The social construction of child maltreatment: the role of medical practitioners

• Summary: This paper explores how medical knowledge in child protection practice operates, in conjunction with social work knowledge and legal knowledge, as a social process of constructing meaning as ‘maltreatment’ (or not) in which the physical body of the child and perceived abnormalities represent ‘evidence’. Through discourse analysis of two case studies, this paper makes explicit and problematizes the social processes by which meanings are given by medical practitioners, social workers, police and parents to material experiences, the preference given to some meanings over others, and the econsequences of particular meanings for children and families and social work practice.

• Findings: Medical, social and legal knowledge are not neutral but embedded in power relations. The case studies show, through a sociological analysis of professional practice in child protection, how preferred versions of knowledge and meaning may override or dismiss alternative meanings, with particular consequences for parents and children and for practice outcomes.

• Applications: The case studies offer opportunities by which critically to engage with child protection knowledge, policy and practice in keeping with contemporary approaches that advocate dialogue, critical reflection and reflexivity, so that professional knowledge and professional power may be deployed constructively rather than oppressively.

Anthropometry, physical performance, and ultrasound patellar tendon abnormality in elite junior basketball players: a cross-sectional study

Objective: Patellar tendinopathy has been reported to be associated with many intrinsic risk factors. Few have been fully investigated. This cross-sectional study examined the anthropometric and physical performance results of elite junior basketball players with normal or abnormal patellar tendons to see if any measures were associated with changes in tendon morphology.

Methods: Agility, leg strength, endurance, and flexibility were measured in 71 male and 64 female players. A blinded radiologist ultrasonographically examined their patellar tendons and athletes were grouped as having normal or abnormal tendons. One-way ANOVA was used to test for differences in anthropometric and physical performance data for athletes whose tendons were normal or abnormal (unilateral or bilateral tendinopathy) on ultrasound.

Results: Results show that females with abnormalities in their tendons had a significantly better vertical jump (50.9±6.8 cm) than those with normal tendons (46.1±5.4 cm) (p = 0.02). This was not found in males. In males, the mean sit and reach in those with normal tendons (13.2±6.7 cm) was greater (p<0.03) than in unilateral tendinopathy (10.3±6.2 cm) or in bilateral tendinopathy (7.8±8.3 cm). In females, those with normal tendons (13.3±4.8 cm) and bilateral tendinopathy (15.8±6.2 cm) were distinctly different from those with unilateral tendinopathy (7.9±6.6 cm).

Conclusion: Flexibility and vertical jump ability are associated with patellar tendinopathy and the findings warrant consideration when managing young, jumping athletes.

Complementary therapies and diabetes

There is increasing recognition that people with diabetes use a range of complementary therapies (CT), for a number of conditions, but do not always inform their conventional health practitioners about their use. Controlling blood glucose levels in people with diabetes is important to reduce the consequent metabolic abnormalities and symptoms and the incidence of long-term complications. Conventional medical and nursing practitioners often incorrectly assume that they are used to control blood glucose levels, e.g. using herbal medicines to increase insulin production or reduce insulin resistance. CT can be beneficial for people with diabetes. They can also lead to adverse events. This paper describes the outcome of monitoring complementary therapy use in our diabetic outpatient services in 2001, the results of a focus group (n=10) to explore issues identified in the monitoring process and a survey undertaken with a convenience sample of diabetes educators (n=40).

Twenty percent of patients used CT and there were three adverse events in the monitoring phase. Eight of the 10 focus group participants used CT and 16 of the diabetes educators used CT in patient care. Only one had a complementary therapy qualification.

Asymptomatic hypoechoic regions on patellar tendon ultrasound : a 4-year clinical and ultrasound followup of 46 tendons

Patellar tendon ultrasound appearance is commonly used in clinical practice to diagnose patellar tendinopathy and guide management. Using a longitudinal study design we examined whether or not the presence of a hypoechoic ultrasonographic lesion in an asymptomatic patellar tendon conferred a risk for developing jumper's knee compared with a tendon that was ultrasonographically normal. Ultrasonographic, symptomatic and anthropometric assessment was completed at baseline and followup. Magnetic resonance imaging was performed on four tendons that resolved ultrasonographically in the study period. Forty-six patellar tendons were followed over 47±11.8 months. Eighteen tendons were hypoechoic at baseline and 28 were ultrasonographically normal. Five tendons resolved ultrasonographically in the study period. Magnetic resonance imaging in four of these tendons was normal. Seven normal patellar tendons at baseline developed a hypoechoic area but only two became symptomatic. Analysis of ultrasonography at baseline and clinical outcome with Fisher's exact test shows there is no association between baseline ultrasound changes and symptoms at followup. In this study there is no statistically significant relationship between ultrasonographic patellar tendon abnormalities and clinical outcome in elite male athletes. Management of jumper's knee should not be solely based on ultrasonographic appearance; clinical assessment remains the cornerstone of appropriate management.

The PKCÁ-D294G mutant found in pituitary and thyroid tumors fails to transduce extracellular signals

Protein kinase C (PKC) is a key regulator of cell proliferation, differentiation, and apoptosis and is one of the drug targets of anticancer therapy. Recently, a single point mutation (D294G) in PKCα has been found in pituitary and thyroid tumors with more invasive phenotype. Although the PKCα-D294G mutant is implicated in the progression of endocrine tumors, no apparent biochemical/cell biological abnormalities underlying tumorigenesis with this mutant have been found. We report here that the PKCα-D294G mutant is unable to bind to cellular membranes tightly despite the fact that it translocates to the membrane as efficiently as the wild-type PKCα upon treatment of phorbol ester. The impaired membrane binding is associated with this mutant's inability to transduce several antitumorigenic signals as it fails to mediate phorbol ester–stimulated translocation of myristoylated alanine–rich protein kinase C substrate (MARCKS), to activate mitogen-activated protein kinase and to augment melatonin-stimulated neurite outgrowth. Thus, the PKCα-D294G is a loss-of-function mutation. We propose that the wild-type PKCα may play important antitumorigenic roles in the progression of endocrine tumors. Therefore, developing selective activators instead of inhibitors of PKCα might provide effective pharmacological interventions for the treatment of certain endocrine tumors.

Hormonal regulation of the Menkes and Wilson copper-transporting ATPases in human placental Jeg-3 cells

Copper deficiency during pregnancy results in early embryonic death and foetal structural abnormalities including skeletal, pulmonary and cardiovascular defects. During pregnancy, copper is transported from the maternal circulation to the foetus by mechanisms which have not been clearly elucidated. Two coppertransporting ATPases, Menkes (ATP7A; MNK) and Wilson (ATP7B; WND), are expressed in the placenta and both are involved in placental copper transport, as copper accumulates in the placenta in both Menkes and Wilson disease. The regulatory mechanisms of MNKand WNDand their exact role in the placenta are unknown. Using a differentiated polarized Jeg-3 cell culture model of placental trophoblasts, MNK and WND were shown to be expressed within these cells. Distinct roles forMNKandWND are suggested on the basis of their opposing responses to insulin. Insulin and oestrogen increased both MNK mRNA and protein levels, altered the localization of MNK towards the basolateral membrane in a copper-independent manner, and increased the transport of copper across this membrane. In contrast, levels of WND were decreased in response to insulin, and the protein was located in a tight perinuclear region, with a corresponding decrease in copper efflux across the apical membrane. These results are consistent with a model of copper transport in the placenta in which MNK delivers copper to the foetus and WND returns excess copper to the maternal circulation. Insulin and oestrogen stimulate copper transport to the foetus by increasing the expression of MNK and reducing the expression of WND. These data show for the first time that MNK and WND are differentially regulated by the hormones insulin and oestrogen in human placental cells.

Estuarine fish health assessment: evidence of wastewater impacts based on nitrogen isotopes and histopathology

Sewage effluent is a powerful agent of ecological change in estuaries. While the effects of sewage pollution on water quality are usually well documented, biological responses of exposed organisms are not. We quantified health impacts in the form of pathological tissue changes across multiple organs in estuarine fish exposed to elevated levels of treated wastewater. Structural pathologies were compared in wild populations of four fish species from two subtropical estuaries on the east coast of Australia that differ substantially in the amount of direct wastewater loadings. Uptake of sewage-derived  nitrogen by fish was traced with stable nitrogen isotopes. Pathologies were common in the liver, spleen, gill, kidney and muscle tissues, and included granulomas, melanomacrophage aggregates, and multiple deformities of the gill epithelia. Tissue deformities were more frequent in fish exposed directly to wastewater discharges. Mullet (Valamugil georgii) were most affected, with only a single specimen free of pathologies in the sewage-impacted estuary. Similarly, in those fish that had structural abnormalities, more deformities were generally found in individuals from sites receiving sewage. These spatial contrasts in impaired fish health correspond to significantly enriched δ₁₅N values in fish muscle as a consequence of fish assimilating sewage-N. Overall, the pattern of lower health and enriched δ₁₅N values in fish from sewage-impacted areas suggests that organism health is lowered by sewage inputs to estuaries. Measurements of organism health are required to understand the effects of sewage on estuarine ecosystems, and histopathology of fishes is a powerful tool to achieve this.

Cultured muscle cells display defects of mitochondrial myopathy ameliorated by anti-oxidants

The mitochondrial DNA A3243G mutation causes neuromuscular disease. To investigate the muscle-specific pathophysiology of mitochondrial disease, rhabdomyosarcoma transmitochondrial hybrid cells (cybrids) were generated that retain the capacity to differentiate to myotubes. In some cases, striated muscle-like fibres were formed after innervation with rat embryonic spinal cord. Myotubes carrying A3243G mtDNA produced more reactive oxygen species than controls, and had altered glutathione homeostasis. Moreover, A3243G mutant myotubes showed evidence of abnormal mitochondrial distribution, which was associated with down-regulation of three genes involved in mitochondrial morphology, Mfn1, Mfn2 and DRP1. Electron microscopy revealed mitochondria with ultrastructural abnormalities and paracrystalline inclusions. All these features were ameliorated by anti-oxidant treatment, with the exception of the paracrystalline inclusions. These data suggest that rhabdomyosarcoma cybrids are a valid cellular model for studying muscle-specific features of mitochondrial disease and that excess reactive oxygen species production is a significant contributor to mitochondrial dysfunction, which is amenable to anti-oxidant therapy.

Low carbohydrate diets: what are the potential short and long term health implications?

Low-carbohydrate diets for weight loss are receiving a lot of attention of late. Reasons for this interest include a plethora of low-carbohydrate diet books, the over-sensationalism of these diets in the media and by celebrities, and the promotion of these diets in fitness centres and health clubs. The re-emergence of low-carbohydrate diets into the spotlight has lead many people in the general public to question whether carbohydrates are inherently 'bad' and should be limited in the diet. Although low-carbohydrate diets were popular in the 1970s they have resurged again yet little scientific fact into the true nature of how these diets work or, more importantly, any potential for serious long-term health risks in adopting this dieting practice appear to have reached the mainstream literature. Evidence abounds that low-carbohydrate diets present no significant advantage over more traditional energy-restricted, nutritionally balanced diets both in terms of weight loss and weight maintenance. Studies examining the efficacy of using low-carbohydrate diets for long-term weight loss are few in number, however few positive benefits exist to promote the adoption of carbohydrate restriction as a realistic, and more importantly, safe means of dieting. While short-term carbohydrate restriction over a period of a week can result in a significant loss of weight (albeit mostly from water and glycogen stores), of serious concern is what potential exists for the following of this type of eating plan for longer periods of months to years. Complications such as heart arrhythmias, cardiac contractile function impairment, sudden death, osteoporosis, kidney damage, increased cancer risk, impairment of physical activity and lipid abnormalities can all be linked to long-term restriction of carbohydrates in the diet. The need to further explore and communicate the untoward side-effects of low-carbohydrate diets should be an important public health message from nutrition professionals.

Malingering pain in the medicolegal context

Malingering—the willful, deliberate, and fraudulent feigning or exaggeration of illness—was originally described as a means of avoiding military service. In present-day clinical practice, malingering may occur in circumstances where the person wishes to avoid legal responsibility or in situations where compensation or some other benefit might be obtained. In law, the term malingering is used in relation to persons to whom military regulations apply; in other situations, malingering is regarded as fraud and may lead to charges of perjury or criminal fraud. Assertions that an individual is malingering are particularly common in clinical settings where the complaint is of a subjective nature and is not accompanied by objectively demonstrable organic abnormalities. This may occur in relation to complaints of pain in situations where the person is entitled to receive pain-contingent compensation or is suing for damages. In this article, we will review the literature on pain and malingering and discuss attempts that have been made to develop methods and guidelines for the detection of malingered pain. There are, however, no valid clinical methods of assessment of possible malingering of pain. In our view, the ultimate issue of the veracity of the plaintiff is for the Court to decide, and epithets such as “malingerer” have no place in reports prepared for legal purposes by health care professionals.

Home-based resistance training is not sufficient to maintain improved glycemic control following supervised training in older individuals with type 2 diabetes

OBJECTIVE—To examine whether improvements in glycemic control and body composition resulting from 6 months of supervised high-intensity progressive resistance training could be maintained after an additional 6 months of home-based resistance training.

RESEARCH DESIGN AND METHODS—We performed a 12-month randomized controlled trial in 36 sedentary, overweight men and women with type 2 diabetes (aged 60–80 years) who were randomly assigned to moderate weight loss plus high-intensity progressive resistance training (RT&WL group) or moderate weight loss plus a control program (WL group). Supervised gymnasium-based training for 6 months was followed by an additional 6 months of home-based training. Glycemic control (HbA_1c), body composition, muscle strength, and metabolic syndrome abnormalities were assessed at 0, 3, 6, 9, and 12 months.

RESULTS—Compared with the WL group, HbA_1c decreased significantly more in the RT&WL group (–0.8%) during 6 months of supervised gymnasium-based training; however, this effect was not maintained after an additional 6 months of home-based training. In contrast, the greater increase in lean body mass (LBM) observed in the RT&WL group compared with the WL group (0.9 kg, P < 0.05) after the gymnasium-based training tended to be maintained after the home-based training (0.8 kg, P = 0.08). Similarly, the gymnasium-based increases in upper body and lower body muscle strength in the RT&WL group were maintained over the 12 months (P < 0.001). There were no between-group differences for changes in body weight, fat mass, fasting glucose, or insulin at 6 or 12 months.

CONCLUSIONS—In older adults with type 2 diabetes, home-based progressive resistance training was effective for maintaining the gymnasium-based improvements in muscle strength and LBM but not glycemic control. Reductions in adherence and exercise training volume and intensity seem to impede the effectiveness of home-based training for maintaining improved glycemic control.

Carpal tunnel syndrome: diagnostic usefulness of sonography

PURPOSE: To prospectively evaluate accuracy of sonography for diagnosis of carpal tunnel syndrome (CTS) in patients clinically suspected of having the disease in one or both hands.
MATERIALS AND METHODS: A prospective cohort of 133 patients suspected of having CTS were referred to a teaching hospital between October 2001 and June 2002 for electrodiagnostic study. One hundred twenty patients (98 women, 22 men; mean age, 49 years; range, 19–83 years) underwent sonography within 1 week after electrodiagnostic study. Radiologist was blinded to electrodiagnostic study results. Seventy-five patients had bilateral symptoms; 23 patients, right-hand symptoms; and 22 patients, left-hand symptoms (total, 195 symptomatic hands). Cross-sectional area of median nerve was measured at three levels: immediately proximal to carpal tunnel inlet, at carpal tunnel inlet, and at carpal tunnel outlet. Flexor retinaculum was used as a landmark to margins of carpal tunnel. Optimal threshold levels (determined with classification and regression tree analysis) for areas proximal to and at tunnel inlet and at tunnel outlet were used to discriminate between patients with and patients without disease. Sensitivity, specificity, and false-positive and false-negative rates were derived on the basis of final diagnosis, which was determined with clinical history and electrodiagnostic study results as reference standard.
RESULTS: For right hands, sonography had sensitivity of 94% (66 of 70); specificity, 65% (17 of 26); false-positive rate, 12% (nine of 75); and false-negative rate, 19% (four of 21) (cutoff, 0.09 cm2 proximal to tunnel inlet and 0.12 cm2 at tunnel outlet). For left hands, sensitivity was 83% (53 of 64); specificity, 73% (24 of 33); false-positive rate, 15% (nine of 62); and false-negative rate, 31% (11 of 35) (cutoff, 0.10 cm2 proximal to tunnel inlet).
CONCLUSION: Sonography is comparable to electrodiagnostic study in diagnosis of CTS and should be considered as initial test of choice for patients suspected of having CTS.

Markers of inflammation in South Asian and European infants from birth to 2 years in Manchester, UK

Inflammatory markers, including serum C-reactive protein (CRP), are predictors of coronary heart disease (CHD) in adults. South Asians in the UK have higher rates of CHD in adulthood than national rates.We tested the hypotheses that South Asian infants would have higher serum concentrations of CRP and homocysteine than European infants up to 2 years of age and that higher infant weight is associated with elevation of inflammatory markers. Infants of South Asian and European origin were investigated in a mixed cross sectional-longitudinal cohort study. Mothers were recruited ante-natally from St Mary’s Hospital,Manchester by postal invitation and telephone call to non-responders. Infants with metabolic or congenital abnormalities, known syndromes or pre-maturity were excluded. Measurements were collected at birth and either 3, 6, 12 or 24 months. High sensitivity CRP and homocysteine were measured by an immulite immunoassay. We used mixed linear modelling to assess whether infant weight, ethnicity, length of follow-up or their interaction were associated with inflammatory makers in infants during follow-up. Data are presented on 306 infants (109 South Asian and 197 European). We found that European infants had higher serum CRP than South Asian infants during follow-up which was of borderline significance.There was no difference in serum homocysteine between ethnic groups during followup and no significant interaction between ethnicity and follow-up. Infant weight was significantly associated with CRP but not homocysteine. In this ongoing longitudinal study,we found little difference in inflammatory markers in infants from birth to 2 years despite markedly higher rates of CHD in South Asian than European adults. Life course exposure to risk factors may play a more dominant role in the development of CHD.

Interaction of Arabidopsis Thaliana with Plasmodiophora Brassicae

Plasmodiophora brassicae is a protistan pathogen that attacks roots of brassicaceous plant species causing devastating disease. Resistance is characterised by restriction of the pathogen and susceptibility by the development of severely malformed roots (‘clubroots’) and stunting of the plant that is associated with alterations in the synthesis of cytokinin and auxin hormones. We are examining the susceptible response in Arabidopsis and whether suppression of key resistance factors by the pathogen contributes to susceptibility. The interaction is being studied using a number of approaches including microscopy of the infection process and development of the pathogen within roots and host gene expression analysis. Quantitative PCR was used to confirm the timing of infection of roots and showed that infection occurred at day four and colonisation increased thereafter to high levels by 23 days after inoculation by which time roots were showing systemic abnormalities. To investigate the basis of this compatible interaction we have conducted a time course experiment following infection of a susceptible ecotype of Arabidopsis (Col-0) to examine whole genome geneexpression changes in the host. Differential gene expression analysis of inoculated versus control roots showed that a higher number of genes had altered expression levels at day four compared to that at day seven and at day ten. At day four the expression levels of several genes known to be important for recognition and signal transduction in resistant interactions and genes involved in the biosynthesis of lignin, phenylpropanoids and ethylene were suppressed. Suppression by P. brassicae of specific plant defence responses appears to be a key component of susceptibility in this system.

Predictors of critical care admission in emergency department patients triaged as low to moderate urgency

Aim. This paper is a report of a study to identify predictors of critical care admission in emergency department patients triaged as low to moderate urgency that may be apparent early in the emergency department episode of care.

Background. Observations of clinical practice show that a number of emergency department patients triaged as low to moderate urgency require critical care admission, raising questions about the relationship between illness severity and physiological status early in the emergency department episode of care.

Methods. A retrospective case control design was used. All participants were aged over 18 years, triaged to Australasian Triage Scale categories 3, 4 or 5, and attended emergency department between 1 July 2004 and 30 June 2005. Cases were admitted to intensive care unit or coronary care unit and controls were admitted to general medical or surgical units. Cases (n = 193) and controls (n = 193) were matched by age, gender, emergency department discharge diagnosis and triage category.

Results. Critical care admission associated with: (i) a presenting complaint of nausea, vomiting and diarrhoea (OR = 3·40, 95%CI:1·22–9·47, P = 0·019), (ii) heart rate abnormalities at triage (OR = 2·10, 95%CI:1·19–3·71, P = 0·011), (iii) temperature abnormalities at triage (OR = 2·87 95%CI:1·05–7·89, P = 0·041), (iv) respiratory rate at first nursing assessment (OR = 1·66, 95%CI:1·05–2·06, P = 0·31) or (v) heart rate abnormalities at first nursing assessment (OR = 1·57, 95%CI = 1·04−2·39, P = 0·033).

Conclusion. Derangements in temperature, respiratory rate and heart appear to increase risk of critical care admission. Further work using a prospective approach is needed to establish which physiological parameters have the highest predictive validity, the level(s) of physiological abnormality with highest clinical utility, and the optimal timing for collection of physiological data.