"First Aid for Scalds" campaign: reaching Sydney''s Chinese, Vietnamese, and Arabic speaking communities

OBJECTIVES: As a serious yet preventable problem, scald injuries in children have been a priority for prevention in Australia and other developed countries. Not only can the occurrence of scalds be prevented, but immediate first aid treatment offers an effective method for secondary prevention, reducing the severity of scalds. Despite the success of scald prevention initiatives, local evidence suggested that first aid knowledge was lacking in some minority ethnic groups. To redress this gap, the "First Aid for Scalds" campaign for those from a non-English speaking background was specifically targeted to three ethnic groups (Vietnamese, Chinese, and Arabic), with the aim of increasing the proportions of parents and caregivers who had correct knowledge of first aid treatment for scalds. The primary strategy was a media campaign, including advertisements on ethnic radio and in ethnic newspapers. METHODS: The evaluation design included formative research and impact evaluation. The impact evaluation study involved random population based telephone surveys with each of the three language groups, before and after the campaign, to assess the reach and effectiveness of the campaign. RESULTS: After the campaign, there were significant increases in the proportion of people who knew the correct first aid treatment for scalds. There were substantial variations in campaign recall and knowledge between each of the three language groups. The largest improvement was found in the Vietnamese group. CONCLUSION: The association between campaign recall and increase in correct knowledge, and the absence of any similar interventions during the campaign period, give credence to the conclusion that the changes observed were a result of the campaign. The results demonstrate the value of community based injury prevention campaigns specifically targeting linguistically diverse communities.     

Neonatal hemangiomatosis and atrial septal defect: a rare cause of right heart failure in infancy

Neonatal hemangiomatosis is a well-recognized cause of left ventricular failure. We describe an infant with neonatal hemangiomatosis and an ostium secundum atrial septal defect who developed severe right heart failure. This was due to the combination of increased flow through the right heart as a result of the atrial septal defect, and the background high cardiac output from the massive arteriovenous shunting and multiple hemangiomas. In addition, the multiple hepatic hemangiomas may exert a vasoactive influence on the pulmonary vasculature.     

Comparative cellular distribution of GABAA and GABAB receptors in the human basal ganglia: immunohistochemical colocalization of the alpha 1 subunit of the GABAA receptor, and the GABABR1 and GABABR2 receptor subunits

The GABA(B) receptor is a G-protein linked metabotropic receptor that is comprised of two major subunits, GABA(B)R1 and GABA(B)R2. In this study, the cellular distribution of the GABA(B)R1 and GABA(B)R2 subunits was investigated in the normal human basal ganglia using single and double immunohistochemical labeling techniques on fixed human brain tissue. The results showed that the GABA(B) receptor subunits GABA(B)R1 and GABA(B)R2 were both found on the same neurons and followed the same distribution patterns. In the striatum, these subunits were found on the five major types of interneurons based on morphology and neurochemical labeling (types 1, 2, 3, 5, 6) and showed weak labeling on the projection neurons (type 4). In the globus pallidus, intense GABA(B)R1 and GABA(B)R2 subunit labeling was found in large pallidal neurons, and in the substantia nigra, both pars compacta and pars reticulata neurons were labeled for both receptor subunits. Studies investigating the colocalization of the GABA(A) alpha(1) subunit and GABA(B) receptor subunits showed that the GABA(A) receptor alpha(1) subunit and the GABA(B)R1 subunit were found together on GABAergic striatal interneurons (type 1 parvalbumin, type 2 calretinin, and type 3 GAD neurons) and on neurons in the globus pallidus and substantia nigra pars reticulata. GABA(B)R1 and GABA(B)R2 were found on substantia nigra pars compacta neurons but the GABA(A) receptor alpha(1) subunit was absent from these neurons. The results of this study provide the morphological basis for GABAergic transmission within the human basal ganglia and provides evidence that GABA acts through both GABA(A) and GABA(B) receptors. That is, GABA acts through GABA(B) receptors, which are located on most of the cell types of the striatum, globus pallidus, and substantia nigra. GABA also acts through GABA(A) receptors containing the alpha(1) subunit on specific striatal GABAergic interneurons and on output neurons of the globus pallidus and substantia nigra pars reticulata.     

Why do cancers have high aerobic glycolysis?

If carcinogenesis occurs by somatic evolution, then common components of the cancer phenotype result from active selection and must, therefore, confer a significant growth advantage. A near-universal property of primary and metastatic cancers is upregulation of glycolysis, resulting in increased glucose consumption, which can be observed with clinical tumour imaging. We propose that persistent metabolism of glucose to lactate even in aerobic conditions is an adaptation to intermittent hypoxia in pre-malignant lesions. However, upregulation of glycolysis leads to microenvironmental acidosis requiring evolution to phenotypes resistant to acid-induced cell toxicity. Subsequent cell populations with upregulated glycolysis and acid resistance have a powerful growth advantage, which promotes unconstrained proliferation and invasion.     

Expanding metabolic screening of newborns: can the health care industry do better than public health?

In Oklahoma since the early 1990s, all newborns have been screened for four metabolic conditions: phenylketonuria, hypothyroidism, galactosemia and hemoglobinopathies. In 2002, 38 affected babies were diagnosed and one expects they are saved from the complications of late diagnosis such as mental retardation or death from sepsis. With advances in genetics and improved biochemical assays, 86% of states now screen for more disorders than Oklahoma, up to 37 in Mississippi. Six recent patient vignettes illustrate the mortality and morbidity of conditions that are screened for elsewhere but not in Oklahoma. In 2001, the Oklahoma Genetics Advisory Council recommended adding three disorders and the State Health Department forecasts that implementation may be complete in 2007. For now, when a patient asks, "Will my baby be screened for as many metabolic conditions as possible?", two answers represent either the public health or the private health care view. The public health answer is, "The state requires screening for four conditions." The health care system answer is, "We can work with you to get 44 conditions tested for, but it will cost money, may not be reimbursed, and has not been proven effective when done on an individual basis." This dilemma, not unique to newborn screening, might be resolved if professional and public opinion strongly supported early expansion.     

Cortical effects of shifting letter position in letter strings of varying length

Neuroimaging and lesion studies suggest that occipito-temporal brain areas play a necessary role in recognizing a wide variety of objects, be they faces, letters, numbers, or household items. However, many questions remain regarding the details of exactly what kinds of information are processed by the occipito-temporal cortex. Here, we address this question with respect to reading. Ten healthy adult subjects performed a single word reading task. We used whole-head magnetoencephalography to measure the spatio-temporal dynamics of brain responses, and investigated their sensitivity to: (1) lexicality (defined here as the difference between words and consonant strings), (2) word length, and (3) variation in letter position. Analysis revealed that midline occipital activity around 100 msec, consistent with low-level visual feature analysis, was insensitive to lexicality and variation in letter position, but was slightly affected by string length. Bilateral occipito-temporal activations around 150 msec were insensitive to lexicality and reacted to word length only in the timing (and not strength) of activation. However, vertical shifts in letter position revealed a hemispheric imbalance: The right hemisphere activation increased with the shifts, whereas the opposite pattern was evident in the left hemisphere. The results are discussed in the light of Caramazza and Hillis's (1990) model of early reading.     

Somatostatin receptor 2 knockout/lacZ knockin mice show impaired motor coordination and reveal sites of somatostatin action within the striatum

The peptide somatostatin can modulate the functional output of the basal ganglia. The exact sites and mechanisms of this action, however, are poorly understood, and the physiological context in which somatostatin acts is unknown. Somatostatin acts as a neuromodulator via a family of five 7-transmembrane G protein-coupled receptors, SSTR1-5, one of which, SSTR2, is known to be functional in the striatum. We have investigated the role of SSTR2 in basal ganglia function using mice in which Sstr2 has been inactivated and replaced by the lacZ reporter gene. Analysis of Sstr2lacZ expression in the brain by beta-galactosidase histochemistry demonstrated a widespread pattern of expression. By comparison to previously published in situ hybridization and immunohistochemical data, Sstr2lacZ expression was shown to accurately recapitulate that of Sstr2 and thus provided a highly sensitive model to investigate cell-type-specific expression of Sstr2. In the striatum, Sstr2 expression was identified in medium spiny projection neurons restricted to the matrix compartment and in cholinergic interneurons. Sstr2 expression was not detected in any other nuclei of the basal ganglia except for a sparse number of nondopaminergic neurons in the substantia nigra. Microdialysis in the striatum showed Sstr2-null mice were selectively refractory to somatostatin-induced dopamine and glutamate release. In behavioural tests, Sstr2-null mice showed normal levels of locomotor activity and normal coordination in undemanding tasks. However, in beam-walking, a test of fine motor control, Sstr2-null mice were severely impaired. Together these data implicate an important neuromodulatory role for SSTR2 in the striatum.