Institution
Louisiana State University
Education•Baton Rouge, Louisiana, United States•
About: Louisiana State University is a education organization based out in Baton Rouge, Louisiana, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 40206 authors who have published 76587 publications receiving 2566076 citations. The organization is also known as: LSU & Louisiana State University and Agricultural and Mechanical College.
Topics: Population, Poison control, Wetland, Autism, Sediment
Papers published on a yearly basis
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TL;DR: The evidence supporting the view that oxidants and leukocytes contribute to the pathogenesis of reperfusion injury is summarized and the mechanisms underlying the protective actions of ischemic preconditioning are discussed.
Abstract: Early restitution of blood flow to ischemic tissues is essential to halt the progression of cellular injury associated with decreased oxygen and nutrient delivery. Recognition of this fact provides the basis for the traditional view that minimizing ischemic time is the only important intervention for diminish ing the extent of ischemic injury. However. it is now clear that reperfusion of ischemic tissues initiates a complex series of reactions that paradoxically injures tissues. Although several mechanisms have been proposed to explain the pathogenesis of ischemialreperfusion (IIR) injury. most attention has fo cused on a role for reactive oxygen metabolites and inflammatory leukocytes. This work has led to the proposal that' free radical ablation or inhibition of postischemic neutrophil infiltration may prove useful for therapeutic interven tion in I1R. In addition to these mechanisms. recent evidence suggests that prior exposure to brief periods of ischemia (ischemic preconditioning) prevents the development of cellular injury induced by a subsequent prolonged inter ruption in blood flow. By elucidating the cellular events underlying precondi tioning. additional mechanisms contributing to the pathogenesis of I/R may become apparent. This review summarizes the evidence supporting the view that oxidants and leukocytes contribute to the pathogenesis of reperfusion injury and discusses the mechanisms underlying the protective actions of ischemic preconditioning.
436 citations
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TL;DR: The study of the fungal microbiota is a new and rapidly emerging field that lags behind the authors' understanding of the bacterial microbiome, especially as a reservoir for blooms of pathogenic microbes when the host is compromised and as a potential cofactor in inflammatory diseases and metabolic disorders.
435 citations
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TL;DR: C cerebral ischemia recruits death-associated protein kinase 1 (DAPK1) into the NMDA receptor NR2B protein complex in the cortex of adult mice and this interaction acts as a central mediator for stroke damage.
434 citations
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Henry Ford Health System1, University of Utah2, Johns Hopkins University3, Virginia Mason Medical Center4, University of Chicago5, Veterans Health Administration6, Saint Louis University7, Pomona College8, Eastern Virginia Medical School9, Cincinnati Children's Hospital Medical Center10, Wayne State University11, Georgetown University12, Wake Forest Baptist Medical Center13, Morehouse School of Medicine14, Florida Atlantic University15, Louisiana State University16
TL;DR: This clinical practice guideline was undertaken to optimize the care of patients with AR by addressing quality improvement opportunities through an evaluation of the available evidence and an assessment of the harm-benefit balance of various diagnostic and management options.
Abstract: Objective. Allergic rhinitis (AR) is one of the most common diseases affecting adults. It is the most common chronic disease in children in the United States today and the fifth most common chronic disease in the United States overall. AR is estimated to affect nearly 1 in every 6 Americans and generates $2 to $5 billion in direct health expenditures annually. It can impair quality of life and, through loss of work and school attendance, is responsible for as much as $2 to $4 billion in lost productivity annually. Not surprisingly, myriad diagnostic tests and treatments are used in managing this disorder, yet there is considerable variation in their use. This clinical practice guideline was undertaken to optimize the care of patients with AR by addressing quality improvement opportunities through an evaluation of the available evidence and an assessment of the harm-benefit balance of various diagnostic and management options. Purpose. The primary purpose of this guideline is to address quality improvement opportunities for all clinicians, in any setting, who are likely to manage patients with AR as well as to optimize patient care, promote effective diagnosis and therapy, and reduce harmful or unnecessary variations in care. The guideline is intended to be applicable for both pediatric and adult patients with AR. Children under the age of 2 years were excluded from the clinical practice guideline because rhinitis in this population may be different than in older patients and is not informed by the same evidence base. The guideline is intended to focus on a limited number of quality improvement opportunities deemed most important by the working group and is not intended to be a comprehensive reference for diagnosing and managing AR. The recommendations outlined in the guideline are not intended to represent the standard of care for patient management, nor are the recommendations intended to limit treatment or care provided to individual patients. Action Statements. The development group made a strong recommendation that clinicians recommend intranasal steroids for patients with a clinical diagnosis of AR whose symptoms affect their quality of life. The development group also made a strong recommendation that clinicians recommend oral second-generation/less sedating antihistamines for patients with AR and primary complaints of sneezing and itching. The panel made the following recommendations: (1) Clinicians should make the clinical diagnosis of AR when patients present with a history and physical examination consistent with an allergic cause and 1 or more of the following symptoms: nasal congestion, runny nose, itchy nose, or sneezing. Findings of AR consistent with an allergic cause include, but are not limited to, clear rhinorrhea, nasal congestion, pale discoloration of the nasal mucosa, and red and watery eyes. (2) Clinicians should perform and interpret, or refer to a clinician who can perform and interpret, specific IgE (skin or blood) allergy testing for patients with a clinical diagnosis of AR who do not respond to empiric treatment, or when the diagnosis is uncertain, or when knowledge of the specific causative allergen is needed to target therapy. (3) Clinicians should assess patients with a clinical diagnosis of AR for, and document in the medical record, the presence of associated conditions such as asthma, atopic dermatitis, sleep-disordered breathing, conjunctivitis, rhinosinusitis, and otitis media. (4) Clinicians should offer, or refer to a clinician who can offer, immunotherapy (sublingual or subcutaneous) for patients with AR who have inadequate response to symptoms with pharmacologic therapy with or without environmental controls.
433 citations
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TL;DR: The change in intestinal lavage fluid volume indicated that reabsorptive processes dominated in the sham and TNBS + L-NAME groups, and secretory responses predominated in TNBS andTNBS + D-NAME animals.
Abstract: Nitric oxide synthesis appears to be elevated in inflammatory bowel disease, but little is known about the contribution of nitric oxide to the pathophysiological process. To address this issue, we included the nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) in the drinking water (10 or 100 micrograms/ml) of guinea pigs immediately after induction of ileitis by intraluminal trinitrobenzenesulfonic acid (TNBS 30 mg/kg in 50% ethanol). Guinea pigs were sacrificed after 7 days of this ad libitum treatment. Control groups received either intraluminal TNBS, saline or ethanol (TNBS vehicle) without L-NAME or TNBS + D-NAME (100 micrograms/ml), the inactive enantiomer. Immediately before sacrifice, guinea pigs were anesthetized and saline was administered intraluminally at the site of TNBS or saline administration and then withdrawn after 30 min. Change in lavage volume and lavage protein and nitrite levels were measured, as well as tissue myeloperoxidase and bowel wall thickness (weight/length). TNBS administration resulted in an increase in tissue thickness, myeloperoxidase and lavage protein and nitrite levels over sham controls. Oral L-NAME prevented these responses. D-NAME was ineffective with the exception of tissue thickness. The change in intestinal lavage fluid volume indicated that reabsorptive processes dominated in the sham and TNBS + L-NAME groups, and secretory responses predominated in TNBS and TNBS + D-NAME animals. In contrast to TNBS-induced ileitis, L-NAME (100 micrograms/ml, p.o., 7 days) administration to intact animals resulted in a local inflammatory response (i.e., increased myeloperoxidase activity and a fluid secretory response).(ABSTRACT TRUNCATED AT 250 WORDS)
432 citations
Authors
Showing all 40485 results
Name | H-index | Papers | Citations |
---|---|---|---|
H. S. Chen | 179 | 2401 | 178529 |
John A. Rogers | 177 | 1341 | 127390 |
Omar M. Yaghi | 165 | 459 | 163918 |
Barry M. Popkin | 157 | 751 | 90453 |
John E. Morley | 154 | 1377 | 97021 |
Claude Bouchard | 153 | 1076 | 115307 |
Ruth J. F. Loos | 142 | 647 | 92485 |
Ali Khademhosseini | 140 | 887 | 76430 |
Shanhui Fan | 139 | 1292 | 82487 |
Joseph E. LeDoux | 139 | 478 | 91500 |
Christopher T. Walsh | 139 | 819 | 74314 |
Kenneth A. Dodge | 138 | 468 | 79640 |
Steven B. Heymsfield | 132 | 679 | 77220 |
George A. Bray | 131 | 896 | 100975 |
Zhanhu Guo | 128 | 886 | 53378 |