J B Furness

University of Melbourne, Melbourne, Victoria, Australia

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Publications (385)1242.4 Total impact

  • R.V. Pustovit · K. Naitou · L.R. Rivera · M.T. Ringuet · J.B. Furness ·

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    ABSTRACT: Background: It has been recently demonstrated that the ghrelin receptor agonist, HM01, caused defecation in rats that were treated to provide a model for the constipation of Parkinson's disease. HM01 significantly increased fecal output and increased Fos activity in neurons of the hypothalamus and hindbrain, but not in the spinal defecation center. Other ghrelin agonists act on the defecation center. Methods: Receptor pharmacology was examined in ghrelin receptor (GHSR1a) transfected cells. Anesthetized rats were used to investigate sites and mechanisms of action. Key results: HM01 activated rat GHSR1a at nanomolar concentrations and was antagonized by the GHSR1a antagonist, YIL781. HM01, intravenous, was potent to activate propulsive colorectal contractions. This was prevented by pelvic nerve section and by intravenous YIL781, but not by spinal cord section rostral to the defecation centers. Direct intrathecal application of HM01 to the defecation center at spinal level L6-S1 initiated propulsive contractions of the colorectum. Conclusions & inferences: HM01 stimulates GHSR1a receptors on neurons in the lumbosacral defecation centers to cause propulsive contractions and emptying of the colorectum. It has greater potency when given systemically, compared with other GHSR1a agonists.
    Neurogastroenterology and Motility 09/2015; DOI:10.1111/nmo.12688 · 3.59 Impact Factor
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    ABSTRACT: Focus Group. To develop a unified, regional spinal cord injury (SCI) research strategy for Australia and New Zealand. Australia. A 1-day structured stakeholder dialogue was convened in 2013 in Melbourne, Australia, by the National Trauma Research Institute in collaboration with the SCI Network of Australia and New Zealand. Twenty-three experts participated, representing local and international research, clinical, consumer, advocacy, government policy and funding perspectives. Preparatory work synthesised evidence and articulated draft principles and options as a starting point for discussion. A regional SCI research strategy was proposed, whose objectives can be summarised under four themes. (1) Collaborative networks and strategic partnerships to increase efficiency, reduce duplication, build capacity and optimise research funding. (2) Research priority setting and coordination to manage competing studies. (3) Mechanisms for greater consumer engagement in research. (4) Resources and infrastructure to further develop SCI data registries, evaluate research translation and assess alignment of research strategy with stakeholder interests. These are consistent with contemporary international SCI research strategy development activities. This first step in a regional SCI research strategy has articulated objectives for further development by the wider SCI research community. The initiative has also reinforced the importance of coordinated, collective action in optimising outcomes following SCI.Spinal Cord advance online publication, 23 June 2015; doi:10.1038/sc.2015.87.
    Spinal Cord 06/2015; 53(10). DOI:10.1038/sc.2015.87 · 1.80 Impact Factor
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    J. B. Furness · J. J. Cottrell · D. M. Bravo ·
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    ABSTRACT: The digestive systems of all species have been shaped by environmental pressures over long evolutionary time spans. Nevertheless, all digestive systems must achieve the same end points, the ingestion of biological material and its conversion to molecules that serve as energy substrates and structural components of tissues. A range of strategies to extract nutrients, including for animals reliant primarily on foregut fermentation, hindgut fermentation, and enzymatic degradation, have evolved. Moreover, animals have adapted to different foodstuffs as herbivores (including frugivores, folivores, granivores, etc.), carnivores, and omnivores. We present evidence that humans have diverged from other omnivores because of the long history of consumption of cooked or otherwise prepared food. We consider them to be cucinivores. We present examples to illustrate that the range of foodstuffs that can be efficiently assimilated by each group or species is limited and is different from that of other groups or species. Differences are reflected in alimentary tract morphology. The digestive systems of each group and of species within the groups are adaptable, with constraints determined by individual digestive physiology. Although overall digestive strategies and systems differ, the building blocks for digestion are remarkably similar. All vertebrates have muscular tubular tracts lined with a single layer of epithelial cells for most of the length, use closely related digestive enzymes and transporters, and control the digestive process through similar hormones and similarly organized nerve pathways. Extrapolations among species that are widely separated in their digestive physiologies are possible when the basis for extrapolation is carefully considered. Divergence is greatest at organ or organismal levels, and similarities are greatest at the cell and molecular level.
    Journal of Animal Science 02/2015; 93(2):485. DOI:10.2527/jas.2014-8481 · 2.11 Impact Factor
  • R. V. Pustovit · J. B. Furness · L. R. Rivera ·
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    ABSTRACT: Background Despite constipation being a common problem, the treatments that are available have side effects and are only partly effective. Recent studies show that centrally penetrant ghrelin receptor agonists cause defecation in humans and other species. Here, we describe some features of a rat model of low fiber-induced constipation, and investigate the effectiveness of the ghrelin agonist, capromorelin.Methods Rats were given low-fiber diets for 5 weeks. Their colorectal responsiveness to distension and to a behavioral test, water avoidance and colon histology were compared to those of rats on a standard diet.Key ResultsAfter the low-fiber diet, distension of the colon produced fewer propulsive contractions, behaviorally induced defecation was reduced, and the lining of the colorectum was inflamed. However, capromorelin was similarly effective in causing defecation in constipated and non-constipated rats.Conclusions & InferencesLow-fiber diet in rats produces a constipation phenotype, characterized by reduced responsiveness of the colorectum to distension and to a behavioral stimulus of defecation, water avoidance. The effectiveness of capromorelin suggests that centrally penetrant ghrelin receptor stimulants may be effective in treating constipation.
    Neurogastroenterology and Motility 01/2015; 27(5). DOI:10.1111/nmo.12517 · 3.59 Impact Factor
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    ABSTRACT: Introduction: Heat stress (HS) compromises intestinal barrier integrity by inducing oxidative stress. Our objective was to evaluate whether supra‐physiological dietary supplementation of selenium (Se) and Vitamin E (VE) can protect gut barrier integrity in heat stressed pigs. Material and methods: Forty‐eight gilts (av. 22.4 kg) were randomly assigned to four diets containing 0.2 ppm Se and 17 IU VE/kg (control), 0.3 ppm Se and 50 IU VE/kg, 0.5 ppm Se and 100 IU VE/kg, or 1.0 ppm Se and 200 IU VE/kg. After 14 d supplementation, six pigs from each dietary group were allocated to climate‐controlled rooms at 20°C (thermoneutral, TN) or HS (35°C, 9 am‐5 pm/ 28°C, rest of day) for 2 d. Respiration rate (RR) and rectal temperature (RT) were monitored between 9 am and 5 pm. After 48 h, pigs were euthanized and small intestinal weights were recorded. Trans‐epithelial resistance (TER) and FITC‐dextran (4 kDa; FD4) permeability were measured in jejunum and ileum samples using an Ussing chamber. Data were analyzed by linear mixed model in Genstat. Results and discussion: Pigs under HS condition had increased RT (P=0.01), RR (P=0.01), FD4 permeability (P=0.03), and decreased TER (P=0.03). Small intestinal weight was not affected (P=0.11). With increasing dose of anti‐oxidants the effects of HS were reduced, as characterized by enhanced TER and lowered FD4 permeability (P=0.02 for both). The highest two doses of anti‐oxidants ameliorated the effects of HS on intestinal integrity. In conclusion, supraphysiological supplementation of Se and VE alleviate heat stress damage to intestinal barrier integrity.
    Digestive Physiology of Pigs, Kliczkow, Poland; 01/2015
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    ABSTRACT: Pigs are comparatively less heat tolerant than other species of production animals, which poses challenges for stock productivity and management during seasonal heat waves that occur in summer. The issues surrounding heat and pig production are predicted to increase, based on the actions of climate change increasing the intensity, frequency and duration of heat waves. Furthermore, future growth areas of pig production are going to be in tropical regions such as South-east Asia and Latin America. Efforts by the pig to dissipate excess body heat come at a cost to health and divert energy away from growth, compromising efficient pig production. Management of heat stress requires multiple strategies, and recent research is improving the understanding of the application of nutritional strategies to ameliorate the effects of heat stress. In particular the use of feed additives is an important, flexible and economical method to alleviate heat stress and the intensive nature of pig production lends itself to the
    Animal Production Science 01/2015; DOI:10.1071/AN15255 · 1.29 Impact Factor
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    ABSTRACT: Introduction: Our experiment showed antioxidants supplementation improved intestinal trans-epithelial resistance (TER) in pigs under heat stress (HS), which is hypothetically due to alleviation of HS-induced oxidative stress (OS). Material and methods: Forty-eight gilts (av. 22.4 kg) were randomly assigned to four diets containing 0.2 ppm Selenium (Se) and 17 IU Vitamin E (VE)/kg (control), 0.3 ppm Se and 50 IU VE/kg, 0.5 ppm Se and 100 IU VE/kg, or 1.0 ppm Se and 200 IU VE/kg. After 14d supplementation, six pigs from each dietary treatment were allocated to climate-controlled rooms at 20°C (thermoneutral) or HS (35°C, 9am-5pm/ 28°C, rest of day) for 2d. Glutathione peroxidase (GPx), glutathione S-transferase (GST), superoxide dismutase (SOD), oxidized glutathione (GSSG), and total glutathione (GSH) were measured in jejunum and ileum homogenates. Data were analysed by ANOVA and correlation in Genstat 16th edition. Results and Discussion: HS attenuated GPx (P<0.01), but not GST or SOD activities. HS induced OS as HS tended to increase GSSG concentration (P=0.08) and increased GSSG/total GSH ratio (P<0.05). Along with increasing dosages, antioxidants linearly improved GPx activity (P<0.05), decreased GSSG (P=0.06) and GSSG/total GSH ratio (P<0.05), but not affect SOD and GST. The highest dose of antioxidants had higher GPx activity (P<0.05), lower GSSH (P=0.06) and GSSG/total GSH ratio (P<0.05) than control diet under HS. GPx and GST activities moderately correlated with TER (correlation=0.45 and -0.44, respectively). In conclusion, 1.0 ppm Se and 200 IU/kg VE alleviated HS-induced OS by improving GPx activity, which partially explained the maintained TER during HS.
    Digestive Physiology of Pigs, Kliczkow, Poland; 01/2015
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    J. B. Furness · J.J. Cottrell · D. M. Bravo ·

  • John Furness ·
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    ABSTRACT: Abstract Text: The optimal utilisation of nutrients requires an integrated response of the gastrointestinal tract to ingested food. Broad mechanisms are similar in all mammals, and involve sensing food components through olfaction, taste and specialised receptors within the stomach and intestines. The sensing of food components leads to release of gut hormones and activation of nerves, which in turn modify digestive functions. Bacteria, viruses, fungi and potentially injurious substances in foods activate tissue defence mechanisms. While the responses to nutrients lead to broadly similar changes in appetite, satiety and food-seeking behaviour, gastrointestinal motility, release of digestive enzymes and induction of nutrient transporters, the requirements in different animals differ. To simplify discussion, we can divide species into ruminant foregut fermenters (such as cattle and sheep), non-ruminant foregut fermenters (e.g., kangaroo, colobus monkey), hind-gut fermenters (such as horse), and auto-enzyme dependent digesters (pig, human) that also gain nutrition from hind-gut fermentation. Ruminants are efficient digesters because the rumenal movements are able to stratify food into gas, fluid and particle components, retaining food to be digested in the forestomach and passing more fully digested material into the abomasum and duodenum, and also being able to return food from the forestomach to the mouth for mastication and limited enzyme exposure. Poultry have multiple stomachs that allow for storage, digestion and tituration, but not fermentation. Ruminants lose efficiency in that most carbohydrate is utilised by gastric bacteria and very little glucose reaches the small intestine. Thus glucose must be synthesised from short chain fatty acids produced by bacteria, whereas species such as pig and human convert carbohydrate to glucose enzymatically. Thus ruminants are more prone than other groups to enter into negative glucose balance, for example during post-partum lactation. Obligatory by-products of fermentation are carbon dioxide and methane. Foregut fermenters are also advantaged by being able to readily utilise vitamins produced by fermentation. It is thought that coprophagy by hind-gut fermenters, such as rabbits, provides access to such vitamins. Foregut fermentation also contributes to detoxification, for which hindgut fermenters and autoenzymic digesters rely primarily on the liver. With these differences in mind, it is necessary to closely consider what information can be readily extrapolated between species. Conversely, we can point to similarities in neural and hormonal signalling systems and products of digestion, achieved in different ways, that are available for energy utilisation and incorporation into tissues. Keywords: digestive physiology; fermentation; glucose; comparative
    2014 ADSA-ASAS-CSAS Joint Annual Meeting; 07/2014
  • John Furness · Hyun-Jung Cho · Samin Kosari · David M Bravo ·
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    ABSTRACT: Abstract Text: Intestinal L cells have key roles in the detection of the chemical environment in the gut lumen, to which they react by the release of hormones that influence appetite, proximal gut motility, insulin secretion and mucosal function (Furness et al, Nature Gastroenterology, 10, 729–740, 2013). Important amongst L cell hormones are glucagon-like peptide1 (GLP-1) and peptide tyrosine-tyrosine (PYY), which are products of separate genes. The conventional description of their localisation is that GLP-1 and PYY are in the same storage vesicles in the same cells. However, GLP-1 and PYY have different functions, particularly in relation to insulin secretion and mucosal function. We have used super-resolution (3D-SIM) microscopy and double-labelling immunohistochemistry to investigate the subcellular localisations of the hormones, and digital scanning microscopy to investigate cell populations. Super-resolution microscopy revealed that GLP-1 and PYY are in separate storage organelles in enteroendocrine cells from mouse, rat, pig and human. The majority of the organelles were 150-170 nm or less in diameter, and are concluded to be secretory vesicles. Only 10-20% of organelles had immunoreactivity for both hormones. Even this may be an overestimate, as touching or very close vesicles may not be effectively resolved, even with super-resolution microscopy. In investigating co-localisation at the cell level, we included glucagon-like insulinotropic peptide (GIP), an incretin of K cells, in the analysis. The work shows that there is a K/L cell gradient in the mouse intestine. From the duodenum to the distal colon, there are populations of cells with GIP alone, GLP alone, PYY alone and all combinations of the three hormones. Greatest numbers of GIP cells were in the doudenum and jejunum, where 30-40% contained only GIP and the remainder also contained GLP-1. A small proportion also contained PYY. Similar patterns of overlap occurred in the proximal and distal ileum, where GLP-1 was the dominant peptide, which was often alone, or co-localised with PYY. In the large intestine the majority of cells contained both GLP-1 and PYY, but cells with only one of these and cells with all three hormones were found. The findings reveal a structural basis for the separate or preferential control of GLP-1, PYY (and possibly GIP) release. A number of physiological studies imply that there can be differential release of GLP-1 and PYY. This should be investigated further. Keywords: enteroendocrine cells, incretins, glucagon like peptide, peptideYY
    2014 ADSA-ASAS-CSAS Joint Annual Meeting; 07/2014
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    ABSTRACT: Background: Disorders of gastrointestinal functions that are controlled by enteric neurons commonly accompany fatty liver disease. Established fatty liver disease is associated with diabetes, which itself induces enteric neuron damage. Here, we investigate the relationship between fatty liver disease and enteric neuropathy, in animals fed a high-fat, high-cholesterol diet in the absence of diabetes. Methods: Mice were fed a high-fat, high-cholesterol diet (21% fat, 2% cholesterol) or normal chow for 33 weeks. Liver injury was assessed by hematoxylin and eosin, picrosirius red staining, and measurement of plasma alanine aminotransaminase (ALT). Quantitative immunohistochemistry was performed for different types of enteric neurons. Key results: The mice developed steatosis, steatohepatitis, fibrosis, and a 10-fold increase in plasma ALT, indicative of liver disease. Oral glucose tolerance was unchanged. Loss and damage to enteric neurons occurred in the myenteric plexus of ileum, cecum, and colon. Total numbers of neurons were reduced by 15-30% and neurons expressing nitric oxide synthase were reduced by 20-40%. The RNA regulating protein, Hu, became more concentrated in the nuclei of enteric neurons after high-fat feeding, which is an indication of stress on the enteric nervous system. There was also disruption of the neuronal cytoskeletal protein, neurofilament medium. Conclusions & inferences: Enteric neuron loss and damage occurs in animals with fatty liver disease in the absence of glucose intolerance. The enteric neuron damage may contribute to the gastrointestinal complications of fatty liver disease.
    Neurogastroenterology and Motility 06/2014; 26(8). DOI:10.1111/nmo.12385 · 3.59 Impact Factor
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    ABSTRACT: Objective: To analyse the temporal bones and implant of the first University of Melbourne's (UOM) patient (MC-1) to receive the multi-channel cochlear prosthesis. Methods: The left cochlea was implanted with the prototype multi-channel cochlear prosthesis on 1 August 1978, and the Cochlear versions CI-22 and CI-24 on 22 June 1983 and 10 November 1998, respectively. MC-1 died in 2007. Results: Plain X-rays of the temporal bones showed that after the CI-22 had been explanted seven electrode bands remained in situ. Micro-CT scans also revealed a partially united fracture transecting the left implanted and right control cochleae. Histology indicated a total loss of the organ of Corti on both sides, and a tear of the left basilar membrane. In addition, there was a dense fibrous capsule with heterotopic bone surrounding one proximal band of the CI-22 array that restricted its removal. This pathology was associated with dark particulate material within macrophages, probably due to the release of platinum from the electrode bands. Scanning electron microscopy (SEM) showed possible corrosion of platinum and surface roughening. Three-dimensional reconstruction of the cochlear histology demonstrated the position of the electrode tracts (C1-22 and CI-24) in relation to the spiral ganglion, which showed 85-90% loss of ganglion cells. Discussion and conclusions: This study confirms our first histopathological findings that our first free-fitting banded electrode array produced moderate trauma to the cochlea when inserted around the scala tympani of the basal turn. The difficulty in extraction was most likely due to one band being surrounded by an unusually large amount of fibrous tissue and bone, with an electrode band caught due to surface irregularities. Some surface corrosion and a small degree of platinum deposition in the tissue may also help explain the outcome for this long-term cochlear implantation.
    Cochlear Implants International 06/2014; 15(S2). DOI:10.1179/1754762814Y.0000000087
  • R V Pustovit · B Callaghan · S Kosari · L R Rivera · H Thomas · J A Brock · J B Furness ·
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    ABSTRACT: Discovery of adequate pharmacological treatments for constipation has proven elusive. Increased numbers of bowel movements were reported as a side-effect of ulimorelin treatment of gastroparesis, but there has been no investigation of the site of action. Anesthetized rats were used to investigate sites and mechanisms of action of ulimorelin. Intravenous ulimorelin (1-5 mg/kg) caused a substantial and prolonged (~1 h) increase in colorectal propulsive activity and expulsion of colonic contents. This was prevented by cutting the nerves emerging from the lumbosacral cord, by the nicotinic receptor antagonist hexamethonium and by antagonists of the ghrelin receptor. The effect of intravenous ulimorelin was mimicked by direct application of ulimorelin (5 μg) to the lumbosacral spinal cord. Ulimorelin is a potent prokinetic that causes propulsive contractions of the colorectum by activating ghrelin receptors of the lumbosacral defecation centers. Its effects are long-lasting, in contrast with other colokinetics that target ghrelin receptors.
    Neurogastroenterology and Motility 11/2013; 26(2). DOI:10.1111/nmo.12259 · 3.59 Impact Factor
  • J B Furness · D P Poole ·
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    ABSTRACT: The functioning of the gastrointestinal tract is under the control of the most extensive system of peripheral neurons in the body, the enteric nervous system, and the largest endocrine system of the body, the GEP endocrine system. The enteric nervous system in large mammals contains 500 million neurons, and the GEP endocrine system produces more than 30 hormones. Numerous enteric neuropathies affecting both humans and animals have been described and digestive disorders affect commercially important species, such as horses and cattle. The most severe enteric neuropathies (e.g., lethal white syndrome in horses or Hirschsprung's disease in humans) can be fatal. Also, horses with ileus or other digestive disorders are commonly euthanized. In this review we discuss examples of enteric neuropathies that affect agricultural animals and humans: prion disease, postoperative ileus, distal enteric aganglionosis, and infective diarrhea. Enteric neurons and glia are a location of prion proteins and are involved in transmission of the infection from gut to brain and brain to gut. Postoperative ileus is a complex disorder involving the local inhibitory effects of sympathetic nervous system activation and the release of opioids, presumably from enteric neurons. Intestinal inflammation, especially of the external muscle that includes enteric ganglia, also occurs in ileus. Congenital distal bowel aganglionosis, responsible for lethal white syndrome in horses, Hirschsprung's disease in humans, and similar conditions in mice and rats, is a fatal condition if untreated. Mutations of the same genes can cause the condition in each of these species. The only effective current treatment is surgical removal of the aganglionic bowel. Infectious diarrheas involve activation of enteric secretomotor neurons by pathogens and the toxins they produce, which causes substantial fluid loss. Strategies to target enteric neurons in the treatment of secretory diarrheas have not been developed. Disorders of enteroendocrine cells, other than GEP endocrine tumors, are less well documented. However, evidence for the involvement of gut endocrine cells in a subset of patients with irritable bowel syndrome, and in the symptomology of celiac disease, has been demonstrated. Further investigation of the involvement of enteric neural and endocrine signaling systems in digestive disorders, especially in agricultural and companion animals, may lead to diagnostic and therapeutic advances.
    Journal of Animal Science 12/2011; 90(4):1203-12. DOI:10.2527/jas.2011-4825 · 2.11 Impact Factor
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    L R Rivera · D P Poole · M Thacker · J B Furness ·
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    ABSTRACT: Nitric oxide (NO), produced by the neural nitric oxide synthase enzyme (nNOS) is a transmitter of inhibitory neurons supplying the muscle of the gastrointestinal tract. Transmission from these neurons is necessary for sphincter relaxation that allows the passage of gut contents, and also for relaxation of muscle during propulsive activity in the colon. There are deficiencies of transmission from NOS neurons to the lower esophageal sphincter in esophageal achalasia, to the pyloric sphincter in hypertrophic pyloric stenosis and to the internal anal sphincter in colonic achalasia. Deficits in NOS neurons are observed in two disorders in which colonic propulsion fails, Hirschsprung's disease and Chagas' disease. In addition, damage to NOS neurons occurs when there is stress to cells, in diabetes, resulting in gastroparesis, and following ischemia and reperfusion. A number of factors may contribute to the propensity of NOS neurons to be involved in enteric neuropathies. One of these is the failure of the neurons to maintain Ca(2+) homeostasis. In neurons in general, stress can increase cytoplasmic Ca(2+), causing a Ca(2+) toxicity. NOS neurons face the additional problem that NOS is activated by Ca(2+). This is hypothesized to produce an excess of NO, whose free radical properties can cause cell damage, which is exacerbated by peroxynitrite formed when NO reacts with oxygen free radicals.
    Neurogastroenterology and Motility 09/2011; 23(11):980-8. DOI:10.1111/j.1365-2982.2011.01780.x · 3.59 Impact Factor
  • L.R. Rivera · M. Thacker · L. Pontell · H.J. Cho · J.B. Furness ·

    Autonomic Neuroscience 09/2011; 163(s 1–2):58–59. DOI:10.1016/j.autneu.2011.05.062 · 1.56 Impact Factor

  • Autonomic Neuroscience 09/2011; 163(1):58-58. DOI:10.1016/j.autneu.2011.05.061 · 1.56 Impact Factor
  • H. S. Al Dera · M. D. Habgood · J. B. Furness · J. A. Brock ·

    Autonomic Neuroscience 09/2011; 163(1):69-69. DOI:10.1016/j.autneu.2011.05.090 · 1.56 Impact Factor

Publication Stats

20k Citations
1,242.40 Total Impact Points


  • 1969-2015
    • University of Melbourne
      • • Department of Anatomy and Neuroscience
      • • School of Botany
      • • Department of Physiology
      • • Department of Zoology
      Melbourne, Victoria, Australia
  • 1971-2002
    • Victoria University Melbourne
      Melbourne, Victoria, Australia
  • 1991
    • The Royal Children's Hospital
      Melbourne, Victoria, Australia
  • 1975-1991
    • Flinders University
      • • Department of Anatomy and Histology
      • • School of Medicine
      • • Centre for Neuroscience
      Tarndarnya, South Australia, Australia
  • 1987
    • Westmead Hospital
      Sydney, New South Wales, Australia
  • 1986
    • Neuroscience Research Australia
      Sydney, New South Wales, Australia
  • 1982
    • University of South Australia
      Tarndarnya, South Australia, Australia
  • 1980
    • National Institute of Mental Health (NIMH)
      • Laboratory of Clinical Science
      Maryland, United States
  • 1977
    • Prince Henry's Institute
      Melbourne, Victoria, Australia
  • 1972
    • University of Birmingham
      Birmingham, England, United Kingdom