Trajectories of depressive symptoms after hip fracture

BACKGROUND: Hip fracture is often complicated by depressive symptoms in older adults. We sought to characterize trajectories of depressive symptoms arising after hip fracture and examine their relationship with functional outcomes and walking ability. We also investigated clinical and psychosocial predictors of these trajectories. METHOD: We enrolled 482 inpatients, aged ≥60 years, who were admitted for hip fracture repair at eight St Louis, MO area hospitals between 2008 and 2012. Participants with current depression diagnosis and/or notable cognitive impairment were excluded. Depressive symptoms and functional recovery were assessed with the Montgomery–Asberg Depression Rating Scale and Functional Recovery Score, respectively, for 52 weeks after fracture. Health, cognitive, and psychosocial variables were gathered at baseline. We modeled depressive symptoms using group-based trajectory analysis and subsequently identified correlates of trajectory group membership. RESULTS: Three trajectories emerged according to the course of depressive symptoms, which we termed ‘resilient’, ‘distressed’, and ‘depressed’. The depressed trajectory (10% of participants) experienced a persistently high level of depressive symptoms and a slower time to recover mobility than the other trajectory groups. Stressful life events prior to the fracture, current smoking, higher anxiety, less social support, antidepressant use, past depression, and type of implant predicted membership of the depressed trajectory. CONCLUSIONS: Depressive symptoms arising after hip fracture are associated with poorer functional status. Clinical and psychosocial variables predicted membership of the depression trajectory. Early identification and intervention of patients in a depressive trajectory may improve functional outcomes after hip fracture

Implementing Care Aims in an integrated team

Care Aims is increasingly being used as a model of care within NHS services, particularly by allied health professionals. This article reports the findings of a pilot study exploring the impact of implementing Care Aims in an integrated community health team. It describes the main findings, and discusses the factors that appeared to impact on the implementation and use of the Care Aims approach in these teams. The model has been traditionally used in uni-professional teams rather than integrated teams. This case study suggests Care Aims has potential to support integrated team working. In this study, clinicians perceived Care Aims was a model that could improve care for patients, support professionals working together and support self-management. However, it is unclear whether it was Care Aims itself or the training and discussion that took place that enabled this team to develop and agree more consistent working practices. Similar to previous studies, this study has shown how team and professional culture can influence how team members work together and provide care in an integrated way. Team and professional cultures are also shown to influence how team members approach and embrace that change. As such, Care Aims may be more challenging to some staff groups to implement

Leprosy and tuberculosis concomitant infection: a poorly understood, age-old relationship

Historically, archaeological evidence, post-mortem findings and retro- spective analysis of leprosy institutions’ data demonstrates a high observed incidence of concomitant infection with leprosy and tuberculosis (TB). However, reports of concomitant infection in the modern literature remain scarce, with estimates of annual new case detection rates of concomitant infection at approximately 0·02 cases per 100,000 population. Whilst the mechanism for this apparent decline in concomitant infections remains unclear, further research on this topic has remained relatively neglected. Modelling of the interaction of the two organisms has suggested that the apparent decline in observations of concomitant infection may be due to the protective effects of cross immunity, whilst more recently others have questioned whether it is a more harmful relationship, predisposing towards increased host mortality. We review recent evidence, comparing it to previously held understanding on the epidemiological relationship and our own experience of concomitant infection. From this discussion, we highlight several under-investigated areas, which may lead to improvements in the future delivery of leprosy management and services, as well as enhance understanding in other fields of infection management. These include, a) highlighting the need for greater understanding of host immunogenetics involved in concomitant infection, b) whether prolonged courses of high dose steroids pre-dispose to TB infection? and, c) whether there is a risk of rifampicin resistance developing in leprosy patients treated in the face of undiagnosed TB and other infections? Longitudinal work is still required to characterise these temporal relationships further and add to the current paucity of literature on this subject matter

An inwardly rectifying K+ channel is required for patterning.

Mutations that disrupt function of the human inwardly rectifying potassium channel KIR2.1 are associated with the craniofacial and digital defects of Andersen-Tawil Syndrome, but the contribution of Kir channels to development is undefined. Deletion of mouse Kir2.1 also causes cleft palate and digital defects. These defects are strikingly similar to phenotypes that result from disrupted TGFβ/BMP signaling. We use Drosophila melanogaster to show that a Kir2.1 homolog, Irk2, affects development by disrupting BMP signaling. Phenotypes of irk2 deficient lines, a mutant irk2 allele, irk2 siRNA and expression of a dominant-negative Irk2 subunit (Irk2DN) all demonstrate that Irk2 function is necessary for development of the adult wing. Compromised Irk2 function causes wing-patterning defects similar to those found when signaling through a Drosophila BMP homolog, Decapentaplegic (Dpp), is disrupted. To determine whether Irk2 plays a role in the Dpp pathway, we generated flies in which both Irk2 and Dpp functions are reduced. Irk2DN phenotypes are enhanced by decreased Dpp signaling. In wild-type flies, Dpp signaling can be detected in stripes along the anterior/posterior boundary of the larval imaginal wing disc. Reducing function of Irk2 with siRNA, an irk2 deletion, or expression of Irk2DN reduces the Dpp signal in the wing disc. As Irk channels contribute to Dpp signaling in flies, a similar role for Kir2.1 in BMP signaling may explain the morphological defects of Andersen-Tawil Syndrome and the Kir2.1 knockout mouse

Mutations in PNKD causing paroxysmal dyskinesia alters protein cleavage and stability.

Paroxysmal non-kinesigenic dyskinesia (PNKD) is a rare autosomal dominant movement disorder triggered by stress, fatigue or consumption of either alcohol or caffeine. Attacks last 1-4 h and consist of dramatic dystonia and choreoathetosis in the limbs, trunk and face. The disease is associated with single amino acid changes (A7V or A9V) in PNKD, a protein of unknown function. Here we studied the stability, cellular localization and enzymatic activity of the PNKD protein in cultured cells and transgenic animals. The N-terminus of the wild-type (WT) long PNKD isoform (PNKD-L) undergoes a cleavage event in vitro, resistance to which is conferred by disease-associated mutations. Mutant PNKD-L protein is degraded faster than the WT protein. These results suggest that the disease mutations underlying PNKD may disrupt protein processing in vivo, a hypothesis supported by our observation of decreased cortical Pnkd-L levels in mutant transgenic mice. Pnkd is homologous to a superfamily of enzymes with conserved β-lactamase domains. It shares highest homology with glyoxalase II but does not catalyze the same reaction. Lower glutathione levels were found in cortex lysates from Pnkd knockout mice versus WT littermates. Taken together, our results suggest an important role for the Pnkd protein in maintaining cellular redox status

Bone Morphogenic Protein Induced Repair of the Premaxillary Cleft

The purpose of this study is to evaluate the bony augmentation of premaxillary clefts in humans using recombinant bone morphogenic protein (rhBMP-2) in a collagen sponge carrier. 12 patients with unilateral cleft alveolar ridges were evaluated pre- and 4 months postoperatively. 10 patients were repaired with rhBMP-2 while two others were grafted with anterior iliac crest particulate marrow cancellous bone (PMCB). Computed tomographic studies were used to evaluate preoperative alveolar cleft volumes, postoperative bone bridge volumes, and pre/post operative volume ratios. A pre/post operative volume ratio for patients repaired with rhBMP-2 ranged from 24.1% to 90.6% with a mean of 71.7%. Patients who were grafted with PMCB had similar pre/post operative volume ratios ranging from 71.3% to 84.9% with a mean of 78.1%. In conclusion, premaxillary alveolar clefts can have repair induced by rhBMP-2 as an effective alternative to conventional anterior iliac particulate marrow cancellous bone

Structural studies of Perfluoroaryldiselenadiazolyl Radicals: Insights into Dithiadiazolyl Chemistry

Synopsis Diselenadiazolyls exhibit a stronger tendency to dimerize in the solid state than their corresponding dithiadiazolyl (DTDA) radicals, reflected in a range of dimerization modes for (p-XC6F4CNSeSeN)2, which contrast with those of the monomeric DTDA radicals, p-XC6F4CNSSN. The structure of (p-NCC6F4CNSeSeN)2 reflects a buildup of molecular strain in order to accommodate both dimerization and structure-directing CN···Se contacts, whereas the suppression of dimerization releases molecular strain yet retains structure-directing CN···S contacts for the corresponding DTDA radical

Climate change anxiety among parents of school-aged children in the UK: Experience as a common predictor of cognitive-emotional and functional impairments

Climate change anxiety (CCA) is distress about climate change and its impacts on the environment and human health. CCA is manifested as cognitive-emotional impairment and functional impairment. CCA has been increasingly recognised in the mental health field, however, how to reduce CCA remains uninformed. Parents of school-aged children are vulnerable to CCA, due to parenting stress and worries for the future. We aimed to identify predictors of the CCA impairment, from experience of climate change, behavioural engagement, and number of children among parents of school-aged children. A convenience sample of 126 parents (82 mothers and 44 fathers) responded to an online survey. Multiple regression analyses were used. After controlling for age and gender, (a) experience of climate change (b=0.16, p< 0.01, 95%CI 0.06-0.27) and behavioural engagement (b=0.31, p<0.05, 95%CI 0.08-0.55) predicted cognitive-emotional impairment, and (b) experience of climate change predicted functional impairment (b=0.20, p<0.01, 95%CI 0.08-0.31). Experience of climate change was a common predictor. Cognitive re-appraisal and compassion practice may help alter the experiential aspect of climate change to mitigate CCA. Future research needs to evaluate the mechanism of climate change experience in order to effectively reduce CCA

Electrochemically stimulating developments in bioelectronic medicine

Cellular homeostasis is in part controlled by biological generated electrical activity. By interfacing biology with electronic devices this electrical activity can be modulated to actuate cellular behaviour. There are current limitations in merging electronics with biology sufficiently well to target and sense specific electrically active components of cells. By addressing this limitation, researchers give rise to new capabilities for facilitating the twoway transduction signalling mechanisms between the electronic and cellular components. This is required to allow significant advancement of bioelectronic technology which offers new ways of treating and diagnosing diseases. Most of the progress that has been achieved to date in developing bioelectronic therapeutics stimulate neural communication, which ultimately orchestrates organ function back to a healthy state. Some devices used in therapeutics include cochlear and retinal implants and vagus nerve stimulators. However, all cells can be effected by electrical inputs which gives rise to the opportunity to broaden the use of bioelectronic medicine for treating disease. Electronic actuation of non-excitable cells has been shown to lead to ‘programmed’ cell behaviour via application of electronic input which alter key biological processes. A neglected form of cellular electrical communication which has not yet been considered when developing bioelectronics therapeutics is faradaic currents. These are generated during redox reactions. A precedent of electrochemical technology being used to modulate these reactions thereby controlling cell behaviour has already been set. In this mini review we highlight the current state of the art of electronic routes to modulating cell behaviour and identify new ways in which electrochemistry could be used to contribute to the new field of bioelectronic medicine