At high concentrations, free radicals and radical-derived, nonradical reactive species are hazardous for living organisms and damage all major cellular constituents. At moderate concentrations, how...

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Free Radicals in the Physiological Control of Cell Function

Allergic rhinitis is a symptomatic disorder of the nose induced after allergen exposure by an IgE-mediated inflammation of the membranes lining the nose. It is a global health problem that causes major illness and disability worldwide. Over 600 million patients from all countries, all ethnic groups and of all ages suffer from allergic rhinitis. It affects social life, sleep, school and work and its economic impact is substantial. Risk factors for allergic rhinitis are well identified. Indoor and outdoor allergens as well as occupational agents cause rhinitis and other allergic diseases. The role of indoor and outdoor pollution is probably very important, but has yet to be fully understood both for the occurrence of the disease and its manifestations.

In 1999, during the Allergic Rhinitis and its Impact on Asthma (ARIA) WHO workshop, the expert panel proposed a new classification for allergic rhinitis which was subdivided into 'intermittent' or 'persistent' disease.

This classification is now validated. The diagnosis of allergic rhinitis is often quite easy, but in some cases it may cause problems and many patients are still under-diagnosed, often because they do not perceive the symptoms of rhinitis as a disease impairing their social life, school and work.

The management of allergic rhinitis is well established and the ARIA expert panel based its recommendations on evidence using an extensive review of the literature available up to December 1999. The statements of evidence for the development of these guidelines followed WHO rules and were based on those of Shekelle et al. A large number of papers have been published since 2000 and are extensively reviewed in the 2008 Update using the same evidence-based system. Recommendations for the management of allergic rhinitis are similar in both the ARIA workshop report and the 2008 Update. In the future, the GRADE approach will be used, but is not yet available.

Another important aspect of the ARIA guidelines was to consider co-morbidities. Both allergic rhinitis and asthma are systemic inflammatory conditions and often co-exist in the same patients. In the 2008 Update, these links have been confirmed.

The ARIA document is not intended to be a standard-of-care document for individual countries. It is provided as a basis for physicians, health care professionals and organizations involved in the treatment of allergic rhinitis and asthma in various countries to facilitate the development of relevant local standard-of-care documents for patients.

/pdf/allergic-rhinitis-and-its-impact-on-asthma-aria-2008-update-13eqfzaw4u.pdf

Allergic rhinitis and its impact on asthma (ARIA) 2008 update (in collaboration with the World Health Organization, GA(2)LEN and AllerGen)

Earnings Management and Investor Protection: An International Comparison

Food intake is regulated by the hypothalamus, including the melanocortin and neuropeptide Y (NPY) systems in the arcuate nucleus. The NPY Y2 receptor (Y2R), a putative inhibitory presynaptic receptor, is highly expressed on NPY neurons in the arcuate nucleus, which is accessible to peripheral hormones. Peptide YY3-36 (PYY3-36), a Y2R agonist, is released from the gastrointestinal tract postprandially in proportion to the calorie content of a meal. Here we show that peripheral injection of PYY3-36 in rats inhibits food intake and reduces weight gain. PYY3-36 also inhibits food intake in mice but not in Y2r-null mice, which suggests that the anorectic effect requires the Y2R. Peripheral administration of PYY3-36 increases c-Fos immunoreactivity in the arcuate nucleus and decreases hypothalamic Npy messenger RNA. Intra-arcuate injection of PYY3-36 inhibits food intake. PYY3-36 also inhibits electrical activity of NPY nerve terminals, thus activating adjacent pro-opiomelanocortin (POMC) neurons. In humans, infusion of normal postprandial concentrations of PYY3-36 significantly decreases appetite and reduces food intake by 33% over 24 h. Thus, postprandial elevation of PYY3-36 may act through the arcuate nucleus Y2R to inhibit feeding in a gut–hypothalamic pathway.

BRIEF COMMUNICATION ARISING: Gut hormone PYY3-36 physiologically inhibits food intake

http://yael-nissan.weebly.com/uploads/5/2/9/2/5292348/the_introduction_to_pain_an_integrative_review_-_millan.pdf

The induction of pain: an integrative review

Signalling and agency theories appear in the accounting literature to be competing theories. This article demonstrates that they are actually consistent theories, in that one set of sufficient conditions of signalling theory is at least consistent with one set of sufficient conditions of agency theory. Indeed, a considerable overlap exists between the two theories: rational behaviour is common to both; information asymmetry in signalling theory is implied by positive monitoring costs in agency theory; ‘quality' in signalling theory can be defined in terms of agency theory variables; and signalling costs are implicit in some bonding devices of agency theory. Examples are given where both theories’ predictions about lobbying, accounting choices, and voluntary auditor selection are added together.

Signalling, Agency Theory and Accounting Policy Choice

Differential distribution of orexin-A and orexin-B immunoreactivity in the rat brain and spinal cord.

Sources and targets of nitric oxide in rat cerebellum

If we are to stand any chance of understanding the circuitry of the superficial dorsal horn, it is imperative that we can identify which classes of interneuron are excitatory and which are inhibitory. Our aim was to test the hypothesis that there is a correlation between the morphology of an interneuron and its postsynaptic action. We used in vitro slice preparations of the rat spinal cord to characterize and label interneurons in laminae I–III with Neurobiotin. Labelled cells (n= 19) were reconstructed in 3D with Neurolucida and classified according to the scheme proposed by Grudt & Perl (2002). We determined if cells were inhibitory or excitatory by reacting their axon terminals with antibodies to reveal glutamate decrboxylase (for GABAergic cells) or the vesicular glutamate transporter 2 (for glutamatergic cells). All five islet cells retrieved were inhibitory. Of the six vertical (stalked) cells analysed, four were excitatory and, surprisingly, two were inhibitory. It was noted that these inhibitory cells had axonal projections confined to lamina II whereas excitatory vertical cells projected to lamina I and II. Of the remaining neurons, three were radial cells (2 inhibitory, 1 excitatory), two were antennae cells (1 inhibitory, 1 excitatory), one was an inhibitory central cell and the remaining two were unclassifiable excitatory cells. Our hypothesis appears to be correct only for islet cells. Other classes of cells have mixed actions, and in the case of vertical cells, the axonal projection appears to be a more important determinant of postsynaptic action.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.2007.140996

Richard Morris

Papers

Signalling, Agency Theory and Accounting Policy Choice

Differential distribution of orexin-A and orexin-B immunoreactivity in the rat brain and spinal cord.

Sources and targets of nitric oxide in rat cerebellum

Morphology of inhibitory and excitatory interneurons in superficial laminae of the rat dorsal horn.

Nitric oxide may act as a messenger between dorsal root ganglion neurones and their satellite cells.