bluuebunny/crossref_metadata_2025_split huggingface dataset:
Field testing of an enhanced direct-fecal polymerase chain reaction procedure, bacterial culture of feces, and a serum enzyme-linked immunosorbent assay for detecting Mycobacterium avium subsp paratuberculosis infection in adult dairy cattle
Authors: Scott H. Morgan , Fosgate Geoffrey T. , Libal Melissa C. , Sneed Lloyd W. , Erol Erdal , Angulo Arthur B. , Jordan Ellen R. 
Published: March 2007

Abstract
Objective—To estimate the sensitivity (Se) and specificity (Sp) for an enhanced direct-fecal PCR procedure, bacterial culture of feces (BCF), and a serum ELISA for detecting Mycobacterium avium subsp paratuberculosis (MAP) infection in adult dairy cattle.
Sample Population—Fecal and serum samples were collected from 669 adult cattle randomly selected from a 4,000-cow dairy herd known to contain animals infected with MAP.
Procedures—Serum samples were evaluated for MAP-specific antibodies via ELISA. Fecal samples were evaluated by BCF and enhanced PCR methods (both gel-based [GB]-PCR and quantitative real-time [qRT]-PCR assays). Fecal samples also were pooled (5:1) and then subjected to GB-PCR assay. Bayesian statistical methods were used to estimate Se and Sp for each diagnostic test without knowledge concerning true MAP infection status.
Results—Adjusting for Se conditional dependence between serum ELISA and BCR, overall Se and Sp were estimated at 33.7% and 95.9%, 51.3% and 99.0%, and 32.2% and 100% for serum ELISA, qRT-PCR, and BCF, respectively.The GB-PCR assay yielded positive results for 38.3% of the pools known to contain feces from at least 1 cow that had positive GBPCR results.
Conclusions and Clinical Relevance—Estimated Se values for the serum ELISA and BCF were slightly lower than those reported elsewhere. The enhanced qRT-PCR method offered relative improvements in Se of 52% and 59% over serum ELISA and microbial culture, respectively. Pooling of fecal samples and testing with the GB-PCR assay are not recommended. Additional studies with qRT-PCR and fecal pools are required.
Changes in platelet function, hemostasis, and prostaglandin expression after treatment with nonsteroidal anti-inflammatory drugs with various cyclooxygenase selectivities in dogs
Authors: Brainard Benjamin M. , Meredith Craig P. , Callan Mary Beth , Budsberg Steven C. , Shofer Francis S. , Driessen Bernd , Otto Cynthia M. 
Published: March 2007

Abstract
Objective—To determine the effects of nonsteroidal anti-inflammatory drugs of various cyclooxygenase selectivities on hemostasis and prostaglandin expression in dogs.
Animals—8 client-owned dogs with clinical signs of osteoarthritis.
Procedures—Dogs received aspirin (5 mg/kg, PO, q 12 h), carprofen (4 mg/kg, PO, q 24 h), deracoxib (2 mg/kg, PO, q 24 h), and meloxicam (0.1 mg/kg, PO, q 24 h) for 10 days each, with an interval of at least 14 days between treatments. On days 0 and 10, blood was collected for platelet aggregation assays, thrombelastography, and measurement of lipopolysaccharide-stimulated prostaglandin E2, platelet thromboxane B2 (TXB2), and free serum TXB2 and 6-keto-prostaglandin F (PGF)-1α concentrations.
Results—Platelet aggregation decreased after treatment with aspirin and carprofen, whereas significant changes from baseline were not detected for the other drugs tested. Thrombelastograms obtained after treatment with carprofen revealed decreased maximum amplitude and α-angle, suggesting hypocoagulability. Maximum amplitude and coagulation index increased after treatment with deracoxib. Plasma concentrations of prostaglandin E2 decreased after treatment with carprofen or deracoxib, and platelet TXB2 production increased after treatment with aspirin. Serum concentrations of the prostacyclin metabolite 6-keto-PGF-1α did not change significantly after treatment with any of the drugs, although the ratio of free TXB2 to 6-keto-PGF-1α decreased slightly after treatment with carprofen and increased slightly after treatment with deracoxib.
Conclusions and Clinical Relevance—At the dosages tested, treatment with meloxicam affected platelet function minimally in dogs with osteoarthritis. Treatment with carprofen decreased clot strength and platelet aggregation. Clot strength was increased after treatment with deracoxib.
Clinical, biochemical, and histologic effects of intra-articular administration of autologous conditioned serum in horses with experimentally induced osteoarthritis
Authors: Frisbie David D. , Kawcak Christopher E. , Werpy Natasha M. , Park Richard D. , McIlwraith C. Wayne 
Published: March 2007

Abstract
Objective—To assess the clinical, biochemical, and histologic effects of intra-articular administration of autologous conditioned serum (ACS) in the treatment of experimentally induced osteoarthritis in horses.
Animals—16 horses.
Procedures—Osteoarthritis was induced arthroscopically in 1 middle carpal joint of all horses. In 8 placebo- and 8 ACS-treated horses, 6 mL of PBS solution or 6 mL of ACS was injected into the osteoarthritis-affected joint on days 14, 21, 28, and 35, respectively; PBS solution was administered in the other sham-operated joints. Evaluations included clinical assessment of lameness and synovial fluid analysis (performed biweekly); gross pathologic and histologic examinations of cartilage and synovial membrane samples were performed at necropsy.
Results—No adverse treatment-related events were detected. Horses that were treated with ACS had significant clinical improvement in lameness, unlike the placebo-treated horses. Among the osteoarthritis-affected joints, ACS treatment significantly decreased synovial membrane hyperplasia, compared with placebo-treated joints; although not significant, the ACS-treated joints also appeared to have less gross cartilage fibrillation and synovial membrane hemorrhage. The synovial fluid concentration of interleukin-1 receptor antagonist (assessed by use of mouse anti–interleukin-1 receptor antagonist antibody) was increased following treatment with ACS.
Conclusions and Clinical Relevance—Results of this controlled study indicated that there was significant clinical and histologic improvement in osteoarthritis-affected joints of horses following treatment with ACS, compared with placebo treatment. On the basis of these findings, further controlled clinical trials to assess this treatment are warranted, and investigation of the mechanisms of action of ACS should be pursued concurrently.
Correlation of ultrasonographic appearance of lesions and cytologic and histologic diagnoses in splenic aspirates from dogs and cats: 32 cases (2002–2005)
Authors: Ballegeer Elizabeth A. , Forrest Lisa J. , Dickinson Ryan M. , Schutten Melissa M. , Delaney Fern A. , Young Karen M. 
Published: March 2007

Abstract
Objective—To determine the accuracy of cytologic diagnosis, compared with histologic diagnosis, in determination of disease in ultrasound-guided fine-needle aspirates of splenic lesions.
Design—Retrospective study.
Sample Population—Splenic specimens from 29 dogs and 3 cats.
Procedures—Records were searched for dogs and cats that had undergone ultrasound-guided splenic aspiration. Criteria for inclusion were ultrasonographic identification of splenic lesions and cytologic and histologic evaluation of tissue from the same lesion. Cytologic samples were obtained by fine-needle aspiration, and histologic specimens were obtained via surgical biopsy, ultrasound-guided biopsy, or necropsy.
Results—Cytologic diagnoses corresponded with histologic diagnoses in 19 of 31 (61.3%) cases and differed in 5 of 31(16.1%) cases, and 1 aspirate was inadequate for evaluation. In 7 of 31 (22.6%) cases, histologic evaluation of tissue architecture was required to distinguish between reactive and neoplastic conditions. On the basis of histologic diagnosis in 14 animals with nonneoplastic conditions, the cytologic diagnosis was correct in 11 cases, not definitive in 2 cases, and incorrect in 1 case. In 17 animals with malignant neoplastic diseases, the cytologic diagnosis was correct in 8 cases, not definitive but consistent with possible neoplasia in 5 cases, and incorrect in 4 cases. Multiple similar-appearing nodules were significantly associated with malignancy, whereas single lesions were more often benign.
Conclusions and Clinical Relevance—Ultrasound-guided aspiration of splenic lesions is a minimally invasive tool for obtaining specimens for cytologic evaluation. Although cytologic diagnoses often reflect histologic results, if missampling or incomplete sampling occurs or tissue architecture is required to distinguish between reactive and neoplastic conditions, accurate diagnosis with fine-needle aspiration may not be possible.
Estrogen regulation and ion dependence of taurine uptake by MCF-7 human breast cancer cells
Authors: Shennan David , Thomson Jean 
Published: March 2007

AbstractIt has been reported that estrogen receptor-positive MCF-7 cells express TauT, a Na+-dependent taurine transporter. However, there is a paucity of information relating to the characteristics of taurine transport in this human breast cancer cell line. Therefore, we have examined the characteristics and regulation of taurine uptake by MCF-7 cells. Taurine uptake by MCF-7 cells showed an absolute dependence upon extracellular Na+. Although taurine uptake was reduced in Cl- free medium a significant portion of taurine uptake persisted in the presence of NO3 -. Taurine uptake by MCF-7 cells was inhibited by extracellular β-alanine but not by L-alanine or L-leucine. 17β-estadiol increased taurine uptake by MCF-7 cells: the Vmax of influx was increased without affecting the Km. The effect of 17β-estradiol on taurine uptake by MCF-7 cells was dependent upon the presence of extracellular Na+. In contrast, 17β-estradiol had no significant effect on the kinetic parameters of taurine uptake by estrogen receptor-negative MDA-MB-231 cells. It appears that estrogen regulates taurine uptake by MCF-7 cells via TauT. In addition, Na+-dependent taurine uptake may not be strictly dependent upon extracellular Cl-.
Soup or Sparks: The History of Drugs and Synapses
Authors: Van der Kloot William 
Published: March 2007

AbstractThe 130 years between Claude Bernard's demonstration that curare blocks neuromuscular transmission, but not nerve conduction or muscular contraction, and the cloning of receptor that binds the drug saw the emergence of neuropharmacology. Propelled by the staggering economic growth of the 19thCentury and public support, the number of scientists and scientific institutions expanded enormously. It became clear that excitable cells interact though one‐way junctions without cytoplasmic continuity: synapses. Drugs were discovered that block transmission at specific synapses or mimic the effects of nerve stimulation. Some thought that drugs bound to specific receptor sites, perhaps on arms of the huge molecule then believed to make up the protoplasm. The crucial step in elucidating the mechanism of transmission and revealing how the drugs act was Loewi's demonstration, in 1921, that stimulated nerves release a chemical that acts on the effector like nerve stimulation. Many concluded that synaptic transmission is chemical. Others argued that this could not be because transmission is so fast—it must be electrical. The argument was finally resolved in the 1950's when it was shown that the potential changes produced by presynaptic nerve stimulation reverse in sign at a set level of postsynaptic potential, demonstrating that the released transmitters open ion channels in the postsynaptic membrane. Transmission is fast because the transmitters bind, open an ion channel, and then are promptly released so the channel closes. These receptors are operated by the high local concentrations of transmitter produced by quanta1 release. Understanding how drugs work at synapses led to new drugs and advances in health care—a stunning record of achievement.
Muscarinic Acetylcholine Receptors
Authors: Wess Jürgen 
Published: March 2007

AbstractThe five muscarinic acetylcholine receptors (M1–M5mAChRs) are prototypical members of the superfamily of G protein‐coupled receptors. The M1–M5mAChRs regulate an extraordinarily large number of central and peripheral functions. The first part of this chapter primarily focuses on how mAChRs function at a molecular level, the diversity of cellular responses following mAChR activation, and the mechanisms that are involved in regulating mAChR activity. The second part of this chapter summarizes recent results obtained with mutant mouse strains deficient in specific mAChR subtypes. These studies have led to a wealth of novel information about the physiological and pathophysiological roles of the individual mAChRs which may pave the way toward the development of novel, clinically useful muscarinic drugs.
Neuropharmacology of Histamine in Brain
Authors: Faucard Raphaël , Schwartz Jean‐Charles 
Published: March 2007

AbstractHistamine is an important neurotransmitter in brain. Histaminergic neurons emanating from the tuberomamillary nucleus in the hypothalamus project diffusely to the whole brain. Histamine acts via stimulation of three receptor subtypes and exerts essentially excitatory effects upon target neurons. The main function of histaminergic neurons is to trigger and maintain wakefulness and pro cognitive responses. Activation of histaminergic neurotransmission in brain is achieved via blockade of H3 receptors, and is currently explored as a treatment of wakefulness and cognitive deficits in several neurological and psychiatric diseases.
Neuropeptides
Authors: Strand Fleur L. 
Published: March 2007

AbstractThe identification, characterization, and evolution of neuropeptides, neuropeptide families, and their receptors are discussed, including new information gleaned by genetic manipulations, peptidomics, and genomics. The flexibility of neuropeptides to act as neurohormones, neurotransmitters, and/or neuromodulators in regulating and modifying synatic events is emphasized. Neuropeptide processing and inactivation are considered and the phenomenon of tissue‐specific processing of prohormones is introduced as an efficient method to achieve diversity in the nervous system. The role of the hypothalamic–pituitary–adrenal system in stress is discussed, as is the importance of the blood–brain barrier, neuropeptide redundancy, and routes of administration.
Antidepressant Treatment and Hippocampal Neurogenesis: Monoamine and Stress Hypotheses of Depression Converge
Authors: Dranovsky Alex , Hen René 
Published: March 2007

AbstractThere are multiple highly effective treatments for depression. Psychosocial treatments focus on the perceptions of stress, stress prevention, and coping mechanisms, whereas most effective pharmacological treatments modulate monoamines in the brain. Numerous research efforts to understand the mechanisms by which psychotherapy and pharmacotherapy treat depression have resulted in the respective “stress” and “monoamine” hypotheses of depression. This chapter will focus on recent findings that stress and monoamine hypotheses of depression converge in their opposing impact on adult hippocampal neurogenesis.
Neuroendocrine Abnormalities in Women with Depression Linked to the Reproductive Cycle
Authors: Parry Barbara L. , Meliska Charles J. , Fernando Martinez L. , Maurer Eva L. , Lopez Ana M. , Sorenson Diane L. 
Published: March 2007

Abstract
In this chapter, the authors focus on reviewing studies that measure the circadian profile of hormonal changes in relation to baseline changes in the reproductive hormones of estradiol, progesterone, follicle‐stimulating hormone (FSH), and luteinizing hormone (LH), comparing DPs with NCs during the menstrual cycle, pregnancy, postpartum, and menopause and across each of these reproductive epochs. Elevated prolactin levels characterize DPs at each reproductive epoch. Increased melatonin levels characterize menopausal and postpartum DPs, whereas decreased melatonin levels characterize premenstrual dysphoric disorder (PMDD) and DPs during pregnancy. Decreased cortisol levels distinguish menopausal DPs from healthy controls. Using circadian measures in well‐defined diagnostic groups, further work is needed in order to identify common versus distinctive neuroendocrine profiles for DPs during each reproductive epoch. This information then could serve as a basis for developing more specific treatment modalities.
Phenomenology and Clinical Science of Schizophrenia
Authors: Ghose Subroto , Tamminga Carol 
Published: March 2007

AbstractSchizophrenia is a clinically well‐characterized illness but of obscure pathophysiology. A shift in conceptual framework from searching for a specific protein defect in schizophrenia to a search for a defect in neural systems is a biologically plausible approach to investigating the pathophysiology of schizophrenia.
Molecular Genetics of Schizophrenia
Authors: Carroll Liam , O'Donovan Michael C. , Owen Michael J. 
Published: March 2007

AbstractMolecular genetic studies of schizophrenia are built upon the firm foundations of reliable diagnostic methodology and a wealth of genetic epidemiological data. The fact that most, if not all, disease genes apparently have only moderate or small effect sizes on the risk of developing the disorder has proved a challenge to their discovery, as it has in the study of other common diseases. However, the sample and technological resources combined with the reagents generated by the human genome project have begun to make complex disease gene discovery studies feasible. This chapter discusses the potential regions of linkage and two associated chromosomal abnormalities that have been identified for schizophrenia, and debates the accumulating evidence favoring several positional candidate genes. Although in no case has the causative variant(s) been identified, the current findings suggest that the positional genetic approach to schizophrenia is at last bearing fruit, and offer grounds for considerable optimism.
Prokineticins: New Pair of Regulatory Peptides
Authors: Cheng Michelle Y. , Zhou Qun‐Yong 
Published: March 2007

AbstractProkineticins are newly discovered regulatory proteins that contain five disulfide bonds. Prokineticins activate a pair of closely related G protein‐coupled receptors. In the last five years, multiple biological functions have been identified for prokineticins. These include functions in peripheral organs such as gastrointestinal motility, pain perception, angiogenesis and hematopoiesis and brain functions such as circadian rhythms and neurogenesis. This chapter gives an overview on the short history of prokineticins, their receptors, followed by discussions of the currently known biological functions of prokineticins.
Pharmacotherapy for Traumatic Brain Injury
Authors: Stein Donald G. , Hoffman Stuart W. 
Published: March 2007

AbstractCurrently there are no clinically approved, safe and effective treatments for traumatic brain injury (TBI) that can rescue damaged nerve cells and enhance functional recovery. This chapter shows that TBI is a complex cascade of events that unfolds over time and no single pharmacological agent has been found to block all the processes that comprise the injury. Here we review the categories of candidate agents and approaches that have been examined for their potential benefits in the treatment of TBI.
Pharmacological Treatment of Multiple Sclerosis
Authors: Keegan B. Mark 
Published: March 2007

AbstractPharmacological therapy for multiple sclerosis includes those aimed at resolution of acute inflammatory relapses of MS, and those for chronic prevention of relapses and new inflammatory MRI lesions. High doses of corticosteroids are the gold standard treatment for resolving acute relapses but, occasionally, therapeutic plasma exchange is used for severe, corticosteroid‐resistant relapses. Type one beta interferons and glatiramer acetate are the standard chronic immunomodulatory treatments for relapse prevention. Mitoxantrone is a chemotherapy agent used mainly in treatment resistant cases and novel monoclonal antibodies such as natalizumab is now reapproved for MS treatment. Innovative uses of medications currently approved for other medical indications are being also pursued as potential MS treatments.
Neuropharmacology of HIV/AIDS
Authors: Houff Sidney A. , Major Eugene O. 
Published: March 2007

AbstractThe development of antiretroviral agents has altered the types of neurological diseases seen in patients with HIV/AIDS. The direct effects of HIV infection on nervous system functions underlie the neurological complications of HIV/AIDS in most patients. These changes have resulted in an increase emphasis on the biochemical and neuropharmacological features of HIV‐associated neurological diseases. The role of the nigra‐striatal system and drugs of abuse in HIV‐associated neurological disease as well as the concurrent development of neurodegenerative diseases will become of increasing importance as the age of patients with HIV/AIDS increases as a result of highly active antiretroviral therapies. In this chapter, we will review the neuropathogenesis of HIV/AIDS related neurological disease emphasizing the role of neuropharmacological pathways in the development and treatment of HIV‐associated neurological disease.
Leptin: A Metabolic Perspective
Authors: Penn Dawn M. , Rooks Cherie R. , Harris Ruth B. S. 
Published: March 2007

AbstractThe history of discovery of leptin is given and current knowledge on the factors that regulate ob gene expression and leptin protein secretion is summarized. The chapter focuses on the metabolic effects of leptin, the pathways involved in the suppression of food intake and stimulation of energy expenditure are described. The role of central activation of sympathetic outflow to peripheral tissues, compared with direct effects of leptin on insulin‐sensitive tissues, in mediating metabolic responses to leptin is discussed. Recent work elucidating the cellular basis for the shift in metabolism of adipose and non‐adipose tissue to lipid oxidation and triglyceride depletion is reviewed.
Ghrelin: Structural and Functional Properties
Authors: Holst Birgitte , Egerod Kristoffer , Schwartz Thue W. 
Published: March 2007

Abstract
Ghrelin is a gastro‐intestinal peptide hormone acting on important brain including the hypothalamus where it modulates appetite, metabolism and the autonomous nervous system. In the pariphery ghrelin has been described as a modulator of the cardiovascular system and various endocrine tissues involved in metabolism. Importantly, ghrelin is the only peptide hormone modified by a fatty acid chain, being essential for its activity. The receptor for ghrelin is a member of the 7TM/G‐protein coupled receptor super family and signal mainly through Gq coupling. Interestingly, the ghrelin receptor is constitutively active providing increased signaling by increased receptor expression independent of thc endogenous ligand.
A novel missense mutation in the NDP gene in a child with Norrie disease and severe neurological involvement including infantile spasms
Authors: Lev Dorit , Weigl Yuval , Hasan Mariana , Gak Eva , Davidovich Michael , Vinkler Chana , Leshinsky‐Silver Esther , Lerman‐Sagie Tally , Watemberg Nathan 
Published: March 2007

AbstractNorrie disease (ND) is a rare X‐linked recessive disorder characterized by congenital blindness and in some cases, mental retardation and deafness. Other neurological complications, particularly epilepsy, are rare. We report on a novel mutation identified in a patient with ND and profound mental retardation. The patient was diagnosed at the age of 6 months due to congenital blindness. At the age of 8 months he developed infantile spasms, which were diagnosed at 11 months as his EEG demonstrated hypsarrhythmia. Mutation analysis of the ND gene (NDP) of the affected child and his mother revealed a novel missense mutation at position c.134T > A resulting in amino acid change at codon V45E. To the best of our knowledge, such severe neurological involvement has not been previously reported in ND patients. The severity of the phenotype may suggest the functional importance of this site of the NDP gene. © 2007 Wiley‐Liss, Inc.