100 research outputs found
Activity-Based Anorexia Reduces Body Weight without Inducing a Separate Food Intake Microstructure or Activity Phenotype in Female Rats—Mediation via an Activation of Distinct Brain Nuclei
Anorexia nervosa (AN) is accompanied by severe somatic and psychosocial complications. However, the underlying pathogenesis is poorly understood, treatment is challenging and often hampered by high relapse. Therefore, more basic research is needed to better understand the disease. Since hyperactivity often plays a role in AN, we characterized an animal model to mimic AN using restricted feeding and hyperactivity. Female Sprague-Dawley rats were divided into four groups: no activity/ad libitum feeding (ad libitum, AL, n=9), activity/ad libitum feeding (activity, AC, n=9), no activity/restricted feeding (RF, n=12) and activity/restricted feeding (activity-based anorexia, ABA, n=11). During the first week all rats were fed ad libitum, ABA and AC had access to a running wheel for 24h/d. From week two ABA and RF only had access to food from 9:00-10:30 am. Body weight was assessed daily, activity and food intake monitored electronically, brain activation assessed using Fos immunohistochemistry at the end of the experiment. While during the first week no body weight differences were observed (p>0.05), after food restriction RF rats showed a body weight decrease: -13% vs. day eight (p0.05). Similarly, the daily physical activity was not different between AC and ABA (p>0.05). The investigation of Fos expression in the brain showed neuronal activation in several brain nuclei such as the supraoptic nucleus, arcuate nucleus, locus coeruleus and nucleus of the solitary tract of ABA compared to AL rats. In conclusion, ABA combining physical activity and restricted feeding likely represents a suited animal model for AN to study pathophysiological alterations and pharmacological treatment options. Nonetheless, cautious interpretation of the data is necessary since rats do not voluntarily reduce their body weight as observed in human AN
Nesfatin-130−59 Injected Intracerebroventricularly Differentially Affects Food Intake Microstructure in Rats Under Normal Weight and Diet-Induced Obese Conditions
Nesfatin-1 is well-established to induce an anorexigenic effect. Recently,
nesfatin-130−59, was identified as active core of full length nesfatin-11−82
in mice, while its role in rats remains unclear. Therefore, we investigated
the effects of nesfatin-130−59 injected intracerebroventricularly (icv) on the
food intake microstructure in rats. To assess whether the effect was also
mediated peripherally we injected nesfatin-130−59 intraperitoneally (ip).
Since obesity affects the signaling of various food intake-regulatory peptides
we investigated the effects of nesfatin-130−59 under conditions of diet-
induced obesity (DIO). Male Sprague–Dawley rats fed ad libitum with standard
diet were icv cannulated and injected with vehicle (5 μl ddH2O) or
nesfatin-130−59 at 0.37, 1.1, and 3.3 μg (0.1, 0.3, 0.9 nmol/rat) and the food
intake microstructure assessed using a food intake monitoring system. Next,
naïve rats were injected ip with vehicle (300 μl saline) or nesfatin-130−59
(8.1, 24.3, 72.9 nmol/kg). Lastly, rats were fed a high fat diet for 10 weeks
and those developing DIO were icv cannulated. Nesfatin-1 (0.9 nmol/rat) or
vehicle (5 μl ddH2O) was injected icv and the food intake microstructure
assessed. In rats fed standard diet, nesfatin-130−59 caused a dose-dependent
reduction of dark phase food intake reaching significance at 0.9 nmol/rat in
the period of 4–8 h post injection (−29%) with the strongest reduction during
the fifth hour (−75%), an effect detectable for 24 h (−12%, p < 0.05 vs.
vehicle). The anorexigenic effect of nesfatin-130−59 was due to a reduction in
meal size (−44%, p < 0.05), while meal frequency was not altered compared to
vehicle. In contrast to icv injection, nesfatin-130−59 injected ip in up to
30-fold higher doses did not alter food intake. In DIO rats fed high fat diet,
nesfatin-130−59 injected icv reduced food intake in the third hour post
injection (−71%), an effect due to a reduced meal frequency (−27%, p < 0.05),
while meal size was not altered. Taken together, nesfatin-130−59 is the active
core of nesfatin-11−82 and acts centrally to reduce food intake in rats. The
anorexigenic effect depends on the metabolic condition with increased
satiation (reduction in meal size) under normal weight conditions, while in
DIO rats satiety (reduction in meal frequency) is induced
Human alveolar echinococcosis after fox population increase, Switzerland
We analyzed databases spanning 50 years, which included retrospective alveolar echinococcosis (AE) case finding studies and databases of the 3 major centers for treatment of AE in Switzerland. A total of 494 cases were recorded. Annual incidence of AE per 100,000 population increased from 0.12-0.15 during 1956-1992 and a mean of 0.10 during 1993-2000 to a mean of 0.26 during 2001-2005. Because the clinical stage of the disease did not change between observation periods, this increase cannot be explained by improved diagnosis. Swiss hunting statistics suggested that the fox population increased 4-fold from 1980 through 1995 and has persisted at these higher levels. Because the period between infection and development of clinical disease is long, the increase in the fox population and high Echinococcus multilocularis prevalence rates in foxes in rural and urban areas may have resulted in an emerging epidemic of AE 10-15 years later
Premature ovarian failure and ovarian autoimmunity
Premature ovarian failure (POF) is defined as a syndrome characterized by
menopause before the age of 40 yr. The patients suffer from anovulation
and hypoestrogenism. Approximately 1% of women will experience menopause
before the age of 40 yr. POF is a heterogeneous disorder with a
multicausal pathogenesis involving chromosomal, genetic, enzymatic,
infectious, and iatrogenic causes. There remains, however, a group of POF
patients without a known etiology, the so-called "idiopathic" form. An
autoimmune etiology is hypothesized for the POF cases with a concomitant
Addison's disease and/or oophoritis. It is concluded in this review that
POF in association with adrenal autoimmunity and/or Addison's disease
(2-10% of the idiopathic POF patients) is indeed an autoimmune disease.
The following evidence warrants this view: 1) The presence of
autoantibodies to steroid-producing cells in these patients; 2) The
characterization of shared autoantigens between adrenal and ovarian
steroid-producing cells; 3) The histological picture of the ovaries of
such cases (lymphoplasmacellular infiltrate around steroid-producing
cells); 4) The existence of various autoimmune animal models for this
syndrome, which underlines the autoimmune nature of the disease. There is
some circumstantial evidence for an autoimmune pathogenesis in idiopathic
POF patients in the absence of adrenal autoimmunity or Addison's disease.
Arguments in support of this are: 1) The presence of cellular immune
abnormalities in this POF patient group reminiscent of endocrine
autoimmune diseases such as IDDM, Graves' disease, and Addison's disease;
2) The more than normal association with IDDM and myasthenia gravis. Data
on the presence of various ovarian autoantibodies and anti-receptor
antibodies in these patients are, however, inconclusive and need further
evaluation. A strong argument against an autoimmune pathogenesis of POF in
these patients is the nearly absent histological confirmation (the
presence of an oophoritis) in these cases (< 3%). However, in animal
models using ZP immunization, similar follicular depletion and fibrosis
(as in the POF women) can be detected. Accepting the concept that POF is a
heterogenous disorder in which some of the idiopathic forms are based on
an abnormal self-recognition by th
Mass campaigns with antimalarial drugs: a modelling comparison of artemether-lumefantrine and DHA-piperaquine with and without primaquine as tools for malaria control and elimination
Cognitive Architecture, Concepts, and Introspection: An Information-Theoretic Solution to the Problem of Phenomenal Consciousness
The Emergence of Emotions
Emotion is conscious experience. It is the affective aspect of consciousness. Emotion arises from sensory stimulation and is typically accompanied by physiological and behavioral changes in the body. Hence an emotion is a complex reaction pattern consisting of three components: a physiological component, a behavioral component, and an experiential (conscious) component. The reactions making up an emotion determine what the emotion will be recognized as. Three processes are involved in generating an emotion: (1) identification of the emotional significance of a sensory stimulus, (2) production of an affective state (emotion), and (3) regulation of the affective state. Two opposing systems in the brain (the reward and punishment systems) establish an affective value or valence (stimulus-reinforcement association) for sensory stimulation. This is process (1), the first step in the generation of an emotion. Development of stimulus-reinforcement associations (affective valence) serves as the basis for emotion expression (process 2), conditioned emotion learning acquisition and expression, memory consolidation, reinforcement-expectations, decision-making, coping responses, and social behavior. The amygdala is critical for the representation of stimulus-reinforcement associations (both reward and punishment-based) for these functions. Three distinct and separate architectural and functional areas of the prefrontal cortex (dorsolateral prefrontal cortex, orbitofrontal cortex, anterior cingulate cortex) are involved in the regulation of emotion (process 3). The regulation of emotion by the prefrontal cortex consists of a positive feedback interaction between the prefrontal cortex and the inferior parietal cortex resulting in the nonlinear emergence of emotion. This positive feedback and nonlinear emergence represents a type of working memory (focal attention) by which perception is reorganized and rerepresented, becoming explicit, functional, and conscious. The explicit emotion states arising may be involved in the production of voluntary new or novel intentional (adaptive) behavior, especially social behavior
Improving basic and translational science by accounting for litter-to-litter variation in animal models
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