’Animal Studies‘, Disziplinarität und die (Post-)Humanities

2013 ◽  
Vol 4 (1) ◽  
Author(s):  
Cary Wolfe

Der Text von Cary Wolfe ist eine gekürzte Übersetzung des Kapitels »Animal Studies«, Disciplinarity, and the (Post)Humanities aus der Monographie What is Posthumanism? (Minnesota 2009). Wolfe diskutiert die Beziehung zwischen (Trans-)Disziplinarität und Posthumanismus im Rückgriff auf Konzepte von Derrida, Foucault und Luhmann, die eine Form von gesellschaftlicher Kommunikation zu denken erlauben, an der menschliche Subjekte zwar noch teilhaben, aber deren souveräne Urheber sie nicht mehr sind </br></br>The paper by Cary Wolfe is an abridged translation of the chapter »Animal Studies«, Disciplinarity, and the (Post)Humanities from the monograph (Minnesota 2009). Wolfe discusses the relation between (trans-)disciplinarity and posthumanism with reference to concepts by Derrida, Foucault and Luhmann, allowing to consider a form of social communication in which human subjects still may participate, but no longer are their sovereign initiators.

1982 ◽  
Vol 28 (9) ◽  
pp. 1899-1904 ◽  
Author(s):  
A H Clemens ◽  
D L Hough ◽  
P A D'Orazio

Abstract The "glucose clamping" technique has been proposed as a method for the early detection of a beginning derangement of glucose homeostasis and thus for the possible prevention of maturity-onset diabetes. This technique interrupts the physiological glucose-insulin relationship by placing a patient's blood glucose concentration under an investigator's control, for quantification of the pancreatic beta-cell response during hyperglycemic clamps and of sensitivity of body tissue to exogenous insulin during normoglycemic clamps. We report the development of a glucose clamping algorithm for use with the Biostator glucose-controlled insulin-infusion system (Horm. Metab. Res., Suppl. 8: 23-33, 1977). This algorithm adds simplicity and precision to the glucose clamping procedure and reduces operator effort to a minimum. We describe the early development of the algorithm with a model system and report evaluations made during animal studies and preliminary investigations with human subjects.


2010 ◽  
Vol 23 (1) ◽  
pp. 4-22 ◽  
Author(s):  
Paul Guilloteau ◽  
Romuald Zabielski ◽  
Harald M. Hammon ◽  
Cornelia C. Metges

The consequences of early-life nutritional programming in man and other mammalian species have been studied chiefly at the metabolic level. Very few studies, if any, have been performed in the gastrointestinal tract (GIT) as the target organ, but extensive GIT studies are needed since the GIT plays a key role in nutrient supply and has an impact on functions of the entire organism. The possible deleterious effects of nutritional programming at the metabolic level were discovered following epidemiological studies in human subjects, and confirmed in animal models. Investigating the impact of programming on GIT structure and function would need appropriate animal models due to ethical restrictions in the use of human subjects. The aim of the present review is to discuss the use of pigs as an animal model as a compromise between ethically acceptable animal studies and the requirement of data which can be interpolated to the human situation. In nutritional programming studies, rodents are the most frequently used model for man, but GIT development and digestive function in rodents are considerably different from those in man. In that aspect, the pig GIT is much closer to the human than that of rodents. The swine species is closely comparable with man in many nutritional and digestive aspects, and thus provides ample opportunity to be used in investigations on the consequences of nutritional programming for the GIT. In particular, the ‘sow–piglets’ dyad could be a useful tool to simulate the ‘human mother–infant’ dyad in studies which examine short-, middle- and long-term effects and is suggested as the reference model.


2021 ◽  
Vol 12 ◽  
Author(s):  
Nevena Draginic ◽  
Vladimir Jakovljevic ◽  
Marijana Andjic ◽  
Jovana Jeremic ◽  
Ivan Srejovic ◽  
...  

This review aimed to provide a summary on the traditional uses, phytochemistry, and pharmacological activities in the cardiovascular system and cardiotoxicity of Melissa officinalis (MO), with the special emphasis on the protective mechanisms in different cardiovascular pathologies. MO is a perennial aromatic herb commonly known as lemon balm, honey balm, or bee balm, which belongs to Lamiaceae family. Active components are mainly located in the leaves or essential oil and include volatile compounds, terpenoid (monoterpenes, sesquiterpenes, triterpenes), and polyphenolic compounds [rosmarinic acid (RA), caffeic acid, protocatechuic acid, quercitrin, rhamnocitrin, luteolin]. For centuries, MO has been traditionally used as a remedy for memory, cognition, anxiety, depression, and heart palpitations. Up until now, several beneficial cardiovascular effects of MO, in the form of extracts (aqueous, alcoholic, and hydroalcoholic), essential oil, and isolated compounds, have been confirmed in preclinical animal studies, such as antiarrhythmogenic, negative chronotropic and dromotropic, hypotensive, vasorelaxant, and infarct size–reducing effects. Nonetheless, MO effects on heart palpitations are the only ones confirmed in human subjects. The main mechanisms proposed for the cardiovascular effects of this plant are antioxidant free radical–scavenging properties of MO polyphenols, amelioration of oxidative stress, anti-inflammatory effects, activation of M2 and antagonism of β1 receptors in the heart, blockage of voltage-dependent Ca2+ channels, stimulation of endothelial nitric oxide synthesis, prevention of fibrotic changes, etc. Additionally, the main active ingredient of MO-RA, per se, has shown substantial cardiovascular effects. Because of the vastness of encouraging data from animal studies, this plant, as well as the main ingredient RA, should be considered and investigated further as a tool for cardioprotection and adjuvant therapy in patients suffering from cardiovascular diseases.


2008 ◽  
Vol 68 (1) ◽  
pp. 71-77 ◽  
Author(s):  
Michael E. Symonds

Whilst previously type 2 diabetes occurred in older adults, its incidence, together with obesity, has increased rapidly in children. An improved understanding of this disease pathway from a developmental view point is critical. It is likely that subtle changes in dietary patterns over an extended period of time contribute to diabetes, although this type of rationale is largely ignored in animal studies aimed at determining the mechanisms involved. Small-animal studies in which large, and often extreme, changes in the diet are imposed at different stages of the life cycle can have substantial effects on fat mass and/or pancreatic functions. These responses are not representative of the much more gradual changes seen in the human population. An increasing number of studies indicate that it is growth rate per se, rather than the type of dietary intervention that determines pancreatic function during development. Epigenetic mechanisms that regulate insulin secretion by the pancreas can be re-set by more extreme changes in dietary supply in early life. The extent to which these changes may contribute to more subtle modulations in glucose homeostasis that can accompany excess fat growth in childhood remains to be established. For human subjects there is much less information as to whether specific dietary components determine disease onset. Indeed, it is highly likely that genotype has a major influence, although recent data relating early diet to physical activity and the FTO gene indicate the difficulty of establishing the relative contribution of diet and changes in body mass to diabetes.


2018 ◽  
Vol 77 (3) ◽  
pp. 223-229 ◽  
Author(s):  
Randy J. Nelson ◽  
Souhad Chbeir

Life on earth has evolved during the past several billion years under relatively bright days and dark night conditions. The wide-spread adoption of electric lights during the past century exposed animals, both human and non-human, to significant light at night for the first time in their evolutionary history. Endogenous circadian clocks depend on light to entrain to the external daily environment and seasonal rhythms depend on clear nightly melatonin signals to assess time of year. Thus, light at night can derange temporal adaptations. Indeed, disruption of naturally evolved light–dark cycles results in several physiological and behavioural changes with potentially serious implications for physiology, behaviour and mood. In this review, data from night-shift workers on their elevated risk for metabolic disorders, as well as data from animal studies will be discussed. Night-shift workers are predisposed to obesity and dysregulated metabolism that may result from disrupted circadian rhythms. Although studies in human subjects are correlative, animal studies have revealed several mechanisms through which light at night may exert its effects on metabolism by disrupting circadian rhythms that are associated with inflammation, both in the brain and in the periphery. Disruption of the typical timing of food intake is a key effect of light at night and subsequent metabolic dysregulation. Strategies to avoid the effects of light at night on body mass dysregulation should be pursued.


2019 ◽  
Vol 8 (7) ◽  
pp. 1061 ◽  
Author(s):  
Mohamed A. Hendaus ◽  
Fatima A. Jomha ◽  
Ahmed H. Alhammadi

Autism spectrum disorder (ASD) is a developmental disability described by diagnostic criteria that comprise deficits in social communication and the existence of repetitive, restricted patterns of behavior, interests, or activities that can last throughout life. Many preclinical studies show the importance of arginine vasopressin (AVP) physiology in social functioning in several mammalian species. Currently, there is a trend to investigate more specific pharmacological agents to improve social functioning in patients with ASD. Neurobiological systems that are crucial for social functioning are the most encouraging conceivable signaling pathways for ASD therapeutic discovery. The AVP signaling pathway is one of the most promising. The purpose of this commentary is to detail the evidence on the use of AVP as an agent that can improve social functioning. The pharmacologic aspects of the drug as well as its potential to ameliorate social functioning characteristics in human and animal studies are described in this manuscript. AVP, especially in its inhaled form, seems to be safe and beneficial in improving social functioning including in children with autism. Larger randomized studies are required to implement a long awaited safe and feasible treatment in people with a deficiency in social functioning.


2010 ◽  
Vol 103 (9) ◽  
pp. 1278-1286 ◽  
Author(s):  
Rachel L. Thompson ◽  
Lisa M. Miles ◽  
Joanne Lunn ◽  
Graham Devereux ◽  
Rebecca J. Dearman ◽  
...  

The aim of the present systematic review was to evaluate the influence of early life exposure (maternal and childhood) to peanuts and the subsequent development of sensitisation or allergy to peanuts during childhood. Studies were identified using electronic databases and bibliography searches. Studies that assessed the impact of non-avoidance compared with avoidance or reduced quantities of peanuts or peanut products on either sensitisation or allergy to peanuts, or both outcomes, were eligible. Six human studies were identified: two randomised controlled trials, two case–control studies and two cross-sectional studies. In addition, published animal and mechanistic studies, relevant to the question of whether early life exposure to peanuts affects the subsequent development of peanut sensitisation, were reviewed narratively. Overall, the evidence reviewed was heterogeneous, and was limited in quality, for example, through lack of adjustment for potentially confounding factors. The nature of the evidence has therefore hindered the development of definitive conclusions. The systematic review of human studies and narrative expert-led reviews of animal studies do not provide clear evidence to suggest that either maternal exposure, or early or delayed introduction of peanuts in the diets of children, has an impact upon subsequent development of sensitisation or allergy to peanuts. Results from some animal studies (and limited evidence from human subjects) suggest that the dose of peanuts is an important mediator of peanut sensitisation and tolerance; low doses tend to lead to sensitisation and higher doses tend to lead to tolerance.


2005 ◽  
Vol 288 (4) ◽  
pp. R819-R827 ◽  
Author(s):  
Terry N. Thrasher

Whether arterial baroreceptors play a role in setting the long-term level of mean arterial pressure (MAP) has been debated for more than 75 years. Because baroreceptor input is reciprocally related to efferent sympathetic nerve activity (SNA), it is obvious that baroreceptor unloading would cause an increase in MAP. Experimental proof of concept is evident acutely after baroreceptor denervation. Chronically, however, baroreceptor denervation is associated with highly variable changes in MAP but not sustained hypertension. The ability of baroreceptors to buffer imposed increases in MAP appears limited by a process termed “resetting,” in which the threshold to fire shifts in the direction of the pressure change and if the pressure elevation is maintained, it leads to a rightward shift in the relationship between baroreceptor firing and MAP. The most common hypothesis linking baroreceptors to changes in MAP proposes that reduced vascular distensibility in baroreceptive areas would cause reduced firing at the same pulsatile pressure and, thus, reflexively increase SNA. This review focuses on effects of baroreceptor denervation in the regulation of MAP in human subjects compared with animal studies; the relationship between vascular compliance, MAP, and baroreceptor resetting; and, finally, the effect of chronic baroreceptor unloading on the regulation of MAP.


1995 ◽  
Vol 2 (1) ◽  
pp. 25-31 ◽  
Author(s):  
David V Bates

Part 1 of this review is concerned with theoretical issues of ozone dosimetry, animal and cellular studies that illustrate the mechanism of action of ozone on living tissues, and with clinical studies. Animal studies have indicated that there are long term effects from low level long term ozone exposure. Clinical studies involve controlled ozone exposures on human subjects, both normals and asthmatics. Exercise concomitant with the ozone exposure increases the effect of the gas. It is concluded that the induction of an inflammatory response in the airway, both in the nose and in the lung, is the striking and earliest feature of ozone exposure. Current unexplained observations include: the dissociation between the inflammatory and function test response; the mechanisms of ‘adaptation’ and of airway hyperresponsiveness; and the phenomena that underlie the effect of ozone on maximal athletic performance.


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