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  • 1990-1994  (6)
  • intracranial pressure  (3)
  • diabetes  (2)
  • Diptera
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 37 (1994), S. 1280-1286 
    ISSN: 1432-0428
    Keywords: Key words Diet ; diabetes ; carbohydrate ; protein ; evolution.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We postulate a critical role for the quantity and quality of dietary carbohydrate in the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM). Our primate ancestors ate a high-carbohydrate diet and the brain and reproductive tissues evolved a specific requirement for glucose as a source of fuel. But the Ice Ages which dominated the last two million years of human evolution brought a low-carbohydrate, high-protein diet. Certain metabolic adaptations were therefore necessary to accommodate the low glucose intake. Studies in both humans and experimental animals indicate that the adaptive (phenotypic) response to low-carbohydrate intake is insulin resistance. This provides the clue that insulin resistance is the mechanism for coping with a shortage of dietary glucose. We propose that the low-carbohydrate carnivorous diet would have disadvantaged reproduction in insulin-sensitive individuals and positively selected for individuals with insulin resistance. Natural selection would therefore result in a high proportion of people with genetically-determined insulin resistance. Other factors, such as geographic isolation, have contributed to further increases in the prevalence of the genotype in some population groups. Europeans may have a low incidence of diabetes because they were among the first to adopt agriculture and their diet has been high in carbohydrate for 10,000 years. The selection pressure for insulin resistance (i. e., a low-carbohydrate diet) was therefore relaxed much sooner in Caucasians than in other populations. Hence the prevalence of genes producing insulin resistance should be lower in the European population and any other group exposed to high-carbohydrate intake for a sufficiently long period of time. [Diabetologia (1994) 37: 1280–1286]
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 105 (1990), S. 158-168 
    ISSN: 0942-0940
    Keywords: Brain edema ; cerebral blood flow ; brain tissue hydraulic resistance ; somatosensory evoked potential ; intracranial pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To evaluate the potency of putative secondary mediators of brain edema and their possible contribution to edema related brain dysfunction an infusion model of brain edema was developed in rats. 100 ul of fluid (saline, 20% nonautologous protein) was infused over one hour into the left forebrain white matter through a stereotaxically placed (+ 1.2 mm ant to bregma, 3 mm lateral and 2.9 mm depth) 25 G needle. Brain tissue hydraulic resistance (Rt), regional cerebral blood flow (rCBF), cortical somatosensory evoked potentials (SEPs) and intracranial pressure (ICP) (intraventricular needle) were monitored during the infusion and rCBF CO2 reactivity (hydrogen clearance), local brain water content (microgravimetry), BBB integrity (Evans Blue 2%) and brain histology (H & E, Solochrome-cyanin) were evaluated after the infusion. Saline infusates caused no physiological dysfunction despite ipsilateral expansion and vacuolation of the subcortical white matter, separation of axonal bundles and a significant decrease (p=3.8×10−5)in local subcortical tissue specific gravity. Cortical histology and specific gravity adjacent to the infusion locus were normal. Rt significantly decreased (p=6.5×10−4) during the infusion but there were only minor increases in ICP. Findings with 20% protein infusates were similar despite a focal 65% decrement in the rCBF CO2 reactivity adjacent to the infusion site. This study has shown that a simple and inexpensive model of infusion brain edema can be created in the rat and that it provides a useful model for assessing the physiological effects of mediator compounds in the infusate. Potential applications and methodological improvements for this model are discussed.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 37 (1994), S. 1280-1286 
    ISSN: 1432-0428
    Keywords: Diet ; diabetes ; carbohydrate ; protein ; evolution
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We postulate a critical role for the quantity and quality of dietary carbohydrate in the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM). Our primate ancestors ate a high-carbohydrate diet and the brain and reproductive tissues evolved a specific requirement for glucose as a source of fuel. But the Ice Ages which dominated the last two million years of human evolution brought a low-carbohydrate, high-protein diet. Certain metabolic adaptations were therefore necessary to accommodate the low glucose intake. Studies in both humans and experimental animals indicate that the adaptive (phenotypic) response to low-carbohydrate intake is insulin resistance. This provides the clue that insulin resistance is the mechanism for coping with a shortage of dietary glucose. We propose that the low-carbohydrate carnivorous diet would have disadvantaged reproduction in insulin-sensitive individuals and positively selected for individuals with insulin resistance. Natural selection would therefore result in a high proportion of people with genetically-determined insulin resistance. Other factors, such as geographic isolation, have contributed to further increases in the prevalence of the genotype in some population groups. Europeans may have a low incidence of diabetes because they were among the first to adopt agriculture and their diet has been high in carbohydrate for 10,000 years. The selection pressure for insulin resistance (i.e., a low-carbohydrate diet) was therefore relaxed much sooner in Caucasians than in other populations. Hence the prevalence of genes producing insulin resistance should be lower in the European population and any other group exposed to high-carbohydrate intake for a sufficiently long period of time.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 0942-0940
    Keywords: Blood brain barrier ; cerebral blood flow ; intracranial pressure ; arachidonic acid ; brain oedema ; evoked potential
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Arachidonic acid solution (2 to 15 mg/ml) was infused into the right forebrain white matter of anaesthetised cats over three hours to evaluate its contribution to the genesis and pathophysiology of vasogenic brain oedema. The 0.6 ml infusion increased local white matter water content by a mean of 11.3 ml/100 g tissue but did not increase cortical water content. Histological studies revealed local expansion and trabeculation of the white matter with aggregations of granulocytic neutrophils in the venules and perivenular brain. The adjacent cortical cytoarchitecture was normal. The white matter around the infusion site was stained lightly and over a variable area (15–20 mm2) by intravenously administered Evans Blue dye 2%. Regional cerebral blood flow (rCBF) adjacent to the frontal infusion did not change significantly during the period of infusion and remained similar to rCBF in the contralateral hemisphere. Following the arachidonic acid infusion regional CBF CO2 reactivity was normal and three was no asymmetry of either cortical somatosensory evoked potential (SEP) or motor evoked potential (MEP) waveforms. The increase in brain water content and changes in the ICP and ICP related biodynamics (pressure-volume index, lumped craniospinal compliance and CSF outflow resistance) were similar to those seen following infusion of 0.6 ml saline. These studies suggest that free intraparenchymal arachidonic acid, at concentrations exceeding those occurring in most neuropathological conditions, can increase the normal brain parenchymal capillary permeability but does not disrupt focal cerebrovascular and electrophysiological function. The clinical implications of these findings are discussed.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 115 (1992), S. 53-59 
    ISSN: 0942-0940
    Keywords: Bradykinin ; intracranial pressure ; evoked potentials ; cerebral blood flow ; brain edema ; blood brain barrier
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The feline infusion model of brain edema was used to evaluate the role of bradykinin in the etiology and pathophysiology of vasogenic brain edema. Bradykinin (3 or 90 ug in 600 μL saline) did not alter normocapnic regional cerebral blood flow (rCBF) nor induce specific changes in either the somatosensory (SEP) or motor (MEP) evoked potentials. The mean increases in ICP (from 4.5 to 16.1 mmHg) and peri-infusion white matter water content (from 69.4 to 79.8 ml/100 g tissue), mean decrease in lumped craniospinal compliance (from 0.040 to 0.014 ml/mmHg) and local histological changes were all similar to those after 600 μL saline infusion. The interstitial bradykinin infusion caused focal blood-brain-barrier (BBB) opening to Evans Blue dye and was chemotaxic for granulocytes. After the infusion there was a global loss of rCBF CO2 reactivity but there was no ischemia at normocapnia. These results show that bradykinin in brain edema fluid, at concentrations greater than those found in neuropathological conditions, can open the BBB of normal cerebral parenchymal capillaries and cause vascular dysregulation. In neuropathological conditions bradykinin may therefore potentiate formation of vasogenic brain edema but does not contribute to perilesional brain dysfunction.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Journal of insect behavior 4 (1991), S. 773-792 
    ISSN: 1572-8889
    Keywords: Delia antiqua ; Anthomyiidae ; Diptera ; herbivore ; egg-laying ; host-finding ; sensory systems ; chemoreception ; n-dipropyl disulfide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Behavioral responses of female onion flies, Delia antiqua (Meigen), to hostplant cues were quantified during encounters of individual flies with onion plants and onion foliar surrogates. The behavioral repertoire of such females included sitting, grooming, running up and down foliar surfaces, extension of the proboscis such that the labellum contacted foliar and soil surfaces, movements of the tip of the abdomen over surfaces (surface probing), subsurface probing of soil crevices with the ovipositor, and oviposition. Sequences of behaviors preceding oviposition were probabilistic rather than highly stereotyped but generally followed the order given above. Foliar surrogates were used to determine the effects of n-dipropyl disulfide (Pr2S2) on the sequence of behaviors leading up to oviposition. The addition of a Pr2S2-treated surrogate to a cage increased the frequency of alighting on that surrogate but also increased alighting on a nearby foliar surrogate without Pr2S2. After alighting, females encountering surrogates treated with Pr2S2 had shorter latencies to proboscis extension and surface probing, spent less time sitting and grooming, and had runs of shorter duration. These females were also more likely to make the transition from probing of surfaces of foliage and soil to subsurface probing of soil crevices and oviposition. Thus, rather than mediating a particular step in the behavioral sequence, Pr2S2 played a role throughout the sequence leading up to oviposition. Collectively, these data and past studies on the onion fly support the hypothesis that egglaying is triggered by a temporal summation of inputs to the central nervous system from various sensory modalities rather than strict behavioral chaining, with each transition effected by some unique cue.
    Type of Medium: Electronic Resource
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