Massively parallel sequencing is unlocking the potential of environmental trace evidence.

Massively parallel sequencing (MPS) has revolutionised the field of genomics enabling substantial advances in human DNA profiling. Further, the advent of MPS now allows biological signatures to be obtained from complex DNA mixtures and trace amounts of low biomass samples. Environmental samples serve as ideal forms of contact trace evidence as detection at a scene can establish a link between a suspect, location and victim. Many studies have applied MPS technology to characterise the biodiversity within high biomass environmental samples (such as soil and water) to address questions related to ecology, conservation, climate change and human health. However, translation of these tools to forensic science remains in its infancy, due in part to the merging of traditional forensic ecology practices with unfamiliar DNA technologies and complex datasets. In addition, people and objects also carry low biomass environmental signals which have recently been shown to reflect a specific individual or location. The sensitivity, and reducing cost, of MPS is now unlocking the power of both high and low biomass environmental DNA (eDNA) samples as useful sources of genetic information in forensic science. This paper discusses the potential of eDNA to forensic science by reviewing the most explored applications that are leading the integration of this technology into the field. We introduce novel areas of forensic ecology that could also benefit from these tools with a focus on linking a suspect to a scene or establishing provenance of an unknown sample and discuss the current limitations and validation recommendations to achieve translation of eDNA into casework.

A randomized controlled trial of four different regimes of biofeedback programme in the treatment of faecal incontinence.

AIM: Biofeedback is an established, effective and non-invasive treatment for faecal incontinence (FI). The aim was to compare the effectiveness of four different biofeedback treatment regimes. METHOD: This was a randomized control trial of patients with FI, stratified into two groups (metropolitan and rural) and then randomized into two subgroups (groups 1 and 2 within metropolitan, groups 3 and 4 within rural) with varying face-to-face and telephone biofeedback components. All patients received standardized counselling and education, dietary modification and the use of anti-diarrhoeal medications. Group 1 received four monthly face-to-face biofeedback treatments, groups 2 and 3 received one face-to-face biofeedback followed by telephone biofeedback and group 4 received a one-off face-to-face biofeedback treatment. Primary outcomes were patient-assessed severity of FI and quality of life as assessed by the 36-item Short Form Health Survey and direct questioning of objectives. Secondary outcomes included St Mark's incontinence score, anxiety, depression and anorectal physiology measures (resting, squeeze pressures; isotonic, isometric fatigue times). RESULTS: Between 2006 and 2012, 351 patients were recruited. One patient died leaving 350 for analysis. 332 (95%) were women. Mean age was 60 (SD = 14). All groups had significant improvements in FI, quality of life, incontinence score and mental status (P < 0.001 each). There were no differences in improvements in FI between groups although patient satisfaction was less with reduced face-to-face contact. There were modest improvements in isotonic and isometric fatigue times suggesting improved sphincter endurance (both P < 0.001). CONCLUSION: Biofeedback is effective for FI. Although face-to-face and telephone biofeedback is not necessary to improve FI, it is important for patient satisfaction.

What is important in cancer care coordination? A qualitative investigation.

Although it is widely recognised that better coordination of cancer care holds considerable potential to improve patients' experience of care and their outcomes, there is no agreed definition of the term 'care coordination' or consensus as to what it entails. An explorative descriptive qualitative study was undertaken to explore the views and experiences of key stakeholders to identify the key components of cancer care coordination. We conducted semi-structured individual and focus groups interviews with patients (n= 20) who have been treated for any cancer and carers (n= 4) as well as clinicians (n= 29) involved in cancer care, using open-ended questions. Data were collected until saturation of concepts was reached. A phenomenological approach based on grounded theory was used to explore the participants' experiences and views. Seven key components were identified: organisation of patient care, access to and navigation through the healthcare system, the allocation of a 'key contact' person, effective communication and cooperation among the multidisciplinary team and other health service providers, delivery of services in a complementary and timely manner, sufficient and timely information to the patient and needs assessment. The components of cancer care coordination identified provide an empirical basis for the development of metrics and interventions to improve this aspect of cancer care.

A unique role: the peer mentor on the spinal cord team at G.F. Strong Rehab Centre.

The peer mentor is a full time paid staff member of the G. F. Strong Rehab Centre Spinal Cord Program. To qualify for the position, an individual with a high lesion spinal cord injury must live a self-managed life in the community. The peer mentor's role bridges professional, lay, and client perspectives, and is a voice for both clients and staff unlike any other team member. This report focuses on the peer mentor's facilitation of communication between clients and staff and on two initiatives that promote clients' perspectives.

The mouse ear inflammatory response to topical arachidonic acid.

Application of arachidonic acid (AA) (0.1-4 mg) to the ears of mice produces immediate vasodilatation and erythema (5 min) followed by the abrupt development of edema which is maximal at 40-60 min. The onset of edema coincides with extravasation of protein and leukocytes. After 1 h, the edema begins to wane rapidly and the inflammatory cells leave the tissue so that by 6 h the ears have returned to near normal except for residual erythema. During the period 6-48 h, AA-treated ears show a greatly diminished response with respect to edema and cell infiltrate when AA is applied a second time. Inhibitor studies show that the inflammatory response is due to formation of AA metabolites via both the cyclooxygenase and lipoxygenase pathways. Under appropriate conditions, AA-induced ear edema can be used as a model to screen for compounds showing in vivo lipoxygenase inhibitory activity. Although relatively large doses of AA were applied topically, there was only a modest stimulation of epidermal DNA synthesis and mitotic index with no consequent hyperplasia. Although arachidonic acid is capable of eliciting most aspects of an inflammatory response, the reaction is abrupt in onset and of short duration. Additional factors appear to be required to produce a prolonged inflammatory response with associated tissue destruction, or inflammatory cell activation and immobilization in situ.

Hyperbaric oxygenation: prosthodontic responsibilities.

This article discussed the use of hyperbaric oxygen in the treatment of chronic osteomyelitis, osteoradionecrosis, and nonhealing wounds. The fabrication of custom-fitted oxygen applicators is presented, and specific recommendations are made for their use. The prosthodontist serves as a valuable member of the hyperbaric treatment team. His professional knowledge and technical expertise allow him to construct treatment applicators which are professionally sound and provide comfort for the patient.

The mitochondrial oxidation of quinol monophosphates.

1. Mitochondria from ox heart and rat liver catalysed a slow cyanide-sensitive oxidation of 2,3-dimethylnaphthaquinol monophosphate, duroquinol monophosphate, menadiol 1-phosphate and menadiol 4-phosphate. 2. The release of P(i) was concomitant with oxygen uptake. 3. The oxidation was somewhat stimulated by Ca(2+) and P(i), and weakly inhibited by 2,4-dinitrophenol. 4. The quinol monophosphates effected a rapid reduction of free cytochrome c, and consequently addition of cytochrome c greatly increased the rate of the mitochondrial oxidation of 2,3-dimethylnaphthaquinol monophosphate. 5. This quinol phosphate interacts with the electron-transport chain at the level of cytochrome c. 6. Polylysine promoted an interaction between 2,3-dimethylnaphthaquinol monophosphate and cytochrome oxidase. Thus, although polylysine blocks mitochondrial oxidations via reduced cytochrome c, the oxidation of the quinol phosphate was strongly stimulated. 7. This stimulation was most effective in the most intact mitochondrial preparations and was inhibited by ADP and by P(i). 8. The implications of these results for factors limiting the rate of quinol phosphate oxidation, the mode of action of stimulators and the mechanism of P(i) formation are discussed.