Mathematical analysis of a model for AVL-HIV co-endemicity.

A model for the transmission dynamics of Anthroponotic Visceral Leishmaniasis (AVL) and human immunodeficiency virus (HIV) in a population is developed and used to assess the impact of the spread of each disease on the overall transmission dynamics. As for other vector-borne disease models, the AVL component of the model undergoes backward bifurcation when the associated reproduction number of the AVL-only sub-model (denoted by RL) is less than unity. Uncertainty and sensitivity analyzes of the model, using data relevant to the dynamics of the two diseases in Ethiopia, show that the top three parameters that drive the AVL infection (with respect to the associated response function, RL) are the average number of times a sandfly bites humans per unit time (σV), carrying capacity of vectors (KV) and transmission probability from infected humans to susceptible sandflies (ß2). The distribution of RL is RL∈[0.06,3.94] with a mean of RL=1.08. Furthermore, the top three parameters that affect HIV dynamics (with respect to the response function RH) are the transmission rate of HIV (ßH), HIV-induced death rate (δH), and the modification parameter for the increase in infectiousness of AIDS individuals in comparison to HIV infected without clinical symptoms of AIDS (ωH). The distribution of RH is RH∈[0.88,2.79] with a mean of RH=1.46. The dominant parameters that affect the dynamics of the full VL-HIV model (with respect to the associated reproduction number, RLH, as the response function) are the transmission rate of HIV (ßH), the average number of times a sandfly bites humans per unit time (σV), and HIV-induced death rate (δH) (the distribution of RLH is RLH∈[0.88,3.94] with a mean of RLH=1.64). Numerical simulations of the model show that the two diseases co-exist (with AVL dominating, but not driving HIV to extinction) whenever the reproduction number of each disease exceeds unity. It is shown that AVL can invade a population at HIV-endemic state if a certain threshold quantity, known as invasion reproduction number, exceeds unity.

An emergency department intervention to protect an overlooked group of children at risk of significant harm.

BACKGROUND: Parental psychiatric disorder, especially depression, personality disorder and deliberate self-harm, is known to put children at greater risk of mental illness, neglect or physical, emotional and sexual abuse. Without a reliable procedure to identify children of parents presenting with these mental health problems, children at high risk of significant harm can be easily overlooked. Although deliberate self-harm constitutes a significant proportion of emergency presentations, there are no guidelines which address the emergency physician's role in identifying and assessing risk to children of these patients. METHODS: A robust system was jointly developed with the local social services child protection team to identify and risk-stratify children of parents with mental illness. This allows us to intervene when we identify children at immediate risk of harm and to ensure that social services are aware of potential risk to all children in this group. The referral process was audited repeatedly to refine the agreed protocol. RESULTS: The proportion of patients asked by the emergency department personnel about dependent children increased and the quality of information received by the social services child protection team improved. CONCLUSIONS: All emergency departments should acknowledge the inadequacy of information available to them regarding patients' children and consider a policy of referral to social services for all children of parents with mental health presentations. This process can only be developed through close liaison within the multidisciplinary child protection team.

Why hypocotyl extension mutants need to be characterized at the cell level: a case study of axr3-1.

Since the discovery of auxin, a debate has taken place as to whether the auxin distribution in elongating organs can account for the distinctive cell elongation profiles that have been found. In an attempt to address this important issue, the elongation profiles of cells have been compared in the hypocotyls of wild-type and auxin-hypersensitive axr3-1 Arabidopsis Columbia ecotype seedlings. Clear differences in cell elongation profiles were found in the two types of seedling, whether they were light- or dark-grown. However, it was not possible unambiguously to ascribe the cell elongation profile differences to the proposition that the axr3-1 mutation causes the hypocotyl to be hypersensitive to auxin. The possibility that the abnormal hypocotyl elongation profile of the mutant was a secondary effect, consequent on a more fundamental effect of the axr3-1 mutation, is considered. It is clear from this study that cell elongation and its control needs to be studied at the cell, and not the organ, level. To characterize a mutant as having a short, or long, hypocotyl is inadequate. To determine which factors control the timing and the magnitude of cell elongation requires the demonstration of correlations between the growth rate of cells and their content of regulating substances or their sensitivity to that substance. Studies of the cell elongation profiles of the many hypocotyl length mutants could also be a very effective means of probing the co-ordination of root and shoot elongation.