Transforming’ the Conversation: Rethinking Fair Use in Academic Course Reserves

The Association of Research Libraries' 2012 publication, Code of Best Practices in Fair Use for Academic and Research Libraries, focuses heavily on the concept of transformative use within the fair use analysis. In some cases, the Association of Research Libraries advocates for using the entire work in an electronic format for course reserves. However, current approaches to electronic course reserves and fair use/transformative use arguments are not conducive to utilizing the Association of Research Libraries' recommendations. This article attempts to reframe the conversation by examining fair use in a broad context and the role of the class in the fair use analysis.

Utilizing Building Usage Assessment: Determining Deployment of Student Workers in an Academic Library

Generating, collecting, and analyzing building usage statistics can greatly increase the ability of an access services unit to meet the changing dynamic of patron needs in an academic library. By analyzing three different data points, the Access Services Unit in Malpass Library at Western Illinois University was able to determine the most effective and efficient way to deploy the student workforce to meet the demonstrated needs of the patron population throughout the day. This article will examine those data points and how they were analyzed in order to improve the services provided by the Access Services Unit.

Brasenose college register. 1509-1909.

"Based primarily on College archives", with additions from other sources; ed. by C. B. Heberden, the principal.

The novels and stories.

v. 1. The late Mrs. Null.--v. 2. The Squirrel Inn. The Merry Chanter.--v. 3. Rudder Grange.--v. 4. The hundredth man.--v. 5. Ardis Claverden.--v. 6. The great war syndicate. The stories of the three burglars. The knife that killed Po Hancy. Dusky philosophy.--v. 7. The house of Martha.--v. 8. Pomona's travels. Euphemia among the pelican's. The Rudder Grangers in England. Pomona's daughter.--v. 9. The adventures of Captain Horn.--v. 10. Mrs. Cliff's yacht.--v. 11. The great stone of Sardis. The water-devil.--v. 12. The girl at Cobhurst.--v. 13. The casting away of Mrs. Lecks and Mrs. Aleshine. The vizier of the two-horned Alexander.--v. 14. The associate hermits.--v. 15. Stories. [v.]1: The lady or the tiger? The discourager of hesitancy. The transferred ghost. The spectral mortgage. Every man his own letter-writer. Thar same old coon. Our story. Derelict. On the training of parents. A borrowed month. The baker of Barnbury. The watchmaker's wife.--v. 16. Stories. [v.]2: A tale of negative gravity. Asaph. The remarkable page. The Cloverfield's carriage. A story of assisted fate. My bull-calf. As one woman to another. Our fire-screen. My terminal moraine. Plain fishing.--v. 17. Stories. [v.]3: The griffin and the minor canon. Old Pipes and the dryad. The bee-man of Orn. The queen's museum. The clocks of Rondaine. Christmas before last; or, the fruit of the fragile palm. Prince Hassak's march. The battle of the third cousins. The banished king. The philopena. Amos Kilbright: his adscititious experiences. The Christmas shadrach. The bishop's ghost and the printer's baby. The philosophy of relative existences.--v. 18. Stories. [v.]4: The magic egg. "His wife's deceased sister." The widow's cruise. Captain Eli's best ear. Love before breakfast. The staying power of Sir Rohan. A piece of red calico. The Christmas wreck. My well and what came out of it. Mr. Tolman. My unwilling neighbor. Our archery club.--v. 19. Afield and afloat: The Buller-Podington compact. The romance of a mule-car. The governor-general. Old Applejoy's ghost. Struck by a boomerang. The skipper and El Capitan. "Come in, new year." A sailor's knot. The great staircase at Landover Hall. The ghosts in my toewer. The landsman's tale.--v. 20. Kate Bonnet: the romance of a pirate's daughter.--v. 21. John Gayther's garden.--v. 22. The captain's toll-gate.--v. 23. A bicycle of Cathay. With a memorial sketch of Mr. Stockton and a bibliography of his works.

Statistical account of the parish of St. Just, in Penwith, in the county of Cornwall: with some notice of its ecclesiastical and druidical antiquities /

Mode of access: Internet.

Minutes of evidence taken under the direction of a general commission of enquiry, for Crown lands and emigration, appointed on the 21st June, 1838, by His Excellency the Right Honourable the Earl of Durham, High Commissioner, and Governor General of Her Majesty's colonies of North America.

Reprint.

Researches on Fungi ...

Vol. 7 published for the Royal Society of Canada by the University of Toronto Press.

Systemic apomorphine alters HPA axis responses to interleukin-1 beta adminstration but not sound stress

Apomorphine is a dopamine receptor agonist that was recently licensed for the treatment of erectile dysfunction. However, although sexual activity can be stressful, there has been little investigation into whether treatments for erectile dysfunction affect stress responses. We have examined whether a single dose of apomorphine, sufficient to produce penile erections (50 mug/kg, i.a.), can alter basal or stress-induced plasma ACTH levels, or activity of central pathways thought to control the hypothalamic-pituitary-adrenal axis in rats. An immune challenge (interleukin-1beta, 1 mug/kg, i.a.) was used as a physical stressor while sound stress (100 dB white noise, 30 min) was used as a psychological stressor. Intravascular administration of apomorphine had no effect on basal ACTH levels but did substantially increase the number of Fos-positive amygdala and nucleus tractus solitarius catecholamine cells. Administration of apomorphine prior to immune challenge augmented the normal ACTH response to this stressor at 90 min and there was a corresponding increase in the number of Fos-positive paraventricular nucleus corticotropin-releasing factor cells, paraventricular nucleus oxytocin cells and nucleus tractus solitarius catecholamine cells. However, apomorphine treatment did not alter ACTH or Fos responses to sound stress. These data suggest that erection-inducing levels of apomorphine interfere with hypothalamic-pituitary-adrenal axis inhibitory feedback mechanisms in response to a physical stressor, but have no effect on the response to a psychological stressor. Consequently, it is likely that apomorphine acts on a hypothalamic-pituitary-adrenal axis control pathway that is unique to physical stressors. A candidate for this site of action is the nucleus tractus solitarius catecholamine cell population and, in particular, A2 noradrenergic neurons. (C) 2003 Elsevier Science Ltd. All rights reserved.

Evidence that the Bed Nucleus of the Stria Terminalis Contributes to the Modulation of Hypophysiotropic Corticotropin-Releasing Factor Cell Responses to Systemic Interleukin-1β

Systemic infection activates the hypothalamic-pituitary-adrenal (HPA) axis, and brainstem catecholamine cells have been shown to contribute to this response. However, recent work also suggests an important role for the central amygdala (CeA). Because direct connections between the CeA and the hypothalamic apex of the HPA axis are minimal, the present study investigated whether the bed nucleus of the stria terminalis (BNST) might act as a relay between them. This was done by using an animal model of acute systemic infection involving intravascular delivery of the proinflammatory cytokine interleukin-1 (IL-1, 1 g/kg). Unilateral ibotenic acid lesions encompassing the ventral BNST significantly reduced both IL-1-induced increases in Fos immunoreactivity in corticotropin-releasing factor (CRF) cells of the hypothalamic paraventricular nucleus (PVN) and corresponding increases in adrenocorticotropic hormone (ACTH) secretion. Similar lesions had no effect on CRF cell responses to physical restraint, suggesting that the effects of BNST lesions were not due to a nonspecific effect on stress responses. In further studies, we examined the functional connections between PVN, BNST, and CeA by combining retrograde tracing with mapping of IL-1-induced increases in Fos in BNST and CeA cells. In the case of the BNST, these studies showed that systemic IL-1 administration recruits ventral BNST cells that project directly to the PVN. In the case of the CeA, the results obtained were consistent with an arrangement whereby lateral CeA cells recruited by systemic IL-1 could regulate the activity of medial CeA cells projecting directly to the BNST. In conclusion, the present findings are consistent with the hypothesis that the BNST acts as a relay between the CeA and PVN, thereby contributing to CeA modulation of hypophysiotropic CRF cell responses to systemic administration of IL-1.

Effect of naloxone-precipitated morphine withdrawal on c-fos expression in rat corticotropin-releasing hormone neurons in the paraventricular hypothalamus and extended amygdala

Morphine withdrawal is characterized by physical symptoms and a negative affective state. The 41 amino acid polypeptide corticotropin-releasing, hormone (CRH) is hypothesized to mediate, in part, both the negative affective state and the physical withdrawal syndrome. Here, by means of dual-immunohistochemical methodology, we examined the co-expression of the c-Fos protein and CRH following naloxone-precipitated morphine withdrawal. Rats were treated with slow-release morphine 50 mg/kg (subcutaneous, s.c.) or vehicle every 48 It for 5 days, then withdrawn with naloxone 5 mg/kg (s.c.) or saline 48 h after the final morphine injection. Two hours after withdrawal rats were perfused transcardially and their brains were removed and processed for immunohistochemistry. We found that naloxone-precipitated withdrawal of morphine-dependent rats increased c-Fos immunoreactivity (IR) in CRH positive neurons in the paraventricular hypothalamus. Withdrawal of morphine-dependent rats also increased c-Fos-IR in the central amygdala and bed nucleus of the stria terminalis. however these were in CRH negative neurons. (C) 2004 Published by Elsevier Ireland Ltd.

Hypothalamic paraventricular nucleus neurons regulate medullary catecholamine cell responses to restraint stress

Both physical and psychological stressors recruit catecholamine cells (CA) located in the ventrolateral medulla (VLM) and the nucleus of the solitary tract (NTS). In the case of physical stressors, this effect is initiated by signals that first access the central nervous system at or below the level of the medulla. For psychological stressors, however, CA cell recruitment depends on higher structures within the neuraxis. Indeed, we have recently provided evidence of a pivotal role for the medial amygdala (MeA) in this regard, although such a role must involve a relay, as MeA neurons do not project directly to the medulla. However, some of the MeA neurons that respond to psychological stress have been found to project to the hypothalamic paraventricular nucleus (PVN), a structure that provides significant input to the medulla. To determine whether the PVN might regulate medullary CA cell responses to psychological stress, animals were prepared with unilateral injections of the neurotoxin ibotenic acid into the PVN (Experiment 1), or with unilateral injections of the retrograde tracer wheat germ agglutinin-gold (WGA-Au) into the CA cell columns of the VLM or NTS (Experiment 2). Seven days later, animals were subjected to a psychological stressor (restraint; 15 minutes), and their brains were subsequently processed for Fos plus appropriate cytoplasmic markers (Experiment 1), or Fos plus WGA-Au (Experiment 2). PVN lesions significantly suppressed the stress-related induction of Fos in both VLM and NTS CA cells, whereas tracer deposits in the VLM or NTS retrogradely labeled substantial numbers of PVN cells that were also Fos-positive after stress. Considered in concert with previous results, these data suggest that the activation of medullary CA cells in response to psychological stress may involve a critical input from the PVN. (C) 2004 Wiley-Liss, Inc.

A critical role for the parabrachial nucleus in generating central nervous system responses elicited by a systemic immune challenge

Using Fos immunolabelling as a marker of neuronal activation, we investigated the role of the parabrachial nucleus in generating central neuronal responses to the systemic administration of the proinflarnmatory cytokine interleukin-1beta (1 mug/kg, i.a.). Relative to intact animals, parabrachial nucleus lesions significantly reduced the number of Fos-positive cells observed in the central amygdala (CeA), the bed nucleus of the stria terminalis (BNST), and the ventrolateral medulla (VLM) after systemic interleukin-1beta. In a subsequent experiment in which animals received parabrachial-directed deposits of a retrograde tracer, it was found that many neurons located in the nucleus tractus solitarius (NTS) and the VLM neurons were both retrogradely labelled and Fos-positive after interleukin-1beta administration. These results suggest that the parabrachial nucleus plays a critical role in interleukin-1beta-induced Fos expression in CeA, BNST and VLM neurons and that neurons of the NTS and VLM may serve to trigger or at least influence changes in parabrachial nucleus activity that follows systemic interleukin-1beta administration. (C) 2004 Elsevier B.V. All rights reserved.

Medial prefrontal cortex control of the Paraventricular hypothalamic nucleus response to psychological stress: Possible role of the bed nucleus of the stria terminalis

The medial prefrontal cortex (mPFC) has been strongly implicated in control of the paraventricular nucleus of the hypothalamus (PVN) response to stress. Because of the paucity of direct projections from the mPFC to the PVN, we sought to investigate possible brain regions that might act as a relay between the two during psychological stress. Bilateral ibotenic acid lesions of the rat mPFC enhanced the number of Fos-immunoreactive cells seen in the PVN after exposure to the psychological stressor, air puff. Altered neuronal recruitment was seen in only one of the candidate relay populations examined, the ventral bed nucleus of the stria terminalis (vBNST). Furthermore, bilateral ibotenic acid lesions of the BNST caused a significant attenuation of the PVN response to air puff. To better characterize the structural relationships between the mPFC and PVN, retrograde tracing studies were conducted examining Fos expression in cells retrogradely labeled with cholera toxin b subunit (CTb) from the PVN and the BNST. Results obtained were consistent with an important role for both the mPFC and BNST in the mpPVN CRF cell response to air puff. We suggest a set of connections whereby a direct PVN projection from the ipsilateral vBNST is involved in the mpPVN response to air puff and this may, in turn, be modulated by an indirect projection from the mPFC to the BNST. (C) 2004 Wiley-Liss, Inc.

Dissection of peripheral and central endogenous opioid modulation of systemic interleukin-1 beta responses using c-fos expression in the rat brain

In opiate addicts or patients receiving morphine treatment, it has been reported that the immune system is often compromised. The mechanisms responsible for the adverse effects of opioids on responses to infection are not clear but it is possible that central and/or peripheral opioid receptors may be important. We have utilised an experimental immune challenge model in rats, the systemic administration of the human pro-inflammatory cytokine interleukin-1 beta (IL-1 beta) to study the effects of selectively blocking peripheral opioid receptors only (using naloxone methiodide) or after blocking both central and peripheral opioid receptors (using naloxone). Pre-treatment with naloxone methiodide decreased (15%) IL-1 beta-induced Fos-immunoreactivity (Fos-IR) in medial parvocellular paraventricular nucleus (mPVN) corticotropin-releasing hormone (CRH) neurons but increased responses in the ventrolateral medulla (VLM) C1 (65%) and nucleus tractus solitarius (NTS) A2 (110%) catecholamine cell groups and area postrema (136%). However no effect of blocking peripheral opioid receptors was detected in the central nucleus of the amygdala (CeA) or dorsal bed nucleus of the stria terminalis (BNST). We next determined the effect of blocking both central and peripheral opioid receptors with naloxone and, when compared to the naloxone methiodide pre-treated group, a further 60% decrease in Fos-IR mPVN CRH neurons induced by IL-1 beta was detected, which was attributed to block of central opioid receptors. Similar comparisons also detected decreases in Fos-IR neurons induced by IL-1 beta in the VLM A1, VLM C1 and NTS A2 catecholamine cell groups, area postrema, and parabrachial nucleus. In contrast, pre-treatment with naloxone increased Fos-IR neurons in CeA (98%) and dorsal BNST (72%). These results provide novel evidence that endogenous opioids can influence central neural responses to systemic IL-1 beta and also suggest that the differential patterns of activation may arise because of actions at central and/or peripheral opioid receptors that might be important in regulating behavioural, hypothalamic-pituitary-adrenal axis and sympathetic nervous system responses during an immune challenge. (c) 2005 Elsevier Ltd. All rights reserved.