A model for community physiotherapy from the perspective of newly graduated physiotherapists as a guide to curriculum revision

Background. Limitations in physiotherapy curricula have been reported. Work-based experiences, especially during compulsory community service, could inform curricula. Objective. To develop a model of community service physiotherapy to guide curriculum reform. Methods. In this appreciative inquiry, trained physiotherapy students conducted tele-interviews with newly graduated physiotherapists. Twelve recently graduated community-service physiotherapists – heterogeneous in gender, mother tongue, university attended and work setting – were purposively recruited. Two coders applied Tesch’s coding technique to the transcripts; one did paper-based work and the other used AtlasTi software. Consensus was reached and a member check done. Results. Four themes identified were: (i) the essence of community physiotherapy; (ii) the collaborative nature of community physiotherapy; (iii) prerequisites for a positive practice environment; and (iv) community physiotherapy as a gateway to personal growth and professional development. Physiotherapists consult clients from varied cultural backgrounds, ages and health and disease profiles. Health education is a key intervention, but clients emphasised therapeutic touch. Team work enhances services, especially within a context of poverty, and prevents isolation. New graduates have to deal with inefficient management, lack of transport, inadequate equipment and needs resilience. They want discipline-specific supervision. Conclusion. Community physiotherapy makes specific demands, especially for novice therapists. Service-learning in authentic diverse contexts would foster professional development and cultural competence. Clinical competency should remain the backbone of the curriculum, complemented by competency in health education. Different ways of reflection would facilitate lifelong learning and growth in attributes such as resilience, which is necessary for dealing with sub-optimal practice environments

Implementing preoperative Botulinum toxin A and progressive pneumoperitoneum through the use of an algorithm in giant ventral hernia repair

Background Repair of large ventral hernias with loss of domain can be facilitated by preoperative Botulinum toxin A (BTA) injections and preoperative progressive pneumoperitoneum (PPP). The aim of this study is to evaluate the outcomes of ventral hernioplasty using a standardized algorithm, including component separation techniques, preoperative BTA and PPP. Methods All patients between June 2014 and August 2018 with giant hernias (either primary or incisional) of more than 12 cm width were treated according to a previously developed standardized algorithm. Retrospective data analysis from a prospectively collected dataset was performed. The primary outcome was closure of the anterior fascia. Secondary outcomes included complications related to the preoperative treatment, postoperative complications, and recurrences. Results Twenty-three patients were included. Median age was 65 years (range 28-77) and median BMI was 31.4 (range 22.7-38.0 kg/m(2)). The median loss of domain was 29% (range 12-226%). For the primary and secondary endpoints, 22 patients were analyzed. Primary closure of the anterior fascia was possible in 82% of all patients. After a median follow-up of 19.5 months (range 10-60 months), 3 patients (14%) developed a hernia recurrence and 16 patients (73%) developed 23 surgical site occurrences, most of which were surgical site infections (54.5%). Conclusion Our algorithm using both anterior or posterior component separation, together with preoperative BTA injections and PPP, achieved an acceptable fascial closure rate. Further studies are needed to explore the individual potential of BTA injections and PPP, and to research whether these methods can prevent the need for component separation, as postoperative wound morbidity remains high in our study

Block of death-receptor apoptosis protects mouse cytomegalovirus from macrophages and is a determinant of virulence in immunodeficient hosts.

The inhibition of death-receptor apoptosis is a conserved viral function. The murine cytomegalovirus (MCMV) gene M36 is a sequence and functional homologue of the human cytomegalovirus gene UL36, and it encodes an inhibitor of apoptosis that binds to caspase-8, blocks downstream signaling and thus contributes to viral fitness in macrophages and in vivo. Here we show a direct link between the inability of mutants lacking the M36 gene (ΔM36) to inhibit apoptosis, poor viral growth in macrophage cell cultures and viral in vivo fitness and virulence. ΔM36 grew poorly in RAG1 knockout mice and in RAG/IL-2-receptor common gamma chain double knockout mice (RAGγC(-/-)), but the depletion of macrophages in either mouse strain rescued the growth of ΔM36 to almost wild-type levels. This was consistent with the observation that activated macrophages were sufficient to impair ΔM36 growth in vitro. Namely, spiking fibroblast cell cultures with activated macrophages had a suppressive effect on ΔM36 growth, which could be reverted by z-VAD-fmk, a chemical apoptosis inhibitor. TNFα from activated macrophages synergized with IFNγ in target cells to inhibit ΔM36 growth. Hence, our data show that poor ΔM36 growth in macrophages does not reflect a defect in tropism, but rather a defect in the suppression of antiviral mediators secreted by macrophages. To the best of our knowledge, this shows for the first time an immune evasion mechanism that protects MCMV selectively from the antiviral activity of macrophages, and thus critically contributes to viral pathogenicity in the immunocompromised host devoid of the adaptive immune system