Oxygen therapy management for patients at risk of respiratory dysfunction

Oxygen therapy is a major intervention used to manage respiratory dysfunction. Research findings revealed a need for health care professionals to review oxygen device selection in specific clinical settings, the importance of involving patients in their care decisions and to document appropriately care that is provided associated with oxygen therapy.

A qualitative evaluation of online chat groups for women completing a psychological intervention for female sexual dysfunction

Because of the embarrassment that can surround female sexual dysfunctions, online interventions offer an anonymous and private treatment alternative. Recently, an online cognitive-behavioral treatment for female sexual dysfunctions was evaluated. Although significant improvements were observed in sexual functioning, the treatment was primarily a behavioral intervention because of difficulties with engaging participants in cognitive therapy over e-mail. To address this limitation, the use of chat groups was incorporated into a new online treatment for female sexual dysfunctions—the PursuingPleasure program. Thirty-eight women participated in the PursuingPleasure chat groups. The goals of the chat groups were to address and overcome challenges as women progressed through PursuingPleasure and to create a social support network where group therapy processes could be used. The chat groups aimed to address misunderstandings, monitor changes, and receive feedback. A qualitative analysis of the chat groups revealed that they helped to facilitate the cognitive-affective aspects of the program, as well as fulfill their other intended functions. This study demonstrates how the use of chat groups in the online treatment of female sexual dysfunctions is a useful addition to Internet-based treatment. Feedback suggests that the chat groups were one of the most helpful aspects of the program, although a small group of women reported finding the groups unhelpful.

The value of impulsivity to define subgroups of addicted individuals differing in personality dysfunction, craving, psychosocial adjustment, and wellbeing: A latent class analysis

High impulsivity is common to substance and gambling addictions. Despite these commonalities, there is still substantial heterogeneity on impulsivity levels within these diagnostic groups, and variations in impulsive levels predict higher severity of symptoms and poorer outcomes. We addressed the question of whether impulsivity scores can yield empirically driven subgroups of addicted individuals that will exhibit different clinical presentations and outcomes. We applied latent class analysis (LCA) to trait (UPPS-P impulsive behavior scale) and cognitive impulsivity (Stroop and d2 tests) scores in three predominantly male addiction diagnostic groups: Cocaine with Personality Disorders, Cocaine Non-comorbid, and Gambling and analyzed the usefulness of the resulting subgroups to differentiate personality beliefs and relevant outcomes: Craving, psychosocial adjustment, and quality of life. In accordance with impulsivity scores, the three addiction diagnostic groups are best represented as two separate classes: Class 1 characterized by greater trait impulsivity and poorer cognitive impulsivity performance and Class 2 characterized by lower trait impulsivity and better cognitive impulsivity performance. The two empirically derived classes showed significant differences on personality features and outcome variables (Class 1 exhibited greater personality dysfunction and worse clinical outcomes), whereas conventional diagnostic groups showed non-significant differences on most of these measures. Trait and cognitive impulsivity scores differentiate subgroups of addicted individuals with more versus less severe personality features and clinical outcomes.

Mitochondrial dysfunction has divergent, cell type-dependent effects on insulin action

The contribution of mitochondrial dysfunction to insulin resistance is a contentious issue in metabolic research. Recent evidence implicates mitochondrial dysfunction as contributing to multiple forms of insulin resistance. However, some models of mitochondrial dysfunction fail to induce insulin resistance, suggesting greater complexity describes mitochondrial regulation of insulin action. We report that mitochondrial dysfunction is not necessary for cellular models of insulin resistance. However, impairment of mitochondrial function is sufficient for insulin resistance in a cell type-dependent manner, with impaired mitochondrial function inducing insulin resistance in adipocytes, but having no effect, or insulin sensitising effects in hepatocytes. The mechanism of mitochondrial impairment was important in determining the impact on insulin action, but was independent of mitochondrial ROS production. These data can account for opposing findings on this issue and highlight the complexity of mitochondrial regulation of cell type-specific insulin action, which is not described by current reductionist paradigms.

Mitochondrial dysfunction in schizophrenia : Pathways, mechanisms and implications.

Mitochondria play a critical role in regulating cellular functions including bioenergetics, calcium homeostasis, redox signalling, and apoptotic cell death. Mitochondria are also essential to many aspects of neurodevelopment and neuronal functions. However, mitochondrial impairment may affect bioenergetics in the developing brain and alter critical neuronal processes leading to neurodevelopmental abnormalities. Schizophrenia is a chronic and severe neuropsychiatric disorder of neurodevelopmental origin. Immuno-inflammatory pathway is one of the widely appreciated mechanisms that has consistently been implicated in the neurodevelopmental origin of schizophrenia. However, the source of inflammation and the underlying neurobiological mechanisms leading to schizophrenia are yet to be fully ascertained. Recent understanding reveals that perturbation of mitochondrial network dynamics might lead to various nervous system disorders with inflammatory pathologies. Mitochondrial deficit, altered redox balance and chronic low-grade inflammation are evident in schizophrenia. It is hypothesized that oxidative/nitrosative stress responses due to mitochondrial dysfunctions might activate immuno-inflammatory pathways and subsequently lead to neuroprogressive changes in schizophrenia. Herein, we summarise the current understanding of molecular links between mitochondrial dysfunctions and pathogenesis of schizophrenia based on evidence from genomics, proteomics and imaging studies, which together support a role for mitochondrial impairment in the pathogenetic pathways of schizophrenia.