Annals of the New York Academy of Sciences
1749-6632
0077-8923
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Cơ quản chủ quản: Wiley-Blackwell , WILEY
Lĩnh vực:
History and Philosophy of ScienceNeuroscience (miscellaneous)Biochemistry, Genetics and Molecular Biology (miscellaneous)
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Published on behalf of the New York Academy of Sciences, Annals of the New York Academy of Sciences provides multidisciplinary perspectives on research of current scientific interest with far-reaching implications for the wider scientific community and society at large. Each special issue assembles the best thinking of key contributors to a field of investigation at a time when emerging developments offer the promise of new insight. Individually themed, Annals special issues stimulate new ways to think about science by providing a neutral forum for discourse—within and across many institutions and fields.
Các bài báo tiêu biểu
What should we call instruments commonly known as payments for environmental services? A review of the literature and a proposal Researchers, policy makers, and practitioners have used various terms to describe instruments that reward the stewardship of ecosystem services that benefit “external” actors. Payments for environmental services , or PES , has been the predominant name. However, critics have challenged both the payments and environmental components of this nomenclature, most commonly proposing markets , compensation , or rewards as alternatives for the former, and ecosystem for the latter. Additional questions arise regarding what to call the agents directly involved in the transaction: sellers and buyers , or stewards and beneficiaries ? For some, concerns about this terminology have emerged from so‐called “pro‐poor PES” debates that ask if actors could and should incorporate poverty alleviation goals into PES instruments. This review of the modulating use of terms and the arguments about which best fit theory and experience points to the key policy and ethical issues at stake as PES programs face critical and timely questions about the direction they will head. The author contends that the choices of terms will influence that direction and proposes a new alternative—rewards for ecosystem service stewardship (RESS)— that better encompasses pro‐poor options.
Tập 1219 Số 1 - Trang 209-225 - 2011
Transforming Growth Factor‐β Is a Potent Negative Regulator of Human Lymphocytes
Tập 628 Số 1 - Trang 345-353 - 1991
Leptin Signaling, Adiposity, and Energy Balance Abstract : A chronic minor imbalance between energy intake and energy expenditure may lead to obesity. Both lean and obese subjects eventually reach energy balance and their body weight regulation implies that the adipose tissue mass is “sensed”, leading to appropriate responses of energy intake and energy expenditure. The cloning of the ob gene and the identification of its encoded protein, leptin, have provided a system signaling the amount of adipose energy stores to the brain. Leptin, a hormone secreted by fat cells, acts in rodents via hypothalamic receptors to inhibit feeding and increase thermogenesis. A feedback regulatory loop with three distinct steps has been identified: (1) a sensor (leptin production by adipose cells) monitors the size of the adipose tissue mass; (2) hypothalamic centers receive and integrate the intensity of the leptin signal through leptin receptors (LRb); (3) effector systems, including the sympathetic nervous system, control the two main determinants of energy balance—energy intake and energy expenditure. While this feedback regulatory loop is well established in rodents, there are many unsolved questions about its applicability to body weight regulation in humans. The rate of leptin production is related to adiposity, but a large portion of the interindividual variability in plasma leptin concentration is independent of body fatness. Gender is an important factor determining plasma leptin, with women having markedly higher leptin concentrations than men for any given degree of fat mass. The ob mRNA expression is also upregulated by glucocorticoids, whereas stimulation of the sympathetic nervous system results in its inhibition. Furthermore, leptin is not a satiety factor in humans because changes in food intake do not induce short‐term increases in plasma leptin levels. After its binding to LRb in the hypothalamus, leptin stimulates a specific signaling cascade that results in the inhibition of several orexigenic neuropeptides, while stimulating several anorexigenic peptides. The orexigenic neuropeptides that are downregulated by leptin are NPY (neuropeptide Y), MCH (melanin‐concentrating hormone), orexins, and AGRP (agouti‐related peptide). The anorexigenic neuropeptides that are upregulated by leptin are α‐MSH (α‐melanocyte‐stimulating hormone), which acts on MC4R (melanocortin‐4 receptor); CART (cocaine and amphetamine‐regulated transcript); and CRH (corticotropin‐releasing‐hormone). Obese humans have high plasma leptin concentrations related to the size of adipose tissue, but this elevated leptin signal does not induce the expected responses (i.e., a reduction in food intake and an increase in energy expenditure). This suggests that obese humans are resistant to the effects of endogenous leptin. This resistance is also shown by the lack of effect of exogenous leptin administration to induce weight loss in obese patients. The mechanisms that may account for leptin resistance in human obesity include a limitation of the blood‐brain‐barrier transport system for leptin and an inhibition of the leptin signaling pathways in leptin‐responsive hypothalamic neurons. During periods of energy deficit, the fall in leptin plasma levels exceeds the rate at which fat stores are decreased. Reduction of the leptin signal induces several neuroendocrine responses that tend to limit weight loss, such as hunger, food‐seeking behavior, and suppression of plasma thyroid hormone levels. Conversely, it is unlikely that leptin has evolved to prevent obesity when plenty of palatable foods are available because the elevated plasma leptin levels resulting from the increased adipose tissue mass do not prevent the development of obesity. In conclusion, in humans, the leptin signaling system appears to be mainly involved in maintenance of adequate energy stores for survival during periods of energy deficit. Its role in the etiology of human obesity is only demonstrated in the very rare situations of absence of the leptin signal (mutations of the leptin gene or of the leptin receptor gene), which produces an internal perception of starvation and results in a chronic stimulation of excessive food intake.
Tập 967 Số 1 - Trang 379-388 - 2002
Multifarious roles of sialic acids in immunity Sialic acids are a diverse family of monosaccharides widely expressed on all cell surfaces of vertebrates and so‐called “higher” invertebrates, and on certain bacteria that interact with vertebrates. This overview surveys examples of biological roles of sialic acids in immunity, with emphasis on an evolutionary perspective. Given the breadth of the subject, the treatment of individual topics is brief. Subjects discussed include biophysical effects regulation of factor H; modulation of leukocyte trafficking via selectins; Siglecs in immune cell activation; sialic acids as ligands for microbes; impact of microbial and endogenous sialidases on immune cell responses; pathogen molecular mimicry of host sialic acids; Siglec recognition of sialylated pathogens; bacteriophage recognition of microbial sialic acids; polysialic acid modulation of immune cells; sialic acids as pathogen decoys or biological masks; modulation of immunity by sialic acid O ‐acetylation; sialic acids as antigens and xeno‐autoantigens; antisialoglycan antibodies in reproductive incompatibility; and sialic‐acid–based blood groups.
Tập 1253 Số 1 - Trang 16-36 - 2012
Inhibition of the Amygdala: Key to Pathological States? Abstract : The amygdala plays an important role in associating sensory stimuli with aversive or appetitive outcomes. Conditioning procedures potentiate inputs to the amygdala, which facilitate emotional responses via subcortical and cortical outputs. Powerful inhibitory circuits exist that control expression of conditioned responses in the amygdala, including inhibition from prefrontal cortex. Deficient inhibitory tone in the amygdala could lead to overexpression of conditioned responses, producing pathological states such as anxiety disorders and drug‐seeking behavior. Support for this comes from several lines of animal research: (1) GABA antagonist‐induced priming of anxiety states, (2) extinction of conditioned fear, (3) modulation of inhibitory avoidance memory, and (4) cue‐induced reinstatement of drug seeking. Cue‐induced craving in humans is associated with feelings of fear and autonomic arousal, suggesting a link between fear and addiction in the amygdala. Future therapies aimed at increasing inhibitory tone in the amygdala, either locally or via the prefrontal cortex, may prevent anxiety disorders and addiction relapse. Novel neuropeptides, which can either excite or inhibit specific components of anxiety responses, offer promise in this regard.
Tập 985 Số 1 - Trang 263-272 - 2003
Serotonin and the Evaluation of Future Rewards Abstract: The ability to select an action by considering both delays and amount of reward outcome is critical for survival and well‐being of animals and humans. Previous animal experiments suggest a role of serotonin in action choice by modulating the evaluation of delayed rewards. It remains unclear, however, through which neural circuits, and through what receptors and intracellular mechanisms, serotonin affects the evaluation of delayed rewards. Here, we review experimental studies and computational theory of decisions under delayed rewards, and propose that serotonin controls the timescale of reward prediction by regulating neural activity in the basal ganglia.
Tập 1104 Số 1 - Trang 289-300 - 2007
CONTROL OF EXPERIMENTAL AND CLINICAL BURN WOUND SEPSIS BY TOPICAL APPLICATION OF SULFAMYLON COMPOUNDS Discussion and Summary The successful control of burn wound sepsis by use of Sulfamylon burn cream has greatly altered the management of the burn wound and its prognosis. The character of the healing wound has altered, with persistence of eschar now seen, due to suppression of microbial debriding action. This problem has been resolved by discontinuing therapy and applying dressings if necessary to hasten eschar separation. The use of a water soluble base, which is 62% water, has resulted in a decrease in evaporative water loss, with a consequent reduction in the metabolic load on the patient. This is evident in the reduction of weight loss in the post‐burn period. The control of local sepsis appears to add to this gain, since it too represents a decrease in metabolic demand. The survival of epithelial islands in deep dermal burns which had previously been converted to full‐thickness injury by infection has resulted in healing of such injuries without resort to skin grafting. The hydrotherapy procedures permit a daily gentle debridement of matured eschar, and a consequent reduction in the frequency of surgical debridement has occurred. The reduction in the need for general anaesthetic has simplified wound management and minimized weight loss due to cancelled meals. The drug is simple to compound and to apply. Areas housing many burn patients are now odorless, in striking contrast to the environment previously existing. The elimination of burn wound sepsis has, however, increased the magnitude of other clinical problems in burn management. The most prominent of these are the pulmonary complications, specifically a diffuse pneumonia. This is not a hematogenous Pseudomonas pneumonia, which was formerly a common complication of burn wound sepsis, but a bronchopneumonia, often associated with patches of atalectasis. The mortality statistics show a consistent reduction of 50% in death rate; most of the change has occurred in burns of less than 50% of body surface. There has been no improvement in death rate of burns of over 60%, although the cause of death has changed from one of wound infection to pneumonia. Burn wound sepsis has been relegated to a minor role in burn mortality by the use of topical Sulfamylon therapy.
Tập 150 Số 3 - Trang 950-960 - 1968