Factors influencing the use and provision of respite care services for older families of people with a severe mental illness

Family carers of people with a severe mental illness play a vital, yet often unrecognized and undervalued role in Australian society. Respite care services can assist these family carers in their role; however, little is known about their access to these services. The paper addresses this knowledge gap. An exploratory field study was conducted throughout the eastern suburbs of Sydney, Australia, to identify and examine the factors influencing the use and provision of respite services for older carers of people with a mental illness. Semistructured, in-depth interviews, and structured self-completed questionnaires were conducted with older family carers, mental health care professionals, and respite care service providers. Additionally, relevant documents (local policies, strategic plans and reports on respite care) were reviewed. It was found that current respite services are problematic for older family carers of Australians with a mental illness, signalling the need for concerted efforts by carers, health professionals, and service providers to improve access. Changes to respite provision and utilization are recommended.     

Involvement of protein kinase A in cannabinoid receptor-mediated protection from oxidative neuronal injury

CB1 cannabinoid receptors (CB1Rs) are involved in protecting the brain from ischemia and related disorders. However, the underlying protective mechanisms are incompletely understood. We investigated the effect of CB1R activation on oxidative injury, which has been implicated in neuronal death after cerebral ischemia and neurodegenerative disorders, in mouse cortical neuron cultures. The CB1R agonist Win 55212-2 [R-(+)-[2,3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4-benzoxazin-yl]-(1-naphthalenyl)methanone mesylate] reduced neuronal death, measured by lactate dehydrogenase release, in cultures treated with 50 microM FeCl2, and its protective effect was attenuated by the CB1R antagonist SR141716A [N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-cichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide hydrochloride]. The endocannabinoid anandamide reproduced the effect of Win 55212-2, as did the antioxidant 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid (Trolox). Neuronal injury was more severe after in vitro or in vivo administration of FeCl2 to CB1R-knockout compared with wild-type mice. Win 55212-2 reduced the formation of reactive oxidative species in cortical neuron cultures treated with FeCl2, consistent with an antioxidant action. Pertussis toxin reduced CB1R-mediated protection, which points to a protective mechanism that involves signaling through G(i/o) proteins. Since CB1R-activated G protein signaling inhibits protein kinase A but activates phosphatidylinositol 3-kinase (PI3K), we tested the involvement of these pathways in CB1R-mediated neuroprotection. Dibutyryl-cyclic adenosine monophosphate (dbcAMP) blocked protection by Win 55212-2, whereas the PI3K inhibitor wortmannin did not, and the effect of dbcAMP was inhibited by the protein kinase A inhibitor H89 [N-[2-((p-bromocinnamyl)amino)ethyl]-5-isoquinolinesulfonamide] (> or =10 nM). CB1R-induced, SR141716A-, pertussis toxin-, and dbcAMP-sensitive protection was also observed for two other oxidative insults, exposure to H2O2 or buthionine sulfoximine. Therefore, receptor-stimulated inhibition of protein kinase A seems to be required for the neuroprotective effect of CB1R activation against oxidative neuronal injury.     

Novel complex class 1 integron bearing an ISCR1 element in an Escherichia coli isolate carrying the blaCTX-M-14 gene

This work identifies an ISCR1-related bla(CTX-M-14) gene, which has never been reported before, from a clinical isolate of Escherichia coli. The bla(CTX-M-14) gene was preceded by an ISCR1 element that was followed by a class 1 integron containing three different insert gene cassettes, i.e., dfrA12, orfF, and aadA2.     

Magnesium ions facilitate integrin alpha 2‐ and alpha 3‐mediated proliferation and enhance alkaline phosphatase expression and activity in hBMSCs

Magnesium metal and its alloys have been proposed as a novel class of bone implant biomaterials because of their biodegradability and mechanical properties. The purpose of this study was to determine whether magnesium ions, which are released abundantly from alloys, affect proliferation and differentiation of human bone marrow‐derived stromal cells (hBMSCs). High levels of magnesium ions did not induce cytotoxicity in hBMSCs, but treatment with 2.5–10 mm magnesium ions for 48–72 h significantly increased hBMSC proliferation. The expression of integrins α2 and α3, but not β1, was upregulated compared with the control and shifted from α3 to α2 in hBMSCs treated with magnesium ions. Knockdown of integrins α2 and/or α3 significantly reduced magnesium‐induced proliferation of hBMSCs. Magnesium exposure profoundly enhanced alkaline phosphatase (ALP) gene expression and activity even at a relatively low magnesium concentration (2.5 mm ). Exposure to magnesium ions facilitated hBMSC proliferation via integrin α2 and α3 expression and partly promoted differentiation into osteoblasts via the alteration of ALP expression and activity. Accordingly, magnesium could be a useful biomaterial for orthopaedic applications such as bone implant biomaterials for repair and regeneration of bone defects in orthopaedic and dental fields. Copyright © 2014 John Wiley & Sons, Ltd.     

Prevalence, clinical correlations, comorbidities, and suicidal tendencies in pathological Korean gamblers: results from the Korean Epidemiologic Catchment Area Study

Objective  

Based on the National Epidemiological Survey of Psychiatric Disorders in South Korea conducted in 2006, we examined the prevalence, clinical correlations, comorbidities, and suicidal tendencies of pathological gamblers in the community.     

Communicating hydrocephalus associated with surgery or radiosurgery for vestibular schwannoma

The purpose of this cohort study was to determine the incidence of communicating hydrocephalus (HCP) associated with the treatment of vestibular schwannoma (VS). Between January 2002 and December 2007, a total of 291 patients diagnosed with VS underwent either surgical resection or gamma knife radiosurgery (GKS). By analyzing the clinical data and MRI scans, we retrospectively reviewed and compared the incidence of communicating HCP between the two treatment modalities. During their clinical course, 10 of 291 patients developed new communicating HCP (3.4%): nine of 90 patients who were treated using GKS (10%) developed communicating HCP post-procedure, while only one of 146 patients who underwent surgical resection alone (0.68%) developed subsequent communicating HCP (p = 0.002). The median event-free survival from the initial treatment with GKS to the development of communicating HCP was 22 months (range: 7–55 months). Three patients who developed new communicating HCP in the GKS group required surgical intervention, including ventriculoperitoneal shunt or endoscopic third ventriculostomy. There was no significant correlation between sex or tumor size and the incidence of communicating HCP in the GKS group (p > 0.05). We found a relatively high incidence of communicating HCP after treatment in patients with VS, particularly for those patients in the GKS group. Therefore, the risk of communicating HCP should be considered in the follow-up of patients who undergo GKS for treatment of VS.     

Postconditioning protects skeletal muscle from ischemia‐reperfusion injury

Ischemia‐reperfusion (I/R) injury caused by abrupt restoration of the circulation after prolonged ischemic insult induces significant morbidity after reconstructive microsurgery. The authors investigated whether a postconditioning (post‐con) procedure attenuated skeletal muscle I/R injury and protected muscular function. Three hours of complete ischemia was induced by occluding the muscular branches of rat extensor digitorum longus (EDL) muscle. The post‐con procedure was started at the end of ischemia and involved six cycles of 15 seconds of reperfusion followed by 15 seconds of re‐occlusion (3 minutes of total intervention) prior to initiating unlimited reperfusion. EDL muscle contractilities were compared with those of normal sides (no ischemic exposure), and experimental group results were also compared with control group results (3 hours of ischemia followed by full reperfusion without post‐con) at 3 hours and 5 days postreperfusion. Muscle wet weights, myeloperoxidase (MPO) activities, and histological results were also evaluated. The muscle contractilities in the post‐con group were significantly preserved at both 3 hours and 5 days postreperfusion as compared with ischemic controls. Decreased inflammatory cell infiltration, MPO activity, and wet weight of postconditioned EDL muscle suggested that post‐con attenuated acute inflammatory reactions induced by I/R. This study demonstrates that post‐con provides effective functional protection to skeletal muscles from I/R injury. © 2010 Wiley‐Liss, Inc. Microsurgery 2010.