Priyadarshini Shanmugam ◽  
Nirupa Soundararajan ◽  
Alice Peace R. ◽  
Perumal Jayaraman

Diagnosis of COVID 19 is based on clinical manifestations, history of exposure, positive CT scan findings and laboratory tests. Inflammation plays a key role in pathogenesis of COVID 19. CRP is an acute phase protein in the serum and is also a surrogate marker for the pro inflammatory cytokine IL 6. Significant rise in CRP indicates clinically relevant inflammation. Aim and Objectives: To analyse the CRP levels in COVID 19 infected patients and to validate CRP as an indicator of the severity of SARS CoV 2 infection. Materials and Methods: This retrospective study was carried out at Chettinad Hospital and Research Institute, a tertiary care hospital situated on the outskirts of Chennai, India, for a period of 4 months. A total of 10263 patients were tested for COVID-19 by RT PCR. Viral RNA Extraction was automated and SARS CoV2 RTPCR performed with ROTOR GENE Q(QIAGEN) using SD Biosensor Real Time PCR kit. The CRP levels were measured using QDx Instacheck Fluorescence immunoassay system, Indianapolis, IN. Results: Among 10263 patients, 2694 (26.2%) patients tested SARS CoV-2 positive. CRP levels were measured for 1472 SARS CoV 2 patients (including both OP and IP). Among them 745 (50.6%) patients were found to be CRP reactive. Of the CRP reactive patients, 7 patients (0.9%) were <18 years, 190 patients (25.5%) were between 18 - 45 years and 548 patients (73.5%) were >45 years. Of the 592 patients with elevated CRP levels, 167 patients were from ICU and 425 patients were from non-ICU. Highly elevated CRP levels of >100mg/L were found in 65% (n=109) of the COVID positive ICU patients and 23% (n=101) of the non-ICU patients. Increased CRP levels were noted in SARS CoV- 2 infected individuals. Elevated CRP was common among elder patients aged >45 years and in males. Conclusion This study concludes that the significant rise of CRP levels was noted in hospitalized SARS CoV 2 positive patients aged > 45 years. Thus, estimating the early rise of serum CRP levels in SARS CoV-2 patients is a well affordable and less invasive parameter to guide the clinicians that is readily available in all the health care centers.


2016 ◽  
Vol 28 (2) ◽  
pp. 237-251 ◽  
Author(s):  
Scott M. Freeman ◽  
Adam R. Aron

Controlling an inappropriate response tendency in the face of a reward-predicting stimulus likely depends on the strength of the reward-driven activation, the strength of a putative top–down control process, and their relative timing. We developed a rewarded go/no-go paradigm to investigate such dynamics. Participants made rapid responses (on go trials) to high versus low reward-predicting stimuli and sometimes had to withhold responding (on no-go trials) in the face of the same stimuli. Behaviorally, for high versus low reward stimuli, responses were faster on go trials, and there were more errors of commission on no-go trials. We used single-pulse TMS to map out the corticospinal excitability dynamics, especially on no-go trials where control is needed. For successful no-go trials, there was an early rise in motor activation that was then sharply reduced beneath baseline. This activation–reduction pattern was more pronounced for high- versus low-reward trials and in individuals with greater motivational drive for reward. A follow-on experiment showed that, when participants were fatigued by an effortful task, they made more errors on no-go trials for high versus low reward stimuli. Together, these studies show that, when a response is inappropriate, reward-predicting stimuli induce early motor activation, followed by a top–down effortful control process (which we interpret as response suppression) that depends on the strength of the preceding activation. Our findings provide novel information about the activation–suppression dynamics during control over reward-driven actions, and they illustrate how fatigue or depletion leads to control failures in the face of reward.


1970 ◽  
Vol 60 (6) ◽  
pp. 1921-1935
Author(s):  
B. M. Gurbuz

Abstract The aim of this paper is to investigate the velocity distribution and structure of the Earth's crust and upper mantle from the close collaboration of theory and experimental results of travel times and spectrum characteristics of body waves. The interpretation was based on 38 seismic records which were obtained from the “Project Early Rise” experiment during July 1966. The results refer to the area bounded by latitudes 49°W and 51°30′ and longitudes 93°W and 98°W. A least-squares analysis of the travel-time data was made and the uncertainties of the slopes, intercept times, and corresponding velocities were determined. The observed wide-angle reflections were used to calculate the root mean square velocities applying the T2 - X2 method. Depth calculations for the velocity discontinuities and seismic depth contour maps were made. A model was constructed, and the validity of the proposed new model was tested by comparing the observed travel times, spectrum-amplitude ratios, and relative phase shifts of body waves with theoretically expected values. Evidence is given for three discontinuities in the Earth's crust with velocities of 6.11 ± 0.01 km/sec, 6.8 ± 0.08 km/sec, and 7.10 ± 0.04 km/sec at average depths 18 ± 2 km and 25.5 ± 0.9 km. Velocities in the uppermost part of the mantle were determined as 7.90 ± 0.05 km/sec and 8.48 ± 0.05 km/sec with interfaces at the average depths of 34 ± 1 km, and 47 ± 1 km, respectively.


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