Social networks,migration, and HIV testing among Latinos in a new immigrant destination: Insights from a qualitative study

Latinos in the U.S. are disproportionately affected by HIV and are more likely than non-Latinos to present with a late diagnosis, which delays engagement in HIV care and treatment. Social networks may provide normative influence and social support for HIV testing, but a contextualised understanding of networks is needed in order to maximise these social resources. We conducted qualitative interviews with foreign-born Latino men and transgender women (n?=?17) in a new immigrant destination to explore their social networks. Most participants described having smaller social networks after migrating. Networks included both local and transnational ties, but most participants had few close ties. Contextual factors including stigma and geographic dispersion limited the re-construction of networks with close ties after migration. HIV testing was not a common topic of discussion with social network ties. Efforts to improve early uptake of HIV testing among Latino immigrants may benefit from engaging with social networks, but such efforts need to address how the context in which networks operate enables access to testing.     

Nurses' satisfaction with medication administration point-of-care technology

Efforts to promote safe care prompted the development point-of-care technology, but successful adoption requires acceptance by nursing staff. To assess the satisfaction of nurses who use point-of-care technology that integrates nurse scanning of bar-coded medications with the patient's electronic medication administration record, the authors examined nurses' satisfaction with barcode/electronic medication administration record before and after introduction in an academic medical center.     

Osimertinib,Surgery, and Radiation Therapy in Treating Patients with Stage IIIB or IV Non-Small Cell Lung Cancer with EGFR Mutations (NORTHSTAR)

Annals of Surgical Oncology -     

Oncogenic AKAP9-BRAF fusion is a novel mechanism of MAPK pathway activation in thyroid cancer

Genes crucial for cancer development can be mutated via various mechanisms, which may reflect the nature of the mutagen. In thyroid papillary carcinomas, mutations of genes coding for effectors along the MAPK pathway are central for transformation. BRAF point mutation is most common in sporadic tumors. By contrast, radiation-induced tumors are associated with paracentric inversions activating the receptor tyrosine kinases RET and NTRK1. We report here a rearrangement of BRAF via paracentric inversion of chromosome 7q resulting in an in-frame fusion between exons 1-8 of the AKAP9 gene and exons 9-18 of BRAF. The fusion protein contains the protein kinase domain and lacks the autoinhibitory N-terminal portion of BRAF. It has elevated kinase activity and transforms NIH3T3 cells, which provides evidence, for the first time to our knowledge, of in vivo activation of an intracellular effector along the MAPK pathway by recombination. The AKAP9-BRAF fusion was preferentially found in radiation-induced papillary carcinomas developing after a short latency, whereas BRAF point mutations were absent in this group. These data indicate that in thyroid cancer, radiation activates components of the MAPK pathway primarily through chromosomal paracentric inversions, whereas in sporadic forms of the disease, effectors along the same pathway are activated predominantly by point mutations.     

Magnetic resonance imaging of perineural spread of head and neck malignancies

Perineural invasion is a common mechanism of spread of head and neck cancers. Imaging plays an important role in detection of this condition because a large number of patients with perineural spread (PNS) are clinically asymptomatic. Accurate detection of PNS requires an understanding of anatomy of commonly involved neural pathways. High level of suspicion on the part of the radiologist, awareness of common imaging signs of PNS and careful attention to imaging technique can aid in earlier detection of this condition.     

Comparative outcomes and cost-utility after surgical treatment of focal lumbar spinal stenosis compared with osteoarthritis of the hip or knee—part 1: long-term change in health-related quality of life

Background contextIt is well accepted that total hip and knee arthroplasty (THA/TKA) for osteoarthritis (OA) is associated with reliable and sustained improvements in postoperative health-related quality of life (HRQoL). Although several studies have demonstrated comparable outcomes with THA/TKA after surgical intervention for lumbar spinal stenosis (LSS), the sustainability of the outcome after LSS surgery compared with THA/TKA remains uncertain.PurposeThe primary purpose of this study is to assess whether improvements in HRQoL after surgical management of focal lumbar spinal stenosis (FLSS) with or without spondylolisthesis are sustainable over the long term compared with that of THA/TKA for OA.Study designSingle-center, retrospective, longitudinal matched cohort study of prospectively collected outcomes, with a minimum of 5-year follow-up (FU).Patient samplePatients who had primary one- to two-level spinal decompression with or without instrumented fusion for FLSS and THA/TKA for primary OA.Outcome measuresPostoperative change from baseline to last FU in Short-Form 36 physical component summary (PCS) and mental component summary (MCS) scores among groups was used as the primary outcome measure.MethodsAn age, sex-matched inception cohort of primary one- to two-level spinal decompression with or without instrumented fusion for FLSS (n=99) was compared with a cohort of primary THA (n=99) and TKA (n=99) for OA and followed for a minimum of 5 years. Linear regression was used for the primary analysis.ResultsMean (percent) FUs in months were 80.5+16.04 (79%), 94.6+16.62 (92%), and 80.6+16.84 (85%) for the FLSS, THA, and TKA cohorts, respectively, with a range of 5 to 10 years for all three cohorts. The number of patients who have undergone revision including those lost to FU for the FLSS, THA, and TKA cohorts were n=20 (20.2%, same site [n=7] and adjacent segment [n=13]) requiring 27 operations, n=3 (3%, same site) requiring 5 operations, and n=8 (8.1%, same site) requiring 12 operations, respectively (p<.01). The average time to first revision was 56/65/43 months, respectively. Mean postoperative PCS (p<.0001) and MCS (p<.02) scores improved significantly and were durable for all groups at the last FU. The mean changes from baseline PCS/MCS scores to last FU were 8.5/6.4, 12.3/7.0, and 8.3/4.9 for FLSS, THA, and TKA, respectively. Adjusting for baseline age, sex, body mass index, PCS score, and MCS score, there was a strong trend in favor of greater sustained change in the PCS score of THA over FLSS (p=.07) and TKA (p=.08). No difference was noted for change in PCS score between FLSS and TKA (p=.95). No differences were noted for change in MCS score among all three cohorts (p>.1).ConclusionsSignificant improvements in HRQoL after surgical treatment of FLSS with or without spondylolisthesis and hip and knee OA are sustained for a mean of 7 to 8 years, with a minimum of 5-year FU. Despite a higher revision rate, patients undergoing surgery for FLSS can expect a comparable long-term average improvement in HRQoL from baseline compared with their peers undergoing TKA and to a lesser extent THA.     

Unravelling mitochondrial pathways to Parkinson's disease

Mitochondria are essential for cellular function due to their role in ATP production, calcium homeostasis and apoptotic signalling. Neurons are heavily reliant on mitochondrial integrity for their complex signalling, plasticity and excitability properties, and to ensure cell survival over decades. The maintenance of a pool of healthy mitochondria that can meet the bioenergetic demands of a neuron, is therefore of critical importance; this is achieved by maintaining a careful balance between mitochondrial biogenesis, mitochondrial trafficking, mitochondrial dynamics and mitophagy. The molecular mechanisms that underlie these processes are gradually being elucidated. It is widely recognized that mitochondrial dysfunction occurs in many neurodegenerative diseases, including Parkinson''s disease. Mitochondrial dysfunction in the form of reduced bioenergetic capacity, increased oxidative stress and reduced resistance to stress, is observed in several Parkinson''s disease models. However, identification of the recessive genes implicated in Parkinson''s disease has revealed a common pathway involving mitochondrial dynamics, transport, turnover and mitophagy. This body of work has led to the hypothesis that the homeostatic mechanisms that ensure a healthy mitochondrial pool are key to neuronal function and integrity. In this paradigm, impaired mitochondrial dynamics and clearance result in the accumulation of damaged and dysfunctional mitochondria, which may directly induce neuronal dysfunction and death. In this review, we consider the mechanisms by which mitochondrial dysfunction may lead to neurodegeneration. In particular, we focus on the mechanisms that underlie mitochondrial homeostasis, and discuss their importance in neuronal integrity and neurodegeneration in Parkinson''s disease.

LINKED ARTICLES

This article is part of a themed issue on Mitochondrial Pharmacology: Energy, Injury & Beyond. To view the other articles in this issue visit http://dx.doi.org/10.1111/bph.2014.171.issue-8