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Institution

Indiana University

EducationBloomington, Indiana, United States
About: Indiana University is a education organization based out in Bloomington, Indiana, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 64480 authors who have published 150058 publications receiving 6392902 citations. The organization is also known as: Indiana University system & indiana.edu.


Papers
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Journal ArticleDOI
TL;DR: More of the public embraces a neurobiological understanding of mental illness, which translates into support for services but not into a decrease in stigma.
Abstract: Objective:Clinicians, advocates, and policy makers have presented mental illnesses as medical diseases in efforts to overcome low service use, poor adherence rates, and stigma. The authors examined the impact of this approach with a 10-year comparison of public endorsement of treatment and prejudice. Method:The authors analyzed responses to vignettes in the mental health modules of the 1996 and 2006 General Social Survey describing individuals meeting DSM-IV criteria for schizophrenia, major depression, and alcohol dependence to explore whether more of the public 1) embraces neurobiological understandings of mental illness; 2) endorses treatment from providers, including psychiatrists; and 3) reports community acceptance or rejection of people with these disorders. Multivariate analyses examined whether acceptance of neurobiological causes increased treatment support and lessened stigma. Results:In 2006, 67% of the public attributed major depression to neurobiological causes, compared with 54% in 1996. Hi...

1,054 citations

Journal ArticleDOI
TL;DR: A variety of potentially therapeutic growth factors were detected and released from the platelets in significant levels in platelet-rich plasma preparations and may be capable of expediting wound healing in a variety of as yet undetermined specific wound applications.
Abstract: Growth factors released from activated platelets initiate and modulate wound healing in both soft and hard tissues. A recent strategy to promote the wound-healing cascade is to prepare an autologous platelet concentrate suspended in plasma, also known as platelet-rich plasma, that contains growth factors and administer it to wound sites. The purpose of this study was to quantitate platelet number and growth factors released from a prepared platelet concentrate. Whole blood was drawn from 10 healthy patients undergoing cosmetic surgery and concentrated into platelet-rich plasma. Platelet counts on whole blood and platelet-rich plasma were determined using a Cell-Dyn 3200. Platelet-derived growth factor-BB, transforming growth factor-[beta]1, vascular endothelial growth factor, endothelial growth factor, and insulin-like growth factor-1 were measured in the platelet-rich plasma using the enzyme-linked immunosorbent assay method. In addition, platelet activation during the concentration procedure was analyzed by measuring P selectin values in blood serum. An 8-fold increase in platelet concentration was found in the platelet-rich plasma compared with that of whole blood (baseline whole blood, 197 ± 42 × 10 3

1,054 citations

Journal ArticleDOI
TL;DR: Relationship between interferon‐γ, indoleamine 2,3‐dioxygenase, and tryptophan catabolism and a possible role for IDO in O2‐radical scavenging and in inflammation is discussed.
Abstract: Interferons have been shown to be potential anti-cancer agents and to inhibit tumor cell growth in culture. The in vivo mechanism of the anti-proliferative effect may be direct or indirect through the immune system; however, in vitro a primary mechanism of cytotoxicity is through the depletion of tryptophan. In particular, interferon-gamma (IFN-gamma) induces an enzyme of tryptophan catabolism, indoleamine 2,3-dioxygenase (IDO), which is responsible for conversion of tryptophan and other indole derivatives to kynurenine. The inhibitory effect of interferon on many intracellular parasites such as Toxoplasma gondii and Chlamydia trachomatis is by the same mechanism. Elevated kynurenine levels have been found in humans in a number of diseases and after interferon treatment, and the enzyme is induced in rodents after administration of interferon inducers, or influenza virus. IDO induction also occurs in vivo during rejection of allogeneic tumors, indicating a possible role for this enzyme in the tumor rejection process. The gene for IDO has been cloned and shown to be differentially regulated by IFN-alpha and IFN-gamma. IDO induction has been correlated with induction of GTP-cyclohydrolase, the key enzyme in pteridine biosynthesis. A direct role for IDO in pteridine synthesis has not been shown, and this parallel induction may reflect coordinate regulation of genes induced by IFN-gamma. A possible role for IDO in O2-radical scavenging and in inflammation is discussed.

1,053 citations

Journal ArticleDOI
TL;DR: A number of methods for detecting modules in both structural and functional brain networks are surveyed and their potential functional roles in brain evolution, wiring minimization, and the emergence of functional specialization and complex dynamics are considered.
Abstract: The development of new technologies for mapping structural and functional brain connectivity has led to the creation of comprehensive network maps of neuronal circuits and systems. The architecture of these brain networks can be examined and analyzed with a large variety of graph theory tools. Methods for detecting modules, or network communities, are of particular interest because they uncover major building blocks or subnetworks that are particularly densely connected, often corresponding to specialized functional components. A large number of methods for community detection have become available and are now widely applied in network neuroscience. This article first surveys a number of these methods, with an emphasis on their advantages and shortcomings; then it summarizes major findings on the existence of modules in both structural and functional brain networks and briefly considers their potential functional roles in brain evolution, wiring minimization, and the emergence of functional specialization...

1,048 citations

Journal ArticleDOI
TL;DR: Results show that SNPs in the mu opioid receptor gene can alter binding and signal transduction in the resulting receptor and may have implications for normal physiology, therapeutics, and vulnerability to develop or protection from diverse diseases including the addictive diseases.
Abstract: Opioid drugs play important roles in the clinical management of pain, as well as in the development and treatment of drug abuse. The mu opioid receptor is the primary site of action for the most commonly used opioids, including morphine, heroin, fentanyl, and methadone. By sequencing DNA from 113 former heroin addicts in methadone maintenance and 39 individuals with no history of drug or alcohol abuse or dependence, we have identified five different single-nucleotide polymorphisms (SNPs) in the coding region of the mu opioid receptor gene. The most prevalent SNP is a nucleotide substitution at position 118 (A118G), predicting an amino acid change at a putative N-glycosylation site. This SNP displays an allelic frequency of approximately 10% in our study population. Significant differences in allele distribution were observed among ethnic groups studied. The variant receptor resulting from the A118G SNP did not show altered binding affinities for most opioid peptides and alkaloids tested. However, the A118G variant receptor binds β-endorphin, an endogenous opioid that activates the mu opioid receptor, approximately three times more tightly than the most common allelic form of the receptor. Furthermore, β-endorphin is approximately three times more potent at the A118G variant receptor than at the most common allelic form in agonist-induced activation of G protein-coupled potassium channels. These results show that SNPs in the mu opioid receptor gene can alter binding and signal transduction in the resulting receptor and may have implications for normal physiology, therapeutics, and vulnerability to develop or protection from diverse diseases including the addictive diseases.

1,048 citations


Authors

Showing all 64884 results

NameH-indexPapersCitations
Frank B. Hu2501675253464
Stuart H. Orkin186715112182
Bruce M. Spiegelman179434158009
David R. Williams1782034138789
D. M. Strom1763167194314
Markus Antonietti1761068127235
Lei Jiang1702244135205
Brenda W.J.H. Penninx1701139119082
Nahum Sonenberg167647104053
Carl W. Cotman165809105323
Yang Yang1642704144071
Jaakko Kaprio1631532126320
Ralph A. DeFronzo160759132993
Gavin Davies1592036149835
Tyler Jacks158463115172
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023127
2022694
20217,272
20207,310
20196,943
20186,496