Institution
University at Buffalo
Education•Buffalo, New York, United States•
About: University at Buffalo is a education organization based out in Buffalo, New York, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 33773 authors who have published 63840 publications receiving 2278954 citations. The organization is also known as: UB & State University of New York at Buffalo.
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University of California, Irvine1, Columbia University2, Ohio State University3, McGill University4, University of California, Los Angeles5, University at Buffalo6, New York University7, Icahn School of Medicine at Mount Sinai8, University of Vermont9, University of Illinois at Chicago10, McGill University Health Centre11, Duke University12, Brookhaven National Laboratory13
TL;DR: Stimulant-naïve school-age children with Combined type attention-deficit/hyperactivity disorder were, as a group, larger than expected from norms before treatment but show stimulant-related decreases in growth rates after initiation of treatment, which appeared to reach asymptotes within 3 years without evidence of growth rebound.
Abstract: Objective: To evaluate the hypothesis of stimulant medication effect on physical growth in the follow-up phase of the Multimodal Treatment Study of Children With ADHD. Method: Naturalistic subgroups were established based on patterns of treatment with stimulant medication at baseline, 14-, 24-, and 36-month assessments: not medicated ( n = 65), newly medicated ( n = 88), consistently medicated ( n = 70), and inconsistently medicated ( n = 147). Analysis of variance was used to evaluate effects of subgroup and assessment time on measures of relative size ( z scores) obtained from growth norms. Results: The subgroup × assessment time interaction was significant for z height ( p z weight ( p z scores significantly >0 at baseline. The newly medicated subgroup showed decreases in relative size that reached asymptotes by the 36-month assessment, when this group showed average growth of 2.0 cm and 2.7 kg less than the not medicated subgroup, which showed slight increases in relative size. Conclusions: Stimulant-naive school-age children with Combined type attention-deficit/hyperactivity disorder were, as a group, larger than expected from norms before treatment but show stimulant-related decreases in growth rates after initiation of treatment, which appeared to reach asymptotes within 3 years without evidence of growth rebound.
307 citations
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TL;DR: Cost-sharing, or the shift in at least part of the higher educational cost burden from governments (or taxpayers) to parents and students, is a worldwide trend manifested in the introduction of (or in sharp increases in) tuition fees, user charges for lodging and food, and in the diminution of student grants.
307 citations
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307 citations
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TL;DR: Observations indicate that somatostatin and some of its analogues can act as growth inhibitors in cancer cells through the activation of tyrosine phosphatase.
Abstract: Several analogues of somatostatin were examined in the Mia PaCa-2 human pancreatic cancer cell line for their ability to promote tyrosine phosphatase activity affecting the receptors for the epidermal growth factor. The inhibition of growth of the Mia PaCa-2 cells in culture was also evaluated to determine the mechanism of action of somatostatin analogues and their relative effectiveness in inhibiting cancer growth. Of the analogues tested D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Trp-NH2 (RC-160) caused the greatest stimulation of tyrosine phosphatase activity. Analogue D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Thr-NH2 (RC-121) had less effect but was more potent than somatostatin-14. Analogue D-Phe-Cys-Phe-D-Trp-Lys-Thr-Cys-Thr(ol) (SMS 201-995) produced no significant dephosphorylation. The analogues displayed the same order of activity in assays on growth inhibition of Mia PaCa-2 cells in cultures. Analogue (SMS-201-995) caused virtually no tyrosine phosphatase stimulation or growth inhibition in this cancer cell line, although it possesses a much higher antisecretory activity than somatostatin-14 in normal tissues. These observations indicate that somatostatin and some of its analogues can act as growth inhibitors in cancer cells through the activation of tyrosine phosphatase. These data reinforce the view that somatostatin analogue RC-160 and related compounds could be used for treatment of pancreatic cancer.
307 citations
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TL;DR: In this paper, the activation energy for crystal growth is 11.0 ± 1.0 kcal mole−1, and the rate is independent of the stirring rate, and photomicrographic evidence is presented in support of the suggestion that the initial surge in the growth curves results from additional nucleation at the surface of the added calcite crystals and in the bulk of the supersaturated solution.
307 citations
Authors
Showing all 34002 results
Name | H-index | Papers | Citations |
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Rakesh K. Jain | 200 | 1467 | 177727 |
Julie E. Buring | 186 | 950 | 132967 |
Anil K. Jain | 183 | 1016 | 192151 |
Donald G. Truhlar | 165 | 1518 | 157965 |
Roger A. Nicoll | 165 | 397 | 84121 |
Bruce L. Miller | 163 | 1153 | 115975 |
David R. Holmes | 161 | 1624 | 114187 |
Suvadeep Bose | 154 | 960 | 129071 |
Ashok Kumar | 151 | 5654 | 164086 |
Philip S. Yu | 148 | 1914 | 107374 |
Hugh A. Sampson | 147 | 816 | 76492 |
Aaron Dominguez | 147 | 1968 | 113224 |
Gregory R Snow | 147 | 1704 | 115677 |
J. S. Keller | 144 | 981 | 98249 |
C. Ronald Kahn | 144 | 525 | 79809 |