Fear of relapse in schizophrenia: a mixed-methods systematic review

Introduction: Fears of relapse in people diagnosed with schizophrenia have long been recognised as an impediment to recovery and wellbeing. However, the extent of the empirical basis for the fear of relapse concept is unclear. A systematic review is required to collate available evidence and define future research directions. Methods: A pre-registered systematic search (PROSPERO CRD42020196964) of four databases (PubMED, MEDLINE-Ovid, PsycINFO-Ovid, and Cochrane Central Register of Controlled Trials) was conducted from their inception to 05/04/2021. Results: We found nine eligible studies. Five were quantitative (4 descriptive and 1 randomised controlled trial), and four were qualitative. The available quantitative evidence suggests that fear of relapse may have concurrent positive relationships with depression (r = 0.72) and suicide ideation (r = 0.48), and negative relationship with self-esteem (r = 0.67). Qualitative synthesis suggests that fear of relapse is a complex phenomenon with behavioural and emotional components which has both direct and indirect effects on wellbeing. Conclusions: Evidence in this area is limited and research with explicit service user and carer involvement is urgently needed to develop new and/or refine existing measurement tools, and to measure wellbeing rather than psychopathology. Nonetheless, clinicians should be aware that fear of relapse exists and appears to be positively associated with depression and suicide ideation, and negatively associated with self-esteem. Fear of relapse can include fears of losing personal autonomy and/or social/occupational functioning. It appears to impact carers as well as those diagnosed with schizophrenia

Origin and Actions of Neuropeptide Y in the Cardiovascular System

The cardiovascular system is richly innervated by sympathetic nerves containing norepinephrine (NE) and neuropeptide Y (NPY). Although NE is considered a major sympathetic neurotransmitter and a primary mediator of cardiovascular functions, the role of NPY is not yet well defined. Over the last several years, evidence has accumulated to indicate that NPY is a sympathetic cotransmitter mediating vasoconstriction independently of catecholamines, as well as being a modulator of autonomic cardiovascular responses (reviews: 1–4). NPY is also abundant in epinephrine-containing chromaffin cells of the adrenal medulla (5) and, under some conditions, may be secreted into the circulation as an adreno-medullary hormone (6). Finally, our (7) and other (8) recent data indicate the extraneuronal presence of NPY, e.g., in platelets, where it may subserve autocrine and paracrine functions in platelet—vascular interactions. Thus, there are at least three potential sources for circulating NPY: the sympathetic nerves, the adrenal medulla, and platelets. The first purpose of this chapter is to discuss the release of NPY from different sources into the cardiovascular system in humans and in other mammalian species, in physiological situations, such as stress, and in disease states, such as hypertension

Seven-year evaluation of idiopathic multiple retinal pigment epithelium detachments

Objective: To analyze a 7-year natural history of idiopathic multiple retinal pigment epithelium (RPE) detachment based on optical coherence tomography (OCT) images. Methods: Case report. SD-OCT imaging (Topcon 3D OCT-1000).Results: A 55-year-old female presented with three foci of pigment epithelium detachment (PED) in her left eye. Her past ophthalmic and medical history was uneventful. The patient’s visual acuity in both eyes was 1.0 throughout the follow-up period. Fluorescein angiography images are shown. Corresponding OCT scans illustrate natural history of the PED foci and retinal structure of the left eye. PED number, location, shape, size and morphology were analyzed. Initially, the dimensions of PEDs were stable, but then a tendency to fluctuate or flatten was observed. Eventually, the lesions have resolved completely. Apart from the detachments, no other structural abnormalities of the retina were found. No PEDs, but sub-, para- and perifoveal RPE protrusions and defects were detected in the right eye.Conclusions: In the hereby presented case:1. OCT proved to be suitable for diagnosis and monitoring of multiple PEDs. 2. Multiple idiopathic PEDs without involvement of the fovea were asymptomatic and regressed spontaneously. As such, they did not require any treatment. However, they were monitored due to potential risk for choroidal neovascularization or serous retinal detachment

Stress hormone epinephrine enhances adipogenesis in murine embryonic stem cells by up-regulating the neuropeptide Y system.

Prenatal stress, psychologically and metabolically, increases the risk of obesity and diabetes in the progeny. However, the mechanisms of the pathogenesis remain unknown. In adult mice, stress activates NPY and its Y2R in a glucocorticoid-dependent manner in the abdominal fat. This increased adipogenesis and angiogenesis, leading to abdominal obesity and metabolic syndrome which were inhibited by intra-fat Y2R inactivation. To determine whether stress elevates NPY system and accelerates adipogenic potential of embryo, here we "stressed" murine embryonic stem cells (mESCs) in vitro with epinephrine (EPI) during their adipogenic differentiation. EPI was added during the commitment stage together with insulin, and followed by dexamethasone in the standard adipogenic differentiation medium. Undifferentiated embryonic bodies (EBs) showed no detectable expression of NPY. EPI markedly up-regulated the expression NPY and the Y1R at the commitment stage, followed by increased Y2R mRNA at the late of the commitment stage and the differentiation stage. EPI significantly increased EB cells proliferation and expression of the preadipocyte marker Pref-1 at the commitment stage. EPI also accelerated and amplified adipogenic differentiation detected by increasing the adipocyte markers FABP4 and PPARγ mRNAs and Oil-red O-staining at the end of the differentiation stage. EPI-induced adipogenesis was completely prevented by antagonists of the NPY receptors (Y1R+Y2R+Y5R), indicating that it was mediated by the NPY system in mESC's. Taken together, these data suggest that stress may play an important role in programming ESCs for accelerated adipogenesis by altering the stress induced hormonal regulation of the NPY system

Mitogenic effect of neuropeptide Y in rat vascular smooth muscle cells

Neuropeptide Y (NPY) is a vasoconstrictor released with norepinephrine from perivascular sympathetic nerves. Since sympathetic nerves appear to play a role in vascular smooth muscle cell (SMC) hypertrophy, we studied the effects of NPY on proliferation of cultured rat aorta- and vena cava-derived SMC. Both cell types displayed high-affinity NPY binding sites with displacement characteristics of [Pro 34]NPY > NPY(13–36) > NPY(18–36) in aorta and [Pro 34]NPY = NPY(13–36) = NPY(18–36) in the vena cava. Incubation with NPY (50–1000 n M) for 48 h increased by up to twofold cell number and [ 3H]-thymidine incorporation in both cell types (aortic more sensitive to NPY than venous). Following incubation with NPY, the disappearance of NPY immunoreactivity (-IR) from media was markedly delayed in the presence of SMC, and cell content of NPY-IR increased in a dose-dependent manner, indicating that SMC either diminish degradation of the peptide (possibly by internalization) or secrete endogenous NPY (or both). Structure-activity relationship studies with NPY(18–36) indicated involvement of Y1 receptors in mitogenesis. Thus, NPY has a mitogenic effect (probably mediated by Y1 receptors) and, therefore, may be a sympathetic trophic factor involved in vascular hypertrophy