Consumers lived experiences and satisfaction with sub-acute mental health residential services.

PURPOSE: Sub-acute recovery-oriented facilities offer short-term residential support for people living with mental illness. They are generally highly regarded by consumers, with emerging evidence indicating that these services may support recovery. The aim of the current study was to explore the relationship between personal recovery and consumers' satisfaction with sub-acute residential services, and consumers' views about service features that aid recovery. METHODS: Consumers at 19 adult Prevention and Recovery Care Services in Victoria, Australia, were invited to complete measures containing sociodemographic information and measures on personal recovery and wellbeing. After going home, participants were invited to complete measures on service satisfaction and experience. RESULTS: Total and intrapersonal scores on the personal recovery measure increased significantly between Time 1 and Time 2, indicating marked improvement. Personal recovery and satisfaction measures were moderately to strongly correlated. Thematically analysed open-ended responses revealed themes of feeling connected, finding meaning and purpose, and self-empowerment as important aspects of these services, with some recommendations for improvements. CONCLUSION: Sub-acute residential mental health care may support individuals' personal recovery; consumer satisfaction indicates these services also offer an acceptable and supportive environment for the provision of recovery-oriented care. Further exploring consumers' experiences of sub-acute residential services is essential to understand their effectiveness, opportunities for improvement and intended impacts on personal recovery.

Intellectual disability and patient activation after release from prison: a prospective cohort study.

BACKGROUND: Intellectual disability and patient activation may be important drivers of inequities in health service access and health outcomes for people with intellectual disability transitioning from prison to the community. We assessed the association between intellectual disability and patient activation after prison release and examined whether this association varied, depending on whether intellectual disability was identified prior to prison release. METHODS: Overall, 936 prisoners were screened for intellectual disability by using the Hayes Ability Screening Index and completed the Patient Activation Measure (PAM) within 6 weeks of prison release and again at 1, 3 and 6 months post-release. We estimated the association between intellectual disability status and PAM scores by using a multilevel linear model, adjusting for sociodemographic, behavioural, health and criminogenic factors. We used propensity score matching to estimate the impact of being identified with intellectual disability prior to release from prison on the change in mean PAM score after prison release. RESULTS: Compared with those who screened negative for intellectual disability, ex-prisoners who screened positive, both with and without prior identification of intellectual disability, had significantly decreased mean PAM scores [(B = -4.3; 95% CI: -6.3, -2.4) and (B = -4.5; 95% CI: -6.8, -2.3), respectively] over 6 months of follow-up. Among those who reported being identified with intellectual disability prior to release from prison, a significant increase in PAM score at the 6-month follow-up interview (B = 5.89; 95% CI: 2.35, 9.42; P = 0.001) was attributable to being identified with intellectual disability prior to release. CONCLUSIONS: Ex-prisoners screening positive for possible intellectual disability have decreased patient activation for at least 6 months after release from prison. However, individuals whose possible intellectual disability is unidentified appear to be particularly vulnerable. Incarceration is a pivotal opportunity for the identification of intellectual disability and for initiating transitional linkages to health and intellectual disability-specific community services for this marginalised population.

Attitudes towards seclusion and restraint in mental health settings: findings from a large, community-based survey of consumers, carers and mental health professionals.

AIMS: There are growing calls to reduce, and where possible eliminate, the use of seclusion and restraint in mental health settings, but the attitudes and beliefs of consumers, carers and mental health professionals towards these practices are not well understood. The aim of this study was to compare the attitudes of mental health service consumers, carers and mental health professionals towards seclusion and restraint in mental health settings. In particular, it aimed to explore beliefs regarding whether elimination of seclusion and restraint was desirable and possible. METHODS: In 2014, an online survey was developed and widely advertised in Australia via the National Mental Health Commission and through mental health networks. The survey adopted a mixed-methods design, including both quantitative and qualitative questions concerning participants' demographic details, the use of seclusion and restraint in practice and their views on strategies for reducing and eliminating these practices. RESULTS: In total 1150 survey responses were analysed. A large majority of participants believed that seclusion and restraint practices were likely to cause harm, breach human rights, compromise trust and potentially cause or trigger past trauma. Consumers were more likely than professionals to view these practices as harmful. The vast majority of participants believed that it was both desirable and feasible to eliminate mechanical restraint. Many participants, particularly professionals, believed that seclusion and some forms of restraint were likely to produce some benefits, including increasing consumer safety, increasing the safety of staff and others and setting behavioural boundaries. CONCLUSIONS: There was strong agreement across participant groups that the use of seclusion and restraint is harmful, breaches human rights and compromises the therapeutic relationship and trust between mental health service providers and those who experience these restrictive practices. However, some benefits were also identified, particularly by professionals. Participants had mixed views regarding the feasibility and desirability of eliminating these practices.

Region II of the Haemophilus influenzae type be capsulation locus is involved in serotype-specific polysaccharide synthesis.

The central (serotype-specific) Region II of the Haemophilus influenzae Type b capsulation locus cap is 8.3 kb long and contains a cluster of four genes. We show that these genes, designated orf1 to orf4, are involved in the biosynthetic steps required for the formation of the Type b capsular polysaccharide and that orf1 probably encodes a CDP-ribitolpyrophosphorylase. We present evidence that growth of polysaccharide chains takes place through the alternating addition of single sugar nucleotides.

PCR for capsular typing of Haemophilus influenzae.

A PCR method for the unequivocal assignment of Haemophilus influenzae capsular type (types a to f) was developed. PCR primers were designed from capsule type-specific DNA sequences cloned from the capsular gene cluster of each of the six capsular types. PCR product was amplified only from the capsular type for which the primers were designed. Product was confirmed by using either an internal oligonucleotide or restriction endonuclease digestion. A total of 172 H. influenzae strains of known capsular type (determined genetically) comprising all capsular types and noncapsulate strains were tested by PCR capsular typing. In all cases the PCR capsular type corresponded to the capsular genotype determined by restriction fragment length polymorphism analysis of the cap region. When used in conjunction with PCR primers derived from the capsular gene bexA, capsulate, noncapsulate, and capsule-deficient type b mutant strains could be differentiated. PCR capsular typing overcomes the problems of cross-reaction and autoagglutination associated with the serotyping of H. influenzae strains. The rapid and unequivocal capsular typing method that is described will be particularly important for typing invasive H. influenzae strains isolated from recipients of H. influenzae type b vaccine.

Direct suppression of phagocytosis by amphipathic polymeric surfactants.

Recent studies have demonstrated that phagocytosis of colloidal particles by the mononuclear phagocytes of the liver and spleen can be controlled by either coating or stabilizing particulate carriers with the amphipathic polymeric surfactants, F108 and T908. These surfactants consist of copolymers of polypropylene oxide (PPO) and polyethylene oxide (PEO) and, when adsorbed to particulate surfaces, significantly decrease sequestration of particulates by the mononuclear phagocytes (MPS) of the liver. To evaluate these observations further, murine peritoneal macrophages were incubated for varying periods with surfactant-coated and noncoated polystyrene particles (PSPs). Phagocytosis was monitored using gamma counting and quantitative fluorescence microscopy. The data show that phagocytosis is decreased when PSPs are coated with F108 and T908. In addition, suppression of phagocytic activity was observed when cells were pretreated with the surfactant and then challenged with noncoated particles. The data confirm previous observations that polymeric surfactants consisting of PEO and PPO protect particulate carriers from rapid uptake by the MPS of the liver. Further, F108 and T908 suppress phagocytosis directly without affecting the integrity, viability, or functional state of the cell.

Role of bradykinin in inflammatory arthritis: identification and functional analysis of bradykinin receptors on human synovial fibroblasts.

Receptor type and function of bradykinin (BK) receptors on human synovial fibroblasts (HSF) was determined. Scatchard analysis of [3H]BK saturation binding to intact synovial cells revealed a single binding site, with a Kd of 3.8 +/- 0.6 nM. HSF express approximately 50,000 BK sites/cell. Specificity of [3H]BK binding was confirmed by the ability of several BK peptide agonists and antagonists to inhibit binding in a dose dependent manner. The rank order of potency for agonist inhibition of [3H]BK and the inability of selective antagonists of the B1-type to displace binding suggest that the BK receptor on HSF is a B2 subtype receptor. The addition of BK to HSF caused a time and concentration dependent increase in PGE2 production. This BK induced PGE2 production was blocked by specific B2 type BK antagonists and not by B1 antagonists. The results of this study identify B2 type BK receptors on synovial fibroblasts and suggest that BK may be a primary mediator in inflammatory arthritis.

Capsulation gene loss and 'rescue' mutations during the Cap+ to Cap- transition in Haemophilus influenzae type b.

Genes for Haemophilus influenzae type b capsule expression are duplicated to form a potentially unstable structure, cap, of directly-repeated chromosomal regions of approximately 17 kb. Capsule-deficient mutants arise in a two-stage process, initiated by rec-dependent reduction of this region from two copies to one. This recombinational event is usually lethal, only about 1/200 surviving to form slow-growing colonies of organisms that continue to synthesize polysaccharide but are defective in its export. A variety of secondary 'rescue' mutations within cap can occur to reduce polysaccharide synthesis and restore normal organism appearance and colony morphology.

Physical symptoms of combination biotherapy: a quality-of-life issue.

Data are available on the principal side effects of individually administered biological response modifiers (BRMs). However, studies on physical symptoms secondary to multiagent regimens (i.e., combinations of BRMs and of BRMs and chemotherapy) are just now appearing in the literature. The combinations of alpha interferon and 5-FU and of alpha interferon and interleukin-2 (IL-2) are the focus of this paper. Published and unpublished reports of side effects associated with these combinations are reviewed, and resulting quality-of-life (QOL) issues examined. Physical side effects that may affect QOL are flu-like symptoms, gastrointestinal (GI) toxicities, and fatigue, which may alter social, physiological, and psychological function and negatively influence the perception of QOL. Nursing interventions to improve these reactions include awareness and assessment of the patient's perception of QOL and strategies to alleviate the symptoms. Numerous opportunities exist for nursing research on improved symptom management and on QOL in combination biotherapy regimens.

Monosodium urate crystals stimulate phospholipase A2 enzyme activities and the synthesis of a phospholipase A2-activating protein.

Eicosanoids are important mediators of the inflammatory response to monosodium urate crystals (MSUC) that results in gout. Phospholipase enzymes cleave fatty acids from membrane phospholipids, and this is thought to be the rate-limiting step in eicosanoid production. To understand better the mechanism of eicosanoid production in this disease, we stimulated human peripheral blood neutrophils and monocytes with MSUC and measured phospholipase enzyme activities. MSUC stimulated both intracellular and secretory phospholipase A2 enzyme activities in a time and concentration-dependent manner. Specificity was observed, as phospholipase C activities were not affected. Pretreatment with colchicine, but not aspirin, indomethacin, allopurinol, or islet activating protein, abrogated the enhanced phospholipase A2 activities. We have recently isolated and characterized a phospholipase A2 activating protein termed PLAP from synovial fluid from patients with rheumatoid arthritis, and from murine and bovine cell lines. PLAP was detected in gouty synovial fluid by immunodot blotting and ELISA assays and expressed the same characteristics as PLAP identified from other sources. To examine the role of PLAP in MSUC-induced phospholipase A2 stimulation, we treated cells with MSUC and observed an increase in immunoreactive PLAP. This response also could be blunted by colchicine, but not other drugs. Both phospholipase A2 and PLAP induced production by human monocytes of PGE2 and leukotriene B4 by neutrophils. These findings suggest that phospholipase A2 activation in response to MSUC requires an intact microtubule structure, and that phospholipase A2 and PLAP may be important modulators of at least a portion of the gouty inflammatory response.

The bex locus in encapsulated Haemophilus influenzae: a chromosomal region involved in capsule polysaccharide export.

The nucleotide sequence of a 5.1 kb region in the Haemophilus influenzae type b capsulation locus has been determined and found to contain four open reading frames: bexD, bexC, bexB, and bexA. Comparison of the deduced products of bexC, bexB, and bexA to known proteins, and TnphoA mutagenesis, suggests that they form components of an ATP-driven polysaccharide export apparatus. Furthermore, close sequence similarity between BexA and BexB and products of the kpsT and kpsM genes at the Escherichia coli K5 capsulation locus (Smith et al., 1990--accompanying paper) suggests that capsulation genes in these organisms may have a common ancestry.

Leukotriene B4 modulates phospholipid methylation and chemotaxis in human polymorphonuclear leukocytes.

Formation of phosphatidylcholine from phosphatidylethanolamine via the S-adenosylmethionine (AdoMet) pathway has been shown to be required for signal transduction of receptor-ligand interactions in a variety of cells. These interactions result in the remodeling of phospholipid pools and phospholipase activation. To extend these observations and to explore the role of the phosphatidylcholine synthesis pathway in transduction of the leukotriene B4 (LTB4) receptor-ligand response, we examined phospholipid methylation in human polymorphonuclear leukocytes (PMN) following stimulation by LTB4, a potent chemotactic agent that is a metabolite of arachidonic acid. At early time points (approximately 3-10 min), formation of methylated phospholipids was enhanced following LTB4 stimulation. The LTB4 analogs 6-trans LTB4 as well as LTB4 epimers induced less methylation compared with LTB4, and the potencies of these analogs in inducing methylation correlated with their diminished ability to induce chemotaxis. Furthermore, the ability of these agonists to induce methylation also correlated with the binding affinity of these agents to the LTB4 receptors on these cells. Synthesis of phosphatidylcholine by the choline transferase pathway was not affected by LTB4. Inhibition of the AdoMet reaction with 3- deazaadenosine, L-homocysteine homolactone, or erythro-9-[2-hydroxy-3-nonyl] adenine (EHNA) abrogated LTB4-induced phospholipid methylation and the chemotactic response. The potencies of these inhibitors in blocking phospholipid methylation also correlated with their ability to abrogate the LTB4-induced chemotactic response. These data suggest that phospholipid methylation and phospholipase activation play an important role in transduction of the LTB4 receptor-ligand interaction in PMN, which results in chemotaxis.

Recent advances in the management of biotherapy-related side effects: fatigue.

Limited information about fatigue patterns in patients with cancer exists in the biotherapy literature. When fatigue is mentioned, it is usually to state whether or not it was a dose-limiting side effect. No further data are provided on how fatigue was measured; which patterns were noted and when; and which relationships were found between fatigue and demographic characteristics, type of biologic response modifier, route of administration, or cumulative dose. Thus, there is little available in the biotherapy literature to guide nursing practice in managing this side effect. Theory that guides practice, however, often emanates from the personal experiences of the patients and from the clinical observations and intuitive hunches of the nurses and physicians participating in clinical trials. These individuals have been most generous in sharing their insights and unpublished data with the authors. This paper presents a comprehensive view of current knowledge on fatigue to guide present nursing practice with patients receiving biotherapy and to provide direction for future nursing and clinical trial research.

A phospholipase A2-activating protein (PLAP) stimulates human neutrophil aggregation and release of lysosomal enzymes, superoxide, and eicosanoids.

We have recently isolated a human phospholipase A2-activating protein (PLAP) that shares antigenic and biochemical similarities with melittin, a well characterized bee venom phospholipase-stimulatory peptide. To explore the potential mechanisms of action of PLAP that extend beyond its effects on eicosanoid synthesis, we examined its effects on the release of human neutrophil lysosomal enzymes and superoxide, and on RBC hemolysis. These results were compared to the effects of melittin, which has been reported to induce enzyme release and hemolysis. We also examined the effects of PLAP on neutrophil aggregation and chemotaxis. PLAP induced neutrophils to release beta-glucuronidase and metalloproteinase enzyme activities as well as produce superoxide ion in both a dose- and time-dependent manner. Eicosanoid synthesis inhibitors did not abrogate these responses. PLAP induced release of arachidonic acid metabolites, but this response could be abrogated by eicosanoid synthesis inhibitors. PLAP also induced neutrophil aggregation and chemokinesis, but not chemotaxis. Concentrations of PLAP that induced these responses did not induce cellular toxicity as determined by light and electron microscopy, lactic dehydrogenase release, trypan blue dye exclusion, and RBC hemolysis. In contrast, prolonged incubation with higher concentrations of PLAP induced cell death that was similar to that observed with melittin. These findings suggest that the mechanisms of action of PLAP extend beyond the eicosanoid synthetic pathway, and that disordered regulation of PLAP may be responsible, at least in part, for chronic immune and inflammatory states.

Statistical analysis of waveguide gratings using Rouard's method.

An analysis of the effects of random aperiodicities on the reflectivity response of a periodic waveguide grating is presented. This analysis is based on our thin film model of the waveguide grating and employs Rouard's method. We show that aperiodicities as small as 1% of the grating period significantly alter the reflectivity response.

Measured TM-TM coupling in waveguide gratings.

We report measurements of the guided-wave reflectivity of a periodic, surface-corrugation, waveguide grating as a function of incidence angle and polarization. We show that the measured response is more accurately described by a coupled-mode theory based on the local-normal-mode expansion of the fields than by that based on the ideal-mode expansion.