The developmental and acute phases of insulin-induced laminitis involve minimal metalloproteinase activity

Metalloproteinases have been implicated in the pathogenesis of equine laminitis and other inflammatory conditions, through their role in the degradation and remodelling of the extracellular matrix environment. Matrix metalloproteinases (MMPs) and their inhibitors are present in normal equine lamellae, with increased secretion and activation of some metalloproteinases reported in horses with laminitis associated with systemic inflammation. It is unknown whether these enzymes are involved in insulin-induced laminitis, which occurs without overt systemic inflammation. In this study, gene expression of MMP-2, MMP-9, MT1-MMP, ADAMTS-4 and TIMP-3 was determined in the lamellar tissue of normal control horses (n = 4) and horses that developed laminitis after 48 h of induced hyperinsulinaemia (n = 4), using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Protein concentrations of MMP-2 and MMP-9 were also examined using gelatin zymography in horses subject to prolonged hyperinsulinaemia for 6 h (n = 4), 12 h (n = 4), 24 h (n = 4) and 48 h (n = 4), and in normal control horses (n = 4). The only change in gene expression observed was an upregulation of MMP-9 (p < 0.05) in horses that developed insulin-induced laminitis (48 h). Zymographical analysis showed an increase (p < 0.05) in pro MMP-9 during the acute phase of laminitis (48 h), whereas pro MMP-2 was present in similar concentration in the tissue of all horses. Thus, MMP-2, MT1-MMP, TIMP-3 and ADAMTS-4 do not appear to play a significant role in the pathogenesis of insulin-induced laminitis. The increased expression of MMP-9 may be associated with the infiltration of inflammatory leukocytes, or may be a direct result of hyperinsulinaemia. The exact role of MMP-9 in basement membrane degradation in laminitis is uncertain as it appears to be present largely in the inactive form.

Food insecurity among Australian children : potential determinants, health and developmental consequences

Children in food-insecure households may be at risk of poor health, developmental or behavioural problems. This study investigated the associations between food insecurity, potential determinants and health and developmental outcomes among children. Data on household food security, socio-demographic characteristics and children’s weight, health and behaviour were collected from households with children aged 3–17 years in socioeconomically disadvantaged suburbs by mail survey using proxy-parental reports (185 households). Data were analysed using logistic regression. Approximately one-in-three households (34%) were food insecure. Low household income was associated with an increased risk of food insecurity [odds ratio (OR), 16.20; 95% confidence interval (CI), 3.52–74.47]. Children with a parent born outside of Australia were less likely to experience food insecurity (OR, 0.42; 95% CI, 0.19–0.93). Children in food-insecure households were more likely to miss days from school or activities (OR, 3.52; 95% CI, 1.46–8.54) and were more likely to have borderline or atypical emotional symptoms (OR, 2.44; 95% CI, 1.11–5.38) or behavioural difficulties (OR, 2.35; 95% CI, 1.04–5.33). Food insecurity may be prevalent among socioeconomically disadvantaged households with children. The potential developmental consequences of food insecurity during childhood may result in serious adverse health and social implications.

Developmental components of resting ventilation among high- and low-altitude Andean children and adults

This paper evaluates the age-associated changes of resting ventilation of 115 high- and low-altitude Aymara subjects, of whom 61 were from the rural Aymara village of Ventilla situated at an average altitude of 4,200 m and 54 from the rural village of Caranavi situated at an average altitude of 900 m. Comparison of the age patterns of resting ventilation suggests the following conclusions: 1) the resting ventilation (ml/kg/min) of high-altitude natives is markedly higher than that of low-altitude natives; 2) the age decline of ventilation is similar in both lowlanders and highlanders, but the starting point and therefore the age decline are much higher at high altitude; 3) the resting ventilation that characterizes high-altitude Andean natives is developmentally expressed in the same manner as it is at low altitude; and 4) the resting ventilation (ml/kg/min) of Aymara high-altitude natives is between 40–80% lower than that of Tibetans. Am J Phys Anthropol 109:295–301, 1999. © 1999 Wiley-Liss, Inc.

Self-regulation and mastery motivation in individuals with developmental disabilities : barriers, supports, and strategies

The development of the capacity for self-regulation represents an important achievement of childhood and is associated with social, behavioral, and academic competence (Bronson, 2001; Cleary & Zimmerman, 2004). Self-regulation evolves as individuals mature, with its final form integrating emotional, cognitive, and behavioral elements working together to achieve self-selected goals. This evolution is closely intertwined with the innate press to master the environment, labeled mastery motivation (Morgan, Harmon, & Maslin-Cole, 1990), as competence is the aim that underpins mastery motivation.

Children with autistic spectrum disorder have an associated risk of depression

Over recent years there has been an increase in the literature examining youth with Autism Spectrum Disorders (ASD). The growth in this area of research has highlighted a significant gap in our understanding of suitable interventions for people with ASD and the treatment of co-occurring psychiatric disorders.1-3 Children with ASD are at increased risk of experiencing depressive symptoms and developing depression; however with very few proven interventions available for preventing and treating depression in children with ASD, there is a need for further research in this area.

From ABCs to ADHD : the role of schooling the construction of behaviour disorder and the production of disorderly objects

Discussion of Attention-Deficit/Hyperactivity Disorder (ADHD) in the media, and thus much popular discourse, typically revolves around the possible causes of disruptive behaviour and the “behaviourally disordered” child. The usual suspects - too much television and video games, food additives, bad parenting, lack of discipline and single mothers – feature prominently as potential contributors to the spiralling rate of ADHD diagnosis in Western industrialised nations, especially the United States and Australia. Conspicuously absent from the field of investigation, however, is the scene of schooling and the influence that the discourses and practices of schooling might bring to bear upon the constitution of “disorderly behaviour” and subsequent recognition of particular children as a particular kind of “disorderly”. This paper reviews a sample of the literature surrounding ADHD, in order to question the function of this absence and, ultimately, make an argument for an interrogation of the school as a site for the production of disorderly objects.

Out of sight, out of mind/out of mind, out of site : Schooling and attention deficit hyperactivity disorder

Attention Deficit Hyperactivity Disorder is a diagnostic term now indelibly scored on the public psyche. In some quarters, a diagnosis of “ADHD” is regarded with derision. In others it is welcomed with relief. Despite intense multi-disciplinary research, the jury is still out with regards to the “truth” of ADHD. Not surprisingly, the rapid increase in diagnosis over the past fifteen years, coupled with an exponential rise in the prescription of restricted class psychopharmaceuticals has stirred virulent debate. Provoking the most interest, it seems, are questions regarding causality. Typically, these revolve around possible antecedents for “disorderly” behaviour – bad food, bad tv and bad parents. Very seldom is the institution of schooling ever in the line of sight. To investigate this gap, I draw on Foucault to question what might be happening in schools and how this may be contributing to the definition, recognition and classification of particular children as a particular kind of “disorderly”.

Histological and morphometric lesions in the pre-clinical, developmental phase of insulin-induced laminitis in Standardbred horses

Lamellar pathology in experimentally-induced equine laminitis associated with euglycaemic hyperinsulinaemia is substantial by the acute, clinical phase (∼48 h post-induction). However, lamellar pathology of the developmental, pre-clinical phase requires evaluation. The aim of this study was to analyse lamellar lesions both qualitatively and quantitatively, 6, 12 and 24 h after the commencement of hyperinsulinaemia. Histological and histomorphometrical analyses of lamellar pathology at each time-point included assessment of lamellar length and width, epidermal cell proliferation and death, basement membrane (BM) pathology and leucocyte infiltration. Archived lamellar tissue from control horses and those with acute, insulin-induced laminitis (48 h) was also assessed for cellular proliferative activity by counting the number of cells showing positive nuclear immuno labelling for TPX2. Decreased secondary epidermal lamellar (SEL) width and increased histomorphological evidence of SEL epidermal basal (and supra-basal) cell death occurred early in disease progression (6 h). Increased cellular proliferation in SELs, infiltration of the dermis with small numbers of leucocytes and BM damage occurred later (24 and 48 h). Some lesions, such as narrowing of the SELs, were progressive over this time period (6–48 h). Cellular pathology preceded leucocyte infiltration and BM pathology, indicating that the latter changes may be secondary or downstream events in hyperinsulinaemic laminitis.

A commentary on the current and future status of educational and developmental psychology in Australia

Educational and developmental psychology faces a number of current and future challenges and opportunities in Australia. In this commentary we consider the identity of educational and developmental psychology in terms of the features that distinguish it from other specialisations, and address issues related to training, specialist endorsement, supervision and rebating under the Australian government's Medicare system. The current status of training in Australia is considered through a review of the four university programs in educational and developmental psychology currently offered, and the employment destinations of their graduates. Although the need for traditional services in settings such as schools, hospitals, disability and community organisations will undoubtedly continue, the role of educational and developmental psychologists is being influenced and to some extent redefined by advances in technology, medicine, genetics, and neuroscience. We review some of these advances and conclude with recommendations for training and professional development that will enable Australian educational and developmental psychologists to meet the challenges ahead.

Developmental lessons from the Capricornia Arts Mob : ‘learning to speak with one voice’

The Capricornia Arts Mob also known as CAM is a collective of Aboriginal and Torres Strait Islander visual artists, sculptors, photographers, carvers and writers based in the Rockhampton Region. Its members are eclectic and include an 18 year old through to Elders. CAM has already had a major exhibition in Rockhampton and is submitting work to a range of arts festivals, events and exhibitions. While their achievements are steadily growing and they have been meeting for 18 months, they have been reluctant to incorporate or implement a formalised structure. In learning how to work together there have been tensions and struggles, there has also been the exhilaration of working collaboratively as artists from diverse Indigenous cultures who utilise different mediums. This has resulted in an incredible vibrancy in creative praxis. Members will share some of CAM’s learnings of the developmental process to date and thoughts and dreams about the future.

Countering the Attention Deficit Hyperactivity Disorder epidemic: a question of ethics?

Recently in Australia, another media skirmish has erupted over the problem we currently call “Attention Deficit Hyperactivity Disorder”. This particular event was precipitated by the comments of a respected District Court judge. His claim that doctors are creating a generation of violent juvenile offenders by prescribing Ritalin to young children created a great deal of excitement, attracting the attention of election-conscious politicians who appear blissfully unaware of the role played by educational policy in creating and maintaining the problem. Given the short (election-driven) attention span of government policymakers, I bypass government to question what those at the front line can do to circumvent the questionable practice of diagnosing and medicating young children for difficulties they experience in schools and with learning.

Unique X-linked familial FSGS with co-segregating heart block disorder is associated with a mutation in the NXF5 gene

Focal segmental glomerulosclerosis (FSGS) is the consequence of a disease process that attacks the kidney's filtering system, causing serious scarring. More than half of FSGS patients develop chronic kidney failure within 10 years, ultimately requiring dialysis or renal transplantation. There are currently several genes known to cause the hereditary forms of FSGS (ACTN4, TRPC6, CD2AP, INF2, MYO1E and NPHS2). This study involves a large, unique, multigenerational Australian pedigree in which FSGS co-segregates with progressive heart block with apparent X-linked recessive inheritance. Through a classical combined approach of linkage and haplotype analysis, we identified a 21.19 cM interval implicated on the X chromosome. We then used a whole exome sequencing approach to identify two mutated genes, NXF5 and ALG13, which are located within this linkage interval. The two mutations NXF5-R113W and ALG13-T141L segregated perfectly with the disease phenotype in the pedigree and were not found in a large healthy control cohort. Analysis using bioinformatics tools predicted the R113W mutation in the NXF5 gene to be deleterious and cellular studies support a role in the stability and localization of the protein suggesting a causative role of this mutation in these co-morbid disorders. Further studies are now required to determine the functional consequence of these novel mutations to development of FSGS and heart block in this pedigree and to determine whether these mutations have implications for more common forms of these diseases in the general population.

A novel immunodeficiency disorder characterized by genetic amplification of interleukin 25

Many primary immunodeficiency disorders of differing etiologies have been well characterized, and much understanding of immunological processes has been gained by investigating the mechanisms of disease. Here, we have used a whole-genome approach, employing single-nucleotide polymorphism and gene expression microarrays, to provide insight into the molecular etiology of a novel immunodeficiency disorder. Using DNA copy number profiling, we define a hyperploid region on 14q11.2 in the immunodeficiency case associated with the interleukin (IL)-25 locus. This alteration was associated with significantly heightened expression of IL25 following T-cell activation. An associated dominant type 2 helper T cell bias in the immunodeficiency case provides a mechanistic explanation for recurrence of infections by pathogens met by Th1-driven responses. Furthermore, this highlights the capacity of IL25 to alter normal human immune responses.